Examine this patient's pulse.



· Palpitations.

· Pre-syncope, dizziness.

· Fatigue.

· Dyspnoea.

· Asymptomatic and atrial fibrillation is discovered incidentally.

· History of ischaemic heart disease, hypertension, valvular heart disease, rheumatic heart disease,

COPD, congenital heart disease (atrial septal defect, ventricular septal defect), thyrotoxicosis (pp


· History of consumption of caffeine, digitalis, theophylline.


· Irregularly irregular pulse (patients are often digitalized and in slow atrial fibrillation).

· Look for:

- malar flush (mitral stenosis)

- mitral valvotomy scar

- warm hands, goitre, pretibial myxoedema (thyrotoxlcosis).

· Elevated JVP without 'a' waves.

· Varying intensity of first heart sound (the intensity is inversely related to the previous RR cycle

length; a longer cycle length produces a softer SI).

· Pulse deficit, which is the difference between the rate of the apex and the pulse rate (because

varying stroke volumes result from varying periods of diastolic filling, not all ventricular beats produce

a palpable peripheral pulse). The pulse deficit is greater when the ventricular rate is high.

· If you are not sure, tell the examiner that you would like to differentiate from ventricular ectopics by

exercising the patient; after exercise, ventricular ectopics diminish in frequency whereas there is no

change in the rhythm of atrial fibrillation.

· Look for the underlying cause:

-Examine the heart for mitral valvular lesion.

-Check the blood pressure for hypertension.

- Ask the patient for history of ischaemic heart disease.

-Check the patient's thyroid status for thyrotoxicosis.


This patient has fast atrial fibrillation (lesion) which is commonly caused by ischaemic heart disease

(aetiology). The patient is short of breath, indicating that he may be in cardiac failure (functional status).

Read this recent review: N Engl J Med 2001; 344: 1067.


What are the common causes of atrial fibrillation ?

· Mitral valvular disease in the young and middle-aged.

· Ischaemic heart disease or hypertension in the elderly.

· Thyrotoxicosis (atrial fibrillation may be the only clinical feature in the elderly).

· Constrictive pericarditis.

· Chronic pulmonary disease.

Mention common sites of systemic embolization.

Brain, leg, kidney, superior mesenteric artery, coronary artery and spleen.

At the bedside, how would you differentiate atrial fibrillation from multiple ventricular ectopics ?

If the patient is not in heart failure, exercise the patient; after exercise, ventricular ectopics tend to

diminish in frequency whereas there is no change in the rhythm of atrial fibrillation.

How would you investigate this patient?


P waves are absent. Fibrillatory or 'f' waves are present at a rate that may vary between 350 and 600

beats/minute and the 'f' waves vary in shape, amplitude and intervals. The RR interval is irregularly

irregular. Narrow QRS complex with varying RR interval (regular unless there is an underlying ventricular

conduction detect).


Useful to determine left atrial size and left ventricular systolic function, and to exclude underlying valvular

heart disease and intracardiac thromboemboli.

Test of thyroid function

To exclude thyrotoxicosis.

Exercise treadmill

When atrial fibrillation is precipitated by exercise.

Holter monitor

Useful in paroxysmal atrial fibrillation to determine whether it was triggered by another arrhythmia such as

when a premature atrial complex during a rapid paroxysmal atrial tachycardia may cause the immediate

onset of atrial fibrillation.


Mention a few causes of irregularly irregular pulse.

· Atrial fibrillation.

· Multiple ventricular ectopics.

· Atrial tlutter with varying block.

· Complete heart block (there is associated bradycardia).

In which congenital disorders is atrial fibrillation common?

Atrial septal defect, Ebstein's anomaly.

What do you understand by the term 'atrial fibrillation'?

Lone atrial fibrillation occurs itl the absence of cardiopulmonary disease or a history of hypertension and

before the age of 60 years. Such patients have a low risk of stroke (0.5% per year).

How would you treat a patient with atrial fibrillation?

Attempt to restore slow ventricular rate:

· In the hypertensive patient use calcium antagonists (verapamil, diltiazem).

· In thyroid disease use a beta-blocker (e.g. propranolol).

