Cardiac Arrythmias Flashcards

Question

Familial Atrial fibrillation is linked to which chromosomal gene defects?

Answer 1

Gene defects linked to chromosomes 10, 6, 5 and 4 have been associated with familial atrial fibrillation.

Answer 2

The ECG shows fine oscillations of the baseline (so-called fibrillation or f waves) and no clear P waves (Fig. 30.46A). The QRS rhythm is rapid and irregular. Untreated, the ventricular rate is usually 120–180/min but it slows with treatment.

Answer 3

The clinical classification of atrial fibrillation includes: • first detected – irrespective of duration or severity of symptoms • paroxysmal – stops spontaneously within 7 days • persistent – continuous \>7 days • longstanding persistent – continuous \>1 year • permanent – continuous, with a joint decision between the patient and the physician to cease further attempts to regain sinus rhythm. The classification is helpful in choosing between rhythm restoration and rate control. Atrial fibrillation may be asymptomatic and the ‘first detected episode’ should not necessarily be regarded as the true onset.

Answer 4

When atrial fibrillation is due to an acute precipitating event, such as alcohol toxicity, chest infection or hyperthyroidism, the provoking cause should be treated. Strategies for the acute management of atrial fibrillation are: • Ventricular rate control, achieved by drugs that block the AV node (see later). • Cardioversion, achieved electrically by DC shock (see p. 1048), or medically by intravenous infusion of an antiarrhythmic drug such as flecainide, propafenone, vernakalant or amiodarone. Cardioversion can also be achieved by giving an oral agent (flecainide or propafenone) previously tested in hospital and found to be safe in a particular patient (‘pill-in- pocket’ approach). The choice depends on: • how well the arrhythmia is tolerated (is cardioversion urgent?) • whether anticoagulation is required before considering elective cardioversion • whether spontaneous cardioversion is likely (previous history? reversible cause?).

Answer 5

Conversion to sinus rhythm can be achieved by electrical DC cardioversion in about 80% of patients. Biphasic waveform defibrillation is more effective than conventional (monophasic) defibrillation, and biphasic defibrillators are now standard. To minimize the risk of thromboembolism associated with cardioversion, patients are fully anticoagulated with warfarin (International Normalized Ratio (INR) 2.0–3.0) or with a direct acting oral anticoagulant agent (DOAC) for 3 weeks before cardioversion (unless atrial fibrillation is of less than 48 hours’ duration) and at least 4 weeks after the procedure. The patient is then assessed for the necessity for long-term anticoagulation based on their thromboembolic risk score (see later). If cardioversion is urgent and the patient is not on any anticoagulation, transoesophageal echocardiography is used to exclude the presence of atrial thrombus.

Answer 6

Two strategies are available: • ‘rate control’ (AV nodal slowing agents plus oral anticoagulation) • ‘rhythm control’ (antiarrhythmic drugs plus DC cardioversion plus oral anticoagulation). Major randomized studies in patients predominantly over the age of 65 years (AFFIRM) or in patients with heart failure (AF-CHF) have shown that there is no net mortality or symptom benefit to be gained from one strategy compared with the other. Which strategy to adopt needs to be assessed for each individual patient. Factors to consider include the likelihood of maintaining sinus rhythm and the safety/tolerability of antiarrhythmic drugs in a particular patient.

Answer 7

This is advocated for younger, symptomatic and physically active patients. Recurrent paroxysms may be prevented with oral medication. In general, patients with no significant heart disease can be treated with any class Ia, Ic or III antiarrhythmic drug, although it is recommended that amiodarone (because of its substantial extracardiac adverse effect profile) should be reserved until other drugs have failed. For patients with heart failure or left ventricular hypertrophy only amiodarone is recommended. Patients with coronary artery disease may be treated with sotalol or amiodarone. Patients with paroxysmal atrial fibrillation or with early persistent atrial fibrillation (little left atrial dilation) may be treated with left atrial ablation.

