The bipolar lead used in transvenous pacing has two electrodes on one catheter (Figure 13-1). The distal, or negative, electrode is at the tip of the pacing lead and is in direct contact with the heart, usually inside the right atrium or ventricle. Approximately 1 cm from the negative electrode is a positive electrode. The negative electrode is attached to the negative terminal, and the positive electrode is attached to the positive terminal of the pulse generator, either directly or by means of a bridging cable (see Figure 13-1, B).

Transcutaneous cardiac pacing involves the use of two large skin electrodes, one placed anteriorly and the other posteriorly on the chest, connected to an external pulse generator. It is a rapid, noninvasive procedure that nurses can perform in the emergency setting and is recommended as a primary intervention in the advanced cardiac life support (ACLS) algorithm for the treatment of symptomatic bradycardia.2 Improved technology related to stimulus delivery and the development of large electrode pads that help disperse the energy have helped reduce the pain associated with cutaneous nerve and muscle stimulation. Discomfort may still be an issue for some patients, particularly when higher energy levels are required to achieve capture. This route is typically used as a short-term therapy until the situation resolves or another route of pacing can be established.

The insertion of temporary epicardial pacing wires has become a routine procedure during most cardiac surgical cases. Ventricular and, in many cases, atrial pacing wires are loosely sewn to the epicardium. The terminal pins of these wires are pulled through the skin before the chest is closed. If both chambers have pacing wires attached, the atrial wires exit subcostally to the right of the sternum and the ventricular wires exit in the same region but to the left of the sternum. These wires can be removed several days after surgery by gentle traction at the skin surface with minimal risk of bleeding.³

The Inter-Society Commission for Heart Disease (ICHD) has a standardized code for describing the various pacing modes. A three-letter code is used to describe temporary pacing modes. The first letter refers to the cardiac chamber that is paced. The second letter designates which chamber is sensed, and the third letter indicates the pacemaker’s response to the sensed event.4

The five-letter pacemaker code contains the three-letter code categories plus two sections that list additional programming functions (Table 13-1).⁴

The nurse inspects for loose connections between the leads and pulse generator on a regular basis.5 Replacement batteries and pulse generators must always be available on the unit. Although the battery has an anticipated life span of 1 month, it probably is sound practice to change the battery if the pacemaker has been operating continually for several days. Newer generators provide a low-battery signal 24 hours before complete loss of battery function occurs to prevent inadvertent interruptions in pacing. The pulse generator must always be labeled with the date on which the battery was replaced.

It is important to be aware of all sources of EMI within the critical care environment that may interfere with the pacemaker’s function. Sources of EMI in the clinical area include electrocautery, defibrillation current, radiation therapy, magnetic resonance imaging devices, and transcutaneous electrical nerve stimulation (TENS) units.3 In most cases, if EMI is suspected of precipitating pacemaker malfunction, conversion to the asynchronous mode (fixed rate) can maintain pacing until the cause of the EMI is removed.

Because the pacing electrode provides a direct, low-resistance path to the heart, the nurse takes special care while handling the external components of the pacing system to avoid conducting stray electrical current from other equipment. Even a small amount of stray current transmitted through the pacing lead could precipitate a lethal dysrhythmia. The possibility of microshock can be minimized by wearing rubber gloves when handling the pacing wires and by proper insulation of terminal pins of pacing wires when they are not in use. The latter precaution can be accomplished by the use of caps provided by the manufacturer or by improvising with a plastic syringe or section of disposable rubber glove. The wires are taped securely to the patient’s chest to prevent accidental electrode displacement. Additional safety measures include using a nonelectric or a properly grounded electric bed, keeping all electrical equipment away from the bed, and permitting the use of only rechargeable electric razors.

During transvenous pacing insertion, a balloon at the tip of the catheter is inflated with air to facilitate transvenous insertion. Once the tip of the pacing catheter is correctly positioned within the heart chamber, the balloon is deflated. It is important that the external balloon port is labeled to avoid inadvertent access.5 A rare complication associated with transvenous pacing is myocardial perforation, which can result in rhythmic hiccoughs or cardiac tamponade.

Patient teaching for the person with a temporary pacemaker emphasizes the prevention of complications. The patient is instructed not to handle any exposed portion of the lead wire and to notify the nurse if the dressing over the insertion site becomes soiled, wet, or dislodged. When epicardial pacemaker wires are removed following cardiac surgery, explain that a pulling sensation may be experienced.6 The patient is advised not to use any electrical devices brought in from home that could interfere with pacemaker functioning.

Patients with temporary transvenous pacemakers need to be taught to restrict movement of the affected extremity to prevent lead displacement.

