Cardiology

24 December 2020

12:23

Pulmonary embolism: investigation

We know from experience that few patients (around 10%) present with the textbook triad of pleuritic chest pain, dyspnoea and haemoptysis. Pulmonary embolism can be difficult to diagnose as it can present with virtually any cardiorespiratory symptom/sign depending on its location and size.

So which features make pulmonary embolism more likely?

The PIOPED study1 in 2007 looked at the frequency of different symptoms and signs in patients who were diagnosed with pulmonary embolism.

The relative frequency of common clinical signs is shown below:

· Tachypnea (respiratory rate >20/min) - 96%

· Crackles - 58%

· Tachycardia (heart rate >100/min) - 44%

· Fever (temperature >37.8°C) - 43%

It is interesting to note that the Well's criteria for diagnosing a PE use tachycardia rather than tachypnoea.

All patients with symptoms or signs suggestive of a PE should have a history taken, examination performed and a chest x-ray to exclude other pathology.

Pulmonary embolism rule-out criteria (PERC)

NICE updated their guidelines on the investigation and management of venous thromboembolism (VTE) in 2020. One of the key changes was the use of the pulmonary embolism rule-out criteria (the PERC rule)

· a copy of criteria can be found in the image below

· all the criteria must be absent to have negative PERC result, i.e. rule-out PE

· this should be done when you think there is a low pre-test probability of PE, but want more reassurance that it isn't the diagnosis

o this low probability is defined as < 15%, although it is clearly difficult to quantify such judgements

· a negative PERC reduces the probability of PE to < 2%

· if your suspicion of PE is greater than this then you should move straight to the 2-level PE Wells score, without doing a PERC

2-level PE Wells score

If a PE is suspected a 2-level PE Wells score should be performed:

Clinical feature	Points
Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins)	3
An alternative diagnosis is less likely than PE	3
Heart rate > 100 beats per minute	1.5
Immobilisation for more than 3 days or surgery in the previous 4 weeks	1.5
Previous DVT/PE	1.5
Haemoptysis	1
Malignancy (on treatment, treated in the last 6 months, or palliative)	1

Clinical probability simplified scores

· PE likely - more than 4 points

· PE unlikely - 4 points or less

If a PE is 'likely' (more than 4 points)

· arrange an immediate computed tomography pulmonary angiogram (CTPA)

· If there is a delay in getting the CTPA then interim therapeutic anticoagulation should be given until the scan is performed.

o interim therapeutic anticoagulation used to mean giving low-molecular-weight heparin

o NICE updated their guidance in 2020. They now recommend using an anticoagulant that can be continued if the result is positive.

o this means normally a direct oral anticoagulant (DOAC) such as apixaban or rivaroxaban

- if the CTPA is positive then a PE is diagnosed

· if the CTPA is negative then consider a proximal leg vein ultrasound scan if DVT is suspected

If a PE is 'unlikely' (4 points or less)

· arranged a D-dimer test

o if positive arrange an immediate computed tomography pulmonary angiogram (CTPA). If there is a delay in getting the CTPA then give interim therapeutic anticoagulation until the scan is performed

o if negative then PE is unlikely - stop anticoagulation and consider an alternative diagnosis

CTPA or V/Q scan?

The consensus view from the British Thoracic Society and NICE guidelines is as follows:

· CTPA is now the recommended initial lung-imaging modality for non-massive PE. Advantages compared to V/Q scans include speed, easier to perform out-of-hours, a reduced need for further imaging and the possibility of providing an alternative diagnosis if PE is excluded

· if the CTPA is negative then patients do not need further investigations or treatment for PE

· V/Q scanning may be used initially if appropriate facilities exist, the chest x-ray is normal, and there is no significant symptomatic concurrent cardiopulmonary disease. V/Q scanning is also the investigation of choice if there is renal impairment (doesn't require the use of contrast unlike CTPA)

Some other points

D-dimers

· sensitivity = 95-98%, but poor specificity

· age-adjusted D-dimer levels should be considered for patients > 50 years

ECG

· the classic ECG changes seen in PE are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III - 'S1Q3T3'. However, this change is seen in no more than 20% of patients

· right bundle branch block and right axis deviation are also associated with PE

· sinus tachycardia may also be seen

Chest x-ray

· a chest x-ray is recommended for all patients to exclude other pathology

· however, it is typically normal in PE

· possible findings include a wedge-shaped opacification

V/Q scan

· sensitivity of around 75% and specificity of 97%

· other causes of mismatch in V/Q include old pulmonary embolisms, AV malformations, vasculitis, previous radiotherapy

· COPD gives matched defects

CTPA

· peripheral emboli affecting subsegmental arteries may be missed

1. Clinical Characteristics of Patients with Acute Pulmonary Embolism(Data from PIOPED II) Am J Med. Oct 2007; 120(10): 871879.

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:23

Angina pectoris: drug management

The management of stable angina comprises lifestyle changes, medication, percutaneous coronary intervention and surgery. NICE produced guidelines in 2011 covering the management of stable angina

Medication

· all patients should receive aspirin and a statin in the absence of any contraindication

· sublingual glyceryl trinitrate to abort angina attacks

· NICE recommend using either a beta-blocker or a calcium channel blocker first-line based on 'comorbidities, contraindications and the person's preference'

· if a calcium channel blocker is used as monotherapy a rate-limiting one such as verapamil or diltiazem should be used. If used in combination with a beta-blocker then use a long-acting dihydropyridine calcium-channel blocker (e.g. modified-release nifedipine). Remember that beta-blockers should not be prescribed concurrently with verapamil (risk of complete heart block)

· if there is a poor response to initial treatment then medication should be increased to the maximum tolerated dose (e.g. for atenolol 100mg od)

· if a patient is still symptomatic after monotherapy with a beta-blocker add a calcium channel blocker and vice versa

· if a patient is on monotherapy and cannot tolerate the addition of a calcium channel blocker or a beta-blocker then consider one of the following drugs: a long-acting nitrate, ivabradine, nicorandil or ranolazine

· if a patient is taking both a beta-blocker and a calcium-channel blocker then only add a third drug whilst a patient is awaiting assessment for PCI or CABG

Nitrate tolerance

· many patients who take nitrates develop tolerance and experience reduced efficacy

· NICE advises that patients who take standard-release isosorbide mononitrate should use an asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours to minimise the development of nitrate tolerance

· this effect is not seen in patients who take once-daily modified-release isosorbide mononitrate

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:48

Acute pericarditis

Pericarditis is one of the differentials of any patient presenting with chest pain.

Features

· chest pain: may be pleuritic. Is often relieved by sitting forwards

· other symptoms include non-productive cough, dyspnoea and flu-like symptoms

· pericardial rub

· tachypnoea

· tachycardia

Causes

· viral infections (Coxsackie)

· tuberculosis

· uraemia (causes 'fibrinous' pericarditis)

· trauma

· post-myocardial infarction, Dressler's syndrome

· connective tissue disease

· hypothyroidism

· malignancy

Investigations

· ECG changes

o the changes in pericarditis are often global/widespread, as opposed to the 'territories' seen in ischaemic events

o 'saddle-shaped' ST elevation

o PR depression: most specific ECG marker for pericarditis

· all patients with suspected acute pericarditis should have transthoracic echocardiography

Management

· treat the underlying cause

· a combination of NSAIDs and colchicine is now generally used for first-line for patients with acute idiopathic or viral pericarditis

© Image used on license from Dr Smith, University of Minnesota

ECG showing pericarditis. Note the widespread nature of the ST elevation and the PR depression

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:49

Long QT syndrome

Long QT syndrome (LQTS) is an inherited condition associated with delayed repolarization of the ventricles. It is important to recognise as it may lead to ventricular tachycardia/torsade de pointes and can therefore cause collapse/sudden death. The most common variants of LQTS (LQT1 & LQT2) are caused by defects in the alpha subunit of the slow delayed rectifier potassium channel. A normal corrected QT interval is less than 430 ms in males and 450 ms in females.

Causes of a prolonged QT interval:

Congenital	Drugs*	Other
· Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel) · Romano-Ward syndrome (no deafness)	· amiodarone, sotalol, class 1a antiarrhythmic drugs · tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram) · methadone · chloroquine · terfenadine** · erythromycin · haloperidol · ondanestron	· electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia · acute myocardial infarction · myocarditis · hypothermia · subarachnoid haemorrhage

Features

· may be picked up on routine ECG or following family screening

· Long QT1 - usually associated with exertional syncope, often swimming

· Long QT2 - often associated with syncope occurring following emotional stress, exercise or auditory stimuli

· Long QT3 - events often occur at night or at rest

· sudden cardiac death

Management

· avoid drugs which prolong the QT interval and other precipitants if appropriate (e.g. Strenuous exercise)

· beta-blockers***

· implantable cardioverter defibrillators in high risk cases

*the usual mechanism by which drugs prolong the QT interval is blockage of potassium channels. See the link for more details

**a non-sedating antihistamine and classic cause of prolonged QT in a patient, especially if also taking P450 enzyme inhibitor, e.g. Patient with a cold takes terfenadine and erythromycin at the same time

***note sotalol may exacerbate long QT syndrome

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:50

Pulmonary embolism: management

NICE updated their guidelines on the management of venous thromboembolism (VTE) in 2020. Some of the key changes include recommending the following:

· the use of direct oral anticoagulants (DOACs) as first-line treatment for most people with VTE

· the use of DOACs in patients with active cancer, as opposed to low-molecular weight heparin as was the previous recommendation

· outpatient treatment in low-risk pulmonary embolism (PE) patients

· routine cancer screening is no longer recommended following a VTE diagnosis

Outpatient treatment in low-risk PE patients

Deep vein thrombosis has for a long time been treated on an outpatient condition. In contrast, patients with any form of PE were typically admitted. However, in recent years patients with a new diagnosis of PE who are deemed low-risk are now increasingly managed as outpatients. NICE formally supported this approach in their latest guidance.

· NICE recommends using a 'validated risk stratification tool' to determine the suitability of outpatient treatment.

o no guidance is given as to what tool should be used

o the 2018 British Society guidelines support the use of the Pulmonary Embolism Severity Index (PESI) score

· key requirements would clearly be haemodynamic stability, lack of comorbidities and support at home

Anticogulant therapy

The cornerstone of VTE management is anticoagulant therapy. This was historically done with warfarin, often preceded by heparin until the INR was stable. However, the development of DOACs, and an evidence base supporting their efficacy, has changed modern management.

Choice of anticoagulant

· the big change in the 2020 guidelines was the increased use of DOACs

· apixaban or rivaroxaban (both DOACs) should be offered first-line following the diagnosis of a PE

o instead of using low-molecular weight heparin (LMWH) until the diagnosis is confirmed, NICE now advocate using a DOAC once a diagnosis is suspected, with this continued if the diagnosis is confirmed

o if neither apixaban or rivaroxaban are suitable then either LMWH followed by dabigatran or edoxaban OR LMWH followed by a vitamin K antagonist (VKA, i.e. warfarin)

· if the patient has active cancer

o previously LMWH was recommended

o the new guidelines now recommend using a DOAC, unless this is contraindicated

· if renal impairment is severe (e.g. < 15/min) then LMWH, unfractionated heparin or LMWH followed by a VKA

· if the patient has antiphospholipid syndrome (specifically 'triple positive' in the guidance) then LMWH followed by a VKA should be used

Length of anticoagulation

· all patients should have anticoagulation for at least 3 months

· continuing anticoagulation after this period is partly determined by whether the VTE was provoked or unprovoked

o a provoked VTE is due to an obvious precipitating event e.g. immobilisation following major surgery. The implication is that this event was transient and the patient is no longer at increased risk

o an unprovoked VTE occurs in the absence of an obvious precipitating event, i.e. there is a possibility that there are unknown factors (e.g. mild thrombophilia) making the patient more at risk from further clots

· if the VTE was provoked the treatment is typically stopped after the initial 3 months (3 to 6 months for people with active cancer)

· if the VTE was unprovoked then treatment is typically continued for up to 3 further months (i.e. 6 months in total)

o NICE recommend that whether a patient has a total of 3-6 months anticoagulant is based upon balancing a person's risk of VTE recurrence and their risk of bleeding

o the HAS-BLED score can be used to help assess the risk of bleeding

o NICE state: 'Explain to people with unprovoked DVT or PE and a low bleeding risk that the benefits of continuing anticoagulation treatment are likely to outweigh the risks. '. The implication of this is that in the absence of a bleeding risk factors, patients are generally better off continuing anticoagulation for a total of 6 months

PE with haemodynamic instability

Thrombolysis

· thrombolysis is now recommended as the first-line treatment for massive PE where there is circulatory failure (e.g. hypotension)

· other invasive approaches should be considered where appropriate facilities exist

Patients who have repeat pulmonary embolisms, despite adequate anticoagulation, may be considered for inferior vena cava (IVC) filters. These work by stopping clots formed in the deep veins of the leg from moving to the pulmonary arteries. IVC filter use is currently supported by NICE but other studies suggest a weak evidence base - please see the link for more details.

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:50

Aortic stenosis

Clinical features of symptomatic disease

· chest pain

· dyspnoea

· syncope

· murmur

o an ejection systolic murmur (ESM) is classically seen in aortic stenosis

o classically radiates to the carotids

o this is decreased following the Valsalva manoeuvre

Features of severe aortic stenosis

· narrow pulse pressure

· slow rising pulse

· delayed ESM

· soft/absent S2

· S4

· thrill

· duration of murmur

· left ventricular hypertrophy or failure

Causes of aortic stenosis

· degenerative calcification (most common cause in older patients > 65 years)

· bicuspid aortic valve (most common cause in younger patients < 65 years)

· William's syndrome (supravalvular aortic stenosis)

· post-rheumatic disease

· subvalvular: HOCM

Management

· if asymptomatic then observe the patient is general rule

· if symptomatic then valve replacement

· if asymptomatic but valvular gradient > 40 mmHg and with features such as left ventricular systolic dysfunction then consider surgery

· cardiovascular disease may coexist. For this reason an angiogram is often done prior to surgery so that the procedures can be combined

· balloon valvuloplasty is limited to patients with critical aortic stenosis who are not fit for valve replacement

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:50

ECG: myocardial ischaemia

One of the main uses of the ECG is to determine whether a patient is having a cardiac event in the context of chest pain. A wide variety of changes can be seen depending on what type of ischaemic event is happening, where it is happening and when it happened.

Acute myocardial infarction (MI)

· hyperacute T waves are often the first sign of MI but often only persists for a few minutes

· ST elevation may then develop

· the T waves typically become inverted within the first 24 hours. The inversion of the T waves can last for days to months

· pathological Q waves develop after several hours to days. This change usually persists indefinitely

Definition of ST elevation myocardial infarction (STEMI)

· clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of:

o 2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years

o 1.5 mm ST elevation in V2-3 in women

o 1 mm ST elevation in other leads

o new LBBB (LBBB should be considered new unless there is evidence otherwise)

A posterior MI causes ST depression not elevation on a 12-lead ECG.

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:51

Warfarin

Warfarin is an oral anticoagulant which inhibits epoxide reductase preventing the reduction of vitamin K to its active hydroquinone form, which in turn acts as a cofactor in the carboxylation of clotting factor II, VII, IX and X (mnemonic = 1972) and protein C.

Indications

· venous thromboembolism: target INR = 2.5, if recurrent 3.5

· atrial fibrillation, target INR = 2.5

· mechanical heart valves, target INR depends on the valve type and location. Mitral valves generally require a higher INR than aortic valves.

Patients on warfarin are monitored using the INR (international normalised ration), the ratio of the prothrombin time for the patient over the normal prothrombin time. Warfarin has a long half-life and achieving a stable INR may take several days. There a variety of loading regimes and computer software is now often used to alter the dose.

Factors that may potentiate warfarin

· liver disease

· P450 enzyme inhibitors, e.g.: amiodarone, ciprofloxacin

· cranberry juice

· drugs which displace warfarin from plasma albumin, e.g. NSAIDs

· inhibit platelet function: NSAIDs

Side-effects

· haemorrhage

· teratogenic, although can be used in breastfeeding mothers

· skin necrosis: when warfarin is first started biosynthesis of protein C is reduced. This results in a temporary procoagulant state after initially starting warfarin, normally avoided by concurrent heparin administration. Thrombosis may occur in venules leading to skin necrosis

· purple toes

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:51

Hypercalcaemia: features

Features

· 'bones, stones, groans and psychic moans'

· corneal calcification

· shortened QT interval on ECG

· hypertension

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:51

Thiazide diuretics

Thiazide diuretics work by inhibiting sodium reabsorption at the beginning of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+-Cl− symporter. Potassium is lost as a result of more sodium reaching the collecting ducts. Thiazide diuretics have a role in the treatment of mild heart failure although loop diuretics are better for reducing overload. The main use of bendroflumethiazide was in the management of hypertension but recent NICE guidelines now recommend other thiazide-like diuretics such as indapamide and chlortalidone.

Common adverse effects

· dehydration

· postural hypotension

· hyponatraemia, hypokalaemia, hypercalcaemia*

· gout

· impaired glucose tolerance

· impotence

Rare adverse effects

· thrombocytopaenia

· agranulocytosis

· photosensitivity rash

· pancreatitis

Flow chart showing the management of hypertension as per current NICE guideliness

*the flip side of this is hypocalciuria, which may be useful in reducing the incidence of renal stones

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:52

Aortic dissection: management

Classification

Stanford classification

· type A - ascending aorta, 2/3 of cases

· type B - descending aorta, distal to left subclavian origin, 1/3 of cases

DeBakey classification

· type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally

· type II - originates in and is confined to the ascending aorta

· type III - originates in descending aorta, rarely extends proximally but will extend distally

Management

Type A

· surgical management, but blood pressure should be controlled to a target systolic of 100-120 mmHg whilst awaiting intervention

Type B*

· conservative management

· bed rest

· reduce blood pressure IV labetalol to prevent progression

Complications

Complications of backward tear

· aortic incompetence/regurgitation

· MI: inferior pattern often seen due to right coronary involvement

Complications of forward tear

· unequal arm pulses and BP

· stroke

· renal failure

© Image used on license from Radiopaedia

An intraluminal tear has formed a 'flap' that can be clearly seen in the ascending aorta. This is a Stanford type A dissection

© Image used on license from Radiopaedia

Stanford type B dissection, seen in the descending aorta

*endovascular repair of type B aortic dissection may have a role in the future

From <https://www.passmedicine.com/review/textbook.php?s=#>

Medical management consists of decreasing heart rate, blood pressure and the shearing forces  of myocardial contractility in order to decrease the propagation of the dissection.

Oral verapamil is not suitable for precise BP control in the acute setting and IV sodium nitroprusside does not slow down the heart rate.

Stanford type A- ascending aorta  dissection

· control BP (IV labetalol) + surgery

Stanford type B - descending aortic  dissection

· control BP (IV labetalol)

From <https://mle.ncl.ac.uk/cases/page/18128/>

24 December 2020

12:52

Atrial fibrillation: post-stroke

NICE issued guidelines on atrial fibrillation (AF) in 2006. They included advice on the management of patients with AF who develop a stroke or transient-ischaemic attack (TIA).

Recommendations include:

· following a stroke or TIA, warfarin or a direct thrombin or factor Xa inhibitor should be given as the anticoagulant of choice. Antiplatelets should only be given if needed for the treatment of other comorbidities

· in acute stroke patients, in the absence of haemorrhage, anticoagulation therapy should be commenced after 2 weeks. If imaging shows a very large cerebral infarction then the initiation of anticoagulation should be delayed

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:52

Chest pain: assessment of patients with suspected cardiac chest pain

NICE updated it's guidelines in 2016 on the 'Assessment and diagnosis of recent onset chest pain or discomfort of suspected cardiac origin'.

Below is a brief summary of the key points. Please see the link for more details.

Patients presenting with acute chest pain

Immediate management of suspected acute coronary syndrome (ACS)

· glyceryl trinitrate

· aspirin 300mg. NICE do not recommend giving other antiplatelet agents (i.e. Clopidogrel) outside of hospital

· do not routinely give oxygen, only give if sats < 94%*

· perform an ECG as soon as possible but do not delay transfer to hospital. A normal ECG does not exclude ACS

Referral

· current chest pain or chest pain in the last 12 hours with an abnormal ECG: emergency admission

· chest pain 12-72 hours ago: refer to hospital the same-day for assessment

· chest pain > 72 hours ago: perform full assessment with ECG and troponin measurement before deciding upon further action

*NICE suggest the following in terms of oxygen therapy:

· do not routinely administer oxygen, but monitor oxygen saturation using pulse oximetry as soon as possible, ideally before hospital admission. Only offer supplemental oxygen to:

· people with oxygen saturation (SpO2) of less than 94% who are not at risk of hypercapnic respiratory failure, aiming for SpO2 of 94-98%

· people with chronic obstructive pulmonary disease who are at risk of hypercapnic respiratory failure, to achieve a target SpO2 of 88-92% until blood gas analysis is available.

Patients presenting with stable chest pain

NICE define anginal pain as the following:

· 1. constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms

· 2. precipitated by physical exertion

· 3. relieved by rest or GTN in about 5 minutes

· patients with all 3 features have typical angina

· patients with 2 of the above features have atypical angina

· patients with 1 or none of the above features have non-anginal chest pain

For patients in whom stable angina cannot be excluded by clinical assessment alone NICE recommend the following (e.g. symptoms consistent with typical/atypical angina OR ECG changes):

· 1st line: CT coronary angiography

· 2nd line: non-invasive functional imaging (looking for reversible myocardial ischaemia)

· 3rd line: invasive coronary angiography

Examples of non-invasive functional imaging:

· myocardial perfusion scintigraphy with single photon emission computed tomography (MPS with SPECT) or

· stress echocardiography or

· first-pass contrast-enhanced magnetic resonance (MR) perfusion or

· MR imaging for stress-induced wall motion abnormalities

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:52

Peri-arrest rhythms: bradycardia

The 2015 Resuscitation Council (UK) guidelines emphasise that the management of bradycardia depends on:

· 1. identifying the presence of signs indicating haemodynamic compromise - 'adverse signs'

· 2. identifying the potential risk of asystole

Adverse signs

The following factors indicate haemodynamic compromise and hence the need for treatment:

· shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness

· syncope

· myocardial ischaemia

· heart failure

Atropine (500mcg IV) is the first line treatment in this situation.

If there is an unsatisfactory response the following interventions may be used:

· atropine, up to maximum of 3mg

· transcutaneous pacing

· isoprenaline/adrenaline infusion titrated to response

Specialist help should be sought for consideration of transvenous pacing if there is no response to the above measures.

Potential risk of asystole

The following are risk factors for asystole. Even if there is a satisfactory response to atropine specialist help is indicated to consider the need for transvenous pacing:

· complete heart block with broad complex QRS

· recent asystole

· Mobitz type II AV block

· ventricular pause > 3 seconds

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:52

Thrombolysis

Thrombolytic drugs activate plasminogen to form plasmin. This in turn degrades fibrin and help breaks up thrombi. They in primarily used in patients who present with a ST elevation myocardial infarction. Other indications include acute ischaemic stroke and pulmonary embolism, although strict inclusion criteria apply.

Examples

· alteplase

· tenecteplase

· streptokinase

Contraindications to thrombolysis

· active internal bleeding

· recent haemorrhage, trauma or surgery (including dental extraction)

· coagulation and bleeding disorders

· intracranial neoplasm

· stroke < 3 months

· aortic dissection

· recent head injury

· severe hypertension

Side-effects

· haemorrhage

· hypotension - more common with streptokinase

· allergic reactions may occur with streptokinase

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:53

Torsades de pointes

Torsades de pointes ('twisting of the points') is a form of polymorphic ventricular tachycardia associated with a long QT interval. It may deteriorate into ventricular fibrillation and hence lead to sudden death.

Causes of long QT interval

· congenital: Jervell-Lange-Nielsen syndrome, Romano-Ward syndrome

· antiarrhythmics: amiodarone, sotalol, class 1a antiarrhythmic drugs

· tricyclic antidepressants

· antipsychotics

· chloroquine

· terfenadine

· erythromycin

· electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia

· myocarditis

· hypothermia

· subarachnoid haemorrhage

Management

· IV magnesium sulphate

© Image used on license from Dr Smith, University of Minnesota

ECG showing torsades de pointes

From <https://www.passmedicine.com/review/textbook.php?s=#>

Pacing is contraindicated in patients with torsades de pointes ventricular tachycardia secondary to reversible causes.

From <https://mle.ncl.ac.uk/cases/page/18128/>

24 December 2020

12:53

Atrial fibrillation: a very basic introduction

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia. It is very common, being present in around 5% of patients over aged 70-75 years and 10% of patients aged 80-85 years. Whilst uncontrolled atrial fibrillation can result in symptomatic palpitations and inefficient cardiac function probably the most important aspect of managing patients with AF is reducing the increased risk of stroke which is present in these patients.

Types of atrial fibrillation

AF may by classified as either first detected episode, paroxysmal, persistent or permanent.

· first detected episode (irrespective of whether it is symptomatic or self-terminating)

· recurrent episodes, when a patient has 2 or more episodes of AF. If episodes of AF terminate spontaneously then the term paroxysmal AF is used. Such episodes last less than 7 days (typically < 24 hours). If the arrhythmia is not self-terminating then the term persistent AF is used. Such episodes usually last greater than 7 days

· in permanent AF there is continuous atrial fibrillation which cannot be cardioverted or if attempts to do so are deemed inappropriate. Treatment goals are therefore rate control and anticoagulation if appropriate

Symptoms and signs

Symptoms

· palpitations

· dyspnoea

· chest pain

Signs

· an irregularly irregular pulse

Investigations

An ECG is essential to make the diagnosis as other conditions can give an irregular pulse, such as ventricular ectopics or sinus arrhythmia.

Management

There are two key parts of managing patients with AF:

· 1. Rate/rhythm control

· 2. Reducing stroke risk

Rate vs. rhythm control

There are two main strategies employed in dealing with the arrhythmia element of atrial fibrillation:

· rate control: accept that the pulse will be irregular, but slow the rate down to avoid negative effects on cardiac function

· rhythm control: try to get the patient back into, and maintain, normal sinus rhythm. This is termed cardioversion. Drugs (pharmacological cardioversion) and synchronised DC electrical shocks (electrical cardioversion) may be used for this purpose

For many years the predominant approach was to try and maintain a patient in sinus rhythm. This approach changed in the early 2000's and now the majority of patients are managed with a rate control strategy. NICE advocate using a rate control strategy except in a number of specific situations such as coexistent heart failure, first onset AF or where there is an obvious reversible cause.

Rate control

A beta-blocker or a rate-limiting calcium channel blocker (e.g. diltiazem) is used first-line to control the rate in AF.

If one drug does not control the rate adequately NICE recommend combination therapy with any 2 of the following:

· a betablocker

· diltiazem

· digoxin

Rhythm control

As mentioned above there are a subgroup of patients for whom a rhythm control strategy should be tried first. Other patients may have had a rate control strategy initially but switch to rhythm control if symptoms/heart rate fails to settle.

When considering cardioversion it is very important to remember that the moment a patient switches from AF to sinus rhythm presents the highest risk for embolism leading to stroke. Imagine the thrombus formed in the fibrillating atrium suddenly being pushed out when sinus rhythm is restored. For this reason patients must either have had a short duration of symptoms (less than 48 hours) or be anticoagulated for a period of time prior to attempting cardioversion.

Reducing stroke risk

Some patients with AF are at a very low risk of stroke whilst others are at a very significant risk. Clinicians use risk stratifying tools such as the CHA2DS2-VASc score to determine the most appropriate anticoagulation strategy.

	Risk factor	Points
C	Congestive heart failure	1
H	Hypertension (or treated hypertension)	1
A2	Age >= 75 years	2
	Age 65-74 years	1
D	Diabetes	1
S2	Prior Stroke or TIA	2
V	Vascular disease (including ischaemic heart disease and peripheral arterial disease)	1
S	Sex (female)	1

The table below shows a suggested anticoagulation strategy based on the score:

Score	Anticoagulation
0	No treatment
1	Males: Consider anticoagulation Females: No treatment (this is because their score of 1 is only reached due to their gender)
2 or more	Offer anticoagulation

NICE recommend that we offer patients a choice of anticoagulation, including warfarin and the novel oral anticoagulants (NOACs).

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:53

ECG: hypokalaemia

ECG features of hypokalaemia

· U waves

· small or absent T waves (occasionally inversion)

· prolong PR interval

· ST depression

· long QT

The ECG below shows typical U waves. Note also the borderline PR interval.

© Image used on license from Dr Smith, University of Minnesota

One registered user suggests the following rhyme

· In Hypokalaemia, U have no Pot and no T, but a long PR and a long QT

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:53

ECG: normal variants

The following ECG changes are considered normal variants in an athlete:

· sinus bradycardia

· junctional rhythm

· first degree heart block

· Wenckebach phenomenon

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:53

Loop diuretics

Furosemide and bumetanide are loop diuretics that act by inhibiting the Na-K-Cl cotransporter (NKCC) in the thick ascending limb of the loop of Henle, reducing the absorption of NaCl. There are two variants of NKCC; loop diuretics act on NKCC2, which is more prevalent in the kidneys.

