Care of the Patient With a Cardiovascular or a Peripheral Vascular Disorder

The cardiovascular (circulatory) system is the transportation system of the body. It delivers oxygen and nutrients to the cells to support their individual activities and transports the cells' waste products to the appropriate organs for disposal. This chapter discusses the structure and function of the blood vessels and the heart.

Heart

The heart is a remarkable organ, not much bigger than a fist (Figure 8-1). It pumps 1000 gallons of blood every day through the closed circuit of blood vessels. It beats 100,000 times a day and transports the blood 60,000 miles through a network of blood vessels. The heart is a hollow organ composed mainly of muscle tissue with a series of one-way valves.

The heart is located in the chest cavity between the lungs in a region called the mediastinum (the organs and tissues separating the lungs; in addition to the heart and its greater vessels, the mediastinum contains the trachea and the esophagus). Two-thirds of the heart lies left of the midline. The wider base of the heart lies superior to and beneath the second rib. The apex, or narrow part, of the heart lies inferiorly, slightly to the left between the fifth and sixth ribs near the diaphragm.

Electrical Conduction System

Heart muscle tissue has an inherent ability to contract in a rhythmic pattern. This ability is called automaticity. If heart muscle cells are removed and placed under a microscope, they continue to beat. In addition, they can respond to a stimulus in the same way that nerve cells do. This unique property is called irritability. Automaticity and irritability are two characteristics that affect the functions of the conduction system. Hormones, ion concentration, and changes in body temperature also affect the conduction of messages around the heart, initiation of heartbeat, and coordination of beating patterns between the atria and the ventricles.

The heartbeat is initiated in the sinoatrial (SA) node, which is located in the upper part of the right atrium, just beneath the opening of the superior vena cava (Figure 8-3). Because it regulates the heartbeat, the SA node is known as the pacemaker. Impulses are passed to the AV node, which is located in the base of the right atrium. The AV node slows the impulses to allow the atrium to complete contraction and to allow the ventricles to fill. The impulses then pass to a group of conduction fibers called the bundle of His, which divides into right and left bundle branches to travel to smaller branches called the Purkinje fibers, which surround the ventricles. The message travels rapidly through the ventricles and causes contractions, which empty the ventricles.

FIGURE 8-3 Conduction system of the heart. Specialized cardiac muscle cells in the wall of the heart rapidly initiate or conduct an electrical impulse throughout the myocardium. The signal is initiated by the sinoatrial (SA) node (pacemaker) and spreads to the rest of the right atrial myocardium directly, to the left atrial myocardium by way of a bundle of interatrial conducting fibers, and to the atrioventricular (AV) node by way of three internodal bundles. The AV node then initiates a signal that is conducted through conduction fibers called the bundle of His, which breaks into right and left bundle branches to travel to smaller branches called the Purkinje fibers, which surround the ventricles. (From Thibodeau GA, Patton KT: Structure and function of the body, ed 14, St. Louis, 2012, Mosby.)

The impulse pathway is as follows:

SA node → AV node → Bundle of His →

Right and left bundle branches → Purkinje fibers

Cardiac Cycle

The cardiac cycle refers to a complete heartbeat. The two atria contract while the two ventricles relax. When the ventricles contract, the two atria relax. The phase of contraction is called systole (Figure 8-4), and the phase of relaxation is called diastole (the period between contraction of the atria or the ventricles during which blood enters the relaxed chambers from the systemic circulation and the lungs [Figure 8-5]). Complete diastole and systole of both atria and ventricles constitute a cardiac cycle; this takes an average of 0.8 second.

FIGURE 8-4 Blood flow during systole. Ao, Aorta; LA, left atrium; LV, left ventricle; PA, pulmonary artery; RA, right atrium; RV, right ventricle. (From Canobbio M: Mosby's clinical nursing series: Cardiovascular disorders, St. Louis, 1990, Mosby.)

FIGURE 8-5 Blood flow during diastole. Ao, Aorta; LA, left atrium; LV, left ventricle; PA, pulmonary artery; RA, right atrium; RV, right ventricle. (From Canobbio M: Mosby's clinical nursing series: Cardiovascular disorders, St. Louis, 1990, Mosby.)

The heart sounds, lubb and dubb, are produced by closure of the valves. The first sound, lubb (long duration and low pitch), is heard when the AV valves close. The second sound, dubb (short duration, sharp sound), is heard when the semilunar valves close. On occasion, a murmur (swishing sound) can be heard. This can be a normal functional phenomenon produced by rapid filling of the ventricles, or it can be an abnormal condition produced by ineffective closure of the valves.

Blood Vessels

Three main types of blood vessels are organized to carry blood to and from the heart: arteries, veins, and capillaries. The heart delivers the blood to large vessels called arteries, which carry blood away from the heart. The arteries branch into smaller vessels called arterioles, which deliver the blood to the tissues. Within the tissues, the arterioles divide into microscopic vessels called capillaries, which form an extensive (50,000-mile) network that allows exchange of products and by-products between the tissues and blood. The capillaries then join to form tiny veins, or venules, that link with larger veins, which carry the blood toward the heart. The pattern is as follows:

Artery → Arteriole → Capillary → Venule → Vein

Circulation

Coronary Blood Supply

To sustain life, the heart must pump blood throughout the body on a continuous basis. As a result, the heart muscle (or myocardium) requires a constant supply of blood containing nutrients and oxygen to function effectively. The delivery of oxygen and nutrient-rich arterial blood to cardiac muscle tissue and the return of oxygen-poor blood from this active tissue to the venous system are called the coronary circulation (Figure 8-6).

FIGURE 8-6 Arterial coronary circulation (anterior). (From Canobbio M: Mosby's clinical nursing series: Cardiovascular disorders, St. Louis, 1990, Mosby.)

Blood flows into the heart muscle by way of two small vessels, the right and left coronary arteries. The coronary arteries wrap around the myocardium (see Figures 8-1 and 8-6). The openings into these vessels lie behind the flaps of the aortic semilunar valves (see Figure 8-6). The coronary arteries bring oxygen and nutrition to the myocardium. Once the circulation is completed and the carbon dioxide and waste products have been collected, the blood flows into a large coronary vein and finally into the coronary sinus, which empties into the right atrium. These two main arteries have many tiny branches that serve the heart muscle. If an artery becomes occluded (blocked or obstructed), these branches provide collateral circulation (alternate routes) to nourish the heart muscle. If the occlusion is severe, surgery and other procedures may be needed. These interventions are discussed later in this chapter.

Systemic Circulation

Systemic circulation occurs when blood is pumped from the left ventricle of the heart through all parts of the body and returns to the right atrium. When the oxygenated blood leaves the left ventricle, it enters the largest artery (1 inch [2.5 cm] in diameter) of the body, the aorta. This is the main trunk of the systemic arterial circulation and is composed of four parts: the ascending aorta, the arch, the thoracic portion of the descending aorta, and the abdominal portion of the descending aorta. As the blood flows through the artery branches, the branches become smaller in diameter (arterioles). The blood continues to flow into the capillaries. The capillaries surround the cells and exchange oxygen and nutrients for carbon dioxide and other waste products. The blood flows to the tiny venules, then to the larger veins, and finally returns to the right atrium via the largest vein, the vena cava (one of two large veins returning blood from the peripheral circulation to the right atrium of the heart).

The blood is now deoxygenated and needs to be replenished with oxygen. In addition, the blood is carrying a high concentration of carbon dioxide. Note that the upper portion of the vena cava (superior vena cava) returns deoxygenated blood from the head, neck, chest, and upper extremities. The inferior vena cava returns deoxygenated blood from parts of the body below the diaphragm.

Pulmonary Circulation

The deoxygenated blood now passes through the pulmonary circulation to pick up the needed oxygen. Blood is pumped from the right atrium to the right ventricle, where it leaves the heart to travel via the pulmonary artery to the lungs. Once the blood reaches the lungs, it travels through arterioles to microscopic capillaries surrounding the alveoli (air sacs), where oxygen diffuses into the bloodstream and carbon dioxide diffuses out. The capillaries then connect with the venules and finally with the four pulmonary veins, which return the oxygenated blood to the left atrium of the heart. It is then pumped to the left ventricle and to the aorta, and the systemic circulation is then repeated. The blood circulation pattern is as follows:

Superior or inferior vena cava → Right atrium →

Tricuspid valve → Right ventricle →

Pulmonary semilunar valve → Pulmonary artery →

Capillaries in the lungs → Pulmonary veins →

Left atrium → Bicuspid valve → Left ventricle →

Aortic semilunar valve → Aorta

Laboratory and Diagnostic Examinations

A number of diagnostic tests are used to evaluate cardiovascular function. The nursing responsibilities are to physically prepare the patient for diagnostic procedures and to explain the examination to the patient.