To facilitate a positive psychological adjustment to the ICD, patient education about the device is vital.17,18 Preoperative teaching for the ICD patient includes information about how the device works and what to expect during the implantation procedure. After implantation, education is focused on aspects of living with an ICD. Patients need information pertaining to scheduled device follow-up and instructions about what to do if they experience a shock. Many institutions have successfully used family support groups for this patient population.

Certain criteria have been developed, based on research findings, to determine the patient population that would most likely benefit from the administration of fibrinolytic therapy. Patients with recent onset of chest pain (<12 hours’ duration) and persistent ST elevation (>0.1 mV in two or more contiguous leads) are considered candidates for fibrinolytic therapy.20 Patients who present with bundle branch blocks that may obscure ST-segment analysis and a history suggesting an acute MI are also considered candidates for therapy. The goal of therapy is to administer fibrinolytic therapy within 30 minutes after presentation at the hospital, described as “door-to-needle” time. Time is crucial because early reperfusion yields the greatest benefit.²¹

Exclusion criteria are usually based on the increased risk of bleeding incurred from the use of fibrinolytics. Patients who have stable clots that might be disrupted by fibrinolytic therapy (recent surgery, trauma, or stroke) usually are not considered candidates for fibrinolytic therapy. Other selection criteria for the use of fibrinolytic therapy are presented in Box 13-3.

Currently, fibrinolytic therapy is not indicated for patients with unstable angina or non-ST-elevation myocardial infarction (NSTEMIs). It is believed that these conditions result from plaque rupture with the formation of an only partially occlusive thrombus. Fibrinolysis breaks up the clot and releases thrombin, and this can paradoxically increase the material necessary for further thrombosis.22 Instead, these patients are treated with antiplatelet agents (e.g., aspirin, clopidogrel, glycoprotein IIb/IIIa inhibitors) and antithrombin drugs (e.g., heparin).

The benefit of fibrinolytic therapy correlates with the degree of restoration of normal blood flow in the infarct-related artery. Coronary artery patency is defined by angiographic perfusion grades developed by the Thrombolysis in Myocardial Infarction (TIMI) study group in 1985 (Box 13-4).²³ Achievement of TIMI grade 3 flow is associated with the best long-term survival. Studies also indicate that rapid restoration of normal blood flow, within 90 minutes after treatment, results in improved LV function and reduced mortality. The three fibrin-specific fibrinolytics have been shown to achieve TIMI 3 flow in 54% to 63% of patients at 90 minutes.²⁴

The area of fibrinolytic therapy continues to evolve, and drug dose ranges and regimens are subject to change when research findings are updated. Whereas fibrinolytic agents target the fibrin portion of the clot, other treatment strategies are focusing on the platelet portion of the clot (see Figure 13-7). Clinical trials evaluating the combination of glycoprotein IIb/IIIa receptor antagonists with fibrinolytic agents (at half-dose) found outcomes equivalent to those of fibrinolytics alone, but with an increased risk for bleeding.²⁵ There was also speculation that a planned strategy for administering fibrinolytics or glycoprotein IIb/IIIa receptor antagonists, or both, to patients who must be transported to another facility for percutaneous intervention would improve outcomes. Although promising in theory, this facilitated approach to revascularization has not been shown to be beneficial and may increase the risk for bleeding complications in some patients.²⁶

Reperfusion of the ischemic myocardium may be observed noninvasively by several means, as follows:

Initially, most institutions required that patients preparing to undergo angioplasty be candidates for coronary artery bypass graft (CABG) surgery. Complications such as intimal dissection with abrupt closure of the vessel could arise during the procedure, requiring the patient to undergo emergency CABG. Today, most dissections are effectively treated with stent placement, with less than 1% of patients requiring emergency bypass surgery. As a result, most institutions use an informal surgical backup plan, such as the first available operating room. Nevertheless, the availability of cardiac surgical services on site is still recommended. The one exception is in institutions that offer PCI only for treatment of acute STEMI. In this setting, an organized plan for emergent transfer to a surgical center may be used in lieu of on-site surgical access.30

Specific interventions are used to prevent subacute stent thrombosis. High-pressure balloon inflations within the stent are employed to fully open the stent within the vessel, so reduced anticoagulation is sufficient to maintain stent patency. Dual antiplatelet therapy (aspirin and thienopyridine) has been shown to be more important than anticoagulation in preventing stent thrombosis.36 These agents are administered before the procedure and continued at discharge.³⁷ Two potent antiplatelet glycoprotein IIb/IIIa inhibitors, eptifibatide (Integrilin) and tirofiban (Aggrastat), also reduce the formation of intracoronary thrombosis and are used across the spectrum of interventional procedures, from PTCA to atherectomy to stenting.³⁷ Indications and dosing of glycoprotein IIb/IIIa inhibitors are provided in Table 13-6.

