Cardiology is a medical speciality dealing with disorders of the heart. It is primarily concerned with ischaemic heart disease (IHD), arrhythmias, and structural heart defects. Try to think of clinical presentations (e.g. chest pain) instead of disease processes (e.g. pericarditis). In a clinical examination, you should deploy a set approach to each possible presentation. Most patients will be actors or providing a retrospective history (see 
p. 875). Fortunately there are only five possible presentations: chest pain, palpitations, shortness of breath, dizziness, and incidental murmurs. Remember, as with all cardiac cases, a full cardiovascular history (see pp. 891–893) and examination (see pp. 900–904) are required.
Chest pain on activity relieved by rest. It is mostly managed in the community by GPs, although you may encounter patients with complex IHD in the clinic.
An umbrella term to describe the spectrum from unstable angina, through non-ST elevation myocardial infarction (NSTEMI) to ST elevation myocardial infarction (STEMI). The former can be seen as referrals to cardiology from other inpatient teams or the ED. STEMIs are mainly seen in large teaching hospitals where the cardiac catheterization labs are situated. Only some institutions can perform percutaneous coronary intervention (PCI) which is part of the optimal early management strategy.
These patients can be seen in the cardiology clinic referred with dyspnoea, angina, ± syncope. Those with critical AS may be referred to cardiothoracic surgeons for consideration of valve replacement.
This is commonly seen in the young (with mitral valve prolapse ± connective tissue disorder), and occasionally post MI (ischaemic necrosis of papillary muscle 
prolapse of mitral valve leaflets). The former cohort is followed up with interval echocardiography.
This condition is almost ubiquitous among the geriatric population. You will see AF in all your clinical attachments but a cardiology placement is the right time to learn how it is managed. Cardiologists may also offer specialist interventions (e.g. chemical/electrical cardioversion and radiofrequency ablation).
Most patients with heart failure have a chronic degree of pump insufficiency. They may be followed up in the clinic for optimization of medication (e.g. diuretics). The cardiology ward will also have patients with acute heart failure and decompensated chronic heart failure.
This can be either transthoracic (TTE) or transoesophageal (TOE) at the ultrasound/echocardiography department. TOE is used if TTE is inconclusive and requires sedation.
Found at the cardiac investigations department.
Speak to the nuclear medicine department to find out when the next list is scheduled.
Look for the dedicated angiography suite; if possible, look for diagnostic (angiogram) and interventional procedures (angioplasty, stent insertion).
This takes place in theatre or the radiology suite.
Perform and interpret a 12-lead ECG (see p. 855). Ask a nurse to show you. You might find yourself with a sick patient without much assistance in which case you will need to know how to perform an ECG (see Fig. 8.1).
Fig. 8.1 ECG complex. Key:
• P wave—atrial depolarization.
• QRS complex—ventricular depolarization.
• Q wave—first downward wave of QRS complex (often absent).
• R wave—initial positive deflection.
• S wave—negative deflection after R wave.
• T wave—ventricular repolarization. Reproduced from https://commons.wikimedia.org. Image in public domain.
Table 8.1 Popular recent studies
| Year | Study title | Comment |
| 2001 | Randomized Evaluation of Mechanical Assistance for the Treatment of Congestive Heart Failure (REMATCH) | Left ventricular assist device reduces mortality compared to medical therapy |
| 2001 | Clopidogrel in Unstable Angina to Prevent Recurrent Events (CURE) | Clopidogrel/aspirin dual therapy reduced mortality and cardiovascular events at risk of  major bleeding |
| 2003 | EURopean trial On reduction of cardiac events with Perindopril in stable coronary Artery disease (EUROPA) | Perindopril reduced mortality and cardiovascular events compared to placebo in stable coronary arterial disease. |
| 2006 | Clopidogrel plus aspirin versus oral anticoagulation for atrial fibrillation in the Atrial fibrillation Clopidogrel Trial with Irbesartan for prevention of Vascular Events (ACTIVE W) | Aspirin/clopidogrel is inferior to warfarin for preventing cardiovascular events and death without improving bleeding risk |
| 2008 | Atrial Fibrillation and Congestive Heart Failure (AF-CHF) | Rhythm control does not reduce mortality (compared to rate control) |
| 2009 | Timing of Intervention in Acute Coronary Syndromes (TIMACS) | Early intervention does not  risk of cardiovascular events and mortality compared to delayed intervention except high-risk patients |
| 2011 | Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Embolism Trial in Atrial Fibrillation (ROCKET AF) | Rivaroxaban is non-inferior to warfarin in preventing thromboembolic events in AF |
| 2012 | Early Surgery versus Conventional Treatment in Infective Endocarditis (EASE) | Surgery reduces mortality in left-sided native valve infective endocarditis |
| 2015 | Comparison of Fondaparinux and Enoxaparin in Acute Coronary Syndromes (OASIS-5) | Fondaparinux is non-inferior to enoxaparin in preventing death and cardiovascular events in NSTEMI |
Defined by BP >140/90 mmHg; optimal BP in diabetics <130/80 mmHg. 95% primary or ‘essential’, 5% secondary such as renal (e.g. renal artery stenosis), endocrine (e.g. Cushing’s syndrome), and drugs (e.g. monoamine oxidase inhibitors). Malignant hypertension (e.g. hypertension plus end-organ damage) may necessitate acute treatment with IV antihypertensives. Treatment options consist of British Hypertensive Society guidelines (see Table 8.2).