Diagnostic Imaging

Radiographic examination (i.e., an x-ray) of the chest provides a film record of heart size, shape, and position and outline of shadows. Lung congestion is also shown, indicating heart failure (HF), perhaps in the earliest stages. Pleural effusion (an abnormal accumulation of fluid in the thoracic cavity between the visceral and parietal pleurae) may be noted in left-sided HF. The nurse's role in preparation for this procedure is to explain the reasons for examination and what the examination will show.

Fluoroscopy allows observation of movement, and is invaluable in pacemaker or intracardial catheter placement. Using a fluoroscope, the motion of internal structures such as the heart is examined with a device that emits x-rays that pass through the patient and fluoresce on a special screen, producing a sort of x-ray–based motion picture.

An angiogram is a series of radiographs taken after a contrast medium (dye) is injected into an artery or vein. Picturing the circulatory process aids in diagnosis of vessel occlusion, pooling in various heart chambers, and congenital anomalies. Angiography allows x-ray visualization of the heart, aorta, inferior vena cava, pulmonary artery and vein, and coronary arteries.

In an aortogram, the abdominal aorta and the major leg arteries are examined by x-ray visualization after a contrast medium is injected via a catheter (a thin, flexible tube) passed through the femoral artery and into the aorta. Aneurysms (abnormal bulges in the wall of a blood vessel) and many other abnormalities can be diagnosed. Contrast media may also be used to visualize the aortic arch and branches.

The nurse's role in preparing the patient for the examination is to explain the procedure. Since dye is involved, it is very important to make sure the patient does not have an allergy to ingredients in the dye. This type of procedure requires the patient's informed consent. After the procedure, the nurse checks the site of catheter insertion (usually the groin area) for excess bleeding, ensures that a compression device is in place, and alerts the health care provider if excess bleeding is noted. The nurse also checks for circulation in the periphery below the site, monitors vital signs, and ensures that the patient remains supine (lying face up) for the recommended amount of time.

Cardiac Catheterization and Angiography

Cardiac catheterization is an invasive procedure used to visualize the heart's chambers, valves, great vessels, and coronary arteries. This procedure aids in diagnosis, prevention of progression of cardiac conditions, and accurate evaluation and treatment of the critically ill patient.

In cardiac catheterization, a catheter is passed through a peripheral vessel and into the vessels or chambers of the heart. It can reveal heart abnormalities, such as valvular defects, arterial occlusion, and congenital anomalies. Cardiac catheterization allows (1) measurement of blood pressure within the heart and (2) assessment of the blood in the heart. Blood samples may also be obtained. Contrast dye may be injected to allow better heart and vessel visualization (angiography). Cardiac catheterization is performed under sterile surgical conditions. Its invasive nature requires a prior signed consent from the patient. Because the contrast medium contains iodine, it is important to determine whether the patient is sensitive to iodine before injection, to avoid an allergic reaction. After the procedure, the nurse assesses the circulation to the extremity used for catheter insertion. Peripheral pulses, color, and sensation of the extremity should be checked every 15 minutes for 1 hour and then with decreasing frequency. The puncture site is observed for hematoma and bleeding. The nurse monitors the vital signs and checks for abnormal heart rate, dysrhythmias, and signs of pulmonary emboli (indicated by respiratory difficulty). The patient lies supine for a designated period with a compression device over the pressure dressing at the insertion site to prevent hemorrhage.

Electrocardiography

The electrocardiogram (ECG or EKG) is a graphic study of the electrical activities of the myocardium to determine transmission of cardiac impulses through the muscles and conduction tissue. Each ECG has three distinct waves, or deflections: the P wave, the QRS complex, and the T wave. Depolarization refers to the electrical activity when the heart contracts. Repolarization is the relaxation phase. The P wave represents the depolarization of the atria. The QRS complex represents the depolarization of the ventricles. The T wave represents the repolarization of the ventricles. Atrial repolarization is not represented but does occur; it is covered by the large QRS complex and cannot be seen on the ECG tracing.

A standard ECG has 12 electrodes attached to the skin surface to measure the total electrical activity of the heart. Each lead records the electrical potential between the limbs or between the heart and limbs. A conductive gel enhances the contact and transmission. The patient is typically placed in the supine position; ambulatory ECGs and exercise stress test ECGs require position variation. The machine, an electrocardiograph or galvanometer, records the energy wave of each heartbeat through a vibrating needle on graph paper, which feeds through the machine at a standard rate. Each ECG waveform represents a single electrical impulse as it travels through the heart (Figure 8-7).

FIGURE 8-7 Normal electrocardiographic (ECG) waves, or deflections (From Thibodeau GA, Patton KT: Structure and function of the body, ed 14, St. Louis, 2012, Mosby.)

The ECG tracing is read or interpreted by a cardiac specialist (cardiologist) or by internal medicine specialists, family practitioners, pediatricians, and emergency department practitioners. The reading can also be displayed on the fluorescent screen (oscilloscope) of a cardiac monitor. A graphic tracing may be printed out by the monitor.

Ambulatory ECGs can be used to monitor heart rhythm over prolonged periods—12, 24, or 48 hours—and compared with various activities or symptoms recorded in a diary kept by the patient. A Holter monitor (small portable recorder) is attached to the patient by leads, with a 2-pound tape recorder carried on a belt or shoulder strap. The monitor operates continuously to record the patterns and rhythms of the patient's heartbeat. In conjunction with the diary, the health care provider can note various events, times, and medication peaks that affect or precipitate dysrhythmias. An ambulatory ECG is particularly useful for patients whose clinical symptoms indicate heart disorders but who may have normal ECG tracings on a resting test. Thorough explanation by the health care provider is essential to ensure proper recordings by the patient, since this is an outpatient procedure.

Cardiac Monitors

It is common practice to continuously assess the cardiac electrical activity of patients who are known or suspected to have dysrhythmias or who are prone to develop dysrhythmias or acute cardiovascular symptoms. A cardiac monitor displays information on the electrical activity of the heart transferred via conductive electrodes placed on the chest.

Most monitors provide a visual display of cardiac electrical activity and the patient's heart rate. Preset alarms warn of heart rates that exceed or drop below limits considered acceptable for each patient and also warn of dysrhythmias.

Ambulatory patients (i.e., patients who are able to walk) are increasingly monitored by battery-powered ECG transmitters that do not directly connect the patient to an oscilloscope. This monitoring is called telemetry, which is the electronic transmission of data to a distant location. The electrodes placed on the patient's chest are attached to a transmitter the patient carries in a pocket or pouch. The transmitter sends a radio signal to a receiver, usually located at the nurse's station or a remote location within a hospital.

Patients need telemetry monitoring for various reasons, including a history of cardiac disease, angina pectoris, suspected dysrhythmias, a change in medications, an electrolyte abnormality, or unexplained syncope. Many of these patients are monitored in a centralized area such as an intermediate care or step-down unit (with monitors at the nurse's station). By remote telemetry, a patient on a medical-surgical unit may be monitored at a separate location, called the home unit, which is usually on a critical care unit. Remote telemetry patients are usually stable; but a stable patient's condition can change rapidly, and telemetry allows continuous heart monitoring to detect abnormalities.

Attachment to a cardiac monitor does not change a patient's need for nursing interventions. The monitoring electrodes are placed on the anterior thorax (chest) rather than the extremities, enabling the patient to be relatively free to carry on usual activities. Pay special attention to the electrode site to ensure a constant tight seal between the electrode and the skin and to note the development of any skin impairment. The conduction gel dries out, even if the pad is sealed; changing electrodes regularly is recommended. Check the telemetry pack for integrity of the lead wires and test the monitoring device's battery with a battery tester. Inform the monitoring area whenever the patient is moved off the unit for a diagnostic test, since the patient may go outside the monitor's range. Another important safety measure is never to remove the telemetry device and allow the patient to shower unless the health care provider has written the order to allow a shower. The patient could be subject to severe dysrhythmia, which would not be detected with the telemetry device removed.

Exercise-stress ECG is another form of monitoring the heart's capability, this time in a laboratory setting while the patient performs a prescribed exercise. Tasks include use of treadmills, stair climbing, and aerobic exercise. While being monitored carefully, the patient is coaxed to a limit of exertion to evaluate myocardial ischemia (reduced oxygen in the heart due to insufficient blood flow), dysrhythmia, and cardiac capability under extreme circumstances. The test sets the limit of exercise tolerance in cardiac disease. If the patient is unable to tolerate activity, a stress test can be done by administering dipyridamole (Persantine) or adenosine (Adenocard), which makes the patient's heart respond as if it were under stress or activity.