In an effort to minimize restenosis, drug-eluting stents (DES) were developed. These stents have polymer coatings impregnated with drugs that are released slowly into the endothelium at the site of stent placement to inhibit cellular proliferation. DES coated with sirolimus (an immunosuppressive drug used to prevent organ transplant rejection) and paclitaxel (an anticancer agent) have been approved by the FDA.38 In initial trials, DES were found to decrease the 6-month restenosis rate to less than 10%, and they soon became the predominant stent, implanted in 90% of patients. Some trials demonstrated similar efficacy between bare metal stents and DES in long-term outcomes (stent thrombosis, MI, or death) and raised concerns regarding the possibility of late stent thrombosis (>1 year) in DES.^39,40 As a result, DES usage has decreased somewhat to between 60% and 70% of patients.³⁰ Because a DES delays endothelialization, dual antiplatelet therapy must be continued for a longer period to prevent stent thrombosis. A DES is also considerably more expensive than a bare metal stent. A comparison of bare metal stents and DES is provided in Table 13-7.

The incidence of serious cardiac complications after PCI, including coronary spasm, coronary artery dissection, and acute coronary thrombosis, has decreased significantly with improvements in technology. Stents have proved efficacious in the repair of coronary dissections, decreasing the need for emergency bypass surgery. Acute thrombosis has decreased with the use of glycoprotein IIb/IIIa inhibitors (see Table 13-6). Other complications that can occur in the period immediately after PCI include bleeding and hematoma formation at the site of vascular cannulation, compromised blood flow to the involved extremity, retroperitoneal bleeding, contrast-induced kidney failure, dysrhythmias, and vasovagal response (hypotension, bradycardia, and diaphoresis) during manipulation or removal of introducer sheaths.

Restenosis after PCI continues to be a problem, although rates are much lower with DES than with angioplasty alone. Patients at greatest risk are those with complex lesions, multivessel disease, or diabetes.41 Treatment options for in-stent restenosis include balloon dilation, debulking with an atherectomy device, implantation of another DES or brachytherapy—the localized delivery of intracoronary radiation through specialized catheters. Because healing within the stent is delayed, late thrombosis may occur in patients with DES. Late thrombosis, although rare, is associated with a 45% mortality rate. Premature discontinuation of antiplatelet therapy is the strongest predictor of late stent thrombosis, especially with DES.³²

It is essential that the nurse observe the patient for recurrent angina or ST elevation, which are clinical indicators of myocardial ischemia. Monitoring leads should be selected that will reflect ischemia in the vessels that were treated during the intervention.29 Angina during interventional cardiology procedures is an expected occurrence at the time of balloon inflation or manipulation within the coronary artery. Intraprocedural angina is caused by the temporary interruption of blood flow through the involved artery, which should subside with deflation or removal of the balloon or nitroglycerin administration, or both. Angina after a coronary interventional procedure may be caused by transient coronary vasospasm, or it may signal a more serious complication—acute thrombosis. In any case, the nurse must act quickly to assess for manifestations of myocardial ischemia and initiate clinical interventions as indicated. The physician usually orders intravenous nitroglycerin to be titrated to alleviate chest pain. Continued angina despite maximal vasodilator therapy usually rules out transient coronary vasospasm as the source of ischemic pain, and a return to the cardiac catheterization laboratory must be considered.

Patients undergoing PCI are exposed to significant amounts of contrast dye, with its associated nephrotoxicity. Renal protective strategies may be implemented before the procedure, especially for patients with evidence of baseline impairment of kidney function. This may include preprocedural hydration, infusion of sodium bicarbonate, and administration of N-acetylcysteine (Mucomyst).42 After PCI, hydration is essential to maintain adequate flow through the kidneys. Intravenous fluids are administered, and patients are encouraged to take oral fluids as tolerated.⁴³

Another point of instruction that must be addressed is the patient’s knowledge deficit related to discharge medications. Patients are sent home on a regimen of antiplatelet drugs and drugs for secondary prevention, such as lipid-lowering agents and blood pressure medications. A nitrate such as isosorbide may be prescribed to promote vasodilation, or, if the patient has demonstrated evidence of a vasospastic component to the disease, calcium channel blockers may be used. It is essential that the patient clearly understand the rationale for therapy and the potential side effects of each drug. Patients also need to understand the importance of not discontinuing their antiplatelet therapy; deaths have been reported when patients discontinued this therapy before elective procedures.46 It is important that patients be provided with written information and a number to call if problems occur.