Table 8.2 British Hypertensive Society guidelines for treatment
| Drug class | Examples | Combinations | |
| A | ACEI or ARB | Ramipril or losartan | A + C in age >55 and Afro-Caribbean |
| B | Beta blocker | Bisoprolol | |
| C | Ca2+ channel blocker | Amlodipine | B + C in younger patients |
| D | Diuretics | Furosemide |
Data from Advanced Paediatric Life Support, 5th Edition, 2011, Wiley.
Resistant hypertension is when a patient still has a poorly controlled BP while on three antihypertensives. Beta blockers are not first-line antihypertensives. B + D combination increases the complication of diabetes mellitus.
Chest discomfort due to myocardial ischaemia brought on by exertion and relieved by rest. Causes are coronary artery disease (majority) and coronary spasm (e.g. Prinzmetal’s). It is distinct from unstable angina which is pain at rest. Standard cardiovascular risk factors apply. Treatment is conservative (lifestyle factors such as moderate exercise, stop smoking), medical (antiplatelet, statins, glyceryl trinitrate (GTN) spray), and revascularization (angioplasty ± stenting, coronary artery bypass graft (CABG)). Prinzmetal’s coronary vasospasm is treated with calcium channel blockers.
All four valves can regurgitate or become stenosed; although one murmur may predominate, often there is mixed valvular disease on echocardiography. Some are encountered rarely (e.g. aortic regurgitation (AR), tricuspid stenosis). Murmurs can be benign (e.g. pregnancy, anaemia, hyperthyroidism) in which case they are typically soft, systolic, and positional. Focus on AS and MR.
AS is commonly due to senile calcification followed by congenital bicuspid and rheumatic heart disease. Classically, AS cardinal signs correlate with prognosis: angina syncope dyspnoea worsening prognosis. If surgery is necessary, the valve is usually replaced.
Common causes of MR are mitral valve prolapse (young females myxomatous degeneration), left ventricular (LV) dilatation, connective tissue disorder, and acute MI ( ischaemic papillary muscle rupture). Presentation ranges from incidental finding (medical student practising clinical examination) to infective endocarditis or acute heart failure.
Honours
Aortic sclerosis is a precursor state of AS. It is caused by senile calcification of the valve. Some consultants will distinguish between sclerosis and stenosis based on auscultation. Classically, AS causes an ejection systolic murmur but the murmur of aortic stenosis radiates to the carotids and is associated with a narrow pulse pressure. Pulse pressure = systolic − diastolic BP.
AF is an irregularly irregular atrial rhythm with intermittent atrioventricular (AV) node response and consequent irregular ventricular rhythm. The ECG appears irregularly irregular without p waves. You diagnose AF on an ECG. Slow AF must be distinguished from fast and often decompensating AF.
Causes of AF include MITRALE:
• Embolism (pulmonary embolism (PE)).
• Recent onset/first diagnosed episode.
• Paroxysmal: self-terminates, usually within 48 hours, recurrent.
• Persistent: lasts >7 days or cardioversion needed to restore sinus rhythm, recurrent.
• Permanent: rhythm control interventions abandoned.
Discussion points
Management of AF can be aimed to restore sinus rhythm (‘rhythm control’) or permitting AF to continue but controlling the heart rate (‘rate control’). Ask your consultant what factors would help determine whether to adopt a policy of rhythm or rate control for individual patients.
• Rhythm control: if AF present for <24 hours to restore normal sinus rhythm cardioversion: (1) chemical: flecainide, amiodarone, vs (2) direct current (DC). If unable to cardiovert immediately, give unfractionated heparin IV and cardiovert on the next working day.
• Rate control: give beta blocker (atenolol, bisoprolol) and add digoxin if rate does not fall sufficiently. Factors considered when deciding between the two are age, comorbidities, structural heart disease, and prolonged AF (over 24 hours).
