The cardiac output, or the amount of blood the heart pumps per minute, is the amount of blood ejected from the left ventricle into the aorta per minute. This is determined by the amount of blood the heart pumps with each stroke (stroke volume) and the number of strokes per minute (heart rate). The heart pumps approximately 70 mL of blood with each stroke at an average rate of 72 strokes per minute; this accounts for an average of more than 5,000 mL of blood per minute. The heart can increase this quantity of blood by about four times by increasing rate, the amount of blood it pumps with each stroke, or both. The heart's ability to do this depends on its ability to time contractions, its ability to contract, and the amount of blood available to pump. These capabilities of the heart first will be described in an overall presentation of blood flow through the heart, contractility of the heart, electrical conduction in the heart, and coronary circulation in relation to anatomy and physiology. Factors outside the heart that influence these variables will be discussed later in relation to their influences on the whole system [2].

The heart actually has three types of muscle fibers: atrial, ventricular, and conducting. Although similar, the atrial and ventricular fibers are completely separated from one another. Their only connection is by way of specialized conducting fibers between the atria and ventricles. The conducting fibers differ from the atrial and ventricular fibers in that they have fewer contractile fibers and therefore have much less contractile ability. They especially are different in their ability to transmit electrical impulses much more rapidly than other kinds of muscle fibers. The point of maximal impulse is located near the apex of the heart [4,5].

The function of the coronary arteries is to provide blood to the myocardium. Like the other cells of the body, the heart needs blood flow to maintain cellular life and perform its work. It receives its blood supply from the left and right coronary arteries, which originate in the root of the aorta just above the left posterior and anterior cusps of the aortic valve. Blood flows into these arteries during ventricular diastole, when the aortic valve is closed by blood pushed backward by the recoil of the aorta at the beginning of ventricular diastole. The duration of ventricular diastole is important to ensure that the heart cells receive sufficient blood supply. Note that when the heart cells contract, the contraction exerts pressure against the coronary vessels and inhibits blood flow [2,3].

The postganglionic parasympathetic nerve fibers primarily secrete acetylcholine and are referred to as cholinergic. The postganglionic sympathetic nerve fibers, which secrete norepinephrine, are referred to as adrenergic. The sympathetic chemical transmitters to the sweat glands and a few blood vessels are cholinergic. This helps explain why sweating is increased with strong sympathetic discharge [2].

An embolism is the obstruction of a blood vessel by a blood clot or foreign substance, such as air or fat. Emboli can occur in arteries or veins (or both). The most common type of embolus is a blood clot (thrombus) that forms in the heart or a blood vessel. The thrombus (or a piece of it) becomes dislodged and travels (then called a thromboembolism) until it arrives in a vessel so small that it cannot move any farther; it then blocks any flow ahead of it. If the embolus is in a vein (or the right side of the heart), it travels through larger and larger vessels until it arrives in the heart, where it moves through the right atrium and ventricle and into vessels in the lungs, which get smaller and smaller. When the embolus reaches a pulmonary vessel too small for it to pass through, it stops. It is then called a pulmonary embolus. When a blood clot breaks off in the left side of the heart or an artery, the thromboembolism travels through smaller and smaller arteries. When it comes to one smaller than itself, it stops and obstructs the blood flow ahead of it. The artery in which it stops may be anywhere in the systemic circulation (e.g., the brain, legs, arms, internal organs). The ultimate result may be death to the tissues ahead of it [3].

Environmental threats to the person with cardiovascular and blood problems include terrain, altitude, and climate. For example, climbing an incline requires more energy expenditure than walking on level ground. Environmental temperature extremes place an additional burden on the cardiac and vascular systems. Cold temperature promotes vasoconstriction and shivering to generate body heat, and a person with an already diminished blood flow may experience ischemia. Shivering increases the metabolic needs and cardiac output. Hot temperatures promote dilation of the vessels near the skin, which also requires an increased cardiac output [13]. A significant increase in altitude results in increased cardiac output, tachycardia, and possibly a slight increase in blood pressure, but no change in stroke volume [16].

