In many patients cardiovascular function may be impaired, even with maximal medical therapy, to the point that they are not able to maintain adequate organ perfusion. These patients may require mechanical support to survive. Cardiovascular support can be as simple as a pacemaker to overcome a myocardial conduction problem or as invasive as artificial circulatory support in a patient awaiting cardiac transplantation. This chapter reviews the basic physiology of these support devices.

Pacemakers are implanted in patients who have symptomatic bradycardia due to a disturbance in normal cardiac conduction or rhythm. Indications include symptomatic bradycardia of any origin including failure of impulse generation or conduction. In some patients, the sinoatrial (SA) node no longer functions properly and does not initiate enough signals to produce an adequate heart rate. The heart has an emergency backup system that kicks in when signals from the SA node are too slow or fail to appear at all. All myocardial cells have the intrinsic ability to automatically depolarize and thus are capable of initiating a wave of depolarization that will result in a heartbeat. Backup heartbeats initiated by myocardial cells other than the SA node are referred to as “escape beats.” Unfortunately, there are two problems with the backup system: (1) the automatic depolarization rate for most myocardial cells is between 30 and 40 per minute, and this may be insufficient to produce an adequate cardiac output, and (2) as discussed in Chapter 7, if depolarization does not begin in the SA node or utilize the myocardial conduction system, the contraction of the heart may not be efficient and results in a smaller stroke volume and lower cardiac output. For example, an escape beat originating in the His-Purkinje system will trigger the ventricles to contract, but not the atria. The loss of atrial contraction and its effect on ventricular filling can severely reduce the cardiac output in some patients. Other escape beats can originate directly from ventricular cells. In this case, not only is atrial contraction lost, but the ventricles themselves may not contract in synchrony or efficiently. In other patients, the SA node may be firing but the signal is blocked in the myocardial conduction system and does not reach the ventricles. These patients may produce ventricular contractions with ventricular escape beats; however, they may not produce an adequate cardiac output.

Both of the cases described above will require mechanical support from an external (temporary) or implanted (permanent) pacemaker to generate electrical currents to stimulate the cardiac chambers to contract. Pacemakers are complex devices, and only a very general description of some of their capabilities is provided here. Pacemakers have two basic functions—sensing and pacing. Pacemaker leads can be placed in the atrium, the ventricle, or both to perform these functions.

Pacemaker leads can be placed to sense and pace from the atrium, the ventricle, or both, depending upon the condition of the patient’s myocardial conduction system. In some patients, the SA node may produce an adequate rate some of the time and at other times be too slow. In these cases, the pacemaker “senses” or is on the lookout for native electrical activity from the SA node. When native electrical activity from the SA node is detected within an appropriate
time interval, the pacemaker will be “inhibited” and will not produce its own electrical signal to pace the heart. In this circumstance, the SA node was able to fire at a sufficient rate and the pacemaker does not need to take over. The pacemaker can be programmed for how slow it allows the native heart rate to drop before taking over. In other cases, there may be a problem in the atrioventricular (AV) node or other portions of the myocardial conduction system. In this case, the pacemaker may sense the SA node signal and then deliver a signal generated from the pacemaker directly to the ventricle bypassing the myocardial conduction system because the native signal could not pass through the diseased conduction system to reach the ventricle.

In 1974, the Intersociety Commission for Heart Disease Resources (ICHD) established a classification code that provided a concise method of communicating pacemaker fundamentals. It initially established a three-letter code that later expanded to a five-letter code in 1981, which is still in use today. Position I reflects the chamber(s) paced (“A” indicates atrium, “V” indicates ventricle, and “D” indicates dual). Position II reflects the chamber(s) sensed (A, V, or “O” indicates absence of sensing). Position III refers to pacemaker response to sensed activity (“I” indicates inhibition of pacer output, “T” indicates trigger in response to sensed activity, “D” indicates dual modes, and “O” indicates no response). Position IV refers to rate modulation of the pacer in response to physiologic activity by the patient (i.e., increase in heart rate in response to exercise). Position V reflects any antitachycardia features that the device offers.

Pacemakers can be set to act asynchronously (no sensing). For example, an AOO pacer is asynchronous (the A in the first position indicates that the atrium is the paced chamber, the O in the second position indicates that sensing is off, and the O in the third position indicates that a response to sensing is turned off). Asynchronous pacing is typically done in emergency situations and can lead to competition with native electrical activity. Pacing spikes can be delivered during ventricular repolarization resulting in ventricular fibrillation. Many patients will have synchronous pacing (e.g., VVI—ventricular sensed, ventricular paced, response to pacing is inhibition) so that the pacer will be inhibited by native conduction; however, if the heart rate falls below a threshold or the patient has complete heart block, the pacer will fire at the preset heart rate on the artificial pacemaker.

A single-chamber mode paces either the ventricle or the atrium. In most dual-chamber pacemakers, there are two leads (one in the right atrium [RA] and one in the right ventricle [RV]) that sense and pace either chamber. AV sequential pacing is more physiologic; however, the RV will pace before the left, which leads to ventricular dyssynchrony and reduced cardiac output. This occurs in all modes in which a single ventricle is paced. Newer pacemakers can have leads in both ventricles (biventricular pacing) to synchronize the contraction of the two ventricles.

Implantable cardioverter-defibrillator (ICD) therapy is used in patients with a history of malignant tachycardia (ventricular tachycardia) or ventricular fibrillation or in patients at increased risk of developing a malignant arrhythmia (congestive heart failure). All ICDs currently implanted also have the capability to pace if bradycardia is present. The internal computer will decide between shocking or pacing the arrhythmia. If pacing does not work for a tachyarrhythmia, the device will switch to delivering a shock. If a shock is chosen (in cases of ventricular tachycardia or ventricular fibrillation), it takes 5-10 seconds to charge the device and deliver the shock.