Page of

Cardiovascular medicine 

Cardiovascular medicine
Chapter:
Cardiovascular medicine
Source:
Oxford Handbook of Clinical Medicine (10 ed.)
Author(s):

Ian B. Wilkinson

, Tim Raine

, Kate Wiles

, Anna Goodhart

, Catriona Hall

, and Harriet O’Neill

DOI:
10.1093/med/9780199689903.003.0003

Fig 3.1 Helen Taussig (1898–1986) battled dyslexia, deafness, and a male-dominated world to become a leading cardiologist. She noticed that ‘blue babies’ with a patent ductus arteriosus (pda) tended to survive longer than those without. This was because many blue babies have congenital obstruction to pulmonary blood flow (eg pulmonary stenosis in tetralogy of Fallot, pTetralogy of Fallot157) and pdas increase blood flow to the lungs, reducing cyanosis. She devised the Blalock–Taussig shunt which creates a passage from the subclavian or carotid artery to one of the pulmonary arteries, mimicing a pda. This dramatically improved survival in babies with tetralogy of Fallot.
One of the joys of cardiology is how often solutions already exist in nature and much of our intervention involves trying to mimic circumstances that can occur naturally. Hence, a good grasp of the underlying physiology is essential for understanding clinical cardiology; as well as interesting to pursue in its own right.

Fig 3.1
Helen Taussig (1898–1986) battled dyslexia, deafness, and a male-dominated world to become a leading cardiologist. She noticed that ‘blue babies’ with a patent ductus arteriosus (pda) tended to survive longer than those without. This was because many blue babies have congenital obstruction to pulmonary blood flow (eg pulmonary stenosis in tetralogy of Fallot, p[link]) and pdas increase blood flow to the lungs, reducing cyanosis. She devised the Blalock–Taussig shunt which creates a passage from the subclavian or carotid artery to one of the pulmonary arteries, mimicing a pda. This dramatically improved survival in babies with tetralogy of Fallot.

One of the joys of cardiology is how often solutions already exist in nature and much of our intervention involves trying to mimic circumstances that can occur naturally. Hence, a good grasp of the underlying physiology is essential for understanding clinical cardiology; as well as interesting to pursue in its own right.

Cardiovascular symptoms

Chest pain

Cardiovascular medicineCardiac-sounding chest pain may have no serious cause, but always think ‘Could this be a myocardial infarction (mi), dissecting aortic aneurysm, pericarditis, or pulmonary embolism?’.

Character:

Constricting suggests angina, oesophageal spasm, or anxiety; a sharp pain may be from the pleura, pericardium, or chest wall. A prolonged (>½h), dull, central crushing pain or pressure suggests mi.

Radiation:

To shoulder, either or both arms, or neck/jaw suggests cardiac ischaemia. The pain of aortic dissection (p[link]) is classically instantaneous, tearing, and interscapular, but may be retrosternal. Epigastric pain may be cardiac.

Precipitants:

Pain associated with cold, exercise, palpitations, or emotion suggests cardiac pain or anxiety; if brought on by food, lying flat, hot drinks, or alcohol, consider oesophageal spasm/disease (but meals can also cause angina).

Relieving factors:

If pain is relieved within minutes by rest or glyceryl trinitrate (gtn), suspect angina (gtn relieves oesophageal spasm more slowly). If antacids help, suspect gi causes. Pericarditic pain improves on leaning forward.

Associations:

Dyspnoea occurs with cardiac pain, pulmonary emboli, pleurisy, or anxiety. mi may cause nausea, vomiting, or sweating. Angina is caused by coronary artery disease—and also by aortic stenosis, hypertrophic cardiomyopathy (hcm), paroxysmal supraventricular tachycardia (svt)—and can be exacerbated by anaemia. Chest pain with tenderness suggests self-limiting Tietze’s syndrome.1 Odd neurological symptoms and atypical chest pain—think aortic dissection.

Pleuritic pain:

Pain exacerbated by inspiration. Implies inflammation of the pleura from pulmonary infection, inflammation, or infarction. It causes us to ‘catch our breath’. ΔΔ‎: musculoskeletal pain;1 fractured rib (pain on respiration, exacerbated by gentle pressure on the sternum); subdiaphragmatic pathology (eg gallstones).

Cardiovascular medicine Chest pain & acutely unwell

(see p[link])

  • Admit

  • Check pulse, bp in both arms (unequal in aortic dissection p[link]), jvp, heart sounds; examine legs for dvt

  • Give O2

  • iv line

  • Relieve pain (eg 5–10mg iv morphine)

  • Cardiac monitor

  • 12-lead ecg

  • cxr

  • Arterial blood gas (abg)

Famous traps:

Aortic dissection; zoster (p[link]); ruptured oesophagus; cardiac tamponade (p[link]); opiate addiction.

Dyspnoea

May be from lvf, pe, any respiratory cause, anaemia, pain, or anxiety.

Severity:

Cardiovascular medicineEmergency presentations: p[link]. Ask about shortness of breath at rest, on exertion, and on lying flat; has their exercise tolerance changed?

Associations:

Specific symptoms associated with heart failure are orthopnoea (ask about number of pillows used at night), paroxysmal nocturnal dyspnoea (waking up at night gasping for breath, p[link]), and peripheral oedema. Pulmonary embolism is associated with acute onset of dyspnoea and pleuritic chest pain; ask about risk factors for dvt.

Palpitation(s)

May be due to ectopics, sinus tachycardia, af, svt, vt, thyrotoxicosis, anxiety, and rarely phaeochromocytoma. See p[link].

History:

Characterize: do they mean their heart was beating fast, hard, or irregularly? Ask about previous episodes, precipitating/relieving factors, duration of symptoms, associated chest pain, dyspnoea, dizziness, or collapse. Did the patient check their pulse?

Syncope

May reflect cardiac or cns events. Vasovagal ‘faints’ are common (pulse↓, pupils dilated). The history from an observer is invaluable in diagnosis.

Prodromal symptoms:

Chest pain, palpitations, or dyspnoea point to a cardiac cause, eg arrhythmia. Aura, headache, dysarthria, and limb weakness indicate cns causes.

During the episode:

Was there a pulse? Limb jerking, tongue biting, or urinary incontinence? nb: hypoxia from lack of cerebral perfusion may cause seizures.

Recovery:

Was this rapid (arrhythmia) or prolonged, with drowsiness (seizure)?

ecg—a methodical approach

Reading an ecg

Cardiovascular medicineFirst confirm the patient’s name and age, and the ecg date. Then (see fig 3.3):

  • Rate: At usual speed (25mm/s) each ‘big square’ is 0.2s; each ‘small square’ is 0.04s. To calculate the rate, divide 300 by the number of big squares between two consecutive r waves (table 3.1). The normal rate is 60–100bpm.

  • Rhythm: If cycles are not clearly regular, use the ‘card method’: lay a card along the ecg, marking positions of three successive r waves. Slide the card to and fro to check that all intervals are equal. If they are not, note if:

    • there is slight but regular lengthening and then shortening (with respiration)—sinus arrhythmia, common in the young

    • there are different rates which are multiples of each other—varying block

    • it is 100% irregular—atrial fibrillation (af) or ventricular fibrillation (vf).

    Sinus rhythm is characterized by a p wave followed by a qrs complex. af has no discernible p waves and qrs complexes are irregularly irregular. Atrial flutter (p[link], fig 3.35 p[link]) has a ‘sawtooth’ baseline of atrial depolarization (~300/min) and regular qrs complexes. Ventricular rhythm has qrs complexes >0.12s with p waves following them or absent (fig 3.12, p[link]).

  • Axis: The overall direction of depolarization across the patient’s anterior chest; this is the sum of all the ventricular electrical forces during ventricular depolarization. See box ‘Determining the ecg axis’. Left axis deviation can result from left anterior hemiblock, inferior mi, vt from a left ventricular focus, wpw, lvh. Right axis deviation can result from rvh, pe, anterolateral mi, wpw and left posterior hemiblock.

  • p wave: Normally precedes each qrs complex, and upright in ii, iii, & avf but inverted in avr. Absent p wave: af, p hidden due to junctional or ventricular rhythm. p mitrale: bifid p wave, indicates left atrial hypertrophy. p pulmonale: peaked p wave, indicates right atrial hypertrophy. Pseudo-p-pulmonale seen if ↑K+.

  • pr interval: Measure from start of p wave to start of qrs. Normal range: 0.12–0.2s (3–5 small squares). A prolonged pr interval implies delayed av conduction (1st degree heart block). A short pr interval implies unusually fast av conduction down an accessory pathway, eg wpw (see fig 3.37, p[link]). See heart block, p[link].

Fig 3.3 Schematic diagram of a normal ecg trace.

Fig 3.3
Schematic diagram of a normal ecg trace.

Fig 3.12 Ventricular tachycardia—regular broad complex tachycardiac indicating a likely ventricular origin for the rhythm.

Fig 3.12
Ventricular tachycardia—regular broad complex tachycardiac indicating a likely ventricular origin for the rhythm.

Fig 3.37 This patient has Wolff-Parkinson-White syndrome as they have delta waves (slurred qrs upstrokes) in beats 1 and 4 of this rhythm strip. the delta wave both broadens the ventricular complex and shortens the pr interval. If a patient with wpw has af, avoid av node blockers such as diltiazem, verapamil, and digoxin—but flecainide may be used.

Fig 3.37
This patient has Wolff-Parkinson-White syndrome as they have delta waves (slurred qrs upstrokes) in beats 1 and 4 of this rhythm strip. the delta wave both broadens the ventricular complex and shortens the pr interval. If a patient with wpw has af, avoid av node blockers such as diltiazem, verapamil, and digoxin—but flecainide may be used.

  • qrs complex: See fig 3.2. Normal duration: <0.12s. qrs >0.12s suggests ventricular conduction defects, eg a bundle branch block (pp[link], [link]), metabolic disturbance, or ventricular origin (eg ventricular ectopic). High-amplitude qrs complexes suggest ventricular hypertrophy (p[link]). Normal q waves are <0.04s wide and <2mm deep; they are often seen in leads i, avl, v5, and v6 and reflect normal septal depolarization. Pathological q waves (deep and wide) may occur within a few hours of an acute mi.

  • qt interval: Measure from start of qrs to end of t wave. It varies with rate. The corrected qt interval (qtc) is the qt interval divided by the square root of the rr interval, ie qtc=qt/√rr. Normal qtc: 0.38–0.42s. For causes of prolonged qt interval see p[link]. Long qt can lead to vt and sudden death.

  • st segment: Usually isoelectric. Planar elevation (>1mm) or depression (>0.5mm) usually implies infarction (p[link], figs 3.9, 3.10, pp[link][link]) or ischaemia, respectively.

  • t wave: Normally inverted in avr, v1, and occasionally v2. Normal if inverted in isolation in lead iii. Abnormal if inverted in i, ii, and v4v6. Peaked in hyperkalaemia (fig 14.4, p[link]) and flattened in hypokalaemia.

  • j wave: See p[link]. The j point is where the s wave finishes and st segment starts. A j wave is a notch at this point. Seen in hypothermia, sah, and ↑Ca2+.

Fig 3.2 ‘qrs’ complexes. If the first deflection from the isoelectric line is negative, it is a q wave. Any positive deflection is an r wave. Any negative deflection after an r is an s.

Fig 3.2
qrs’ complexes. If the first deflection from the isoelectric line is negative, it is a q wave. Any positive deflection is an r wave. Any negative deflection after an r is an s.

Fig 3.9 Acute infero-lateral myocardial infarction: marked st elevation in the inferior leads (ii, iii, avf), but also in v5 and v6, indicating lateral involvement. There is a ‘reciprocal change’ of st-segment depression in leads i and avl; this is often seen with a large inferior myocardial infarction.

Fig 3.9
Acute infero-lateral myocardial infarction: marked st elevation in the inferior leads (ii, iii, avf), but also in v5 and v6, indicating lateral involvement. There is a ‘reciprocal change’ of st-segment depression in leads i and avl; this is often seen with a large inferior myocardial infarction.

Fig 3.10 Acute anterior myocardial infarction—st segment elevation and evolving q waves (the first qrs deflection is negative) in leads v1-4.

Fig 3.10
Acute anterior myocardial infarction—st segment elevation and evolving q waves (the first qrs deflection is negative) in leads v1-4.

ecg—abnormalities

Sinus tachycardia

All impulses are initiated in the sinoatrial node (‘sinus rhythm’) hence all qrss are preceeded by a normal p wave with a normal pr interval. Tachycardia means rate >100bpm. See p[link].

Sinus bradycardia

Sinus rhythm at a rate <60bpm.

Causes:

Physical fitness, vasovagal attacks, sick sinus syndrome, drugs (β‎-blockers, digoxin, amiodarone), hypothyroidism, hypothermia, ↑intracranial pressure, cholestasis. See p[link].

AF

(ecg p[link]) Common causes: ihd, thyrotoxicosis, hypertension, obesity, heart failure, alcohol. See p[link].

Heart block (hb)

(See fig 3.5.) Disrupted passage of electrical impulse through the av node.

Fig 3.5 Rhythm strips of heart blocks.

Fig 3.5
Rhythm strips of heart blocks.

1st-degree hb:

The pr interval is prolonged and unchanging; no missed beats.

2nd-degree hb: Mobitz i:

The pr interval becomes longer and longer until a qrs is missed, the pattern then resets. This is Wenckebach phenomenon.

2nd-degree hb: Mobitz ii:

qrss are regularly missed. eg p - qrs - p - - p - qrs - p - - this would be Mobitz ii with 2:1 block (2p:1qrs). This is a dangerous rhythm as it may progress to complete heart block.

1st- and 2nd-degree hb may be caused by: normal variant, athletes, sick sinus syndrome, ihd (esp inferior mi), acute myocarditis, drugs (digoxin, β‎-blockers).

3rd-degree hb: Complete heart block:

No impulses are passed from atria to ventricles so p waves and qrss appear independently of each other. As tissue distal to the avn paces slowly, the patient becomes very bradycardic, and may develop haemodynamic compromise. Urgent treatment is required. Causes: ihd (esp inferior mi), idiopathic (fibrosis), congenital, aortic valve calcification, cardiac surgery/trauma, digoxin toxicity, infiltration (abscesses, granulomas, tumours, parasites).

st elevation

Normal variant (high take-off), acute mi (stemi), Prinzmetal’s angina (p[link]), acute pericarditis (saddle-shaped), left ventricular aneurysm.

st depression

Normal variant (upward sloping), digoxin toxicity (downward sloping), ischaemic (horizontal): angina, nstemi, acute posterior mi (st depression in v1v3).

t inversion

In v1v3: normal (black patients and children), right bundle branch block (rbbb), rv strain (eg secondary to pe). In v2v5: anterior ischaemia, hcm, subarachnoid haemorrhage, lithium. In v4v6 and avl: lateral ischaemia, lvh, left bundle branch block (lbbb). In ii, iii and avf: inferior ischaemia.

nb: st- and t-wave changes are often non-specific, and must be interpreted in the light of the clinical context.

Myocardial infarction

(See p[link] and fig 3.21; example ecgs figs 3.9, 3.10)

  • Within hours, the t wave may become peaked and st segments may begin to rise.

  • Within 24h, the t wave inverts. st elevation rarely persists, unless a left ventricular aneurysm develops. t-wave inversion may or may not persist.

  • Within a few days, pathological q waves begin to form. q waves usually persist, but may resolve in 10% of patients.

  • The location of these changes indicates the ischaemic area location, see table 3.2.

Fig 3.21 Sequential ecg changes following acute mi.

Fig 3.21
Sequential ecg changes following acute mi.

Pulmonary embolism

(fig 3.11) ecg findings may include: sinus tachycardia (commonest), rbbb (p[link]), right ventricular strain pattern (r-axis deviation, dominant r wave and t-wave inversion/st depression in v1 and v2,). Rarely, the ‘sIqIIItIII’ pattern occurs: deep s waves in i, pathological q waves in iii, inverted t waves in iii.

Fig 3.11 Changes seen in pulmonary hypertension (eg after a pe).

• Right axis deviation (qrs more negative than positive in lead I);
• Positive qrs complexes (‘dominant r waves’) in v1 and v2 suggesting right ventricular hypertrophy;
• st depression and t-wave inversion in the right precordial leads (v1-3) suggesting right ventricular strain;
• Peaked p waves (p pulmonale) suggesting right atrial hypertrophy.

Fig 3.11
Changes seen in pulmonary hypertension (eg after a pe).

  • Right axis deviation (qrs more negative than positive in lead I);

  • Positive qrs complexes (‘dominant r waves’) in v1 and v2 suggesting right ventricular hypertrophy;

  • st depression and t-wave inversion in the right precordial leads (v1-3) suggesting right ventricular strain;

  • Peaked p waves (p pulmonale) suggesting right atrial hypertrophy.

Reproduced from Handler et al., Pulmonary Hypertension, 2012, with permission from Oxford University Press.

Metabolic abnormalities

Digoxin effect:

Down-sloping st depression and inverted t wave in v5v6 (‘reversed tick’, see fig 3.19). In digoxin toxicity, any arrhythmia may occur (ventricular ectopics and nodal bradycardia are common).

Fig 3.19 This ecg shows the classic ‘reverse tick’ of digoxin toxicity: downsloping st wave with rapid upstroke back to isoelectric line. The bradycardia is also suggestive of digoxin toxicity.