Paroxysmal nocturnal dyspnea occurs during sleep. The patient usually awakens suddenly, breathing with difficulty and having a sensation of suffocation. This usually occurs two to five hours after the onset of sleep and happens only once during the night. Paroxysmal nocturnal dyspnea occurs in patients with CHF and is due to pump failure of the left ventricle, which leads to fluid accumulation in the lungs. It is relieved by sitting upright with legs over the side of the bed or by walking around the room. It usually subsides within 20 minutes without aftereffects, and the patient can sleep the remainder of the night [18].

Orthopnea is a form of dyspnea that develops when the patient lies down and is an indicator of left ventricular failure. It is relieved within minutes by sitting up or standing. Patients with orthopnea often require several pillows at night to elevate the head and prevent nocturnal breathlessness. In fact, the severity of the condition was often informally measured by the number of pillows necessary. As heart disease advances and CHF progresses, the severity of this symptom increases. In severe heart failure, the patient is unable to lie down and usually sleeps in a chair. To obtain information about this symptom, ask the patient how well she or he sleeps, and determine how many pillows the patient normally uses and whether the number necessary to provide breathing comfort during the night has increased [18].

During auscultation, a normal physiologic splitting of the first heart sound (S₁) and the second heart sound (S₂) may be heard. The simultaneous closure of the mitral and tricuspid valve is heard as S₁. The normal splitting of S₁ is more difficult to hear, although it may be heard occasionally in the tricuspid area. An easily heard S₁ splitting is abnormal. Often, the sound is actually a diastolic S₄ heart sound [37,38].

Murmurs heard throughout systole are referred to as holosystolic or pansystolic. These murmurs are associated with mitral or tricuspid regurgitation or with a ventricular septal defect. Mitral regurgitation is the most common of these and can be caused by rheumatic heart disease, mitral valve prolapse, calcification, or most commonly, left ventricular failure. S₃ with gallop rhythm is indicative of left ventricular failure. This murmur is loud, high pitched, and blowing, and is heard best at the apex, radiating to the left axilla [38].

Found in high concentrations in both skeletal and heart muscle, CK is the most useful enzyme measurement in the early diagnosis of MI. When the myocardium is injured, the serum CK level rises 3 to 6 hours after the event, peaks at 24 hours, and usually returns to normal within 72 to 96 hours. The specificity of CK activity is increased with the identification of the three CK isoenzymes: CK-BB, found primarily in nervous and smooth muscle tissue; CK-MM, found mainly in skeletal muscle; and CK-MB, which has the highest concentration in the cardiac muscle and is specific to the heart. Elevation in CK-MB is diagnostic of MI and appears within 4 to 6 hours after the onset of chest pain, peaks within 24 hours, and returns to normal within 48 to 72 hours. If the patient is not hospitalized within 24 hours from the onset of chest pain, the rise and peak of CK-MB may not be detected. CK-MM also increases with MI and persists for approximately five days. Serial documentation of CK and CK isoenzyme measurements provides a continuous assessment of myocardial necrosis [40,41].

Found in high concentrations in both skeletal and heart muscle, CK is the most useful enzyme measurement in the early diagnosis of MI. When the myocardium is injured, the serum CK level rises 3 to 6 hours after the event, peaks at 24 hours, and usually returns to normal within 72 to 96 hours. The specificity of CK activity is increased with the identification of the three CK isoenzymes: CK-BB, found primarily in nervous and smooth muscle tissue; CK-MM, found mainly in skeletal muscle; and CK-MB, which has the highest concentration in the cardiac muscle and is specific to the heart. Elevation in CK-MB is diagnostic of MI and appears within 4 to 6 hours after the onset of chest pain, peaks within 24 hours, and returns to normal within 48 to 72 hours. If the patient is not hospitalized within 24 hours from the onset of chest pain, the rise and peak of CK-MB may not be detected. CK-MM also increases with MI and persists for approximately five days. Serial documentation of CK and CK isoenzyme measurements provides a continuous assessment of myocardial necrosis [40,41].