Indications

· heart failure: both acute (usually intravenously) and chronic (usually orally)

· resistant hypertension, particularly in patients with renal impairment

Adverse effects

· hypotension

· hyponatraemia

· hypokalaemia, hypomagnesaemia

· hypochloraemic alkalosis

· ototoxicity

· hypocalcaemia

· renal impairment (from dehydration + direct toxic effect)

· hyperglycaemia (less common than with thiazides)

· gout

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:54

Myocardial infarction: secondary prevention

NICE produced guidelines on the management of patients following a myocardial infarction (MI) in 2013. Some key points are listed below

All patients should be offered the following drugs:

· dual antiplatelet therapy (aspirin plus a second antiplatelet agent)

· ACE inhibitor

· beta-blocker

· statin

Some selected lifestyle points:

· diet: advise a Mediterranean style diet, switch butter and cheese for plant oil based products. Do not recommend omega-3 supplements or eating oily fish

· exercise: advise 20-30 mins a day until patients are 'slightly breathless'

· sexual activity may resume 4 weeks after an uncomplicated MI. Reassure patients that sex does not increase their likelihood of a further MI. PDE5 inhibitors (e.g, sildenafil) may be used 6 months after a MI. They should however be avoided in patient prescribed either nitrates or nicorandil

Most patients who've had an acute coronary syndrome are now given dual antiplatelet therapy (DAPT). Clopidogrel was previously the second antiplatelet of choice. Now ticagrelor and prasugrel (also ADP-receptor inhibitors) are more widely used. The NICE Clinical Knowledge Summaries now recommend:

· post acute coronary syndrome (medically managed): add ticagrelor to aspirin, stop ticagrelor after 12 months

· post percutaneous coronary intervention: add prasugrel or ticagrelor to aspirin, stop the second antiplatelet after 12 months

· this 12 month period may be altered for people at a high-risk of bleeding or those who at high-risk of further ischaemic events

Aldosterone antagonists

· patients who have had an acute MI and who have symptoms and/or signs of heart failure and left ventricular systolic dysfunction, treatment with an aldosterone antagonist licensed for post-MI treatment (e.g. eplerenone) should be initiated within 3-14 days of the MI, preferably after ACE inhibitor therapy

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:54

Scoring systems

There are now numerous scoring systems used in medicine. The table below lists some of the more common ones:

Scoring system	Notes
CHA2DS2-VASc	Used to determine the need to anticoagulate a patient in atrial fibrillation
ABCD2	Prognostic score for risk stratifying patients who've had a suspected TIA
NYHA	Heart failure severity scale
DAS28	Measure of disease activity in rheumatoid arthritis
Child-Pugh classification	A scoring system used to assess the severity of liver cirrhosis
Wells score	Helps estimate the risk of a patient having a deep vein thrombosis
MMSE	Mini-mental state examination - used to assess cognitive impairment
HAD	Hospital Anxiety and Depression (HAD) scale - assesses severity of anxiety and depression symptoms
PHQ-9	Patient Health Questionnaire - assesses severity of depression symptoms
GAD-7	Used as a screening tool and severity measure for generalised anxiety disorder
Edinburgh Postnatal Depression Score	Used to screen for postnatal depression
SCOFF	Questionnaire used to detect eating disorders and aid treatment
AUDIT	Alcohol screening tool
CAGE	Alcohol screening tool
FAST*	Alcohol screening tool
CURB-65	Used to assess the prognosis of a patient with pneumonia
Epworth Sleepiness Scale	Used in the assessment of suspected obstructive sleep apnoea
IPSS	International prostate symptom score
Gleason score	Indicates prognosis in prostate cancer
APGAR	Assesses the health of a newborn immediately after birth
Bishop score	Used to help assess the whether induction of labour will be required
Waterlow score	Assesses the risk of a patient developing a pressure sore
FRAX	Risk assessment tool developed by WHO which calculates a patients 10-year risk of developing an osteoporosis related fracture
Ranson criteria	Acute pancreatitis
MUST	Malnutrition

*FAST is also mnemonic to help patients/relatives identify the symptoms of a stroke

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:55

Warfarin: interactions

Interactions of warfarin are important both clinically and in terms of exams.

General factors that may potentiate warfarin

· liver disease

· P450 enzyme inhibitors (see below)

· cranberry juice

· drugs which displace warfarin from plasma albumin, e.g. NSAIDs

· inhibit platelet function: NSAIDs

Drugs which either inhibit or induce the P450 system may affect the metabolism of warfarin and hence the INR:

Inducers of the P450 system include - INR will decrease	Inhibitors of the P450 system include - INR will increase
· antiepileptics: phenytoin, carbamazepine · barbiturates: phenobarbitone · rifampicin · St John's Wort · chronic alcohol intake · griseofulvin · smoking (affects CYP1A2, reason why smokers require more aminophylline)	· antibiotics: ciprofloxacin, clarithromycine/erythromycin · isoniazid · cimetidine,omeprazole · amiodarone · allopurinol · imidazoles: ketoconazole, fluconazole · SSRIs: fluoxetine, sertraline · ritonavir · sodium valproate · acute alcohol intake · quinupristin

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:55

Adenosine

Adenosine is most commonly used to terminate supraventricular tachycardias. The effects of adenosine are enhanced by dipyridamole (antiplatelet agent) and blocked by theophyllines. It should be avoided in asthmatics due to possible bronchospasm.

Mechanism of action

· causes transient heart block in the AV node

· agonist of the A1 receptor in the atrioventricular node, which inhibits adenylyl cyclase thus reducing cAMP and causing hyperpolarization by increasing outward potassium flux

· adenosine has a very short half-life of about 8-10 seconds

Adenosine should ideally be infused via a large-calibre cannula due to it's short half-life,

Adverse effects

· chest pain

· bronchospasm

· transient flushing

· can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:55

Amiodarone

Amiodarone is a class III antiarrhythmic agent used in the treatment of atrial, nodal and ventricular tachycardias. The main mechanism of action is by blocking potassium channels which inhibits repolarisation and hence prolongs the action potential. Amiodarone also has other actions such as blocking sodium channels (a class I effect)

The use of amiodarone is limited by a number of factors

· very long half-life (20-100 days). For this reason, loading doses are frequently used

· should ideally be given into central veins (causes thrombophlebitis)

· has proarrhythmic effects due to lengthening of the QT interval

· interacts with drugs commonly used concurrently (p450 inhibitor) e.g. Decreases metabolism of warfarin

· numerous long-term adverse effects (see below)

Monitoring of patients taking amiodarone

· TFT, LFT, U&E, CXR prior to treatment

· TFT, LFT every 6 months

Adverse effects of amiodarone use

· thyroid dysfunction: both hypothyroidism and hyper-thyroidism

· corneal deposits

· pulmonary fibrosis/pneumonitis

· liver fibrosis/hepatitis

· peripheral neuropathy, myopathy

· photosensitivity

· 'slate-grey' appearance

· thrombophlebitis and injection site reactions

· bradycardia

· lengths QT interval

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:55

Aortic regurgitation

Features

· early diastolic murmur: intensity of the murmur is increased by the handgrip manoeuvre

· collapsing pulse

· wide pulse pressure

· Quincke's sign (nailbed pulsation)

· De Musset's sign (head bobbing)

· mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams

Causes (due to valve disease)

· rheumatic fever

· infective endocarditis

· connective tissue diseases e.g. RA/SLE

· bicuspid aortic valve

Causes (due to aortic root disease)

· aortic dissection

· spondylarthropathies (e.g. ankylosing spondylitis)

· hypertension

· syphilis

· Marfan's, Ehler-Danlos syndrome

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:55

Chest pain

The table below gives characteristic exam question features for conditions causing chest pain

Condition	Characteristic exam feature
Myocardial infarction	Cardiac-sounding pain · heavy, central chest pain they may radiate to the neck and left arm · nausea, sweating · elderly patients and diabetics may experience no pain Risk factors for cardiovascular disease
Pneumothorax	History of asthma, Marfan's etc Sudden dyspnoea and pleuritic chest pain
Pulmonary embolism	Sudden dyspnoea and pleuritic chest pain Calf pain/swelling Current combined pill user, malignancy
Pericarditis	Sharp pain relieved by sitting forwards May be pleuritic in nature
Dissecting aortic aneurysm	'Tearing' chest pain radiating through to the back Unequal upper limb blood pressure
Gastro-oesophageal reflux disease	Burning retrosternal pain Other possible symptoms include regurgitation and dysphagia
Musculoskeletal chest pain	One of the most common diagnoses made in the Emergency Department. The pain is often worse on movement or palpation. May be precipitated by trauma or coughing
Shingles	Pain often precedes the rash

Further notes:

Aortic dissection

· This occurs when there is a flap or filling defect within the aortic intima. Blood tracks into the medial layer and splits the tissues with the subsequent creation of a false lumen. It most commonly occurs in the ascending aorta or just distal to the left subclavian artery (less common). It is most common in Afro-carribean males aged 50-70 years.

· Patients usually present with a tearing intrascapular pain, which may be similar to the pain of a myocardial infarct.

· The dissection may spread either proximally or distally with subsequent disruption to the arterial branches that are encountered.

· In the Stanford classification system the disease is classified into lesions with a proximal origin (Type A) and those that commence distal to the left subclavian (Type B).

· Diagnosis may be suggested by a chest x-ray showing a widened mediastinum. Confirmation of the diagnosis is usually made by use of CT angiography

· Proximal (Type A) lesions are usually treated surgically, type B lesions are usually managed non operatively.

Pulmonary embolism

· Typically sudden onset of chest pain, haemoptysis, hypoxia and small pleural effusions may be present.

· Most patients will have an underlying deep vein thrombosis

· Diagnosis may be suggested by various ECG findings including S waves in lead I, Q waves in lead III and inverted T waves in lead III. Confirmation of the diagnosis is usually made through use of CT pulmonary angiography.

· Treatment is with anticoagulation, in those patients who develop a cardiac arrest or severe compromise from their PE, consideration may be given to thrombolysis.

Myocardial infarction

· Traditionally described as sudden onset of central, crushing chest pain. It may radiate into the neck and down the left arm. Signs of autonomic dysfunction may be present. The presenting features may be atypical in the elderly and those with diabetes.

· Diagnosis is made through identification of new and usually dynamic ECG changes (and cardiac enzyme changes). Inferior and anterior infarcts may be distinguished by the presence of specific ECG changes (usually II, III and aVF for inferior, leads V1-V5 for anterior).

· Treatment is with oral antiplatelet agents, primary coronary angioplasty and/ or thrombolysis.

Perforated peptic ulcer

· Patients usually develop sudden onset of epigastric abdominal pain, it may be soon followed by generalised abdominal pain.

· There may be features of antecendant abdominal discomfort, the pain of gastric ulcer is typically worse immediately after eating.

· Diagnosis may be made by erect chest x-ray which may show a small amount of free intra-abdominal air (very large amounts of air are more typically associated with colonic perforation).

· Treatment is usually with a laparotomy, small defects may be excised and overlaid with an omental patch, larger defects are best managed with a partial gastrectomy.

Boerhaaves syndrome

· Spontaneous rupture of the oesophagus that occurs as a result of repeated episodes of vomiting.

· The rupture is usually distally sited and on the left side.

· Patients usually give a history of sudden onset of severe chest pain that may complicate severe vomiting.

· Severe sepsis occurs secondary to mediastinitis.

· Diagnosis is CT contrast swallow.

· Treatment is with thoracotomy and lavage, if less than 12 hours after onset then primary repair is usually feasible, surgery delayed beyond 12 hours is best managed by insertion of a T tube to create a controlled fistula between oesophagus and skin.

· Delays beyond 24 hours are associated with a very high mortality rate.

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:55

Complete heart block

Features

· syncope

· heart failure

· regular bradycardia (30-50 bpm)

· wide pulse pressure

· JVP: cannon waves in neck

· variable intensity of S1

Types of heart block

First degree heart block

· PR interval > 0.2 seconds

Second degree heart block

· type 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped beat occurs

· type 2 (Mobitz II): PR interval is constant but the P wave is often not followed by a QRS complex

Third degree (complete) heart block

· there is no association between the P waves and QRS complexes

© Image used on license from Dr Smith, University of Minnesota

ECG showing third degree (complete) heart block

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:55

Constrictive pericarditis

Causes

· any cause of pericarditis

· particularly TB

Features

· dyspnoea

· right heart failure: elevated JVP, ascites, oedema, hepatomegaly

· JVP shows prominent x and y descent

· pericardial knock - loud S3

· Kussmaul's sign is positive

CXR

· pericardial calcification

The key differences between constrictive pericarditis and cardiac tamponade are summarized in the table below:

	Cardiac tamponade	Constrictive pericarditis
JVP	Absent Y descent	X + Y present
Pulsus paradoxus	Present	Absent
Kussmaul's sign*	Rare	Present
Characteristic features		Pericardial calcification on CXR

A commonly used mnemonic to remember the absent Y descent in cardiac tamponade is TAMponade = TAMpaX

*a paradoxical rise in JVP during inspiration

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:58

Dabigatran

Dabigatran is an oral anticoagulant that works by being a direct thrombin inhibitor. It is one of the drugs developed over the past 20 years as an alternative to warfarin, with the advantage that it does not require regular monitoring.

What is dabigatran used for?

Dabigatran is currently used for two main indications.

Firstly it is an option in the prophylaxis of venous thromboembolism following hip or knee replacement surgery.

Secondly, it is also licensed in the UK for prevention of stroke in patients with non-valvular atrial fibrillation who have one or more of the following risk factors present:

· previous stroke, transient ischaemic attack or systemic embolism

· left ventricular ejection fraction below 40%

· symptomatic heart failure of New York Heart Association (NYHA) class 2 or above

· age 75 years or older

· age 65 years or older with one of the following: diabetes mellitus, coronary artery disease or hypertension

What are the known side-effects of dabigatran?

Unsurprisingly haemorrhage is the major adverse effect.

Doses should be reduced in chronic kidney disease and dabigatran should not be prescribed if the creatinine clearance is < 30 ml/min.

Reversing the effects

Idarucizumab can be used for rapid reversal of the anticoagulant effects of dabigatran.

Drug Safety Update 2013

The RE-ALIGN study showed significantly higher bleeding and thrombotic events in patients with recent mechanical heart valve replacement using dabigatran compared with warfarin.

Previously there had been no guidance to support the use of dabigatran in patients with prosthetic heart valves but the advice has now changed to dabigatran being contraindicated in such patients.

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:58

ECG: bi/tri-fascicular block

Bifascicular block

· combination of RBBB with left anterior or posterior hemiblock

· e.g. RBBB with left axis deviation

Trifascicular block

· features of bifascicular block as above + 1st-degree heart block

© Image used on license from Dr Smith, University of Minnesota

ECG showing trifascicular block: RBBB + left anterior hemiblock + 1st-degree heart block

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:59

ECG: hypothermia

The following ECG changes may be seen in hypothermia

· bradycardia

· 'J' wave - small hump at the end of the QRS complex

· first degree heart block

· long QT interval

· atrial and ventricular arrhythmias

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:59

Heart failure: NYHA classification

The New York Heart Association (NYHA) classification is widely used to classify the severity of heart failure:

NYHA Class I

· no symptoms

· no limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations

NYHA Class II

· mild symptoms

· slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea

NYHA Class III

· moderate symptoms

· marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms

NYHA Class IV

· severe symptoms

· unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:59

Pulses

Pulsus paradoxus

· greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration → faint or absent pulse in inspiration

· severe asthma, cardiac tamponade

Slow-rising/plateau

· aortic stenosis

Collapsing

· aortic regurgitation

· patent ductus arteriosus

· hyperkinetic states (anaemia, thyrotoxic, fever, exercise/pregnancy)

Pulsus alternans

· regular alternation of the force of the arterial pulse

· severe LVF

Bisferiens pulse

· 'double pulse' - two systolic peaks

· mixed aortic valve disease

'Jerky' pulse

· hypertrophic obstructive cardiomyopathy*

*HOCM may occasionally be associated with a bisferiens pulse

From <https://www.passmedicine.com/review/textbook.php?s=#>

Bounding	CO2 retention, liver failure, sepsis
Bisferiens	mixed aortic stenosis and regurgitation
Anacrotic	Aortic stenosis
Collapsing	Aortic regurgitation

From <https://mle.ncl.ac.uk/cases/page/18128/>

Jerky- HOCM

24 December 2020

12:59

Rheumatic fever

Rheumatic fever develops following an immunological reaction to recent (2-6 weeks ago) Streptococcus pyogenes infection.

Pathogenesis

· Streptococcus pyogenes infection → activation of the innate immune system leading to antigen presentation to T cells

· B and T cells produce IgG and IgM antibodies and CD4+ T cells are activated

· there is then a cross-reactive immune response (a form of type II hypersensitivity) thought to be mediated by molecular mimicry

· the cell wall of Streptococcus pyogenes includes M protein, a virulence factor that is highly antigenic. It is thought that the antibodies against M protein cross-react with myosin and the smooth muscle of arteries

· this response leads to the clinical features of rheumatic fever

· Aschoff bodies describes the granulomatous nodules found in rheumatic heart fever

Diagnosis is based on evidence of recent streptococcal infection accompanied by:

· 2 major criteria

· 1 major with 2 minor criteria

Evidence of recent streptococcal infection

· raised or rising streptococci antibodies,

· positive throat swab

· positive rapid group A streptococcal antigen test

Major criteria

· erythema marginatum

· Sydenham's chorea: this is often a late feature

· polyarthritis

· carditis and valvulitis (eg, pancarditis)*

· subcutaneous nodules

Minor criteria

· raised ESR or CRP

· pyrexia

· arthralgia (not if arthritis a major criteria)

· prolonged PR interval

© Image used on license from DermNet NZ

Erythema marginatum is seen in around 10% of children with rheumatic fever. It is rare in adults

*The latest iteration of the Jones criteria (published in 2015) state that rheumatic carditis cannot be based on pericarditis or myocarditis alone and that there must be evidence of endocarditis (the clinical correlate of which is valvulitis which manifests as a regurgitant murmur).

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:59

Ventricular tachycardia

Ventricular tachycardia (VT) is broad-complex tachycardia originating from a ventricular ectopic focus. It has the potential to precipitate ventricular fibrillation and hence requires urgent treatment.

There are two main types of VT:

· monomorphic VT: most commonly caused by myocardial infarction

· polymorphic VT: A subtype of polymorphic VT is torsades de pointes which is precipitated by prolongation of the QT interval. The causes of a long QT interval are listed below

Causes of a prolonged QT interval

Congenital	Drugs	Other
· Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel) · Romano-Ward syndrome (no deafness)	· amiodarone, sotalol, class 1a antiarrhythmic drugs · tricyclic antidepressants, fluoxetine · chloroquine · terfenadine · erythromycin	· electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia · acute myocardial infarction · myocarditis · hypothermia · subarachnoid haemorrhage

Management

If the patient has adverse signs (systolic BP < 90 mmHg, chest pain, heart failure) then immediate cardioversion is indicated. In the absence of such signs antiarrhythmics may be used. If these fail, then electrical cardioversion may be needed with synchronised DC shocks

Drug therapy

· amiodarone: ideally administered through a central line

· lidocaine: use with caution in severe left ventricular impairment

· procainamide

Verapamil should NOT be used in VT

If drug therapy fails

· electrophysiological study (EPS)

· implant able cardioverter-defibrillator (ICD) - this is particularly indicated in patients with significantly impaired LV function

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:59

Acute coronary syndrome: a very basic introduction

Acute coronary syndrome (ACS) is an umbrella term covering a number of acute presentations of ischaemic heart disease.

It covers a number of presentations, including

· ST elevation myocardial infarction (STEMI)

· non-ST elevation myocardial infarction (NSTEMI)

· unstable angina

Before we go into more detail into these presentations it's useful to take a step back and consider how such conditions develop.

ACS generally develops in patients who have ischaemic heart disease, either known or previously undetected. Ischaemic heart disease is a term synonymous with coronary heart disease and coronary artery disease. It describes the gradually build up of fatty plaques within the walls of the coronary arteries. This leads to two main problems:

· 1. Gradual narrowing, resulting in less blood and therefore oxygen reaching the myocardium at times of increased demand. This results in angina, i.e. chest pain due to insufficient oxygen reaching the myocardium during exertion

· 2. The risk of sudden plaque rupture. The fatty plaques which have built up in the endothelium may rupture leading to sudden occlusion of the artery. This can result in no blood/oxygen reaching the area of myocardium.

Remember that there are a large number of factors which can increase the chance of a patient developing ischaemic heart disease:

Unmodifiable risk factors	Modifiable risk factors
Increasing age Male gender Family history	Smoking Diabetes mellitus Hypertension Hypercholesterolaemia Obesity

Pathophysiology

Ischaemic heart disease is a complex process which develops over a number of years. A number of changes can be seen:

· initial endothelial dysfunction is triggered by a number of factors such as smoking, hypertension and hyperglycaemia

· this results in a number of changes to the endothelium including pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability

· fatty infiltration of the subendothelial space by low-density lipoprotein (LDL) particles

· monocytes migrate from the blood and differentiate into macrophages. These macrophages then phagocytose oxidized LDL, slowly turning into large 'foam cells'. As these macrophages die the result can further propagate the inflammatory process.

· smooth muscle proliferation and migration from the tunica media into the intima results in formation of a fibrous capsule covering the fatty plaque.

Image sourced from Wikipedia

Diagram showing the progression of atherosclerosis in the coronary arteries with associated complications on the right.

Image sourced from Wikipedia

Slide showing a markedly narrowed coronary artery secondary to atherosclerosis. Stained with Masson's trichrome.

Complications of atherosclerosis

Once a plaque has formed a number of complications can develop:

· the plaque forms a physical blockage in the lumen of the coronary artery. This may cause reduced blood flow and hence oxygen to the myocardium, particularly at times of increased demand, resulting clinically in angina

· the plaque may rupture, potentially causing a complete occlusion of the coronary artery. This may result in a myocardial infarction

© Image used on license from PathoPic

Ruptured coronary artery plaque resulting in thrombosis and associated myocardial infarction.

© Image used on license from PathoPic

Pathological specimen showing infarction of the anteroseptal and lateral wall of the left ventricle. There is a background of biventricular myocardial hypertrophy.

Symptoms and signs

The classic and most common feature of ACS is chest pain.

· typically central/left-sided

· may radiate to the jaw or the left arm

· often described as 'heavy' or constricting, 'like an elephant on my chest'

· it should be noted however in real clinical practice patients present with a wide variety of types of chest pain and patients/doctors may confuse ischaemic pain for other causes such as dyspepsia

· certain patients e.g. diabetics/elderly may not experience any chest pain

Other symptoms in ACS include

· dyspnoea

· sweating

· nausea and vomiting

Patients presenting with ACS often have very few physical signs to ellicit:

· pulse, blood pressure, temperature and oxygen saturations are often normal or only mildly altered e.g. tachycardia

· if complications of the ACS have developed e.g. cardiac failure then clearly there may a number of findings

· the patient may appear pale and clammy

Investigations

The two most important investigations when assessing a patient with chest pain are:

· ECG

· cardiac markers e.g. troponin

ECG showing a ST elevation myocardial infarction (STEMI). Note by how looking at which leads are affected (in this case II, III and aVF) we are able to tell which coronary arteries are blocked (the right coronary artery in this case). A blockage of the left anterior descending (LAD) artery would cause elevation of V1-V4, what is often termed an 'anterior' myocardial infarction.

© Image used on license from Dr Smith, University of Minnesota

ECG showing a non-ST elevation myocardial infarction (NSTEMI). On the ECG there is deep ST depression in I-III, aVF, and V3-V6. aVR also has ST elevation. Deep and widespread ST depression is associated with very high mortality because it signifies severe ischemia usually of LAD or left main stem.

The table below shows a simplified correlation between ECG changes and coronary territories:

	ECG changes	Coronary artery
Anterior	V1-V4	Left anterior descending
Inferior	II, III, aVF	Right coronary
Lateral	I, V5-6	Left circumflex

Diagram showing the correlation between ECG changes and coronary territories in acute coronary syndrome

Management

Once a diagnosis of ACS has been made there are a number of elements to treatment:

· prevent worsening of presentation (i.e. further occlusion of coronary vessel)

· revascularise (i.e. 'unblock') the vessel if occluded (patients presenting with a STEMI)

· treat pain

A commonly taught mnemonic for the treatment of ACS is MONA:

· Morphine

· Oxygen

· Nitrates

· Aspirin

Whilst useful it should be remember that not all patients require oxygen therapy. British Thoracic Society guidelines are now widely adopted and oxygen should only be given if the oxygen saturations are < 94%.

For patients who've had a STEMI (i.e. one of the coronary arteries has become occluded) the priority of management is to reopen, or revascularise, the blocked vessel.

· a second antiplatelet drug should be given in addition to aspirin. Options include clopidogrel, prasugrel and ticagrelor

· for many years the treatment of choice was thrombolysis. This involved the intravenous administration of a thrombolytic or 'clot-busting' drug to breakdown the thrombus blocking the coronary artery

· since the early 2000's thrombolysis has been superseded by percutaneous coronary intervention (PCI). In this procedure the blocked arteries are opened up using a balloon (angioplasty) following which a stent may be deployed to prevent the artery occluding again in the future. This is done via a catheter inserted into either the radial or femoral artery

If a patient presents with an NSTEMI then a risk stratification too (such as GRACE) is used to decide upon further management. If a patient is considered high-risk or is clinically unstable then coronary angiography will be performed during the admission. Lower risk patients may have a coronary angiogram at a later date.

Secondary prevention

Patients who've had an ACS require lifelong drug therapy to help reduce the risk of a further event. Standard therapy comprises the following as a minimum:

· aspirin

· a second antiplatelet if appropriate (e.g. clopidogrel)

· a beta-blocker

· an ACE inhibitor

· a statin

Further images

The following images show the progress of coronary artery atherosclerosis:

© Image used on license from PathoPic

Normal coronary artery with blood in the lumen.

© Image used on license from PathoPic

Slightly stenosed coronary artery

© Image used on license from PathoPic

Moderately stenosed coronary artery, beetween 50-75%

© Image used on license from PathoPic

Severely stenosed coronary artery

© Image used on license from PathoPic

Recanalised old atherothrombotic occlusion of a coronary artery. Numerous small neolumina recanalising the organised occluding thrombus (indicated with arrows)

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

12:59

Acute coronary syndrome: prognostic factors

The 2006 Global Registry of Acute Coronary Events (GRACE) study has been used to derive regression models to predict death in hospital and death after discharge in patients with acute coronary syndrome

Poor prognostic factors

· age

· development (or history) of heart failure

· peripheral vascular disease

· reduced systolic blood pressure

· Killip class*

· initial serum creatinine concentration

· elevated initial cardiac markers

· cardiac arrest on admission

· ST segment deviation

*Killip class - system used to stratify risk post myocardial infarction

Killip class	Features	30 day mortality
I	No clinical signs heart failure	6%
II	Lung crackles, S3	17%
III	Frank pulmonary oedema	38%
IV	Cardiogenic shock	81%

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:00

Atrial fibrillation: pharmacological cardioversion

NICE published guidelines on the management of atrial fibrillation (AF) in 2014. The following is also based on the joint American Heart Association (AHA), American College of Cardiology (ACC) and European Society of Cardiology (ESC) 2016 guidelines

Agents with proven efficacy in the pharmacological cardioversion of atrial fibrillation

· amiodarone

· flecainide (if no structural heart disease)

· others (less commonly used in UK): quinidine, dofetilide, ibutilide, propafenone

Less effective agents

· beta-blockers (including sotalol)

· calcium channel blockers

· digoxin

· disopyramide

· procainamide

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:00

Atrial septal defects

Atrial septal defects (ASDs) are the most likely congenital heart defect to be found in adulthood. They carry a significant mortality, with 50% of patients being dead at 50 years. Two types of ASDs are recognised, ostium secundum and ostium primum. Ostium secundum are the most common

Features

· ejection systolic murmur, fixed splitting of S2

· embolism may pass from venous system to left side of heart causing a stroke

Ostium secundum (70% of ASDs)

· associated with Holt-Oram syndrome (tri-phalangeal thumbs)

· ECG: RBBB with RAD

Ostium primum

· present earlier than ostium secundum defects

· associated with abnormal AV valves

· ECG: RBBB with LAD, prolonged PR interval

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:01

B-type natriuretic peptide

B-type natriuretic peptide (BNP) is a hormone produced mainly by the left ventricular myocardium in response to strain.

Whilst heart failure is the most obvious cause of raised BNP levels any cause of left ventricular dysfunction such as myocardial ischaemia or valvular disease may raise levels. Raised levels may also be seen due to reduced excretion in patients with chronic kidney disease. Factors which reduce BNP levels include treatment with ACE inhibitors, angiotensin-2 receptor blockers and diuretics.

Effects of BNP

· vasodilator

· diuretic and natriuretic

· suppresses both sympathetic tone and the renin-angiotensin-aldosterone system

Clinical uses of BNP

Diagnosing patients with acute dyspnoea

· a low concentration of BNP(< 100pg/ml) makes a diagnosis of heart failure unlikely, but raised levels should prompt further investigation to confirm the diagnosis

· NICE currently recommends BNP as a helpful test to rule out a diagnosis of heart failure

Prognosis in patients with chronic heart failure

· initial evidence suggests BNP is an extremely useful marker of prognosis

Guiding treatment in patients with chronic heart failure

· effective treatment lowers BNP levels

Screening for cardiac dysfunction

· not currently recommended for population screening

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:01

Cardiac enzymes and protein markers

Interpretation of the various cardiac enzymes has now largely been superceded by the introduction of troponin T and I. Questions still however commonly appear in exams.

Key points for the exam

· myoglobin is the first to rise

· CK-MB is useful to look for reinfarction as it returns to normal after 2-3 days (troponin T remains elevated for up to 10 days)

	Begins to rise	Peak value	Returns to normal
Myoglobin	1-2 hours	6-8 hours	1-2 days
CK-MB	2-6 hours	16-20 hours	2-3 days
CK	4-8 hours	16-24 hours	3-4 days
Trop T	4-6 hours	12-24 hours	7-10 days
AST	12-24 hours	36-48 hours	3-4 days
LDH	24-48 hours	72 hours	8-10 days

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:01

Chronic heart failure: diagnosis

NICE issued updated guidelines on diagnosis and management in 2018. Previously the first-line investigation was determined by whether the patient has previously had a myocardial infarction or not this is no longer the case - all patients should have an N-terminal pro-B-type natriuretic peptide (NT‑proBNP) blood test first-line.

Interpreting the test

· if levels are 'high' arrange specialist assessment (including transthoracic echocardiography) within 2 weeks

· if levels are 'raised' arrange specialist assessment (including transthoracic echocardiography) echocardiogram within 6 weeks

Serum natriuretic peptides

B-type natriuretic peptide (BNP) is a hormone produced mainly by the left ventricular myocardium in response to strain. Very high levels are associated with a poor prognosis.