Fig 3.19
This ecg shows the classic ‘reverse tick’ of digoxin toxicity: downsloping st wave with rapid upstroke back to isoelectric line. The bradycardia is also suggestive of digoxin toxicity.

Hyperkalaemia:

Tall, tented t wave, widened qrs, absent p waves, ‘sine wave’ appearance (see fig 14.4, p[link]).

Hypokalaemia:

Small t waves, prominent u waves, peaked p waves.

Hypercalcaemia:

Short qt interval.

Hypocalcaemia:

Long qt interval, small t waves. See p[link] for causes of long qt intervals.

ecg—additional points

Where to place the chest leads

(See fig 3.6.)

  • v1: Right sternal edge, 4th intercostal space.

  • v2: Left sternal edge, 4th intercostal space.

  • v3: Half-way between v2 and v4.

  • v4: 5th intercostal space, mid-clavicular line; all subsequent leads are in the same horizontal plane as v4.

  • v5: Anterior axillary line.

  • v6: Mid-axillary line (v7: posterior axillary line).

Fig 3.6 Placement of ecg leads.

Fig 3.6
Placement of ecg leads.

Good skin preparation (clean with non-alcoholic wipe, shave if hairy, etc.) will improve ecg quality. Finish 12-lead ecgs with a long rhythm strip in lead ii.

qrs complexes: the long and the short

qrs complexes represent ventricular depolarization, and width represents time, so a broader qrs complex means depolarization of the ventricles is taking longer. Normally, a wave of depolarization reaches the ventricles via the specialist conduction pathways—the bundles of His. This delivers the electrical activity to certain points of the ventricles, meaning the waves of depolarization need travel as short a distance as possible to depolarize all the ventricular myocardium. This allows rapid spread of depolarization and thus an efficient contraction action as both ventricles contract from apex to outflow tracts together. Hence, the qrs complex is narrow (<120ms).

Ventricular depolarization takes longer when depolarization is not initiated in this pattern. For example, if it originates in the ventricles (eg ventricular ectopics, vt) or if one or more branches of the bundles of His are blocked—bundle branch blocks—meaning depolarization is initiated in one ventricle but not the other, so it has to travel the long (in time and space) path from one ventricle to the other.

Ventricular depolarization also takes longer if all conduction is slowed. This may happen in some electrolyte imbalances, eg hyperkalaemia.

Right bundle branch block:

(p[link], fig 3.8) qrs >0.12s, ‘rsr’ pattern in v1; dominant r in v1; inverted t waves in v1v3 or v4; wide, slurred s wave in v6. Causes: normal variant (isolated rbbb), pulmonary embolism, cor pulmonale.

Fig 3.8 Right bundle branch block—broad qrs, M pattern in v1 and sloped s wave (with the eye of faith, a ‘W’ shape) in v5. MaRRoW = RBBB.

Fig 3.8
Right bundle branch block—broad qrs, M pattern in v1 and sloped s wave (with the eye of faith, a ‘W’ shape) in v5. MaRRoW = RBBB.

Left bundle branch block:

(p[link], fig 3.7) qrs >0.12s, ‘m’ pattern in v5, dominant s in v1, inverted t waves in i, avl, v5v6. Causes: ihd, hypertension, cardiomyopathy, idiopathic fibrosis. Cardiovascular medicinenb: if there is lbbb, no comment can be made on the st segment or t wave. Cardiovascular medicineNew lbbb may represent a stemi, see p[link].

Fig 3.7 Left bundle branch block: wide qrs with a W pattern in v1 (slight notching in upstroke of s wave—clearer in v3) and the M pattern in v6. WiLLiaM = LBBB.

Fig 3.7
Left bundle branch block: wide qrs with a W pattern in v1 (slight notching in upstroke of s wave—clearer in v3) and the M pattern in v6. WiLLiaM = LBBB.

Bifascicular block:

The combination of rbbb and left bundle hemiblock, manifest as an axis deviation, eg left axis deviation in the case of left anterior hemiblock.

Trifascicular block:

Bifascicular block plus 1st-degree hb. Cardiovascular medicineMay need pacing (p[link]).

Suspect left ventricular hypertrophy (lvh) if the r wave in v6 is >25mm or the sum of the s wave in v1 and the r wave in v6 is >35mm (see fig 3.41).

Fig 3.41 Left ventricular hypertrophy—this is from a patient with malignant hypertension—note the sum of the s-wave in v2 and r-wave in v6 is greater than 35mm.

Fig 3.41
Left ventricular hypertrophy—this is from a patient with malignant hypertension—note the sum of the s-wave in v2 and r-wave in v6 is greater than 35mm.

Suspect right ventricular hypertrophy (rvh) if dominant r wave in v1, t wave inversion in v1v3 or v4, deep s wave in v6, right axis deviation.

Other causes of dominant r wave in v1: rbbb, posterior mi, type a wpw syndrome (p[link]).

Causes of low-voltage qrs complex:

(qrs <5mm in all limb leads.) Hypothyroidism, chronic obstructive pulmonary disease (copd), ↑haematocrit (intracardiac blood resistivity is related to haematocrit), changes in chest wall impedance (eg in renal failure & subcutaneous emphysema but not obesity), pulmonary embolism, bundle branch block, carcinoid heart disease, myocarditis, cardiac amyloid, doxorubicin cardiotoxicity, and other heart muscle diseases, pericardial effusion, pericarditis.5

See lifeinthefastlane.com for excellent ecg tutorials, cases, and examples.

Cardiac imaging

There are many heart conditions associated with structural defects, eg valve defects, congenital heart diseases, and some muscle disorders (eg hypertrophic cardiomyopathy (hcm)). Whilst clues to these can sometimes be found on history, examination, and ecg, it is imaging that gives the diagnosis. Imaging is also helpful for conditions that are not primarily due to deformities but which affect the way the heart functions. For example, after an mi the affected territory may be hypokinetic. Stress techniques allow us to observe the heart at rest and then under stress, comparing the perfusion and function in the two states. Cardiac mri is a rapidly expanding area although not yet available in all major hospitals.

Chest x-ray

The humble chest x-ray provides just a snapshot of the heart and little detail but can be an important source of information and is often the only immediately accessible imaging modality for a new or newly unwell patient. An enlarged heart (cardiothoracic ratio >0.5) suggests congestive heart failure; signs of pulmonary oedema suggest decompensated heart failure (see fig 3.38); a globular heart may indicate pericardial effusion (fig 3.14); metal wires and valves will show up, evidencing previous cardiothoracic surgery; dextrocardia may explain a bizarre ecg; and rib notching may be an important clue in coarctation of the aorta (p[link]).

Fig 3.38 (a) The cxr in left ventricular failure. These features can be remembered as a b c d e. Alveolar oedema, classically this is perihilar ‘bat’s wing’ shadowing. Kerley B lines—now known as septal lines. These are variously attributed to interstitial oedema and engorged peripheral lymphatics. Cardiomegaly—cardiothoracic ratio >50% on a pa film. Dilated prominent upper lobe veins (upper lobe diversion). Pleural Effusions. Other features include peribronchial cuffing (thickened bronchial walls) and fluid in the fissures. (b) ‘Bat’s wing’, peri-hilar pulmonary oedema indicating heart failure and fluid overload.

Fig 3.38
(a) The cxr in left ventricular failure. These features can be remembered as a b c d e. Alveolar oedema, classically this is perihilar ‘bat’s wing’ shadowing. Kerley B lines—now known as septal lines. These are variously attributed to interstitial oedema and engorged peripheral lymphatics. Cardiomegaly—cardiothoracic ratio >50% on a pa film. Dilated prominent upper lobe veins (upper lobe diversion). Pleural Effusions. Other features include peribronchial cuffing (thickened bronchial walls) and fluid in the fissures. (b) ‘Bat’s wing’, peri-hilar pulmonary oedema indicating heart failure and fluid overload.

Fig 3.14 Two chest x-rays of the same patient, the one on the right was taken 6 months after the one on the left. On the later image, a pericardial effusion has expanded the cardiac shadow and given it a ‘globular’ shape.

Fig 3.14
Two chest x-rays of the same patient, the one on the right was taken 6 months after the one on the left. On the later image, a pericardial effusion has expanded the cardiac shadow and given it a ‘globular’ shape.

Reproduced from Leeson, Cardiovascular Imaging, 2011, with permission from Oxford University Press.

Echocardiography

This is the workhorse of cardiological imaging. Ultrasound is used to give real-time images of the moving heart. This can be transthoracic (tte) or transoesophageal (toe), at rest, during exercise, or after infusion of a pharmacological stressor (eg dobutamine). If the patient is too unwell to be moved, an echo machine can be brought to them and continuous toe imaging may be used as a guide during surgery. Increasingly pocket-sized echo machines are used for a quick assessment of an unwell patient, to be followed by a formal scan later. See p[link].

Cardiac ct

This can provide detailed information about cardiac structure and function. ct angiography (fig 3.15) permits contrast-enhanced imaging of coronary arteries during a single breath hold with very low radiation doses. It can diagnose significant (>50%) stenosis in coronary artery disease with an accuracy of 89%. ct coronary angiography has a negative predictive value of >99%, which makes it an effective non-invasive alternative to routine transcatheter coronary angiography to rule out coronary artery disease.6 Medications are often given to slow the heart down and the imaging may be ‘gated’, meaning the scanner is programmed to take images at times corresponding to certain points on the patient’s ecg. This allows characterization of the heart at different points in the cardiac cycle. See p[link].

Fig 3.15 Cardiac ct demonstrating coronary artery stenosis.

Fig 3.15
Cardiac ct demonstrating coronary artery stenosis.

Reproduced from Camm et al., esc Textbook of Cardiovascular Medicine, 2009, with permission from Oxford University Press.

Cardiac mr

A radiation-free method of characterizing cardiac structure and function including viability of myocardium. By varying the settings, different defects can be found. mr is the first-choice imaging method to look at diseases that directly affect the myocardium (fig 3.16). Nowadays, pacemakers are available which are safe for mr scanning—check mr safety with your cardiac technicians before requesting mr for patients with pacemakers in situ. See p[link].

Fig 3.16 Cardiac mr image demonstrating the asymmetrical left ventricular wall thickening typical of hypertrophic cardiomyopathy.

Fig 3.16
Cardiac mr image demonstrating the asymmetrical left ventricular wall thickening typical of hypertrophic cardiomyopathy.

Reproduced from Myerson et al., Cardiovascular Magnetic Resonance, 2013, with permission from Oxford University Press.

Nuclear imaging

Perfusion is assessed at rest and with exercise- or pharmacologically-induced stress. This test is particularly useful for assessing whether myocardium distal to a blockage is viable and so whether stenting or cabg will be of value. If hypoperfusion is ‘fixed’, ie present at rest and under stress, the hypoperfused area is probably scar tissue and so non-viable. If hypoperfusion is ‘reversible’ at rest, the myocardium may benefit from improved blood supply. See p[link].

Echocardiography

This non-invasive technique uses the differing ability of various structures within the heart to reflect ultrasound waves. It not only demonstrates anatomy but also provides a continuous display of the functioning heart throughout its cycle.

Types of scan

m-mode (motion mode):

A single-dimension image.

Two-dimensional (real time):

A 2d, fan-shaped image of a segment of the heart is produced on the screen (fig 3.17); the moving image may be ‘frozen’. Several views are possible, including long axis, short axis, 4-chamber, and subcostal. 2d echocardiography is good for visualizing conditions such as: congenital heart disease, lv aneurysm, mural thrombus, la myxoma, septal defects.

Fig 3.17 Echo images. (a) A normal heart seen with the parasternal long-axis view. (b) Diagram of what can be seen in (a). (c) A normal heart seen in apical four-chamber view. (d) Diagram of what can be seen in (c).

Fig 3.17
Echo images. (a) A normal heart seen with the parasternal long-axis view. (b) Diagram of what can be seen in (a). (c) A normal heart seen in apical four-chamber view. (d) Diagram of what can be seen in (c).

Reproduced from Leeson et al., Echocardiography, 2012, with permission from Oxford University Press.

3d echocardiography:

Now possible with matrix array probes, and is termed 4d (3d + time) if the images are moving.

Doppler and colour-flow echocardiography:

Different coloured jets illustrate flow and gradients across valves and septal defects (p[link]) (Doppler effect, p[link]).

Tissue Doppler imaging:

This employs Doppler ultrasound to measure the velocity of myocardial segments over the cardiac cycle. It is particularly useful for assessing longitudinal motion—and hence long-axis ventricular function, which is a sensitive marker of systolic and diastolic heart failure.

Transoesophageal echocardiography (toe):

More sensitive than transthoracic echocardiography (tte) as the transducer is nearer to the heart. Indications: diagnosing aortic dissections; assessing prosthetic valves; finding cardiac source of emboli, and ie/sbe. Contraindicated in oesophageal disease and cervical spine instability.

Stress echocardiography:

Used to evaluate ventricular function, ejection fraction, myocardial thickening, regional wall motion pre- and post-exercise, and to characterize valvular lesions. Dobutamine or dipyridamole may be used if the patient cannot exercise. Inexpensive and as sensitive/specific as a thallium scan (p[link]).

Uses of echocardiography

Quantification of global lv function:

Heart failure may be due to systolic or diastolic ventricular impairment (or both). Echo helps by measuring end-diastolic volume. If this is large, systolic dysfunction is the likely cause. If small, diastolic. Pure forms of diastolic dysfunction are rare. Differentiation is important because vasodilators are less useful in diastolic dysfunction as a high ventricular filling pressure is required.

Echo is also useful for detecting focal and global hypokinesia, lv aneurysm, mural thrombus, and lvh (echo is 5–10 times more sensitive than ecg in detecting this).

Estimating right heart haemodynamics:

Doppler studies of pulmonary artery flow and tricuspid regurgitation allow evaluation of rv function and pressures.

Valve disease:

The technique of choice for measuring pressure gradients and valve orifice areas in stenotic lesions. Detecting valvular regurgitation and estimating its significance is less accurate. Evaluating function of prosthetic valves is another role.

Congenital heart disease:

Establishing the presence of lesions, and significance.

Endocarditis:

Vegetations may not be seen if <2mm in size. tte with colour Doppler is best for aortic regurgitation (ar). toe is useful for visualizing mitral valve vegetations, leaflet perforation, or looking for an aortic root abscess.

Pericardial effusion:

Best diagnosed by echo. Fluid may first accumulate between the posterior pericardium and the left ventricle, then anterior to both ventricles and anterior and lateral to the right atrium. There may be paradoxical septal motion.

HCM:

(p[link]) Echo features include asymmetrical septal hypertrophy, small lv cavity, dilated left atrium, and systolic anterior motion of the mitral valve.

Cardiac catheterization

This involves the insertion of a catheter into the heart via the femoral or radial artery or venous system, and manipulating it within the heart and great vessels to:

  • Inject radiopaque contrast medium to image cardiac anatomy and blood flow, see fig 3.18a.

  • Perform angioplasty (ballooning and stenting), valvuloplasty (eg transcatheter aortic valve implantation (tavi, fig 3.45)), cardiac biopsies, transcatheter septal defect closure.

  • Perform electrophysiology studies and radiofrequency ablations.

  • Sample blood to assess oxygen saturation and measure pressures.

  • Perform intravascular ultrasound or echocardiography.

Fig 3.18 (a) Coronary artery anatomy. (b) and (c) Images from angiography. (b) shows stenosis of the left anterior descending artery (lad). In (c), the same patient has had their lad stented, allowing contrast to flow freely through to the distal vessel. The stenting is a type of angioplasty (a procedure to widen the lumen of a blood vessel); in the context of coronary arteries, it is called pci (percutaneous coronary intervention). ppci (primary pci) is pci performed acutely for a patient with acute coronary syndrome (acs), see pManagement of acs120.

Fig 3.18
(a) Coronary artery anatomy. (b) and (c) Images from angiography. (b) shows stenosis of the left anterior descending artery (lad). In (c), the same patient has had their lad stented, allowing contrast to flow freely through to the distal vessel. The stenting is a type of angioplasty (a procedure to widen the lumen of a blood vessel); in the context of coronary arteries, it is called pci (percutaneous coronary intervention). ppci (primary pci) is pci performed acutely for a patient with acute coronary syndrome (acs), see p[link].

Images (b) and (c) reproduced from Ramrakha et al., Oxford Handbook of Cardiology, 2012, with permission from Oxford University Press.

Fig 3.45 This is one of the two main types of transcatheter aortic valve implants: animal valve leaflets mounted on metal stents. This extraordinary stucture must be resilient against the movement of the heart walls and the powerful flow of blood; it must avoid obstructing forward flow of blood whilst providing a near-complete block to backflow; and it has surfaces of foreign material yet must avoid triggering clots or allowing microbial growth. On top of this, it must be able to fold down over a wire to allow safe passage through the arterial tree from the groin to the heart, before being opened out by an inflated balloon.

Fig 3.45
This is one of the two main types of transcatheter aortic valve implants: animal valve leaflets mounted on metal stents. This extraordinary stucture must be resilient against the movement of the heart walls and the powerful flow of blood; it must avoid obstructing forward flow of blood whilst providing a near-complete block to backflow; and it has surfaces of foreign material yet must avoid triggering clots or allowing microbial growth. On top of this, it must be able to fold down over a wire to allow safe passage through the arterial tree from the groin to the heart, before being opened out by an inflated balloon.