Answer 8

As a primary strategy, this is appropriate in patients who: • have the permanent form of the arrhythmia associated with symptoms that can be further improved by slowing heart rate, or are older than 65 years with recurrent atrial tachyarrhythmias (‘accepted’ atrial fibrillation) • have persistent tachyarrhythmias and have failed cardioversion(s) and serial prophylactic antiarrhythmic drug therapy, and in whom the risk/benefit ratio from using specific antiarrhythmic agents is shifted towards increased risk. Rate control is usually achieved with a combination of digoxin, beta-blockers or non-dihydropyridine calcium-channel blockers (verapamil or diltiazem). Digoxin monotherapy may be sufficient for elderly, non-ambulant patients. In younger patients the effect of catecholamines easily overwhelms the vagotonic effect of digoxin and additional AV nodal slowing agents are needed. The ventricular rate response is generally considered to be controlled if the resting heart rate is below 110 b.p.m. but stricter control, between 60 and 80 b.p.m. at rest and below 110 b.p.m. during moderate exercise, may be needed if symptoms persist. To assess the adequacy of rate control, an ECG rhythm strip may be sufficient in an elderly patient but ambulatory 24-hour Holter monitoring and an exercise stress test (treadmill) are needed in younger individuals. Older patients with poor rate control despite optimal medical therapy should be considered for AV node ablation and pacemaker implantation (‘ablate and pace’ strategy). These patients usually experience a marked symptomatic improvement but require life-long anticoagulation because of the on-going risk of thromboembolism.

Answer 9

A scoring system known as CHA2DS2VASc is used (Box 30.15) as the first step in determining the need for anticoagulation. Long-term prophylaxis against ischaemic stroke with oral anticoagulation must be balanced against the risk of haemorrhage. The HAS-BLED score is recommended by European, Canadian and UK (NICE) guidelines. A high HAS-BLED score identifies patients with a high risk of bleeding (Box 30.16 and Fig. 30.47), and where risk factors exist, attempts may be made to modify them for instance by controlling hypertension and minimising alcohol intake. When oral anticoagulation is required, either warfarin (dose adjusted to maintain an INR between 2.0 and 3.0) or one of the direct oral anticoagulants (the DOACs) can be used. These latter agents fall into two classes: direct thrombin inhibitors (e.g. dabigatran) and oral direct factor Xa inhibitors (e.g. rivaroxaban and apixaban). DOACs specifically block a single step in the coagulation cascade, in contrast to warfarin, which blocks several vitamin K-dependent factors (II, VII, IX and X). In comparison with warfarin, the DOACs have a rapid onset of action, shorter half-life and fewer food and drug interactions, and do not require INR testing. Trial data have shown them to be equally effective as, and maybe safer than, warfarin. Antiplatelet agents should not be used to reduce stroke risk. Percutaneous left atrial appendage occlusion (LAAO) may be offered where anticoagulation is contraindicated or not tolerated.

Answer 10

Atrial flutter is usually an organized atrial rhythm with an atrial rate typically between 250 and 350 b.p.m. Typical, or isthmus-dependent, atrial flutter involves a macro re-entrant right atrial circuit around the tricuspid annulus. The wavefront circulates down the lateral wall of the right atrium, through the Eustachian ridge between the tricuspid annulus and the inferior vena cava, and up the interatrial septum, giving rise to the most frequent pattern, referred to as counter-clockwise flutter. Re-entry can also occur in the opposite direction (clockwise or reverse flutter).

Answer 11

The ECG shows regular sawtooth-like atrial flutter waves (F waves) between QRS complexes (see Fig. 30.46B). In typical counter-clockwise atrial flutter the F waves are negative in the inferior leads and positive in leads V1 and V2. In clockwise atrial flutter the deflection of the F waves is the opposite. If F waves are not clearly visible, it is worth trying to reveal them by slowing AV conduction by carotid sinus massage or by administering AV nodal blocking drugs such as adenosine or verapamil.

