Examine this patient's cardiovascular system.

This patient has a permanent pacemaker (lesion) for previous heart block (aetiology) which is functioning

adequately (functional status).

· Symptomatic bradyarrhythmias (heart rate <40 beats/min or documented periods of asystole >30

seconds when awake). Symptoms include syncope, pre-syncope, confusion, seizures, or congestive

heart failure and they must be clearly related to the bradycardia.

· Asymptomatic Mobitz type I1 atrioventricular block (N Engl d Med 1998; 338: 1147-8).

· Complete heart block.

* They are connected to the heart by one or two electrodes and are powered by long-lasting (5-10

years) solid-state lithium batteries. Most pacemakers are designed to pace and sense the ventricles -

called the VVI pacemakers because they pace the ventricle (V), sense the ventricle (V) and are

inhibited (I) by the ventricular signal. They are inserted under local anaesthesia and fluoroscopic

guidance, subcutaneously under the pectoral muscles.

· In symptomatic sinus tachycardia, an atrial pacemaker may sometimes be implanted (AAI).

· In sick sinus syndrome, a dual-chamber pacemaker DDD (because it paces two or dual chambers, senses both (D) and reacts in two (D) ways, i.e. pacing in the same chamber is inhibited by

spontaneous atrial and ventricular signals, and ventricular pacing is triggered by spontaneous atrial events) is implanted.

· Rate-responsive pacemakers measure activity, respiration, biochemical and electrical indicators, and change their pacing rate so that it is suitable for that level of exertion.

The patient may not drive until the pacemaker has been shown to be functioning correctly for at least I month after implantation. Patients must inform driving licensing authorities and the motor insurers.

· Dual chamber pacing has been used to optimize cardiac output and minimize the outflow tract

gradient in patients with hypertrophic obstructive cardiomyopathy.

· Dual chamber pacing is currently being investigated in dilated cardiomyopathy with heart failure and intraventricular conduction delay to optimize AV delay and improve cardiac output.

· Erosion through the skin due to mechanical factors.

· Infection.

· Lead displacement or lead fracture (the most common site of pacing lead fracture is between the

first rib and the clavicle).

· Pacemaker malfunction.

· Electromagnetic interference.

· Pain/ecchymoses at the site of insertion.

· Pneumothorax.

The,~e inclucle he:wy electric rnotor~ nn¢t nrc welding Device~ ~;nch a~ airport security devices and ham radios cause single-beat inhibition but they should not cause significant clinical interference.

Microwave ovens do not interfere with pacemakers. Cellular phones and anti-theft devices or electronic article surveillance equipment can potentially interlere with pacemakers (N Engl J Meal 1997; 336: 1518-19; N Engl J Med 1997; 336: 1473-9). Analogue phones are less likely to cause interference than phones based on digital technology. Patients should avoid carrying a cellular phone in a pocket directly over the pacemaker.

It is seen in individuals with a single-chamber pacemaker who experience symptoms of low cardia output (dizziness, etc.) when erect; it is attributed to the lack of atrial kick. Pacemaker syndrome is caused by haemodynamic changes as a consequence of inappropriate use of ventricular pacing: it occurs when ventricular pacing is uncoupled from atrial contraction. It is most common when the VVI mode is used in patients with sinus rhythm but can occur in any pacing mode when atrioventricular

synchrony is lost. Levels of atrial natriuretic factor are high in pacemaker syndrome.

If pacemaker syndrome occurs in a patient with a VV1 pacemaker the only definitive treatment is to convert to a dual-chamber pacemaker. If the patient has occasional bradycardia then often symptoms may be ameliorated by programming the pacemaker to a lower limit and programming with hysteresis 'on'. This allows the patient to stay in normal sinus rhythm for longer periods by minimizing the pacing.

Placement of a separate pacemaker into a patient who has a defibrillator has the potential to cause serious pacemaker-defibrillator interactions. The most commonly implanted defibrillators have the

additional ability to attempt termination of ven-tricular tachycardia with antitachycardia pacing. The obvious advantage of this feature is that an arrhythmia can be terminated painlessly without delivery of a shock. If antitachycardia pacing is unsuccessful then the device will administer a shock.

· Cardiac arrest resulting from ventricular tachyarrhythmia not due to a reversible or transient cause

(remember: patients who have cardiac arrest unrelated to acute myocardial infarction have

approximately a 35% chance of recurrent ventricular arrhythmias within the first year).

· Spontaneous sustained ventricular tachycardia.

· Syncope of undetermined origin with inducible sustained ventricular tachycardia on

electrophysiological study and when drug therapy is not effective or tolerated.

· Non-sustained ventricular tachycardia with coronary artery disease and inducible ventricular

tachycardia on electrophysiological study that is not suppressible by a class I antiarrhythmic drug.

· Magnetic resonance imaging.

· Lithotripsy, if the pulse generator is in the field.

INSTRUCTION

Examine this patient's cardiovascular system.

This patient has constrictive pericarditis (lesion) caused by radiation therapy for previous Hodgkin's

disease (aetiology) and is now limited by dyspnoea and marked ascites (functional status).

· Tuberculosis (<15% of patients).

· Connective tissue disorder.

· Neoplastic infiltration.

· Radiation therapy (often years earlier).

· Postpurulent pericariditis.

· Haemopericardium after surgery (rare).

· Chronic renal failure.

It is caused by the abrupt halting of rapid ventricular filling.

· Loud P2 (see p. 103).

· S3 gallop (see p. 39).

· Opening snap (mitral stenosis).

· Pericardial sound.

· Tumour plop (atrial myxoma).

The presence of low arterial blood pressure, high venous pressure and absent apex

in cardiac tamponade is known as Beck's triad.

· Chest radiograph typically shows normal heart size and pericardial calcification (note: the combination

of pulsus paradoxus, pericardial knock and pericardial calcification favours the diagnosis of

constrictive pericarditis).

· ECG shows low voltage complexes, non-specific T wave flattening or atrial fibrillation.

· Echocardiogram shows myocardial thickness is normal and may reveal thickened pericardium;

normal ventricular dimensions with enlarged atria and good systolic and poor diastolic dysfunction.

Doppler shows increased right ventricular systolic and decreased left ventricular systolic velocity with

inspiration, expiratory aug-mentation of hepatic vein diastolic flow reversal.

· CT scan or MRI: shows normal myocardial thickness usually, and pericardial thickening and

calcification.

· Cardiac catheterization typically shows identical left and right ventricular filling pressures and

pulmonary artery systolic pressure usually <45 mmHg, with normal myocardial biopsy.

Haemodynamic tracings show rapid 'y' descent in atrial pressure and early dip in diastolic pressure,

with pressure rise to plateau in mid or late diastole.

· Surgery is the only satisfactory treatment: Complete surgical resection of the pericardium (myocardial

inflammation or fibrosis may delay symptomatic response).

Patients with tuberculous pericarditis should be pre-treated with antituberculosis therapy; if the

diagnosis is confirmed after pericardial resection, full anti-tuberculous therapy should be continued for

6-12 months after resection.

C.S. Beck (1894-1971), surgeon, Peter Bent Brigham Hospital in Boston.

W. Broadbent(1868-1951), English physician who qualified from St Mary's Hospital Medical School,

London. He described the Broadbent sign in constrictive pericarditis, which is an indrawing of the 11th

and 12th left ribs with a narrowing and retraction of the intercostal space posteriorly; this occurs as a

result of pericardial adhesions to the diaphragm.