Image courtesy of Edwards Lifesciences LLC, Irvine, CA. Edwards, Edwards Lifesciences, Edwards SAPIEN, SAPIEN, SAPIEN XT and SAPIEN 3 are trademarks of Edwards Lifesciences Corporation.

During the procedure, ecg and arterial pressures are monitored continuously. In the uk, the majority are performed as day-case procedures.

Indications

  • Coronary artery disease: diagnostic (assessment of coronary vessels and graft patency); therapeutic (angioplasty, stent insertion), fig 3.18b.

  • Valvular disease: diagnostic (pressures indicate severity); therapeutic valvuloplasty (if the patient is too ill or declines valve surgery).

  • Congenital heart disease: diagnostic (assessment of severity of lesions by measuring pressures and saturations); therapeutic (balloon dilatation or septostomy).

  • Other: cardiomyopathy; pericardial disease; endomyocardial biopsy.

Pre-procedure checks

  • Brief history/examination; nb: peripheral pulses, bruits, aneurysms.

  • Investigations: fbc, u&e, lft, clotting screen, cxr, ecg.

  • Consent for procedure, including possible extra procedures, eg consent for angioplasty if planning to do angiography as you may find a lesion that needs stenting. Explain reason for procedure and possible complications.

  • iv access, ideally in the left hand.

  • Patient should be nil by mouth (nbm) from 6h before the procedure.

  • Patients should take all their morning drugs (and pre-medication if needed)—but withhold oral hypoglycaemics.

Post-procedure checks

  • Pulse, bp, arterial puncture site (for bruising or swelling), foot pulses.

  • Investigations: fbc and clotting (if suspected blood loss), ecg.

Complications

  • Haemorrhage: apply firm pressure over puncture site. If you suspect a false aneurysm, ultrasound the swelling and consider surgical repair. Haematomas are high risk for infections.

  • Contrast reaction: this is usually mild with modern contrast agents.

  • Loss of peripheral pulse: may be due to dissection, thrombosis, or arterial spasm. Occurs in <1% of brachial catheterizations. Rare with femoral catheterization.

  • Angina: may occur during or after cardiac catheterization. Usually responds to sublingual gtn; if not, give analgesia and iv nitrates.

  • Arrhythmias: usually transient. Manage along standard lines.

  • Pericardial effusion: suspect if unexplained continued chest pain. May need drain depending on severity and haemodynamic status.

  • Pericardial tamponade: rare, but should be suspected if the patient becomes hypotensive and anuric. ΔΔ‎ Urgent pericardial drain.

  • Infection: post-catheter pyrexia is usually due to a contrast reaction. If it persists for >24h, take blood cultures before giving antibiotics.

Mortality

<1 in 1000 patients, in most centres.

Intracardiac electrophysiology

This catheter technique can determine types and origins of arrhythmias, and locate and ablate problem areas, eg aberrant pathways in wpw or arrhythmogenic foci. Arrhythmias may be induced, and the effectiveness of control by drugs assessed.

Cardiovascular drugs

Antiplatelet drugs

Aspirin irreversibly acetylates cyclo-oxygenase, preventing production of thromboxane a2, thereby inhibiting platelet aggregation. Used in low dose (eg 75mg/24h po) for secondary prevention following mi, tia/stroke, and for patients with angina or peripheral vascular disease. May have a role in primary prevention.7 adp receptor antagonists (eg clopidogrel, prasugrel, ticagrelor) also block platelet aggregation, but may cause less gastric irritation. They have a role if truly intolerant of aspirin; with aspirin after coronary stent insertion; and in acute coronary syndrome. Glycoprotein iib/iiia antagonists (eg tirofiban) have a role in unstable angina/mi.8

Anticoagulants

See p[link]. Direct oral anticoagulants (doacs, previously noacs), eg Xa inhibitors (eg apixaban) and direct thrombin inhibitors (dabigatran), are increasingly replacing warfarin9 for treatment of af and clots, see p[link]. Warfarin remains the anticoagulant of choice for mechanical valves. Anticoagulants used in acs include treatment dose lmwh, fondaparinux (Xa inhibitor), & bivalirudin (thrombin inhibitor).

β‎-blockers

Block β‎-adrenoceptors, thus antagonizing the sympathetic nervous system. Blocking β‎1-receptors is negatively inotropic and chronotropic; blocking β‎2-receptors induces peripheral vasoconstriction and bronchoconstriction. Drugs vary in their β‎1/β‎2 selectivity (eg propranolol is non-selective, and bisoprolol relatively β‎1 selective), but this does not seem to alter their clinical efficacy.

Uses:

Angina, hypertension, antidysrhythmic, post mi (↓mortality), heart failure (with caution).

CI:

Severe asthma/copd, heart block.

ses:

Lethargy, erectile dysfunction, ↓joie de vivre, nightmares, headache.

ace inhibitors

These are used in hypertension (ht), heart failure, and post-mi. First dose ht is a concern in patients with severe ccf and malignant ht. In ccf patients, reduce diuretic dose initially and use long-acting ace-i. Monitor u&e when starting or raising ace-i dose, a creatinine rise of >20% is concerning. If the patient starts ace-i prior to discharge, ask the gp to check u&e in 1–2 weeks. If renal function deteriorates markedly, consider investigating for renal artery stenosis. The risk to the kidneys is greater when the patient is unwell. Hold in aki and hyperkalaemia; avoid starting if the patient is dehydrated.

ses:

Include dry cough and urticaria.

Diuretics

  • Loop diuretics (eg furosemide) are used in heart failure, and inhibit the Na/2Cl/K co-transporter. ses: dehydration, ↓Na+,↓K+, ↓Ca2+, ototoxic

  • Thiazides and thiazide-like diuretics are used in hypertension (eg indapamide) and heart failure (eg metolazone). se: ↓K+, ↑Ca2+, ↓Mg2+, ↑urate (±gout), impotence (nb: small doses, eg chlortalidone 25mg/24h rarely cause significant ses)

  • Potassium-sparing diuretics: aldosterone antagonists (eg spironolactone, eplerenone) directly block aldosterone receptors; amiloride blocks the epithelial sodium channel in the distal convoluted tubules.

Vasodilators

Used in heart failure, ihd, and hypertension. Nitrates (p[link]) preferentially dilate veins and the large arteries, ↓ filling pressure (pre-load), while hydralazine (often used with nitrates) primarily dilates the resistance vessels, thus ↓ bp (after-load). Prazosin (an α‎-blocker) dilates arteries and veins.

Calcium antagonists

These ↓ cell entry of Ca2+ via voltage-sensitive channels in smooth muscle, thereby promoting coronary and peripheral vasodilation and reducing myocardial oxygen consumption. All current drugs block l-type Ca2+ channels. However, their effects differ because of differential binding properties.

  • The dihydropyridines, eg nifedipine, amlodipine, are mainly peripheral vasodilators (also dilate coronary arteries) and cause a reflex tachycardia, so are often used with a β‎-blocker. They are used mainly in hypertension and angina.

  • The non-dihydropyridines—verapamil and diltiazem—also slow conduction at the av and sa nodes and may be used to treat hypertension, angina, and dysrhythmias. Δ‎ Don’t give non-dihydropyridines with β‎-blockers (risk of severe bradycardia ± lvf).

ses:

Flushes, headache, ankle oedema (diuretic unresponsive), ↓lv function, gingival hypertrophy.

CI:

Heart block.

Digoxin

Blocks the Na+/K+ pump. It is used to slow the pulse in fast af (p[link]; aim for ≲100). As it is a weak +ve inotrope, its role in heart failure in sinus rhythm may be best reserved if symptomatic despite optimal ace-i therapy;10 here there is little benefit vis-à-vis mortality (but admissions for worsening ccf are ↓ by ~25%).11 Elderly people are at ↑risk of toxicity: use lower doses. Measure plasma levels >6h post-dose (p[link]). Typical dose: 500mcg stat po, repeated after 12h, then 125mcg (if elderly) to 250mcg/d po od (62.5mcg/d is almost never enough). iv dose: 0.75–1mg in 0.9% NaCl over 2h. ↑Toxicity risk if: ↓K+, ↓Mg2+, or ↑Ca2+. t½ ≈ 36h. If on digoxin, use less energy in cardioversion (start at 5J). Cardiovascular medicineIf on amiodarone, halve the dose of digoxin.

ses:

Any arrhythmia (supraventricular tachycardia with av block is suggestive), nausea, ↓appetite, yellow vision, confusion, gynaecomastia. If toxicity is suspected, do an ecg (fig 3.19), digoxin levels, and check K+, Mg2+, and Ca2+. If toxicity is confirmed, stop digoxin, correct electrolyte imbalances, treat arrhythmias, and consider iv DigiFab® (p[link]).

cis:

hcm; wpw syndrome (p[link]).

Sodium channel blockers

Class i anti-arrhythmics. Procainamide (1a) and lidocaine (1b) can be used to terminate vt. nb qt interval may be prolonged. Flecainide (1c) is useful for af cardioversion in patients without contraindications, and for arrhythmia prophylaxis in patients with wpw or troublesome paroxysmal af.

cis:

Heart failure, ihd, valve disease, and heart block.

Amiodarone

A class iii anti-arrhythmic. Amiodarone prolongs the cardiac action potential, reducing the potential for tachyarrhythmias. Used in both supra-ventricular and ventricular tachycardias, including during cardiac arrest. Broad range of side effects incl. thyroid disease, liver disease, pulmonary fibrosis and peripheral neuropathy. Monitor tfts and lfts every 6 months.

Ivabradine

Blocks the pacemaker ‘funny current’, slowing pulse rate without significantly dropping blood pressure. Used in angina, heart failure, and (off-licence) in autonomic tachycardia syndromes.

cis:

Acute mi, bradycardia, long qt syndrome, shock. Many drug interactions, including with calcium antagonists.

Statins

Statins (eg simvastatin, p[link]) inhibit the enzyme hmg-coa reductase, which causes de novo synthesis of cholesterol in the liver. This increases ldl receptor expression by hepatocytes leading to ↓circulating ldl cholesterol. More effective if given at night, but optimum dose and target plasma cholesterol are unknown.

ses:

Muscle aches, abdominal discomfort, ↑transaminases (eg alt), ↑ck, myositis, rarely rhabdomyolysis (more common if used with fibrates). Statins are generally well tolerated. There are currently ~3 million people taking statins in England, which saves ~10 000 lives a year. See also hyperlipidaemia, pp[link][link], fig 14.13.

Anti-anginal drugs

p[link].

Antihypertensives

p[link].

Angina pectoris

Cardiovascular medicineIf acs is a possible diagnosis (including unstable angina), see pp [link][link].

Angina12 is symptomatic reversible myocardial ischaemia. Features:

  1. 1 Constricting/heavy discomfort to the chest, jaw, neck, shoulders, or arms.

  2. 2 Symptoms brought on by exertion.

  3. 3 Symptoms relieved within 5min by rest or gtn.

All 3 features = typical angina; 2 features = atypical angina; 0–1 features = non-anginal chest pain.

Other precipitants: emotion, cold weather, and heavy meals. Associated symptoms: dyspnoea, nausea, sweatiness, faintness. Features that make angina less likely: pain that is continuous, pleuritic or worse with swallowing; pain associated with palpitations, dizziness or tingling.

Causes

Atheroma. Rarely: anaemia; coronary artery spasm; as; tachyarrhythmias; hcm; arteritis/small vessel disease (microvascular angina/cardiac syndrome x).

Types of angina

Stable angina:

Induced by effort, relieved by rest. Good prognosis.

Unstable angina:

(Crescendo angina.) Angina of increasing frequency or severity; occurs on minimal exertion or at rest; associated with ↑↑risk of mi.

Decubitus angina:

Precipitated by lying flat.

Variant (Prinzmetal) angina:

(box ‘Vasospastic angina’) Caused by coronary artery spasm (rare; may coexist with fixed stenoses).

Tests

ecg usually normal, but may show st depression; flat or inverted t waves; signs of past mi.

Blood tests:

fbc, u&e, tfts, lipids, Hba1c. Consider echo and chest x-ray. Further investigations are usually necessary to confirm an ihd diagnosis—see box.

Management

Address exacerbating factors:

Anaemia, tachycardia (eg fast af), thyrotoxicosis.

Secondary prevention of cardiovascular disease:

  • Stop smoking; exercise; dietary advice; optimize hypertension and diabetes control.

  • 75mg aspirin daily if not contraindicated.

  • Address hyperlipidaemia—see p[link].

  • Consider ace inhibitors, eg if diabetic.

prn symptom relief:

Glyceryl trinitrate (gtn) spray or sublingual tabs. Advise the patient to repeat the dose if the pain has not gone after 5min and to call an ambulance if the pain is still present 5min after the second dose. se: headaches, bp↓.

Anti-anginal medication:

(p[link]) First line: β‎-blocker and/or calcium channel blocker (Cardiovascular medicinedo not combine β‎-blockers with non-dihydropyridine calcium antagonists). If these fail to control symptoms or are not tolerated, trial other agents.

  • β‎-blockers: eg atenolol 50mg bd or bisoprolol 5–10mg od.

  • Calcium antagonists: amlodipine—start at 5mg od; diltiazem—dose depends on formulation.

  • Long-acting nitrates: eg isosorbide mononitrate—starting regimen depends on formulation. Alternatives: gtn skin patches. ses: headaches, ↓bp.

  • Ivabradine: reduces heart rate with minimal impact on bp. Patient must be in sinus rhythm. Start with 5mg bd (2.5mg in elderly).

  • Ranolazine: inhibits late Na+ current. Start at 375mg bd. Caution if heart failure, elderly, weight <60kg or prolonged qt interval.

  • Nicorandil: a K+ channel activator. Start with 5–10mg bd. ci: acute pulmonary oedema, severe hypotension, hypovolaemia, lv failure.

Revascularization:

Considered when optimal medical therapy proves inadequate.

  • Percutaneous coronary intervention (pci): (p[link]) a balloon is inflated inside the stenosed vessel, opening the lumen. A stent is usually inserted to reduce the risk of re-stenosis. Dual antiplatelet therapy (dapt; usually aspirin and clopidogel) is recommended for at least 12 months after stent insertion to reduce the risk of instent thrombosis. Specialist advice should be sought regarding antiplatelets if the patient has a high bleeding risk or requires surgery.

  • cabg: (p[link]) compared to pci, patients undergoing cabg are less likely to need repeat revascularization and those with multivessel disease can expect better outcomes. However, cabg is open heart surgery and so recovery is slower and the patient is left with two large wounds (sternal and vein harvesting).

Acute coronary syndromes (acs)

Definitions

acs includes unstable angina and myocardial infarctions (mis). These share a common underlying pathology—plaque rupture, thrombosis, and inflammation. However, acs may rarely be due to emboli, coronary spasm, or vasculitis (p[link]) in normal coronary arteries. Myocardial infarction means there is myocardial cell death, releasing troponin. Ischaemia means a lack of blood supply, ±cell death. mis have troponin rises, unstable angina does not. An mi may be a stemiacs with st-segment elevation (may only be present in v7v9 if posterior stemi) or new-onset lbbb; or an nstemi—trop-positive acs without st-segment elevation—the ecg may show st depression, t-wave inversion, non-specific changes, or be normal. The degree of irreversible myocyte death varies, and significant necrosis can occur without st elevation.

Risk factors

Non-modifiable: age, ♂ gender, family history of ihd (mi in 1st-degree relative <55yrs). Modifiable: smoking, hypertension, dm, hyperlipidaemia, obesity, sedentary lifestyle, cocaine use. Controversial risk factors include: stress, type a personality, lvh, fibrinogen↑, hyperinsulinaemia, ↑homocysteine levels, ace genotype.

Incidence

5/1000 per annum (uk) for st-segment elevation (declining in uk & usa).

Diagnosis

An increase in cardiac biomarkers (eg troponin) and either: symptoms of ischaemia, ecg changes of new ischaemia, development of pathological q waves, new loss of myocardium, or regional wall motion abnormalities on imaging.

Symptoms

Acute central chest pain, lasting >20min, often associated with nausea, sweatiness, dyspnoea, palpitations. acs without chest pain is called ‘silent’; mostly seen in elderly and diabetic patients. Silent mis may present with: syncope, pulmonary oedema, epigastric pain and vomiting, post-operative hypotension or oliguria, acute confusional state, stroke, and diabetic hyperglycaemic states.

Signs

Distress, anxiety, pallor, sweatiness, pulse ↑ or ↓, bp ↑ or ↓, 4th heart sound. There may be signs of heart failure (↑jvp, 3rd heart sound, basal crepitations) or a pansystolic murmur (papillary muscle dysfunction/rupture, vsd). Low-grade fever may be present. Later, a pericardial friction rub or peripheral oedema may develop.

Tests

ECG:

(See fig 3.21.) stemi: classically, hyperacute (tall) t waves, st elevation, or new lbbb occur within hours. t-wave inversion and pathological q waves follow over hours to days (p[link]). nstemi/unstable angina: st depression, t wave inversion, non-specific changes, or normal. Cardiovascular medicineIn 20% of mi, the ecg may be normal initially. Paced ecgs and ecgs with chronic bundle branch block are unhelpful for diagnosing nstemis14 and may hinder stemi15 diagnosis; in these cases, clinical assessment and troponin levels are especially important.