Answer 12

Management of a symptomatic acute paroxysm is by electrical cardioversion. Patients who have been in atrial flutter for more than 1–2 days should be treated in a similar manner to those with atrial fibrillation and anticoagulated for 3 weeks prior to cardioversion. Acute pharmacological cardioversion can be achieved using class Ic (flecainide, propafenone) or certain class III antiarrhythmic agents (dofetilide, ibutilide; these have better efficacy than in atrial fibrillation but are not available in many countries) Recurrent paroxysms may be prevented by class III antiarrhythmic agents (sotalol, amiodarone). AV nodal blocking agents may be used to control the ventricular rate if the arrhythmia persists. However, the treatment of choice for patients with recurrent atrial flutter is catheter ablation (see p. 1059), which permanently interrupts re-entry by creating a line of conduction block within the isthmus between the inferior vena cava and the tricuspid valve ring. This technique offers patients whose only arrhythmia is typical atrial flutter an almost certain chance of a cure, although the later occurrence of atrial fibrillation is not uncommon.

Answer 13

This is an uncommon arrhythmia. Its prevalence is believed to be less than 1% in patients with arrhythmias. It is usually associated with structural heart disease but in many cases it is referred to as idiopathic. Macro re-entrant tachycardia often occurs after surgery for congenital heart disease. Atrial tachycardia with block is often a result of digitalis poisoning. The mechanisms of atrial tachycardia are attributed to enhanced automaticity, triggered activity or intra-atrial re-entry. Atrial re-entrant tachycardia is usually relatively slow (125–150 b.p.m.) and can be initiated and terminated by atrial premature beats. The P′P′ intervals are regular. The PR interval depends on the rate of tachycardia and is longer than in sinus rhythm at the same rate. Atrial tachycardia is typically caused by a focus that is frequently located along the crista terminalis in the right atrium, adjacent to a pulmonary vein in the left atrium, or around one of the atrial appendages. Short runs of atrial tachycardia may provoke more sustained episodes of atrial fibrillation.

Answer 14

Carotid sinus massage may increase AV block during tachycardia, thereby facilitating the diagnosis, but does not usually terminate the arrhythmia.

Answer 15

Management options include cardioversion, antiarrhythmic drug therapy to maintain sinus rhythm, AV nodal slowing agents to control rate and, in selected cases, radiofrequency catheter ablation.

Answer 16

Sustained ventricular tachycardia (\>30 sec) often results in pre-syncope (dizziness), syncope, hypotension and cardiac arrest, although it may be remarkably well tolerated in some patients. Examination reveals a pulse rate typically between 120 and 220 b.p.m. Usually, there are clinical signs of atrioventricular dissociation (i.e. intermittent cannon ‘a’ waves in the neck and variable intensity of the first heart sound).

Answer 17

The ECG shows a rapid ventricular rhythm with broad (often ≥0.14 sec), abnormal QRS complexes. AV dissociation may result in visible P waves, which appear to march through the tachycardia, capture beats (an intermittent narrow QRS complex owing to normal ventricular activation via the AV node and conducting system) and fusion beats (intermediate between ventricular tachycardia beat and capture beat).

Answer 18

Treatment may be urgent, depending on the haemodynamic situation. If the patient is haemodynamically compromised (e.g. hypotensive or pulmonary oedema), emergency DC cardioversion may be required. On the other hand, if the blood pressure and cardiac output are well maintained, intravenous therapy with beta-blockers (esmolol), class I drugs or amiodarone is usually used. DC cardioversion is necessary if medical therapy is unsuccessful.

Answer 19

This involves very rapid and irregular ventricular activation with no mechanical effect. The patient is pulseless and becomes rapidly unconscious; respiration ceases (cardiac arrest).

Answer 20

The ECG shows shapeless, rapid oscillations and there is no hint of organized complexes.

Answer 21

The only effective treatment is electrical defibrillation. Basic and advanced cardiac life support is needed.

Answer 22

This inheritable condition accounts for part of a group of patients with idiopathic ventricular fibrillation who have no evidence of causative structural cardiac disease. It is more common in young male adults and in South-east Asia. The diagnosis is made by identifying the classic ECG changes that may be present spontaneously or may be provoked by the administration of a class I antiarrhythmic (flecainide or ajmaline – principally used as a diagnostic agent in suspected Brugada patients): right bundle branch block with coved ST elevation in leads V1–V3 (Fig. 30.49). Atrial fibrillation may occur. It can present with sudden death during sleep, resuscitated cardiac arrest and syncope, or the patient may be asymptomatic and diagnosed incidentally or during familial assessment. The only successful treatment is an ICD. Beta-blockade is not helpful and may be harmful.