Thallium Scanning

Thallium-201 is a radioactive isotope (radioisotope) that is actively transported into normal cells. If the cells are ischemic or infarcted, the thallium will not be picked up. Thallium concentrates in tissue with normal blood flow; tissue with inadequate perfusion appears as dark areas on scanning—a “cold spot.” The radioisotope is injected intravenously while the patient exercises on a treadmill. (Note: Breast tissue in the female can produce artifact, leading to a false-positive result. Technetium-99 m sestamibi may be used instead of thallium to minimize artifact and thus improve accuracy.) In a patient who cannot tolerate physical exercise, dipyridamole is given before the thallium to physiologically simulate exercise-induced stress. After the procedure is over, caution the patient to avoid driving for the next 4 hours, and to stand slowly from a sitting or lying position to avoid orthostatic hypotension during that time.

Echocardiography

Echocardiography uses high-frequency ultrasound directed at the heart. The echo, or reflected sound, is graphically recorded as a sonogram, outlining the size, shape, and position of cardiac structures. This test is used to detect pericardial effusion (collection of blood or other fluid in the pericardial sac), ventricular function, cardiac chamber size and contents, ventricular muscle and septal motion and thickness, cardiac output (ejection fraction), cardiac tumors, valvular function, and congenital heart disorder.

The ventricular ejection fraction (EF) on an echocardiogram can be gauged as follows:

• Normal: 55% to 70%

• Moderate HF: 40% to 55% (indicates damage, perhaps from a previous heart attack but not necessarily heart failure)

• Moderate to severe HF: Less than 40%

Positron Emission Tomography

Positron emission tomography (PET) is a computerized radiographic technique that uses radioactive substances to examine the metabolic activity of various body structures. In PET studies the patient either inhales or is injected with a radioactive biochemical substance. A computer interprets the data, depicting the various levels of metabolic activity as color-coded images. Used to study dementia, stroke, epilepsy, and tumors, PET is also useful in the diagnosis and treatment of cardiac disease. The ability of PET to distinguish between viable and nonviable myocardial tissue allows health care providers to identify the most appropriate candidates for bypass surgery or angioplasty. PET is also able to accurately detect coronary artery disease (CAD) noninvasively in an asymptomatic patient, prompting early intervention that can salvage a potentially ischemic myocardium.

MUGA Scan

A MUGA (multigated acquisition) scan uses a radioactive tracer and a special camera. The camera takes pictures of the heart as it pumps. The test may be done while the patient is resting, exercising, or both. This test is considered a noninvasive procedure, although a radioisotope is injected to assess the ejection fraction of the left ventricle.

Before the procedure begins, the nurse ensures that the patient has had no food or drink for at least 6 hours before the test and has avoided caffeine and tobacco use as well.

After the scan is done, the nurse should encourage the patient to drink plenty of fluids to flush out the radioactive dye. The patient should be able to resume normal activities after the procedure.

Laboratory Tests

The history, physical examination, and blood studies help the health care provider diagnose and monitor the cardiovascular disease process. The nurse's responsibility is to prepare the patient by explaining what the tests are for and the preparation required for each test.

Blood cultures to detect growth of bacteria in the blood are crucial to the diagnosis of infective endocarditis.

A complete blood count (CBC) is a determination of the number of red blood cells (erythrocytes) and white blood cells (WBCs; leukocytes) per cubic millimeter, as well as the proportions of the various kinds of white blood cells (the WBC differential), platelets, hemoglobin, and hematocrit (the volume percentage of red blood cells in whole blood). Lower hemoglobin levels reduce the ability of the blood to carry oxygen to the cells, resulting in anemia. An elevated WBC count indicates infection or inflammation. An elevated red blood cell count indicates that the body is compensating for chronic hypoxemia (an abnormal deficiency of oxygen in the arterial blood) by stimulating red blood cell production by the bone marrow, leading to secondary polycythemia (an abnormal increase in the number of red blood cells in the blood). Chronic hypoxemia is often found in heart failure.

Coagulation studies include prothrombin time (PT), international normalized ratio (INR), and partial thromboplastin time (PTT). These studies are used to monitor the patient receiving anticoagulant drug therapy, which is prescribed for patients after a myocardial infarction (MI) to dissolve the thrombus. Coagulation studies are also used in patients with chronic atrial fibrillation or those with atrial fibrillation who are undergoing electrical cardioversion (restoring the heart's normal sinus rhythm by delivering a synchronized electric shock through two metal paddles placed on the patient's chest).

The erythrocyte sedimentation rate (ESR) is determined to monitor or rule out inflammatory/infective conditions. The ESR is elevated with MI and infective endocarditis and decreases when healing begins. The ESR also indicates the extent of inflammation and infection in rheumatic fever.

Serum electrolyte tests focus on the body's balance of sodium, potassium, calcium, and magnesium, which are necessary for myocardial muscle function. Sodium (Na⁺) helps maintain fluid balance. Potassium (K⁺) is required for relaxation of cardiac muscle, and calcium (Ca²⁺) is necessary for contraction of cardiac muscle. Magnesium (Mg²⁺) helps maintain the correct level of electric excitability in the nerves and the muscles, including the myocardium and the cardiac conduction system. The health care provider compares serum electrolyte levels with ECG changes.

Serum lipids are associated with vascular disease, particularly CAD. Cholesterol and triglycerides bound to plasma proteins are found in the blood as lipoproteins. Density levels vary according to the protein-to-fat ratio. An elevated level of high-density lipoprotein (HDL) is desired, but an elevated level of low-density lipoprotein (LDL) or very-low-density lipoprotein (VLDL) increases the risk for cardiovascular disease (Box 8-1).

Box 8-1

Cholesterol Numbers

What Do They Mean?

YOUR TOTAL CHOLESTEROL NUMBER	TOTAL CHOLESTEROL LEVEL
A total cholesterol level less than 200 mg/dL is considered desirable	Desirable: Less than 200 mg/dL Borderline: 200 mg/dL to 239 mg/dL High: 240 mg/dL or greater
HDL CHOLESTEROL NUMBER	HDL CHOLESTEROL LEVEL
The higher the HDL cholesterol level, the better, because this means that there are more good lipoproteins to remove adhered cholesterol from the arteries	Low: Less than 40 mg/dL in men and Less than 50 mg/dL in women. High: Greater than 60 mg/dL
LDL CHOLESTEROL NUMBER	LDL CHOLESTEROL LEVEL
The higher the number of bad lipoproteins, or LDLs, in the blood, the more likely it is that cholesterol is beginning to adhere to the arteries. Monitor risk factors to assess for probability of development of heart disease	Optimal: Less than 100 mg/dL Near to above optimal: 100-129 mg/dL Borderline high: 130-159 mg/dL High: 160-189 mg/dL Very high: Greater than 190 mg/dL
SET LDL CHOLESTEROL GOAL
Once the LDL cholesterol number is known, one can change the diet to help lower the amount of cholesterol in the blood. The table below shows the target LDL cholesterol goal. Reducing the risk factors is important too, so health care providers must make recommendations to assist the patient in maintaining acceptable cholesterol levels.

	START DIET TREATMENT IF:
RISK FACTORS	LDL CHOLESTEROL IS:	THE LDL GOAL IS:
No heart disease and fewer than two risk factors other than high LDL cholesterol	160 mg/dL or more	Less than 160 mg/dL
No heart disease but two or more risk factors other than high LDL cholesterol	130 mg/dL or more	100 mg/dL or less
Definite heart disease or arterial disease	100 mg/dL or more	Less than 130 mg/dL

HDL, High-density lipoprotein; LDL, low-density lipoprotein.

Modified from Third Report of the Palmaz-Schatz stent, an articulated stainless steel mesh deployed by balloon inflation. (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults, 2001.

Arterial blood gases are measured to monitor oxygenation (PaO₂, the partial pressure of oxygen in the blood; and PaCO₂, the partial pressure of carbon dioxide in the blood) and acid-base balance (pH). These tests are used to monitor blood oxygenation in patients with unstable cardiac conditions and to evaluate patients in cardiac failure.

Serum cardiac markers are certain proteins released into the circulation in large quantities when cardiac cells die (National Library of Medicine, 2012a). These markers, specifically serum cardiac enzymes and troponin I, are important screening diagnostic criteria for an acute MI. The increase in serum cardiac enzymes that occurs after cell death can show whether cardiac damage is present and the approximate extent of the damage. The levels of cardiac enzyme creatine kinase (CK) and its isoenzyme, creatine phosphokinase (CK-MB), start to rise within 2 to 3 hours after the beginning of an MI, peak in 24 hours, and return to normal within 24 to 40 hours. CK and CK-MB have been the “gold standard” for years, but they have been replaced with troponins I and T. CK-MB is also found in skeletal muscle and its blood level can be elevated by surgery, muscle trauma, and muscle diseases, making the differential diagnosis more difficult, so it is not a specific indicator for MI.