Saphenous vein grafting involves the anastomosis of an excised portion of the saphenous vein proximal to the aorta and distal to the coronary artery below the obstruction (Figure 13-11). Traditionally, the saphenous vein graft was obtained through an open incision, but endoscopic harvesting of this vessel is now possible. This minimally invasive technique of graft procurement decreases postoperative pain and reduces leg wound infection.⁵⁴

The IMA, which usually remains attached to its origin at the subclavian artery, is swung down and anastomosed distal to the coronary artery (Figure 13-12). Either the right IMA or the left IMA may be used as a conduit. Of note, emergency CABG may preclude the use of the IMA because of the extra time required to mobilize the artery and the inability to effect cardioplegia through this conduit. However, the current trend is to use arterial conduits such as the IMA whenever possible, because their long-term patency rates are superior to those of the saphenous vein graft.⁵⁵

The right gastroepiploic artery (GEA) has also been introduced as an alternative conduit for CABG. The artery, which is a branch of the gastroduodenal artery, is pulled up through the diaphragm to the pericardial cavity, and anastomosed to a distal portion of the coronary artery. Although it is a little smaller in diameter than the IMA, studies indicate that patency rates are excellent.56 Because of its size and anatomic location, the gastroepiploic artery is well suited for bypassing the right coronary artery, the circumflex artery, or the posterior descending artery. However, the technical aspects of obtaining this conduit may limit its widespread use.

The potential benefit of long-term patency associated with arterial conduits has revived interest in the use of radial artery grafts. First introduced as a potential conduit for myocardial revascularization in the 1970s, radial artery grafts were abandoned because of a high incidence of early graft occlusion and vasospasm. Current early patency rates of 90% or better have been attributed to improved harvesting techniques and the use of postoperative calcium channel blockers to minimize vasospasm.57 A comparison of conduits used for myocardial revascularization is provided in Table 13-9.

Postoperative bleeding from the mediastinal chest tubes can be caused by inadequate hemostasis, disruption of suture lines, or coagulopathy associated with cardiopulmonary bypass or hypothermia. Bleeding is more likely to occur with IMA grafts as a result of the extensive chest wall dissection required to free the IMA. If bleeding in excess of 150 mL/hr occurs early in the postoperative period, clotting factors (fresh-frozen plasma, fibrinogen, and platelets) and additional protamine (used to reverse the effects of heparin) may be administered, along with prompt blood replacement. Other medications used in the treatment of postoperative bleeding are described in Table 13-11.

Autotransfusion devices, which facilitate the collection and reinfusion of shed mediastinal blood, were used in some institutions in the past. Routine autotransfusion of shed mediastinal blood is no longer recommended, because it may further exacerbate bleeding by activating the extrinsic clotting pathway and increase the risk of infection.⁶⁵ The use of positive end-expiratory pressure (PEEP) in conjunction with mechanical ventilation may be helpful in controlling excessive bleeding in some cases by increasing the intrathoracic pressure enough to effect tamponade of oozing mediastinal blood vessels.⁶⁵ Rewarming the patient reverses the depressed manufacture and release of clotting factors that results from hypothermia. However, persistent mediastinal bleeding—usually in excess of 500 mL in 1 hour or 300 mL/hr for 2 consecutive hours despite normalization of clotting studies—is an indication for reexploration of the surgical site.

Until recently, overnight intubation to facilitate lung expansion and optimize gas exchange was common for patients who had undergone cardiac surgery. Newer protocols that facilitate early extubation (within the first 4 to 8 hours) have been implemented in most institutions.66 Early extubation requires a multidisciplinary approach that incorporates anesthesiologists, surgeons, nurses, and respiratory therapists. Potential candidates must be identified before surgery so that the anesthetic regimen can be modified to support early extubation. One approach is to use short-acting anesthetic agents such as propofol (Diprivan) at the end of the surgery and to minimize the use of opioids. Another option is to administer neostigmine and glycopyrrolate at the end of the surgery to reverse the neuromuscular blockade used during the procedure.

After surgery, patients are evaluated for hemodynamic stability, adequate control of bleeding, and normothermia. After these criteria have been met, the patient is weaned off propofol or given neuromuscular reversal agents, and ventilator weaning can begin. If needed, opioids are given in small increments to manage pain and anxiety. Patients who exhibit hemodynamic instability or intraoperative complications or who have underlying pulmonary disease related to long-term valvular dysfunction may require longer periods of mechanical ventilation. After extubation, supplemental oxygen is administered, and patients are medicated for incisional pain to facilitate adequate coughing and deep breathing.