Answer 23

Two major syndromes have been described, one that is (Jervell– Lange-Nielsen syndrome) and one that is not (Romano–Ward syndrome) associated with congenital deafness. • Jervell–Lange-Nielsen syndrome (autosomal recessive) • Romano–Ward syndrome (autosomal dominant)

Answer 24

• LQT1 (KCNQ1 gene mutation affecting the Iksα subunit), in which the arrhythmia is usually provoked by exercise, particularly swimming • LQT2 (KCNH2 gene mutation affecting the Ikrα subunit), in which arrhythmia provocation is associated with emotion and acoustic stimuli • LQT3 (SCN5A gene mutation affecting the INaα subunit), in which the arrhythmias occur during rest or when asleep.

Answer 25

QT prolongation and torsades de pointes are usually provoked by bradycardia.

Answer 26

Patients with a long QT develop syncope and palpitations as a result of polymorphic ventricular tachycardia (torsades de pointes). They usually terminate spontaneously but may degenerate to ventricular fibrillation, resulting in sudden death.

Answer 27

Torsades de pointes is characterized on the ECG by rapid, irregular, sharp complexes that continuously change from an upright to an inverted position (Fig. 30.50B). Between spells of tachycardia, or immediately preceding the onset of tachycardia, the ECG shows a prolonged QT interval; the corrected QT (see Box 30.9) is usually over 0.50 sec.

Answer 28

Acute (acquired) long QT syndrome is treated as follows: • Any electrolyte disturbance is corrected. • Causative drugs are stopped. • The heart rate is maintained with atrial or ventricular pacing. • Magnesium sulphate 8 mmol (Mg2+) is given over 10–15 min for acquired long QT. • Intravenous isoprenaline may be effective when QT prolongation is acquired (isoprenaline is contraindicated for congenital long QT syndrome). Long-term, congenital long QT syndrome is generally treated by beta-blockade, pacemaker therapy and, occasionally, left cardiac sympathetic denervation. LQT1 patients seem to respond well to beta-blockade while LQT3 patients are better treated with sodium-channel blockers. All long QT patients should avoid drugs known to prolong the QT interval. Patients who remain symptomatic despite conventional therapy, and those with marked QT prolongation or a strong family history of sudden death, usually need ICD therapy.

Answer 29

Five types have been described; they are caused by genetic abnormalities that lead to faster repolarization. Ventricular arrhythmias and sudden death may occur and an ICD is the best treatment.

