Implantable Cardiac Pulse Generators: Pacemakers and Cardioverter-Defibrillators

Pacemakers

Pacemakers are devices placed for bradyarrhythmias, and they remain the only effective treatment for ameliorating symptomatic bradycardia due to sinus node dysfunction (e.g., sick sinus syndrome) or a failure of impulse propagation (e.g., complete heart block). Advances in technology and understanding of cardiac conduction physiology have led to the development of more physiologic pacing. Pacemakers have become sophisticated at maintaining the normal atrial-ventricular activation over various heart rate ranges, varying the heart rate in response to metabolic demands, and preserving natural ventricular activation. Pacemakers have many additional features that correspond to the changing needs of patients throughout the day, including rate responsiveness to increase pacing during times of increased physical exertion and sleep functions to decrease pacing rate during times of rest. Standard pacemakers have either one or two (atrial and ventricular) leads. A patient is considered to be pacemaker dependent if they suffer significant symptoms or even cardiac arrest upon the cessation of pacing.

The dual chamber pacemakers are capable of pacing and sensing in both the ventricle and the atrium. Such capability permits the pacemaker to ensure not only an adequate ventricular rate, but to preserve the atrial contraction before each ventricular contraction. These pacemakers guarantee a minimum atrial rate and also ensure that a ventricular contraction occurs within a specified amount of time after each atrial contraction. Limitations on ventricular rate are usually built in the circuitry and are programmable. Most pacemakers have the capability of varying the pacing rate. In the rate adaptive mode, the pacemakers sense the patient’s level of activity and accordingly adjust the pacing rate using sensors that are typically piezoelectric and detect body motion transmitted from underlying muscles. Another method of determining the presence of physical activity utilizes detection of the respiratory rate and/or volume using bioimpedance sensors.

All pacemakers generate a pulse of current to depolarize a small region of the myocardium; the wave then spontaneously spreads to the rest of the myocardium. The pacing capture threshold is the minimum electrical energy needed to consistently capture the heart outside of the refractory period and is determined by (1) the intrinsic excitability of the myocardium, (2) the current density at the electrode-tissue interface, and (3) the duration of the electric pulse.

The North American Society of Pacing and Electrophysiology (NASPE) and the British Pacing and Electrophysiology Group (BPEG) initially published a generic pacemaker code (NBG code) in 1987. In 2002 the NBG code was subsequently revised ( Table 38.1 ). Common perioperative pacing modes include dual chamber, adaptive-rate pacing (DDDR), dual chamber pacing without atrium synchronous ventricular pacing (DDIR), and dual chamber asynchronous pacing with no rate modulation or multisite pacing (DOO).

• 1.

  DDDR pacing defines a pacemaker programmed to pace the atrium and/or ventricle, sense the atrium and/or ventricle, inhibit or trigger pacing output in response to a sensed event, and have a rate responsive sensor that is able to alter paced rates due to changes in perceived metabolic demand. DDDR is a very common program configuration for patients with sick sinus syndrome and/or heart block.

• 2.

  DDIR is a common pacing mode for patients with supraventricular tachyarrhythmias (SVTs). If a patient is set to DDD, the ventricle response depends on the atrial rate. During SVT in DDD mode, rapid ventricular pacing may occur. In DDI, the pacemaker paces and senses both the atrium and ventricle; however, the device will not pace the ventricle at an identical rate if the patient has SVT. The response to a fast rate in the atrium will lead to inhibition of pacing in the ventricle—hence the I in the third designation. Most modern pacemakers have built-in automatic mode switching during episodes of SVT. They will switch from DDD to DDI to avoid SVT with a rapid ventricular response.

• 3.

  For some perioperative care, devices will be placed in an asynchronous mode like DOO. An asynchronous mode or nontracking mode will pace the atrium and ventricle at a set rate, regardless of the underlying rate and rhythm. This is advantageous in the perioperative environment in order to avoid the pacemaker from oversensing the monopolar electrocautery as intrinsic cardiac conduction. Asynchronous modes avoid oversensing (and under pacing) hearts that are pacemaker dependent and inhibited from pacing due to monopolar electrocautery ( Table 38.2 ).