• Refractory AF: may be managed by radiofrequency ablation.
• Thromboembolic risk reduction since AF increases the risk of thromboembolic events (cerebrovascular accident (CVA), ischaemic bowel).
Honours
Patients with AF are at risk of stroke and may be treated prophylactically with anticoagulant (e.g. warfarin) or antiplatelet (e.g. aspirin) agents. This decision is informed by the CHA2DS2-VASc score developed from the Euro Heart Survey1 of 5000+ patients in 35 countries. Scores of 0–9 equate to 0–15% risk respectively. Adults with non-valvular AF and a CHA2DS2-VASc stroke risk score of ≥2 are offered anticoagulation (warfarin, target international normalized ratio (INR) 2–3). Consider if score = 1. The factors are listed in Table 8.3.
Table 8.3 CHA2DS2-VASc risk factors
| Risk factor | Points |
| Congestive heart failure | 1 |
| Hypertension | 1 |
| Age >75 years | 2 |
| Diabetes mellitus | 1 |
| Stroke/TIA/VTE | 2 |
| Vascular disease | 1 |
| Age: 65–74 years | 1 |
| Sex category | 1 if female |
| Total | 9 |
TIA, transient ischaemic attack; VTE, venous thromboembolism.
Lip GY et al. (2010). Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: the euro heart survey on atrial fibrillation. Chest 137:263–72.
Heart block describes a failure of electrical conduction in the heart. Atrioventricular nodal block can be divided into first degree, second degree (two types: Mobitz I/Wenckebach and Mobitz II), and third degree. Mobitz II and third-degree heart blocks are associated with sudden cardiac death and may require a pacemaker. See Fig. 8.2.
Fig. 8.2 ECG basics—heart blocks. Reproduced from https://commons.wikimedia.org/wiki/File:Heart_block.png under the Creative Commons Attribution-Share Alike 4.0 International.
Honours
A potentially fatal disease characterized by (1) prolonged PR interval (first-degree AV block), (2) right bundle branch block, and (3) left anterior or posterior fascicular block. May need pacemaker.
Chronic heart failure is a clinical syndrome characterized by inadequate cardiac output to meet the body's metabolic needs. Essentially this means pump failure. In left heart failure, there is back pressure to the pulmonary circulation ( haemoptysis, orthopnoea, and paroxysmal nocturnal dyspnoea), while right heart failure causes back pressure to venous return ( peripheral oedema, ascites, and raised jugular venous pressure (JVP)). Congestive cardiac failure refers to coexisting left- and right-sided heart failure. Chronic heart failure is gradual (e.g. cardiomyopathy vs acute heart failure develops suddenly post MI). Management aims to treat the cause (e.g. valvulopathy) and optimize cardiac function (beta blocker, digoxin, diuretics, GTN), where failure cardiothoracic intervention.
Honours
Heart failure patients often find themselves taking a concoction of different medications, some of which are at first glance surprising:
• Diuretics (e.g. furosemide) remove excess fluid through urination.
• ACE inhibitors control blood pressure and are thought to aid myocardial ‘remodeling’. A number of RCTs showed that they reduce mortality in heart failure patients.
• Beta-blockers protect the heart from damaging effects of catecholamines. Some beta-blockers have been found to increase ejection fraction and reduce both hospitalisations and mortality.
• Aldosterone antagonists (e.g. spironolactone) work in a similar way to diuretics (as well as potassium-sparing) but also reduce heart failure mortality.
These are a class of diseases of the heart muscle itself. Key types are hypertrophic (AD inheritance or sporadic) angina, sudden death in athletes, dilated (alcohol, peripartum, congenital), and restrictive (due to infiltration (e.g. amyloidosis, haemochromatosis). Presentations vary but may show signs of heart failure.
Regulatory protein involved in myocyte contraction but released in infarction. Differential diagnoses for raised troponin are PE, critical illness (e.g. sepsis), heart failure, pericarditis, trauma, and renal impairment. Serial measurements are required since it can take 12 hours to peak. Troponin has replaced creatine kinase (CK) measurements.
Released upon ventricular stretch and seen in heart failure. Higher normal intervals correlate with increasing age and false positives are common.
You should be able to perform an ECG (see p. 855). Have your own method of analysing and presenting your ECG. Dedicate specific days to finding and reading ECGs on the cardiology ward, in the ED, and coronary care unit. Go with a colleague and read each ECG systematically. Present a number of interesting ECGs to a senior doctor if possible. When presenting an ECG, please adopt a system. The most common system is name, age, time, indication, rate, rhythm, axis, PR interval, QRS complexes, ST/T wave segments, QT intervals, and summary (see Fig. 8.4). For the purposes of working as a doctor, you must recognize AF and ischaemic changes (T-wave inversion, ST elevation/depression, new left bundle branch block (LBBB)). Find patients in hospital with acute coronary syndrome (ACS) and examine the ECGs that led to their diagnosis.