Answer 30

``` Monomorphic ventricular tachycardia in patients with structurally normal hearts (idiopathic ventricular tachycardia) is usually a benign condition with an excellent long-term prognosis. ``` Occasionally, it is incessant (so called Gallavardin’s tachycardia) and, if untreated, may lead to cardiomyopathy. Normal heart ventricular tachycardia arises from a focus in either the right ventricular outflow tract or the left ventricular septum. Treatment of symptoms is usually with beta-blockers. There is a special form of verapamil-sensitive tachycardia that responds well to non-dihydropyridine calcium antagonists. In symptomatic patients, radiofrequency catheter ablation is highly effective, resulting in a cure in over 90% of cases. It is sometimes difficult to distinguish arrhythmogenic right ventricular hypertrophy (see p. 1121) from this seemingly benign disorder.

Answer 31

Non-sustained ventricular tachycardia (NSVT) is defined as ventricular tachycardia that is 5 consecutive beats or more but lasts for less than 30 seconds (Fig. 30.51A). NSVT can be found in 6% of patients with normal hearts and usually does not require treatment. It is documented in up to 60–80% of patients with heart disease. There is insufficient evidence on prognosis but an ICD has been shown to improve survival of patients with particularly poor left ventricular function (ejection fraction ≤30%) by preventing arrhythmic death. Antiarrhythmic suppression of NSVT is not usually advocated but beta-blockers may improve quality of life in symptomatic individuals.

Answer 32

These may be uncomfortable, especially when frequent. The patient complains of extra beats, missed beats or heavy beats because it may be the premature beat, the post-ectopic pause or the next sinus beat that is noticed. The pulse is irregular owing to the premature beats. Some early beats may not be felt at the wrist. When a premature beat occurs regularly after every normal beat, ‘pulsus bigeminus’ may occur. If premature ventricular beats are highly symptomatic, treatment with beta-blockade may be helpful. If the ectopics are very frequent, left ventricular dysfunction may develop; if the ectopics stem from a single focus, especially when in the right ventricle, catheter ablation can be very effective. These premature beats (Fig. 30.51B–D) have a broad (\>0.12 sec) and bizarre QRS complex because they arise from an abnormal (ectopic) site in the ventricular myocardium. Following a premature beat, there is usually a complete compensatory pause because the AV node or ventricle is refractory to the next sinus impulse. Early ‘R-on- T’ ventricular premature beats (occurring simultaneously with the upstroke or peak of the T wave of the previous beat) may induce ventricular fibrillation in patients with heart disease, particularly following myocardial infarction. Ventricular premature beats are usually treated only if symptomatic. Simple measures, such as reassurance and beta-blocker therapy, are normally all that is required.

Answer 33

These are membrane-depressant drugs that reduce the rate of entry of sodium into the cell (sodium-channel blockers). They may slow conduction, delay recovery or reduce the spontaneous discharge rate of myocardial cells. Class I agents have been found to increase mortality compared to placebo in post-myocardial infarction patients with ventricular ectopy (Cardiac Arrhythmia Suppression Trial (CAST) trials – class Ic agents) and in patients treated for atrial fibrillation (class Ia agent, quinidine). In view of this, class Ic agents, such as flecainide, and all other class I drugs should be reserved for patients who do not have significant coronary artery disease, left ventricular dysfunction or other forms of significant structural heart disease.

Answer 34

These antisympathetic drugs prevent the effects of catecholamines on the action potential. Most are β-adrenoceptor antagonists. Cardioselective beta-blockers (β1) include metoprolol, bisoprolol, atenolol and acebutolol. Beta-blockers suppress AV node conduction, which may be effective in preventing attacks of junctional tachycardia, and may help to control the ventricular rate during paroxysms of other forms of SVT (e.g. atrial fibrillation). In general, beta-blockers are anti-ischaemic and anti-adrenergic, and have proven beneficial effects in patients post myocardial infarction (by preventing ventricular fibrillation) and in those with congestive heart failure. It is therefore advisable to use beta-blocker therapy either alone or in combination with other antiarrhythmic drugs in patients with symptomatic tachyarrhythmias, particularly those with coronary artery disease.

Answer 35

These prolong the action potential, usually by blocking the rapid component of the delayed rectifier potassium current (IKr), and do not affect sodium transport through the membrane. The drugs in this class are amiodarone and sotalol. Sotalol is also a beta-blocker. Sotalol may result in acquired long QT syndrome and torsades de pointes. The risk of torsades is increased in the setting of hypokalaemia, and particular care should be taken in patients taking diuretic therapy. Amiodarone therapy, in contrast to most other antiarrhythmic drugs, carries a low risk of proarrhythmia in patients with significant structural heart disease, but its use may be limited due to toxic and potentially serious side-effects. Dronedarone is a multichannel-blocking drug that suppresses the recurrence of atrial fibrillation and reduces hospital admissions in patients with cardiovascular risk. However, it has proven harmful in patients with left ventricular dysfunction and is contraindicated in heart failure. Vernakalant is a multichannel blocker that is approved for the rapid intravenous medical cardioversion of new-onset atrial fibrillation.

Answer 36

The non-dihydropyridine calcium-channel blockers are particularly effective at slowing conduction in nodal tissue. These drugs can prevent attacks of junctional tachycardia (AVNRT and AVRT) and may help to control ventricular rates during paroxysms of other forms of SVT (e.g. atrial fibrillation).