The ECG graphically represents the electrical activity of the heart. Cellular activity of the cardiac muscle generates electrical impulses that flow through the heart, causing cardiac contraction and relaxation. The flow of electrical impulses that leads to contraction is called depolarization. The straight line after the T wave of one pattern and before the P wave of the next pattern corresponds to the resting state. Electrical recovery of the heart muscle is referred to as repolarization. This electrical activity of the heart muscle can be measured by a system of electrodes placed at specific points on the body surface. Only electrical activity generated by the atria and ventricles can be recorded by the body-surface ECG; the specialized conducing tissues within the heart do not provide enough voltage to be detected by body-surface electrodes. The ECG displays the electrical activity as waveforms. As the electrical impulses travel through the atria, depolarization of the atria occurs. The ECG displays this activity as a P wave. The impulses continue through the heart to the ventricles. Ventricular depolarization is represented by a three-wave complex called a QRS complex. Because there are more muscle cells in the ventricles, ventricular repolarization can be measured on ECG and is recorded as a T wave [45].

The ECG recording is a valuable aid in cardiovascular assessment. For each pulse to be palpable with the QRS complex, ventricular contraction had to occur. Not only does it illustrate the rate and rhythm of the heart and conduction through the heart, it also indicates enlargement of the atrial and ventricular chambers, inflammation of the pericardium, electrolyte (potassium) disturbance, or damage to the myocardium. A depressed T wave indicates a low serum potassium level. Any influence on the heart's ability to contract and relax can be documented by the ECG. In a normal physical exam, the 12-lead ECG reading is obtained for baseline information. To monitor effectiveness of cardiac drugs, serial ECGs may be performed [45].

The diary forms provided to patients should include headings for time, type of activity, and symptoms. The patient should be instructed to note the time and to record activities of daily living, including eating, walking, watching television, and sleeping, and to note any associated symptoms (e.g., dizziness, chest pain, fainting, palpitations). The patient may perform the usual activities but should avoid operating heavy machinery, microwave ovens, or electric shavers as well as bathing or showering, as these activities may interfere with the electrical signals of the ECG recorder. The patient may also be shown how to replace the electrodes if they are accidentally removed.

The purpose of the procedure should be explained fully. The nurse should relate that the major purpose for a cardiac catheterization procedure is to visualize the disease process in the coronary arteries and that the information obtained by this procedure is necessary to facilitate the patient's treatment. The patient will be required to recover for a few hours after the procedure. Standard preoperative tests (e.g., chest x-ray, ECG, CBC, urinalysis) are usually performed. The patient receives nothing by mouth after midnight or has only a liquid breakfast if the cardiac catheterization is scheduled for the afternoon. A mild sedative is usually given before the test. Nursing assessment includes the patient's vital signs, evaluation of peripheral pulses, and auscultation of heart and lung sounds. The site of catheter insertion is prepared, the area is shaved if necessary, and usually an antiseptic scrub is done [17].

The most important nursing action following cardiac catheterization is assessing the groin for bleeding and the leg for color, warmth (circulation) and pulse. Postcatheterization care involves monitoring vital signs every 15 minutes for an hour, then every 30 minutes for an hour or until stable. Peripheral pulses and possible bleeding at catheter insertion sites should be assessed with the vital signs. An IV line for medication and fluid replacement is usually required. The patient is kept on bed rest (supine) for a few hours following the procedure [17].