Intended to ‘capture’ arrhythmias over a longer period than a snapshot given by an ECG. One problem is that arrhythmias may not occur during the 24-hour monitored period—alternatives include a 48-hour monitor or an implantable recorder.
Ultrasound of the heart to discern structure and function, performed either as TTE or TOE. A normal range of LV ejection fraction is 55–70%. Attend a clinic to understand the principles of imaging.
ECG and BP assessment using a treadmill (‘Bruce protocol’) or by chemical stress (e.g. dobutamine) used to confirm and quantify IHD. The test might be stopped if symptomatic (e.g. chest pain) or significant ECG changes (e.g. ST elevation).
Non-invasive technetium-99 scan to assess myocardial blood flow often following exercise or chemical stress test (as previously mentioned) to determine hypoperfusion.
Fig. 8.3 Left coronary angiogram. LAD, left anterior descending coronary artery; LCX, left circumflex coronary artery. Reproduced with permission from Matsunaga et al. Angiostatin is negatively associated with coronary collateral growth in patients with coronary artery disease. Am J Physiol Heart Circ Physiol. 2005 May;288(5):H2042–6.
Fig. 8.4 Basic ECG rhythms. AF, atrial fibrillation; SVT, supraventricular tachycardia; VF, ventricular fibrillation; VT, ventricular tachycardia. Reproduced with permission from Tim Raine et al, Oxford Handbook for the Foundation Programme 4e, 2014, Oxford University Press.
Assess and manage airway using manoeuvres/adjuncts.
Assess respiratory effort, 15 L/min O2, if no respiratory effort call arrest team.
CRT, pulse, heart sounds, BP, if no pulse call arrest team.
ACS is a spectrum of coronary arterial disease from unstable angina (ischaemic chest pain at rest) to myocardial infarction (chest pain and cardiac ischaemia with elevated cardiac enzymes). MI is often classified by ST elevation (or new LBBB), STEMI, or those without ST elevation (NSTEMI, subendocardial infarction), but often with other ischaemic changes (e.g. T-wave inversion, ST depression). Both result in infarction of myocytes and the release of cardiac enzymes (e.g. troponin).
Pain in chest and/or arms, back, jaw lasting >15 min, nausea, vomiting, marked sweating, breathlessness, and haemodynamic instability. Beware that MI can be ‘silent’ (painless), especially in the elderly and diabetics.
Male sex, increasing age, hypercholesterolaemia, hypertension, diabetes mellitus, smoking, family history of coronary artery disease, obesity.
History of typical cardiac pain and:
• ≥1 mm ST elevation in at least two adjacent limb leads or
• ≥2 mm ST elevation in at least two contiguous precordial leads or
You must be able to recognize a STEMI on an ECG for your exams—this is a very common question (see 
http://lifeinthefastlane.com/).
Raised troponin ± ischaemic ECG changes, but do not fulfil STEMI criteria.
Worsening angina or a single episode of ‘crescendo angina’, with a high risk of impending MI. Features include angina at rest, frequency, duration, and severity of pain (including response to GTN).
• ECG (within 5 min of arrival). It is helpful to review previous ECGs to look for new changes, e.g. LBBB. Repeat the ECG every 15 min to look for dynamic changes, especially if further pain.
• Full blood count (FBC), urea and electrolytes (U&E), glucose, INR, activated partial thromboplastin time (APTT), troponin T or I on arrival and at 12 hours after symptom onset (or presentation if unknown). Note, high-sensitivity troponins are being used to rule out ACS earlier.
• CXR—only if there are clinical features of LV failure and if it will not delay PCI/thrombolysis.
• The Global Registry of Acute Coronary Events (GRACE) score is used to risk stratify patients with diagnosed ACS.
• Sit the patient up, give O2 if hypoxic, attach cardiac monitor.
• Aspirin 300 mg PO stat (get senior advice if patient on warfarin).
• GTN spray sublingually: try one or two puffs (400 mcg per puff).
• Diamorphine or morphine IV (± metoclopramide) as required.
• Clopidogrel 300 mg PO stat if ischaemic ECG or raised troponin (600 mg or prasugrel 60 mg if going for PCI).
• IV infusion GTN if pain continues and systolic BP >90 mmHg (start at 0.6 mg/hour and as necessary).
• Atenolol IV or PO unless contraindicated.