	BNP	NTproBNP
High levels	> 400 pg/ml (116 pmol/litre)	> 2000 pg/ml (236 pmol/litre)
Raised levels	100-400 pg/ml (29-116 pmol/litre)	400-2000 pg/ml (47-236 pmol/litre)
Normal levels	< 100 pg/ml (29 pmol/litre)	< 400 pg/ml (47 pmol/litre)

Factors which alter the BNP level:

Increase BNP levels	Decrease BNP levels
Left ventricular hypertrophy Ischaemia Tachycardia Right ventricular overload Hypoxaemia (including pulmonary embolism) GFR < 60 ml/min Sepsis COPD Diabetes Age > 70 Liver cirrhosis	Obesity Diuretics ACE inhibitors Beta-blockers Angiotensin 2 receptor blockers Aldosterone antagonists

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:01

DVLA: cardiovascular disorders

The guidelines below relate to car/motorcycle use unless specifically stated. For obvious reasons, the rules relating to drivers of heavy goods vehicles tend to be much stricter

Specific rules

· hypertension

o can drive unless treatment causes unacceptable side effects, no need to notify DVLA

o if Group 2 Entitlement the disqualifies from driving if resting BP consistently 180 mmHg systolic or more and/or 100 mm Hg diastolic or more

· angioplasty (elective) - 1 week off driving

· CABG - 4 weeks off driving

· acute coronary syndrome- 4 weeks off driving

o 1 week if successfully treated by angioplasty

· angina - driving must cease if symptoms occur at rest/at the wheel

· pacemaker insertion - 1 week off driving

· implantable cardioverter-defibrillator (ICD)

o if implanted for sustained ventricular arrhythmia: cease driving for 6 months

o if implanted prophylactically then cease driving for 1 month. Having an ICD results in a permanent bar for Group 2 drivers

· successful catheter ablation for an arrhythmia- 2 days off driving

· aortic aneurysm of 6cm or more - notify DVLA. Licensing will be permitted subject to annual review.

o an aortic diameter of 6.5 cm or more disqualifies patients from driving

· heart transplant: do not drive for 6 weeks, no need to notify DVLA

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:09

Eisenmenger's syndrome

Eisenmenger's syndrome describes the reversal of a left-to-right shunt in a congenital heart defect due to pulmonary hypertension. This occurs when an uncorrected left-to-right leads to remodeling of the pulmonary microvasculature, eventually causing obstruction to pulmonary blood and pulmonary hypertension.

Associated with

· ventricular septal defect

· atrial septal defect

· patent ductus arteriosus

Features

· original murmur may disappear

· cyanosis

· clubbing

· right ventricular failure

· haemoptysis, embolism

Management

· heart-lung transplantation is required

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:09

Heart failure: acute management

Management options in acute heart failure include:

· oxygen

· IV loop diuretics

· opiates

· vasodilators

· inotropic agents

· CPAP

· ultrafiltration

· mechanical circulatory assistance: e.g. intra-aortic balloon counterpulsation or ventricular assist devices

Consideration should be given to discontinuing beta-blockers in the short-term.

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:09

Heart sounds

The first heart sound (S1) is caused by closure of the mitral and tricuspid valves whilst the second heart sound (S2) is due to aortic and pulmonary valve closure

S1

· closure of mitral and tricuspid valves

· soft if long PR or mitral regurgitation

· loud in mitral stenosis

S2

· closure of aortic and pulmonary valves

· soft in aortic stenosis

· splitting during inspiration is normal

S3 (third heart sound)

· caused by diastolic filling of the ventricle

· considered normal if < 30 years old (may persist in women up to 50 years old)

· heard in left ventricular failure (e.g. dilated cardiomyopathy), constrictive pericarditis (called a pericardial knock) and mitral regurgitation

S4 (fourth heart sound)

· may be heard in aortic stenosis, HOCM, hypertension

· caused by atrial contraction against a stiff ventricle

o therefore coincides with the P wave on ECG

· in HOCM a double apical impulse may be felt as a result of a palpable S4

Sites of auscultation

Valve	Site
Pulmonary valve	Left second intercostal space, at the upper sternal border
Aortic valve	Right second intercostal space, at the upper sternal border
Mitral valve	Left fifth intercostal space, just medial to mid clavicular line
Tricuspid valve	Left fourth intercostal space, at the lower left sternal border

The diagram below demonstrates where the various cardiac valves are best heard.

Image sourced from Wikipedia

From <https://www.passmedicine.com/review/textbook.php?s=#>

Left ventricular volume overload causes a third heart sound.

Cannon waves occur when the atrium contracts against a closing tricuspid valve.

Cannon waves happen only when P waves fall within QT intervals in ECG. P wave represents atrial systolic  contraction and QT represents ventricular systole. When the atrium contracts against a closed tricuspid  valve during a ventricular contraction, a cannon wave projecting into the neck is seen.

From <https://mle.ncl.ac.uk/cases/page/18128/>

24 December 2020

13:09

Hypothermia

Hypothermia is an unintentional reduction of core body temperature below the normal physiological limits. In initial stages, thermoreceptors in the skin and subcutaneous tissues sense the low temperature and cause a regional vasoconstriction. This causes the hypothalamus to stimulate the release of TSH and ACTH. It also stimulates heat production by promoting shivering.

Definitions:

· Mild hypothermia: 32-35°C

· Moderate or severe hypothermia: < 32°C

Epidemiology:

· The incidence of hypothermia varies globally. In the UK, the estimated annual number of hypothermia-related deaths is 300/year, whereas in Canada, it is 8000/year.

· Hypothermia is most common during the winter, and the elderly are particularly susceptible (see further risk factors below). Many cases of hypothermia also occur indoors, due to poor heating facilities.

Causes can include:

· Exposure to cold in the environment is the major cause

· Inadequate insulation in the operating room

· Cardiopulmonary bypass

· Newborn babies.

Risk factors:

· General anaesthesia

· Substance abuse

· Hypothyroidism

· Impaired mental status

· Homelessness

· Extremes of age

Signs of hypothermia include:

· shivering

· cold and pale skin. Frostbite occurs when the skin and subcutaneous tissue freeze, causing damage to cells.

· slurred speech

· tachypnoea, tachycardia and hypertension (if mild)

· respiratory depression, bradycardia and hypothermia (if moderate)

· confusion/ impaired mental state

Babies with hypothermia can look healthy. However, they may be limp, unusually quiet and refuse to feed. Heat loss in newborns is extremely common, hence a hat and clothing/ blankets will be applied soon after birth.

Investigations:

· Temperature. Special low-reading rectal thermometers or thermistor probes are preferred for measuring core body temperature. The patient's temperature should be tracked over time, to check for improvement.

· 12 lead ECG. As the core temperature approaches 32°C to 33°C, acute ST-elevation and J waves or Osborn waves may appear

· FBC, serum electrolytes. Haemoglobin and haematocrit can be elevated (due to haemoconcentration). Platelets and WBCs are low due to sequestration in the spleen. Monitoring potassium is advised as hypothermic patients can be hypokalaemic due to a shift of potassium into the intracellular space.

· Blood glucose. Stress hormones are increased, and the body can have more peripheral resistance to insulin.

· Arterial blood gas

· Coagulation factors

· Chest X-ray

Initial management includes:

· Removing the patient from the cold environment and removing any wet/cold clothing,

· Warming the body with blankets

· Securing the airway and monitoring breathing,

· If the patient is not responding well to passive warming, you may consider maintaining circulation using warm IV fluids or applying forced warm air directly to the patient's body

+ rapid re-warming can lead to peripheral vasodilation and shock

· In severe cases, be prepared to conduct CPR. IV drugs should be avoided if possible, as the patient is more likely to have a drastic response to the drug.

For reference, the NHS also provides advice to the public for what NOT to do when a person has hypothermia (due to the risk of cardiac arrest):

· Don't put the person into a hot bath.

· Don't massage their limbs.

· Don't use heating lamps.

· Don't give them alcohol to drink.

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:09

Infective endocarditis: features

Modified Duke criteria

Infective endocarditis diagnosed if

· pathological criteria positive, or

· 2 major criteria, or

· 1 major and 3 minor criteria, or

· 5 minor criteria

Pathological criteria

Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content)

Major criteria

Positive blood cultures

· two positive blood cultures showing typical organisms consistent with infective endocarditis, such as Streptococcus viridans and the HACEK group, or

· persistent bacteraemia from two blood cultures taken > 12 hours apart or three or more positive blood cultures where the pathogen is less specific such as Staph aureus and Staph epidermidis, or

· positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci, or

· positive molecular assays for specific gene targets

Evidence of endocardial involvement

· positive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves), or

· new valvular regurgitation

Minor criteria

· predisposing heart condition or intravenous drug use

· microbiological evidence does not meet major criteria

· fever > 38ºC

· vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura

· immunological phenomena: glomerulonephritis, Osler's nodes, Roth spots

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:10

Infective endocarditis: prophylaxis

The 2008 guidelines from NICE have radically changed the list of procedures for which antibiotic prophylaxis is recommended

NICE recommends the following procedures do not require prophylaxis:

· dental procedures

· upper and lower gastrointestinal tract procedures

· genitourinary tract; this includes urological, gynaecological and obstetric procedures and childbirth

· upper and lower respiratory tract; this includes ear, nose and throat procedures and bronchoscopy

The guidelines do however suggest:

· any episodes of infection in people at risk of infective endocarditis should be investigated and treated promptly to reduce the risk of endocarditis developing

· if a person at risk of infective endocarditis is receiving antimicrobial therapy because they are undergoing a gastrointestinal or genitourinary procedure at a site where there is a suspected infection they should be given an antibiotic that covers organisms that cause infective endocarditis

It is important to note that these recommendations are not in keeping with the American Heart Association/European Society of Cardiology guidelines which still advocate antibiotic prophylaxis for high-risk patients who are undergoing dental procedures.

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:10

Postural hypotension

Postural hypotension may be defined as a fall of systolic blood pressure > 20 mmHg on standing.

Causes

· hypovolaemia

· autonomic dysfunction: diabetes, Parkinson's

· drugs: diuretics, antihypertensives, L-dopa, phenothiazines, antidepressants, sedatives

· alcohol

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:10

Pulmonary embolism

Potential features of pulmonary embolism include:

· chest pain

o typically pleuritic

· dyspnoea

· haemoptysis

· tachycardia

· tachypnoea

· respiratory examination

o classically the chest will be clear

o however, in real-world clinical practice findings are often found (see below for more details)

We know from experience that few patients (around 10%) present with the medical student textbook triad of pleuritic chest pain, dyspnoea and haemoptysis. Pulmonary embolism can be difficult to diagnose as it can present with virtually any cardiorespiratory symptom/sign depending on it's location and size.

So which features make pulmonary embolism more likely?

The PIOPED study1 in 2007 looked at the frequency of different symptoms and signs in patients who were diagnosed with pulmonary embolism.

The relative frequency of common clinical signs is shown below:

· Tachypnea (respiratory rate >16/min) - 96%

· Crackles - 58%

· Tachycardia (heart rate >100/min) - 44%

· Fever (temperature >37.8°C) - 43%

It is interesting to note that the Well's criteria for diagnosing a PE use tachycardia rather than tachypnoea.

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:10

Takayasu's arteritis

pulseless disease of Asian young females

Takayasu's arteritis is a large vessel vasculitis. It typically causes occlusion of the aorta and questions commonly refer to an absent limb pulse. It is more common in females and Asian people

Features

· systemic features of a vasculitis e.g. malaise, headache

· unequal blood pressure in the upper limbs

· carotid bruit

· intermittent claudication

· aortic regurgitation (around 20%)

Investigation:

magnetic resonance angiography.

Angiography showing multiple stenoses in the branches of the aorta secondary to Takayasu's arteritis

Associations

· renal artery stenosis

Management

· steroids

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:10

Ventricular septal defect

Ventricular septal defects (VSD) are the most common cause of congenital heart disease. They close spontaneously in around 50% of cases. Congenital VSDs are associated with chromosomal disorders (e.g. Down's syndrome, Edward's syndrome, Patau syndrome) and single gene disorders such as Non-congenital causes include post myocardial infarction

Features

· classically a pan-systolic murmur which is louder in smaller defects

Complications

· aortic regurgitation*

· infective endocarditis

· Eisenmenger's complex

· right heart failure

· pulmonary hypertension: pregnancy is contraindicated in women with pulmonary hypertension as it carries a 30-50% risk of mortality

*aortic regurgitation is due to a poorly supported right coronary cusp resulting in cusp prolapse

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:10

Abdominal aorta aneurysm

- Abdominal aortic aneurysms are a common problem in vascular surgery.

· They may occur as either true or false aneurysm. With the former all 3 layers of the arterial wall are involved, in the latter only a single layer of fibrous tissue forms the aneurysm wall.

· True abdominal aortic aneurysms have an approximate incidence of 0.06 per 1000 people. They are commonest in elderly men and for this reason the UK is now introducing the aneurysm screening program with the aim of performing an abdominal aortic ultrasound measurement in all men aged 65 years.

Causes

· Several different groups of patients suffer from aneurysmal disease.

· The commonest group is those who suffer from standard arterial disease, i.e. Those who are hypertensive, have diabetes and have been or are smokers.

· Other patients such as those suffering from connective tissue diseases such as Marfan's may also develop aneurysms. In patients with abdominal aortic aneurysms the extracellular matrix becomes disrupted with a change in the balance of collagen and elastic fibres.

Management

· Most abdominal aortic aneurysms are an incidental finding.

· Symptoms most often relate to rupture or impending rupture.

· 20% rupture anteriorly into the peritoneal cavity. Very poor prognosis.

· 80% rupture posteriorly into the retroperitoneal space

· The risk of rupture is related to aneurysm size, only 2% of aneurysms measuring less than 4cm in diameter will rupture over a 5 year period. This contrasts with 75% of aneurysms measuring over 7cm in diameter.

· This is well explained by Laplaces' law which relates size to transmural pressure.

· For this reason most vascular surgeons will subject patients with an aneurysm size of 5cm or greater to CT scanning of the chest, abdomen and pelvis with the aim of delineating anatomy and planning treatment. Depending upon co-morbidities, surgery is generally offered once the aneurysm is between 5.5cm and 6cm.

A CT reconstruction showing an infrarenal abdominal aortic aneurysm. The walls of the sac are calcified which may facilitate identification on plain x-rays

Image sourced from Wikipedia

Indications for surgery

· Symptomatic aneurysms (80% annual mortality if untreated)

· Increasing size above 5.5cm if asymptomatic

· Rupture (100% mortality without surgery)

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:10

Acute coronary syndrome: clincial features

Features of acute coronary syndrome (ACS) include:

· chest pain: classically on the left side of the chest. May radiate to the left arm or neck. This may not be present in elderly or diabetic patients

· dyspnoea

· nausea and vomiting

· sweating

· palpitations

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:11

Antiplatelets: summary of latest guidance

The table below summarises the most recent guidelines regarding antiplatelets:

Diagnosis	1st line	2nd line
Acute coronary syndrome (medically treated)	Aspirin (lifelong) & ticagrelor (12 months)	If aspirin contraindicated, clopidogrel (lifelong)
Percutaneous coronary intervention	Aspirin (lifelong) & prasurgrel or ticagrelor (12 months)	If aspirin contraindicated, clopidogrel (lifelong)
TIA	Clopidogrel (lifelong)	Aspirin (lifelong) & dipyridamole (lifelong)
Ischaemic stroke	Clopidogrel (lifelong)	Aspirin (lifelong) & dipyridamole (lifelong)
Peripheral arterial disease	Clopidogrel (lifelong)	Asprin (lifelong)

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:11

Atrial myxoma

Atrial myxoma is the most common primary cardiac tumour.

Overview

· 75% occur in left atrium, most commonly attached to the fossa ovalis

· more common in females

Features

· systemic: dyspnoea, fatigue, weight loss, pyrexia of unknown origin, clubbing

· emboli

· atrial fibrillation

· mid-diastolic murmur, 'tumour plop'

· echo: pedunculated heterogeneous mass typically attached to the fossa ovalis region of the interatrial septum

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:11

Atrioventricular block

In atrioventricular (AV) block, or heart block, there is impaired electrical conduction between the atria and ventricles. There are three types:

First-degree heart block

· PR interval > 0.2 seconds

· asymptomatic first-degree heart block is relatively common and does not need treatment

Second-degree heart block

· type 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped beat occurs

· type 2 (Mobitz II): PR interval is constant but the P wave is often not followed by a QRS complex

Third-degree (complete) heart block

· there is no association between the P waves and QRS complexes

ECG showing types of heart block

Type 1 (Wenckebach)

Sinus tachycardia with complete AV block and resulting junctional escape

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:11

Cardiac imaging: non-invasive techniques excluding echocardiography

The ability to image the heart using non-invasive techniques such as MRI, CT and radionuclides has evolved rapidly over recent years.

Nuclear imaging

These techniques use radiotracers which are extracted by normal myocardium. Examples include:

· thallium

· technetium (99mTc) sestamibi: a coordination complex of the radioisotope technetium-99m with the ligand methoxyisobutyl isonitrile (MIBI), used in 'MIBI' or cardiac Single Photon Emission Computed Tomography (SPECT) scans

· fluorodeoxyglucose (FDG): used in Positron Emission Tomography (PET) scans

The primary role of SPECT is to assess myocardial perfusion and myocardial viability. Two sets of images are usually acquired. First the myocardium at rest followed by images of the myocardium during stress (either exercise or following adenosine / dipyridamole). By comparing the rest with stress images any areas of ischaemia can classified as reversible or fixed (e.g. Following a myocardial infarction). Cardiac PET is predominately a research tool at the current time

MUGA

· Multi Gated Acquisition Scan, also known as radionuclide angiography

· radionuclide (technetium-99m) is injected intravenously

· the patient is placed under a gamma camera

· may be performed as a stress test

· can accurately measure left ventricular ejection fraction. Typically used before and after cardiotoxic drugs are used

Cardiac Computed Tomography (CT)

Cardiac CT is useful for assessing suspected ischaemic heart disease, using two main methods:

· calcium score: there is known to be a correlation between the amount of atherosclerotic plaque calcium and the risk of future ischaemic events. Cardiac CT can quantify the amount of calcium producing a 'calcium score'

· contrast enhanced CT: allows visualisation of the coronary artery lumen

If these two techniques are combined cardiac CT has a very high negative predictive value for ischaemic heart disease.

Cardiac MRI

Cardiac MRI (commonly termed CMR) has become the gold standard for providing structural images of the heart. It is particularly useful when assessing congenital heart disease, determining right and left ventricular mass and differentiating forms of cardiomyopathy. Myocardial perfusion can also be assessed following the administration of gadolinium. Currently CMR provides limited data on the extent of coronary artery disease.

Please also see the British Heart Foundation link for an excellent summary.

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:49

Choking

Partial or complete airway obstruction is a life-threatening emergency. Episodes often occur whilst eating and patients will often clutch their neck. The first step is to ask the patient 'Are you choking?'

Features of airway obstruction (taken from the Resus Council)

Mild airway obstruction	Severe airway obstruction
Response to question 'Are you choking?' · victim speaks and answers yes Other signs · victim is able to speak, cough, and breathe	Response to question 'Are you choking?' · victim unable to speak · victim may respond by nodding Other signs · victim unable to breathe · breathing sounds wheezy · attempts at coughing are silent · victim may be unconscious

If mild airway obstruction

· encourage the patient to cough

If severe airway obstruction and is conscious:

· give up to 5 back-blows

· if unsuccessful give up to 5 abdominal thrusts

· if unsuccessful continue the above cycle

If unconscious

· call for an ambulance

· start cardiopulmonary resuscitation (CPR)

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:49

Combination antiplatelet and anticoagulant therapy

With the increase in comorbidity, it is now common to find that a patient has an indication for both an antiplatelet (e.g. established cardiovascular disease) and an anticoagulant (e.g. atrial fibrillation, venous thromboembolism or valvular heart disease). However, combination therapy increases the risk of bleeding and may not be needed in all cases. How should this be managed?

Whilst there are not guidelines to cover every scenario a recent review in the BMJ offered an expert opinion outlining the approach in common scenarios.

Secondary prevention of stable cardiovascular disease with an indication for an anticoagulant

· normally in this situation, all patients are recommended to be prescribed an antiplatelet

· if an indication for anticoagulant exists (for example atrial fibrillation) it is indicated that anticoagulant monotherapy is given without the addition of antiplatelets

Post-acute coronary syndrome/percutaneous coronary intervention

· in these patients, there is a much stronger indication for antiplatelet therapy

· generally patients are given triple therapy (2 antiplatelets + 1 anticoagulant) for 4 weeks-6 months after the event and dual therapy (1 antiplatelet + 1 anticoagulant) to complete 12 months

· there is variation from patient to patient however given that the stroke risk in atrial fibrillation varies according to risk factors.

Venous thromboembolism (VTE)

· if a patient on antiplatelets develops a VTE they are likely to be prescribed anticoagulants for 3-6 months

· a HAS-BLED score should be calculated. Those with a low risk of bleeding may continue antiplatelets. In patients with an intermediate or high risk of bleeding consideration should be given to stopping the antiplatelets

For more information please see BMJ 2017;358:j3782

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:49

Dilated cardiomyopathy

Dilated cardiomyopathy (DCM) is the most common form of cardiomyopathy, accounting for 90% of cases.

Causes:

· idiopathic: the most common cause

· myocarditis: e.g. Coxsackie B, HIV, diphtheria, Chagas disease

· ischaemic heart disease

· peripartum

· hypertension

· iatrogenic: e.g. doxorubicin

· substance abuse: e.g. alcohol, cocaine

· inherited: either a familial genetic predisposition to DCM or a specific syndrome e.g. Duchenne muscular dystrophy

o around a third of patients with DCM are thought to have a genetic predisposition

o a large number of heterogeneous defects have been identified

o the majority of defects are inherited in an autosomal dominant fashion although other patterns of inheritance are seen

· infiltrative e.g. haemochromatosis, sarcoidosis

+ these causes may also lead to restrictive cardiomyopathy

· nutritional e.g. wet beriberi (thiamine deficiency)

Pathophysiology

· dilated heart leading to predominately systolic dysfunction

· all 4 chambers are dilated, but the left ventricle more so than right ventricle

· eccentric hypertrophy (sarcomeres added in series) is seen

Features

· classic findings of heart failure

· systolic murmur: stretching of the valves may result in mitral and tricuspid regurgitation

· S3

· 'balloon' appearance of the heart on the chest x-ray

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:49

ECG: digoxin

ECG features

· down-sloping ST depression ('reverse tick', 'scooped out')

· flattened/inverted T waves

· short QT interval

· arrhythmias e.g. AV block, bradycardia

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:49

ECG: right bundle branch block

Right bundle branch block is a common feature seen on ECGs.

One of the most common ways to remember the difference between LBBB and RBBB is WiLLiaM MaRRoW

· in LBBB there is a 'W' in V1 and a 'M' in V6

· in RBBB there is a 'M' in V1 and a 'W' in V6

Causes of RBBB

· normal variant - more common with increasing age

· right ventricular hypertrophy

· chronically increased right ventricular pressure - e.g. cor pulmonale

· pulmonary embolism

· myocardial infarction

· atrial septal defect (ostium secundum)

· cardiomyopathy or myocarditis

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:49

Glycoprotein IIb/IIIa receptor antagonists

Examples include;

· abciximab

· eptifibatide

· tirofiban

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:49

Heart failure (acute): features

Acute heart failure (AHF) is life-threatening emergency. AHF is a term used to describe the sudden onset or worsening of the symptoms of heart failure. Thus it may present with or without a background history of pre-existing heart failure. AHF without a past history of heart failure is called de-novo AHF. Decompensated AHF is more common (66-75%) and presents with a background history of HF.

It usually presents after the age of 65-years and is a major cause for unplanned hospital admission in such patients.

AHF is usually caused by a reduced cardiac output that results from a functional or structural abnormality.

De-novo heart failure is caused by and increased cardiac filling pressures and myocardial dysfunction usually as a result of ischaemia. This causes reduced cardiac output and therefore hypoperfusion. This, in turn can cause pulmonary oedema. Other less common causes of de-novo AHF are:

· Viral myopathy

· Toxins

· Valve dysfunction

Decompensated heart failure accounts for most cases of AHF. The most common precipitating causes of acute AHF are:

· Acute coronary syndrome

· Hypertensive crisis

· Acute arrhythmia

· Valvular disease

There is generally a history of pre-existing cardiomyopathy. It usually presents with signs of fluid congestion, weight gain, orthopnoea and breathlessness.

Patient with heart failure are broadly characterised into 1 of 4 groups based on whether they present:

· With or without hypoperfusion

· With or without fluid congestion

Classifying patients into one of these 4 groups is clinically useful as it determines the therapeutic approach.

Generally speaking, the signs and symptoms of AHF are as follows:

Symptoms	Signs
Breathlessness	Cyanosis
Reduced exercise tolerance	Tachycardia
Oedema	Elevated jugular venous pressure
Faitgue	Displaced apex beat
	Chest signs: classically bibasal crackles but may also cause a wheeze
	S3-heart sound

Sometimes the presentation will be that of the underlying cause (e.g: chest pain, viral infection)

Over 90% of patients with AHF have a normal or increased blood pressure (mmHg).

The diagnostic workup for patients with AHF includes:

· Blood tests – this is to look for any underlying abnormality such as anaemia, abnormal electrolytes or infection.

· Chest X-ray – findings include pulmonary venous congestion, interstitial oedema and cardiomegaly

· Echocardiogram – this will identify pericardial effusion and cardiac tamponade

· B-type natriuretic peptide – raised levels (>100mg/litre) indicate myocardial damage and are supportive of the diagnosis.

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:49

Heart failure (chronic): features

Features:

· dyspnoea

· cough: may be worse at night and associated with pink/frothy sputum

· orthopnoea

· paroxysmal nocturnal dyspnoea

· wheeze ('cardiac wheeze')

· weight loss ('cardiac cachexia'): occurs in up to 15% of patients. Remember this may be hidden by weight gained secondary to oedema

· bibasal crackles on examination

· signs of right-sided heart failure: raised JVP, ankle oedema and hepatomegaly

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:49

Heart sounds: S2

S2 is caused by the closure of the aortic valve (A2) closely followed by that of the pulmonary valve (P2)

Causes of a loud S2

· hypertension: systemic (loud A2) or pulmonary (loud P2)

· hyperdynamic states

· atrial septal defect without pulmonary hypertension

Causes of a soft S2

· aortic stenosis

Causes of fixed split S2

· atrial septal defect

Causes of a widely split S2

· deep inspiration

· RBBB

· pulmonary stenosis

· severe mitral regurgitation

Causes of a reversed (paradoxical) split S2 (P2 occurs before A2)

· LBBB

· severe aortic stenosis

· right ventricular pacing

· WPW type B (causes early P2)

· patent ductus arteriosus

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:49

Hyperlipidaemia: xanthomata

Characteristic xanthomata seen in hyperlipidaemia:

Palmar xanthoma

· remnant hyperlipidaemia

· may less commonly be seen in familial hypercholesterolaemia

Eruptive xanthoma are due to high triglyceride levels and present as multiple red/yellow vesicles on the extensor surfaces (e.g. elbows, knees)

Causes of eruptive xanthoma

· familial hypertriglyceridaemia

· lipoprotein lipase deficiency

Tendon xanthoma, tuberous xanthoma, xanthelasma

· familial hypercholesterolaemia

· remnant hyperlipidaemia

Xanthelasma are also seen without lipid abnormalities

Management of xanthelasma, options include:

· surgical excision

· topical trichloroacetic acid

· laser therapy

· electrodesiccation

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:50

Hypertension: a very basic introduction

Hypertension is one of the most common medical conditions encountered in the developed world. Whilst there is a degree of normal variation in blood pressure according to the time of day and whether we are exerting ourselves hypertension describes a chronically raised blood pressure. The main relevance of hypertension lies in the fact that it is an important risk factor for the development of cardiovascular disease such as ischaemic heart disease and stroke. Unless the blood pressure is very high it is unusual for patients to experience any symptoms.

What is a 'normal' blood pressure?

Normal blood pressure can vary widely according to age, gender and individual physiology. Most healthy people have a blood pressure between 90/60 mmHg and 140/90 mmHg.

NICE define hypertension as follows:

· a clinic reading persistently above >= 140/90 mmHg, or:

· a 24 hour blood pressure average reading >= 135/85 mmHg

Why do some patients have an elevated blood pressure?

Patients with hypertension may be divided into two categories. The vast majority (around 90-95%) have primary, or essential, hypertension. This is where there is no single disease causing the rise in blood pressure but rather a series of complex physiological changes which occur as we get older.

Secondary hypertension may be caused by a wide variety of endocrine, renal and other causes. The table below lists some of the conditions that may cause secondary hypertension

Renal disease	Endocrine disorders	Other causes
• Glomerulonephritis • Chronic pyelonephritis • Adult polycystic kidney disease • Renal artery stenosis	• Primary hyperaldosteronism • Phaeochromocytoma • Cushing's syndrome • Liddle's syndrome • Congenital adrenal hyperplasia (11-beta hydroxylase deficiency) • Acromegaly	• Glucocorticoids • NSAIDs • Pregnancy • Coarctation of the aorta • Combined oral contraceptive pill

Symptoms and signs

As mentioned earlier, hypertension does not typically cause symptoms unless it is very high, for example > 200/120 mmHg. If very raised patients may experience:

· headaches

· visual disturbance

· seizures

In terms of signs hypertension is obviously usually detected when checking someones blood pressure. For diagnosing longstanding blood pressure there has been a move in recent years to using 24 hour blood pressure monitors. These avoid cases of so called 'white coat' hypertension where a patients blood pressure rises when they are in a clinical setting, for example a GP surgery. Studies have shown that readings from 24 hour blood pressure monitors correlate better with clinical outcomes and hence should be used to guide decisions about treatment.

It also also important when assessing a patient with newly diagnosed hypertension to ensure they do not have any end-organ damage:

· fundoscopy: to check for hypertensive retinopathy

· urine dipstick: to check for renal disease, either as a cause or consequence of hypertension

· ECG: to check for left ventricular hypertrophy or ischaemic heart disease

Investigations

As mentioned previously 24 hour blood pressure is now recommend for the diagnosis of hypertension. If 24 hour blood pressure monitoring is not available then home readings using an automated sphygmomanometer are useful.