Troponins are myocardial muscle proteins released into the circulation after a myocardial injury. In the heart there are two subtypes: cardiac-specific troponin T and troponin I. These sensitive markers can indicate a very small amount of myocardial damage. Troponin T appears in the blood 3 to 5 hours after an MI, and its level may remain elevated for up to 21 days. Like CK-MB, the level of troponin T is affected by skeletal muscle injury and renal disease. Troponin I is a sensitive and specific cardiac marker, not influenced by skeletal muscle trauma or renal failure. The troponin I level rises 3 hours after MI, peaks at 14 to 18 hours, and returns to normal in 5 to 7 days. Troponin I is useful in diagnosing an MI (American Heart Association, 2013a). The ability to measure the myocardial contractile proteins (troponins) in serum, which are often present in very small amounts, is a major advance in the diagnosis of acute MI and acute myocardial damage.

Myoglobin is released into circulation within a few hours after an MI. Although it is one of the first serum cardiac markers that increase after an MI, myoglobin is also present in skeletal muscle, so an increase can be associated with noncardiac causes. In addition, it is rapidly excreted in urine, and blood levels return to normal range within 24 hours after an MI.

B-type natriuretic peptide (BNP) is a hormone secreted by the heart in response to ventricular expansion and pressure overload. A BNP level above 100 pg/mL indicates HF. The higher the BNP level, the more severe the HF (American Heart Association, 2013a).

Homocysteine is an amino acid produced during protein digestion. Normal values range from 4 to 14 µmol/L. Elevated blood levels of homocysteine may be an independent risk factor for ischemic heart disease, cerebrovascular disease, peripheral arterial disease (PAD), and venous thrombosis. Homocysteine appears to promote the progression of atherosclerosis by causing endothelial damage, promoting LDL deposits, and stimulating vascular smooth muscle growth. Homocysteine plays an important role in blood clotting. An elevated level results in increased platelet aggregation. Screening for elevated homocysteine levels (greater than 14 µmol/L) should be considered in patients with progressive and unexplained atherosclerosis despite normal levels of lipoproteins and who have no other risk factors. It is also recommended in patients with an unusual family history of atherosclerosis, especially at a young age.

Dietary deficiency of vitamins B₆ (pyridoxine), B₁₂ (cobalamin), or folate is the most common cause of elevated homocysteine. Some researchers believe that an elevated level of homocysteine can be treated by giving vitamins B₆, B₁₂, and folate. Whether this treatment will reduce the incidence of MI remains to be proven (American Heart Association, 2013a).

The liver produces C-reactive protein (CRP) during periods of acute inflammation. The presence of CRP is a predictor of cardiac events and is emerging as an independent risk factor for CAD. People with diabetes mellitus are already at high risk for developing cardiovascular disease. If a patient has both an elevated level of CRP and diabetes, the risk for a cardiovascular disorder becomes even greater (Pagana and Pagana, 2008).

Disorders of the Cardiovascular System

Cardiovascular disorders are a major health care problem in the United States. Public awareness, modifications in lifestyle, and improvements in medical treatment have contributed to a decline in overall deaths. The nurse's role in caring for patients with cardiovascular disorders includes being aware of the prevalence of cardiac disease, risk factors, and the disease process; implementing nursing interventions; and patient teaching.

Effects of Normal Aging on the Cardiovascular System

By the time an individual reaches the age of 65 years, physiologic changes have reduced the heart's efficiency as a pump. Yet the heart still is capable of functioning adequately unless there is underlying cardiac disease (see Lifespan Considerations box). According to the National Heart, Lung, and Blood Institute (2011), all Americans should have their cholesterol levels checked once every 5 years. Older adults with high cholesterol should take steps to lower their cholesterol levels, including taking cholesterol-lowering medications, stopping smoking, increasing their activity levels, continuing their blood pressure medications, decreasing their weight, and, if they have diabetes, continuing to control their blood glucose level.

Lifespan Considerations

Older Adults

Cardiac Disease

• Changes in the cardiac musculature lead to reduced efficiency and strength, resulting in decreased cardiac output.

• Disorientation, syncope, and decreased tissue perfusion to organs and other body tissues can occur as a result of decreased cardiac output.

• Aging causes sclerotic changes in blood vessels and leads to decreased elasticity and narrowing of the lumen. Arterial disease resulting from the aging process causes hypertension because of the increased cardiac effort needed to pump blood through the circulatory system.

• Progressive coronary artery changes can lead to the development of collateral coronary circulation. This can modify the severity of signs and symptoms seen in MI. Angina symptoms may be less pronounced, and dyspnea may replace angina as a key symptom of acute infarction.

• Heart failure can result from rapid intravenous infusion.

• Edema secondary to heart failure may cause tissue impairment in the immobile older adult. Immobility leads to venous stasis (i.e., a slowing or stoppage of venous blood flow), venous ulcer, and poor wound healing. It also increases the risk of venous thrombosis and embolus formation.

• Older adults with cardiac disease often receive several medications, which are often prescribed at lower doses than for younger adults. Even with lower doses of medications, observe the older adult closely for signs of toxicity, since the rate of drug metabolism and excretion decreases with age.

• Independent older adults with cardiac conditions should receive adequate teaching regarding medication, diet, and warning signs of complications. Encourage them to maintain regular contact with the health care provider and to seek care at the first sign of problems.

Risk Factors

Risk factors indicate predispositions for developing cardiovascular disease. The presence of more than one risk factor is associated with an increased risk for developing cardiovascular disease. Risk factors are classified as nonmodifiable and modifiable.

Nonmodifiable Factors

An important aspect of caring for the patient with a cardiovascular disorder is understanding the risk factors for cardiovascular disease and incorporating them into patient teaching. The nonmodifiable risk factors (risk factors that cannot be changed) associated with cardiovascular disorders include age, genetics, and heredity.

Family history.

A family member such as a parent or sibling who has a cardiovascular problem before 50 years of age puts the patient at greater risk for developing cardiovascular disease.

Age.

Normal physiologic changes that occur with aging and past lifestyle habits increase the patient's risk for developing cardiovascular disease with advancing age. CAD and MI occur most frequently among white, middle-aged men.

Gender.

Middle-aged men are at greater risk of developing cardiovascular disease than middle-aged women. Although the incidence in men and women equalizes after age 65, cardiovascular disease is a more common cause of death in women than in men. Women develop CAD about 10 years later than men because natural estrogen may have a cardioprotective effect before menopause. Despite this, the incidence of cardiovascular disease in women 50 years of age and older is increasing. Factors possibly responsible are increased social and economic pressures on women and changes in lifestyle. Ten times more women die from heart disease than die from breast cancer. The mortality rate for women with CAD has remained relatively constant even though cardiovascular disease remains the leading cause of death. Despite this statistic, only 15% of women consider CAD their greatest health risk. Recent research on CAD has shown that women often do not have the same signs and symptoms of an acute coronary event as those that are commonly seen in men (American Heart Association, 2012a).

Cultural and ethnic considerations.

African American men have a higher incidence of hypertension than do white men. African American women have a higher incidence of CAD, with greater severity and higher death rates, than do white women (American Heart Association, 2012a). Hispanics have rates similar to those of African Americans and whites. Heart disease is second only to cancer in American Indians, Alaska Natives, Asians, and/or Pacific Islanders (Centers for Disease Control and Prevention [CDC], 2011).

Modifiable Factors

Smoking.

Individuals who smoke cigarettes have a two to three times greater risk of developing cardiovascular disease than nonsmokers. The degree of risk is proportional to the number of cigarettes smoked. Individuals who quit smoking decrease their risk. Tobacco smoke contains nicotine, which causes the release of catecholamine (i.e., epinephrine, norepinephrine). Catecholamine release causes tachycardia, hypertension, and vasoconstriction of the peripheral arteries, which in turn increase the work of the heart and result in greater myocardial oxygen consumption (American Heart Association, 2011). Nicotine reduces the amount of available oxygen to the heart muscle. Nicotine also increases platelet adhesion, which results in increased risk of embolism (American Heart Association, 2011).

Hyperlipidemia.

Hyperlipidemia is elevated concentrations of any or all lipids in the plasma. The ratio of HDL to LDL is the best predictor for the development of cardiovascular disease. Density levels vary according to the protein-to-fat ratio:

• VLDL contains more fat than protein (primarily triglycerides); triglycerides are the main storage form of lipids and constitute approximately 95% of fatty tissue.

• LDL contains an equal amount of fat and protein (approximately 50%) with moderate amounts of phospholipid cholesterol.