• Glycaemic control: patients with clinical MI and diabetes mellitus or marked hyperglycaemia (>11.0 mmol/L) should have immediate blood glucose control, continued for at least 24 hours.
• Management of STEMI can be according to MONACLES:
• Low-molecular-weight heparin (LMWH), e.g. Enoxaparin
• Refer for immediate primary PCI (pPCI), ideally to be performed within 90 min of first medical contact. This is superior to thrombolysis.
• Glycoprotein IIb/IIIa inhibitor (e.g. IV abciximab) if undergoing pPCI.
• When pPCI cannot be provided within 120 min, administer immediate thrombolysis (e.g. reteplase), unless contraindicated.
• If not having pPCI, give fondaparinux 2.5 mg IV initially, then subcutaneously (SC) daily.
• LMWH, e.g. enoxaparin 1 mg/kg SC every 12 hours or fondaparinux 2.5 mg SC daily.
• If medium or high risk of early recurrent cardiovascular events, organize early PCI.
• Consider a glycoprotein IIb/IIIa inhibitor e.g. eptifibatide (IV) for high-risk patients, particularly if they are undergoing PCI—seek expert advice.
Unstable angina is managed according to degree of risk: antiplatelets, nitrates, beta blockers, ± angiography.
Assess LV function in all MI patients (e.g. echocardiography).
If acute MI is confirmed, offer:
• aspirin plus a second antiplatelet agent, e.g. clopidogrel
• beta blocker, e.g. bisoprolol once stable, titrate up
• consider stress testing in low-risk patients with ACS.
Complication of MI are INFARCT:
• Inflamed pericardium (pericarditis, Dressler’s syndrome weeks later).
• New murmur (e.g. papillary muscle rupture MR, septal rupture ventricular septal defect (VSD)).
• Failure (cardiogenic shock).
• Rupture of LV pericardial effusion/tamponade.
• Thromboembolism (mural thrombi systemic emboli, e.g. gut ischaemia).
This is acute onset of pump failure due to intercurrent illness (e.g. sepsis), post MI, arrhythmias, or decompensation of chronic heart failure. Patient presents with breathlessness and fatigue associated with cardiac disease. It is often accompanied by fluid retention, as indicated by an elevated JVP and oedema. Acute heart failure develops quickly, while chronic failure develops over a longer period. Causes: systolic LV dysfunction (i.e. pump failure), diastolic LV dysfunction, congenital heart disease, pericardial or endocardial disease, valvular problems, rhythm/conduction disturbance, and hypertension.
• ECG: not often normal and may give clues to the cause (e.g. Q waves and poor R-wave progression in previous MI, LVH in hypertension/AS, low-voltage QRS in pericardial disease. Also LBBB, AF, AV block, bradyarrhythmia).
• CXR: cardiomegaly, pulmonary oedema, pleural effusion, upper lobe diversion, ‘bat’s wing’ hilar shadows, Kerley B lines, pleural effusions, fluid in interlobar fissure (a popular exam question).
• Arterial blood gases (ABGs): if hypoxic.
• FBC, U&E, consider liver function tests (LFTs) and thyroid function tests (TFTs).
• BNP: rules out if <100 ng/L.
• Echocardiography: within 48 hours of admission for those with a new diagnosis of heart failure (raised BNP).
Acute treatment is LMNOP:
Treatment of the underlying cause and other steps include the following:
• Sit patient up, give O2, and attach cardiac monitor.
• Furosemide IV 20–40 mg (more if renal impairment or already on diuretics).
• Monitor U&E, weight, and urine output while on diuretics.
• The National Institute for Health and Care Excellence (NICE) do not recommend routinely using nitrates, but consider GTN IV infusion if there is concomitant myocardial ischaemia, severe hypertension, or regurgitant aortic or mitral valve disease. Monitor BP closely (keep systolic BP >90 mmHg). New guidelines are cautious about the use of morphine but this is dependent on judicious use for the patient.
• Non-invasive ventilation (NIV) (continuous positive airway pressure (CPAP)): for cardiogenic pulmonary oedema with severe dyspnoea and acidaemia.
• Invasive ventilation indications: respiratory failure, reduced consciousness, or exhaustion despite treatment.
• Beta blocker: start when stable (i.e. not requiring diuretics) if there is LV systolic dysfunction unless HR <50, second- or third-degree heart block, or shock.
• ACEI and an aldosterone antagonist (e.g. spironolactone) if reduced LV ejection fraction.
• Limit fluid intake to 2 L/day.
• Moderate regular exercise and weight loss if overweight.
• Stop smoking and avoid alcohol.