Following diagnosis patients typically have the following tests:

· urea and electrolytes: check for renal disease, either as a cause or consequence of hypertension

· HbA1c: check for co-existing diabetes mellitus, another important risk factor for cardiovascular disease

· lipids: check for hyperlipidaemia, again another important risk factor for cardiovascular disease

· ECG

· urine dipstick

Management

The management of patients with hypertension involves several aspects:

· drug therapy using antihypertensives

· modification of other risk factors to reduce the overall risk of cardiovascular disease

· monitoring the patient for the development of complications of hypertension

The table below shows the common drugs used to treat hypertension:

Drug	Mechanism of action	Common side-effects	Notes
Angiotensin-converting enzyme (ACE) inhibitors	Inhibit the conversion angiotensin I to angiotensin II	Cough Angioedema Hyperkalaemia	First-line treatment in younger patients (< 55 years old) Less effective in Afro-Caribbean patients Must be avoided in pregnant women Renal function must be check 2-3 weeks after starting due to the risk of worsening renal function in patients with renovascular disease Drug names end in '-pril'
Calcium channel blockers	Block voltage-gated calcium channels relaxing vascular smooth muscle and force of myocardial contraction	Flushing Ankle swelling Headache	First-line treatment in older patients (>= 55 years old)
Thiazide type diuretics	Inhibit sodium absorption at the beginning of the distal convoluted tubule	Hyponatraemia Hypokalaemia Dehydration	Although technically a diuretic, thiazides have a very weak diuretic action
Angiotensin II receptor blockers (A2RB)	Block effects of angiotensin II at the AT1 receptor	Hyperkalaemia	Angiotensin II receptor blockers are generally used in situations where patients have not tolerated an ACE inhibitor, usually due to the development of a cough Drug names end in '-sartan'

Drug therapy is decided by well established NICE guidelines, which advocate a step-wise approach:

Flow chart showing the management of hypertension as per current NICE guideliness

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:50

Hypertension: secondary causes

It is thought that between 5-10% of patients diagnosed with hypertension have primary hyperaldosteronism, including Conn's syndrome. This makes it the single most common cause of secondary hypertension.

Renal disease accounts for a large percentage of the other cases of secondary hypertension. Conditions which may increase the blood pressure include:

· glomerulonephritis

· pyelonephritis

· adult polycystic kidney disease

· renal artery stenosis

Endocrine disorders (other than primary hyperaldosteronism) may also result in increased blood pressure:

· phaeochromocytoma

· Cushing's syndrome

· Liddle's syndrome

· congenital adrenal hyperplasia (11-beta hydroxylase deficiency)

· acromegaly

Drug causes:

· steroids

· monoamine oxidase inhibitors

· the combined oral contraceptive pill

· NSAIDs

· leflunomide

Other causes include:

· pregnancy

· coarctation of the aorta

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:50

Hypertrophic obstructive cardiomyopathy: management

Hypertrophic obstructive cardiomyopathy (HOCM) is an autosomal dominant disorder of muscle tissue caused by defects in the genes encoding contractile proteins. The estimated prevalence is 1 in 500.

Management

· Amiodarone

· Beta-blockers or verapamil for symptoms

· Cardioverter defibrillator

· Dual chamber pacemaker

· Endocarditis prophylaxis*

Maintain fluid at all times

Drugs to avoid

· nitrates

· ACE-inhibitors

· inotropes

*although see the 2008 NICE guidelines on infective endocarditis prophylaxis

From <https://www.passmedicine.com/review/textbook.php?s=#>

MR SAM ASH

insertion of an implantable cardioverter defibrillator to lower the risk of sudden cardiac death

From <https://mle.ncl.ac.uk/cases/page/18128/>

HOCM is the most common cause of sudden cardiac death in young people.

Surgery:

Surgical myectomy

Alcohol septal ablation

24 December 2020

13:50

Infective endocarditis: prognosis and management

Poor prognostic factors

· Staphylococcus aureus infection (see below)

· prosthetic valve (especially 'early', acquired during surgery)

· culture negative endocarditis

· low complement levels

Mortality according to organism

· staphylococci - 30%

· bowel organisms - 15%

· streptococci - 5%

Current antibiotic guidelines (source: British National Formulary)

Scenario	Suggested antibiotic therapy
Initial blind therapy	Native valve · amoxicillin, consider adding low-dose gentamicin If penicillin allergic, MRSA or severe sepsis · vancomycin + low-dose gentamicin If prosthetic valve · vancomycin + rifampicin + low-dose gentamicin
Native valve endocarditis caused by staphylococci	Flucloxacillin If penicillin allergic or MRSA · vancomycin + rifampicin
Prosthetic valve endocarditis caused by staphylococci	Flucloxacillin + rifampicin + low-dose gentamicin If penicillin allergic or MRSA · vancomycin + rifampicin + low-dose gentamicin
Endocarditis caused by fully-sensitive streptococci (e.g. viridans)	Benzylpenicillin If penicillin allergic · vancomycin + low-dose gentamicin
Endocarditis caused by less sensitive streptococci	Benzylpenicillin + low-dose gentamicin If penicillin allergic · vancomycin + low-dose gentamicin

Indications for surgery

· severe valvular incompetence

· aortic abscess (often indicated by a lengthening PR interval)

· infections resistant to antibiotics/fungal infections

· cardiac failure refractory to standard medical treatment

· recurrent emboli after antibiotic therapy

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:50

Inhaled foreign body

This typically occurs in younger children. Whilst the presentation if often acute it can sometimes go unnoticed, with up to a third of cases being diagnosed after a few days.

Features

· cough

· stridor

· dyspnoea

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:50

Investigating palpitations

Palpitations are a common presenting symptom.

Possible causes include

· arrhythmias

· stress

· increased awareness of normal heart beat / extrasystoles

First-line investigations include:

· 12-lead ECG: this will only capture the heart rhythm for a few seconds and hence is likely to miss episodic arrhythmias. However, other abnormalities linked to the underlying arrhythmia (for example a prolonged QT interval or PR interval, or changes suggesting recent myocardial ischaemia) may be seen.

· thyroid function tests: thyrotoxicosis may precipitate atrial fibrillation and other arrhythmias

· urea and electrolytes: looking for disturbances such as a low potassium

· full blood count

Capturing episodic arrhythmias

First-line investigations are often normal in patients complaining of palpitations. The next step is to exclude an episode arrhythmia.

The most common investigation is Holter monitoring

· portable battery operated device

· continuously records ECG from 2-3 leads

· usually done for 24 hours but may be used for longer if symptoms are less than daily

· patients are asked to keep a diary to record any symptomatic palpitations. This can later be compared to the rhythm strip at the time of the symptoms

· at the end of the monitoring a report is generated summarising a number of parameters including heart rate, arrhythmias and changes in ECG waveform

If no abnormality is found on the Holter monitor, and symptoms continue, other options include:

· external loop recorder

· implantable loop recorder

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:50

Isolated systolic hypertension

Isolated systolic hypertension (ISH) is common in the elderly, affecting around 50% of people older than 70 years old. The Systolic Hypertension in the Elderly Program (SHEP) back in 1991 established that treating ISH reduced both strokes and ischaemic heart disease. Drugs such as thiazides were recommended as first line agents. This approach is contradicated by the 2011 NICE guidelines which recommends treating ISH in the same stepwise fashion as standard hypertension.

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:50

Ivabradine

Ivabradine is a class of anti-anginal drug which works by reducing the heart rate. It acts on the If ('funny') ion current which is highly expressed in the sinoatrial node, reducing cardiac pacemaker activity.

Adverse effects

· visual effects, particular luminous phenomena, are common

· headache

· bradycardia, heart block

There is no evidence currently of superiority over existing treatments of stable angina.

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:50

Mitral regurgitation

Also known as mitral insufficiency, mitral regurgitation (MR) occurs when blood leaks back through the mitral valve on systole. It is the second most common valve disease after aortic stenosis. The mitral valve is located between the left atrium and ventricle, and regurgitation leads to a less efficient heart as less blood is pumped through the body with each contraction. This said, MR is common in otherwise healthy patients to a trivial degree and does not need treatment.

As the degree of regurgitation becomes more severe, the body’s oxygen demands may exceed what the heart can supply and as a result, the myocardium can thicken over time. While this may be benign initially, patients may find themselves increasingly fatigued as a thicker myometrium becomes less efficient, and eventually go into irreversible heart failure.

Risk factors

· Female sex

· Lower body mass

· Age

· Renal dysfunction

· Prior myocardial infarction

· Prior mitral stenosis or valve prolapse

· Collagen disorders e.g. Marfan's Syndrome and Ehlers-Danlos syndrome

Causes

· Following coronary artery disease or post-MI: if the papillary muscles or chordae tendinae are affected by a cardiac insult, mitral valve disease may ensue as a result of damage to its supporting structures.

· Mitral valve prolapse: Occurs when the leaflets of the mitral valve is deformed so the valve does not close properly and allows for backflow. Most patients with this have a trivial degree of mitral regurgitation.

· Infective endocarditis: When vegetations from the organisms colonising the heart grow on the mitral valve, it is prevented from closing properly. Patients with abnormal valves are more likely to develop endocarditis as opposed to their peers.

· Rheumatic fever: While this is uncommon in developed countries, rheumatic fever can cause inflammation of the valves and therefore result in mitral regurgitation.

· Congenital

Symptoms

· Most patients with MR are asymptomatic, and patients suffering from mild to moderate MR may stay largely asymptomatic indefinitely. Symptoms tend to be due to failure of the left ventricle, arrhythmias or pulmonary hypertension. This may present as fatigue, shortness of breath and oedema.

Signs

· The murmur heard on auscultation of the chest is typically a pansystolic murmur described as “blowing”. It is heard best at the apex and radiating into the axilla. S1 may be quiet as a result of incomplete closure of the valve. Severe MR may cause a widely split S2

Investigations

· ECG may show a broad P wave, indicative of atrial enlargement

· Cardiomegaly may be seen on chest x-ray, with an enlarged left atrium and ventricle

· Echocardiography is crucial to diagnosis and to assess severity

Treatment options

· Medical management in acute cases involves nitrates, diuretics, positive inotropes and an intra-aortic balloon pump to increase cardiac output

· If patients are in heart failure, ACE inhibitors may be considered along with beta-blockers and spironolactone

· In acute, severe regurgitation, surgery is indicated

· The evidence for repair over replacement is strong in degenerative regurgitation, and is demonstrated through lower mortality and higher survival rates

· When this is not possible, valve replacement with either an artificial valve or a pig valve is considered

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:50

Mitral valve prolapse

Mitral valve prolapse is common, occurring in around 5-10 % of the population. It is usually idiopathic but may be associated with a wide variety of cardiovascular disease and other conditions

Associations

· congenital heart disease: PDA, ASD

· cardiomyopathy

· Turner's syndrome

· Marfan's syndrome, Fragile X

· osteogenesis imperfecta

· pseudoxanthoma elasticum

· Wolff-Parkinson White syndrome

· long-QT syndrome

· Ehlers-Danlos Syndrome

· polycystic kidney disease

Features

· patients may complain of atypical chest pain or palpitations

· mid-systolic click (occurs later if patient squatting)

· late systolic murmur (longer if patient standing)

· complications: mitral regurgitation, arrhythmias (including long QT), emboli, sudden death

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:50

Myocarditis

Myocarditis describes inflammation of the myocardium. There are a wide range of underlying causes. It should be particularly considered in younger patients who present with chest pain.

Causes

· viral: coxsackie B, HIV

· bacteria: diphtheria, clostridia

· spirochaetes: Lyme disease

· protozoa: Chagas' disease, toxoplasmosis

· autoimmune

· drugs: doxorubicin

Presentation

· usually young patient with an acute history

· chest pain

· dyspnoea

· arrhythmias

Investigations

· bloods

o ↑ inflammatory markers in 99%

o ↑ cardiac enzymes

o ↑ BNP

· ECG

o tachycardia

o arrhythmias

o ST/T wave changes including ST-segment elevation and T wave inversion

Management

· treatment of underlying cause e.g. antibiotics if bacterial cause

· supportive treatment e.g. of heart failure or arrhythmias

Complications

· heart failure

· arrhythmia, possibly leading to sudden death

· dilated cardiomyopathy: usually a late complication

From <https://www.passmedicine.com/review/textbook.php?s=#>

Cyclophosphamide is known to be associated with haemorrhagic myocarditis

From <https://mle.ncl.ac.uk/cases/page/18128/>

24 December 2020

13:51

Nitrates

Nitrates are a group of drugs which have vasodilating effects. The main indications for their use is in the management of angina and the acute treatment of heart failure. Sublingual glyceryl trinitrate is the most common drug used in patients with ischaemic heart disease to relieve angina attacks.

Mechanism of action

· nitrates cause the release of nitric oxide in smooth muscle, activating guanylate cyclase which then converts GTP to cGMP, which in turn leads to a fall in intracellular calcium levels

· in angina they both dilate the coronary arteries and also reduce venous return which in turn reduces left ventricular work, reducing myocardial oxygen demand

Side-effects

· hypotension

· tachycardia

· headaches

· flushing

Nitrate tolerance

· many patients who take nitrates develop tolerance and experience reduced efficacy

· the BNF advises that patients who develop tolerance should take the second dose of isosorbide mononitrate after 8 hours, rather than after 12 hours. This allows blood-nitrate levels to fall for 4 hours and maintains effectiveness

· this effect is not seen in patients who take modified release isosorbide mononitrate

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:51

Orthostatic hypotension

Orthostatic hypotension is more common in older people and patients who have neurodegenerative disease (e.g. Parkinson's) diabetes, or hypertension

Iatrogenic causes include alpha-blockers (e.g. for benign prostatic hyperplasia).

Features

· a drop in BP (usually >20/10 mm Hg) within three minutes of standing

· presyncope

· syncope

Management

· treatment options include midodrine and fludrocortisone

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:51

Parenteral anticoagulation

Parenteral anticoagulants are used for the prevention of venous thromboembolism and in the management of acute coronary syndrome.

Unfractionated heparin and low molecular weight heparin are discussed in detail so this note will focus on fondaparinux and direct thrombin inhibitors.

Fondaparinux

Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa. It is given subcutaneously.

Direct thrombin inhibitors

Examples include bivalirudin. These are generally given intravenously.

Dabigatran is a type of direct thrombin inhibitor that is taken orally. It is often grouped alongside the direct oral anticoagulants (DOACs).

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:51

Pulmonary artery occlusion pressure monitoring

The pulmonary artery occlusion pressure is an indirect measure of left atrial pressure, and thus filling pressure of the left heart. The low resistance within the pulmonary venous system allows this useful measurement to be made. The most accurate trace is made by inflating the balloon at the catheter tip and 'floating' it so that it occludes the vessel. If it is not possible to occlude the vessel in this way then the measurement gained will be the pulmonary artery end diastolic pressure.

Interpretation of PAOP

PAOP	mmHg	Scenario
Normal	8-12
Low	<5	Hypovolaemia
Low with pulmonary oedema	<5	ARDS
High	>18	Overload

When combined with measurements of systemic vascular resistance and cardiac output it is possible to accurately classify patients.

Systemic vascular resistance

Derived from aortic pressure, right atrial pressure and cardiac output.

SVR=80(mean aortic pressure-mean right atrial pressure)/cardiac output

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:51

Saphenous vein

Long saphenous vein

This vein may be harvested for bypass surgery, or removed as treatment for varicose veins with saphenofemoral junction incompetence.

· Originates at the 1st digit where the dorsal vein merges with the dorsal venous arch of the foot

· Passes anterior to the medial malleolus and runs up the medial side of the leg

· At the knee, it runs over the posterior border of the medial epicondyle of the femur bone

· Then passes laterally to lie on the anterior surface of the thigh before entering an opening in the fascia lata called the saphenous opening

· It joins with the femoral vein in the region of the femoral triangle at the saphenofemoral junction

Tributaries

· Medial marginal

· Superficial epigastric

· Superficial iliac circumflex

· Superficial external pudendal veins

Short saphenous vein

· Originates at the 5th digit where the dorsal vein merges with the dorsal venous arch of the foot, which attaches to the great saphenous vein.

· It passes around the lateral aspect of the foot (inferior and posterior to the lateral malleolus) and runs along the posterior aspect of the leg (with the sural nerve)

· Passes between the heads of the gastrocnemius muscle, and drains into the popliteal vein, approximately at or above the level of the knee joint.

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:51

Subclavian artery

Path

· The left subclavian comes directly off the arch of aorta

· The right subclavian arises from the brachiocephalic artery (trunk) when it bifurcates into the subclavian and the right common carotid artery.

· From its origin, the subclavian artery travels laterally, passing between anterior and middle scalene muscles, deep to scalenus anterior and anterior to scalenus medius. As the subclavian artery crosses the lateral border of the first rib, it becomes the axillary artery. At this point it is superficial and within the subclavian triangle.

Image sourced from Wikipedia

Branches

· Vertebral artery

· Internal thoracic artery

· Thyrocervical trunk

· Costocervical trunk

· Dorsal scapular artery

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:51

Takotsubo cardiomyopathy

Takotsubo cardiomyopathy is a type of non-ischaemic cardiomyopathy associated with a transient, apical ballooning of the myocardium. It may be triggered by stress.

Pathophysiology

· Takotsubo is a Japanese word that describes an octopus trap

· the apical ballooning appearance occurs due to severe hypokinesis of the mid and apical segments with preservation of activity of the basal segments. In simple terms, the bottom of the heart (the apex) does not contract and therefore appears to balloon out. However, the area closer to the top (the base) continues to contract (creating the neck of the octopus trap)

Features

· chest pain

· features of heart failure

· ECG: ST-elevation

· normal coronary angiogram

Treatment is supportive.

Prognosis

· the majority of patients improve with supportive treatment

From <https://www.passmedicine.com/review/textbook.php?s=#>

24 December 2020

13:51

Travel-related thrombosis

It is not uncommon for us to be asked by patients whether they should take aspirin prior to a long haul flight. So called 'economy class syndrome' as a concept has increased in the public's mind over the past 10 years or so. It is certainly true that long-haul air travel is associated with an increased risk of VTE. A 2001 study in the New England Journal of Medicine1 showed the following risk of pulmonary embolism:

· 0.01 cases per million for travel under 5,000 km

· 1.5 cases per million for travel between 5,000 - 10,000 km

· 4.8 cases per million for travel over 10,000 km

The Civil Aviation Authority do not give specific guidance relating to venous thromboembolism. The British Committee for Standards in Haematology did however produce guidelines in 2005 as did SIGN in 2010 and Clinical Knowledge Summaries (CKS) in 2013. Unfortunately, there is no universal agreement on what to advise patients.

The most recent CKS guidelines advise that we take a risk based approach. For example, a patient with no major risk factors for VTE (i.e. the average person) then no special measures are needed.

Patients with major risk factors should consider wearing anti-embolism stockings. These can either be bought by the patient or prescribed (class I). Clearly if the risk is very high (e.g. a long-haul flight following recent major surgery) then consideration should be given to delaying the flight or specialist advice sought regarding the use of low-molecular weight heparin.

All guidelines agree there is no role for aspirin in low, medium or high risk patients.

From <https://www.passmedicine.com/review/textbook.php?s=#>

22 December 2020

16:11

Hypertension: management

NICE published updated guidelines for the management of hypertension in 2019. Some of the key changes include:

· lowering the threshold for treating stage 1 hypertension in patients < 80 years from 20% to 10%

· angiotensin receptor blockers can be used instead of ACE-inhibitors where indicated

· if a patient is already taking an ACE-inhibitor or angiotensin receptor blocker, then a calcium channel blocker OR a thiazide-like diuretic can be used. Previously only a calcium channel blocker was recommended

Blood pressure classification

This becomes relevant later in some of the management decisions that NICE advocate.

Stage	Criteria
Stage 1 hypertension	Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg
Stage 2 hypertension	Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg
Severe hypertension	Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 110 mmHg

Flow chart showing simplified schematic for diagnosis hypertension following NICE guidelines

Managing hypertension

Lifestyle advice should not be forgotten and is frequently tested in exams:

· a low salt diet is recommended, aiming for less than 6g/day, ideally 3g/day. The average adult in the UK consumes around 8-12g/day of salt. A recent BMJ paper* showed that lowering salt intake can have a significant effect on blood pressure. For example, reducing salt intake by 6g/day can lower systolic blood pressure by 10mmHg

· caffeine intake should be reduced

· the other general bits of advice remain: stop smoking, drink less alcohol, eat a balanced diet rich in fruit and vegetables, exercise more, lose weight

ABPM/HBPM >= 135/85 mmHg (i.e. stage 1 hypertension)

· treat if < 80 years of age AND any of the following apply; target organ damage, established cardiovascular disease, renal disease, diabetes or a 10-year cardiovascular risk equivalent to 10% or greater

· in 2019, NICE made a further recommendation, suggesting that we should 'consider antihypertensive drug treatment in addition to lifestyle advice for adults aged under 60 with stage 1 hypertension and an estimated 10-year risk below 10%. '. This seems to be due to evidence that QRISK may underestimate the lifetime probability of developing cardiovascular disease

ABPM/HBPM >= 150/95 mmHg (i.e. stage 2 hypertension)

· offer drug treatment regardless of age

For patients < 40 years consider specialist referral to exclude secondary causes.

Flow chart showing the management of hypertension as per current NICE guideliness

Step 1 treatment

· patients < 55-years-old or a background of type 2 diabetes mellitus: ACE inhibitor or a Angiotensin receptor blocker (ACE-i or ARB): (A)

o angiotensin receptor blockers should be used where ACE inhibitors are not tolerated (e.g. due to a cough)

· patients >= 55-years-old or of black African or African–Caribbean origin: Calcium channel blocker (C)

o ACE inhibitors have reduced efficacy in patients of black African or African–Caribbean origin are therefore not used first-line

Step 2 treatment

· if already taking an ACE-i or ARB add a Calcium channel blocker or a thiazide-like Diuretic

· if already taking a Calcium channel blocker add an ACE-i or ARB

o for patients of black African or African–Caribbean origin taking a calcium channel blocker for hypertension, if they require a second agent consider an angiotensin receptor blocker in preference to an ACE inhibitor

· (A + C) or (A + D)

Step 3 treatment

· add a third drug to make, i.e.:

o if already taking an (A + C) then add a D

o if already (A + D) then add a C

· (A + C + D)

Step 4 treatment

· NICE define step 4 as resistant hypertension and suggest either adding a 4th drug (as below) or seeking specialist advice

· first, check for:

o confirm elevated clinic BP with ABPM or HBPM

o assess for postural hypotension.

o discuss adherence

· if potassium < 4.5 mmol/l add low-dose spironolactone

· if potassium > 4.5 mmol/l add an alpha- or beta-blocker

Patients who fail to respond to step 4 measures should be referred to a specialist. NICE recommend:

If blood pressure remains uncontrolled with the optimal or maximum tolerated doses of four drugs, seek expert advice if it has not yet been obtained.

Blood pressure targets

	Clinic BP	ABPM / HBPM
Age < 80 years	140/90 mmHg	135/85 mmHg
Age > 80 years	150/90 mmHg	145/85 mmHg

New drugs

Direct renin inhibitors

· e.g. Aliskiren (branded as Rasilez)

· by inhibiting renin blocks the conversion of angiotensinogen to angiotensin I

· no trials have looked at mortality data yet. Trials have only investigated fall in blood pressure. Initial trials suggest aliskiren reduces blood pressure to a similar extent as angiotensin converting enzyme (ACE) inhibitors or angiotensin-II receptor antagonists

· adverse effects were uncommon in trials although diarrhoea was occasionally seen

· only current role would seem to be in patients who are intolerant of more established antihypertensive drugs

From <https://www.passmedicine.com/question/questions.php?q=0>

21 December 2020

21:47

Heart failure: drug management

NICE issued updated guidelines on management in 2018, key points are summarised here

Whilst loop diuretics play an important role in managing fluid overload it should be remembered that no long-term reduction in mortality has been demonstrated for loop diuretics such as furosemide.

The first-line treatment for all patients is both an ACE-inhibitor and a beta-blocker

· generally, one drug should be started at a time. NICE advise that clinical judgement is used when determining which one to start first

· beta-blockers licensed to treat heart failure in the UK include bisoprolol, carvedilol, and nebivolol.

· ACE-inhibitors and beta-blockers have no effect on mortality in heart failure with preserved ejection fraction

Second-line treatment is an aldosterone antagonist

· these are sometimes referred to as mineralocorticoid receptor antagonists. Examples include spironolactone and eplerenone

· it should be remember that both ACE inhibitors (which the patient is likely to already be on) and aldosterone antagonists both cause hyperkalaemia - therefore potassium should be monitored

Third-line treatment should be initiated by a specialist. Options include ivabradine, sacubitril-valsartan, hydralazine in combination with nitrate, digoxin and cardiac resynchronisation therapy

· ivabradine

o criteria: sinus rhythm > 75/min and a left ventricular fraction < 35%

· sacubitril-valsartan

o criteria: left ventricular fraction < 35%

o is considered in heart failure with reduced ejection fraction who are symptomatic on ACE inhibitors or ARBs

o should be initiated following ACEi or ARB wash-out period

· digoxin

o digoxin has also not been proven to reduce mortality in patients with heart failure. It may however improve symptoms due to its inotropic properties

o it is strongly indicated if there is coexistent atrial fibrillation

· hydralazine in combination with nitrate

o this may be particularly indicated in Afro-Caribbean patients

· cardiac resynchronisation therapy

o indications include a widened QRS (e.g. left bundle branch block) complex on ECG

Other treatments

· offer annual influenza vaccine

· offer one-off pneumococcal vaccine

o adults usually require just one dose but those with asplenia, splenic dysfunction or chronic kidney disease need a booster every 5 years

From <https://www.passmedicine.com/review/textbook.php?s=#>

In acute decompensated heart failure, the negative inotropic effects  of beta blockers can worsen stroke volume and therefore aggravate  heart failure.

Chronic beta-blocker use in stable heart failure is associated with  significantly improved survival in patients but should be deferred  until patient is no longer congested after treatment with appropriate  diuresis and post-load reduction.

From <https://mle.ncl.ac.uk/cases/page/18128/>

Haemodynamic profile is that of wet decompensated heart failure. Intravenous loop diuretic is more effective than oral diuretic in clearing the congestion.

Beta-blocker is not advisable in patients with acute decompensated heart  failure.

From <https://mle.ncl.ac.uk/cases/page/18128/>

N-type pro B-type natriuretic peptide

· >2000ng/L refer for specialist assessment urgently, transthoracic echo within 2 weeks

· 400-2000ng/L refer for specialist assessment within 6 weeks

· <400ng/L, diagnosis of heart failure less likely

Reduced levels in obese, African-Caribbean, patients on diuretics, ACEi, beta-blockers

Need to rule out other causes (>70 years old, LVH, ischaemia, pulmonary embolism) in patients with high natriuretic peptide levels

From <https://mle.ncl.ac.uk/cases/page/17993/>

21 December 2020

22:11

Statins

Statins inhibit the action of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis.

Adverse effects

· myopathy: includes myalgia, myositis, rhabdomyolysis and asymptomatic raised creatine kinase. Risks factors for myopathy include advanced age, female sex, low body mass index and presence of multisystem disease such as diabetes mellitus. Myopathy is more common in lipophilic statins (simvastatin, atorvastatin) than relatively hydrophilic statins (rosuvastatin, pravastatin, fluvastatin)

· liver impairment: the 2014 NICE guidelines recommend checking LFTs at baseline, 3 months and 12 months. Treatment should be discontinued if serum transaminase concentrations rise to and persist at 3 times the upper limit of the reference range

· there is some evidence that statins may increase the risk of intracerebral haemorrhage in patients who've previously had a stroke. This effect is not seen in primary prevention. For this reason the Royal College of Physicians recommend avoiding statins in patients with a history of intracerebral haemorrhage

Contraindications

· macrolides (e.g. erythromycin, clarithromycin) are an important interaction. Statins should be stopped until patients complete the course

· pregnancy

Who should receive a statin?

· all people with established cardiovascular disease (stroke, TIA, ischaemic heart disease, peripheral arterial disease)

· following the 2014 update, NICE recommend anyone with a 10-year cardiovascular risk >= 10%

· patients with type 2 diabetes mellitus should now be assessed using QRISK2 like other patients are, to determine whether they should be started on statins

· patients with type 1 diabetes mellitus who were diagnosed more than 10 years ago OR are aged over 40 OR have established nephropathy

Statins should be taken at night as this is when the majority of cholesterol synthesis takes place. This is especially true for simvastatin which has a shorter half-life than other statins.

NICE currently recommends the following for the prevention of cardiovascular disease::

· atorvastatin 20mg for primary prevention

o increase the dose if non-HDL has not reduced for >= 40%

· atorvastatin 80mg for secondary prevention

From <https://www.passmedicine.com/question/questions.php?q=0>

21 December 2020

21:54

Warfarin: management of high INR

The following is based on the BNF guidelines, which in turn take into account the British Committee for Standards in Haematology (BCSH) guidelines.

Situation	Management
Major bleeding	Stop warfarin Give intravenous vitamin K 5mg Prothrombin complex concentrate - if not available then FFP*
INR > 8.0 Minor bleeding	Stop warfarin Give intravenous vitamin K 1-3mg Repeat dose of vitamin K if INR still too high after 24 hours Restart warfarin when INR < 5.0
INR > 8.0 No bleeding	Stop warfarin Give vitamin K 1-5mg by mouth, using the intravenous preparation orally Repeat dose of vitamin K if INR still too high after 24 hours Restart when INR < 5.0
INR 5.0-8.0 Minor bleeding	Stop warfarin Give intravenous vitamin K 1-3mg Restart when INR < 5.0
INR 5.0-8.0 No bleeding	Withhold 1 or 2 doses of warfarin Reduce subsequent maintenance dose

*as FFP can take time to defrost prothrombin complex concentrate should be considered in cases of intracranial haemorrhage

From <https://www.passmedicine.com/question/questions.php?q=0>

22 December 2020

17:56

ECG: coronary territories

The table below shows the correlation between ECG changes and coronary territories:

	ECG changes	Coronary artery
Anteroseptal	V1-V4	Left anterior descending
Inferior	II, III, aVF	Right coronary
Anterolateral	V4-6, I, aVL	Left anterior descending or left circumflex
Lateral	I, aVL +/- V5-6	Left circumflex
Posterior	Tall R waves V1-2	Usually left circumflex, also right coronary

It should be remembered that a new left bundle branch block (LBBB) may point towards a diagnosis of acute coronary syndrome.

Diagram showing the correlation between ECG changes and coronary territories in acute coronary syndrome

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From <https://www.passmedicine.com/question/questions.php?q=0>

21 December 2020

21:54

Atrial fibrillation: rate control and maintenance of sinus rhythm

The Royal College of Physicians and NICE published guidelines on the management of atrial fibrillation (AF) in 2006. The following is also based on the joint American Heart Association (AHA), American College of Cardiology (ACC) and European Society of Cardiology (ESC) 2012 guidelines

Medication

Agents used to control rate in patients with atrial fibrillation

· beta-blockers

o a common contraindication for beta-blockers is asthma

· calcium channel blockers

· digoxin

o not considered first-line anymore as they are less effective at controlling the heart rate during exercise

o however, they are the preferred choice if the patient has coexistent heart failure

Agents used to maintain sinus rhythm in patients with a history of atrial fibrillation

· sotalol

· amiodarone

· flecainide

· others (less commonly used in UK): disopyramide, dofetilide, procainamide, propafenone, quinidine

The table below indicates some of the factors which may be considered when considering either a rate control or rhythm control strategy

Factors favouring rate control	Factors favouring rhythm control
Older than 65 years History of ischaemic heart disease	Younger than 65 years Symptomatic First presentation Lone AF or AF secondary to a corrected precipitant (e.g. Alcohol) Congestive heart failure

Catheter ablation

NICE recommends the use of catheter ablation for those with AF who have not responded to or wish to avoid, antiarrhythmic medication.