Less than 100 mg/dL	Optimal
100 to 129 mg/dL	Near optimal to above optimal
130 to 159 mg/dL	Borderline high
160 to 189 mg/dL	High
More than 190 mg/dL	Very high

• HDL contains more protein than fat (which serves a protective function, removing cholesterol from tissues). It is suspected that HDL also removes cholesterol from the peripheral tissues and transports it to the liver for excretion. HDL may have a protective effect by preventing cellular uptake of cholesterol and lipids. Low levels (less than 40 mg/dL) are believed to increase a person's risk for CAD, whereas high levels (more than 60 mg/dL) are considered protective (see Box 8-1).

A diet high in saturated fat, cholesterol, and calories contributes to hyperlipidemia. Therefore dietary control is an important aspect in modifying this risk factor. An overall serum cholesterol level of less than 200 mg/dL is desirable, 200 to 239 mg/dL is borderline high, and more than 239 mg/dL is high.

Change in diet is probably the most important method of lowering cholesterol level. Weight reduction in overweight patients with abnormal lipid profiles is an essential element of dietary intervention. In addition to lowering LDL levels, weight reduction leads to decreases in triglyceride level and blood pressure. A combination of weight reduction and physical exercise improves the lipid profile, with a decrease in LDL level, an increase in HDL level, and a decrease in triglyceride levels. Low HDL levels are often familial and only somewhat modifiable.

Cholesterol-lowering drugs are often included in treatment of hyperlipidemia. Cholesterol-lowering drugs are divided into six classes: (1) bile acid sequestrants; (2) nicotinic acid (niacin); (3) statins such as simvastatin (Zocor), pravastatin (Pravachol), and rosuvastatin (Crestor); (4) fibric acid derivatives such as gemfibrozil (Lopid) and probucol (Lorelco); (5) the cholesterol absorption inhibitor ezetimibe (Zetia); and (6) combination drugs such as ezetimibe and simvastatin (Vytorin). Pravastatin reduces the risk of a first MI by about one-third in hypercholesterolemic patients with no history of coronary disease. Simvastatin is now allowed by the U.S. Food and Drug Administration (FDA) to add a label statement that the drug can reduce deaths by lowering cholesterol.

Hypertension.

Hypertension is called the “silent killer” because a patient with elevated blood pressure does not display signs and symptoms of heart disease until damage has begun to develop. This damage increases the risks of heart disease, stroke, heart failure, or cardiovascular death. Prehypertension is defined as blood pressure of 120 to 139/80 to 89 mm Hg, which requires monitoring yearly to decrease a patient's risk of developing cardiac disease.

Hypertension is blood pressure higher than 140/90 mm Hg, taken on two separate occasions. Adhering to diet, exercise, and the prescribed pharmacological therapies to control elevated blood pressure helps modify the individual's risk.

Diabetes mellitus.

Cardiac disease has been found to be more prevalent in individuals with diabetes mellitus. Diabetes poses a greater risk than other factors, possibly because an elevated blood glucose level damages the arterial intima (the innermost layer of an artery) and contributes to atherosclerosis. Patients with diabetes also have alterations in lipid metabolism and tend to have high cholesterol and triglyceride levels. Keeping the blood glucose level under control helps modify the individual's risk. The CDC estimates that 68% of people with diabetes over the age of 65 will have heart disease (CDC, 2010). Adults with diabetes and heart disease are two to four times more likely than adults without diabetes to die from cardiac-related complications. Blood pressure control decreases these risks by 33% to 50%. In general, every 10-mm Hg drop in systolic blood pressure decreases the risk by 12%. Patients with diabetes who decrease their diastolic blood pressure by 10 mm Hg decrease their chance of a cardiovascular event by 50%.

Obesity.

Excess body weight increases the workload of the heart. It also contributes to the severity of other risk factors. The CDC estimates that 35.7% of Americans are obese. This correlates to 97 million Americans with a body mass index (BMI) of 30 or above. As the BMI increases, so do the risk factors for developing diabetes, cardiovascular events, and stroke. A weight reduction program and maintaining an ideal body weight help modify the individual's risk.

Sedentary lifestyle.

Lack of regular exercise has been correlated with an increased risk of developing cardiovascular disease. Regular aerobic exercise can improve the heart's efficiency and help lower the blood glucose level, improve the ratio of HDLs to LDLs, reduce weight, lower blood pressure, reduce stress, and improve overall feelings of well-being. Individuals with sedentary lifestyles should work with their health care provider to plan an exercise program that fits their lifestyle. Some health care providers define regular physical exercise as exercising at least three to five times a week for at least 30 minutes, causing perspiration and an increase in heart rate by 30 to 50 beats per minute (bpm). Yoga has been receiving increasing research as a form of exercise that increases musculoskeletal strengthening, flexibility, and relaxation. Yoga movements also have therapeutic cognitive effects of distraction and mindfulness, thereby reducing stress on the body. Another form of exercise receiving national attention is walking. Walking is one of the best forms of exercise because it is the simplest and easiest way to exercise. Walking can strengthen bones, tune up the cardiovascular system, and clear a cluttered mind. Walking is a remedy for stress as well.

Stress.

The body's stress response releases catecholamines that increase the heart rate. Catecholamines are hormones produced by the adrenal glands and released during times of physical and emotional stress. Catecholamines also affect myocardial cells and may cause cellular damage. The vasoconstriction that occurs may contribute to the development of cardiovascular disease. Stress reduction measures may help modify an individual's risk.

Psychosocial factors.

In the early 1970s, health care providers used the term “type A personality” to describe a person who is always in a hurry, impatient, and irritable, or always angry or hostile. Recent studies have found that the term type A does not always fit the person with cardiovascular risks. More recent studies have found that the type D personality is more likely to suffer from increased cardiovascular symptoms. The person with a type D personality has chronic negative emotions, is pessimistic, and socially inhibited. Type D personalities tend to have increased levels of anxiety, irritation, and depressed mood across most situations and times. Type D people do not share their feelings because they fear disapproval, thereby increasing their chance of a cardiovascular event.

Cardiac Dysrhythmias

A cardiac dysrhythmia (or arrhythmia) is any cardiac rhythm that deviates from normal sinus rhythm. Normal sinus rhythm originates in the SA node and is characterized by the following:

• Rate: 60 to 100 bpm

• P waves: Precede each QRS complex (atrial depolarization)

• P-R interval: Interval between atrial and ventricular repolarization

• QRS complex: Ventricular depolarization

• T wave: Ventricular repolarization

• Rhythm: Regular

A dysrhythmia is the result of an alteration in the formation of impulses through the SA node to the rest of the myocardium. It also results from irritation of the myocardial cells that generate impulses, independent of the conduction system. Signs and symptoms of dysrhythmia vary, as do treatment options, depending on the type and severity of the dysrhythmia. A short overview of each dysrhythmia follows.

Types of Cardiac Dysrhythmias

Sinus tachycardia.

Sinus tachycardia is a rapid, regular rhythm originating in the SA node. It is characterized by a heartbeat of 100 to 150 bpm or more.

Causes of sinus tachycardia include exercise, anxiety, fever, shock, medications, HF, excessive caffeine, recreational drugs, and tobacco use. Tachycardia increases the amount of oxygen delivered to the cells by increasing the amount of blood circulated through the vessels.

Clinical manifestations include occasional palpitations. Many patients are asymptomatic. Other signs and symptoms may include hypotension and angina, if cardiovascular disease is also present.

Medical management is directed at the primary cause. This is a normal rhythm and is not usually caused by a cardiac problem.

Sinus bradycardia.

Sinus bradycardia is a slow rhythm originating in the SA node. It is characterized by a pulse rate of less than 60 bpm. Bradycardia can be life-threatening if the cause is not found. Bradycardia caused by an SA node dysfunction or other undetermined causes may be managed by the insertion of a pacemaker. Causes of sinus bradycardia include obstructive sleep apnea, vomiting, intracranial tumors, MI, medications (especially overuse of digitalis, beta-adrenergic blockers, or calcium channel blockers), carotid sinus massage, vagal stimulation, endocrine disturbances, increased intracranial pressure, and hypothermia. When found in association with MI, it is a beneficial rhythm because it reduces myocardial oxygen demand. An athlete's resting heart rhythm may normally be slow, because of the training the athlete undergoes.

Clinical manifestations of bradycardia may not be manifested in some patients until the heart drops to the 50s and may include fatigue, lightheadedness, and syncope. Some patients are asymptomatic.

Medical management is directed toward the primary cause of the problem and maintaining cardiac output. If the cause is determined to be vagal stimulation, such as when bearing down with a bowel movement or vomiting, a stool softener is given or medication to stop the vomiting, and the patient is taught how to stop vagal stimulation. Atropine (Atreza, Sal-Tropine) may be prescribed to increase the heart rate. A temporary or permanent, implantable pacemaker is sometimes necessary (Figures 8-8 and 8-9). If the cause is suspected to be drug related, blood is drawn and the drug concentration is determined; if necessary, the drug is withheld.