DSA is a newer approach to the traditional angiograms, requiring less patient observation during the procedure. Instead of injecting contrast dye directly into an artery, dye is injected into the venous system via the superior vena cava so it circulates through the heart and into the arterial system. A fluoroscopic image-intensifier displays the vessels and focuses (intensifies) the image. A computer then converts images into measurements. The first image obtained before the injection of the contrast dye is subtracted from the postinjection images. The image obtained from the computer subtraction is an enhanced image of the arterial system. Several vessels rather than one vessel can be evaluated with one injection of contrast dye. DSA is commonly used to diagnose abdominal aneurysms; thoracic aneurysms are more frequently diagnosed by magnetic resonance imaging (MRI) [59].

Intracardiac pressures can be measured and monitored continuously at the bedside in many critical care units. A balloon-tipped, flow-directed catheter is inserted percutaneously or by a venous cutdown into a large vein, such as the internal jugular or the subclavian, femoral, or brachial veins. The catheter (most commonly a Swan-Ganz catheter) is slowly advanced toward the right atrium. When it enters the right atrium, the balloon is inflated. Then, the flow of blood carries the catheter through the tricuspid valve, the right ventricle, and the pulmonary valve into the pulmonary artery. The balloon finally wedges into a branch of the pulmonary artery. The pulmonary artery wedge pressure (PAWP) is obtained, and the balloon is quickly deflated. The catheter floats back into the pulmonary artery and remains in this position for continuous monitoring. The pressures routinely monitored are the pulmonary artery systolic pressure (PASP) and diastolic pressure (PADP), PAWP, and cardiac output. The PASP represents the pressure generated by the contraction of the right ventricle, whereas the PADP represents the filling pressure of the right ventricle. These pressures are monitored to assess right-sided heart function and pulmonary resistance. In the absence of lung dysfunction and mitral valve stenosis, PAWP reflects left atrial pressure and left ventricular end-diastolic filling pressure. Thus, the function of the left heart can be assessed. The best hemodynamic indicator of left ventricular hypertrophy is the measurement of pulmonary capillary wedge pressure (PCWP) [37,38].

Angina pectoris is defined as chest pain caused by myocardial ischemia from reduced blood flow, reduced oxygen supply for demand of myocardium, or a temporary or reversible cause. It is classified as stable, unstable, or Prinzmetal and is the most common symptom of CHD. The pain of angina may last from 30 seconds to 30 minutes. It has been described as a heaviness; a squeezing, viselike pain; or a crushing pain over or near the sternum. The pain may radiate into the left arm, neck, jaw, or back. Difficulty breathing may accompany the pain. Angina usually occurs with increased activity or exposure to a cold environment, when myocardial oxygen need increases. Treatment may be medical, surgical, or a combination of the two. Causes include CHD, coronary spasms, thrombi, or any condition that creates an imbalance between oxygen supply and demand of myocardium [65].

Duration of pain is important in distinguishing MI from angina pectoris. The sudden onset of pain, usually not associated with activity, may awaken the patient in the middle of night. Tachycardia is the result of the increased need of oxygen for cardiac tissue. Diaphoresis, tachypnea, dyspnea, elevated temperature, change in level of consciousness, anxiety, feeling of impending doom, and nausea/vomiting may also occur. ECG changes include depressed or elevated ST segment (most common), inverted T wave, and/or formation of Q waves [68,69]. Arrhythmias, PVCs, and ventricular tachycardia may be present [69].

Prognosis related to the extent of heart damage is determined by the presence or absence of collateral circulation [68,69].

Most patients with MI are administered nitroglycerin for vasodilatation, often in the form of sublingual/topical spray, Nitrol drip, and/or Nitrol paste. Analgesics are given as needed for pain relief. Morphine sulfate is indicated if the blood pressure is too low or pain is unrelieved by nitroglycerin. The scheduled dose of morphine should be held if the patient's respiratory rate is 10 breaths per minute or less. Other usual medications include stool softeners, calcium channel blockers, beta blockers, antihypertensives, and anticoagulants such as heparin, warfarin, or low-molecular-weight heparin (e.g., enoxaparin) [66,67]. Thrombolysis should be considered.