Infection of heart valves characterized by a new murmur and evidence of infection. Organisms include Streptococcus viridans (commonest), Staphylococcus aureus (e.g. IV drug user (IVDU), early prosthetic valve infection), and Staphylococcus epidermidis (late prosthetic valve infection). Risk factors include valvulopathy, prosthetic valve, and recurrent bacteraemia (IVDU, poor dentition). Treatment is with broad-spectrum IV antibiotics (e.g. benzylpenicillin, flucloxacillin, and gentamicin). It is possible to get through a whole cardiology attachment without seeing a patient with confirmed infective endocarditis.
Honours
A confident clinical diagnosis of infective endocarditis requires two major criteria, one major and three minor criteria, or five minor criteria.
• Two separate blood cultures growing microorganisms typical for infective endocarditis.
• Echocardiographic evidence of endocardial infection.
• Predisposing condition (e.g. valvular disease).
• Embolic phenomenon (e.g. Janeway lesions).
• Immunological phenomenon (e.g. Osler’s nodes).
• Microbiological evidence (e.g. single positive blood culture).
Fig. 8.5 Echocardiogram confirming infective endocarditis. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle. Reproduced with permission from Cabell CH et al. Bacterial endocarditis: the disease, treatment, and prevention. Circulation. 2003 May 27;107(20):e185–7. http://circ.ahajournals.org/content/107/20/e185
Sinus tachycardia—usually rate is <150 bpm. Can be due to fever, pain, anxiety, hypovolaemia, anaemia, heart failure, or thyrotoxicosis. The treatment approach for unstable patients is similar regardless of the specific tachyarrhythmia. Unstable patients (e.g. with shock, syncope, MI, heart failure), require DC cardioversion. Otherwise, distinguish between broad and narrow complex tachyarrhythmias. Narrow complex (QRS <120 ms): supraventricular tachycardia (SVT) and atrial flutter (regular), AF (irregularly irregular). Broad complex (QRS >120 ms): ventricular tachycardia (VT), torsades de pointes (regular), and ventricular fibrillation (VF) (irregular). Interventions vagal manoeuvers (carotid massage, Valsalva) and IV adenosine (SVT (usually >150 bpm)) and IV amiodarone (VT). With adenosine, warn the patient they will briefly feel terrible. You may need to spend some time in the resuscitation area, intensive therapy unit (ITU), or coronary care unit to see these unstable patients.
Causes of sinus bradycardia include inferior MI, drugs (e.g. digoxin), and hypothyroidism. Unstable bradyarrhythmia (hypotension, syncope, heart failure) requires urgent pharmacological treatment (e.g. atropine 500 mcg IV) and/or transcutaneous pacing.
Inflammation of the pericardium which may be idiopathic or caused by infection or post MI. It is characterized by pleuritic chest pain relieved by sitting forward and ECG might show saddle-shaped (concave-ST segment) elevation. It is typically treated with NSAIDs and these patients are not regularly admitted or followed up in clinic so the ED is your best chance of finding this condition.
Characterize pain, e.g. using SOCRATES: site, onset, character, radiation, associations, time course, exacerbating/relieving factors, severity. Determine whether chest pain is ischaemic. Pleurisy (sharp pain on inspiration, relieved by sitting forward) is caused by the four Ps: pericarditis, PE, pneumothorax, and pneumonia.
• Central (± radiating to left arm, neck, jaw).
• Sudden onset, crushing, ‘elephant sitting on chest’, or heavy.
• Associated with heartburn/nausea/sweating.
When taking a history, consider cardiac (ACS, pericarditis, AS, aortic dissection), respiratory (PE, pneumothorax, pneumonia), GI (GORD, oesophageal spasm, oesophagitis, cholecystitis, peptic ulcer), and MSk (fracture, costochondritis) causes. Ask about key features (worse on breathing/eating/moving) to satisfy examiners that you are thinking more broadly than cardiac causes alone. Stable angina is the most likely encounter in clinical examinations (see p. 181).
Honours
A genetic cardiac disease also known as ‘sudden death syndrome’ due to sodium channelopathy leading to fatal VF. ECG shows right bundle branch block, prolonged PR and ST elevation mainly anteriorly (in V1–V3).
Most patients with shortness of breath have a respiratory cause. Acute heart failure is very unlikely in an examination setting, but consider chronic heart failure in any patient with a cardiovascular history (e.g. MI) or coronary risk factors. Classification for difficulty in breathing (dyspnoea) is by New York Heart Association (NYHA) classes or Medical Research Council (MRC) grades (see Table 8.4).