Technical aspects

· the aim is to ablate the faulty electrical pathways that are resulting in atrial fibrillation. This is typically due to aberrant electrical activity between the pulmonary veins and left atrium

· the procedure is performed percutaneously, typically via the groin

· both radiofrequency (uses heat generated from medium frequency alternating current) and cryotherapy can be used to ablate the tissue

Anticoagulation

· should be used 4 weeks before and during the procedure

· it should be remember that catheter ablation controls the rhythm but does not reduce the stroke risk, even if patients remain in sinus rhythm. Therefore, patients still require anticoagulation as per there CHA2DS2-VASc score

o if score = 0: 2 months anticoagulation recommended

o if score > 1: longterm anticoagulation recommended

Outcome

· notable complications include

o cardiac tamponade

o stroke

o pulmonary valve stenosis

· success rate

o around 50% of patients experience an early recurrence (within 3 months) of AF that often resolves spontaneously

o longer term, after 3 years, around 55% of patients who've had a single procedure remain in sinus rhythm. Of patient who've undergone multiple procedures around 80% are in sinus rhythm

From <https://www.passmedicine.com/question/questions.php?q=0>

Wednesday, 23 December 2020

01:07

ACE inhibitors

Angiotensin-converting enzyme (ACE) inhibitors are now the established first-line treatment in younger patients with hypertension and are also extensively used to treat heart failure. They are known to be less effective in treating hypertensive Afro-Caribbean patients. ACE inhibitors are also used to treat diabetic nephropathy and have a role in the secondary prevention of ischaemic heart disease.

Mechanism of action:

· inhibit the conversion angiotensin I to angiotensin II

· ACE inhibitors are activated by phase 1 metabolism in the liver

Side-effects:

· cough

o occurs in around 15% of patients and may occur up to a year after starting treatment

o thought to be due to increased bradykinin levels

· angioedema: may occur up to a year after starting treatment

· hyperkalaemia

· first-dose hypotension: more common in patients taking diuretics

Cautions and contraindications

· pregnancy and breastfeeding - avoid

· renovascular disease - may result in renal impairment

· aortic stenosis - may result in hypotension

· hereditary of idiopathic angioedema

· specialist advice should be sought before starting ACE inhibitors in patients with a potassium >= 5.0 mmol/L

Interactions

· patients receiving high-dose diuretic therapy (more than 80 mg of furosemide a day)

o significantly increases the risk of hypotension

Monitoring

· urea and electrolytes should be checked before treatment is initiated and after increasing the dose

o a rise in the creatinine and potassium may be expected after starting ACE inhibitors

o acceptable changes are an increase in serum creatinine, up to 30% from baseline and an increase in potassium up to 5.5 mmol/l.

o significant renal impairment may occur in patients who have undiagnosed bilateral renal artery stenosis

Flow chart showing the management of hypertension as per current NICE guideliness

22 December 2020

16:57

Hypertension: diagnosis

NICE published updated guidelines for the management of hypertension in 2019. This builds on the significant guidelines released in 2011 that recommended:

· classifying hypertension into stages

· recommending the use of ambulatory blood pressure monitoring (ABPM) and home blood pressure monitoring (HBPM)

Flow chart showing simplified schematic for diagnosis hypertension following NICE guidelines

Why were these guidelines needed?

It has long been recognised by doctors that there is a subgroup of patients whose blood pressure climbs 20 mmHg whenever they enter a clinical setting, so called 'white coat hypertension'. If we just rely on clinic readings then such patients may be diagnosed as having hypertension when, the vast majority of the time, their blood pressure is normal.

This has led to the use of both ambulatory blood pressure monitoring (ABPM) and home blood pressure monitoring (HBPM) to confirm the diagnosis of hypertension. These techniques allow a more accurate assessment of a patients' overall blood pressure. Not only does this help prevent overdiagnosis of hypertension - ABPM has been shown to be a more accurate predictor of cardiovascular events than clinic readings.

Blood pressure classification

This becomes relevant later in some of the management decisions that NICE advocate.

Stage	Criteria
Stage 1 hypertension	Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg
Stage 2 hypertension	Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg
Severe hypertension	Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 120 mmHg

Diagnosing hypertension

Firstly, NICE recommend measuring blood pressure in both arms when considering a diagnosis of hypertension.

If the difference in readings between arms is more than 20 mmHg then the measurements should be repeated. If the difference remains > 20 mmHg then subsequent blood pressures should be recorded from the arm with the higher reading.

It should of course be remember that there are pathological causes of unequal blood pressure readings from the arms, such as supravalvular aortic stenosis. It is therefore prudent to listen to the heart sounds if a difference exists and further investigation if a very large difference is noted.

NICE also recommend taking a second reading during the consultation, if the first reading is > 140/90 mmHg. The lower reading of the two should determine further management.

NICE suggest offering ABPM or HBPM to any patient with a blood pressure >= 140/90 mmHg.

If the blood pressure is >= 180/120 mmHg:

· admit for specialist assessment if:

o signs of retinal haemorrhage or papilloedema (accelerated hypertension) or

o life-threatening symptoms such as new-onset confusion, chest pain, signs of heart failure, or acute kidney injury

· NICE also recommend referral if a phaeochromocytoma is suspected (labile or postural hypotension, headache, palpitations, pallor and diaphoresis)

· if none of the above then arrange urgent investigations for end-organ damage (e.g. bloods, urine ACR, ECG)

o if target organ damage is identified, consider starting antihypertensive drug treatment immediately, without waiting for the results of ABPM or HBPM.

o if no target organ damage is identified, repeat clinic blood pressure measurement within 7 days

Ambulatory blood pressure monitoring (ABPM)

· at least 2 measurements per hour during the person's usual waking hours (for example, between 08:00 and 22:00)

· use the average value of at least 14 measurements

If ABPM is not tolerated or declined HBPM should be offered.

Home blood pressure monitoring (HBPM)

· for each BP recording, two consecutive measurements need to be taken, at least 1 minute apart and with the person seated

· BP should be recorded twice daily, ideally in the morning and evening

· BP should be recorded for at least 4 days, ideally for 7 days

· discard the measurements taken on the first day and use the average value of all the remaining measurements

Interpreting the results

ABPM/HBPM >= 135/85 mmHg (i.e. stage 1 hypertension)

· treat if < 80 years of age AND any of the following apply; target organ damage, established cardiovascular disease, renal disease, diabetes or a 10-year cardiovascular risk equivalent to 10% or greater

· in 2019, NICE made a further recommendation, suggesting that we should 'consider antihypertensive drug treatment in addition to lifestyle advice for adults aged under 60 with stage 1 hypertension and an estimated 10-year risk below 10%. '. This seems to be due to evidence that QRISK may underestimate the lifetime probability of developing cardiovascular disease

ABPM/HBPM >= 150/95 mmHg (i.e. stage 2 hypertension)

· offer drug treatment regardless of age

From <https://www.passmedicine.com/question/questions.php?q=0>

21 December 2020

21:47

Beta-blockers

Beta-blockers are an important class of drug used mainly in the management of cardiovascular disorders.

Indications

· angina

· post-myocardial infarction

· heart failure: beta-blockers were previously avoided in heart failure but there is now strong evidence that certain beta-blockers improve both symptoms and mortality

· arrhythmias: beta-blockers have now replaced digoxin as the rate-control drug of choice in atrial fibrillation

· hypertension: the role of beta-blockers has diminished in recent years due to a lack of evidence in terms of reducing stroke and myocardial infarction.

· thyrotoxicosis

· migraine prophylaxis

· anxiety

Examples

· atenolol

· propranolol: one of the first beta-blockers to be developed. Lipid soluble therefore crosses the blood-brain barrier

Side-effects

· bronchospasm

· cold peripheries

· fatigue

· sleep disturbances, including nightmares

· erectile dysfunction

Contraindications

· uncontrolled heart failure

· asthma

· sick sinus syndrome

· concurrent verapamil use: may precipitate severe bradycardia

From <https://www.passmedicine.com/review/textbook.php?s=#>

21 December 2020

21:48

Peri-arrest rhythms: tachycardia

The 2015 Resuscitation Council (UK) guidelines have simplified the advice given for the management of peri-arrest tachycardias. Separate algorithms for the management of broad-complex tachycardia, narrow complex tachycardia and atrial fibrillation have been replaced by one unified treatment algorithm

Following basic ABC assessment, patients are classified as being stable or unstable according to the presence of any adverse signs:

· shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness

· syncope

· myocardial ischaemia

· heart failure

If any of the above adverse signs are present then synchronised DC shocks should be given

Treatment following this is given according to whether the QRS complex is narrow or broad and whether the rhythm is regular or irregular. The full treatment algorithm can be found at the Resuscitation Council website, below is a very limited summary:

Broad-complex tachycardia

Regular

· assume ventricular tachycardia (unless previously confirmed SVT with bundle branch block)

· loading dose of amiodarone followed by 24 hour infusion

Irregular

· 1. AF with bundle branch block - treat as for narrow complex tachycardia

· 2. Polymorphic VT (e.g. Torsade de pointes) - IV magnesium

Narrow-complex tachycardia

Regular

· vagal manoeuvres followed by IV adenosine

· if above unsuccessful consider diagnosis of atrial flutter and control rate (e.g. Beta-blockers)

Irregular

· probable atrial fibrillation

· if onset < 48 hr consider electrical or chemical cardioversion

· rate control (e.g. Beta-blocker or digoxin) and anticoagulation

From <https://www.passmedicine.com/review/textbook.php?s=#>

21 December 2020

22:38

Acute coronary syndrome: initial management

Acute coronary syndrome (ACS) is a very common and important presentation in medicine. The management of ACS has evolved over recent years, with the development of new drugs and procedures such as primary coronary intervention (PCI).

Emergency departments often have their own protocols based around local factors such as availability of PCI and hospital drug formularies. The following is based around the 2020 update to the NICE ACS guidelines.

Acute coronary syndrome can be classified as follows:

· ST-elevation myocardial infarction (STEMI): ST-segment elevation + elevated biomarkers of myocardial damage

· non ST-elevation myocardial infarction (NSTEMI): ECG changes but no ST-segment elevation + elevated biomarkers of myocardial damage

· unstable angina

The management of ACS depends on the particular subtype. NICE management guidance groups the patients into two groups:

· 1. STEMI

· 2. NSTEM/unstable angina

Common management of all patients with ACS

· aspirin 300mg

· oxygen should only be given if the patient has oxygen saturations < 94% in keeping with British Thoracic Society oxygen therapy guidelines

· morphine should only be given for patients with severe pain

o previously IV morphine was given routinely

o evidence, however, suggests that this may be associated with adverse outcomes

· nitrates

o can be given either sublingually or intravenously

o useful if the patient has ongoing chest or hypertension

o should be used in caution if patient hypotensive

The next step in managing a patient with suspected ACS is to determine whether they meet the ECG criteria for STEMI. It is, of course, important to recognise that these should be interpreted in the context of the clinical history.

STEMI criteria

· clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of:

o 2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years

o 1.5 mm ST elevation in V2-3 in women

o 1 mm ST elevation in other leads

o new LBBB (LBBB should be considered new unless there is evidence otherwise)

Management of STEMI

Once a STEMI has been confirmed the first step is to immediately assess eligibility for coronary reperfusion therapy. There are two types of coronary reperfusion therapy:

· primary coronary intervention

o should be offered if the presentation is within 12 hours of onset of symptoms AND PCI can be delivered within 120 minutes of the time when thrombolysis could have been given (i.e. consider thrombolysis if there is a significant delay in being able to provide PCI)

o if patients present after 12 hours and still have evidence of ongoing ischaemia then PCI should still be considered

o drug-eluting stents are now used. Previously 'bare-metal' stents were sometimes used but have higher rates of restenosis

o radial access is preferred to femoral access

· thrombolysis

o should be offered within 12 hours of onset of symptoms if primary PCI cannot be delivered within 120 minutes of the time when thrombolysis could have been given

o a practical example may be a patient who presents with a STEMI to a small district general hospital (DGH) which does not have facilities for PCI. If they cannot be transferred to a larger hospital for PCI within 120 minutes then thrombolysis should be given. If the patient's ECG taken 90 minutes after thrombolysis failed to show resolution of the ST elevation then they would then require transfer for PCI

If patients are eligible this should be offered as soon as possible.

Primary coronary intervention for patients with STEMI

Further antiplatelet prior to PCI

· this is termed 'dual antiplatelet therapy', i.e. aspirin + another drug

· if the patient is not taking an oral anticoagulant: prasugrel

· if taking an oral anticoagulant: clopidogrel

Drug therapy during PCI

· patients undergoing PCI with radial access:

o unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI) - this is the action of using a GPI during the procedure when it was not intended from the outset, e.g. because of worsening or persistent thrombus

· patients undergoing PCI with femoral access:

o bivalirudin with bailout GPI

Other procedures during PCI

· thrombus aspiration, but not mechanical thrombus extraction, should be considered

· complete revascularisation should be considered for patients with multivessel coronary artery disease without cardiogenic shock

Thrombolysis for patients with STEMI

Thrombolysis used to be the only form of coronary reperfusion therapy available. However, it is used much less commonly now given the widespread availability of PCI.

The contraindications to thrombolysis and other factors are described in other notes.

Patients undergoing thrombolysis should also be given an antithrombin drug.

If patients have persistent myocardial ischaemia following thrombolysis then PCI should be considered.

Management of NSTEMI/unstable

The management of NSTEMI/unstable is complicated and depends on individual patient factors and a risk assessment. The summary below provides an overview but the full NICE guidelines should be reviewed for further details.

Further drug therapy

· antithrombin treatment

o fondaparinux should be offered to patients who are not at a high risk of bleeding and who are not having angiography immediately

o if immediate angiography is planned or a patients creatinine is > 265 µmol/L then unfractionated heparin should be given

Risk assessment

The Global Registry of Acute Coronary Events (GRACE) is the most widely used tool for risk assessment. It can be calculated using online tools and takes into account the following factors:

· age

· heart rate, blood pressure

· cardiac (Killip class) and renal function (serum creatinine)

· cardiac arrest on presentation

· ECG findings

· troponin levels

This results in the patient being risk stratified as follows:

Predicted 6‑month mortality	Risk of future adverse cardiovascular events
1.5% or below	Lowest
> 1.5% to 3.0%	Low
> 3.0% to 6.0%	Intermediate
> 6.0% to 9.0%	High
over 9.0%	Highest

Based on this risk assessment key decisions are made regarding whether a patient has coronary angiography (with follow-on PCI if necessary) or has conservative management. The detailed pros/cons of this descision are covered in other notes.

Which patients with NSTEMI/unstable angina should have a coronary angiography (with follow-on PCI if necessary)?

· immediate: patient who are clinically unstable (e.g. hypotensive)

· within 72 hours: patients with a GRACE score > 3% i.e. those at immediate, high or highest risk

· coronary angiography should also be considered for patients is ischaemia is subsequently experienced after admission

Primary coronary intervention for patients with NSTEMI/unstable angina

Further drug therapy

· unfractionated heparin should be given regardless of whether the patient has had fondaparinux or not

· further antiplatelet ('dual antiplatelet therapy', i.e. aspirin + another drug) prior to PCI

o if the patient is not taking an oral anticoagulant: prasugrel or ticagrelor

o if taking an oral anticoagulant: clopidogrel

Conservative management for patients with NSTEMI/unstable angina

Further drug therapy

· further antiplatelet ('dual antiplatelet therapy', i.e. aspirin + another drug)

o if the patient is not at a high-risk of bleeding: ticagrelor

o if the patient is at a high-risk of bleeding: clopidogrel

From <https://www.passmedicine.com/question/questions.php?q=0>

22 December 2020

17:22

Coarctation of the aorta

Coarctation of the aorta describes a congenital narrowing of the descending aorta.

Overview

· more common in males (despite association with Turner's syndrome)

Features

· infancy: heart failure

· adult: hypertension

· radio-femoral delay

· mid systolic murmur, maximal over back

· apical click from the aortic valve

· notching of the inferior border of the ribs (due to collateral vessels) is not seen in young children

Associations

· Turner's syndrome

· bicuspid aortic valve

· berry aneurysms

· neurofibromatosis

From <https://www.passmedicine.com/question/questions.php?q=0>

21 December 2020

22:49

Atrial fibrillation: anticoagulation

NICE updated their guidelines on the management of atrial fibrillation (AF) in 2014. They suggest using the CHA2DS2-VASc score to determine the most appropriate anticoagulation strategy. This scoring system superceded the CHADS2 score.

	Risk factor	Points
C	Congestive heart failure	1
H	Hypertension (or treated hypertension)	1
A2	Age >= 75 years	2
	Age 65-74 years	1
D	Diabetes	1
S2	Prior Stroke or TIA	2
V	Vascular disease (including ischaemic heart disease and peripheral arterial disease)	1
S	Sex (female)	1

The table below shows a suggested anticoagulation strategy based on the score:

Score	Anticoagulation
0	No treatment
1	Males: Consider anticoagulation Females: No treatment (this is because their score of 1 is only reached due to their gender)
2 or more	Offer anticoagulation

Remember that if a CHA2DS2-VASc score suggests no need for anticoagulation it is important to ensure a transthoracic echocardiogram has been done to exclude valvular heart disease, which in combination with AF is an absolute indication for anticoagulation.

NICE recommend that we offer patients a choice of anticoagulation, including warfarin and the novel oral anticoagulants (NOACs). There are complicated rules surrounding which NOAC is licensed for which risk factor - these can be found in the NICE guidelines. Aspirin is no longer recommended for reducing stroke risk in patients with AF

Doctors have always thought carefully about the risk/benefit profile of starting someone on warfarin. A history of falls, old age, alcohol excess and a history of previous bleeding are common things that make us consider whether warfarinisation is in the best interests of the patient. NICE now recommend we formalise this risk assessment using the HASBLED scoring system.

	Risk factor	Points
H	Hypertension, uncontrolled, systolic BP > 160 mmHg	1
A	Abnormal renal function (dialysis or creatinine > 200) Or Abnormal liver function (cirrhosis, bilirubin > 2 times normal, ALT/AST/ALP > 3 times normal	1 for any renal abnormalities 1 for any liver abnormalities
S	Stroke, history of	1
B	Bleeding, history of bleeding or tendency to bleed	1
L	Labile INRs (unstable/high INRs, time in therapeutic range < 60%)	1
E	Elderly (> 65 years)	1
D	Drugs Predisposing to Bleeding (Antiplatelet agents, NSAIDs) Or Alcohol Use (>8 drinks/week)	1 for drugs 1 for alcohol

There are no formal rules on how we act on the HAS-BLED score although a score of >= 3 indicates a 'high risk' of bleeding, defined as intracranial haemorrhage, hospitalisation, haemoglobin decrease >2 g/L, and/or transfusion.

From <https://www.passmedicine.com/question/questions.php?q=0>

For anyone struggling with remember CHA2DS2-VASc, I find SADCHAVS easier to remember. The top two in the list are the 2 point scores, and the rest 1.

Stroke 2

Age >75 2

Diabetes 1

Congestive Heart Failure 1

HTN 1

Age >65 1

Vascular Hx 1

Sex Female 1

From <https://www.passmedicine.com/question/questions.php?q=0>

22 December 2020

18:06

Infective endocarditis

The strongest risk factor for developing infective endocarditis is a previous episode of endocarditis. The following types of patients are affected:

· previously normal valves (50%, typically acute presentation)

o the mitral valve is most commonly affected

· rheumatic valve disease (30%)

· prosthetic valves

· congenital heart defects

· intravenous drug users (IVDUs, e.g. typically causing tricuspid lesion)

· others: recent piercings

Causes

· historically Streptococcus viridans was the most common cause of infective endocarditis. This is no longer the case, except in developing countries. Staphylococcus aureus is now the most common cause of infective endocarditis. Staphylococcus aureus is also particularly common in acute presentation and IVDUs

· coagulase-negative Staphylococci such as Staphylococcus epidermidis commonly colonize indwelling lines and are the most cause of endocarditis in patients following prosthetic valve surgery, usually the result of perioperative contamination. After 2 months the spectrum of organisms which cause endocarditis return to normal (i.e. Staphylococcus aureus is the most common cause)

· Streptococcus viridans still accounts for around 20% of cases. Technically Streptococcus viridans is a pseudotaxonomic term, referring to viridans streptococci, rather than a particular organism. The two most notable viridans streptococci are Streptococcus mitis and Streptococcus sanguinis. They are both commonly found in the mouth and in particular dental plaque so endocarditis caused by these organisms is linked with poor dental hygiene or following a dental procedure

· Streptococcus bovis is associated with colorectal cancer

o the subtype Streptococcus gallolyticus is most linked with colorectal cancer

· non-infective: systemic lupus erythematosus (Libman-Sacks), malignancy: marantic endocarditis

Culture negative causes

· prior antibiotic therapy

· Coxiella burnetii

· Bartonella

· Brucella

· HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)

*Lancet 2016; 387: 882-93 Infective Endocarditis

From <https://www.passmedicine.com/question/questions.php?q=0>

21 December 2020

21:47

Murmurs

Ejection systolic

· louder on expiration

o aortic stenosis

o hypertrophic obstructive cardiomyopathy

· louder on inspiration

o pulmonary stenosis

o atrial septal defect

· also: tetralogy of Fallot

Holosystolic (pansystolic)

· mitral/tricuspid regurgitation (high-pitched and 'blowing' in character)

o tricuspid regurgitation becomes louder during inspiration, unlike mitral stenosis

o during inspiration, the venous blood flow into the right atrium and ventricle are increased → increases the stroke volume of the right ventricle during systole

· ventricular septal defect ('harsh' in character)

Late systolic

· mitral valve prolapse

· coarctation of aorta

Early diastolic

· aortic regurgitation (high-pitched and 'blowing' in character)

· Graham-Steel murmur (pulmonary regurgitation, again high-pitched and 'blowing' in character)

Mid-late diastolic

· mitral stenosis ('rumbling' in character)

· Austin-Flint murmur (severe aortic regurgitation, again is 'rumbling' in character)

Continuous machine-like murmur

· patent ductus arteriosus

Image sourced from Wikipedia

From <https://www.passmedicine.com/review/textbook.php?s=#>

22 December 2020

17:38

Supraventricular tachycardia

Whilst strictly speaking the term supraventricular tachycardia (SVT) refers to any tachycardia that is not ventricular in origin the term is generally used in the context of paroxysmal SVT. Episodes are characterised by the sudden onset of a narrow complex tachycardia, typically an atrioventricular nodal re-entry tachycardia (AVNRT). Other causes include atrioventricular re-entry tachycardias (AVRT) and junctional tachycardias.

Acute management

· vagal manoeuvres: e.g. Valsalva manoeuvre, carotid sinus massage

· intravenous adenosine 6mg → 12mg → 12mg: contraindicated in asthmatics - verapamil is a preferable option

· electrical cardioversion

Prevention of episodes

· beta-blockers

· radio-frequency ablation

From <https://www.passmedicine.com/question/questions.php?q=0>

21 December 2020

22:04

Syncope

Syncope may be defined as a transient loss of consciousness due to global cerebral hypoperfusion with rapid onset, short duration and spontaneous complete recovery. Note how this definition excludes other causes of collapse such as epilepsy.

The European Society of Cardiology published guidelines in 2009 on the investigation and management of syncope. They suggested the following classification:

Reflex syncope (neurally mediated)

· vasovagal: triggered by emotion, pain or stress. Often referred to as 'fainting'

· situational: cough, micturition, gastrointestinal

· carotid sinus syncope

Orthostatic syncope

· primary autonomic failure: Parkinson's disease, Lewy body dementia

· secondary autonomic failure: e.g. Diabetic neuropathy, amyloidosis, uraemia

· drug-induced: diuretics, alcohol, vasodilators

· volume depletion: haemorrhage, diarrhoea

Cardiac syncope

· arrhythmias: bradycardias (sinus node dysfunction, AV conduction disorders) or tachycardias (supraventricular, ventricular)

· structural: valvular, myocardial infarction, hypertrophic obstructive cardiomyopathy

· others: pulmonary embolism

Reflex syncope is the most common cause in all age groups although orthostatic and cardiac causes become progressively more common in older patients.

Evaluation

· cardiovascular examination

· postural blood pressure readings: a symptomatic fall in systolic BP > 20 mmHg or diastolic BP > 10 mmHg or decrease in systolic BP < 90 mmHg is considered diagnostic

· ECG

· carotid sinus massage

· tilt table test

· 24 hour ECG

From <https://www.passmedicine.com/question/questions.php?q=0>

22 December 2020

16:25

Atrial fibrillation: cardioversion

There are two scenarios where cardioversion may be used in atrial fibrillation:

· electrical cardioversion as an emergency if the patient is haemodynamically unstable

· electrical or pharmacological cardioversion as an elective procedure where a rhythm control strategy is preferred.

The notes below refer to cardioversion being used in the elective scenario for rhythm control. The wording of the 2014 NICE guidelines is as follows:

offer rate or rhythm control if the onset of the arrhythmia is less than 48 hours, and start rate control if it is more than 48 hours or is uncertain

Onset < 48 hours

If the atrial fibrillation (AF) is definitely of less than 48 hours onset patients should be heparinised. Patients who have risk factors for ischaemic stroke should be put on lifelong oral anticoagulation. Otherwise, patients may be cardioverted using either:

· electrical - 'DC cardioversion'

· pharmacology - amiodarone if structural heart disease, flecainide or amiodarone in those without structural heart disease

Following electrical cardioversion if AF is confirmed as being less than 48 hours duration then further anticoagulation is unnecessary

Onset > 48 hours

If the patient has been in AF for more than 48 hours then anticoagulation should be given for at least 3 weeks prior to cardioversion. An alternative strategy is to perform a transoesophageal echo (TOE) to exclude a left atrial appendage (LAA) thrombus. If excluded patients may be heparinised and cardioverted immediately.

NICE recommend electrical cardioversion in this scenario, rather than pharmacological.

If there is a high risk of cardioversion failure (e.g. Previous failure or AF recurrence) then it is recommend to have at least 4 weeks amiodarone or sotalol prior to electrical cardioversion

Following electrical cardioversion patients should be anticoagulated for at least 4 weeks. After this time decisions about anticoagulation should be taken on an individual basis depending on the risk of recurrence

From <https://www.passmedicine.com/question/questions.php?q=0>

22 December 2020

16:20

Cardiac tamponade

Cardiac tamponade is characterized by the accumulation of pericardial fluid under pressure.

Classical features - Beck's triad:

· hypotension

· raised JVP

· muffled heart sounds

Other features:

· dyspnoea

· tachycardia

· an absent Y descent on the JVP - this is due to the limited right ventricular filling

· pulsus paradoxus - an abnormally large drop in BP during inspiration

· Kussmaul's sign - much debate about this

· ECG: electrical alternans

The key differences between constrictive pericarditis and cardiac tamponade are summarised in the table below:

	Cardiac tamponade	Constrictive pericarditis
JVP	Absent Y descent	X + Y present
Pulsus paradoxus	Present	Absent
Kussmaul's sign	Rare	Present
Characteristic features		Pericardial calcification on CXR

A commonly used mnemonic to remember the absent Y descent in cardiac tamponade is TAMponade = TAMpaX

Management

· urgent pericardiocentesis

© Image used on license from Dr Smith, University of Minnesota

An ECG demonstrating electrical alternans. Note the alternation of QRS complex amplitude between beats.

From <https://www.passmedicine.com/question/questions.php?q=0>

21 December 2020

22:46

Diabetes mellitus: hypertension management

Patient diabetes mellitus have traditionally had their blood pressure controlled more aggressively to help reduce their overall cardiovascular risk. However, a 2013 Cochrane review casted doubt on the wisdom of lower blood pressure targets for patients with diabetes. It compared patients who had tight blood pressure control (targets < 130/85 mmHg) with more relaxed control (< 140-160/90-100 mmHg). Patients who were more tightly controlled had a slightly reduced rate of stroke but otherwise outcomes were not significantly different.

In light of this, NICE recommends a blood pressure target of < 140/90 mmHg for type 2 diabetics, the same as for patients without diabetes.

For patients with type 1 diabetes, NICE recommends:

Intervention levels for recommending blood pressure management should be 135/85 mmHg unless the adult with type 1 diabetes has albuminuria or 2 or more features of metabolic syndrome, in which case it should be 130/80 mmHg

Because ACE-inhibitors have a renoprotective effect in diabetes they are the first-line antihypertensives recommended for NICE. Patients of African or Caribbean family origin should be offered an ACE-inhibitor plus either a thiazide diuretic or calcium channel blocker. Further management then reverts to that of non-diabetic patients, as discussed earlier in the module.

Remember than autonomic neuropathy may result in more postural symptoms in patients taking antihypertensive therapy.

The routine use of beta-blockers in uncomplicated hypertension should be avoided, particularly when given in combination with thiazides, as they may cause insulin resistance, impair insulin secretion and alter the autonomic response to hypoglycaemia.

From <https://www.passmedicine.com/question/questions.php?q=0>

21 December 2020

21:47

Myocardial infarction: STEMI management

A number of studies over the past 10 years have provided an evidence for the management of ST-elevation myocardial infarction (STEMI)

In the absence of contraindications, all patients should be given

· aspirin

· P2Y12-receptor antagonist. Clopidogrel was the first P2Y12-receptor antagonist to be widely used but now ticagrelor is often favoured as studies have shown improved outcomes compared to clopidogrel, but at the expense of slightly higher rates of bleeding. This approached is supported in SIGN's 2016 guidelines. They also recommend that prasugrel (another P2Y12-receptor antagonist) could be considered if the patient is going to have a percutaneous coronary intervention

· unfractionated heparin is usually given for patients who're are going to have a PCI. Alternatives include low-molecular weight heparin

NICE suggest the following in terms of oxygen therapy:

· do not routinely administer oxygen, but monitor oxygen saturation using pulse oximetry as soon as possible, ideally before hospital admission. Only offer supplemental oxygen to:

· people with oxygen saturation (SpO2) of less than 94% who are not at risk of hypercapnic respiratory failure, aiming for SpO2 of 94-98%

· people with chronic obstructive pulmonary disease who are at risk of hypercapnic respiratory failure, to achieve a target SpO2 of 88-92% until blood gas analysis is available.