FIGURE 8-8 A, Ventricular pacing. Impulses are initiated in the right ventricle. B, Atrial pacing. Impulses are initiated in the right atrium and travel to the ventricles via the normal conduction system through the atrioventricular (AV) node. LA, Left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

FIGURE 8-9 A, A dual-chamber, rate-responsive pacemaker from Medtronic, Inc., is designed to detect body movement and automatically increase or decrease paced heart rates based on the level of physical activity. B, Cardiac leads, in both the atrium and the ventricle, enable a dual-chamber pacemaker to sense and pace in both heart chambers. (From Black JM, Hawks JH: Medical-surgical nursing: Clinical management for positive outcomes, ed 8, St. Louis, 2009, Mosby.)

Supraventricular tachycardia.

Supraventricular tachycardia (SVT) is the sudden onset of a rapid heartbeat. It originates in the atria. It is characterized by a pulse rate of 150 to 250 bpm.

Causes of SVT include medications, alcohol, mitral valve prolapse, emotional stress, smoking, and hormone imbalance such as decreases in estrogen in postmenopausal women. The cause is typically not associated with heart disease. Clinical manifestations include palpitations, lightheadedness, dyspnea, and anginal pain.

Medical management first looks at how well the patient tolerates the dysrhythmia and at the overall clinical picture. The focus is aimed at decreasing the heart rate and eliminating the underlying cause. Specific treatments may include carotid sinus pressure, adenosine, digoxin (Lanoxin), calcium channel blockers (e.g., diltiazem [Cardizem]), beta-adrenergic blockers, propranolol (Inderal), antidysrhythmics, amiodarone (Cordarone), and cardioversion. Persistent, recurring SVT caused by the presence of an accessory pathway (i.e., a second, abnormal electrical conduction pathway; see Electrical Conduction System, above) may ultimately be treated by radiofrequency catheter ablation (i.e., cutting away or eradication) of the accessory pathway.

Atrial fibrillation.

In atrial fibrillation, electrical activity in the atria is disorganized, causing the atria to fibrillate, or quiver, rather than contract as a unit. Atrial fibrillation is a very rapid production of atrial impulses. The atria beat chaotically and are not contracting properly. It is characterized by an atrial rate of 350 to 600 bpm. If untreated, the ventricular response rate may be 100 to 180 bpm.

Causes of atrial fibrillation include cardiac surgery, longstanding hypertension, pulmonary embolism, atherosclerosis, mitral valve disease, HF, cardiomyopathy, congenital abnormalities, chronic obstructive pulmonary disease, and thyrotoxicosis. Clinical manifestations include pulse deficit, palpitations, dyspnea, angina, lightheadedness, syncope, fatigue, change in level of consciousness, and pulmonary edema. Because of ventricular rhythm irregularity and ineffective atrial contractions, decreased cardiac output may be noted, resulting in HF, angina, and shock. Thrombi (blood clots) may form in the atria as a result of ineffective atrial contraction and cause emboli (i.e., thrombi that have moved from one point in the body to another), thus affecting the lungs or periphery. An embolized clot may pass to the brain, causing a stroke. Risk of stroke increases fivefold with atrial fibrillation. Risk of stroke is even higher in patients who have structural heart disease, hypertension, and are over 65 years of age.

Medical management focuses on treating the irritability of the atria, slowing the ventricular response to atrial stimulation, and correcting the primary cause. The goal of therapy is to prevent atrial thrombi from developing and embolizing, such as in the lungs or periphery. Specific pharmacologic treatments to achieve cardioversion may include (1) digitalis; (2) calcium channel blockers such as intravenous (IV) diltiazem (Cardizem) and verapamil (Calan, Isoptin); (3) antidysrhythmics such as procainamide (Procan SR, Pronestyl), amiodarone (Cordarone), dofetilide (Tikosyn), flecainide (Tambocor), and propafenone (Rythmol) (American Heart Association, 2012); and anticoagulants such as heparin and warfarin (Coumadin). Outpatients typically take oral warfarin to maintain anticoagulation. The goal of anticoagulation is to maintain an INR between 2 and 3. If pharmacologic cardioversion fails, the patient may need electrical cardioversion. Transesophageal echocardiography (TEE) is used to detect a thrombus in the atria before proceeding with electrical cardioversion. The Joint Commission recommends that patients with atrial fibrillation be prescribed warfarin and long-term antidysrhythmic medication therapy at discharge.

There are several new anticoagulants on the market that are also being prescribed to treat deep-vein thrombosis (DVT) and atrial fibrillation. Pradaxa (dabigatran etexilate mesylate) and Xarelto (rivaroxaban) are two of the newest that have been approved for this use. Unlike warfarin (Coumadin), these drugs do not require continuing modification of the dosages. Although these drugs do not require modification of dosages and long-term determination of PT, PT/INR blood levels, there are still issues with the drugs. Please see the Safety Alert box for drugs that interact unfavorably with Xarelto.

For patients who do not respond to medication therapy or electrical conversion, catheter ablation (cutting or removal) with radiofrequency energy is used to destroy the areas in the atria that trigger abnormal electrical signals. The catheter is inserted into the femoral vein and threaded via fluoroscopy to the heart. The special ablation catheter is placed in strategic areas, and bursts of radiofrequency energy destroy the irritable area (American Heart Association, 2012b).

Catheter ablation to treat atrial fibrillation is usually performed on younger patients because of a better response rate and fewer complications than in the older adult. After the catheter ablation procedure, perform neurovascular assessment checks at the peripheral sites distal to the catheter insertion site (American Heart Association, 2011).

Atrioventricular block.

AV block occurs when a defect in the AV junction slows or impairs conduction of impulses from the SA node to the ventricles. Three types of blocks are seen: first degree, second degree, and third degree. A third-degree block indicates worsening of the impairment at the AV junction and a complete heart block.

Common causes of AV block include atherosclerotic heart disease (ASHD), MI, and heart failure (HF). Other causes may be digitalis toxicity, congenital abnormality, drugs, and hypokalemia (low potassium in the blood).

First-degree heart block is often asymptomatic. Vertigo, weakness, and irregular pulse are seen with second-degree block. Disease that is progressing, as with third-degree block, will be accompanied by hypotension, angina, and bradycardia. The heart rate is often quite low, often in the 30s.

Medical management involves evaluating the patient's response and determining the cause of the dysrhythmia. Atropine and isoproterenol may be prescribed. A pacemaker frequently is needed with third-degree block (see Figure 8-8).

Premature ventricular contractions.

Premature ventricular contractions (PVCs) are abnormal heartbeats that arise from the right or left ventricle. PVCs are early ventricular beats that occur in conjunction with the underlying rhythm, which is unchanged except for the PVC itself.

PVCs may originate from more than one location in the ventricles and be caused by irritability of the ventricular musculature, exercise, stress, electrolyte imbalance, digitalis toxicity, hypoxia, and MI.

Clinical manifestations depend on the frequency of PVCs and their effect on the heart's ability to pump blood effectively. Some patients are asymptomatic; others may experience palpitations, weakness, and lightheadedness. Other symptoms are associated with decreased cardiac output.

Medical management focuses on treating the underlying heart condition. Symptomatic PVCs can be treated with beta-adrenergic blockers such as carvedilol (Coreg), antianginals, propranolol (Inderal), and antidysrhythmics such as procainamide, amiodarone, or lidocaine (Xylocaine).

A PVC may be a single event or may occur several times in a minute or in pairs or strings. PVCs that last long enough to cause ventricular tachycardia may lead to death.

Ventricular tachycardia.

Ventricular tachycardia (VT) occurs when three or more successive PVCs occur. In VT the ventricular rate is greater than 100 bpm (usually 140 to 240 bpm). The rhythm is regular or slightly irregular. Conditions that can cause its occurrence include hypoxemia, drug toxicity such as with digitalis or quinidine, electrolyte imbalance (e.g., potassium, magnesium), and bradycardia. Repeated and prolonged episodes of VT in the second week after MI may be a warning of ventricular fibrillation and require aggressive evaluation and treatment.

Medical management focuses on intravenously administered procainamide or amiodarone. These drugs depress excitability of cardiac muscle to electrical stimulation and slow conduction in the atria, bundle of His, and ventricles. Lidocaine is used only if acute myocardial ischemia or MI is considered to be the cause of VT. If pharmacologic measures are unsuccessful, the alternative is cardioversion. Catheter ablation can be helpful. Ongoing VT suppression is obtained with oral beta-adrenergic blockers or calcium channel blockers.

Ventricular fibrillation.

Ventricular fibrillation occurs when the ventricular musculature of the heart is quivering. This medical emergency is characterized by rapid and disorganized ventricle pulsation.