The transient neurological dysfunction often seen in patients who have had cardiac surgery has been attributed to decreased cerebral perfusion, cerebral microemboli, and the systemic inflammatory response. It was once thought to be primarily caused by cardiopulmonary bypass, but newer evidence indicates that cognitive decline may be influenced more by patient-related factors such as the degree of preexisting cerebral vascular disease or diabetes.67 Compounding these are environmental factors such as sensory deprivation and sensory overload associated with being in a critical care unit. The term postcardiotomy delirium has been used to describe this postoperative syndrome that initially may manifest as only a mild impairment of orientation but that may progress to agitation, hallucinations, and paranoid delusions. One study indicated that mild preoperative cognitive impairment might be a useful predictor of who is likely to develop postcardiotomy delirium.⁶⁸

Treatment of delirium may require the use of medications such as benzodiazepines or haloperidol (Haldol). Environmental modifications such as noise reduction, restoring normal day/night lighting patterns, and placing familiar objects at the bedside may help to calm and reorient the patient. Liberalization of visitation policies to allow family members a prolonged presence at the bedside is also highly desirable. Nursing management is organized to maximize optimal sleep patterns whenever possible.

Postoperative fever is fairly common after cardiopulmonary bypass. However, persistent temperature elevation to greater than 101° F (38.3° C) must be investigated. Sternal wound infections and infective endocarditis are the most devastating infectious complications, but leg wound infection, pneumonia, and urinary tract infection also can occur. Infection rates are greater in diabetic patients. Studies have shown that maintaining the blood glucose concentration between 80 and 110 mg/dL in the perioperative period by means of a continuous insulin infusion may decrease the risk of infection in this population.69

The American College of Cardiology and the American Heart Association have developed a set of clinical practice guidelines for care of the patient undergoing CABG.51 These guidelines are designed to support clinical decision making with research evidence (Evidence-Based Collaborative Practice box on Coronary Artery Bypass Graft Surgery).

In an effort to avoid the adverse effects of cardiopulmonary bypass, off-pump coronary artery bypass (OPCAB) is performed in approximately 20% to 30% of cases.70 A variety of incisional approaches can be used. In minimally invasive direct coronary artery bypass graft (MIDCABG) surgery, a small left anterior thoracotomy incision is used to directly harvest the left IMA, which is then anastomosed to the LAD artery. Alternative approaches may use a segment of saphenous vein or radial artery, one end of which is attached to the left IMA and the other to accessible coronary arteries.⁷⁰ Some surgeons may opt for a standard median sternotomy approach to allow for bypassing of distal vessels. Several techniques are used to stabilize the operative area during an OPCAB procedure. Immobilization devices that use compression or suction to create an immobile area have been developed to stabilize cardiac wall motion at the site of the anastomosis. Drugs that temporarily decrease the heart rate (e.g., esmolol, diltiazem) or cause transient cardiac asystole (e.g., adenosine) may also be used to further limit cardiac motion.⁷¹

Results from OPCAB surgery have been mixed. Some studies have demonstrated improvements in morbidity, including decreased transfusion requirements, shortened time on the ventilator, decreased length of stay, and a lower incidence of stroke and renal complications.⁷² Others have shown no advantage over conventional surgery.^73,74 OPCAB may be most beneficial in patients with significant comorbid conditions and in those with contraindications to cardiopulmonary bypass.⁷⁵

Minimally invasive procedures will continue to be refined with the use of robotic equipment in cardiac surgery, currently under clinical investigation at a small number of centers. Robotic-assisted surgery allows the surgeon to view a computer-enhanced image while manipulating instruments through small portholes using robotic arms. This provides increased surgical precision and the ability to perform conventional procedures with smaller incisions.⁷⁰

The ECG and arterial pressure tracings are constantly monitored to verify the timing and effect of balloon counterpulsation. For counterpulsation to occur, the pump must receive a trigger signal to identify the beginning of a new cardiac cycle. The trigger can be the R wave of the ECG, the upstroke of the arterial pressure waveform, or a pacemaker spike.76 Dysrhythmias can adversely affect the timing of balloon inflation and deflation, so rhythm disturbances must be detected and treated promptly. Modern IABPs have automatic timing features that use internal algorithms to adjust inflation and deflation in response to changes in the patient’s heart rate or rhythm. New catheters are available that incorporate a fiberoptic sensor to enhance the quality of the arterial waveform obtained from the IAB catheter and improve timing. Mean arterial pressure is ideally maintained at approximately 80 mm Hg with adequate pumping.

