Symptomatic bradycardias unresponsive to atropine are treated with a cardiac pacemaker. A temporary pacemaker (external unit) may be connected to the myocardium by a thin (French gauge 5 or 6), bipolar pacing electrode wire inserted via a subclavian or internal jugular vein and manipulated into the right ventricular apex using cardiac fluoroscopy. The energy needed for successful pacing (the pacing threshold) is assessed by reducing the energy until the pacemaker fails to stimulate the tissue (loss of capture). The output energy is then set at three times the threshold value to prevent inadvertent loss of capture. If the threshold increases above 5 V, the pacemaker wire should be re-sited. A temporary pacemaker unit is almost always set to work ‘on demand’, i.e. to fire only when a spontaneous beat has not occurred. The rate of temporary pacing is usually 60-80 b.p.m. Permanent pacing Permanent pacemakers are fully implanted in the body and connected to the heart by one or two electrode leads. The pacemaker is powered by solid-state lithium batteries, which usually last from 5 to 10 years. Modern pacemakers are often ‘programmable’. This means that their operating characteristics (e.g. the pacing rate) can be changed by a programmer that transmits specific electromagnetic signals through the skin. The pacemaker leads are passed transvenously to the right heart chambers. Most pacemakers are designed to pace and sense the ventricles. Such pacemakers are described as ‘vvr’ units because they pace the ventricle (V), sense the ventricle (V) and are inhibited (I) by the ventricular signal. Occasionally, e.g. in symptomatic sinus bradycardia, an atrial pacemaker (AAI) may be implanted. Pacemakers that are connected to both the right atrium and ventricle (‘dual chamber’ pacemaker) are increasingly being used in order to simulate the natural pacemaker and activation sequence of the heart. This form of pacemaker is called DD because it paces the two (Dual) chambers, senses both (D) and reacts in two (D) ways-pacing in the same chamber is inhibited by spontaneous atrial and ventricular signals, and ventricular pacing is triggered by spontaneous atrial events. Another form of ‘physiological’ pacemaker is the ‘rate-responsive’ system, which, by measuring activity, respiration, biochemical or electrical indicators, changes its rate of pacing so that it is appropriate to the level of exertion. The choice of pacemaker mostly depends on the underlying condition (e.g. sick sinus syndrome must be treated with a dual chamber device) and the general condition of the patient (old and infirm patients do not usually benefit from the most sophisticated units).
Permanent pacemakers are inserted under local anaesthetic using fluoroscopy to guide the insertion of the electrode leads. The pacemaker is usually positioned subcutaneously in front of the pectoral muscle. Following surgery, which usually takes 30 min to 1 hour, the patient rests in bed for 6–24 hours before being discharged. Patients may not drive until the pacemaker has been shown to be working correctly at least 1 month after implantation, and must inform the licensing authorities and their motor insurers. Antibiotics may be prescribed prophylactically.
Complications are few but include:
INFECTION. When a pacemaker system is infected, antibiotic treatment is not sufficient and the pacemaker must usually be removed before antibiotics will subdue the infection. Another pacemaker is fitted later. EROSION. The pacemaker may erode through the skin. This is usually due to a low-grade infection. Mechanical factors may also be responsible.
LEAD DISPLACEMENT. In most cases the pacing lead is securely wedged into the trabeculae of the right ventricle. It rarely displaces but when it does it may lead to sudden loss of pacing and a recurrence of prepacing symptoms.
PACEMAKER MALFUNCTION. This is now a very uncommon complication but requires the replacement of the pacemaker. Electromagnetic interference of the function of a modern pacemaker is not common, except in the hospital or industrial environment. High tension cables, high energy radars and some medical equipment, such as MRI machines and lithotripters, may transiently inhibit the output of a pacemaker or convert it to interference mode (continuous pacing despite an adequate underlying rhythm).
A pericardial effusion is an accumulation of fluid between the parietal and visceral layers of pericardium. Fluid is removed to relieve symptoms due to haemodynamic embarrassment or for diagnostic purposes. Pericardial aspiration or pericardiocentesis is performed by inserting a needle into the pericardial space, usually via a subxiphisternal route. If a large volume of fluid is to be removed, a wide-bore needle and cannula are inserted. The needle may be removed and the cannula left in situ to drain the fluid. Fluid that is removed is sent for chemical analysis, microscopy, including cytology, and culture. If a reaccumulation of pericardial fluid is anticipated, the cannula may be left in place for several days or an operation can be performed to cut a window in the parietal pericardium (fenestration) or to remove a large section of the pericardium.
Right heart bedside catheterization
Bedside catheterization of the pulmonary artery with a Swan-Ganz catheter may be performed in patients with:
• Cardiac failure
• Cardiogenic shock
• Doubtful fluid status
The catheter is used to measure cardiac output, pulmonary artery pressure, right atrial pressure and the pulmonary artery wedge pressure (an indirect measurement of left atrial pressure). The measurement of these pressures and the cardiac output allows appropriate therapy to be prescribed and the effects of that therapy to be monitored. The catheter also provides a route for the delivery of drugs to the central circulation.
Intra-aortic balloon pumping
This is a technique used to assist temporarily the failing left ventricle. A catheter with a long sausage-shaped balloon at its tip is introduced percutaneously into the femoral artery and manipulated under X-ray control so that the balloon lies in the descending aorta just below the aortic arch. The balloon is rhythmically deflated and inflated with carbon dioxide gas. Using the ECG or intraaortic pressure changes, the inflation is timed to occur during ventricular diastole to increase diastolic aortic pressure and consequently to improve coronary and cerebral blood flow. During systole the balloon is deflated, resulting in a reduction in the resistance to left ventricular emptying.
Balloon pumping is used:
To IMPROVE CARDIAC OUTPUT when there is a transient or reversible depression of left ventricular function, e.g. in a patient with severe mitral valve regurgitation who is awaiting surgical replacement of the mitral valve or in a patient with a ventricular septal defect due to septal infarction.
To TREAT UNSTABLE ANGINA PECTORIS by improving coronary flow and decreasing myocardial oxygen consumption by reducing the ‘after-load’. This technique may be successful, even when medical therapy has failed. It is followed by early arteriography and appropriate definitive therapy such as surgery or coronary angioplasty.
Balloon pumping should not be used when there is no remediable cause of cardiac dysfunction. It is also unsuit able in patients with aortic valve regurgitation or dissection of the aorta.
Complications of balloon pumping occur in about 20% of patients and include aortic dissection, leg ischaemia, emboli from the balloon, and balloon rupture. Embolic complications are reduced by anticoagulation with heparin.