The output dial regulates the amount of electrical current, measured in milliamperes (mA), that is delivered to the heart to initiate depolarization. The point at which depolarization occurs, called threshold, is indicated by a myocardial response to the pacing stimulus (i.e., capture). Threshold can be determined by gradually decreasing the output setting until 1 : 1 capture is lost. The output setting is then slowly increased until 1 : 1 capture is reestablished; this threshold to pace is less than 1 mA with a properly positioned pacing electrode. The output is set two to three times higher than threshold, because thresholds tend to fluctuate over time. Box 13-1 details the procedure for measuring pacing thresholds. Separate output controls for atrium and ventricle are used with a dual-chamber pulse generator.

The sensitivity control regulates the ability of the pacemaker to detect the heart’s intrinsic electrical activity. Sensitivity is measured in millivolts (mV) and determines the size of the intracardiac signal that the generator will recognize. If the sensitivity is adjusted to its most sensitive setting—a setting of 0.5 to 1.0 mV—the pacemaker can respond even to low-amplitude electrical signals coming from the heart. Turning the sensitivity to its least sensitive setting (i.e., adjusting the dial to a setting of 20 mV or to the area labeled async) results in inability of the pacemaker to sense any intrinsic electrical activity and causes the pacemaker to function at a fixed rate. A sense indicator (often a light) on the pulse generator signals each time intrinsic cardiac electrical activity is sensed. A pulse generator may be designed to sense atrial activity, ventricular activity, or both. Box 13-2 describes the procedure for measuring sensitivity.

The AV interval control (available only on dual-chamber generators) regulates the time interval between the atrial and ventricular pacing stimuli. This interval is analogous to the PR interval that occurs in the intrinsic ECG. Proper adjustment of this interval to between 150 and 250 milliseconds (msec) preserves AV synchrony and permits maximal ventricular stroke volume and enhanced cardiac output.

Temporary DDD pacemakers have several other digital controls that are unique to this type of temporary pulse generator. The lower rate, or base rate, determines the rate at which the generator will pace when intrinsic activity falls below the set rate of the pacemaker. The upper rate determines the fastest ventricular rate the pacemaker will deliver in response to sensed atrial activity. This setting is needed to protect the patient’s heart from being paced in response to rapid atrial dysrhythmias. The pulse width, which can be adjusted from 0.05 to 2 msec, controls the length of time that the pacing stimulus is delivered to the heart. There is also an atrial refractory period, programmable from 150 to 500 msec, which regulates the length of time, after a sensed or paced ventricular event, during which the pacemaker cannot respond to another atrial stimulus. An emergency button is also available on most models to allow for rapid initiation of asynchronous (DOO) pacing during an emergency.

On all temporary pacemakers, an on/off switch is provided with a safety feature that prevents the accidental termination of pacing. Also a “lock” feature is used to prevent unintended changes to the prescribed settings.

All patients with temporary pacemakers require continuous ECG monitoring. The pacing artifact is the spike that is seen on the ECG tracing as the pacing stimulus is delivered to the heart. A P wave is visible after the pacing artifact if the atrium is being paced (Figure 13-2, A). Similarly, a QRS complex follows a ventricular pacing artifact (see Figure 13-2, B). With dual-chamber pacing, a pacing artifact precedes both the P wave and the QRS complex (see Figure 13-2, C).

About one third of patients with severe heart failure have ventricular conduction delays (prolonged QRS duration or bundle branch block). These conduction delays have been shown to create a lack of synchrony between the contractions of the LV and RV. The hemodynamic consequences of this dyssynchrony include impaired ventricular filling with decreased ejection fraction, cardiac output, and mean arterial pressure.9 Cardiac resynchronization therapy (CRT) uses atrial pacing plus stimulation of both the LV and RV (biventricular pacing), in an attempt to optimize atrial and ventricular mechanical activity. The CRT device uses three pacing leads, one each in the right atrium and the RV and a specially designed transvenous lead that is inserted through the coronary sinus to pace the LV.⁹ Because many patients with heart failure are also at risk for sudden cardiac death, biventricular pacing is available on some implantable cardioverter defibrillators (ICDs). A number of clinical trials have shown symptomatic and structural cardiac improvement with this new therapy.¹⁰

There is a growing incidence of atrial fibrillation, and atrial pacing has been proposed as a possible preventative therapy for this dysrhythmia in selected patients. Atrial pacing in patients with bradycardia has been shown to lower the recurrence of atrial fibrillation, especially compared with ventricular pacing.11 Most pacemakers can be programmed to mode switch to a non-P wave tracking mode if rapid atrial rates are sensed.¹ Strategies for patients with paroxysmal atrial fibrillation, which include pacing both atriums (bi-atrial pacing) and transiently pacing the atrium at a rate higher than the patient’s intrinsic sinus rate, require further study.¹²