CHF usually begins in the left ventricular region of the heart and manifests as pulmonary congestion and edema. It is defined as the inability of the heart to pump sufficiently to meet the metabolic needs of the body, causing decreased tissue perfusion due to decreased cardiac output. Heart failure indicates that the heart is unable to adequately perform its function of pumping blood throughout the circulatory system [70]. Left heart failure and right heart failure describe the side of the heart that has the primary impairment. It is helpful to think of heart failure as left or right because the symptoms and signs may provide clues as to the location of the primary problem. Keep in mind, however, that failure of one side of the heart usually leads to failure of the other side. CHF may be acute (pulmonary edema or cardiogenic shock), chronic, or both [71].

Signs and symptoms of left heart failure include [71,72]:

A popular trick for remembering the usual pulmonary manifestation of left-side heart failure is to recall that both of the words "left" and "lung" begin with the letter L.

Right-sided heart failure is caused by pulmonary hypertension (cor pulmonale), left-sided heart failure, or right ventricular infarction. Pulmonary hypertension causes increased pressure the right ventricle must pump against. As a result, the right ventricle cannot empty, leading to hypertrophy and dilation. Right ventricular distention leads to blood accumulating in the systemic venous system. The trick to remembering this correlation is the letter R, for "right" and "rest of the body" [71,72].

Increased venous pressure causes abdominal organ congestion and peripheral edema [72]. Lower extremity edema occurs in patients who are ambulatory, while bedridden patients will experience sacral edema. Liver engorgement will lead to right upper quadrant pain. Anorexia and nausea occur with gastrointestinal venous congestion.

Biventricular failure occurs when a patient experiences signs and symptoms of both left and right failure and jugular venous distention occurs. Peripheral edema is reabsorbed into circulation when the patient goes to bed and feet are elevated, causing fluid overload, pulmonary congestion, and paroxysmal nocturnal dyspnea. In addition, severe heart failure predisposes the patient to dyspnea at rest. S₃ and S₄ heart sounds may be heard [71,72].

Hepatomegaly and splenomegaly result from abdominal engorgement or congestion. Signs include increased abdominal pressure, gastrointestinal problems (e.g., anorexia, nausea, vomiting), decreased digestion, and impaired absorption of nutrients. Dysrhythmias may develop from myocardial distention causing interference with conduction and lowering cardiac output. Cardiogenic shock or acute pulmonary edema may develop as cardiac function deteriorates [71,72].

Nursing assessment includes vital signs, hemodynamic monitoring, heart rhythm, pulse quality (e.g., full, bounding, thready), respiratory status (e.g., dyspnea, shortness of breath, tachypnea), lung sounds (e.g., crackles, rhonchi, wheezing), heart sounds (e.g., S₃ or S₄, murmur or rub), jugular neck vein distention, abdominal assessment (e.g., palpation, distention, ascites), edema, and activity tolerance [73,74]. Diagnostic tests include:

S₁ and S₂ may be diminished as cardiac function fails. S₃ (ventricular gallop) is an early sign of heart failure, and S₄ (atrial gallop) may also be present. Basilar crackles may be heard. Increasing crackles and dyspnea mean worsening of condition and should be reported immediately when heard [19].

Notify the physician if output is equal to or less than 30 cc/hour. Use of diuretics reduces circulating volume and can produce hypovolemia even in the presence of peripheral edema. Decreased urinary output could indicate decreased cardiac output and renal ischemia [18].

Sinus tachycardia has the same configuration as normal sinus rhythm, but the rate is greater than 100 bpm. This can be an early warning sign of cardiac dysfunction, such as heart failure. Patients with sinus tachycardia may be asymptomatic or may experience a "racing" feeling, syncope, and/or dyspnea. This dysrhythmia may be related to episodes of hypotension [76,77].