CXR:

Look for cardiomegaly, pulmonary oedema, or a widened mediastinum. Don’t routinely delay treatment whilst waiting for a cxr.

Blood:

fbc, u&e, glucose, lipids, cardiac enzymes.

Cardiac enzymes:

(See box ’Troponin‘.) Cardiac troponin levels (t and i) are the most sensitive and specific markers of myocardial necrosis. Different hospitals use different assays: check the required timing of troponin blood samples where you work (eg two samples 3h apart). Other cardiac enzymes (see fig 3.22) are sensitive but less specific; their role in acs diagnosis is decreasing as troponin testing improves.

Fig 3.22 Enzyme changes following acute mi. Increasingly, high-sensitivity troponins are used alone for routine investigation of acs.

Fig 3.22
Enzyme changes following acute mi. Increasingly, high-sensitivity troponins are used alone for routine investigation of acs.

Echo:

Regional wall abnormalities.

Differential diagnosis

(p[link].) Stable angina, pericarditis, myocarditis, Takotsubo cardiomyopathy (p[link]), aortic dissection (p[link]), pe, oesophageal reflux/spasm, pneumothorax, musculoskeletal pain, pancreatitis.

Management

See p[link], pp[link][link].

Mortality

50% of deaths occur within 2h of onset of symptoms. Up to 7% die before discharge. Worse prognosis if: elderly, lv failure, and st changes.16

Management of acs

acs management depends on whether the acs is ‘st elevated’ or not:

  1. 1 st elevated myocardial infarction (stemi): this category includes acs with st elevation on ecg (fig 3.9) but also acs with new lbbb (fig 3.7); and posterior mis (fig 3.24) where st elevation may only be seen with extra leads (v7v9). Urgent revascularization is essential. Cardiovascular medicinep[link].

  2. 2 acs without st elevation: serial troponins are needed to differentiate non-st elevated mis (nstemis) (trop rise) from unstable angina (no trop rise). Cardiovascular medicinep[link].

Fig 3.24 Acute postero-lateral mi. The posterior infarct is evidenced by the reciprocal changes seen in v1-3: dominant r waves (‘upside-down’ pathological q waves) and st depression (‘upside-down’ st elevation). If extra chest leads were added (v7-9), we would see the classic st elevation pattern, see p ecg—abnormalities98. The st elevation in v6 suggests lateral infarction. A blockage in the circumflex coronary artery could explain both the posterior and lateral changes.

Fig 3.24
Acute postero-lateral mi. The posterior infarct is evidenced by the reciprocal changes seen in v1-3: dominant r waves (‘upside-down’ pathological q waves) and st depression (‘upside-down’ st elevation). If extra chest leads were added (v7-9), we would see the classic st elevation pattern, see p [link]. The st elevation in v6 suggests lateral infarction. A blockage in the circumflex coronary artery could explain both the posterior and lateral changes.

After the immediate actions described on pp[link][link], treatment of acs17 focuses on managing symptoms, secondary prevention of further cardiovascular disease, revascularization (if not already undertaken), and addressing complications.

Symptom control

Manage chest pain with prn gtn and opiates. If this proves insufficient, consider a gtn infusion (monitor bp, omit if recent sildenafil use). If pain is deteriorating, seek senior help. Manage symptomatic heart failure, p[link].

Modify risk factors

  • Patients should be strongly advised and helped to stop smoking (p[link]).

  • Identify and treat diabetes mellitus, hypertension, and hyperlipidaemia.

  • Advise a diet high in oily fish, fruit, vegetables, & fibre, and low in saturated fats.

  • Encourage daily exercise. Refer to a cardiac rehab programme.

  • Mental health: flag to the patient’s gp if depression or anxiety are present—these are independently associated with poor cardiovascular outcomes.

Optimize cardioprotective medications

  • Antiplatelets: aspirin (75mg od) and a second antiplatelet agent (eg clopidogrel) for at least 12 months to ↓vascular events (eg mi, stroke). Consider adding a ppi (eg lansoprazole) for gastric protection.

  • Anticoagulate, eg with fondaparinux, until discharge.

  • β‎-blockade reduces myocardial oxygen demand. Start low and increase slowly, monitoring pulse and bp. If contraindicated, consider verapamil or diltiazem.

  • ace-i in patients with lv dysfunction, hypertension, or diabetes unless not tolerated (consider arb). Titrate up slowly, monitoring renal function.

  • High-dose statin, eg atorvastatin 80mg.

  • Do an echo to assess lv function. Eplerenone improves outcomes in mi patients with heart failure (ejection fraction <40%).

Revascularization

  • stemi patients and very high-risk nstemi patients (eg haemodynamically unstable) should receive immediate angiography ± pci. nstemi patients who are high risk (eg grace score >140) should have angiography within 24h; intermediate risk (eg grace 109–140) within 3d; low-risk patients may be considered for non-invasive testing.

  • Patients with multivessel disease may be considered for cabg instead of pci (p[link]).

Manage complications

See p[link].

Discharge

Address any questions the patient has. Discuss ‘red flag’ symptoms and where to seek medical advice should they arise. Ensure the management plan is communicated to the patient’s gp. Book clinic and cardiac rehab appointments.

General advice

  • Driving:18 drivers with group 1 licences (car and motorcycle) can resume driving 1wk after successful angioplasty, or 4wk after acs without successful angioplasty, if their ejection fraction is >40%. Group 2 licence holders must inform the dvla of their acs and stop driving; depending on the results of functional tests, they may be able to restart after 6wk.

  • Work: how soon a patient can return to work will depend on their clinical progress and the nature of their work. They should be encouraged to discuss speed of return ± changes in duties (eg to lighter work if manual labour) with their employer. Some occupations cannot be restarted post-mi: eg airline pilots & air traffic controllers. Drivers of public service or heavy goods vehicles will have to undergo functional testing (eg exercise test), as mentioned previously.

Complications of mi

Cardiac arrest

(See p[link], fig A3.)

Cardiogenic shock

(p[link].)

Left ventricular failure

(p[link], p[link], p[link].)

Bradyarrhythmias

Sinus bradycardia:

See p[link]. Patients with inferior mis may suffer atropine-unresponsive bradycardia due to infarction of nodal tissue.

1st-degree av block:

Most commonly seen in inferior mi. Observe closely as approximately 40% develop higher degrees of av block (in which case calcium channel blockers and β‎-blockers should be stopped).

Wenckebach phenomenon:

(Mobitz type i) Does not require pacing unless poorly tolerated.

Mobitz type ii block:

Carries a high risk of developing sudden complete av block; should be paced.

Complete av block:

Usually resolves within a few days. Insert pacemaker (may not be necessary after inferior mi if narrow qrs, reasonably stable and pulse ≳40–50).

Bundle branch block:

mi complicated by trifascicular block or non-adjacent bifascicular disease (p[link]) should be paced.

Tachyarrhythmias

nb: ↓K+, hypoxia, and acidosis all predispose to arrhythmias and should be corrected.

Sinus tachycardia:

Can ↑ myocardial O2 demand, treat causes (pain, hypoxia, sepsis, etc.) and add β‎-blocker if not contraindicated.

SVT:

p[link].

af or flutter:

If compromised, dc cardioversion. Otherwise, medical therapy as per p[link]. Frequent pvcs (premature ventricular complexes) and non-sustained vt (≥3 consecutive pvcs >100bpm and lasting <30s) are common after acute mi and are associated with increased risk of sudden death. Correct hypokalaemia and hypomagnesaemia and ensure the patient is on β‎-blockers, if not contraindicated.19

Sustained vt:

(Consecutive pvcs >100bpm and lasting >30s.) Treat with synchronized dc shock (if no pulse, treat as per advanced life support algorithm, see p[link], fig A3). Use anti-arrhythmics only if vt recurrent and not controlled with shocks. Consider ablation +/or icd.

Ventricular fibrillation:

80% occurs within 12h. vf occuring after 48h usually indicates pump failure or cardiogenic shock. · dc shock (see p[link], fig A3), consider icd.

Right ventricular failure (rvf)/infarction

Presents with low cardiac output and ↑jvp. Fluid is key; avoid vasodilators (eg nitrates) and diuretics.20 Inotropes are required in some cases.

Pericarditis

Central chest pain, relieved by sitting forwards. ecg: saddle-shaped st elevation, see fig 3.51, p[link]. Treatment: nsaids. Echo to check for effusion.

Fig 3.51 Pericarditis. Note the widespread ‘saddle-shaped’ st elevation—particularly clear in v5 and v6.

Fig 3.51
Pericarditis. Note the widespread ‘saddle-shaped’ st elevation—particularly clear in v5 and v6.

Systemic embolism

May arise from lv mural thrombus. After large anterior mi, consider anticoagulation with warfarin for 3 months.

Cardiac tamponade

(p[link]) Presents with low cardiac output, pulsus paradoxus, Kussmaul’s sign,3 muffled heart sounds. Diagnosis: echo. Treatment: pericardial aspiration (provides temporary relief, Cardiovascular medicinesee p[link] for technique), surgery.

Mitral regurgitation

May be mild (minor papillary muscle dysfunction) or severe (chordal or papillary muscle rupture secondary to ischaemia). Presentation: pulmonary oedema. Treat lvf (p[link]) and consider valve replacement.

Ventricular septal defect

Presents with pansystolic murmur, ↑jvp, cardiac failure. Diagnosis: echo. Treatment: surgery. 50% mortality in first week.

Late malignant ventricular arrhythmias

Occur 1–3wks post-mi and are the cardiologist’s nightmare. Avoid hypokalaemia, the most easily avoidable cause. Consider 24h ecg monitoring prior to discharge if large mi.

Dressler’s syndrome

(p[link]) Recurrent pericarditis, pleural effusions, fever, anaemia, and ↑esr 1–3wks post-mi. Treatment: consider nsaids; steroids if severe.

Left ventricular aneurysm

This occurs late (4–6wks post-mi), and presents with lvf, angina, recurrent vt, or systemic embolism. ecg: persistent st-segment elevation. Treatment: anticoagulate, consider excision.

Arrhythmias—overview

Disturbances of cardiac rhythm (arrhythmias) are:

  • common

  • often benign (but may reflect underlying heart disease)

  • often intermittent, causing diagnostic difficulty see box ‘Continuous ecg monitoring’

  • occasionally severe, causing cardiac compromise which may be fatal.

Cardiovascular medicineEmergency management: pp[link][link].

Causes

Cardiac:

Ischaemic heart disease (ihd); structural changes, eg left atrial dilatation secondary to mitral regurgitation; cardiomyopathy; pericarditis; myocarditis; aberrant conduction pathways.

Non-cardiac:

Caffeine; smoking; alcohol; pneumonia; drugs (β‎2-agonists, digoxin, l-dopa, tricyclics, doxorubicin); metabolic imbalance (K+, Ca2+, Mg2+, hypoxia, hypercapnia, metabolic acidosis, thyroid disease); and phaeochromocytoma.

Presentation

Palpitations, chest pain, presyncope/syncope, hypotension, or pulmonary oedema. Some arrhythmias may be asymptomatic, incidental findings, eg af.

History

Take a detailed history of palpitations (p[link]). Ask about precipitating factors, onset/offset, nature (fast or slow, regular or irregular), duration, associated symptoms (chest pain, dyspnoea, collapse). Review drug history. Ask about past medical history and family history of cardiac disease and sudden death. Syncope occuring during exercise is always concerning; the patient may have a condition predisposing them to sudden cardiac death (eg long qt syndrome).

Tests

fbc, u&e, glucose, Ca2+, Mg2+, tsh, ecg: Look for signs of ihd, af, short pr interval (wpw syndrome), long qt interval (metabolic imbalance, drugs, congenital), u waves (hypokalaemia). 24h ecg monitoring or other continuous ecg monitoring (see box ‘Continuous ecg monitoring’). Echo to look for structural heart disease, eg mitral stenosis, hcm. Provocation tests: exercise ecg, cardiac catheterization ± electrophysiological studies may be needed.

Cardiovascular medicineNarrow complex tachycardias:

See pp[link][link], [link].

Cardiovascular medicineAtrial fibrillation and flutter:

See pp[link][link], [link].

Cardiovascular medicineBroad complex tachycardias:

See pp[link][link], [link].

Cardiovascular medicineBradycardia:

See p[link] (causes and management of acute bradycardia) and p[link] (heart block). Intermittent, self-resolving bradycardic episodes can cause significant problems (eg recurrent syncope). Continuous ecg monitoring (box ‘Continuous ecg monitoring’) will be needed to assist the diagnosis ±specialist tests (eg tilt table testing for reflex syncope). Seek out reversible causes, eg hypothyroidism or medications such as β‎-blockers. In some cases, no reversible cause is found and the intermittent bradycardia is sufficiently dangerous to warrant a permanent pacemaker (p[link]). See box, ‘Sick sinus syndrome’.

Management

Some arrhythmias can be managed conservatively, eg by reducing alcohol intake. Many arrhythmias respond to medical management with regular tablets or a ‘pill in the pocket’. Interventional management may include pacemakers (p[link]), ablation (eg of accessory pathways or arrhythmogenic foci), or implantable cardioverter defibrillators (icds), eg in patients with ventricular arrhythmias post-mi and in those with congenital arrhythmogenic conditions (p[link]).

Narrow complex tachycardia

Definition

ecg shows rate of >100bpm and qrs complex duration of <120ms. Narrow qrs complexes occur when the ventricles are depolarized via the normal conduction pathways (fig 3.26).

Differential diagnosis

Regular narrow complex tachycardias:

See fig 3.27.

Irregular narrow complex tachycardias:

  • Normal variant: sinus arrhythmia (rate changes with inspiration/expiration); sinus rhythm with frequent ectopic beats.

  • Atrial fibrillation (af): p[link], fig 3.35.

  • Atrial flutter with variable block: eg pppqrsppqrs (3:1 block then 2:1 block). The atrial rhythm is regular but the ventricular rhythm (hence pulse) is irregular.

  • Multifocal atrial tachycardia: like focal atrial tachycardia but there are multiple groups of atrial cells taking it in turns to initiate a cardiac cycle. p-wave morphology and p-p intervals vary. Usually associated with copd.

Principles of management

See p[link].

Cardiovascular medicineIf the patient is compromised, use dc cardioversion (p[link]).

  • Identify and treat the underlying rhythm: eg treating sinus tachycardia secondary to dehydration with iv fluids; treating multifocal sinus tachycardia secondary to copd by correcting hypoxia and hypercapnia; treating focal atrial tachycardia secondary to digoxin toxicity with digoxin-specific antibody fragments; treating avrt secondary to wpw with flecainide, propafenone, or amiodarone; for atrial fibrillation (af) and flutter see p[link].

  • If avnrt or avrt are suspected, consider transiently blocking the avn. This should break the circuit of an atrio-ventricular re-entry rhythm, allowing sinus rhythm to re-establish. If the underlying rhythm is actually atrial in origin (eg flutter or atrial tachycardia), avn blockade will not treat the rhythm but the paused ventricular activity will unmask the atrial rhythm (fig 3.28), aiding diagnosis and management. avn blockade can be achieved by:

    1. 1 Vagal manoeuvres: carotid sinus massage, Valsalva manoeuvre (eg blowing into a syringe).

    2. 2 iv adenosine: see p[link].

  • In some cases, narrow complex tachyarrhythmias cause symptomatic episodes of sufficient severity and frequency to warrant more invasive treatment, eg ablation therapy for accessory pathways.

Fig 3.28 This patient was given adenosine for tachycardia thought to be due to avrt or avnrt. The adenosine has slowed the ventricular rate, revealing flutter waves (sawtooth appearance), disproving an avrt/avnrt diagnosis.

Fig 3.28
This patient was given adenosine for tachycardia thought to be due to avrt or avnrt. The adenosine has slowed the ventricular rate, revealing flutter waves (sawtooth appearance), disproving an avrt/avnrt diagnosis.

Image courtesy of Dr Ed Burns, www.lifeinthefastlane.com.

Broad complex tachycardia

Definition

ecg shows rate of >100 and qrs complexes >120ms. If no clear qrs complexes, it is vf or asystole (or problems with the ecg machine or stickers).

Principles of management

Cardiovascular medicineIf the patient is unstable or you are uncertain of what to do, get help fast—the patient may be periarrest (p[link]).

  • Identify the underlying rhythm and treat accordingly.

  • If in doubt, treat as ventricular tachycardia (vt)—the commonest cause.

  • Giving avn blocking agents to treat svt with aberrancy when the patient is in vt can cause dangerous haemodynamic instability. Treating for vt when the patient is actually in svt has less potential for deterioration.

  • If wpw is suspected, avoid drugs that slow av conduction—see p[link].

Differential diagnosis

  • Ventricular fibrillation—chaotic, no pattern, fig 3.29.

  • Ventricular tachycardia (vt), figs 3.12, 3.30.

  • Torsade de pointes (polymorphic vt)—vt with varying axis (see fig 3.31), may look like vf. ↑qt interval is a predisposing factor.

  • Any cause of narrow complex tachycardias (p[link]) when in combination with bundle branch block or metabolic causes of broad qrs.

  • Antidromic avrt (eg wpw), p[link].