Nursing management for patients after permanent pacemaker implantation includes monitoring for complications related to insertion and for pacemaker malfunction. Postoperative complications are rare but include cardiac perforation and tamponade, pneumothorax, hematoma, lead displacement, and infection.13,14

Identification of permanent pacemaker malfunction is the same as that described previously for temporary pacemakers. To evaluate pacemaker function, the nurse must know at least the pacemaker’s programmed mode of pacing and the lower rate setting. With permanent pacemakers, settings are adjusted noninvasively through a specialized programmer that uses pulsed magnetic fields or an RF signal. If a pacemaker problem is suspected, ECG strips are obtained, and the physician is notified so that the pacemaker settings can be reprogrammed as needed. If the patient experiences symptoms of decreased cardiac output, he or she may require support with temporary transcutaneous pacing until the problem is corrected.

Critical care nurses also may be involved in monitoring patients with permanent pacemakers after discharge. Some units are equipped with transtelephonic monitoring equipment that allows patients to transmit information over the telephone from a monitoring device in their home. Transmission of the patient’s ECG can provide information to confirm proper pacemaker function (capture and sensing) and to determine battery status (rate). Newer technology that uses an Internet-based remote monitoring system for pacemaker follow-up may soon replace standard transtelephonic ECG evaluation.¹⁵

The foregoing discussion provides an introduction to the basic concepts of pacemaker therapy. However, the nurse who cares for patients with permanent or temporary pacemakers must be familiar with even the most sophisticated modes of pacemaker function. Only by keeping pace with current technology can the nurse accurately interpret pacer function and thereby safely and effectively care for patients with pacemakers.

The ICD system contains (1) sensing electrodes to recognize the dysrhythmia and (2) defibrillation electrodes or patches that are in contact with the heart and can deliver a shock. These electrodes are connected to a generator that is surgically placed in the subcutaneous tissue of the pectoral region in the upper chest (Figure 13-6). The early-model generators could defibrillate or cardiovert only lethal dysrhythmias. The current generation of devices delivers a tiered therapy, with options for programmable antitachycardia pacing, bradycardia backup pacing, low-energy cardioversion, and high-energy defibrillation. With tiered therapy, antitachycardia pacing is used as the first line of treatment in some cases of VT. If the VT can be pace-terminated successfully, the patient will not receive a shock from the generator and may not even realize that the ICD terminated the dysrhythmia. If programmed bursts of pacing do not terminate the VT, the ICD will cardiovert the rhythm. If the dysrhythmia deteriorates into VF, the ICD is programmed to defibrillate at a higher energy. If the dysrhythmia terminates spontaneously, the device will not discharge. Occasionally, the electrical rhythm may deteriorate to asystole or a slow idioventricular rhythm; in such cases, the bradycardia backup pacing function is activated.

ICDs are dual-chamber devices with leads in both atria and ventricles. The atrial leads allows for dual-chamber pacing to optimize hemodynamic performance and atrial sensing to more accurately discriminate between atrial and ventricular tachycardias and to decrease the incidence of inappropriate shocks. Implantable defibrillators with atrial capabilities may also be used to deliver therapies such as cardioversion or antitachycardia pacing to patients with atrial tachydysrhythmias, but their use may be limited because of the painful nature of the shocks.¹² ICDs may also incorporate triple-lead systems (leads in one atrium and both ventricles) to allow for CRT and defibrillation in one device. Other developments in ICD technology include improved diagnostic and telemetry functions, such as the ability to provide real-time electrograms obtained from the ICD electrodes or the ability to perform remote device interrogation by telephone or Internet.¹⁶

It is important to know the type of ICD implanted, how the device functions, and whether it is activated (i.e., on). If the patient experiences a shockable rhythm, the nurse should be prepared to defibrillate in the rare event that the device fails. During external defibrillation, the paddles or patches should not be placed directly over the ICD generator. Standard paddle placement may need to be altered in patients with ICDs to achieve successful defibrillation.2 Most patients continue to take antidysrhythmic medications to decrease the number of shocks required and to slow the rate of the tachycardia. Complications associated with the permanent ICD include infection from the implanted system,¹⁴ broken leads, and sensing of supraventricular tachydysrhythmias resulting in unneeded discharges.

Four fibrinolytic agents are currently available for intravenous treatment of acute STEMI. All of these agents stimulate lysis of the clot by converting inactive plasminogen to plasmin, an enzyme responsible for degradation of fibrin. Streptokinase (SK) and urokinase were the first generation of fibrinolytic agents and had their primary effect on circulating plasminogen. Urokinase availability has been limited because of manufacturing problems. Newer fibrinolytic agents (e.g., alteplase, reteplase, tenecteplase) have a greater effect on clot plasminogen than on circulating plasminogen and are described as clot selective. A comparison of currently approved fibrinolytic agents is provided in Table 13-4.