Chaotic atrial activity causing the atria to quiver (400 to 600 impulses) instead of contracting normally is referred to as atrial fibrillation. It may be intermittent or a chronic rhythm disturbance. In patients with atrial fibrillation, rapid impulse firing from the atrial wall bombards the AV node, resulting in a wavy baseline between rate and rhythm, no visible consistent P waves, and an irregular ventricular response pattern. Atrial fibrillation is most likely to increase the ventricular rate, which decreases diastolic filling time and cardiac output. Clinical signs and symptoms depend on the ventricular response. Peripheral pulses will be irregular and variable in quality. Signs and symptoms of decreased cardiac output are common, including hypotension, shortness of breath, fatigue, angina, syncope, and heart failure. Patients with atrial fibrillation are at high risk for thromboembolic formations due to pooling of blood in the atria and the absence of "atrial kick." Synchronized electrical cardioversion is often necessary to correct atrial fibrillation [76,77].

Premature junctional contraction is an early impulse in the cycle, originating in the AV node. This dysrhythmia originates in the AV node with inverted P waves that may fall before, during, or after the QRS. It is a failsafe mechanism when the SA node does not fire, but it should not remain as the dominant pacemaker. Depolarization of the atria is through retrograde conduction, so any visible P wave will be inverted on the ECG strip. The P wave may be absent or inverted before or behind the QRS. Premature junctional contraction is usually asymptomatic and presents with a slower heart rate (40 to 60 bpm). Some patients will experience signs and symptoms of decreased cardiac output from the absence of "atrial kick" and decreased myocardial tissue perfusion leading to ischemia and potentially signs of heart failure [76,77].

As may be assumed, ventricular dysrhythmias originate in the ventricles (i.e., idioventricular rhythm). They are denoted by wide and bizarre QRS complexes that are greater than 0.12 seconds in duration with increased amplitude, abnormal ST segment, and a T wave that has an opposite deflection from the QRS complex. The P wave will have no relationship to the QRS complex. The inherent rate is 20 to 40 bpm [76,77].

The most common dysrhythmias are PVCs. These dysrhythmias come early in the cycle and are frequently caused by hypokalemia [76,77]. PVCs are usually clinically insignificant in older adults, but frequent, recurrent, or multimodal PVCs indicate myocardial irritability and may precipitate lethal dysrhythmias. If present, signs and symptoms include a feeling of "skipped beats," chest discomfort, dyspnea, hypotension, and dizziness. The incidence is greatest following myocardial ischemia, MI, hypertrophy, or infection. These dysrhythmias may be unifocal or multimodal (i.e., coming from different sites in the ventricular wall). PVCs may also follow specific patterns [76,77]:

Ventricular tachycardia is a rapid ventricular rhythm disturbance defined as three or more consecutive PVCs. It may be a short burst or sustained. The rhythm is usually regular with a rate greater than 100 bpm, and the typical cause is re-entry mechanism. Signs and symptoms include fluttering in the chest, palpitations, shortness of breath, signs of decreased cardiac output, hypotension, loss of consciousness, and no palpable pulses. If left untreated, ventricular tachycardia may deteriorate into lethal rhythm [76,77].

Third-degree AV block (also called complete heart block) occurs when P waves and QRS complexes (ventricular rhythm) are regular but are in no way related to each other. There may or may not be more P waves than QRS complexes, and the PR interval constantly varies. Signs and symptoms are associated with bradycardia, as the rate can be as low as 30 bpm, and decreased cardiac output, including light-headedness, confusion, and syncope. This type of block requires intervention and can be life-threatening, with an 80% mortality rate [76,77].

Many dysrhythmias are treated with the placement of a permanent pacemaker. The most common types of pacemakers in use are atrial demand pacemakers, ventricular demand pacemakers, dual-chamber pacemakers, and ventricular-paced/dual-sensing single chamber pacemakers. Demand pacemakers are used most often. These devices are set at a rate that is individualized for each patient and begin to fire when the patient's heart rate falls to or below a set rate [37].