Primary percutaneous coronary intervention (PCI) has emerged as the gold-standard treatment for STEMI but is not available in all centres. Thrombolysis should be performed in patients without access to primary PCI

With regards to thrombolysis:

· tissue plasminogen activator (tPA) has been shown to offer clear mortality benefits over streptokinase

· tenecteplase is easier to administer and has been shown to have non-inferior efficacy to alteplase with a similar adverse effect profile

An ECG should be performed 90 minutes following thrombolysis to assess whether there has been a greater than 50% resolution in the ST elevation

· if there has not been adequate resolution then rescue PCI is superior to repeat thrombolysis

· for patients successfully treated with thrombolysis PCI has been shown to be beneficial. The optimal timing of this is still under investigation

Glycaemic control in patients with diabetes mellitus

· in 2011 NICE issued guidance on the management of hyperglycaemia in acute coronary syndromes

· it recommends using a dose-adjusted insulin infusion with regular monitoring of blood glucose levels to glucose below 11.0 mmol/l

· intensive insulin therapy (an intravenous infusion of insulin and glucose with or without potassium, sometimes referred to as 'DIGAMI') regimes are not recommended routinely

From <https://www.passmedicine.com/review/textbook.php?s=#>

21 December 2020

21:47

Aortic dissection

Aortic dissection is a rare but serious cause of chest pain.

Pathophysiology

· tear in the tunica intima of the wall of the aorta

Associations

· hypertension: the most important risk factor

· trauma

· bicuspid aortic valve

· collagens: Marfan's syndrome, Ehlers-Danlos syndrome

· Turner's and Noonan's syndrome

· pregnancy

· syphilis

Features:

· chest pain: typically severe, radiates through to the back and 'tearing' in nature

· aortic regurgitation

· hypertension

· other features may result from the involvement of specific arteries. For example coronary arteries → angina, spinal arteries → paraplegia, distal aorta → limb ischaemia

· the majority of patients have no or non-specific ECG changes. In a minority of patients, ST-segment elevation may be seen in the inferior leads

Classification

Stanford classification

· type A - ascending aorta, 2/3 of cases

· type B - descending aorta, distal to left subclavian origin, 1/3 of cases

DeBakey classification

· type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally

· type II - originates in and is confined to the ascending aorta

· type III - originates in descending aorta, rarely extends proximally but will extend distally

© Image used on license from Radiopaedia

Stanford type A / DeBakey type I

© Image used on license from Radiopaedia

Stanford type A / DeBakey type II

© Image used on license from Radiopaedia

Stanford type B / DeBakey type III

From <https://www.passmedicine.com/review/textbook.php?s=#>

22 December 2020

17:03

Atrial flutter

Atrial flutter is a form of supraventricular tachycardia characterised by a succession of rapid atrial depolarisation waves.

ECG findings

· 'sawtooth' appearance

· as the underlying atrial rate is often around 300/min the ventricular or heart rate is dependent on the degree of AV block. For example if there is 2:1 block the ventricular rate will be 150/min

· flutter waves may be visible following carotid sinus massage or adenosine

Management

· is similar to that of atrial fibrillation although medication may be less effective

· atrial flutter is more sensitive to cardioversion however so lower energy levels may be used

· radiofrequency ablation of the tricuspid valve isthmus is curative for most patients

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From <https://www.passmedicine.com/question/questions.php?q=0>

21 December 2020

22:54

Mitral stenosis

It is said that the causes of mitral stenosis are rheumatic fever, rheumatic fever and rheumatic fever. Rarer causes that may be seen in the exam include mucopolysaccharidoses, carcinoid and endocardial fibroelastosis

Features

· mid-late diastolic murmur (best heard in expiration)

· loud S1, opening snap

· low volume pulse

· malar flush

· atrial fibrillation

Features of severe MS

· length of murmur increases

· opening snap becomes closer to S2

Chest x-ray

· left atrial enlargement may be seen

Echocardiography

· the normal cross sectional area of the mitral valve is 4-6 sq cm. A 'tight' mitral stenosis implies a cross sectional area of < 1 sq cm

© Image used on license from Radiopaedia

Chest x-ray from a patient with mitral stenosis. This patient has had a sternotomy and a prosthetic mitral valve. There is splaying of the carina with elevation of the left main bronchus, a double right heart border and cardiomegaly. The features are those of left atrial enlargement. Although the entire heart is enlarged, a double contour is seen through the right side of the heart. The more medial line is the enlarged left atrium (white dotted line) and the heart heart border is more lateral (blue dotted line).

From <https://www.passmedicine.com/question/questions.php?q=0>

22 December 2020

16:31

Cardiomyopathies: key points

The old classification of dilated, restricted and hypertrophic cardiomyopathy has been largely abandoned due to the high degree of overlap. The latest classification of cardiomyopathy by the WHO and American Heart Association reflect this.

The tables below shows a very limited set of exam related facts for the various cardiomyopathies:

Primary cardiomyopathies - predominately involving the heart

Genetic - both conditions listed below are autosomal dominant. An implantable cardioverter-defibrillator is often inserted to reduce the incidence of sudden cardiac death.

Type of cardiomyopathy	Selected points
Hypertrophic obstructive cardiomyopathy	Leading cause of sudden cardiac death in young athletes Usually due to a mutation in the gene encoding β-myosin heavy chain protein Common cause of sudden death Echo findings include MR, systolic anterior motion (SAM) of the anterior mitral valve and asymmetric septal hypertrophy
Arrhythmogenic right ventricular dysplasia	Right ventricular myocardium is replaced by fatty and fibrofatty tissue Around 50% of patients have a mutation of one of the several genes which encode components of desmosome ECG abnormalities in V1-3, typically T wave inversion. An epsilon wave is found in about 50% of those with ARV - this is best described as a terminal notch in the QRS complex

Mixed - rather confusingly most of the causes of dilated and restrictive cardiomyopathy are now listed separately in the 'secondary' causes. This category servers as a reminder that many patients will have a genetic predisposition to cardiomyopathy which is then triggered by the secondary process, hence the 'mixed' category

Type of cardiomyopathy	Selected causes/points
Dilated cardiomyopathy	Classic causes include · alcohol · Coxsackie B virus · wet beri beri · doxorubicin
Restrictive cardiomyopathy	Classic causes include · amyloidosis · post-radiotherapy · Loeffler's endocarditis

Familial restrictive cardiomyopathy demonstrates autosomal dominant inheritance in the majority of cases.

Acquired

Type of cardiomyopathy	Selected points
Peripartum cardiomyopathy	Typical develops between last month of pregnancy and 5 months post-partum More common in older women, greater parity and multiple gestations
Takotsubo cardiomyopathy	'Stress'-induced cardiomyopathy e.g. patient just found out family member dies then develops chest pain and features of heart failure Transient, apical ballooning of the myocardium Treatment is supportive

Secondary cardiomyopathies- pathological myocardial involvement as part of a generalized systemic disorder

Type of cardiomyopathy	Selected causes/points
Infective	Coxsackie B virus Chagas disease
Infiltrative	Amyloidosis
Storage	Haemochromatosis
Toxicity	Doxorubicin Alcoholic cardiomyopathy
Inflammatory (granulomatous)	Sarcoidosis
Endocrine	Diabetes mellitus Thyrotoxicosis Acromegaly
Neuromuscular	Friedreich's ataxia Duchenne-Becker muscular dystrophy Myotonic dystrophy
Nutritional deficiencies	Beriberi (thiamine)
Autoimmune	Systemic lupus erythematosis

From <https://www.passmedicine.com/question/questions.php?q=0>

Arrhythmogenic right ventricular cardiomyopathy is characterised by right ventricular  myocardium replacement by fatty and fibrofatty tissue.

Arrhythmogenic right ventricular cardiomyopathy in late stages may cause dilation of the ventricles but not initially.

From <https://mle.ncl.ac.uk/cases/page/18128/>

Progressive deterioration of AV block risk is high in myotonic muscular dystrophy.

Permanent pacemaker for AV block first degree

From <https://mle.ncl.ac.uk/cases/page/18128/>

Reversible cardiomyopathies: (not exhaustive)

Viral myocarditis

PVC-induced cardiomyopathy

Tachycardia cardiomyopathy

Alcohol cardiomyopathy

24 December 2020

13:09

ECG: ST elevation

Causes of ST elevation

· myocardial infarction

· pericarditis/myocarditis

· normal variant - 'high take-off'

· left ventricular aneurysm

· Prinzmetal's angina (coronary artery spasm)

· Takotsubo cardiomyopathy

· rare: subarachnoid haemorrhage

From <https://www.passmedicine.com/review/textbook.php?s=#>

22 December 2020

17:25

ECG: P wave changes

Increased P wave amplitude

· cor pulmonale

From <https://www.passmedicine.com/question/questions.php?q=0>

21 December 2020

22:35

ECG: T wave changes

Peaked T waves

· hyperkalaemia

· myocardial ischaemia

Inverted T waves

· myocardial ischaemia

· digoxin toxicity

· subarachnoid haemorrhage

· arrhythmogenic right ventricular cardiomyopathy

· pulmonary embolism ('S1Q3T3')

· Brugada syndrome

From <https://www.passmedicine.com/question/questions.php?q=0>

22 December 2020

17:13

Buerger's disease

Buerger's disease (also known as thromboangiitis obliterans) is a small and medium vessel vasculitis that is strongly associated with smoking.

Features

· extremity ischaemia

o intermittent claudication

o ischaemic ulcers

· superficial thrombophlebitis

· Raynaud's phenomenon

From <https://www.passmedicine.com/question/questions.php?q=0>

Categorized as Vasculitis: Highly inflammatory thrombus with sparing of vessel walls.

Common in young men

Tobacco use

Non Atherosclerotic/ Segmental

Small/medium sized arteries/veins

Upper/lower Extremities

Young smokers- 15-45 years old, 9:1 male

Presents with- foot claudication, rest pain/ digital ulcers, superficial phlebitis

Treatment-

Smoking cessation

Digital protection

Arterial pumping

Non-surgical candidate

Wound care

Auto amputation

Endothelin receptor antagonists

28 December 2020

22:03

Endothelin receptor antagonists decrease pulmonary vascular resistance. The aim of endothelin  receptor antagonist therapy is to reduce pulmonary vascular resistance and hence reduce the  strain on the right-sided cardiac chambers. Right ventricular failure is the commonest cause of  death in primary pulmonary hypertension.

From <https://mle.ncl.ac.uk/cases/page/18128/>

Catecholaminergic polymorphic ventricular

28 December 2020

22:02

HOCM is the most common cause of sudden cardiac death in young people.

Catecholaminergic polymorphic ventricular

Inherited cardiac disease associated with sudden cardiac death autosomal dominant with prevalence of 1:10,000.

Brugada

More common in South East Asia. Sodium channelopathy.

Arrhythmogenic right ventricular dysplasia

Fibro fatty infiltration of right ventricle. Cause of sudden death

Long QT

Inherited and acquired. Family history with inherited form. Usually preceded by history of recurrent syncopes. Severe forms may cause sudden deaths.

Prostacyclins

28 December 2020

22:05

Prostacyclins are used in the treatment of primary pulmonary hypertension.

Hydrochlorothiazide is not used to treat PAH but may be used for heart failure and systemic  hypertension.

Aspirin does not affect PAH.

Lisinopril and carvedilol are first line drugs for heart failure treatment.

From <https://mle.ncl.ac.uk/cases/page/18128/>

occupational asthma

28 December 2020

22:14

Industrial chemicals like isocyanates are the most common cause of occupational asthma.

From <https://mle.ncl.ac.uk/cases/page/18128/>

ICD implantation

28 December 2020

23:05

Obesity venous insufficiency

28 December 2020

23:08

Exertional dyspnoea walking up an incline is  likely due to morbid obesity.

diurnal variation to his ankle swelling, worse at night  compared to morning plus venous varicosities, probably secondary to obesity.

From <https://mle.ncl.ac.uk/cases/page/18128/>

Mitochrondrial cardiomyopathy

28 December 2020

23:13

Retinitis pigmentosa may be present

Maternal inheritance

Nuclear genes coding mitochondrial proteins may be mutated

Neuromuscular manifestations are often apparent

Diastolic dysfunction in hypertrophic cardiomyopathy

28 December 2020

23:14

Cause:

Increased LV stiffness

Impairment of ventricular relaxation

Compromised myocardial energy metabolism

Impairment of coronary blood flow

Sudden cardiac death with HCM

28 December 2020

23:15

Associations:

· Unexplained syncope

· History of premature SCD in a first-degree relative with hypertrophic cardiomyopathy

· Non-sustained ventricular tachycardia on Holter

· Previous history of cardiac arrest

Pulmonary hypertension Classification

28 December 2020

15:57

Defined as mean pulmonary artery pressure (mPAP) ≥ 20mmHg at rest (measured by right heart catheterisation)

Considered severe when:

· mPAP ≥35 mmHg

· mPAP ≥20 mmHg + elevated right atrial pressure

+/- cardiac index <2L/min/m²

Cardiac index-

· More accurate picture of heart function relative to individual body size

· Cardiac index (L/min/m²)

·

· Normal range 2.5-4.0 L/min/m²

· Minimum cardiac index of 2.0 L/ min/ m² required to maintain life without mechanical support

Risk factors-

· Family history of pulmonary arterial hypertension

· Congenital heart disease

· Connective tissue disease (systemic sclerosis, SLE)

· Drugs and toxins

· Aminorex, Methamphetamine, Fenfluramine

o Aminorex =a type of SSRI, stimulates weight loss

o Fenfluramine= appetite suppressant

· Human Immunodeficiency Virus (HIV)

· Mechanism not known

· Portal hypertension

Clinical classifications-

Group 1: Pulmonary Arterial Hypertension (PAH) with Pulmonary Artery Occlusion Pressure <15mmHg

· Idiopathic PAH

· Hereditary PAH

· Drug and toxin-induced PAH

PAH associated with

· Connective tissue disease

· HIV infection

· Portal hypertension

· Congenital Heart Disease

· Schistosomiasis

Group 2: Pulmonary Hypertension due to left heart disease

· Heart failure with preserved ejection fraction

· Heart failure with reduced ejection fraction

· Valvular heart diseases

Group 3: Pulmonary Hypertension due to lung diseases/ hypoxia

· Obstructive lung disease

· Restrictive lung disease

· Other lung disease with mixed restrictive/ obstructive pattern

· Developmental lung disorders

Group 4: Pulmonary Hypertension due to pulmonary artery obstructions

· Chronic thromboembolic pulmonary hypertension (CTEPH)

· Other pulmonary artery obstructions

Group 5: Pulmonary Hypertension with unclear/ multifactorial mechanism

· Systemic and metabolic disorders

· Others

· Complex congenital heart diseases

Investigation:

Gold standard: cardiac catheterisation.

Right heart pressure measurements are required via cardiac catheterisation.

Management:

Pulmonary arterial hypertension patients with negative response to vasodilator testing may be treated with prostacyclin analogues, endothelin receptor antagonists or phosphodiesterase inhibitors. Combination therapy is often necessary.

Pulmonary arterial hypertension patients with positive response to vasodilator testing are  treated with calcium channel blockers e.g.  nifedipine, felodipine.

Prostacyclin analogues

Iloprost, epoprostenol

Endothelin receptor antagonists (sentans)

Bosentan, ambrisentan

Phosphodiesterase inhibitor (afils)

Sildenafil, tadalafil, vardenafil

Pulmonary Arterial Hypertension (PAH)

29 December 2020

00:05

Problem comes from pulmonary artery

BMPR2 gene

Can be genetically passed on

Female sex important factor

Risk factors-

Collagen vascular disease

Congenital heart disease

Portal hypertension

HIV infection

Drugs and toxins

Pregnancy

Susceptibility- Abnormal BMPR2 gene + other genetic factors

Vascular injury-

Endothelial dysfunction- reduced nitric oxide synthase, reduced prostacyclin production, increased thromboxane production, increased endothelin 1 production

Vascular smooth muscle dysfunction- impaired voltage-gated potassium channel

Disease progression- loss of response to short acting vasodilator trial

Idiopathic Pulmonary Arterial Hypertension

29 December 2020

12:18

· Most common among group 1 PAH

· Female : Male = >3:1

· No known triggering factor

· Not associated with family history of PAH

· Pathology mainly in distal arteries

· Hypertrophy of tunica media

· Proliferation and fibrotic changes in tunica intima

· Thickened tunica adventitia with perivascular infiltrates, as well as complex and thrombotic lesions

· Pulmonary veins unaffected

Hereditary Pulmonary Arterial Hypertension

29 December 2020

12:18

· 6-10% patients with PH

· Female > Male

· Autosomal dominance inheritance with incomplete penetrance

· 20% carriers will develop disease

· BMPR2

· 1^st PAH-predisposing gene

· Regulates growth, differentiation and apoptosis of pulmonary artery endothelial and smooth muscle cells

· Associated with KCNK3 channelopathy

BMPR2 gene

· Most commonly associated genetic mutation in hereditary PAH

· Highly expressed in pulmonary vascular endothelium

· Forms complexes with ALK1/ ALK2 receptors

· Female sex important factor in penetrance of BMPR2 mutations

Pulmonary Hypertension due to left heart diseases

29 December 2020

12:27

Problems come from left side of the heart

Most common cause of Pulmonary hypertension

Backward transmission of Left Arterial pressure to the pulmonary vasculature leads to pulmonary vascular resistance (PVH)

Enlarged and thickened pulmonary veins, pulmonary capillary dilation

Alveolar hemorrhage, lymphatic and lymph node enlargement

Distal arteries may be affected by medial hypertrophy and intimal fibrosis

Trans pulmonary gradient mPAP-PAWP= <12mmHg

Primary or pathognomic vascular changes in arterial wall may be present

Pulmonary Hypertension due to lung disorders

29 December 2020

15:34

Problems come from the lungs

Chronic inflammation causing alveolar hypoxic + loss of capillaries d/t due to emphysema

Mechanical injury due to hyperinflation

Muscularization of small resistance vessels

Chronic Thromboembolic Pulmonary hypertension CTEPH

29 December 2020

15:55

Definition is based on findings described after 3 months of effective anti-coagulation to discriminate from acute

Pre-capillary PH and at least one segmental perfusion defect detected by V/Q scan, MDCT angiography, or Pulmonary angiography

Due to obstruction of major Pulmonary Artery by Pulmonary embolism which can be symptomatic or asymptomatic, acute or chronic

Pulmonary Arterial hypertension due to Multifactorial causes

29 December 2020

15:58

Chronic Haemolytic anaemia

Myeloproliferative disorders

Splenectomy

Sarcoidosis

Pulmonary LCH Langerhans cell histiocytosis

NF1

Gaucher's disease

Tumoral obstruction of Pulmonary Artery

CRF chronic renal failure?

Pulmonary Arterial Hypertension with Connective Tissue Disease

Maximum in Scleroderma patients

Long duration of disease > 8 years

Limited scleroderma> diffuse scleroderma

8-12% prevalence

Poor prognosis

Patient with limited scleroderma have the risk of developing progressive blood vessel narrowing in the lungs frequently in the absence of lung scarring and inflammation

Low DLCO<55% predicted - Diffusing Capacity for Carbon Monoxide

Forced Vital Capacity FVC%/ DLCO% >1.6

Anti-centromere

Antinuclear pattern on ANA

High resolution CT findings in scleroderma

Scarring and inflammation of lungs (ILD)- both diffuse and limited scleroderma

Lungs have no scar but larger blood vessels are dilated, typical of pulmonary arterial hypertension which is seen mainly in limited scleroderma

Pulmonary Arterial Hypertension - Portal hypertension

29 December 2020

16:08

6% of patients with Portal hypertension develop Pulmonary Arterial Hypertension

Problem for liver transplantation as PAH increases mortality during and after surgery

Poor prognosis as 3 year survival is only 40%

Females, autoimmune hepatitis have increased risk while HCV (Hep C virus) has decreased risk

Independent of the cause of the portal hypertension

Severity of underlying liver disease does not correlate with the severity of PAH

Hyperdynamic circulation and high CO lead to increased shear stress on Pulmonary Circulation

The histological abnormalities are similar to Idiopathic PAH

Portosystemic shunts may allow the shunting of ET-1, VIP, 5HT, TXA2, IL1 and escape metabolism

Pulmonary arterial hypertension associated with Congenital heart disease

29 December 2020

16:13

Right ventricular adaptive response

In Congenital heart disease du to very early onset of PAH-

Marked hypertrophy of Right ventricle

Sustain increased afterload with better right ventricle function than for many decades than those who develop PAH in later life

Survival of patient with Eisenmenger is better than those with Idiopathic PAH

Eisenmenger's syndrome describes the reversal of a left-to-right shunt in a congenital heart defect due to pulmonary hypertension. This occurs when an uncorrected left-to-right leads to remodeling of the pulmonary microvasculature, eventually causing obstruction to pulmonary blood and pulmonary hypertension.

Associated with

· ventricular septal defect

· atrial septal defect

· patent ductus arteriosus

Features

· original murmur may disappear

· cyanosis

· clubbing

· right ventricular failure

· haemoptysis, embolism

Management

· heart-lung transplantation is required

· Right ventricle adaptive response to early onset PAH

· Early onset PAH cause marked right ventricular hypertrophy

· Hypertrophied right ventricle can better sustain increased afterload compared to patients developing PAH in later life

· Survival of patient with Eisenmenger Syndrome better than patients with Idiopathic Pulmonary Arterial Hypertension

Pulmonary Veno-Occlusive Disease

29 December 2020

17:00

Most devastating form of PH

Median survival 84 fays

71% dead in 6 months

10% of PHs are PVOD

Luminal narrowing and occlusion of pulmonary veins

Difficult to distinguish from PH

-profound hypoxia at rest

-CT chest: septal thickening and ground glass

Vasodilators NOT used due to pulmonary oedema risk

LUNG TRANSPLANTATION management

Rare disease

Characterized pathologically by evidence of repeated pulmonary venous thrombosis

The characteristic histologic feature of pulmonary veno-occlusive disease is obstruction of pulmonary venules and veins by intima fibrosis; intravascular fibrous septa are nearly always present

Etiology of disease is unknown

Drugs given in IPAH is contraindicated here

Pulmonary oedema after giving PAH therapy is 1st clue

Pulmonary Hypertension symptoms

29 December 2020

17:12

Shortness of breath

Chest pain

Dizziness

Syncope

Fatigue

Oedema

Dry cough

Raynaud’s phenomenon (associated with CTDs) (connective tissue diseases)

Skin- Telangiectasias, Raynaud’s phenomena, Sclerodactyly (when associated with CTD)

Increased jugular venous pressure (JVP)

Hepatojugular reflux

Peripheral oedema +/- ascites

Heart sounds:

Accentuated split S2

Third heart sound present

Tricuspid regurgitation- heard best at left lower sternal border

Pulmonary Arterial Hypertension Screening, Investigation, Diagnosis and Assessment

29 December 2020

17:43

ECG screening- electrocardiogram not recommended

RV strain may show

Prognostic information

Right heart disease

May show right axis deviation

Insufficiently sensitive as a screening tool

Echocardiography screening- RV enlargement, decreased LV capacity size, abnormal septal configuration consistent with RV overload, marked dependence on atrial systole for ventricular filling

Right heart catheterization is MANDATORY to confirm and characterize disease

PAH is defined by

· mPAP >25mmHg at rest

· mPAP >30mmHg with exercise

· PCWP <15mmHg (Pulmonary Capillary Wedge Pressure= indirectly measure left atrial pressure)

· PVR >3 units (Pulmonary vascular resistance)

o Cardiac output is required to calculate PVR

Screening with CX-ray

Large central pulmonary arteries

Peripheral pruning

Enlarged right heart

Asymptomatic patients may have normal chest xray

May reveal underlying cause of PH

Ventilation perfusion lung scan- check perfusion defects

CTEPH- pulmonary angiography

Chronic thromboembolic pulmonary hypertension

Assess thrombus accessibility

Confirm diagnosis

Angiographic patterns- Web narrowing, post stenotic dilatation, proximal occlusion, pouch defects

cMRI-

Access RV morphology and function

RV systolic and diastolic dysfunction- poor prognostic indicator

Management of Pulmonary Hypertension

29 December 2020

17:54

Acute Vasoreactivity test- idiopathic, Hereditary, Drug induced

Vasoactive- CCB therapy, Calcium channel blocker

Non vasoactive

Low risk- oral monotherapy/ combo therapy

High risk- combo therapy including IV PC

Inadequate response= double/triple sequential therapy

Lung transplant

Therapy for PAH

Low level graded aerobic exercise- not heavy exertion, may provoke syncope

Oxygen supplementation

Sodium restricted diet

Routine immunization- influenza and pneumococcal pneumonia

Nitric oxide-

Inhaled form

Acts as direct smooth muscle relaxant via activation of guanylate cyclase system

Short therapeutic half-life

Ameliorates hypoxemia and lowers PVR by direct pulmonary vasodilatation

Specific measure for Idiopathic PAH-

Long term anticoagulation with warfarin 1.5.2.5 inr

Pulmonary vasodilators- calcium channel blockers, prostacyclin, nitric oxide pathway (PD5 inhib, ER antagonists)

Prostacyclin analogues

Iloprost, epoprostenol

Endothelin receptor antagonists (sentans)

Bosentan, ambrisentan

Phosphodiesterase inhibitor (afils)

Sildenafil, tadalafil, vardenafil

Non-vasoreactive patients-

Depends on WHO functional class

Class I

PAH specific agent e.g. PDE5I

Class II or III

Dual therapy e.g. endothelin receptor antagonist plus a PDE5I

Class IV

Combination therapy to include a parenteral prostainoid e.g. iv                 epoprostenol (alternatives: iv, sub-cut or inhaled treprostinil,                 inhaled iloprost)                       

Lung transplant indications-

New York Heart Association (NYHA) functional class III

or IV

Mean right atrial pressure >10mmHg

Mean pulmonary arterial pressure >50 mmHg

Failure to improve functionally despite medical therapy

Rapidly progressive disease

Cardiomyopathy Causes

29 December 2020

18:08

Morphologically and functionally abnormal myocardium

· In absence of any other diseases sufficient to explain the observed phenotype

Divided into Primary and Secondary Cardiomyopathy

Primary-

· Pathology predominantly involves the heart

· Examples:

· Dilated cardiomyopathy

· Hypertrophic cardiomyopathy

· Restrictive cardiomyopathy

· Arrhythmogenic right ventricular cardiomyopathy

· Obliterative cardiomyopathy

Secondary-

Dilated Cardiomyopathy

29 December 2020

18:19

systolic dysfunction + ventricular dilation

Autosomal Dominant inheritance

1:2500 prevalence

Presentation:

Heart failure

Cardiac arrythmia

Thromboembolism

Sudden death- family history obtained

Conduction defects

Investigations:

Bedside ECG

-nonspecific ST segment and T wave changes

-Sinus tachycardia

-Arrhythmias

· Atrial Fibrillation, Ventricular tachycardia

Imaging

CXR- generalized cardiac enlargement

Echocardiogram

-LV +/- RV dilation

Decreased ventricular wall motility

Tricuspid and mitral valve insufficiency (Doppler)

Poor global function

Cardiac MRI

Coronary angiography- to exclude coronary artery disease

Endomyocardial Biopsy indications-

Acute dilated cardiomyopathy + refractory heart failure symptoms

Dilated cardiomyopathy in presence of systemic diseases- SLE Polymyositis, sarcoidosis

Rapidly progressive ventricular dysfunction

-in unexplained, recent onset cardiomyopathy

New onset cardiomyopathy + recurrent VT/high grade heart block

Heart failure in setting of fever, rash, and peripheral eosinophilia

Management

Manage symptoms of cardiac failure

Implantable Cardioverter Defibrillator (ICD)

Cardiac transplant

Hypertrophic Cardiomyopathy

29 December 2020

19:00

Myocardium hypertrophy of ventricular walls > 15mm

Ventricles volume decreased

Most common cause of sudden death among young athletes

Left ventricular hypertrophy

· In absence of causative hemodynamic factors

o (Hypertension, aortic valve diseases, systemic diseases, storage diseases)

· 1:500-1:1000 prevalence

o Men>women 2:1

o Black> White

Autosomal dominant with incomplete penetrance

Mutation in genes encoding for sarcomere proteins

· Myosin, actin, troponin, tropomyosin

· Genetic basis does not directly correlate with prognostic risk stratification

Obstructive HCM-

· Subaortic obstruction HCM

· Mid ventricular Obstructive HCM

Non-obstructive HCM-

· Normal systolic function

· Impaired systolic function

MR- mitral regurgitation

SAM- Systolic Anterior motion of mitral valve

ASH- asymmetric hypertrophy of interventricular septum

Symmetric hypertrophy or apical hypertrophy

4 interrelated processes:

Left Ventricular Outflow Obstruction

Mitral regurgitation

Diastolic dysfunction

Myocardial ischemia

Left Ventricular Outflow Obstruction

Clinical features:

Asymmetrical hypertrophy of interventricular septum (ASH)

Systolic anterior motion (SAM) of mitral valve

Leaflets of mitral valve move towards enlarged septum during systole

Mitral valve leaflets obstructs blood flow from ventricles to aorta

Narrowing of outflow tract

https://youtu.be/_K1F3bHyELo?t=131 (2:11-2:39)

Major determinant for heart failure symptoms, and death

Complications- LV Outflow Obstruction

Elevated intraventricular pressure

Prolonged ventricular relaxation

· Leads to diastolic dysfunction

Increased myocardial wall stress

Increased bodily oxygen demand

Decreased cardiac output

Mitral Regurgitation

Result from systolic anterior motion of mitral valve

Severity directly proportional to outflow obstruction

Patients complain of dyspnoea and orthopnoea

Diastolic Dysfunction

Impaired ventricular relaxation

· High systolic contraction load

· Contraction/ relaxation of ventricles not uniform

Exertional dyspnoea symptoms

· Abnormal diastolic filling

· Increased pulmonary venous pressure

Myocardial Ischemia

Often occurs without atherosclerotic coronary artery disease

Postulated mechanism:

Abnormally small +/- partially obliterated intramural coronary arteries

Due to hypertrophy

Inadequate number of capillaries for the degree of mass

Symptoms* some asymptomatic

Chest pain

Dyspnoea

Syncope with exertion

Pulmonary oedema

Cardiac arrhythmias

· e.g. atrial fibrillation

Sudden death

Signs- Palpation of pulses

Double apical pulsation

· Forceful atrial contraction

Jerky carotid pulse

· Short upstroke, prolonged systolic ejection

Jugular venous pulse

· Prominent a wave: decreased ventricular compliance

Signs- Auscultation

Fourth heart sound (S4)