Fig 3.30 vt with a rate of 235/min.

Fig 3.30
vt with a rate of 235/min.

Fig 3.31 Torsade de pointes tachycardia.

Fig 3.31
Torsade de pointes tachycardia.

Differentiatingvt from svt with aberrancy

This may be difficult; seek expert help. Diagnosis is based on the history (ihd increases the likelihood of a ventricular arrhythmia), a 12-lead ecg, and the response (or lack thereof) to certain medications. ecg findings in favour of vt:

  • +ve or −ve qrs concordance in all chest leads (ie all +ve (r) or all −ve (qs)).

  • qrs >160ms.

  • Marked left axis deviation, or ‘northwest axis’ (qrs positive in avr).

  • av dissociation (ps independent of qrss) or 2:1 or 3:1 Mobitz ii heart block.

  • Fusion beats or capture beats (figs 3.32, 3.33).

  • rsr’ pattern where r is taller than r’. (r’ taller than r suggests rbbb.)

Fig 3.32 A fusion beat (*)—a ‘normal beat’ fuses with a vt complex creating an unusual complex.

Fig 3.32
A fusion beat (*)—a ‘normal beat’ fuses with a vt complex creating an unusual complex.

Fig 3.33 A capture beat (*)—a normal qrs amongst runs of vt. This would not be expected if the qrs breadth were down to bundle branch block or metabolic causes.

Fig 3.33
A capture beat (*)—a normal qrs amongst runs of vt. This would not be expected if the qrs breadth were down to bundle branch block or metabolic causes.

Management

See page 805.

Ventricular extrasystoles (ectopics)

These are common and can be symptomatic—patients describe palpitations, a thumping sensation, or their heart ‘missing a beat’. The pulse may feel irregular if there are frequent ectopics. On ecg, ventricular ectopics are broad qrs complexes; they may be single or occur in patterns:

  • Bigeminy—ectopic every other beat, see fig 3.34. ecg machines may disregard the second qrs and so calculate the rate to be half the true value.

  • Trigeminy—every third beat is an ectopic.

  • Couplet—two ectopics together.

  • Triplet—three ectopics together.

Fig 3.34 Bigeminy—a normal qrs is followed by a ventricular ectopic beat * then a compensatory pause, this pattern then repeats. The ectopic beats have the same morphology as each other so probably all share an origin.

Fig 3.34
Bigeminy—a normal qrs is followed by a ventricular ectopic beat * then a compensatory pause, this pattern then repeats. The ectopic beats have the same morphology as each other so probably all share an origin.

Occasional ventricular ectopics24 in otherwise healthy people are extremely common and rarely significant. Frequent ectopics (>60/hour), particularly couplets and triplets, should prompt testing for underlying cardiac conditions. Post-mi, ventricular ectopics are associated with increased risk of dangerous arrhythmias. Pay attention to whether the ectopics all ‘look’ the same on the ecg suggesting a single focus (monomorphic) or may come from multiple foci (polymorphic). Causes and management can be different.

Atrial fibrillation (af) and flutter

af25 is a chaotic, irregular atrial rhythm at 300–600bpm (fig 3.35); the av node responds intermittently, hence an irregular ventricular rhythm. Cardiac output drops by 10–20% as the ventricles aren’t primed reliably by the atria. af is common in the elderly (≤9%). The main risk is embolic stroke. Warfarin reduces this to 1%/yr from 4%. So, do an ecg on everyone with an irregular pulse (±24h ecg if dizzy, faints, palpitations, etc.). If af started more than 48h ago, intracardiac clots may have formed, necessitating anticoagulation prior to cardioversion. see box ‘Anticoagulation and af’.

Causes

Heart failure; hypertension; ihd (seen in 22% mi patients);26 pe; mitral valve disease; pneumonia; hyperthyroidism; caffeine; alcohol; post-op; ↓K+; ↓Mg2+.

Rare causes:

Cardiomyopathy; constrictive pericarditis; sick sinus syndrome; lung cancer; endocarditis; haemochromatosis; sarcoid. ‘Lone’ af means no cause found.

Symptoms

May be asymptomatic or cause chest pain, palpitations, dyspnoea, or faintness.

Signs

Irregularly irregular pulse, the apical pulse rate is greater than the radial rate, and the 1st heart sound is of variable intensity; signs of lvf (p[link]). Cardiovascular medicineExamine the whole patient: af is often associated with non-cardiac disease.

Tests

ecg shows absent p waves, irregular qrs complexes, fig 3.35. Blood tests: u&e, cardiac enzymes, thyroid function tests. Echo to look for left atrial enlargement, mitral valve disease, poor lv function, and other structural abnormalities.

Managing acute af

  • If the patient has adverse signs (shock, myocardial ischaemia (chest pain or ecg changes), syncope, heart failure): Cardiovascular medicineabcde, get senior input Cardiovascular medicinedc cardioversion (synchronized shock, start at 120–150J) ± amiodarone if unsuccessful (p[link]); do not delay treatment in order to start anticoagulation.

  • If the patient is stable & af started <48h ago: rate or rhythm control may be tried. For rhythm control, dc cardiovert or give flecainide (ci: structural heart disease, ihd) or amiodarone. Start heparin in case cardioversion is delayed (see box ‘Anticoagulation and af’).

  • If the patient is stable & af started >48h ago or unclear time of onset: rate control (eg with bisoprolol or diltiazem). If rhythm control is chosen, the patient must be anticoagulated for >3wks first.

  • Correct electrolyte imbalances (K+, Mg2+, Ca2+); ℞ associated illnesses (eg mi, pneumonia); and consider anticoagulation (see box ‘Anticoagulation and af’).

Managing chronic af

The main goals are rate control and anticoagulation. Rate control is at least as good as rhythm control,27 but rhythm control may be appropriate if

  • symptomatic or ccf

  • younger

  • presenting for 1st time with lone af

  • af from a corrected precipitant (eg ↑↓u&e).

Anticoagulation:

See box ‘Anticoagulation and af’.

Rate control:

β‎-blocker or rate-limiting Ca2+ blocker are 1st choice. If this fails, add digoxin (p[link]), then consider amiodarone. Digoxin as monotherapy in chronic af is only acceptable in sedentary patients. Cardiovascular medicineDo not give β‎-blockers with verapamil. Aim for heart rate <90bpm at rest and 200 minus age (yrs) bpm on exertion. Avoid getting fixated on a target heart rate.

Rhythm control:

Elective dc cardioversion: do echo first to check for intracardiac thrombi. If there is ↑risk of cardioversion failure (past failure, or past recurrence) give amiodarone for 4wks before the procedure and 12 months after. Elective pharmacological cardioversion: flecainide is 1st choice (ci if structural heart disease, eg scar tissue from mi: use iv amiodarone instead). In refractory cases, avn ablation with pacing, pulmonary vein ablation, or the maze procedure may be considered.28

Paroxysmal af:

‘Pill in the pocket’ (eg sotalol or flecainide prn) may be tried if: infrequent af, bp >100mmHg systolic, no past lv dysfunction. Anticoagulate (See box ‘Anticoagulation and af’). Consider ablation if symptomatic or frequent episodes.

Atrial flutter

See pp[link][link], fig 3.35.

Treatment:

Similar to af regarding rate and rhythm control and the need for anticoagulation.29 dc cardioversion is preferred to pharmacological cardioversion; start with 70–120J. iv amiodarone may be needed if rate control is proving difficult. Recurrence rates are high so radiofrequency ablation is often recommended for long-term management.

Pacemakers

In normal circumstances the san plays the role of pacemaker. On occasion, other areas of myocardium will set the pace (see earlier in chapter). If the heart is not pacing itself fast enough, artificial pacing may be required. Options include ‘percussion pacing’—fist strikes to the precordium, used only in periarrest situations; transcutaneous pacing—electrical stimulation via defibrillator pads (p[link]); temporary transvenous pacing (p[link]); and a subcutaneously implanted permanent pacemaker.

Indications for temporary cardiac pacing include

  • Symptomatic bradycardia, unresponsive to atropine.

  • After acute anterior mi, prophylactic pacing is required in:

    • complete av block

    • Mobitz type i av block (Wenckebach)

    • Mobitz type ii av block

    • non-adjacent bifascicular, or trifascicular block (p[link]).

  • After inferior mi, pacing may not be needed in complete av block if reasonably stable, rate is >40–50, and qrs complexes are narrow.

  • Suppression of drug-resistant tachyarrhythmias by overdrive pacing, eg svt, vt.

  • Special situations: during general anaesthesia; during cardiac surgery; during electrophysiological studies; drug overdose (eg digoxin, β‎-blockers, verapamil).

Cardiovascular medicineSee p[link] for further details and insertion technique.

Indications for a permanent pacemaker (ppm) include

  • Complete av block (Stokes–Adams attacks, asymptomatic, congenital).

  • Mobitz type ii av block (p[link]).

  • Persistent av block after anterior mi.

  • Symptomatic bradycardias (eg sick sinus syndrome, p[link]).

  • Heart failure (cardiac resynchronization therapy).

  • Drug-resistant tachyarrhythmias.

Pre-operative assessment

Bloods (fbc, clotting screen, renal function), iv cannula, consent, antibiotics as per local protocol.

Post-operative management

Prior to discharge, check wound for bleeding or haematoma; check lead positions and for pneumothorax on cxr; check pacemaker function. During 1st week, inspect for wound haematoma or dehiscence. Other problems: lead fracture or dislodgement; pacemaker interference (eg from patient’s muscles); infected device. The battery needs changing every 5–10 years. For driving rules see p[link].

Pacemaker letter codes

These enable pacemaker identification (min is 3 letters):

  • 1st letter the chamber paced (a=atria, v=ventricles, d=dual chamber).

  • 2nd letter the chamber sensed (a=atria, v=ventricles, d=dual chamber, o=none).

  • 3rd letter the pacemaker response (t=triggered, i=inhibited, d=dual).

  • 4th letter (r=rate modulation, p=programmable, m=multiprogrammable).

  • 5th letter (p means that in tachycardia the pacemaker will pace the patient. s means that in tachycardia the pace-maker shocks the patient. d=dual ability to pace and shock. o=neither of these).

Cardiac resynchronization therapy (crt)

Improves the synchronization of cardiac contraction and reduces mortality31 in people with symptomatic heart failure who have an ejection fraction <35% and a qrs duration >120ms.32 It involves biventricular pacing (both septal and lateral walls of the lv) and, if required, also an atrial lead. It may be combined with a defibrillator (crt-d).

ecg of paced rhythms

(fig 3.13 and fig 3.36). Pacemaker input appears as a vertical ‘spike’ on the ecg. This spike can be very small with modern bipolar pacing systems. Ventricular pacing usually has a broad qrs morphology (similar to lbbb). Systems are usually programmed ‘on demand’ so will only pace when necessary. Modern systems are generally very reliable but pacing spikes with no capture afterwards suggests a problem. Programming of devices is complicated so seek help early if concerned. Many pacemakers store intracardiac electrograms which can be accessed to correlate rhythm with any symptoms.

Fig 3.13 Dual chamber pacemaker. Pacing spikes occur before each p wave and each qrs complex. Paced qrs complexes are broad as the impulse starts in the ventricles.

Fig 3.13
Dual chamber pacemaker. Pacing spikes occur before each p wave and each qrs complex. Paced qrs complexes are broad as the impulse starts in the ventricles.

Reproduced from Myerson et al., Emergencies in Cardiology, 2012, with permission from Oxford University Press.

Fig 3.36 ecg of a paced rhythm.

Fig 3.36
ecg of a paced rhythm.

Heart failure—basic concepts

Definition

Cardiac output is inadequate for the body’s requirements.33

Prevalence

1–3% of the general population; ~10% among elderly patients.34

Key classifications

Systolic failure:

Inability of the ventricle to contract normally, resulting in ↓cardiac output. Ejection fraction (ef) is <40%. Causes: ihd, mi, cardiomyopathy.

Diastolic failure:

Inability of the ventricle to relax and fill normally, causing ↑filling pressures. Typically ef is >50%, this is termed hfpef (heart failure with preserved ef). Causes: ventricular hypertrophy, constrictive pericarditis, tamponade, restrictive cardiomyopathy, obesity. nb: systolic and diastolic failure pathophysiology often coexists.

Left ventricular failure (lvf):

Symptoms: dyspnoea, poor exercise tolerance, fatigue, orthopnoea, paroxysmal nocturnal dyspnoea (pnd), nocturnal cough (± pink frothy sputum), wheeze (cardiac ‘asthma’), nocturia, cold peripheries, weight loss.

Right ventricular failure (rvf):

Causes: lvf, pulmonary stenosis, lung disease (cor pulmonale, see p[link]). Symptoms: peripheral oedema (up to thighs, sacrum, abdominal wall), ascites, nausea, anorexia, facial engorgement, epistaxis.

lvf and rvf may occur independently, or together as congestive cardiac failure (ccf).

Acute heart failure:

Often used exclusively to mean new-onset acute or decompensation of chronic heart failure characterized by pulmonary and/or peripheral oedema with or without signs of peripheral hypoperfusion.

Chronic heart failure:

Develops or progresses slowly. Venous congestion is common but arterial pressure is well maintained until very late.

Low-output heart failure:

Cardiac output is ↓ and fails to ↑ normally with exertion. Causes:

  • Excessive preload: eg mitral regurgitation or fluid overload (eg renal failure or too rapid iv infusions, particularly in the elderly and those with established hf).

  • Pump failure: systolic and/or diastolic hf (see above), ↓heart rate (eg β‎-blockers, heart block, post mi), negatively inotropic drugs (eg most antiarrhythmic agents).

  • Chronic excessive afterload: eg aortic stenosis, hypertension.

Excessive preload can cause ventricular dilatation, this exacerbates pump failure.

Excessive afterload prompts ventricular muscle thickening (ventricular hypertrophy), resulting in stiff walls and diastolic dysfunction.

High-output heart failure:

This is rare. Here, output is normal or increased in the face of ↑↑needs. Failure occurs when cardiac output fails to meet these needs. It will occur with a normal heart, but even earlier if there is heart disease. Causes: anaemia, pregnancy, hyperthyroidism, Paget’s disease, arteriovenous malformation, beriberi. Consequences: initially features of rvf; later lvf becomes evident.

Diagnosis

Requires symptoms of failure (see above) and objective evidence of cardiac dysfunction at rest. For ccf, use the Framingham criteria.35

Signs

As described previously plus cyanosis, ↓bp, narrow pulse pressure, pulsus alternans, displaced apex (lv dilatation), rv heave (pulmonary hypertension), signs of valve diseases. Severity can be graded using the New York classification (see box).

Investigations

According to nice,33 if ecg and b-type natriuretic peptide (bnp; p[link]) are normal, heart failure is unlikely, and an alternative diagnosis should be considered; if either is abnormal, then echocardiography (p[link]) is required.

Tests

fbc; u&e; bnp; cxr (see fig 3.38); ecg; echo. ecg may indicate cause (look for evidence of ischaemia, mi, or ventricular hypertrophy). It is rare to get a completely normal ecg in chronic heart failure. Echocardiography is the key investigation.36 It may indicate the cause (mi, valvular heart disease) and can confirm the presence or absence of lv dysfunction. Endomyocardial biopsy is rarely needed.

Prognosis

Poor with ~25–50% of patients dying within 5yrs of diagnosis. If admission is needed, 5yr mortality ≈75%. Be realistic: in one study, 54% of those dying in the next 72h had been expected to live for >6months.37

Heart failure—management

Acute heart failure

Cardiovascular medicineThis is a medical emergency (p[link]).

Chronic heart failure

Cardiovascular medicineStop smoking. Stop drinking alcohol. Eat less salt. Optimize weight & nutrition.33

  • Treat the cause (eg if dysrhythmias; valve disease).

  • Treat exacerbating factors (anaemia, thyroid disease, infection, ↑bp).

  • Avoid exacerbating factors, eg nsaids (fluid retention) and verapamil (−ve inotrope).

  • Annual ’flu vaccine, one-off pneumococcal vaccine.

  • Drugs:

    1. 1 Diuretics: Give loop diuretics to relieve symptoms, eg furosemide 40mg/24h po or bumetanide 1–2mg/24h po. Increase dose as necessary. se: K+↓, renal impairment. Monitor u&e and add K+-sparing diuretic (eg spironolactone) if K+ <3.2mmol/L, predisposition to arrhythmias, concurrent digoxin therapy, or pre-existing K+-losing conditions. If refractory oedema, consider adding a thiazide, eg metolazone 5–20mg/24h po. Diuretics improve symptoms but studies showing mortality benefit are lacking.

    2. 2 ace-i: Consider in all those with left ventricular systolic dysfunction (lvsd); improves symptoms and prolongs life (see p[link][link]). If cough is a problem, an angiotensin receptor blocker (arb) may be substituted. se: ↑K+.

    3. 3 β‎-blockers: (eg carvedilol) ↓mortality in heart failure—benefit additional to those of ace-i in patients with systolic dysfunction.38 Use with caution: ‘start low and go slow’; if in doubt seek specialist advice first; wait ≥2weeks between each dose increment. β‎-blocker therapy in patients hospitalized with decompensated heart failure is associated with lower post-discharge mortality risk and improved treatment rates.39

    4. 4 Mineralocorticoid receptor antagonists: Spironolactone (25mg/24h po) ↓mortality by 30% when added to conventional therapy.40 Use in those still symptomatic despite optimal therapy as listed previously, and in post-mi patients with lvsd. Spironolactone is K+-sparing, but there is little risk of significant hyperkalaemia, even when given with ace-i. Nevertheless, u&e should be monitored, particularly if the patient has known ckd. Eplerenone is an alternative if spironolactone is not tolerated.