The most common complication of IABP support is lower extremity ischemia resulting from occlusion of the femoral artery by the catheter itself or by emboli caused by thrombus formation on the balloon.77 Although ischemic complications have decreased with sheathless insertion techniques and the introduction of smaller balloon catheters (7.5 versus 9.5 Fr), evaluation of peripheral circulation remains an important nursing assessment.⁷⁸ The presence and quality of peripheral pulses distal to the catheter insertion site are assessed frequently, along with color, temperature, and capillary refill of the involved extremity. Doppler localization of peripheral pulses may be required if pulses are difficult to palpate on the cannulated extremity. Signs of diminished perfusion must be reported immediately. Anticoagulation (e.g., heparin infusion) may be prescribed to decrease the incidence of thrombosis. Other vascular complications associated with IABP include acute aortic dissection and the development of pseudoaneurysms at the catheter insertion site.

Weaning from the IABP is considered after hemodynamic stability has been achieved with no, or only minimal, pharmacological support. One weaning procedure consists of slowly decreasing the pumping frequency from every beat to every eighth beat, as tolerated. Another weaning method involves a gradual decrease in balloon volume.79 To prevent thrombus formation on the balloon surface, the IABP must remain at a minimal pumping ratio (or volume) until its removal.

Class II drugs are β-adrenergic blockers (beta-blockers). They inhibit dysrhythmias mediated by the sympathetic nervous system by competing with endogenous catecholamines for available receptor sites. As a result, spontaneous depolarization during the resting phase (phase 4) is depressed, and AV conduction is slowed. Drugs in this class can be further subdivided into cardioselective agents (those that block only β₁-receptors) and noncardioselective agents (those that block both β₁– and β₂-receptors). Knowledge of the effects of adrenergic-receptor stimulation allows for anticipation of both the therapeutic responses brought about by beta-blockade and the potential adverse effects of these agents (Table 13-13). For example, bronchospasm can be precipitated by noncardioselective beta-blockers in a patient with chronic obstructive pulmonary disease (COPD) caused by blockade of the effects of β₂-receptors in the lungs. Beta-blockers also are negative inotropes and must be used cautiously in patients with LV dysfunction. Although numerous beta-blockers are marketed, only esmolol, metoprolol, and propranolol are available as intravenous agents for the treatment of acute dysrhythmias. Of these, esmolol (Brevibloc) offers significant advantages for the critically ill patient because of its short half-life (approximately 9 minutes). It is used in the treatment of supraventricular tachycardias, such as atrial fibrillation and atrial flutter.

Class III agents include amiodarone, dofetilide, ibutilide, and sotalol. These agents markedly slow the rate of phase 3 repolarization, increasing the effective refractory period and the action potential duration. Although their effects on the action potential are similar, these drugs differ greatly in their mechanism of action and their side effects. At this time, sotalol is approved only for oral use. Intravenous amiodarone was originally approved for the treatment of serious ventricular dysrhythmias refractory to other medications. Because of its effectiveness, it is now used for both atrial and ventricular dysrhythmias.80 Dofetilide (Tikosyn) is a new class III antidysrhythmic agent used for the conversion to and maintenance of normal sinus rhythm in patients with highly symptomatic atrial fibrillation or atrial flutter. Because dofetilide prolongs the refractoriness of both atrial and ventricular tissue, prolongation of the QT interval can occur and is associated with an increased risk of torsades de pointes.⁸¹ Therapy with dofetilide is initiated in a hospital setting under close monitoring. Ibutilide (Covert) is a short-term antidysrhythmic agent used for the rapid conversion of acute atrial fibrillation or atrial flutter to sinus rhythm. The drug is administered as a 10-minute infusion in a carefully monitored clinical setting. The most serious side effect of ibutilide is its potential for inducing life-threatening dysrhythmias, especially torsades de pointes.⁸²

Class IV agents are calcium channel blockers that inhibit the influx of calcium through slow calcium channels during the plateau phase (phase 2). This effect occurs primarily in tissue in which slow calcium channels predominate, primarily the sinus and AV nodes and the atrial tissue. Verapamil was the first drug in this category available as an intravenous antidysrhythmic. It depresses sinus and AV node conduction and is effective in terminating supraventricular tachycardias caused by AV nodal reentry. Diltiazem (Cardizem) has become available in intravenous form and is thought to be as effective as verapamil in treating supraventricular dysrhythmias, with fewer hypotensive side effects. Because accessory pathways are not affected by calcium channel blockade, both of these agents must be avoided when treating atrial fibrillation in patients with Wolff-Parkinson-White syndrome.80

Adenosine (Adenocard) is an antidysrhythmic agent that remains unclassified under the current system. Adenosine occurs endogenously in the body as a building block of adenosine triphosphate (ATP). Given in intravenous boluses, adenosine slows conduction through the AV node, causing transient AV block. It is used clinically to convert supraventricular tachycardias and to facilitate differential diagnosis of rapid dysrhythmias. Because of its short half-life, the drug is administered intravenously as a rapid bolus, followed by a saline flush. The bolus is delivered as centrally as possible, so that the drug reaches the heart before it is metabolized.80 Side effects are transient, because the drug is rapidly taken up by the cells and is cleared from the body within 10 seconds.