  Table 38.2

  Common Pacemaker Settings

  Examples	Chamber Paced	Chamber Sensed	Response to Sensing	Rate Modulation	Multisite Pacing	Common Clinical Utilization
  AAI	Atrium	Atrium	Intrinsic atrial beat inhibits atrial pacing	None	None	Sick sinus syndrome with intact atrioventricular conduction
  DDDR	Both	Both	Intrinsic beat will inhibit output; atrial beat will trigger ventricular pacing if lack of intrinsic ventricular beat	Present	None	Atrioventricular block
  VVIRV	Ventricle	Ventricle	Intrinsic ventricular beat will inhibit ventricular pacing	Present	Multisite ventricular pacing	Heart failure with prolonged QRS
  DOO	Both	None	None	None	None	Perioperative asynchronous setting to avoid electromagnetic interference

Implantable Cardioverter-Defibrillators

ICDs are implanted in patients for primary or secondary prevention of cardiac arrest. Primary prevention refers to ICD placement for patients who have not had any episodes of ventricular arrhythmias but who are at risk for future events. Secondary prevention refers to ICD placement for patients who have had prior ventricular arrhythmias. There is strong evidence that ICDs implanted for primary prevention improve mortality in high-risk patients, including patients with a left ventricular ejection fraction less than 40% who are on optimal medical therapy. For patients with ischemic and nonischemic cardiomyopathy, ICDs reduce mortality approximately 23% to 55%. Certain groups of patients do not benefit from ICD implantation, including patients with recent myocardial infarction and patients who have received coronary artery bypass grafting. In addition, many of the patients in the decisive trials for ICD placement were younger (mean or median age between 58 and 67 years for the MADIT-II, CABG-PATCH, DINAMIT), whereas many patients currently receiving ICDs are over the age of 70.

ICDs have four main functions. They sense atrial or ventricular electrical activity, classify these signals to various programmed “heart rate zones,” deliver tiered therapies to terminate ventricular tachycardia (VT) or fibrillation, and pace for bradycardia. All modern ICDs are pacemakers, and this has important perioperative applications. Although ICDs improve survival in many patients, unnecessary shocks are very detrimental. They are proarrhythmic, can lead to anxiety and depression, and decrease patient quality of life. Inappropriate shocks are common (30% to 50% of all shocks) as a result of inappropriate treatment of SVT, oversensing physiologic T waves, or lead fracture. The discrimination between VT and SVT is critical for ICDs to avoid inappropriate therapy. There are several methods by which ICDs discriminate between SVT and VT. Single chamber ventricular ICDs utilize ventricular–ventricular timing intervals and QRS morphology. Dual chamber ICDs use atrial–atrial timing intervals and the chamber of onset. Subcutaneous ICDs assess surface electrocardiogram (ECG). The sensitivity and specificity for VT detection by QRS morphology is more than 90%.

ICDs terminate ventricular arrhythmias by either antitachycardiac pacing (ATP) or defibrillation. ATP terminates reentrant VT by blocking reentry and it terminates slow VT (<188 to 200) approximately 90% of the time. ATP is desirable because it reduces inappropriate shocks and prolongs battery life. For VT that is not terminated by ATP or for ventricular fibrillation (VF), defibrillation is the treatment of choice. The energy for defibrillation may be incrementally increased or set to maximum energy for each shock.

Cardiac Resynchronization Therapy Devices

CRT plays an important role in the management of heart failure and is becoming a device commonly encountered by anesthesiologists because of the large prevalence of heart failure in this country. These devices are indicated in select patients with heart failure, systolic dysfunction, and a prolonged QRS. Conduction abnormalities are frequently seen in systolic heart failure, with approximately 25% to 40% of these patients having a prolonged QRS complex (>120 ms). In these patients, cardiac depolarization spreads slowly through the myocardium without a healthy Purkinje conduction system, leading to intraventricular dyssynchrony. During intraventricular dyssynchrony, the left ventricular (LV) septal wall contracts earlier than the lateral wall, which leads to less efficient ejection from the left ventricle in addition to decreased diastolic filling. The goal of CRT is to restore synchronous contraction of the left ventricle and to optimize timing of LV and right ventricular (RV) ejection. This is accomplished through biventricular pacing using a standard RV lead and an LV lead placed adjacent to the lateral wall via the coronary sinus. Biventricular pacing in the right ventricle and the left ventricle leads to improved hemodynamic variables, including systolic blood pressure, stroke volume, cardiac output, and rate of rise of LV pressure (d P /d t ). In contrast to pharmacologic means of improving systolic function, CRT improves cardiac performance with reductions rather than with increases in myocardial metabolic demand. In addition, CRT has been shown to improve mitral regurgitation (MR) and New York Heart Association (NYHA) function class because of reverse ventricular remodeling over time. Standard indications for CRT are LV ejection fraction (LVEF) less than 35% with QRS greater than 120 ms, sinus rhythm, and NYHA class III or IV after optimal medical therapy. Left bundle branch block is the most common conduction abnormality in patients undergoing CRT. Approximately 30% of patients meeting selection criteria for CRT do not respond to biventricular pacing. Risk factors for failure to respond to CRT include ischemic cardiomyopathy, sustained VT, severe MR, and dilated LV cavity. CRT has been shown to reduce mortality, heart failure symptoms, and also heart failure hospitalizations. Patients with CRT should be considered pacemaker-dependent because of the constant pacing they undergo to synchronize the ventricle.