    5. 5 Digoxin: Helps symptoms even in those with sinus rhythm, and should be considered for patients with lvsd who have signs or symptoms of heart failure while receiving standard therapy, including ace-i and β‎-blockers, or in patients with af. Dose example: 125mcg/24h po if sinus rhythm. Monitor u&e; maintain K+ at 4–5mmol/L as ↓K+ risks digoxin toxicity, and vice versa. Digoxin levels: p[link]. Other inotropes are unhelpful in terms of outcome.

    6. 6 Vasodilators: The combination of hydralazine (se: drug-induced lupus) and isosorbide dinitrate should be used if intolerant of ace-i and arbs as it reduces mortality. It also reduces mortality when added to standard therapy (including ace-i) in black patients with heart failure.41

Intractable heart failure

Reassess the cause. Are they taking the drugs?—at maximum dose? Switching furosemide to bumetanide (one 5mg tab≈200mg furosemide) might help. Inpatient management may include:

  • Minimal exertion; Na+ & fluid restriction (1.5L/24h po).

  • Metolazone (as above) and iv furosemide (p[link]).

  • Opiates and iv nitrates may relieve symptoms (p[link]).

  • Weigh daily. Do frequent u&e (beware ↓K+).

  • Give dvt prophylaxis: heparin + ted stockings (p[link]).

In extremis:

Try iv inotropes (p[link]; it may be difficult to wean patients off them).

Consider:

Cardiac resynchronization (p[link]), lv assist device (box ‘Pulseless patients’), or transplantation.

Palliative care

Treat/prevent comorbidities (eg ’flu vaccination). Good nutrition (allow alcohol!). Involve gp: continuity of care and discussion of prognosis is much appreciated.42 Dyspnoea, pain (from liver capsule stretching), nausea, constipation, and ↓mood all need tackling.43 Opiates improve pain and dyspnoea. O2 may help.

Hypertension

Hypertension44 is the most important risk factor for premature death and cvd; causing ~50% of all vascular deaths (8×106/yr). Usually asymptomatic, so regular screening (eg 3-yrly) is a vital task—most preventable deaths are in areas without universal screening.45

Defining hypertension

bp has a skewed normal distribution (p[link]) within the population, and risk is continuously related to bp, so it is impossible to define ‘hypertension’.46 We choose to select a value above which risk is significantly increased and the benefit of treatment is clear cut, see below. Don’t rely on a single reading—assess over a period of time (how long depends on the bp and the presence of other risk factors or end-organ damage). Confirm with 24hr ambulatory bp monitoring (abpm); or a week of home readings. nb: the diagnostic threshold is lower ~135/85mmHg.

Whom to treat

All with bp ≥160/100mmHg (or abpm ≥150/95mmHg). For those ≥140/90, the decision depends on the risk of coronary events, presence of diabetes, or end-organ damage; see fig 3.40.44 The hyvet study showed that there is even substantial benefit in treating the over-80s.47 Lower thresholds may be appropriate for young people—bp is on average lower in young people (eg 100–110/60–70 in 18-year-olds) and they have a ‘lifetime’ of risk ahead of them; but evidence to treat is lacking.

White-coat hypertension

Refers to an elevated clinic pressure, but normal abpm (day average <135/85). nice says don’t treat; but more likely to develop hypertension in future, and may have ↑risk of cvd. Masked hypertension is the opposite.

‘Malignant’ or accelerated phase hypertension:

A rapid rise in bp leading to vascular damage (pathological hallmark is fibrinoid necrosis). Usually there is severe hypertension (eg systolic >200, diastolic>130mmHg) + bilateral retinal haemorrhages and exudates; papilloedema may or may not be present. Symptoms are common, eg headache ± visual disturbance. It requires urgent treatment, and may also precipitate acute kidney injury, heart failure, or encephalopathy, which are hypertensive emergencies. Untreated, 90% die in 1yr; treated, 70% survive 5yrs. It is more common in younger and in black subjects. Look hard for any underlying cause.

Primary or ‘essential’ hypertension:

(Cause unknown.) ~95% of cases.

Secondary hypertension:

~5% of cases. Causes include:

  • Renal disease: the most common secondary cause. 75% are from intrinsic renal disease: glomerulonephritis, polyarteritis nodosa (pan), systemic sclerosis, chronic pyelonephritis, or polycystic kidneys. 25% are due to renovascular disease, most frequently atheromatous (elderly ♂ cigarette smokers, eg with peripheral vascular disease) or rarely fibromuscular dysplasia (young ♀).

  • Endocrine disease: Cushing’s (p[link]) and Conn’s syndromes (p[link]), phaeochromocytoma (p[link]), acromegaly, hyperparathyroidism.

  • Others: coarctation (p[link]), pregnancy (ohcs p[link]), liquorice, drugs: steroids, maoi, oral contraceptive pill, cocaine, amphetamines.

Signs and symptoms

Usually asymptomatic (except malignant hypertension, see earlier in topic). Headache is no more common than in the general population. Always examine the cvs fully and check for retinopathy. Are there features of an underlying cause (phaeochromocytoma, p[link], etc.), signs of renal disease, radiofemoral delay, or weak femoral pulses (coarctation), renal bruits, palpable kidneys, or Cushing’s syndrome? Look for end-organ damage: lvh, retinopathy and proteinuria—indicates severity and duration of hypertension and associated with a poorer prognosis.

Tests

To confirm diagnosis:

abpm or home bp monitoring.

To help quantify overall risk:

Fasting glucose; cholesterol.

To look for end-organ damage:

ecg or echo (any lv hypertrophy? past mi?); urine analysis (protein, blood).

To ‘exclude’ secondary causes:

u&e (eg K+↓ in Conn’s); Ca2+ (↑ in hyperparathyroidism).

Special tests:

Renal ultrasound/arteriography (renal artery stenosis); 24h urinary meta-adrenaline (p[link]); urinary free cortisol (p[link]); renin; aldosterone; mr aorta (coarctation).

Hypertension—management

Look for and treat underlying causes (eg renal disease, ↑alcohol: see p[link]). Drug therapy reduces the risk of cvd and death. Almost any adult over 50 would benefit from antihypertensives, whatever their starting bp.48 Treatment is especially important if: bp is persistently ≥160/100mmHg or cardiovascular risk ↑ (10yr risk of vascular disease ≥20%), or existing vascular disease or target organ damage (eg brain, kidney, heart, retina) with bp >140/90mmHg. Essential hypertension is not ‘curable’ and long-term treatment is needed.

Treatment goal

<140/90mmHg (<130/80 in diabetes, 150/90 if aged >80). Reduce blood pressure slowly; rapid reduction can be fatal, especially in the context of an acute stroke. These may fall—sprint49 showed a target of 120/80 was beneficial.

Lifestyle changes

↓Concomitant risk factors: stop smoking; low-fat diet. Reduce alcohol and salt intake; increase exercise; reduce weight if obese.

Drugs

The allhat study suggests that adequate bp reduction is more important than the specific drug used.50 However, β‎-blockers seem to be less effective than other drugs at reducing major cardiovascular events, particularly stroke. β‎-blockers and thiazides may increase the risk of new-onset diabetes, Ca2+-channel blockers appear neutral, and ace-i or arb may reduce the risk.44

Monotherapy:

If ≥55yrs, and in black patients of any age, 1st choice is a Ca2+-channel antagonist or thiazide. If <55, 1st choice is ace-i (or arb if ace-i intolerant, eg cough). β‎-blockers are not 1st line for hypertension, but consider in younger people, particularly if: intolerance or contraindication to ace-i/arb, she is a woman of child-bearing potential, or there is ↑sympathetic drive.

Combination ℞:

ace-i + Ca2+-channel antagonist or diuretic is logical, and has been commonly used in trials. There is little evidence on using 3 drugs but current recommendation is ace-i, Ca2+-channel antagonist, and thiazide.44 If bp still uncontrolled on adequate doses of 3 drugs, add a 4th—consider: spironolactone 25–50mg/24h or higher-dose thiazide, but monitor u&e. Alternatively, β‎-blocker, or selective α‎-blocker and get help. Check compliance (urinary drug screen, or observed ℞).

Drug examples

Thiazides:

Eg chlortalidone 25–50mg/24h po mané. se: ↓K+, ↓Na+, impotence. ci: gout.

Ca2+-channel antagonists:

Eg nifedipine mr, 30–60mg/24h po. se: flushes, fatigue, gum hyperplasia, ankle oedema; avoid short-acting form.

ace-i:

Eg lisinopril 10–40mg/24h po (max 40mg/d). ace-i may be 1st choice if co-existing lvf, or in diabetics (esp. if microalbuminuria, p[link]) or proteinuria. se: cough, ↑K+, renal failure, angio-oedema. ci: bilateral renal artery or aortic valve stenosis; p[link].

arb:

Candesartan (8–32mg/d); caution if valve disease or cardiomyopathy; monitor K+. se: vertigo, urticaria, pruritus. Useful if ace-i induces cough.

β‎-blockers:

Eg bisoprolol 2.5–5mg/24h po. se: bronchospasm, heart failure, cold peripheries, lethargy, impotence. ci: asthma; caution in heart failure. Consider aspirin when bp controlled, if aged >55yrs. Add a statin if cholesterol raised. Cardiovascular medicineMost drugs take 4–8wks to gain maximum effect: don’t assess efficacy with just one bp measurement.

Malignant hypertension

(fig 3.41) In general, use oral therapy, unless there is encephalopathy or ccf. The aim is for a controlled reduction in bp over days, not hours. Avoid sudden drops in bp as cerebral autoregulation is poor (↑stroke risk). Bed rest; there is no ideal hypotensive, but atenolol or long-acting Ca2+ blockers may be used po.

Encephalopathy:

(Headache, focal cns signs, seizures, coma.) Aim to reduce bp to ~110mmHg diastolic over 4h. Admit to monitored area. Insert intra-arterial line for pressure monitoring. Either iv labetalol (eg 50mg iv over 1min, repeated every 5min, max 200mg) or sodium nitroprusside infusion (0.5mcg/kg/min ivi titrated up to 8mcg/kg/min, eg 50mg in 1L glucose 5%; expect to give 100–200mL/h for a few hours only, to avoid cyanide risk).

Cardiovascular medicineNever use sublingual nifedipine to reduce bp (rapid drop in bp may cause stroke).51

Rheumatic fever (rf)

This systemic infection is still common in developing countries but increasingly rare in the West. Peak incidence: 5–15yrs. Tends to recur unless prevented. Pharyngeal infection with Lancefield group a β‎-haemolytic streptococci triggers rheumatic fever 2–4wks later, in the susceptible 2% of the population. An antibody to the carbohydrate cell wall of the streptococcus cross-reacts with valve tissue (antigenic mimicry) and may cause permanent damage to the heart valves.

Diagnosis

Use the revised Jones criteria (may be over-rigorous). There must be evidence of recent strep infection plus 2 major criteria, or 1 major + 2 minor.

Evidence of group a β‎-haemolytic streptococcal infection:

  • Positive throat culture (usually negative by the time rf symptoms appear).

  • Rapid streptococcal antigen test +ve.

  • Elevated or rising streptococcal antibody titre (eg anti-streptolysin O (aso) or dnase b titre).

  • Recent scarlet fever.

Major criteria:

  • Carditis: tachycardia, murmurs (mitral or aortic regurgitation, Carey Coombs’ murmur, p[link]), pericardial rub, ccf, cardiomegaly, conduction defects (45–70%). An apical systolic murmur may be the only sign.52

  • Arthritis: a migratory, ‘flitting’ polyarthritis; usually affects larger joints (75%).

  • Subcutaneous nodules: small, mobile, painless nodules on extensor surfaces of joints and spine (2–20%).

  • Erythema marginatum: (fig 3.42) geographical-type rash with red, raised edges and clear centre; occurs mainly on trunk, thighs and arms in 2–10% (p[link]).

  • Sydenham’s chorea (St Vitus’ dance): occurs late in 10%. Unilateral or bilateral involuntary semi-purposeful movements. May be preceded by emotional lability and uncharacteristic behaviour.

Fig 3.42 Erythema marginatum.

Fig 3.42
Erythema marginatum.

Image courtesy of Dr Maria Angelica Binotto.

Minor criteria:

  • Fever.

  • Raised esr or crp.

  • Arthralgia (but not if arthritis is one of the major criteria).

  • Prolonged pr interval (but not if carditis is major criterion).

  • Previous rheumatic fever.

Management

  • Bed rest until crp normal for 2wks (may be 3 months).

  • Benzylpenicillin 0.6–1.2g iv stat, then phenoxymethylpenicillin 250–500mg 4 times daily po for 10 days (if allergic to penicillin, give erythromycin or azithromycin for 10 days).

  • Analgesia for carditis/arthritis: aspirin 100mg/kg/d po in divided doses (max 4–8g/d) for 2d, then 70mg/kg/d for 6wks. Monitor salicylate level. Toxicity causes tinnitus, hyperventilation, and metabolic acidosis. Risk of Reye syndrome in children. Alternative: nsaids (p[link]). If moderate-to-severe carditis is present (cardiomegaly, ccf, or 3rd-degree heart block), add oral prednisolone to salicylate therapy. In case of heart failure, treat appropriately (p[link]), with severe valve disease, surgery may be required.

  • Immobilize joints in severe arthritis.

  • Haloperidol (0.5mg/8h po) or diazepam for the chorea.

Prognosis

60% with carditis develop chronic rheumatic heart disease. This correlates with the severity of the carditis.53 Acute attacks last an average of 3 months. Recurrence may be precipitated by further streptococcal infections, pregnancy, or use of the oral contraceptive pill. Cardiac sequelae affect mitral (70%), aortic (40%), tricuspid (10%), and pulmonary (2%) valves. Incompetent lesions develop during the attack, stenoses years later.

Secondary prophylaxis

Penicillin v 250mg/12h po. Alternatives: sulfadiazine 1g daily (0.5g if <30kg) or erythromycin 250mg twice daily (if penicillin allergic). Duration: If carditis+persistent valvular disease, continue at least until age of 40 (sometimes lifelong). If carditis but no valvular disease, continue for 10yrs. If there is no carditis, 5yrs of prophylaxis (until age of 21) is sufficient.

Mitral valve disease

Mitral regurgitation (mr)

Backflow through the mitral valve during systole.

Causes:

Functional (lv dilatation); annular calcification (elderly); rheumatic fever; infective endocarditis; mitral valve prolapse; ruptured chordae tendinae; papillary muscle dysfunction/rupture (eg post-mi); connective tissue disorders (Ehlers–Danlos, Marfan’s); cardiomyopathy; congenital (may be associated with other defects, eg asd, av canal); appetite suppressants (eg fenfluramine, phentermine).

Symptoms:

Dyspnoea; fatigue; palpitations; symptoms of causative factor (eg fever).

Signs:

af; displaced, hyperdynamic apex; pansystolic murmur at apex radiating to axilla; soft s1; split s2; loud p2 (pulmonary hypertension). Severity: the more severe, the larger the left ventricle.

Tests:

ecg: af; p-mitrale if in sinus rhythm (may mean ↑left atrial size); lvh. cxr: big la & lv; mitral valve calcification; pulmonary oedema.

Echocardiogram:

To assess lv function and mr severity and aetiology (transoesophageal to assess severity and suitability for repair rather than replacement). Cardiac catheterization to confirm diagnosis, exclude other valve disease, and assess coronary artery disease (can combine cabg with valve surgery).

Management:

Control rate if fast af. Anticoagulate if: af; history of embolism; prosthetic valve; additional mitral stenosis. Diuretics improve symptoms. Surgery4 for deteriorating symptoms; aim to repair or replace the valve before lv is irreversibly impaired.

Mitral valve prolapse:

Is the most common valvular abnormality (prevalence: ~5%). Occurs alone or with: asd, patent ductus arteriosus, cardiomyopathy, Turner’s syndrome, Marfan’s syndrome, osteogenesis imperfecta, pseudoxanthoma elasticum, wpw (p[link]).

Symptoms:

Usually asymptomatic. May develop atypical chest pain, palpitations, and autonomic dysfunction symptoms.

Signs:

Mid-systolic click and/or a late systolic murmur.

Complications:

mr, cerebral emboli, arrhythmias, sudden death.

Tests:

Echo is diagnostic. ecg may show inferior t-wave inversion.

℞:

β‎-blockers may help palpitations and chest pain. Surgery if severe mr.

Mitral stenosis

Causes:

Rheumatic fever, congenital, mucopolysaccharidoses, endocardial fibroelastosis, malignant carcinoid (p[link]; rare), prosthetic valve.

Presentation:

Normal mitral valve orifice area is ~4–6cm2. Symptoms usually begin when the orifice becomes <2cm2. Pulmonary hypertension causes dyspnoea, haemoptysis, chronic bronchitis-like picture; pressure from large left atrium on local structures causes hoarseness (recurrent laryngeal nerve), dysphagia (oesophagus), bronchial obstruction; also fatigue, palpitations, chest pain, systemic emboli, infective endocarditis (rare).