Table 8.4 NYHA vs modified MRC classification grades
| Class | NYHA | Grade | MRC |
| I | Presence of cardiac disease without limitation to physical activity | 0 | No dyspnoea except with strenuous exercise |
| II | Presence of cardiac disease with slight limitation to physical activity | 1 | Dyspnoea when hurrying on level or walking uphill |
| III | Presence of cardiac disease with marked limitation to physical activity | 2 | Walks slower than contemporaries or has to stop on level ground due to dyspnoea |
| 3 | Stops for breath after walking 100 m or after a few minutes on level ground | ||
| IV | Presence of cardiac disease resulting in the inability to carry on with physical activity without discomfort | 4 | Too breathless to leave the house or to dress/undress oneself |
Patients experience an abnormal awareness of the heart beating. The patient will complain of ‘missing a beat’ or ‘heart fluttering’. Adapt your standard history of presenting complaint and ask them to tap out the rhythm. Your aim is to establish whether the beat is regular or accelerated during episodes. Tachyarrhythmias cause palpitations but bradyarrhythmias do not. There are three broad causes and a good history will distinguish between these.
• Hyperdynamic circulation: thyrotoxicosis, pyrexia, anaemia, pregnancy.
• Sympathetic overdrive: anxiety, phaeochromocytoma.
• Dysrhythmias: AF, atrial flutter, SVT, VT, VF, heart block.
It is important to ask about associated symptoms (shortness of breath, chest pain, blackouts, and feeling unwell) and family history (close relative with history of sudden cardiac death at a young age). Again, these are necessary to be considered ‘safe’. Examiners’ favourites include AF. Other dysrhythmias (SVT, VT, VF) are potentially unstable and unlikely to appear in clinical examinations.
This is caused by cerebral hypoperfusion (e.g. hypoxia, hypotension). It is a complicated presentation, so learn the important causes. When taking a syncope history, organize your questions in terms of what was happening before, during, and after the attack.
An emotionally charged situation points to vasovagal syncope; standing up quickly or for a long time suggests orthostatic/postural hypotension. Syncope on exercise is sinister and indicates cardiac outflow obstruction (e.g. AS). Associated symptoms during (or immediately before) the attack include aura (i.e. warning of impending syncope), nausea, sweating, visual disturbance, fingertip/lip tingling, palpitations, and chest pain.
Drugs commonly causing syncope include antihypertensives (e.g. diuretics, nitrates, beta blockers) and tricyclic antidepressants (e.g. amitriptyline).
• Often during times of stress (e.g. fasting, coughing, exercise).
• Dysrhythmias (e.g. heart blocks, Wolff–Parkinson–White syndrome, VT).
• Obstructive lesions (e.g. AS, septal hypertrophy).
• Bradycardia (e.g. sick sinus syndrome, Stokes–Adams attacks).
• Standing up too quickly or for too long.
• Primary autonomic failure (e.g. Parkinson’s disease).
• Secondary autonomic failure (e.g. autonomic neuropathy in diabetes).
Cardiology is all about clinical signs; you are very unlikely to see a number of these throughout your entire career but that should not stop you from looking!
You need to be able to recognize important clinical signs which may be presented in photograph form or in actual patients. You may not see these in the outpatient department so visit other resources such as books and online references.
Albeit rare signs, look for splinter haemorrhages (dark ‘pen marks’ under nailbed), clubbing, Janeway lesions (painless haemorrhagic macules on palms/soles, septic embolic microhaemorrhages), Osler’s nodes (tender papules on pulps from immunological complex deposits), Roth spots (seen on fundoscopy), and new murmur (acutely regurgitation followed by stenosis from chronic inflammation). Other signs include splenomegaly as well as microscopic haematuria and strokes from septic emboli.
Obesity, tar staining, high BP, and signs of hypercholesterolaemia: corneal arcus (grey ring around iris), tendon xanthomata (small yellow papules, usually knuckles), and xanthelasma (small yellow papules on eyelids). Bear in mind that corneal arcus is pathological below the age of 50 years but geriatric patients have physiological corneal senilis.
Do not fear murmurs—they commonly appear in finals and are only difficult when unnecessarily complicated. It is rarely necessary to correctly diagnosis the valve lesion from auscultation alone—recognizing the existence of a murmur may be sufficient to pass. Suspect a murmur in all cardiac patients. Use the history to predict what murmur to expect. Commonly encountered cases are MR (young, endocarditis, connective tissue disorder, or post MI) and mechanical aortic valves. Diastolic murmurs (e.g. tricuspid stenosis, pulmonary regurgitation) are rarer, quieter, and less likely to appear in examinations. If you hear a murmur, state whether it is systolic or diastolic. Feel the carotid pulse while auscultating the chest. If the murmur and pulse are synchronous, it is systolic. If they are asynchronous, the murmur is diastolic. You must distinguish between these in real patients before finals—listening to recorded heart sounds is not sufficient. Do not obsess between a pansystolic (MR) vs mid-systolic ejection (AS) murmur. You can mention the difference characteristics between both murmurs but it is never that clear cut in practice.