Magnesium is also unclassified under the present system. Although its action as an antidysrhythmic agent is not entirely understood, clinical studies suggest that it may reduce the incidence of both ventricular and supraventricular dysrhythmias in selected patient populations. It is considered the treatment of choice in patients with torsades de pointes. For acute treatment, 1 to 2 g of magnesium is administered over 1 to 2 minutes. In patients with confirmed hypomagnesemia, this bolus may be followed with a 24-hour infusion.⁸⁰

Antidysrhythmic drugs carry the risk of serious side effects, some of which can be life threatening. The major side effects of the intravenous antidysrhythmic agents are listed in Table 13-14. The most severe complication is the potential for a prodysrhythmic effect. This may result in worsening of the underlying dysrhythmia, the occurrence of a new dysrhythmia, or the development of a bradydysrhythmia. For example, torsades de pointes is a prodysrhythmia caused by a number of drugs. Because the development of a prodysrhythmia is unpredictable, the nurse plays an important role in evaluating ECG changes, monitoring drug levels, and assessing patient symptoms. Antidysrhythmic agents may also alter the amount of energy required for defibrillation and pacing. For example, increases in the dose of an antidysrhythmic drug may increase the amount of output (mA) required to depolarize the myocardium.

More than 2 million people in the United States have atrial fibrillation, and extensive research has been done on the treatment of this disorder. The goals of pharmacological therapy for atrial fibrillation include reestablishing and maintaining sinus rhythm, decreasing the rapid ventricular response during episodes of atrial fibrillation, and preventing the risk of thromboembolism. Table 13-15 reviews current drugs used in the treatment of atrial fibrillation. Results of some clinical trials suggest that rate control is equivalent to restoration of sinus rhythm in terms of mortality.^82,83

Sympathomimetic agents stimulate adrenergic receptors, thereby simulating the effects of sympathetic nerve stimulation. Included in this category are naturally occurring catecholamines (epinephrine, dopamine, and norepinephrine) and synthetic catecholamines (dobutamine and isoproterenol). The cardiovascular effects of these drugs, which vary according to their selectivity for specific receptor sites, are often dose dependent as well. Table 13-16 describes the cardiovascular effects of sympathomimetic drugs at various dosages.

Phosphodiesterase inhibitors are inotropic agents that also are potent vasodilators (inodilators). Drugs in this classification inhibit the enzyme phosphodiesterase, resulting in increased levels of cyclic adenosine monophosphate (AMP) and intracellular calcium. Amrinone (Inocor) and milrinone (Primacor) were the first of these agents approved for use in the United States. Increases in cardiac output occur as a result of increased contractility (inotropic effects) and decreased afterload (vasodilative effects). Filling pressures tend to decrease, while heart rate and blood pressure remain fairly constant. Amrinone may cause thrombocytopenia, so platelet counts are monitored and patients are observed for hemorrhagic complications. Milrinone is associated with a lower rate of thrombocytopenia but can induce ventricular dysrhythmias (PVCs, VT) in a significant number of patients.85

Direct-acting vasodilators include sodium nitroprusside, nitroglycerin, and hydralazine. These drugs produce relaxation of vascular smooth muscle through the activation of nitric oxide, which results in decreased systemic vascular resistance (SVR). Hypotension may occur as a result of peripheral vasodilation, and headaches may be caused by cerebral vasodilation. Compensatory mechanisms can occur in response to the drop in blood pressure. These include baroreceptor activation that causes reflex tachycardia and activation of the renin-angiotensin-aldosterone system (RAAS) (see Figure 12-14 in Chapter 12), with resultant sodium and water retention.

Calcium channel blockers are a chemically diverse group of drugs with differing pharmacological effects (Table 13-18).

Nifedipine (Procardia) and nicardipine (Cardene) are dihydropyridines. Drugs in this group of calcium channel blockers (with the suffix pine) are used primarily as arterial vasodilators. These agents reduce the influx of calcium in the arterial resistance vessels. Both coronary and peripheral arteries are affected. They are used in the critical care setting to treat hypertension. Nifedipine is available only in an oral form, but in the past it was prescribed sublingually during hypertensive emergencies. Reports of adverse events associated with sublingual nifedipine have prompted the FDA to strongly discourage sublingual use.⁸⁷ Nicardipine has become available as an intravenous calcium channel blocker, and it offers more accurate titration for effective control of hypertension. Side effects of nifedipine and nicardipine are related to vasodilation and include hypotension, reflex tachycardia, flushing, headache, and ankle edema.