· In ischaemic heart disease use a beta-blocker or diltiazem, verapamil.

· In heart failure use digoxin or verapamil.

· In hypertrophic cardiomyopathy use a beta-blocker or calcium antagonists.

· In those who are intolerant of or do not respond to drugs, radiofrequency catheter ablation of the

atrioventricular node (with a cardiac pacemaker) may provide symptomatic relief; however, it does not

change the risk of systemic emboli or the need for anticoagulation (N Engl J Med 1999; 340: 534).

· More recently, radiofrequency ablation of the pulmonary veins has been shown to be effective in

paroxysmal atrial fibrillation when the ectopic focus is in the pulmonary veins.

Attempt to restore sinus rhythm by cardioversion if the following conditions apply:

· Left atrial size by echocardiogram is less than 4.5 cm (left atrial size >4.5 cm is not associated with

long-term maintenance of sinus rhythm).

· Short duration of the arrhythmia (acute atrial fibrillation is likely to remain in sinus rhythm).

· Drugs used to restore sinus rhythm or prevent recurrence include quinidine, procainamide,

disopyramide, propafenone, sotalol, fiecainide, amiodarone and ibutilide (N Engl J Med 2000;

342:913-20; Circulation 1996; 94:1613).

Anticoagulation with warfarin is advised for certain patients':

· Undergoing cardioversion (electrical or drug).

· With underlying mitral valve disease.

· In left ventricular failure.

· With cardiomyopathy.

· Above the age of 60 years.

Mention a few drugs used to restore sinus rhythm.

Procainamide, disopyramide or quinidine for 2-3 days restores sinus rhythm in up to 30% of patients.

What is the role of oral anticoagulants in chronic atrial fibrillation?

Non-rheumatic atrial fibrillation is an important risk factor for stroke, even though it is recognized that only

80% of strokes in such patients

the heart. All patients with non-rheumatic atrial fibrillation should be anticoagulated with warfarin unless

there are contraindications (Br J Hosp Med 1993: 50: 452-7).

What is the role of surgery in the treatment of atrial fibrillation?

· A novel surgical technique, the Maze procedure, has recently been described in which multiple

incisions are made in the atria to prevent re-entrant loops (Clin Curdiol 1991; 14:827 34). This

procedure is highly effective in preventing atrial fibrillation: only one patient out of 65 suffered a

clinical recurrence of the arrhythmia three or more months after the procedure. Although the

long-term outcome is not known, it remains a promising procedure when atrial fibrillation is not

controlled by medical therapy or in those cases complicated by recurrent thromboembolism.

· The 'corridor' procedure effectively isolates both the left and right atrium, leaving a strip of

myocardium connecting the sinus node to the atrioventricular node. This procedure does not prevent

atrial fibrillation but isolates the fibrillating atria. Although a 70% 'cure' rate is reported, sequential

atrioventricular contraction is not restored (with the consequent haemodynamic effects and the risk of


What do you know about holiday heart syndrome?

It is the occurrence of supraventricnlar arrhythmias, usually atrial fibrillation anti atrial flutter, folk)wing an

acute alcoholic binge in chronic alcoholics. These are usually transient.

It was James Mackenzie, a Scottish general practitioner working in Burnley, England, utilizing an

ink-polygraph to record and label jugular venous pulses, who pioneered the deciphering of normal and

abnormal cardiac rhythms. His key observation that the jugular 'a' wave disappeared in a patient who

went from a normal to an irregular rhythm provided the first insight into the mechanism of atrial fibrillation.

In 1924, Willem Einthoven (1860-1927) of Leyden University, The Netherlands, was awarded the Nobel

Prize for his discovery of the mechanism of electrocardiography (Am J CardJo11994; 7:]: 384-9).

In 1909, Lewis in England and Rothberger and Winterberg in Vienna, taking advantage of Einthoven's

newly developed string galvanometer, were the first to establish electrocardiographically that auricular

fibrillation was the cause of pulsus irregularis perpetuus.

Rodney Falk is Professor of Cardiology at Boston University. He trained in England and his main interests

are amyloidosis and atrial fibrillation.