Because patients with an area of plaque disruption are still at risk for clot formation and reocclusion, fibrinolytic therapy is used in conjunction with anticoagulants and antiplatelet agents. Current guidelines recommend that heparin be administered for a minimum of 48 hours after fibrinolytic therapy. Low-molecular-weight heparin (LMWH) is considered an acceptable alternative in patients younger than 75 years who have adequate kidney function. Antiplatelet therapy with clopidogrel is recommended for 14 days, and aspirin should be continued indefinitely²⁰ (Table 13-5).

In the cardiac catheterization laboratory, the blood flow of a vessel that has been occluded by a thrombus and then opened by fibrinolytic therapy can be observed directly under fluoroscopy. The adequacy of the flow of blood through the coronary artery is described using the standardized thrombolysis in myocardial infarction (TIMI) scale (Box 13-4).

Indications for catheter-based interventions have been considerably broadened since the initial application of balloon angioplasty. Whereas only patients with single-vessel CAD were once considered for PTCA, patients with multivessel disease, even those who have previously undergone saphenous vein grafting, internal mammary artery (IMA) grafting, or fibrinolytic therapy for acute MI, may now be candidates for catheter intervention. Previously seen as a rescue procedure to reduce a severe stenosis that persisted after fibrinolytic therapy, PCI is now preferred as the initial method of treatment for acute MI (primary PCI) when this therapy is available in the hospital.29 See “Coronary Artery Disease” in Chapter 12.

PTCA involves the use of a balloon-tipped catheter that, when advanced through an atherosclerotic lesion (atheroma), can be inflated intermittently for the purpose of dilating the stenotic area and improving blood flow through it (Figure 13-8). The high inflation pressure of the balloon stretches the vessel wall, fractures the plaque, and enlarges the vessel lumen. After balloon deflation, the vessel exhibits some degree of elastic recoil, resulting in a residual stenosis of approximately 30%.³¹ A successful angioplasty procedure is one in which the stenosis is reduced to less than 50% of the vessel lumen diameter.³⁰

Restenosis occurred in more than one third of patients who underwent PTCA as a solo procedure. Restenosis within the first 6 months was diagnosed when patients experienced a recurrence of anginal symptoms.³² Studies showed that restenosis was influenced by the final lumen diameter after PTCA, the severity of elastic recoil of the vessel walls in response to the balloon inflation, and the amount of intimal hyperplasia that occurred as the vessel healed over the treated area. Patient characteristics such as a history of diabetes or unstable angina were also found to increase the risk of restenosis.³³ Today, PTCA is rarely used alone as an intervention, except to treat lesions in very small coronary arteries.³¹ Nevertheless, balloon angioplasty remains an essential technique in PCI for dilating vessels and for deploying intracoronary stents.

Atherectomy is the excision and removal of the atherosclerotic plaque by cutting, shaving, or grinding. Specialized coronary catheters are used. Initially, atherectomy devices were used alone in an attempt to avoid the trauma to the vessel that was known to occur with balloon angioplasty and to more efficiently remove the atherosclerotic plaque, thereby decreasing the rate of restenosis. Later, as restenosis was also found to occur with these devices, balloon angioplasty was added as an adjunctive therapy to optimize the diameter of the vessel lumen and offset the intimal hyperplasia that occurred as a result of the procedure. Despite significant improvements in initial procedural success, atherectomy failed to significantly reduce the rate of restenosis.34 In the current era of stenting, atherectomy devices are used in less than 5% of procedures.³¹

Two atherectomy devices are used in PCI: directional coronary atherectomy (DCA) (Figure 13-9, A) and rotational ablation (Rotablator) (Figure 13-9, B). A randomized clinical trial showed no clinical benefit for the use of DCA in combination with stent, compared with stenting alone.³⁵ As a result, DCA is currently used only for noncalcified lesions that involve a bifurcation of a major side branch or in the ostium of the left anterior descending (LAD) artery.²⁸ Rotational atherectomy is used for chronic total occlusion and for calcified bifurcation lesions.²⁸

A major development in the field of interventional cardiology has been the coronary stent prosthesis. A stent is a metal structure that is introduced into the coronary artery over a guidewire and expanded into the vessel wall at the site of the lesion (Figure 13-10). Bare metal stents were first used to treat acute or threatened vessel closure after failed PTCA.³² The stent acted as a scaffold to tack dissection flaps against the vessel wall and provided mechanical support to minimize elastic recoil. Multiple stents may be implanted sequentially within a vessel to fully cover the area of the lesion. Stents are currently the predominant form of PCI and are used in more than 90% of all interventional procedures.⁷ Numerous stent models are available. They are composed of various types of metal (stainless steel, titanium, cobalt chromium) and come in a variety of configurations (e.g., mesh, coil). Most stents are balloon expandable (see Figure 13-10).