Signs:

Malar flush on cheeks (due to ↓cardiac output); low-volume pulse; af common (due to enlarged la); tapping, non-displaced, apex beat (palpable s1); rv heave. On auscultation: loud s1; opening snap (pliable valve); rumbling mid-diastolic murmur (heard best in expiration, with patient on left side). Graham Steell murmur (p[link]) may occur. Severity: the more severe the stenosis, the longer the diastolic murmur, and the closer the opening snap is to s2.

Tests:

ecg: af; p-mitrale; rvh; progressive rad. cxr: left atrial enlargement (double shadow in right cardiac silhouette); pulmonary oedema; mitral valve calcification. Echo is diagnostic. Significant stenosis exists if the valve orifice is <1cm2/m2 body surface area. Indications for cardiac catheterization: previous valvotomy; signs of other valve disease; angina; severe pulmonary hypertension; calcified mitral valve.

Management:

If in af, rate control (p[link]) is crucial; anticoagulate with warfarin (p[link]). Diuretics ↓ preload and pulmonary venous congestion. If this fails to control symptoms, balloon valvuloplasty (if pliable, non-calcified valve), open mitral valvotomy, or valve replacement.

Aortic valve disease

Aortic stenosis (as)

Causes:

Senile calcification is the commonest.57 Others: congenital (bicuspid valve, Williams syndrome, p[link]), rheumatic heart disease.

Presentation:

Think of as in any elderly person with chest pain, exertional dyspnoea, or syncope. The classic triad includes angina, syncope, and heart failure. Also: dyspnoea; dizziness; faints; systemic emboli if infective endocarditis; sudden death.

Signs:

Slow rising pulse with narrow pulse pressure (feel for diminished and delayed carotid upstroke—parvus et tardus); heaving, non-displaced apex beat; lv heave; aortic thrill; ejection systolic murmur (heard at the base, left sternal edge and the aortic area, radiates to the carotids). s1 is usually normal. As stenosis worsens, a2 is increasingly delayed, giving first a single s2 and then reversed splitting. But this sign is rare. More common is a quiet a2. In severe as, a2 may be inaudible (calcified valve). There may be an ejection click (pliable valve) or an s4.

Tests:

ecg: lvh with strain pattern; p-mitrale; lad; poor r-wave progression; lbbb or complete av block (calcified ring). cxr: lvh; calcified aortic valve (fig 3.44); post-stenotic dilatation of ascending aorta. Echo: diagnostic (p[link]). Doppler echo can estimate the gradient across valves: severe stenosis if peak gradient ≳40mmHg (but beware the poor left ventricle not able to generate gradient) and valve area <1cm2. If the aortic jet velocity is >4m/s (or is increasing by >0.3m/s per yr) risk of complications is increased.57 Cardiac catheter can assess: valve gradient; lv function; coronary artery disease; risks: emboli generation.

Fig 3.44 Severely calcified aortic valve.

Fig 3.44
Severely calcified aortic valve.

Reproduced with permission from Hamid Reza Taghipour.

Differential diagnosis:

Hypertrophic cardiomyopathy (hcm, p[link]); aortic sclerosis.

Management:

If symptomatic, prognosis is poor without surgery: 2–3yr survival if angina/syncope; 1–2yr if cardiac failure. If moderate-to-severe and treated medically, mortality can be as high as 50% at 2yrs, therefore prompt valve replacement (p[link]) is usually recommended. In asymptomatic patients with severe as and a deteriorating ecg, valve replacement is also recommended. If the patient is not medically fit for surgery, percutaneous valvuloplasty/replacement (tavi = transcatheter aortic valve implantation) may be attempted (fig 3.45).

Aortic sclerosis

Senile degeneration of the valve. There is an ejection systolic murmur; but no carotid radiation, and normal pulse (character and volume) and s2.

Aortic regurgitation (ar)

Acute:

Infective endocarditis, ascending aortic dissection, chest trauma.

Chronic:

Congenital, connective tissue disorders (Marfan’s syndrome, Ehlers–Danlos), rheumatic fever, Takayasu arteritis, rheumatoid arthritis, sle, pseudoxanthoma elasticum, appetite suppressants (eg fenfluramine, phentermine), seronegative arthritides (ankylosing spondylitis, Reiter’s syndrome, psoriatic arthropathy), hypertension, osteogenesis imperfecta, syphilitic aortitis.

Symptoms:

Exertional dyspnoea, orthopnoea, and pnd. Also: palpitations, angina, syncope, ccf.

Signs:

Collapsing (water-hammer) pulse (p[link]); wide pulse pressure; displaced, hyperdynamic apex beat; high-pitched early diastolic murmur (heard best in expiration, with patient sat forward). Eponyms: Corrigan’s sign: carotid pulsation; de Musset’s sign: head nodding with each heart beat; Quincke’s sign: capillary pulsations in nail beds; Duroziez’s sign: in the groin, a finger compressing the femoral artery 2cm proximal to the stethoscope gives a systolic murmur; if 2cm distal, it gives a diastolic murmur as blood flows backwards; Traube’s sign: ‘pistol shot’ sound over femoral arteries; an Austin Flint murmur (p[link]) denotes severe ar.

Tests:

ecg: lvh. cxr: cardiomegaly; dilated ascending aorta; pulmonary oedema. Echo is diagnostic. Cardiac catheterization to assess: severity of lesion; anatomy of aortic root; lv function; coronary artery disease; other valve disease.

Management:

The main goal of medical therapy is to reduce systolic hypertension; ace-i are helpful. Echo every 6–12 months to monitor. Indications for surgery: severe ar with enlarged ascending aorta, increasing symptoms, enlarging lv or deteriorating lv function on echo; or infective endocarditis refractory to medical therapy. Aim to replace the valve before significant lv dysfunction occurs. Predictors of poor post-operative survival: ejection fraction <50%, nyha class iii or iv (p[link]), duration of ccf >12 months.

Right heart valve disease

Tricuspid regurgitation

Causes:

Functional (rv dilatation; eg due to pulmonary hypertension induced by lv failure or pe); rheumatic fever; infective endocarditis (iv drug abuser5); carcinoid syndrome; congenital (eg asd, av canal, Ebstein’s anomaly (downward displacement of the tricuspid valve—see ohcs p[link])); drugs (eg ergot-derived dopamine agonists, p[link]; fenfluramine).

Symptoms:

Fatigue; hepatic pain on exertion (due to hepatic congestion); ascites; oedema and symptoms of the causative condition.

Signs:

Giant v waves and prominent y descent in jvp (p[link]); rv heave; pansystolic murmur, heard best at lower sternal edge in inspiration; pulsatile hepatomegaly; jaundice; ascites.

Management:

Drugs: diuretics for systemic congestion; drugs to treat underlying cause. Valve repair or replacement (~10% 30-day mortality). Tricuspid regurgitation resulting from myocardial dysfunction or dilatation has a mortality of up to 50% at 5 yrs.

Tricuspid stenosis

Causes:

Main cause is rheumatic fever, which almost always occurs with mitral or aortic valve disease. Also: congenital, infective endocarditis.

Symptoms:

Fatigue, ascites, oedema.

Signs:

Giant a wave and slow y descent in jvp (p[link]); opening snap, early diastolic murmur heard at the left sternal edge in inspiration. af can also occur.

Diagnosis:

Echo.

Treatment:

Diuretics; surgical repair.

Pulmonary stenosis

Causes:

Usually congenital (Turner syndrome, Noonan syndrome, Williams syndrome, Fallot’s tetralogy, rubella). Acquired causes: rheumatic fever, carcinoid syndrome.

Symptoms:

Dyspnoea; fatigue; oedema; ascites.

Signs:

Dysmorphic facies (congenital causes); prominent a wave in jvp; rv heave. In mild stenosis, there is an ejection click, ejection systolic murmur (which radiates to the left shoulder); widely split s2. In severe stenosis, the murmur becomes longer and obscures a2. p2 becomes softer and may be inaudible.

Tests:

ecg: rad, p-pulmonale, rvh, rbbb; echo/toe (p[link]); cxr: prominent pulmonary arteries caused by post-stenotic dilatation. Cardiac catheterization is diagnostic.

Treatment:

Pulmonary valvuloplasty or valvotomy.

Pulmonary regurgitation

Causes:

Any cause of pulmonary hypertension (p[link]).

Signs:

Decrescendo murmur in early diastole at the left sternal edge (the Graham Steell murmur if associated with mitral stenosis and pulmonary hypertension).

Cardiac surgery

Cardiac surgery has come on a long way since 1923 when Dr Henry Souttar58,59 used his finger to open a stenosed mitral valve in a beating heart.6 Cardiac bypass allows prolonged access to the open, static heart, during which complex and high-precision repair and replacement of valves and aortic roots can occur. Transcatheter procedures are playing an increasing role in the management of cardiovascular disease. Key open heart procedures include:

Valve replacements

Mechanical valves may be of the ball-cage (Starr–Edwards), tilting disc (Bjork–Shiley), or double tilting disc (St Jude) type. These valves are very durable but the risk of thromboembolism is high; patients require lifelong anticoagulation. Xenografts are made from porcine valves or pericardium. These valves are less durable and may require replacement at 8–10yrs but have the advantage of not necessitating anticoagulation. Homografts are cadaveric valves. They are particularly useful in young patients and in the replacement of infected valves. Complications of prosthetic valves: systemic embolism, infective endocarditis, haemolysis, structural valve failure, arrhythmias.

CABG

See p[link].

Cardiac transplantation

Consider this when cardiac disease is severely curtailing quality of life, and survival is not expected beyond 6–12 months.

Surgery for congenital heart defects

See p[link].

Aortic root surgery

Replacement/repair if dissection or aneurysmal.

Infective endocarditis (ie)

Cardiovascular medicineFever + new murmur = endocarditis until proven otherwise. Any fever lasting >1wk in those known to be at risk7 must prompt blood cultures.61 Acute infective endocarditis (ie) tends to occur on ‘normal’ valves and may present with acute heart failure ± emboli; the commonest organism is Staph. aureus. Risk factors: skin breaches (dermatitis, iv lines, wounds); renal failure; immunosuppression; dm. Mortality: 5–50% (related to age and embolic events). Endocarditis on abnormal valves tends to run a subacute course. Risk factors: aortic or mitral valve disease; tricuspid valves in iv drug users; coarctation; patent ductus arteriosus; vsd; prosthetic valves. Endocarditis on prosthetic valves may be ‘early’ (within 60d of surgery, usually Staph. epidermidis, poor prognosis) or ‘late’.

Causes

Bacteria:

Bacteraemia occurs all the time, eg when we chew (not just during dentistry or medical interventions—which is why routine prophylaxis for such procedures does not make sense).61 Strep. viridans is the commonest (usually subacute) followed by Staph. aureus, Strep. bovis (need colonoscopy ?tumour), Enterococci and Coxiella burnetii. Rarely: HACEK Gram −ve bacteria (HaemophilusActinobacillusCardiobacteriumEikenellaKingella); diphtheroids; Chlamydia.

Fungi:

Candida; Aspergillus; Histoplasma. Usually in iv drug abusers, immunocompromised patients or those with prosthetic valves. High mortality, need surgical management.

Other:

sle (Libman–Sacks endocarditis); malignancy.

Signs

Septic signs:

Fever, rigors, night sweats, malaise, weight loss, anaemia, splenomegaly, and clubbing (fig 3.46).

Fig 3.46 Clubbing with endocarditis.

Fig 3.46
Clubbing with endocarditis.

Cardiac lesions:

Any new murmur, or a change in pre-existing murmur, should raise the suspicion of endocarditis. Vegetations may cause valve destruction and severe regurgitation, or valve obstruction. An aortic root abscess causes prolongation of the pr interval, and may lead to complete av block. lvf is a common cause of death.

Immune complex deposition:

Vasculitis (p[link]) may affect any vessel. Microscopic haematuria is common; glomerulonephritis and acute kidney injury may occur. Roth spots (boat-shaped retinal haemorrhage with pale centre); splinter haemorrhages (fig 3.47); Osler’s nodes (painful pulp infarcts in fingers or toes).

Fig 3.47 Splinter haemorrhages are normally seen under the fingernails or toenails. They are usually red-brown in colour.

Fig 3.47
Splinter haemorrhages are normally seen under the fingernails or toenails. They are usually red-brown in colour.

Embolic phenomena:

Emboli may cause abscesses in the relevant organ, eg brain, heart, kidney, spleen, gut (or lung if right-sided ie) or skin: termed Janeway lesions (fig 3.48; painless palmar or plantar macules), which, together with Osler’s nodes, are pathognomonic.

Fig 3.48 Janeway’s lesions are non-tender erythematous, haemorrhagic, or pustular spots, eg on the palms or soles.

Fig 3.48
Janeway’s lesions are non-tender erythematous, haemorrhagic, or pustular spots, eg on the palms or soles.

Diagnosis

Use the Modified Duke criteria (box ‘Modified Duke criteria’).62,63

Blood cultures:

Do three sets at different times from different sites at peak of fever. 85–90% are diagnosed from the 1st two sets; 10% are culture-negative.

Blood tests:

Normochromic, normocytic anaemia, neutrophilia, high esr/crp. Rheumatoid factor positive (an immunological phenomenon). Also check u&e, Mg2+, lft.

Urinalysis:

For microscopic haematuria.

cxr:

Cardiomegaly, pulmonary oedema.

Regular ecgs:

To look for heart block.

Echocardiogram:

tte (p[link]) may show vegetations, but only if >2mm. toe (p[link]) is more sensitive, and better for visualizing mitral lesions and possible development of aortic root abscess.

CT:

To look for emboli (spleen, brain, etc.).

Treatment

Liaise early with microbiologists and cardiologists.62 Antibiotics: see box ‘Antibiotic therapy for infective endocarditis’.

Surgery if:

Heart failure, valvular obstruction; repeated emboli; fungal ie; persistent bacteraemia; myocardial abscess; unstable infected prosthetic valve.64

Prognosis

50% require surgery. 20% inhospital mortality (Staphs 30%; bowel bacteria 14%; Streps 6%). 15% recurrence at 2yrs.

Prevention

Antibiotic prophylaxis is no longer recommended for those at risk of ie undergoing invasive procedures. However, if they are given antibiotics for other reasons during a procedure, the antibiotic should cover the common ie organisms.

Recommendations

Give clear information about prevention, including:

  • The importance of maintaining good oral health.

  • Symptoms that may indicate ie and when to seek expert advice.

  • The risks of invasive procedures, including non-medical procedures such as body piercing or tattooing.65

Diseases of heart muscle

Acute myocarditis

This is inflammation of myocardium, often associated with pericardial inflammation (myopericarditis).67

Causes:

See table 3.3.

Symptoms and signs:

acs-like symptoms, heart failure symptoms, palpitations, tachycardia, soft s1, s4 gallop (p[link]).

Tests:

ecg: st changes and t-wave inversion, atrial arrhythmias, transient av block, qt prolongation. Bloods: crp, esr, & troponin may be raised; viral serology and tests for other likely causes. Echo: diastolic dysfunction, regional wall abnormalities. Cardiac mr if clinically stable. Endomyocardial biopsy is gold standard.

℞:

Supportive. Treat the underlying cause. Treat arrhythmias and heart failure (p[link]). nsaid use is controversial. Avoid exercise as this can precipitate arrhythmias.

Prognosis:

50% will recover within 4wks. 12–25% will develop dcm and severe heart failure. dcm can occur years after apparent recovery.

Dilated cardiomyopathy (dcm)

A dilated, flabby heart of unknown cause. Associations: alcohol, ↑bp, chemotherapeutics, haemochromatosis, viral infection, autoimmune, peri- or postpartum, thyrotoxicosis, congenital (x-linked).

Prevalence:

0.2%.

Presentation:

Fatigue, dyspnoea, pulmonary oedema, rvf, emboli, af, vt.

Signs:

↑Pulse, ↓bp, ↑jvp, displaced and diffuse apex, s3 gallop, mitral or tricuspid regurgitation (mr/tr), pleural effusion, oedema, jaundice, hepatomegaly, ascites.

Tests:

Blood: bnp (p[link]), ↓Na+ indicates a poor prognosis. cxr: cardiomegaly, pulmonary oedema. ecg: tachycardia, non-specific t-wave changes, poor r-wave progression. Echo: globally dilated hypokinetic heart and low ejection fraction. Look for mr, tr, lv mural thrombus.

℞:

Bed rest, diuretics, β‎-blockers, ace-i, anticoagulation, biventricular pacing, icds, lvads, transplantation.

Mortality:

Variable, eg 40% in 2yrs.

Hypertrophic cardiomyopathy (hcm)

lv outflow tract (lvot) obstruction from asymmetric septal hypertrophy. hcm is the leading cause of sudden cardiac death in the young.

Prevalence:

0.2%. Autosomal dominant inheritance, but 50% are sporadic. 70% have mutations in genes encoding β‎-myosin, α‎-tropomyosin, and troponin t. May present at any age. Ask about family history of sudden death.

Symptoms and signs:

Sudden death may be the first manifestation of hcm in many patients (vf is amenable to implantable defibrillators), angina, dyspnoea, palpitation, syncope, ccf. Jerky pulse; a wave in jvp; double-apex beat; systolic thrill at lower left sternal edge; harsh ejection systolic murmur.