· Cardiac hypertrophy

Ejection systolic murmur

· Along left lower sternal border

· Intensity increase with decreased preload (Valsalva manoeuvre), vice versa (during squatting)

Mitral regurgitation

· Secondary to SAM (systolic anterior motion)

Investigation-

ECG

· Left ventricular hypertrophy

· Presence of septal Q waves

Echocardiography

Used for:

· Diagnosis

· Haemodynamic assessment

· Clinical risk stratification

· Interventional management

Findings:

· Left ventricular hypertrophy (LVH)

· Asymmetrical septal hypertrophy (ASH)

· Systolic Anterior Motion (SAM)

Echocardiographic Diagnosis for HCM:

LVH ≥15mm (Asymmetric > Symmetric)

Absence of other cardiovascular/ systemic disease associated with LVH/myocardial wall thickening

Cardiac Magnetic Resonance (CMR)

Indicated when ECHO views are limited

· Due to unusual distribution of hypertrophy

· Detect milder magnitudes of hypertrophy

Demonstrates myocardial scarring

· Differentiate hypertrophic cardiomyopathy from other LVH

· Gadolinium enhanced imaging detect myocardial scarring in ~2/3 of patients with hypertrophic obstructive cardiomyopathy (HOCM)

Cardiac Catheterization-

Not typically necessary in HCM

Hyperdynamic systole function results in almost complete obliteration of left ventricular cavity

Management

Aims:

Treat symptoms

Prevent sudden death

Options:

· Medications

· Dual-chamber pacing

· Implantable Cardioverter Defibrillator (ICD)

· Surgery-

o Surgical septal myomectomy

o Alcohol septal ablation

Medications-

Beta-blockers

· During chest pain

· Increase ventricular diastolic filling/ relaxation

· Decrease myocardial oxygen consumption

· Not been shown to reduce incidence of sudden cardiac death

Verapamil

· During chest pain

· Augments ventricular diastolic filling/ relaxation

Disopyramide

· Class 1a anti-arrhythmic agent

· Sodium channel blocker

· Negative inotrope

· Used in combination with beta blocker

Amiodarone

· Anti-arrhythmia

Diuretics

· Relieve heart failure symptoms

Avoid vasodilators

· Vasodilators may aggravate left ventricular outflow obstruction

Surgery-

For severe symptoms with large outflow gradient (>50mmHg)

Does not prevent sudden cardiac death

Types:

· Surgical septal myomectomy

· Remove small portion of upper septum

· +/- mitral valve replacement

· 5-year symptomatic benefit in ~70% patients

Alcohol septal ablation

· Successful short-term outcomes

o Left ventricular outflow tract gradient reduced to <20mmHg

o Symptomatic improvements

o Increased exercise tolerance

o Long-term data unavailable

· Complications:

o Complete heart block

o Large myocardial infarctions

· RCT for alcohol septal ablation vs surgical myomectomy unavailable

Complications-

Atrial Fibrillation

· Prevalent in up to 30% older patients

· Cardiac output decreases by 40%

Autonomic Dysfunction

· 25% of patients with HCM

· Associated with poor prognosis

Endocarditis

· 4-5% of patients with HCM

· Usually mitral valve affected

Heart failure

· 10-15% patients progress to NYHA Class III-IV

· 3% end-stage heart failure with systolic dysfunction

Sudden cardiac death in HCM-

· Nonsustained ventricular tachycardia- rest, exercise on 24 hours Holter monitoring

· >30mm on ECHO LV hypertrophy

· Abnormal exercise blood pressure response

· Unexplained syncope

· Family history of sudden death

Restrictive cardiomyopathy

29 December 2020

21:51

Diastolic insufficiency

Impaired ventricular filling

· Ventricles stiff and rigid

· Increased tension of ventricular filling

· Systolic function normal in early stages

Intraventricular pressure rises precipitously with small increase in volume

Morphology

Hypertrophy of myocardium

· Myocardium becomes firm

Thickening of endocardium

Both atrium dilated

· Due to diastolic disturbances

Ventricle size slightly enlarged

· No dilation of cavities

Ventricle walls loss elasticity

Patchy/ diffuse interstitial fibrosis/ amyloid

Aetiology

Primary restrictive cardiomyopathy

· Idiopathic

· Loeffler eosinophilic endomyocardial disease (for your interest)

Secondary restrictive cardiomyopathy

· Amyloidosis

· Sarcoidosis

· Haemochromatosis

· Scleroderma

· Glycogen storage disease of the heart

· Carcinoid heart disease

Symptoms

Fatigue

Dyspnoea

Tachypnoea

Examination findings

Increased JVP

Hepatic enlargement

Ascites

Oedema

S4 heart sounds

ECG

Low voltage QRS, ST and T-wave changes

Chest X-Ray

Cardiomegaly

Pulmonary venous congestion

Echocardiography

Symmetrical myocardial thickening

Impaired ventricular filling

Cardiac Magnetic Resonance

Myocardial fibrosis in amyloidosis

Endomyocardial biopsy

Management-

No specific treatment

Manage cardiac failure and embolic manifestations

Cardiac transplant in selected cases

Melphalan, prednisolone, colchicine may improve survival in primary amyloidosis

Obliterative Cardiomyopathy

29 December 2020

21:56

Rare form of restrictive cardiomyopathy

Thrombosis + fibrosis + obliteration of ventricular cavities

· Involves endocardium of one or both ventricles

· Endocardium thickens

Features:

· Mitral + tricuspid valve regurgitation

· Heart failure

· Pulmonary embolism

· Systemic embolism

Associated with:

Eosinophilic leukaemia

Chrug-Strauss syndrome

Management:

Anticoagulants + antiplatelets

Manage heart failure

Tricuspid and mitral valve replacement +/- decortication of endocardium

Arrhythmogenic Right Ventricular Cardiomyopathy

29 December 2020

21:57

Predominantly affects right ventricle

Population prevalence 1 : 5000

Autosomal dominant inheritance

Fatty/ fibro-fatty replacement of myocytes

· Leads to ventricular dilation

Most patients asymptomatic

Symptoms (if present):

· Ventricular arrhythmia

· Syncope

· Right heart failure

Increased risk of sudden death

ECG

· Usually normal

· May show T-wave inversion in right ventricular leads (V1, V2)/ features of RBBB

24-hours Holter monitoring

· Non-sustained ventricular tachycardia

Echocardiography

· Right ventricular dilation + aneurysm formation (in advanced cases)

Cardiac Magnetic Resonance

· Fibrofatty infiltration

Treatment

Amiodarone

· Symptomatic arrhythmias

Beta blockers

· Non-life threatening arrhythmias

Implantable Cardioverter Defibrillator (ICD)

· Life threatening arrythmias

Cardiac transplant

· Intractable arrhythmia

· Cardiac failure

Left Ventricular Noncompaction

29 December 2020

21:58

Prominent trabeculations, deep recesses in apex of left ventricle

Thin compact epicardium, thickened endocardium

Increased risk of thrombosis, heart failure, ventricular tachycardia and sudden death

Risk of offspring inheriting disease

Alcoholic Cardiomyopathy

29 December 2020

21:58

1/3 of dilated cardiomyopathy cases in the Western world

Risk increases with alcohol consumption >10 years

· Advice early alcohol abstinence

Chronic, insidious onset

Result of

· Direct toxin from alcohol

· Thiamine deficiency

Presentation:

Dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea

Palpitation

Syncope

Chest pain

Pleural effusion

ECG findings:

Atrial fibrillation/ Atrial flutter

QT prolongation

Poor R-wave progression

Premature ventricular contraction

LBBB/RBBB

1st degree atrioventricular block

Long history of alcohol consumption prior to diagnosis is associated with cardiomyopathy

·

Peripartum Cardiomyopathy

28 December 2020

21:02

· Systolic heart failure (LVEF <45% / fractional shortening <30%)

· In the last month of pregnancy/ within 5 months of delivery

· Other determinable aetiology of heart failure absent

· Absence of any heart disease before last month of pregnancy

Fractional shortening:

Reduction of length of end-diastolic diameter by the end of systole

Measures heart’s muscular contractility

Efficiency of heart in ejecting blood impaired when diameter fails to shorten by >28%

LVEF- Left ventricular ejection fraction

Fractional shortening

The reduction of the length of the end-diastolic diameter that occurs by the end of systole. Like the ejection fraction, this is a measure of the heart's muscular contractility. If the diameter fails to shorten by at least 28%, the efficiency of the heart in ejecting blood is impaired.

Criteria for diagnosis:

· Cardiomyopathy must be temporally related to recent pregnancy; onset within five months postpartum or in the last month of pregnancy

· No other detectable cause for heart failure

· Pre-existing heart disease must be absent

· Left ventricular dysfunction demonstrable

Inherited Infiltrative Disorders

29 December 2020

21:59

· Haemochromatosis:

· Ventricular and cardiac conduction system involvement

· Complications: ventricular wall thickening, dilated cardiomyopathy, restrictive cardiomyopathy

· Fabry disease:

· Glycolipid deposition in endothelium, myocardium, mitral valve

· Complications: hypertension, mitral regurgitation, heart failure

· Gaucher disease:

· Cerebrosides (glycosphingolipids) deposition

· Complications: left ventricular dysfunction, haemorrhagic pericardial effusion

Peripheral vascular disease

29 December 2020

22:06

Definition

Arterial- Arteriosclerosis of the arteries impedes circulation from the heart to the lower extremities, causing ischemia of the muscles in the lower extremities, also known as peripheral artery disease (PAD)

Venous- valve weakening, venous stasis, venous clot formation, chronic venous insufficiency & deep vein thromboembolism are the major types of venous PVD. There are different degrees of PVD and they are characterized by a variety of signs and symptoms

Risk factors-

Smoking, Diabetes, advanced age, High blood pressure, excess weight, family history of PAD, high cholesterol

Arterial Occlusive Disease

Plaque in arterial blood vessel wall narrows over time

Clinical presentation of PAD

Common to least common

Asymptomatic PAD

Stable Claudication

Chronic Limb Ischemia

Acute Limb Ischaemia

PAD symptoms:

40% Mostly asymptomatic

10% typical symptoms (intermittent claudication)

· Exercise calf pain- not present at rest, relieved within 10 minutes by rest

50% Atypical symptoms- Occlusion may develop slowly, allowing collateral circulation to develop

Intermittent claudication

Exertional pain: fatigue, cramping, tightness

Calf> Thigh> Buttock

Relief when standing, symptoms consistent from day to day

Lower extremity arterial pulse exam-

Femoral

Popliteal(medial)

Dorsalis pedis

Post tibial

Bruit, symmetrical, asymmetrical?

0 absent

1 faint

2 reduced

3 normal

4 bounding

Buerger test- chronic arterial insufficiency

Provoke test- Raynaud's disease

Ice- white, warm blue

Cap refill time- 20-30 severe ischaemia

Venous filling time normal 5 sec, veins collapse in ischemic limb

Fontaine

Rutherford scores

Ankle Brachial Index (ABI)

Confirm PAD diagnosis

Assesses the functional severity of claudication

May unmask PAD

Duplex Ultrasonography and Doppler Color -flow imaging

Measure blood vessels and blood flow PVD

Localizing diseased segments and spectral imaging can assess lesion severity

MR Angiography

Advantages

Non invasive

No iodinated contrast

Disadvantages

Less specific (overcalls stenosis)

No angioplasty/stenting

Nephrogenic systemic fibrosis- 30ml/min creatinine clearance cutoff

CT Angiography

Advantages

Non invasive

Accuracy

Multi-assessment

Disadvantages

No angioplasty/stenting

Iodinated contrast

Conventional Angiography

Advantages- most sensitive (calcified vessels)

Angioplasty/ stenting

Disadvantages

Invasive, iodinated contrast, 1:1000 bad outcome

Management-

the key modifiable risk factors, such as smoking, control of diabetes, hyperlipidemia, diet, body weight and exercise

manage pain

depression and anxiety.

Genebased therapy

Interventional radiology treatments- angioplasty, stents, thrombolytic therapy, stent-grafts

Amputation: indication

Absolute: Severe rest pain with no revascularization option

Limb gangrene

Life threatening infection

Relative:

Lifestyle limiting symptoms

Critical limb ischaemia

Estimated life expectancy <=2 years or autogenous vein is not available, balloon angioplasty is reasonable

Estimated life expectancy > 2 years and autogenous vein is available bypass surgery is reasonable

Poor invasive or surgical candidate

Medical comorbidity, lack of suitable outflow vessel, patient preferencec

Cardiac gaited pump or non cardiac gaited pump optional??

27 December 2020

19:40

Ankle-brachial pressure index

Ankle Brachial Index (ABI)

The ankle-brachial pressure index (ABPI) is the ratio of the systolic blood pressure in the lower leg to that in the arms. Lower blood pressure in the legs (result in a ABPI < 1) is an indicator of peripheral arterial disease (PAD). ABPI is therefore useful in evaluating patients with suspected PAD, for example a male smoker who presents with intermittent claudication.

It is also important to determine the ABPI in patients with leg ulcers. Venous ulcers are often treated with compression bandaging. Doing this in a patient with PAD could however be harmful as it would further restrict the blood supply to the foot. ABPIs should therefore always be measured in patients with leg ulcers.

Interpretation of ABPI

· > 1.2: may indicate calcified, stiff arteries. This may be seen with advanced age or PAD

· 1.0 - 1.2: normal

· 0.9 - 1.0: acceptable

· < 0.9: likely PAD. Values < 0.5 indicate severe disease which should be referred urgently

The ABPI is a good test, values less than 0.90 have been shown to have a sensitivity of 90% and a specificity of 98%* for PAD.

Compression bandaging is generally considered acceptable if the ABPI >= 0.8.

*Yao ST, Hobbs JT, Irvine WT. Ankle systolic pressure measurements in arterial disease affecting the lower extremities. Br J Surg. Sep 1969;56(9):676-9.

From <https://www.passmedicine.com/review/textbook.php?s=#>

Heart transplant

30 December 2020

00:29

· Cardiac Transplantation is indicated when predicted quality of life is better after transplantation than it would be continuing other treatment methods

· Not always an easy decision

· Heart transplant patients have a long hard road ahead of them after surgery

· Transplants are the last resort to saving a patient’s life

· Limited number of donor hearts leads to rationing based on

need and survival expectations

· Very selective criteria for being eligible to receive a donor heart, window closes fast for these patients

Contraindications:

· Severe Pulmonary HTN

· >6 Wood units not responsive to vasodilators

· Active infection

· Uncontrolled Malignancy

· Irreversible end-organ disease

· Hepatic, Renal, Pulmonary

· Pulmonary Infarction

· Age >60 years

· Diabetes mellitus with end-organ damage

· Severe Cerebral and Peripheral Vascular Disease

Donor selection criteria

Most Donor Hearts come from MVAs where patient has severe brain damage

Donor Criteria-

· Age- birth to 53 years (<45 ideally)

· Size- donor and recipient must have a size difference of < 20 kg

· ABO Bloodtype-

· <10-15% reactivity on the test allows transplant to

· proceed

· >15% reactivity needs a lymphocyte cross-match test which takes 6 hours and can delay procedure

Pre-Operative Considerations

· Reversible Renal Dysfunction-

· LV failure causes systemic hypoperfusion which can cause Kidney failure (reversible or not?)

· ↑ BUN, ↑ Creatinine (signs of renal dysfunction)

· Reversible Hepatic Dysfunction-

· RV and LV failure lead to venous congestion, especially in Liver, decreased Liver perfusion

· Patient Medications-

· Digitalis and diuretics- cause hypokalemia which causes arrhythmias

· Anti-arrhythmics cause decreased ventricular contractility

· ACE Inhibitors lead to a decrease in PVR

· Coumadin causes a need for Vitamin K and FFP during procedure

Waiting list:

· Status 1A

· On an artificial heart, VAD, ECMO, IABP for <30 days

· Mechanical Ventilation

· High dose inotropes

· Life expectancy < 7 days w/o transplant

· Status 1B

· On extracorporeal device for > 30 days

· Continuous inotropes

· Status II

· All other patients

Harvesting donor heart procedure:

Must maximize hemodynamics to prevent myocardial injury

· Keep CVP <10 mm Hg (prevent distention)

· Keep MAPs normal to high range

· Avoid volume depletion

· Treat Diabetes Insipidus with Vasopressin

· Occurs a lot in brain damage victims

· Keep pH and electrolyte levels normal

Recipient operation

All recipients are given Cyclosporine f or immunosuppression

Induction may be difficult due to failing heart

· Must keep heart rate high to maintain higher C.O. with patients with low stroke volume

Surgical Techniques:

· Orthotopic Heart Transplant- (Most Common)

· Native heart completely removed - and replaced

· Heterotopic Heart Transplant-

· Donor heart placed in parallel with native – two hearts

Acute rejection:

· No longer worried about IgM ABO reactions

· Vigorous blood typing prevents this

· Cause of Hyperacute Rejection is due to pre-existing IgG antibodies usually directed against donor HLA (human leukocyte antigens) proteins.

· Antibodies present due to previous blood cell transfusions (multidonor platelets most dangerous)

· IgG antibodies attack new donor heart tissue

· This is why we absolutely try to refrain from giving a

transplant candidate donor blood products

·

·

·

·

·

·

·

· Opportunistic infection after heart transplant

CMV

· Toxoplasma gondii

· Pneumocystis carinii

· Aspergillus organism

·

Post transplantation lymphoproliferative disorder (PTLD)

· Skin cancer

·

·

·

·

· Tricuspid regurgitation after heart transplant

·

·

·

·

Cardiac CT

30 December 2020

10:46

Includes

Cardiac Calcium scoring (without contrast)

Cardiac Angiography (with Contrast)

To begin with a cardiac calcium scoring is done without contrast. Depending on the score, further need for angiography is decided.

E.g.. If the score is 0 or >400: No need for further Angiography.

If intermediate, then proceed with angiography.

Indications: CAD

· We divide the patients according to the risks and probability of CAD

Low Probability (<10%)

· Asymptomatic men & women irrespective of age

· Women >50years with atypical chest pain

Intermediate (10-90%)

· Men of all ages with atypical angina

· Women>50yrs with atypical angina

· Women 30-50years with typical angina

High Probability(>90%)

· Men>40years with typical Angina

· Women>50years with typical Angina

Calcium scoring

· It is done without a contrast.

· It measures whether calcified atherosclerotic plaque is present in the vessels or not.

· Based on the principle that

· Obstructive atherosclerotic plaques are calcified.

· Calcium is not present in the walls of a normal coronary artery.

It is a semi-automated measure. We have to look at the coronary arteries, one by one and click on the visible hyperdensity(calcium), and a automated score is obtained . The scores of all the vessels are added up to get a final score.

Coronary CT angiography

· Multidetector row CT (MDCT) is necessary to perform a cardiac CT.

· The sensitivity and specificity depends on the Machine

It is done under the guidance of ECG ( ECG gated Study: ECG leads are placed before the start of the study)

The Most important pre-requisite is the good image quality which depends on

Heart Rate: (less than 60BPM)

Synchronization with ECG

Breath Holding: Depends on the Machine (9s for 64slice scanner)

Proper scan and post processing protocols.

Images are acquired

3D volume rendering

Maximum intensity projection-MIP

Multiplanar reformatting -MPR

Other indications-

Post CABG assessment

Assessment of aorta

Assessment of pulmonary vessels

Congenital anomalies of the heart and Vessels

Assessment of valves/prosthetic valves

Assessment of cardiac masses

Assessment of pericardium(mass, effusion, pericarditis

Advantages

· Non invasive

· Fast

· Calcium scoring

· 3D reconstruction

· Can see beyond the lumen(atheroma imaging)

Disadvantages/Limitations

· Contrast requirement(adequate renal function)

· Limited spatial resolution

· Radiation

· Requires slow heart rate(preferably<60BPM)

· No hemodynamic information

· Movement artefacts

· Limitation if high amount of calcium is present in the vessels.

· Obese and Unco-operative patient

· Stents

RIGHT CORONARY ARTERY

Lung transplant

30 December 2020

12:04

When is a lung transplant indicated?

End stage pulmonary disease (ESPD)

Parenchymal ESPD- Obstrucive- COPD, Emphysema; Restrictive- idiopathic fibrosis; Infectious- cystic fibrosis

Vascular ESPD- Eisonmenger's Syndrome L>R Shunt become R>L; Pulmonary hypertension; rare disease with increased PVR due to atresia of pulmonary artery

Lung transplant indications

· Failure of medical and surgical improvement of disease

· Less than a 2 year expected survival from disease

· Progressive exercise intolerance

· CO2 retention

· Increased O2 requirements

· Right Heart Failure

In patients with COPD, NICE recommends

· have severe COPD, with FEV1 less than 50% and breathlessness that affects their quality of life despite optimal medical treatment and

· do not smoke and

· have completed pulmonary rehabilitation and

· do not have contraindications for transplantation (for example, comorbidities or frailty).

Lung transplant contraindications

Incurable Malignancy

Old Age

Active or incurable infection

–        HIV, Hep C…

Other major organ system damage (kidney, liver)

Morbid obesity

Alcohol, smoking or drug abuse

Previous CT surgery (case by case)

Diseases:

Chronic Obstructive Pulmonary Disease (COPD) (36%)

Idiopathic Pulmonary Fibrosis (20%)

Cystic Fibrosis (16%)

Idiopathic Pulmonary Arterial HTN (3.3%)

Sarcoidosis

Bronchiectasis

Donor selection:

Only 20% of all organ donors have lungs that are oedema and infection free

Evaluation:

· Age <50 (<40 for heart-lung combo)

· Infection free

–        PaO2 > 300 on 100% O2

· Peak Inspiratory Pressures < 30 cm H2O

· Smoking history < 20 pack years with no COPD

Wait list:

Patients should be seen every 3-6 months for review

Must live several hours from transplant center

Strict ABO compatibility

Matching donor to recipient height is used for

selection

–        Must be within 4cm of each other

⚫ If the donor is longer, you can downsize it by lobectomy or

wedge resection

Follow up appointment:

Lung Biopsies done at 2 weeks, 4-6 weeks and 12 weeks, 6 months, and then yearly

Acute Rejection usually happens within the first year

Occurs in 36% of transplants

Acute rejection symptoms – fever, dyspnoea, impaired gas exchange, decreased FEV

Infection:

Infections are the leading cause of morbidity and mortality in lung transplants

· Bacterial, Viral, and Fungal Infections

Infection rate in lung transplant is higher than any other transplant

· Due to airway colonization having direct exposure to the lung allograft

· ⚫ lack of the cough relfex

· Bacterial infections often originate from the donor lungs

· Recipient can provide their own infections pre-op, common in Cystic Fibrosis patients

Complication of heart lung transplant:

⚫        HTN- 88%%

Renal Dysfunction- 28%

Hyperlipidemia- 66%

Diabetes- 21%

Bronchiolitis Obliterans- 27%

Coronary Artery vasculopathy- 8%

Survival Rates:

· 72% at 3 months

· 64% at 1 year

Future:

Ex vivo lung perfusion

Transplant after a non-heart beating donation

Cardiac conduction disorders

30 December 2020

12:29

Classified according to:

· Electrophysiological mechanism of arrhythmogenesis

· Anatomic site of origin + pattern of conduction in cardiac chambers

Types:

· Rhythm disorders

· Impulse conduction disorders

Causes

· Congenital defects in conduction system

· Fluid and electrolyte imbalances

· Side effects of drugs/ medications

· Myocardial infarction + Myocardial ischemia

· Degenerative changes in conduction system

Impulse formation disorders- error in impulse formation from SA node causing arrhythmias

Sinus node pathologies

· Sick sinus syndrome

· Brady/Tachy Syndrome

· Sinus arrhythmia

· Sinus arrest

Atrial arrhythmias

Management of arrhythmias

Pharmacological treatment

Pacemaker

Cardioversion

· Defibrillation

· Synchronised

Radiofrequency Ablations

Surgical Interventions

Pharmacological treatment:

· Class I anti-arrhythmias: Block fast Na⁺ channels

· Class II anti-arrhythmias: ß-adrenergic-blocking drugs

· Blunt sympathetic nervous system stimulation on the heart

· Class III anti-arrhythmias: Extend action potential and refractory period

· Class IV anti-arrhythmias: Block slow Ca²⁺ channels

· Depress phase 4, lengthen phase 1 and 2

Pacemaker:

· Permanent pacemaker: battery under the skin

· Temporary pacemaker: battery outside the body

· Types

· Transvenous

· Epicardial- inserted during bypass surgery

· Transcutaneous- emergency

· Modes

· Asynchronous: at preset time and rate

· Synchronous/ on demand: when heart rate goes below rate set

Problems:

· Oversensing

· Inappropriate sensing of extraneous electrical signs

Undersensing

Fail to recognise intrinsic myocardial depolarisation

Impulse Conduction Disorders

Impulse generated normally,

but slowed/ blocked as it makes its way through the conduction system

Sick Sinus Syndrome

30 December 2020

13:16

· Also known as “Lazy Sinus Syndrome” or “Sinus Nodal Dysfunction Syndrome”

· Results from dysfunction of sinus node automaticity

· Abnormal conduction/ blockage of impulse from nodal region

· Rhythm disturbance may be intermittent/ chronic

· Refers to wide spectrum of SA node abnormalities

· Failure of sinues node to increase heart rate with exercise

· Sinus bradycardia +/- tachycardia

· Sinus arrest

· SA block

· Atrial tachyarrhythmias

o Atrial fibrillation

o Atrial flutter

Sick sinus syndrome can produce a variety of ECG manifestations consisting of atrial bradyarrhythmias, atrial tachyarrhythmias, and alternating bradyarrhythmias and tachyarrhythmias7 (Table 3).3

Supraventricular bradyarrhythmias may include sinus bradycardia, sinus arrest with or without junctional escape, sinoatrial exit block, ectopic atrial bradycardia, and atrial fibrillation with slow ventricular response. The sinus bradycardia that occurs in patients with sick sinus syndrome is inappropriate and not caused by medications.2,5 The sino-atrial exit block that occurs in patients with sick sinus syndrome may demonstrate a Mobitz type I block (Wenckebach block) and a Mobitz type II block.2 The ECG may reveal a long pause following cardioversion of atrial tachyarrhythmias, and a greater-than three-second pause following carotid massage.5 Sixty percent of patients have tachyarrhythmias.8

Brady/Tachy Syndrome

30 December 2020

13:18

· Intermittent episodes of bradycardia and tachycardia

· Patients may have periods of atrial fibrillation, and periods of chronotropic incompetence

· 75-80% patients have pacemaker implanted

Sinus arrhythmia

30 December 2020

13:19

· Most commonly associated with phases of respiration

· Respiratory sinus arrhythmia

· Normal physiological phenomenon

· Most marked in young persons

· Normal P-QRS-T complexes, with alternating period of gradually lengthening P-P intervals (towards end of expiration) and gradually shortening P-P intervals (towards end of inspiration)

· Arrhythmias accentuated by vagotonic procedures (digitalis administration, carotid sinus compression), abolished by vagolytic procedures (exercise, atropine administration)

Atrial arrhythmias

30 December 2020

13:21

Mechanism:

Enhanced automaticity

Re-entry

Triggered activity

Types

· Premature atrial contraction

· Atrial tachycardia

· Multifocal atrial tachycardia

· Paroxysmal atrial tachycardia

· Atrial flutter

· Atrial fibrillation

· Wandering Pacemaker

Premature Atrial Contraction (PAC) also known as Atrial Premature Complex (APC)

· Conducted through AV node and the rest of the heart

· Depend on prematurity and status of AV node and intraventricular conduction system

· Non-conducted/ blocked PAC don’t trigger QRS complex

· PAC arising close to AV node (low atrial ectopic) activate atria retrogradely

· Produce inverted P wave, with short P-R interval (>120ms)

o P-R interval < 120ms classified as pre-junctional complex (PJC)

Sino-atrial block

30 December 2020

13:30

· In sino-atrial block, SA node discharges impulse at regular intervals

· However, some impulses are delayed on their way to the atria

· Categorised based on length of impulse conduction delay

· First degree SA block

· Second degree Type I block

· Second degree Type II block

· Third degree block

· First degree SA block

· Delay between sinus node firing, and depolarisation of atria

· Could not detect first degree SA block on surface ECG

· Surface ECG does not show sinus node activity

Second Degree (Type I) block (Wenkebach)

· Conduction time between sinus node and surrounding atrial tissue becomes progressively short, until an entire cycle is dropped

· P-wave blocked in SA node, and would not appear on ECG

· Rhythm is irregular, and P-P interval gets progressively shorter

· Eventually, entire PQRST complex is dropped

Second-degree (Type II) SA block

· Conduction time between sinus node and atrial tissue normal until an impulse is blocked

Third degree SA block

· Some impulses are blocked causing long sinus pauses

· Pauses last for indefinite period, and ends with sinus beat

Third degree SA block vs Sinus arrest

· In both case, the atrial activity stops, and ECG appears similar

· However, both cases result from different cause

Third-degree SA block

· Impulse conduction failure

· Pause lasts for indefinite period, ends with sinus beat

Sinus arrest

· Impulse formation failure

· Pause ends with junctional escape beat

·

Atrio-ventricular block

30 December 2020

13:38

Delay/ failure in transmission of cardiac impulse from atrium to ventricle

Causes:

· Idiopathic fibrosis of conduction system

· Ischemic heart disease

· Inferior MI leads to transient AV blocks, resolve within 7 days

· Anterior MI leads to permanent AV blocks

· Structural heart diseases

· Myocarditis, cardiomyopathy, valvular diseases

· Rheumatic fever

· Hyperkalaemia/ hypokalaemia

· Drugs

Digoxin toxicity

Verapamil, amiodarone

· Types:

· First degree AV block (P-R interval progressively increases)

· Second degree AV block

· Mobitz Type I (P-R interval progressively increases)

· Mobitz Type II (P-R interval constant)

· Third degree AV block (complete heart block)

First degree AV block

· Delayed conduction through AV node

· PR interval >200ms (Prolonged PR interval)

· Almost asymptomatic

· Not indicated for pacemaker

Second-degree (Type I) AV block- Mobitz I

· a.k.a Wenckebach block

· Happens post inferior MI

· Presence of AV node ischemia

· Progressively prolonged PR interval

· Until there is failure to conduct, and a ventricular beat dropped (skipped QRS)