Endocarditis may result from invasion of pathogenic organisms or injury to the lining of the heart. Infective endocarditis is usually caused by streptococci or staphylococci. Any part of the endothelial lining of the heart may be affected, but the mitral valve is most susceptible. The condition may be classified as either acute or subacute. The process begins with platelet-fibrin vegetation on healthy valves (acute) and on damaged valves or endocardium tissue (subacute). Signs and symptoms of infective endocarditis are murmur, cough, shortness of breath, anorexia, abdominal pain, anemia, splenomegaly, fever (greater than 101.5o F), chills, night sweats, flu-like symptoms, joint pain, mitral valve murmur, arterial emboli, and petechiae in the skin or mucous membranes. With arterial emboli, the patient may present with decreased or absent pulses in the affected extremity, cerebrovascular symptoms related to stroke, abdominal pain related to bowel or spleen infarctions, back pain related to infarction of the kidney, or chest pain related to MI [60,61].

Valvular heart disease encompasses any conditions that interfere with the unidirectional blood flow within the heart. The underlying cause may be either acute (e.g., endocarditis, calcium deposits) or chronic (e.g., rheumatic heart disease). Valvular heart disease presents as stenosis, regurgitation, incompetency of the valve, or a combination of these factors. A stenotic valve impedes blood flow forward, while an incompetent valve does not close after blood has entered the chamber and should be moving forward. Both stenotic and incompetent valves may lead to heart failure. Specific valvular disorders include [2,80]:

The goal of care in the immediate postoperative period is the prevention or early detection of complications of cardiac surgery. Assessment of arterial pressure, pulmonary artery pressures, heart rate, and heart rhythm is done every 15 minutes. A slow rate can indicate heart block. Chest drainage and urinary flow are measured hourly. Blood counts, clotting studies, and ABG measurements are performed regularly. Assessment of neurovascular, abdominal, and pulmonary functions and the circulatory function of the operated leg are performed as ordered. The patient's fluid and electrolyte balances should be monitored. Pulmonary status is particularly important, as atelectasis in the early postoperative period is documented by decreased breath sounds and fever. When patients are extubated, they should perform deep-breathing and coughing exercises every two hours and use an incentive spirometer hourly. Patients on bed rest should perform range-of-motion exercises. Activity will be gradually increased to full accomplishment of activities of daily living.

Four to six hours postprocedure, the most important aspect of nursing care is observing the patient for signs of coronary artery occlusion/ischemia, including chest pain, ECG changes, dysrhythmias, and hypotension. Monitor vital signs every 15 minutes for an hour and then every 30 minutes until stable. A 12-lead ECG should be taken every eight hours over the next 24 hours, and continuous ECG monitoring may be done. Assess the patient's peripheral circulation (e.g., color, warmth, pulses, sensation), mobility, and catheter insertion (for bleeding, hematoma, or infection) every hour for four hours, then every two hours for eight hours, and finally every four hours. Monitor the patient's urinary output every hour and breath sounds every two hours. Maintain pressure on the catheter insertion site until all bleeding has ceased, and keep the head of the bed below 30 degrees. Encourage fluids to assist in the elimination of contrast media used in the procedure. When discharged, teach the patient about the signs and symptoms to report, including chest pressure or heaviness, recurrence of angina pectoris, dizziness, or light-headedness.

It is important to note that the recipient's transplanted heart will have two P waves on the ECG, a higher resting heart rate than normal, and a slower heart response to exercise. Infection is the primary cause of death after heart transplantation, with the highest risk noted in the first three months after surgery. Rejection is the second most common cause of death and may be acute or chronic.

The signs and symptoms of regurgitation may vary based on the affected valve. Mitral valve regurgitation may cause dyspnea, pulmonary hypertension, decreased cardiac output, dizziness, fatigue, tachycardia, angina, murmur or rub, and/or an S₃ or S₄ heart sound [2,80]. If the aortic valve is involved, the patient may present with wide pulse pressure, hyperkinetic (strong, bounding) peripheral pulses, signs and symptoms of CHF, and angina.