Tests:

  • ecg: lvh; progressive t-wave inversion; deep q waves (inferior + lateral leads); af; wpw syndrome (p[link]); ventricular ectopics; vt.

  • Echo: asymmetrical septal hypertrophy; small lv cavity with hypercontractile posterior wall; midsystolic closure of aortic valve; systolic anterior movement of mitral valve.

  • mri: see fig 3.16.

  • Cardiac catheterization helps assess: severity of gradient; coronary artery disease or mitral regurgitation, but may provoke vt.

  • Electrophysiological studies may be needed (eg if wpw, p[link]).

  • Exercise test ± Holter monitor (p[link]) to risk stratify

℞:

β‎-blockers or verapamil for symptoms (the aim is reducing ventricular contractility). Amiodarone (p[link]) for arrhythmias (af, vt). Anticoagulate for paroxysmal af or systemic emboli. Septal myomectomy (surgical or chemical (with alcohol) to ↓lv outflow tract gradient) is reserved for those with severe symptoms. Consider implantable defibrillator—use http://www.doc2do.com/hcm/webHCM.html to assess risk of sudden cardiac death.

Mortality:

5.9%/yr if <14yrs; 2.5%/yr if >14yrs. Poor prognostic factors: age <14yrs or syncope at presentation; family history of hcm/sudden death.

Restrictive cardiomyopathy

Causes:

Idiopathic; amyloidosis; haemochromatosis; sarcoidosis; scleroderma; Löffler’s eosinophilic endocarditis; endomyocardial fibrosis.

Presentation:

Is like constrictive pericarditis (p[link]). Features of rvf predominate: ↑jvp, with prominent x and y descents; hepatomegaly; oedema; ascites.

Diagnosis:

Echo, mri, cardiac catheterization.

℞:

Treat the cause.

Cardiac myxoma

(figs 3.49, 3.50) Rare benign cardiac tumour. Prevalence ≤5/10 000, ♀:♂≈2:1. Usually sporadic, but may be familial (Carney complex: cardiac and cutaneous myxomas, skin pigmentation, endocrinopathy, etc., p[link]). It may mimic infective endocarditis (fever, weight loss, clubbing, ↑esr, systemic emboli), or mitral stenosis (left atrial obstruction, af). A ‘tumour plop’ may be heard, and signs may vary according to posture.

Fig 3.49 Echocardiogram of a 35-yr-old patient who presented with severe exertional dyspnoea and several episodes of syncope. Look at the large mass (cardiac myxoma) in left atrium. Abbreviations: rv: right ventricle; lv: left ventricle; av: aortic valve; ao: aorta; mv: mitral valve.

Fig 3.49
Echocardiogram of a 35-yr-old patient who presented with severe exertional dyspnoea and several episodes of syncope. Look at the large mass (cardiac myxoma) in left atrium. Abbreviations: rv: right ventricle; lv: left ventricle; av: aortic valve; ao: aorta; mv: mitral valve.

Reproduced with permission from Hamid Reza Taghipour.

Fig 3.50 Echocardiogram of the same patient as fig 3.49 during diastole. Notice how the large mass of myxoma protrudes into the left ventricle during diastole, and obstructs the mitral valve almost completely. Abbreviations: rv: right ventricle; lv: left ventricle; ao: aorta.

Fig 3.50
Echocardiogram of the same patient as fig 3.49 during diastole. Notice how the large mass of myxoma protrudes into the left ventricle during diastole, and obstructs the mitral valve almost completely. Abbreviations: rv: right ventricle; lv: left ventricle; ao: aorta.

Reproduced with permission from Hamid Reza Taghipour.

Tests:

Echo.

℞:

Excision.

Pericardial diseases

Acute pericarditis

This is inflammation of the pericardium.68

Causes:

Idiopathic or secondary to:

  • Viruses: eg coxsackie, echovirus, ebv, cmv, adenovirus, mumps, varicella, hiv.

  • Bacteria: eg tb—commonest cause worldwide, Lyme disease, q fever, pneumonia, rheumatic fever, Staphs, Streps, mycoplasma, legionella, mai in hiv.

  • Fungi and parasitic: v rare, usually in immunocompromised.

  • Autoimmune: systemic autoimmune diseases eg sle, ra; vasculitides eg Behçet, Takayasu; ibd; sarcoid; amyloid; Dressler’s (p[link]).

  • Drugs: eg procainamide, hydralazine, penicillin, isoniazid, chemotherapy.

  • Metabolic: uraemia, hypothyroidism, anorexia nervosa.

  • Others: trauma, surgery, malignancy, radiotherapy, mi, chronic heart failure.

Clinical features:

Central chest pain worse on inspiration or lying flat ± relief by sitting forward. A pericardial friction rub (p[link]) may be heard. Look for evidence of a pericardial effusion or cardiac tamponade (see later in topic). Fever may occur.

Tests:

ecg classically shows concave (saddle-shaped) st segment elevation and pr depression, but may be normal or non-specific (10%); see fig 3.51. Blood tests: fbc, esr, u&e, cardiac enzymes (nb: troponin may be raised); tests relating to possible aetiologies. Cardiomegaly on cxr may indicate a pericardial effusion. Echo (if suspected pericardial effusion). cmr and ct may show localized inflammation.

Treatment:

nsaids or aspirin with gastric protection for 1–2weeks. Add colchicine 500mcg od or bd for 3 months to reduce the risk of recurrence. Rest until symptoms resolve. Treat the cause. If not improving or autoimmune, consider steroids (may increase the risk of recurrence) or other immunosuppressive therapies.

Pericardial effusion

Accumulation of fluid in the pericardial sac (normally 10–50mL).68

Causes:

Pericarditis, myocardial rupture (haemopericardium—surgical, stab wound, post-mi); aortic dissection; pericardium filling with pus; malignancy.

Clinical features:

Dyspnoea, chest pain, signs of local structures being compressed—hiccoughs (phrenic n), nausea (diaphragm), bronchial breathing at left base (Ewart’s sign: compressed left lower lobe). Muffled heart sounds. Look for signs of cardiac tamponade (below).

Diagnosis:

cxr shows an enlarged, globular heart if effusion >300mL; fig 3.14. ecg shows low-voltage qrs complexes and may have alternating qrs morphologies (electrical alternans). Echocardiography shows an echo-free zone surrounding the heart.

Management:

Treat the cause. Pericardiocentesis may be diagnostic (suspected bacterial pericarditis) or therapeutic (cardiac tamponade). See p[link]. Send pericardial fluid for culture, zn stain/tb culture, and cytology.

Constrictive pericarditis

The heart is encased in a rigid pericardium.68

Causes:

Often unknown (uk); elsewhere tb, or after any pericarditis.

Clinical features:

These are mainly of right heart failure with ↑jvp (with prominent x and y descents, p[link]); Kussmaul’s sign (jvp rising paradoxically with inspiration); soft, diffuse apex beat; quiet heart sounds; s3; diastolic pericardial knock, hepatosplenomegaly, ascites, and oedema.

Tests:

cxr: small heart ± pericardial calcification. ct/mri—helps distinguish from restrictive cardiomyopathy. Echo. Cardiac catheterization.

Management:

Surgical excision. Medical ℞ to address the cause and symptoms.

Cardiac tamponade

A pericardial effusion that raises intrapericardial pressure, reducing ventricular filling and thus dropping cardiac output.68 ΔΔ‎ Can lead rapidly to cardiac arrest.

Signs:

↑Pulse, ↓bp, pulsus paradoxus, ↑jvp, Kussmaul’s sign, muffled s1 and s2.

Diagnosis:

Beck’s triad: falling bp; rising jvp; muffled heart sounds. ecg: low-voltage qrs ± electrical alternans. Echo is diagnostic: echo-free zone (>2cm, or >1cm if acute) around the heart ± diastolic collapse of right atrium and right ventricle.

Management:

Seek expert help. The pericardial effusion needs urgent drainage (p[link]). Send fluid for culture, zn stain/tb culture, and cytology.

Adult congenital heart disease (achd)

This is a growing area of cardiology as increasing numbers of children with congenital heart defects survive to adulthood, sometimes as a result of complex restructuring procedures which have their own physiological implications (see box ‘Patients with one ventricle’). achd69 patients are at increased risk of many conditions described elsewhere, for which many of the ‘standard’ investigations and therapies will apply: including arrhythmias (p[link]), heart failure (p[link]), and infective endocarditis (p[link]).

Investigations

Echocardiography (± bubble contrast) is first line. Increasingly, cardiac ct and mr are used to provide precise anatomical and functional information. Cardiac catheterization generates data on oxygen saturation and pressure in different vessels and chambers. Exercise testing assesses functional capacity.

A few of the more common achds are discussed below:

Bicuspid aortic valve

These work well at birth and go undetected. Many eventually develop aortic stenosis (needing valve replacement) ± aortic regurgitation predisposing to ie/sbe ± aortic dilatation/dissection. Intense exercise may accelerate complications, so do yearly echocardiograms on affected athletes.70

Atrial septal defect (asd)

A hole connects the atria.

  • Ostium secundum defects: 80% cases; hole high in the septum; often asymptomatic until adulthood when a lr shunt develops. Shunting depends on the compliance of the ventricles. lv compliance decreases with age (esp. if ↑bp), so augmenting lr shunting; hence dyspnoea/heart failure, typically aged 40–60yrs.

  • Ostium primum defects: associated with av valve anomalies, eg in Down’s syndrome; present in childhood.

Signs and symptoms:

Chest pain, palpitations, dyspnoea. Arrhythmias incl. af; ↑jvp; wide, fixed split s2; pulmonary systolic flow murmur. Pulmonary hypertension may cause pulmonary or tricuspid regurgitation, dyspnoea and haemoptysis. ↑Frequency of migraine.

Simple tests:

ecg: rbbb with lad (primum defect) or rad (secundum defect). cxr: small aortic knuckle, pulmonary plethora, atrial enlargement.

Complications:

  • Reversal of left-to-right shunt, ie Eisenmenger’s complex: initial lr shunt leads to pulmonary hypertension which increases right heart pressures until they exceed left heart pressures, hence shunt reversal. This causes cyanosis as deoxygenated blood enters systemic circulation.

  • Paradoxical emboli eg causing cvas (vein→artery via asd; rare).

Treatment:

May close spontaenously. If not, primum defects are usually closed in childhood. Secundum defects should be closed if symptomatic or signs of rv overload. Transcatheter closure is more common than surgical.

Ventricular septal defect (vsd)

A hole connects the ventricles.

Causes:

Congenital (prevalence 2:1000 births); acquired (post-mi).

Symptoms:

May present with severe heart failure in infancy, or remain asymptomatic and be detected incidentally in later life.

Signs:

Classically, a harsh pansystolic murmur is heard at the left sternal edge, with a systolic thrill, ± left parasternal heave. Smaller holes, which are haemodynamically less significant, give louder murmurs. Signs of pulmonary hypertension.

Complications:

ar, ie/sbe, pulmonary hypertension, Eisenmenger’s complex (above), heart failure from volume overload.

Tests:

ecg: normal, lad, lvh, rvh. cxr: normal heart size ± mild pulmonary plethora (small vsd) or cardiomegaly, large pulmonary arteries and marked pulmonary plethora (large vsd). Cardiac catheter: step up in O2 saturation in right ventricle.

Treatment:

Initially medical as many close spontaneously. Indications for surgical closure: failed medical therapy, symptomatic vsd, shunt >3:1, sbe/ie. Endovascular closure may be possible.71

Coarctation of the aorta

Congenital narrowing of the descending aorta; usually occurs just distal to the origin of the left subclavian artery. More common in boys.

Associations:

Bicuspid aortic valve; Turner’s syndrome.

Signs:

Radiofemoral delay; weak femoral pulse; ↑bp; scapular bruit; systolic murmur (best heard over the left scapula); cold feet.

Complications:

Heart failure from high afterload; ie; intracerebral haemorrhage.

Tests:

ct or mri-aortogram; cxr may show rib notching as blood diverts down intercostal arteries to reach the lower body, causing these vessels to dilate and erode local rib bone.

Treatment:

Surgery, or balloon dilatation ± stenting.

Tetralogy of Fallot

See p[link].

Driving and the heart

uk licences are inscribed ‘You are required by law to inform Drivers Medical Branch, dvla, Swansea sa99 1at at once if you have any disability (physical or medical), which is, or may become likely to affect your fitness as a driver, unless you do not expect it to last more than 3 months’. It is the responsibility of drivers to inform the dvla (the uk Driving and Vehicle Licensing Authority), and that of their doctors to advise patients that medical conditions74 (and drugs) may affect their ability to drive and for which conditions patients should inform the dvla. Drivers should also inform their insurance company of any condition disclosed to the dvla. If in doubt, ask your defence union.

The following are examples of the guidance for holders of standard licences; different rules apply for group 2 vehicle licence-holders (eg lorries, buses). More can be found at https://www.gov.uk/guidance/cardiovascular-disorders-assessing-fitness-to-drive.

Angina

Driving must cease when symptoms occur at rest or with emotion. Driving may recommence when satisfactory symptom control is achieved. dvla need not be notified.

Angioplasty

Driving must cease for 1wk, and may recommence thereafter provided no other disqualifying condition. dvla need not be notified.

MI

If successfully treated with angioplasty, cease driving for 1 week provided urgent intervention not planned and lvef (left ventricular ejection fraction) >40%, and no other disqualifying condition. Otherwise, driving must cease for 1 month. dvla need not be notified.

Dysrhythmias

Including sinoatrial disease, af/flutter, atrioventricular conduction defects, and narrow or broad complex tachycardias. Driving must cease if the dysrhythmia has caused or is likely to cause incapacity. Driving may recommence 4wks after successful control provided there is no other disqualifying condition.

Pacemaker implant

Stop driving for 1wk, the patient must notify the dvla.

Implanted cardioverter/defibrillator

The licence is subject to annual review. Driving may occur when these criteria can be met:

  • 6 months have passed since icd implanted for secondary prevention.

  • 1 month has passed since icd implanted for primary prophylaxis.

  • The device has not administered therapy (shock and/or symptomatic antitachycardia pacing) within the last 6 months (except during testing).

  • No therapy (shock) in the last 2 years has been accompanied by incapacity (whether caused by the device or arrhythmia)—unless this was a result of device malfunction which has been corrected for at least 1 month or steps have been taken to avoid recurrence (eg ablation) which have been successful for at least 6 months.

  • A period of 1 month off driving must occur following any revision of the device (generator and/or electrode) or alteration of antiarrhythmics.

  • The device is subject to regular review with interrogation.

  • There is no other disqualifying condition.

Syncope

Simple faint:

No restriction.

Unexplained syncope:

With probable cardiac aetiology—4wks off driving if cause identified and treated; otherwise 6 months off. Loss of consciousness or altered awareness associated with signs of seizure requires 6 months off driving. If the patient is known to be epileptic or has had another such episode in the preceeding 5yrs, they must abstain from driving for 1yr. See driving and epilepsy (box). Patients who have had a single episode of loss of consciousness with no cause found despite neurological and cardiac investigations, must abstain from driving for 6 months.

Hypertension

Driving may continue unless treatment causes unacceptable side-effects. dvla need not be notified.

Notes:

We thank Dr Parag Gajendragadkar, our Specialist Reader, for his contribution to this chapter.

1 25% of non-cardiac chest pain is musculoskeletal: look for pain on specific postures or activity. Aim to reproduce the pain by movement and, sometimes, palpation over the structure causing it. Focal injection of local anaesthetic helps diagnostically and is therapeutic. Tietze’s syndrome: self-limiting costochondritis ± costosternal joint swelling. Causes: idiopathic; microtrauma; infection; psoriatic/rheumatoid arthritis. ℞: nsaids or steroid injections. Tenderness is also caused by: fibrositis, lymphoma, chondrosarcoma, myeloma, metastases, rib tb. Imaging: bone scintigraphy; ct.

2 Dialogue-transformed symptoms explain one of the junior doctor’s main vexations: when patients retell symptoms to a consultant in the light of day, they bear no resemblance to what you originally heard. But do not be vexed: your dialogue may have helped the patient far more than any ward round.

3 jvp rises during inspiration. Adolf Kussmaul was a prominent 19th-century physician and the first to attempt gastroscopy. Inspired by a sword swallower he passed a rigid tube into the stomach, however light technology was limited and it was not until years later that gastroscopists could visualize the stomach.

4 In patients with severe symptoms for whom open surgery is too dangerous, consider transcatheter valve repair, eg with MitraClip®. This is only available in specialist centres.

5 Remember that it is the tricuspid valve which is the valve most vulnerable to events arriving by vein, eg pathogens from iv drug abusers or hormones (particularly 5-ht) from carcinoid tumours.

6 Souttar’s own description of this landmark case is available online: H S Souttar. The surgical treatment of mitral stenosis. bmj 1925: 2(3379): 603–606.

7 Past ie or rheumatic fever; iv drug abuser; damaged or replaced valve; ppm or icd; structural congenital heart disease (but not simple asd, fully repaired vsd, or patent ductus); hypertrophic cardiomyopathy.

8 If Strep bovis is cultured, do colonoscopy, as a colon neoplasm is the likely portal of entry (table 6.3, p[link]).

Copyright © 2020. All rights reserved.