Diltiazem (Cardizem) is from the benzothiazepine group of calcium channel blockers. Verapamil (Calan, Isoptin) is part of the phenylalkylamine group. The different classifications account for the differing actions of these calcium channel blockers. These drugs dilate coronary arteries but have little effect on the peripheral vasculature. They are used in the treatment of angina, especially that which has a vasospastic component, and as antidysrhythmics in the treatment of supraventricular tachycardias.

Nesiritide (Natrecor) is a new vasodilator used in the treatment of acute heart failure. This agent is a recombinant form of human brain natriuretic peptide (BNP), the hormone released by cardiac cells in response to ventricular distention. The primary effects of nesiritide include decreased filling pressures (PAOP, CVP), reduced SVR, and increased urine output. Compared with traditional vasodilator therapy for acute heart failure, nesiritide reportedly is as effective as the traditional agents and has fewer side effects (e.g., headache).85 The recommended dose is an intravenous bolus of 2 mcg/kg, followed by a continuous infusion of 0.01 mcg/kg/min. The primary side effect is hypotension. If this occurs, nesiritide may need to be discontinued for a time and then restarted at a lower dose after the patient has stabilized.⁸⁵ Low-dose nesiritide may have a protective effect on kidney function.⁸⁸ High dose administration is associated with hypotension and dysrythmias.⁸⁸

Labetalol (Normodyne), a combined peripheral alpha-blocker and cardioselective beta-blocker, is used in the treatment of acute stroke and hypertensive emergencies.89 Because the blockade of β₁-receptors permits the decrease of blood pressure without the risk of reflexive tachycardia and increased cardiac output, this drug is also useful in the treatment of acute aortic dissection.⁹⁰

Phentolamine (Regitine) is a nonselective peripheral alpha-blocker that decreases blood pressure through arterial vasodilation. The half-life is 19 minutes when given intravenously. It is administered by slow IV push, 1 to 5 mg every 6 hours to reduce blood pressure.⁸⁶ This drug is used only in very specific circumstances. Phentolamine is the drug of choice to control blood pressure and sweating caused by pheochromocytoma, an epinephrine (adrenaline)-secreting tumor that can arise from the adrenal medulla.⁸⁶

Phentolamine also is used to treat the extravasation of dopamine or other vasopressors into peripheral tissues. If this occurs, 5 to 10 mg is diluted in 10 mL normal saline and administered intradermally into the infiltrated area as soon as possible following the extravasation.

Fenoldopam (Corlopam) is the first of a new class of vasodilators called selective, specific dopamine (D₁) receptor agonists.86 The drug is a potent vasodilator that affects peripheral, renal, and mesenteric arteries. It is administered by continuous intravenous infusion beginning at 0.1 mcg/kg/min and titrated up to the desired blood pressure effect, with a maximum recommended dose of 1.6 mcg/kg/min. It can be administered as an alternative to sodium nitroprusside or other antihypertensives in the treatment of hypertensive emergencies. Fenoldopam can be used safely in patients with kidney dysfunction.⁸⁶

Vasopressin, also known as antidiuretic hormone (ADH), has become popular in the critical care setting for its vasoconstrictive effects. At higher doses, vasopressin directly stimulates V1 receptors in vascular smooth muscle, resulting in vasoconstriction of capillaries and small arterioles. A one-time dose of 40 units intravenously is recommended in the ACLS guidelines as first-line drug therapy for VF, pulseless VT asystole, or pulseless electrical activity (PEA).91 Continuous infusions of 0.02 unit/min up to 0.1 unit/min have been used in the treatment of vasodilatory shock in patients with refractory hypotension after cardiopulmonary bypass.⁶²

In septic shock, vasopressin levels have been reported to be lower than anticipated for a shock state.⁹² Vasopressin continuous infusion of 0.03 unit/min may be added to the norepinephrine infusion in refractory shock per the 2008 surviving sepsis guidelines.⁹² Patients must be assessed for side effects such as heart failure caused by the antidiuretic effects, and monitored for increased risk of ischemia in the myocardium, spleen, and periphery.⁹² Vasopressin should be infused through a central line to avoid the risk of peripheral extravasation and resultant tissue necrosis. Placement of an arterial line in shock states to monitor blood pressure and SVR is recommended.⁹²