The cause is usually myocardial ischemia or infarction. Other causes are untreated VT, electrolyte imbalances, digitalis or quinidine toxicity, and hypothermia. It may also occur with coronary reperfusion after thrombolytic therapy.

Clinical manifestations are the result of no cardiac output and include loss of consciousness, lack of a pulse, decreases in blood pressure and respirations, possible seizures, and sudden death if untreated.

Medical management focuses on providing emergency treatment, including cardiopulmonary resuscitation (CPR), defibrillation (the termination of ventricular fibrillation by delivering a direct electrical countershock to the patient's precordium, i.e., that part of the patient's body surface covering the heart and stomach), and medications such as lidocaine or procainamide. Defibrillation is the most effective method of ending ventricular fibrillation and should ideally be performed within 15 to 20 seconds of onset to avoid brain damage from the lack of blood flow.

Assessment

Subjective data for the patient with a cardiac dysrhythmia include the patient's report of symptoms associated with the specific dysrhythmia. Symptoms may include palpitations, skipped beats, nausea, lightheadedness, vertigo, anxiety, dyspnea, fatigue, and chest discomfort.

Collection of objective data includes immediate visual observation of the patient when ECG monitoring indicates a dysrhythmia. Signs may include syncope, irregular pulse, tachycardia, and tachypnea. Noting the patient's response to the dysrhythmia is important to plan and implement appropriate nursing interventions. Monitor vital signs and observe for signs of decreased cardiac output.

Diagnostic Tests

Prior to treating a patient with a dysrhythmia, the health care provider needs to know if this is an abnormal or normal conduction occurrence of the heart. To find the cause or abnormality diagnostic tests are scheduled. Some of these can be performed without hospitalization.

ECG monitoring, telemetry, and Holter monitoring are commonly used to confirm the diagnosis of cardiac dysrhythmias and can be done without hospitalization. Laboratory work is also done to detect a medication toxicity. Treatment is aimed at the findings of the diagnostic tests.

Medical Management

Treatment varies according to the type of cardiac dysrhythmia (Table 8-1).

Table 8-1

Medications for Cardiac Dysrhythmias

Generic Name (Trade Name)	Action	Nursing Interventions
Cardiac Glycoside
digoxin (Lanoxin)	Used to control rapid ventricular rate in atrial fibrillation and to convert paroxysmal supraventricular tachycardia to normal sinus rhythm Increases cardiac force and efficiency, slows heart rate, increases cardiac output	Monitor apical pulse to ensure rate is above 60 bpm (call health care provider if digoxin withheld) Monitor for digitalis toxicity (nausea, vomiting, anorexia, dysrhythmias, bradycardia, tachycardia, headache, fatigue, visual disturbance)
Antidysrhythmic Agents
procainamide (Pronestyl, Procan SR)	IV solutions given for severe ventricular dysrhythmias	Observe for new dysrhythmias, dry mouth, blurred vision, bradycardia, hypotension, nausea, anorexia, dizziness, visual disturbances
procainamide (Pronestyl, Procan SR)	Depresses excitability of cardiac muscle to electrical stimulation and slows conduction in atrium, bundle of His, and ventricle, thus increasing refractory period
lidocaine (IV)	Suppresses the impulse that triggers dysrhythmias	Monitor heart rate and BP closely
disopyramide (Norpace CR)	Provides long-term treatment of premature ventricular contractions, ventricular tachycardia, and atrial fibrillation	Monitor BP and apical pulse
adenosine (Adenocard)	Slows conduction through AV node, can interrupt reentry pathways through AV node, and can restore normal sinus rhythm in patients with paroxysmal supraventricular tachycardia (PSVT)	Monitor BP, pulse rate, and respirations Assess patient for headache, dizziness, gastrointestinal complaints, new dysrhythmias Do not give caffeine within 4-6 hr of adenosine because caffeine inhibits the effect of the drug
amiodarone (Cordarone, Pacerone)	Prolongs duration of action potential and effective refractory period; provides noncompetitive alpha- and beta-adrenergic inhibition; increases P-R and Q-T intervals; decreases sinus rate; decreases peripheral vascular resistance. Used for severe ventricular tachycardia, supraventricular tachycardia, atrial fibrillation, ventricular fibrillation not controlled by first-line agents, cardiac arrest	Observe for headache, dizziness, hypotension, bradycardia, sinus arrest, heart failure, dysrhythmia Assess BP continuously for hypotension or hypertension Report dysrhythmia or bradycardia Monitor for dyspnea, chest pain
mexiletine (Mexitil) propafenone (Rythmol)	Decrease excitability of cardiac muscle	Monitor pulse, BP Monitor for diarrhea, visual disturbances, respiratory distress
tocainide (Tonocard)	Suppresses automaticity of conduction tissue	Notify health care provider if cough, wheezing, or shortness of breath occurs
Beta-Adrenergic Blockers
propranolol (Inderal) sotalol (Betapace) acebutolol (Sectral) esmolol (Brevibloc) metoprolol (Lopressor) carvedilol (Coreg)	Used to treat supraventricular and ventricular dysrhythmias, persistent sinus tachycardia Decrease myocardial oxygen demand, decrease workload of the heart, decrease heart rate	Monitor heart rate and BP carefully. Use caution with patient with bronchospastic disease Monitor for bradycardia, hypotension, new dysrhythmias, dizziness, headache, nausea, diarrhea, sleep disturbances
Calcium Channel Blockers
verapamil (Calan, Isoptin) diltiazem (Cardizem)	Treat supraventricular tachycardia and control rapid rates in atrial tachycardia Produce relaxation of coronary vascular smooth muscle, dilate coronary arteries	Use caution in patients with CHF Monitor apical pulse and BP Watch for fatigue, headache, dizziness, peripheral edema, nausea, tachycardia Both verapamil and diltiazem increase the toxicity of digoxin
Inotropic Agent
dobutamine (Dobutrex) (IV) dopamine (Intropin) (IV)	Used in severe CHF with pulmonary edema Increase myocardial contractility Increase cardiac output, increase BP, and improve renal blood flow	Monitor BP, heart rate, and urinary output continuously during the administration Palpate peripheral pulses; notify health care provider if extremities become cold or mottled
Anticoagulant
warfarin (Coumadin)	Used in treatment of atrial fibrillation with embolization to prevent complication of stroke	Assess patient for signs of bleeding and hemorrhage Monitor prothrombin time and International Normalized Ratio (PT/INR) frequently during therapy Review foods high in vitamin K. Patient should have consistently limited intake of these foods because these foods will cause levels to fluctuate

AV, Atrioventricular; BP, blood pressure; bpm, beats per minute; CHF, congestive heart failure; HCl, hydrochloride; IV, intravenous.

Nursing Interventions and Patient Teaching

Nursing interventions focus on symptomatic relief, promotion of comfort, relief of anxiety, emergency action as needed, and patient teaching.

Assess the patient's apical pulse to obtain an accurate pulse rate when dysrhythmias are present. Because the rhythm is irregular, take the apical pulse for 1 minute. Assess the patient's anxiety and degree of understanding, noting both verbal and nonverbal expressions regarding diagnosis, procedures, and treatments.

Explain the diagnostic and monitoring devices in use. Monitor heart rate and rhythm. Administer antidysrhythmic agents as ordered and monitor response. Maintain a quiet environment; administer sedation or analgesic medication as ordered. Administer oxygen per protocol.

Nursing diagnoses and interventions for the patient with a cardiac dysrhythmia include but are not limited to the following:

Nursing Diagnosis	Nursing Interventions
Pain, related to ischemia	Administer medications as ordered
	Teach relaxation techniques
	Institute position change and support
	Administer prescribed oxygen
Decreased cardiac output, related to cardiac insufficiency	Monitor heart rate and rhythm
	Reduce cardiac workload by encouraging bed rest
	Elevate head of bed 30 to 45 degrees for comfort
	Restrict activities as ordered; plan care to avoid fatigue
	Administer antidysrhythmic agents as ordered
	Monitor for signs of drug toxicity
Ineffective coping, related to fear of and uncertainty about disease process	Assist patient in identifying strengths and coping skills
	Supply emotional support
	Teach relaxation techniques
	Assess coping ability and level of family support
	Explain purpose of care as related to specific dysrhythmia

Teach the patient the importance of lifestyle changes such as avoiding or stopping smoking or use of nicotine products. Teach the patient about medication therapy and its purposes, desired effects, and dosage and the side effects to report to the health care provider. Explain the reason for and method of taking pulse rate and rhythm. Explain the need to avoid exercising beyond the tolerance level, to avoid strenuous or isometric activity, and to check with the health care provider regarding limitations and allowances. Instruct the patient regarding conserving energy for activities of daily living (ADLs): taking regular rest periods between activities and for 1 hour after meals; when possible, sitting rather than standing while performing a task; and stopping an activity or task if symptoms such as fatigue, dyspnea, or palpitations begin. Stress management is important to promote healing and prevent further cardiac events.