Honours
Patients with prosthetic aortic valves (tissue or metal) often appear in examinations because they are stable, well known to the hospital, and have more obvious clinical signs. On inspecting the chest, you will see a large scar in the chest midline (median sternotomy). At this point you could divert your routine (briefly) to examine the legs for evidence of great saphenous vein harvesting. A leg scar suggests previous CABG but no scar indicates another cardiac procedure (e.g. valve replacement). Aortic valves are routinely replaced and mitral valves are usually repaired first. If there is no evidence of great saphenous vein harvesting, listen carefully and you may be rewarded by the soft ‘click’ of a metallic aortic valve. Report this constellation of findings out loud to the examiner—diagnosing a metallic aortic valve replacement without laying a hand (or stethoscope) on the patient has to be worth bonus points!
You are unlikely to commit the signs of each valve lesion to your long-term memory by rote learning alone. Try to think mechanically about why each sign exists. AS means blood (at high pressure being ejected from the heart) squeezing through a tight hole. The result is a loud noise on ejection (the ejection systolic murmur best heard in the aortic area at the right second intercostal space or parasternal edge) which radiates to the carotids, a slow-rising ‘anacrotic’ pulse (as the column of blood squeezes through the narrowed hole), and a narrow pulse pressure (systolic and diastolic pressures close together). By contrast, in AR, blood pumped from the heart falls backwards through the incompetent aortic valve leading to a ‘collapsing’ or ‘waterhammer’ pulse, wide pulse pressure, and an early diastolic murmur in the aortic area. Consider reading up on the eponymous signs associated with AR. The key feature of MR is a pansystolic murmur that radiates to the axilla. You should learn signs of other murmurs (e.g. MS, but the signs of AS, AR, and MR are particularly high yield). (See Table 8.5 for Levine’s grading).
Table 8.5 Levine’s grading of heart murmurs
| Grade | Examination finding |
| I | Barely audible on auscultation |
| II | Faint but audible on auscultation |
| III | Easily heard without a thrill |
| IV | Loud murmur with a palpable thrill |
| V | Louder murmur heard over a wide area with a thrill |
| VI | Murmur heard without stethoscope (e.g. metallic valve) |
Almost regardless of presentation, the investigation of cardiac complaints is universal. Send routine bloods (e.g. FBC, U&E) and consider thyroid function tests (hyperthyroidism worsens angina and is a cause of AF). Most patients should have a CXR, ECG, and echocardiogram. Cardiac ischaemia may require an exercise tolerance test, and intermittent dysrhythmias should be investigated with a 24-hour Holter monitor.
Depends largely on the underlying pathology but may include monitoring, medication, antibiotics for infective endocarditis, and surgery (replacement with xenograft or metal).
Honours
There are many eponymous signs of AR which are unlikely to appear in formal exams but are beloved by consultants and senior trainees alike. You are unlikely to ever see them (hence their disappearance from exams) and it has been said that the last person to have seen De Musset’s sign was De Musset himself! They nevertheless remain part of the rich historical tapestry of medical education:
• Corrigan’s sign: abrupt distension and collapse of carotid arteries.
• De Musset’s sign: rhythmic nodding of the head in synchrony with the heart beating.
• Müller’s sign: pulsation of the uvula.
• Quincke’s sign: capillary pulsation in the nailbeds visible on applying gentle pressure.
• Traube’s sign: ‘pistol shot’ sound on auscultating femoral pulse.
Although it is a simple concept, heart failure is often misunderstood by students and poorly explained by their teachers. It essentially means the pump is not working effectively enough to propel blood around the body. One major consequence is that the column of blood backs up and fluid is squeezed out of the arterial circulation into inappropriate spaces. Signs of heart failure are often described as being caused by ‘left-’ or ‘right-sided’ heart failure, although these rarely present as isolated entities. Most patients will have mixed ‘congestive cardiac failure’. In right ventricular failure, blood backs up along the inferior and superior vena cavae which leads to raised JVP, hepatomegaly, ascites, and peripheral oedema. In LV failure, blood backs up along the pulmonary veins. The signs (and symptoms) are therefore primarily respiratory, such as dyspnoea, respiratory distress, bibasal crepitations, pleural effusion, pleural oedema, and hypoxia.