· Patient might experience palpitations and fatigue

· Not indicated for pacemaker

· as long as no bradycardia

Second-degree (Type II) AV Block

· a.k.a “high grade” block (2:1 block / 3:1 block)

· Regularly dropped ventricular beats (QRS complex missing)

· P-R interval normal

· May progress to third-degree AV block (complete heart block)

· Usually indicated for pacemaker

·

Intermittent loss of QRS complex- p-wave not transmitted beyond AV node

Normal P-R interval

Third-degree AV block

· Complete heart block

· No impulse conduction from atria to ventricles

· Atria and ventricles have independent impulses

o Complete atrio-ventricular dissociation

· Atria beats faster (~100 beats per minute) than ventricles (~40 beats per minute)

· Narrow QRS complex if AV node acts as pacemaker (proximal block)

· Wide QRS complex if ventricle sets the pace (distal block)

·

Symptoms:

· Dizziness

· Angina

· Heart failure

· Adams-Stokes Syndrome (in severe cases)

· Periodic syncopal attacks due to sudden but pronounced decrease in cardiac output

· Usually patients with high-grade arrhythmia/ complete heart block

Acute Management- AV blocks

· Manage bradycardia and reduced cardiac output

· Atropine 0.5mg IV

· May have effect if block located at AV node

· Otherwise will aggravate block if the block is distal to AV node

· Isoprenaline 5μg/min

· Caution in cases of acute coronary syndromes: may trigger ventricular tachycardia

· Transcutaneous/ transvenous pacemaker if sinus bradycardia/ asystole

· Despite attempts with atropine and isoprenaline

Indications for Pacemaker in AV block (unless there is a reversible cause)

· AV block types II and III

· AV block type I if there is symptomatic haemodynamic compromise (usually associated with PR >0.3s, and wide QRS)

Intraventricular Block

30 December 2020

13:49

Bundle branch block

Fascicular branch block

Intraventricular Conduction System

Left bundle branch block (LBBB)

Complete LBBB

Incomplete LBBB

Right bundle branch block (RBBB)

Complete RBBB

Incomplete RBBB

Left anterior fascicular branch

Left posterior fascicular branch

· Left Bundle Branch Block

· Presence of regional wall motion abnormalities in most patients with LBBB

· Akinetic/ dyskinetic segments in septum, anterior wall of myocardium, apex

· Even if coronary artery disease/ cardiomyopathy is absent

Causes:

· Hypertrophy/ dilation/ fibrosis of left ventricular myocardium

· Ischemic heart diseases

· Cardiomyopathy

· Advanced valvular heart diseases

· Inflammatory changes of the heart

· Hyperkalaemia

· Digitalis toxicity

· Degenerative changes of conducting system (Lenegre disease)

ECG diagnostic criteria- LBBB

· QRS ≥ 120millisecond

· Leads V5, V6, aVL show broad and notched / slurred R waves

· “Rabbit-ear” sign

· Q-wave absent in left-sided leads

· Except lead aVL

· Reciprocal changes in V1 and V2 leads

· Left axis deviation may be present

·

Incomplete LBBB

· QRS duration >100 ms, <120ms

· Q-wave absent in leads V5, V6 and I

Right Bundle Branch Block (RBBB)

Causes

· Post VSD repair

· Post right ventriculotomy

· Right ventricular hypertrophy

· Large ASD (secundum type)

· Brugada Syndrome

· Ebstein’s anomaly

· Congenital abnormality of tricuspid valve leading to atrialisation of right ventricle

· Increased incidence of RBBB among population at high altitude

ECG diagnostic criteria:

· QRS ≥ 120 ms

· rsr’, rsR’ or rSR’ pattern in lead V1 or V2, and occasionally wide and notched R wave

· “M-shaped sign”

· Reciprocal changes in leads V5, V6, I and aVL

· “W-shaped sign”

·

·

Incomplete RBBB

Same as RBBB, but QRS complex <120ms

21 December 2020

22:02

Wolff-Parkinson White

· Presence of congenital accessory pathway + tachyarrhythmia episodes

· a.k.a. pre-excitation syndrome

Wolff-Parkinson White (WPW) syndrome is caused by a congenital accessory conducting pathway between the atria and ventricles leading to a atrioventricular re-entry tachycardia (AVRT). As the accessory pathway does not slow conduction AF can degenerate rapidly to VF

Possible ECG features include:

· short PR interval

· wide QRS complexes with a slurred upstroke - 'delta wave'

· left axis deviation if right-sided accessory pathway*

· right axis deviation if left-sided accessory pathway*

© Image used on license from Dr Smith, University of Minnesota

ECG showing short PR interval associated with a slurred upstroke (delta wave). Note the non-specific ST-T changes which are common in WPW and may be mistaken for ischaemia. The left axis deviation means that this is type B WPW, implying a right-sided pathway

© Image used on license from Dr Smith, University of Minnesota

Further example showing a characteristic delta wave

Differentiating between type A and type B**

· type A (left-sided pathway): dominant R wave in V1

· type B (right-sided pathway): no dominant R wave in V1

Image sourced from Wikipedia

Associations of WPW

· HOCM

· mitral valve prolapse

· Ebstein's anomaly

· thyrotoxicosis

· secundum ASD

Management

· definitive treatment: radiofrequency ablation of the accessory pathway

· medical therapy: sotalol***, amiodarone, flecainide

*in the majority of cases, or in a question without qualification, Wolff-Parkinson-White syndrome is associated with left axis deviation

**there is a rare type C WPW, WPW in which the delta waves are upright in leads V1-V4 but negative in leads V5-V6

***sotalol should be avoided if there is coexistent atrial fibrillation as prolonging the refractory period at the AV node may increase the rate of transmission through the accessory pathway, increasing the ventricular rate and potentially deteriorating into ventricular fibrillation

From <https://www.passmedicine.com/question/questions.php?q=0>

· Pre-excitation: early activation of ventricles as impulse bypass AV node via accessory pathways

· Accessory pathway (bypass tract):

o Abnormal conduction pathway formed during cardiac development

o Types of pathways:

§ Bundle of Kent (atria to ventricles) (most common in Wolff-Parkinson White Syndrome)

§ James bundle (atria to bundle of HIS) (more common in Lown-Ganong- Levine Syndrome)

§ Mahaim fibres (right atrium/ AV node to right bundle branch)

ECG:

· Abnormally short PR intervals (<0.12seconds)

· Wide QRS complex with “slurred upstroke” (delta-wave)

· Delta wave due to accessory conduction pathway (bundle of Kent)

· Conduction from atria to ventricles bypassing AV node

·

Symptoms:

· Palpitation, syncope, dizziness, tachyarrhythmia

· Tachyarrhythmia:

· ~70% Atrioventricular Re-entry Tachycardia (AVRT)

o Paroxysmal supraventricular tachycardia

· ~20% atrial fibrillation

· 7% atrial flutter

· May induce ventricular fibrillation

Management:

· Procainamide: Class Ia anti-arrhythmia drugs

· Class III anti-arrhythmia drugs

· Radiofrequency ablation

Lown-Ganong-Levine Syndrome

30 December 2020

14:05

· Another type of pre-excitation syndrome

· Grouped with Wolff-Parkinson White syndrome as AVRT

· Intranodal accessory pathway (James fibre)

· Bypasses delay within AV node

· Results in short PR interval (<0.12s)

· Ventricular conduction occurs through usual ventricular conduction pathways

· Unlike Wolff-Parkinson White Syndrome, there is no region of ventricular myocardium depolarised independently of the rest of ventricles

· Therefore no delta wave in Lown-Ganong Levine Syndrome

· QRS complex is normal (not-widened)

Ion Channel Defects

30 December 2020

14:06

· Long QT syndrome

· Brugada syndrome

Long QT syndrome

Congenital

· Genetic defect in potassium K⁺ channel (involved in repolarisation)

Examples:

Romano Ward Syndrome, Jervell and Lange-Nielson Syndrome

Acquired

· Drugs

· Hypocalcaemia

· Acute myocarditis/ acute myocardial infarction

· Hypothermia

· Hypertrophic Obstructive Cardiomyopathy

· Advanced atrioventricular blocks

May cause Torsades de Pointes

· a.k.a. Polymorphic Ventricular Tachycardia

· Associated with prolonged QT interval

· Increased risk of sudden cardiac death

·

Aortic Aneurysm

30 December 2020

14:12

Aortic aneurysm refers to pathologic dilatation of aortic segment.

The extent of dilatation is debatable but one criterion is an increase in the diameter of at least 50% greater than that expected for the same aortic segment in unaffected individuals of same age and sex

According to location, TAAs are classified into aortic root or ascending aortic aneurysms, which are most common (≈60%), followed by aneurysms of the descending aorta (≈35%) and aortic arch (<10%)

Risk factors:

Genetic:

· Marfan syndrome

· Bicuspid aortic valve

· Loeys-Dietz syndrome

· Hereditary thoracic AA or dissection

· Vascular Ehlers- Danlos syndrome

Congenital diseases or syndromes

· Coarctation of aorta

· Turner syndrome (dissection at small aortic dimensions)

· Tetralogy of Fallot

Atherosclerosis

· Penetrating atherosclerotic ulcer

Trauma, blunt or iatrogenic

· Catheter or stent

· Intra-aortic balloon pump

· Aortic or vascular surgery

· Motor vehicle accident

· CABG or AVR

Cocaine use

Inflammatory or infectious disease

· Giant cell arteritis

· Takayasu arteritis

· Bechet disease

· Aortitis

· Syphilis

Pregnancy (typically in third trimester)

Tearing pain

Investigations

Blood tests:

FBC, clotting screen, renal function.

ESR and/or CRP if an inflammatory cause is suspected.

LFTs and amylase, if embolisation or dissection is suspected

Investigate for a suspected cause, if relevant - eg, syphilis or HIV serology, connective tissue disease.

ECG.

Lung function tests.

Ultrasound:

Transthoracic echocardiogram shows aortic valve and aortic root.

Transoesophageal echocardiogram shows from the aortic valve to the proximal descending aorta.

Abdominal ultrasound - to look for associated abdominal aneurysms.

Scans:

CT scan with contrast medium is the most widely used diagnostic tool. This defines the precise anatomy and can show the aneurysm, dissection, thrombus or haematoma. Detailed views are needed for endovascular repair planning.

CT angiography is possible and non-invasive, although the contrast material is nephrotoxic.

Magnetic resonance imaging (MRI) also shows the anatomy well; the advantage is that magnetic resonance angiography is not nephrotoxic.

Coronary angiography may be appropriate when assessing fitness for surgery or the possible need for coronary artery bypass grafting (CABG) in addition to aortic surgery.

Medical management:

· Regular monitoring of the aneurysm - eg, by CT or MRI scans every six months.

· Rigorous blood pressure control with use of beta-blockers to reduce shear stress across the aortic wall.

· Smoking cessation.

· Treating the underlying cause where feasible - eg, infection.

· Treating other cardiovascular risk factors - eg, hyperlipidaemia.

Asymptomatic indications for surgery:

· Asymptomatic TAAs are assessed to evaluate the relative risks/benefits of surgery. The risk of rupture depends on:

· Aneurysm diameter. This is the most important factor predicting rupture. Generally, aneurysms of diameter >5.5 cm (ascending aorta) or >6 cm (descending aorta) merit repair.

· Using body surface area as well as aneurysm diameter gives a more accurate risk profile.

· Patients with Marfan's syndrome or a strong family history of TAA merit surgery earlier (at a smaller aneurysm diameter).

· The rate of expansion is also important.

Immediate/urgent surgery is needed for:

· Ruptured TAA.

· Some types of aortic dissection.

· Acute symptoms (because these suggest expansion and impending rupture/dissection).

· Symptomatic TAAs merit surgery regardless of their size (because there is a higher risk that they will rupture or dissect).

Surgical repair:

· This involves thoracotomy to replace the diseased aorta with a Dacron® graft.

· Replacement of the aortic root ± the aortic valve may also be necessary.

Endovascular repair:

· Endovascular repair is also known as 'endovascular stenting', EVAR (= endovascular aneurysm/aortic repair) or TEVAR (= thoracic endovascular aneurysm/aortic repair).

· complications, ie endoleaks, stent fractures, stent graft migration, iliac artery rupture, retrograde dissection and aorto-oesophageal fistula. These may require re-intervention.

· Patients receiving stents require frequent follow-up with CT scans.

· Improves outcomes

Prevalence

· The incidence is approximately 3-4 per 100,000 per year.

· The males > female

· It is most common between the ages of 50-70, being rare below the age of 40.

· Aortic dissection is very rare in children but it has been reported in association with coarctation of the aorta

Management:

For acute type A (types I and II) dissection, surgery aims to prevent aortic rupture and pericardial tamponade and to relieve aortic regurgitation^.

· Implantation of a composite graft in the ascending aorta, with or without re-implantation of coronary arteries, is performed.

· Either total aortic arch replacement or partial or hemiarch replacement may be considered.

For type B aortic dissection, thoracic endovascular aortic repair (TEVAR)

Initial management:

Immediate ICU care

BP control and monitoring

· Central line, arterial line, urine output

Imaging studies

Daily chest xray, weekly ct scan

Pharmacologic therapy

Vasodilators: sodium nitroprusside

Beta blockers: Esmolol

Endovascular stent graft:

· Indications

· Poor surgical candidates for thoracic aneurysm

· Expected survival time <5 years

· Problem

· Endoleaks, exclusion of intercostal arteries, lack of long term data

· Results: early mortality :9%, stroke, paraplegia, early endoleak, reintervention

The long-term prognosis

stable type B (not involving the ascending aorta) dissections

· significant aortic aneurysm formation in 25-30% within four years

· survival rates from 50-80% at five years

· 30-60% at 10 years

D-dimer levels:

Rise in acute aortic dissection as in pulmonary embolism

Level >1,600 ng/mL within first 6 hours - positive likelihood ratio of 12.8 for dissection

In first 24 hours after symptom onset - D-dimer level < 500 ng/Ml has negative predictive value of 95%

Inadequate to exclude Dissection

MRI:

· Sensitivity of 98% and specificity of 98% with diagnostic odds ratio of 6.8

· Capable of multiplanar imaging with 3D reconstruction

· Cine MRI visualize blood flow, differentiating slow flow and clot and AR

· MRA -detect and quantify AR & branch vessel morphology

Aortography:

· Identify intimal flap, true and false lumen

· Thickened wall (thrombosed false lumen)

· AR, branch vessel involvement

· Diagnostic accuracy 90-95%

· 5-10% false negative rate

– thrombosed false lumen

– simultaneous opacification of both lumens

– misses IMH

· Risks of procedure

TEE:

· Accurately visualise entire thoracic aorta (sensitivity 98.0%, specificity 95.0%, diagnostic odds ratio 6.1)

· 2 lumens separated by flap

· Visualize coronary ostia

· AR

· Pericardial effusion

· LV & RV function

· May not adequately visualize distal ascending aorta and aortic arch

Obstructive Sleep Apnoea/ Hypopnoea Syndrome

30 December 2020

17:46

· Frequent, interrupted sleep

· Due to repeated collapse of upper airways

o e.g.: tongue falling backwards blocking air entry through pharynx

o Airway collapse can be:

§ Complete with cessation of airflow (apnoea)

§ Partial with significant hypoventilation (hypopnoea)

· Oxygen saturation in the body drops

· Patient complains of excessive daytime sleepiness, reduced concentration etc

Apnoea

· Cessation of airflow for at least 10 seconds

· Reduction in >80% airflow

Hypopnoea

· Reduction of airflow (30-50%)

· Moderate reduction of airflow (<50%) + oxygen desaturation >3%

· Evidence of arousal in EEG + oxygen desaturation at least 10 seconds

In patients with apnoea :

· Upper airway is smaller in retropalatal & retroglossal region

· Amount of subcutaneous fat (white area at the back of neck) is thicker

Prevalence

· Common among males, middle-aged, elderly and overweight population

· Affects >2.5 million adults in the UK (5% total population)

· Mostly undiagnosed

· Associated with hypertension, diabetes, stroke and heart disease

· Complications: shortened life expectancy, road-traffic accidents by sleepy drivers

· ~2.4% Malaysian population (2011)*

· Highest among Malays

· Prevalence among middle-aged men (9%) and women (4%)

Aetiology

Anatomical factors

Micrognathia (Mandibular hypoplasia)

Undersized (small) lower jaw

Retrognathia

Lower jaw located more posteriorly compared to upper jaw

Macroglossia

Unusually large tongue

Tonsillar hypertrophy

Enlarged adenoids

Long soft palate

Neuromuscular factors

· Decreased activities of pharyngeal dilator muscles

· Inhibition of muscle activity during REM sleep

· Use of alcohol, sedatives, muscle relaxants

Risk factors:

· Obesity (Strongest Risk Factor)

· Male

· Middle age (30-50 years old)

· Hypothyroidism

· Acromegaly

· Use of sedatives/ narcotics/ alcohol

· Smoking

Severity definition:

· Number of apnoea episodes

· % reduction in oxygen saturation

Complications:

Increased risk of vascular diseases:

· Systemic hypertension

· Pulmonary hypertension (due to hypercapnia)

· Arrhythmia

· Nocturnal bradycardia during apnoea, tachycardia upon resolution

· Myocardial infarction

· Heart failure

· Stroke

· Sudden death

Excessive daytime sleepiness

· Reduced concentration in daily activities

· Road-traffic accidents due to driver sleepiness (risk 7x greater)

OSA and hypertension:

· Repetitive hypoxemia and hypercapnia

· Reduced airflow into lungs

· Subsequent bodily oxygen desaturation

· Chemoreflex mediated sympathetic activation

· Increased sympathetic nerve activity + increased catecholamine

· Increased cardiac output & vasoconstriction

· BP could rise to 220/130mmHg during apnoea

· Diastolic nocturnal hypertension

· Loss of nocturnal dipping of blood pressure

Symptoms history

· Snoring

· Restless sleep & Insomnia

Waking up frequently gasping for air at night

· Complains of unrefreshing sleep

· Morning headache and tiredness

· Impaired memory and concentration

OSA Cardinal Symptoms (3S):

· Snoring

· Sleepiness

· Sleep Apnoea Episodes

Epworth Sleepiness Scale (ESS)

· Self-administered 8-question questionnaire

· Respondents asked to rate from 0-3 on their usual chance of dozing off while doing activities listed on questionnaire

· Scores:

· 0-10: normal daytime sleepiness

· 11-12: mild excessive daytime sleepiness

· 13-15: moderate excessive daytime sleepiness

· 16-24: severe excessive daytime sleepiness

Inspection

· Obesity

· Micrognathia/ retrognathia (small, receding lower jaws)

· Macroglossia (enlarged tongue)

· Neck size >17 inches

· Nasal congestion/ nasal polyps

· Tonsillar hypertrophy

· Adenoid enlargement

Bedside

· Blood pressure

· Assess systemic hypertension (complications of OSA)

· ECG

· Rule out arrhythmias, myocardial infarction etc (complications of OSA)

· Arterial blood gas

· Look for pO₂ and pCO₂ (patient with OSA experience hypoxemia and hypercapnia)

Bloods

· Full blood count

· Patient might have polycythaemia secondary to chronic hypoxemia

· Thyroid function test

· Hypothyroidism- risk factor of OSA

Imaging

· Echocardiography

· Assess presence of left ventricular hypertrophy (complication of OSA)

· CT/MRI

· Cephalometric analysis

· Look at structure of airways, adenoids, tongue etc

Current practice diagnosing Obstructive sleep apnea OSA NICE Guideline

· Diagnosis made through overnight sleep study

· Overnight sleep study of varying complexity could be performed

· Depending on patient preference and local arrangements

· Inpatients

· At home

Polysomnography/

Overnight Sleep Studies

· Gold standard investigation for OSA

· Simultaneous recordings of multiple physiological signals during sleep

· Obstructive apnoea

· Absence of airflow despite persistent ventilatory effort

· Central apnoea

· Absence of airflow due to lack of ventilatory effort

· Mixed apnoea

· Central + obstructive apnoea

· Usually central apnoea followed by obstructive apnoea

Diagnostic Criteria of OSA

(American Academy of Sleep Medicine)

· Excessive daytime sleepiness not better explained by other factors

· 2 or more of (not better explained by other factors):

· Choking during sleep

· Recurrent awakening

· Unrefreshing sleep

· Daytime fatigue

· Impaired concentration

· Apnoea-Hypopnoea Index (AHI)>5

Indications for Treatment

(American Academy of Sleep Medicine)

· Apnoea-Hypopnoea Index (AHI) 15 or more (moderate-severe)

· AHI 5-14 (mild) with documented symptoms of:

· Excessive daytime sleepiness or;

· Impaired cognition, mood disorders, insomnia or;

· Documented hypertension, ischaemic heart disease, history of stroke

Management:

· Patients need to be managed by experienced teams in respiratory medicine department, usually in secondary care

· Continuous airway positive pressure (CPAP) for symptomatic patients

· Adjuncts (e.g. intraoral mandibular advancement devices)

· Advice on weight reduction

· Bariatric surgery in patients with severe obesity

· Symptom improvement

· Weight reduction

· Exercise, diet

· 10-15% weight loss lead to 50% reduction in sleep apnoea severity in obese male patients

· Avoid CNS depressants (alcohol, sedatives)

· Smoking cessation

· Avoid sleeping in supine position

· Prevent tongue from blocking the airways

Continuous Positive Airway Pressure (CPAP)

Maintain pharyngeal airway patency

· Prevent collapse of pharyngeal tissues through positive pressure into airway

Average setting about

5-15 cmH₂O

CPAP problems:

· Mask discomfort to patient

· Facial skin abrasion/ discomfort

· Difficult to exhale (due to positive pressure)

· Nasal dryness

· Sore throat

· Patient might not accept treatment

· Claustrophobia

Adjuncts:

Nasal pillows

Tongue Retaining Device

Maintain tongue in protruded position while sleeping

Mandibular Advancement Device

Reposition mandible to increase airway space, improving upper airway patency

· Surgery:

· Uvulopalatopharyngoplasty (UPPP)

· 1^st line treatment for retropalatal collapse

· Excise tonsils and portions of soft palate, reorientate tonsillar pillars to enlarge oropharyngeal space

· Nasal reconstruction

· Adenotonsillectomy

· Preferred treatment in children

· Partial Glossectomy

· Limited for macroglossia

· Tongue reduction surgery from midline of posterior tongue to free margin of epiglottis

· Tracheostomy

· Only if more conservative treatments failed

· Presence of life threatening cardiopulmonary complications

· Bypass upper airway

Occupational lung disease

30 December 2020

19:29

“Disease contracted as a result of exposure to risk factors arising from work activity”

International Labour Organisation (ILO)

Particle size of air contaminates

· Particles >10μm diameter do not penetrate beyond the nose and throat

· Coarse particles: 2.5-10 μm

· Silica, aluminium, iron

· Deposit relatively high in tracheobronchial tree

· Fine particles: <2.5 μm

· Burning fossil fuels, high temperature industrial processes, gases, fumes

· Deposited at lower airways

· Ultra-fine particles: <0.1 μm

· Deposit in lungs and alveolar walls

· Can be carried to extrapulmonary sites via blood circulation

Work-related Asthma

Occupational asthma

· New onset asthma caused by high-dose/ long-term exposure to particles in work environment

Work-exacerbated asthma

· Condition of asthma in patients with known cases of asthma worsens (increased disease frequency/ severity) as a result of work exposure

Irritant- induced Occupational Asthma

· a.k.a. Reactive airways dysfunction syndrome

· Develops after single, high exposure to irritant chemicals

· Irritant agents are non-specific

· Manifest asthmatic symptoms within 24 hours of exposure

· Non-specific bronchial hyperreactivity

· Improve over time, may go over entirely (~3 months)

· Persistent complications are possible if symptoms persist >6 months

Sensitised Occupational Asthma

· Sensitisation: become allergic to specific chemical agent in workplace

· Can be low molecular weight or high molecular weight chemicals

· Exposure occurs over a period of time

· Latency period several weeks to several years

· Greatest risk at first 2 years of exposure

· Presence of bronchial inflammation

Occupational Asthma- Diagnostic Criteria:

· Defined occupational history

· Exposure to sensitizing agents

· Absence of asthma symptoms before beginning of employment

· Documented relationship between development of symptoms at workplace, and reduction of symptoms upon withdrawal (leaving) from workplace

Pneumoconiosis: Lung tissue reaction to presence of

dust accumulation in lungs – An Overview

Essential factors for clinical pneumoconiosis:

· Exposure to specific substance:

· Silica and asbestos: Potent biological effect

· Coal: May accumulate to considerable amounts, but minimal tissue response

· Size of particles between 1-5 μm

· Commonly retained in lungs

· Exposure for sufficient length of time

· ~10 years

· Silicosis

· Coal worker pneumoconiosis

· Asbestosis

Asbestosis

· Very high incidence before 1980s

· Asbestos widely used to construct ceiling, walls and flooring of houses/ buildings

· Provide insulation and fire protection

· Latency period

· Several years before pleural thickening develops

· >20 years for fibrosis & plaque

Parenchymal Asbestosis

· Diffuse interstitial fibrosis with restrictive pattern on pulmonary function test

· Impaired gas exchange in alveoli

· Presents with progressive exertional dyspnoea and fatigue

· Takes >10 years for radiographic changes to develop

Asbestos-Related Pleural Abnormalities

· Types of abnormalities:

· Pleural plaques

· Benign asbestos pleural effusion

· Diffuse pleural thickening

· Rounded atelectasis

· Mostly asymptomatic

· Some patients may develop progressive dyspnoea, intermittent chest pain, cough

Hypersensitivity Pneumonitis

· Hypersensitivity reaction in the lungs

· In response to inhaled organic dust

· Exposure can be occupational/ environmental

· Can be Type III (immune-mediated) or Type IV (delayed reaction) hypersensitivity

Pathology:

· Infiltration of alveolar walls with lymphocytes, plasma cells and histiocytes

· Loosely formed granulomas

· Fibrotic changes in advanced stages

Acute Hypersensitivity Pneumonitis

· Dyspnoea, fever, malaise, cough ~4-6 hours after exposure

· Symptoms continue 24-48 hours

· Physical examination: fine crackles throughout the lungs

· Chest radiography: may be normal/ show reticular nodular infiltration

· Have excellent prognosis

Chronic Hypersensitivity Pneumonitis

· Progressive dyspnoea over the years

· Physical examination: bilateral fine inspiratory crackles

· Blood gas: hypoxaemia (↓O₂ in blood) (worse on exercise)

· Chest radiography: reticular nodular infiltration + fibrosis (predominantly in upper lobes)

· Pulmonary function test- restrictive pattern

· May progress to end-stage fibrosis

·

· Management

· Remove triggering antigen from the environment or;

· Remove patient from environment

· Corticosteroids in severe cases

Chronic Obstructive Pulmonary Disease (COPD)

Relationship with Occupational Lung Disease

· Occupational Lung Disease vs COPD

· Difficult to establish work-relatedness of COPD in individual patients

· Diagnosis by exclusion

· Mostly based on epidemiological evidence

· Diagnosis process easier if patient is non-smoker

o Often not possible to apportion effect of smoking from effect of occupational exposure that cause COPD to smokers

Malignancies

· Lung cancer

· Mesothelioma

· Lung Carcinoma

· Latency period 20-40 years

· Risk depends on:

· Level, frequency, duration of exposure

· Age at time of exposure

· Individual susceptibility factors (family history of malignancy etc.)

· Smoking highly increases risk of lung carcinoma

Occupational Lung Cancer Carcinogens

· Arsenic

· Asbestos

· Beryllium

· Cadmium

· Silica dust

· Nickel

· Ionising radiation (Radon)

· Polycyclic aromatic hydrocarbons

· Soot

· Coal tar

· Diesel exhaust

High risk occupations

· Aluminium production

· Coal gasification

· Iron and steel founders

· Rubber production

· Painting

Mesothelioma

· Malignancy/ thickening at pleural lining of lungs

· Usually linked to chronic asbestos exposure

· Symptoms:

· Normally asymptomatic until advance stages

· Dyspnoea, chest pain, fatigue

·

High-resolution CT

Indications:

· Significant symptoms but chest radiograph findings unremarkable

· Pleural obscuring abnormalities

Typical findings:

· Intralobular/ interlobular thickening

· Radiopaque subpleural lines

· Ground-glass appearance

· Honeycombing

Management

· Supportive therapy:

· Bronchodilator: Ipratropium bromide, inhaled corticosteroids

· Oxygen supplementation

· Treat infections

· Stop exposure to triggering agents

· Smoking cessation

· Influenza and pneumococcal vaccines

Preventing against Occupational Lung Disease

· Personal Protective Equipment (PPE)

HFrEF and HFpEF management

05 January 2021

16:56

First-line treatment for heart failure with reduced ejection fraction (HFrEF):

ACEi + beta blocker - Do not offer ACEi if there is haemodynamically significant valvular disease

Monitoring:

ACEi

· Blood pressure (every dose increment)

· Sodium, potassium, renal function (before starting ACEi, after 1-2 weeks starting ACEi, and at every dose increment)

Beta blocker

· Heart rate and blood pressure (every dose increment)

ARB - if ACEi not tolerated

Hydralazine with nitrate -  if both ACEi and ARB not tolerated

Aldosterone antagonist - in addition to ACEi + beta blocker if patient continue to have heart failure symptoms. Consider lower doses for patients with eGFR <45ml/min/1.73m2

Specialist Treatment for heart failure with reduced ejection fraction (HFrEF):

Ivabradine

· Patients with NYHA class II-IV stable chronic heart failure with systolic dysfunction and; sinus rhythm 75 bpm and; in combination with first-line treatment and; left ventricular ejection fraction <35%

· Initiated 4 weeks after starting ACEi, beta-blockers and aldosterone antagonist

Sacubitril valsartan

· Patients with NYHA class II-IV symptoms and; with left ventricular ejection fraction <35% and; already on stable dose of ACEi/ ARB

Hydralazine with nitrate

· If patient is of African-Caribbean origin

· Has NYHA class III-IV heart failure with reduced ejection fraction

Digoxin

· Worsening/ severe heart failure with reduced ejection fraction despite first-line treatment

Surgical interventions

· Implantable devices. Implantable cardiac defibrillator (ICD), cardiac resynchronisation therapy (CRT) with defibrillator (CRT-D) or with pacing (CRT-P) recommended for patients with heart failure with left ventricular dysfunction, and left ventricular ejection fraction <35%

Cardiac transplant

· Considered for patients with severe refractory cardiogenic shock

From <https://mle.ncl.ac.uk/cases/page/18007/>