Cardiac Arrest

The sudden cessation of cardiac output and circulatory process is termed cardiac arrest. Conditions leading to cardiac arrest are severe ventricular tachycardia, ventricular fibrillation, and ventricular asystole. The absence of oxygen–carbon dioxide exchange leads to symptoms of anaerobic tissue cell metabolism and respiratory and metabolic acidosis. Thus immediate CPR is necessary to prevent major organ damage. Signs and symptoms of cardiac arrest include abrupt loss of consciousness with no response to stimuli, gasping respirations followed by apnea, absence of pulse (radial, carotid, femoral, and apical), absence of blood pressure, pupil dilation, and pallor and cyanosis.

CPR is initiated by the first person to discover the condition. The aim is to reestablish circulation and ventilation. Prevention of severe damage to the brain, heart, liver, and kidneys as a result of anoxia (lack of oxygen) is of primary concern. Remember the CAB of CPR: C, circulation; A, restore airway; and B, restore breathing. Resuscitation measures are divided into two components: basic cardiac life support in the form of CPR and advanced cardiac life support (ACLS).

ACLS is a systematic approach to provide early treatment of cardiac emergencies. ACLS includes (1) basic life support, (2) the use of adjunctive equipment and special techniques for establishing and maintaining effective ventilation and circulation, (3) ECG monitoring and dysrhythmia recognition, (4) therapies for emergency treatment of patient with cardiac or respiratory arrest, and (5) treatment of patient with suspected acute MI.

Artificial Cardiac Pacemakers

A pacemaker is made of titanium with computer circuits that control the pacing system; one or more leads are placed into the heart and a lithium battery is used (American Heart Association, 2012). It initiates and controls the heart rate by delivering an electrical impulse via an electrode to the myocardium. These catheter-like electrodes are placed within the area to be paced: right atrium, right ventricle, or both (see Figures 8-8 and 8-9). A permanent pacemaker power source is placed subcutaneously, usually over the pectoral muscle on the patient's nondominant side (American Heart Association, 2013a). Most are demand pacemakers, which send electrical stimuli to pace the heart when the heartbeat decreases below a preset rate. Some pacemakers have a single-chamber device with one lead that paces the right atrium or right ventricle; other pacemakers are dual-chamber with separate leads that connect to both the right atrium and the right ventricle (American Heart Association, 2013a).

Another pacemaker, the biventricular pacemaker, has three leads, one lead for each ventricle and one lead for the right atrium. This device restores normal simultaneous contraction of the ventricles. A biventricular pacemaker significantly improves left ventricular ejection fraction and exercise tolerance. It improves the quality of life for patients with worsening HF (American Heart Association, 2013a).

A pacemaker maintains a regular cardiac rhythm by electrically stimulating the heart muscle. It is used when patients experience adverse symptoms because of dysrhythmias that cannot be managed by medications alone. These include second- and third-degree AV block, bradydysrhythmia (slow and/or irregular heartbeat), and tachydysrhythmia (rapid heartbeat that can be regular or irregular).

An external pacemaker is used in emergency situations on a short-term basis. Temporary pacemakers are used for cardiac support after some MIs or open-heart surgery. A permanent pacemaker is placed when other measures have failed to convert the dysrhythmia or conduction problem. The batteries used in permanent pacemakers today are small, weighing less than 1 ounce, and can last 15 years or more.

Nursing Interventions and Patient Teaching

After placement of a pacemaker, closely monitor heart rate and rhythm by apical pulse and by ECG patterns. Check vital signs and level of consciousness frequently until stable. Observe the insertion site for erythema, edema, and tenderness, which could indicate infection. The patient may be on bed rest with the arm on the pacemaker side immobilized for the first few hours. Discharge teaching includes instructions not to lift the arm on the surgical side over the head for 6 to 8 weeks. The patient needs to refrain from swimming, golfing, and weight lifting until given permission by the health care provider (American Heart Association, 2013a).

Inform the patient of the necessity to continue medical management, and advise that he or she wear medical-alert identification and carry pacemaker information. Emphasize the importance of reporting signs and symptoms of pacemaker failure: weakness, vertigo, chest pain, and pulse changes.

Teach the patient to avoid potentially hazardous situations. Each pacemaker manufacturer can provide a list of devices that patients with pacemakers should avoid getting close to, such as high-output electrical generators or large magnets such as a magnetic resonance imaging (MRI) scanner. This may cause interference, placing the pacemaker in a fixed mode and interfering with its functioning. Instruct the patient to move away from any device that may cause untoward symptoms such as vertigo.

The pacemaker's pulse generator is set to produce a heart rate appropriate to the patient's clinical condition and the desired therapeutic goal. With rare exceptions, the rate is set between 70 and 80 bpm. If the heart rate falls below the preset level, notify the health care provider.

Teach the patient how and when to take a radial pulse. The pulse should be taken at the same time each day and when symptoms of vertigo or weakness occur. During patient education, remember to (1) list symptoms to expect and to report to the health care provider, (2) promote understanding of medication administration, (3) explain treatment outcomes, (4) explain the importance of maintaining prescribed diet and fluid amounts, and (5) explain the importance of not smoking. Teach the patient that shortness of breath occurring with exercise or exertion can be significant, because of the heart's inability to provide enough oxygen to the cells.

Prognosis

The patient can expect to lead a reasonably normal life with full resumption of most activities as prescribed by the health care provider.

Disorders of the Heart

Coronary Atherosclerotic Heart Disease

The coronary arteries arise from the base of the aorta just below the semilunar valves (see Figure 8-6). These arteries curve and branch to adequately supply the heart muscle with oxygen and nutrients. The shapes, contours, and arrangements of the vessels allow for easy entrapment of substances that interfere with blood flow.

Coronary artery disease (CAD) is the term used to describe a variety of conditions that obstruct blood flow in the coronary arteries. Atherosclerosis (a common arterial disorder characterized by yellowish plaques of cholesterol, lipids, and cellular debris in the inner layers of the walls of large and medium-size arteries) is the primary cause of ASHD. The lumen (a cavity or channel within any organ of the body) of the vessel narrows as the disease progresses. Blood flow to the heart is obstructed when this process occurs in the coronary arteries.

Atherosclerosis, the basic underlying disease affecting coronary lumen size, is characterized by changes in the intimal lining (the innermost layer) of the arteries. The severity of the disease is measured by the degree of obstruction within each artery and by the number of vessels involved. Obstructions exceeding 75% of the lumen of one or more of the three coronary arteries increase the risk of death.

The basic physiologic changes of the atherosclerotic process result in problems with myocardial oxygen supply and demand. When the myocardial oxygen demand exceeds the supply delivered by the coronary arteries, ischemia results (Figure 8-10). The artery walls also become less elastic and less responsive to blood flow (see Cultural Considerations box).

FIGURE 8-10 Progressive development of coronary atherosclerosis. A, Injury to intimal wall. B, Lipoprotein invasion of smooth muscle cells. C, Development of fatty streak and fibrous plaque. D, Development of complicated lesion. (From Black JM, Hawks JH: Medical-surgical nursing: Clinical management for positive outcomes, ed 8, St. Louis, 2009, Mosby.)

Angina Pectoris

Etiology and Pathophysiology

Angina means a spasmodic, cramplike, choking feeling. Pectoris refers to the breast or chest area. Angina pectoris refers to the paroxysmal (severe, usually episodic) thoracic pain and choking feeling caused by decreased oxygen flow to or lack of oxygen (anoxia) of the myocardium.

Angina pectoris occurs when the cardiac muscle is deprived of oxygen. Atherosclerosis of the coronary arteries is the most common cause. The narrowed lumina of the coronary arteries are unable to deliver enough oxygen-rich blood to the myocardium. When the myocardial oxygen demand exceeds the supply, ischemia (decreased blood supply to a body organ or part, often marked by pain and organ dysfunction) of the heart muscle occurs, resulting in chest pain or angina. Typically angina occurs with an increased cardiac workload brought on by exposure to intense cold, exercise, unusually heavy meals, emotional stress, or any other strenuous activity.

CAD is the number one killer in the United States. Many people who die from the disease, however, experience several episodes of unstable angina first. If unstable angina were accurately diagnosed and promptly managed, many deaths and much of the disability associated with CAD could be avoided.

Cultural Considerations

Cardiovascular Disorder

• White, middle-aged men have the highest incidence of coronary artery disease (CAD).

• African Americans and Hispanics have a higher incidence of hypertension than do white Americans.

• African Americans have an early age of onset of CAD.

• African American women have a higher incidence of CAD than do white American women.

• Native Americans younger than 35 years of age have a heart disease mortality rate twice as high as that of other Americans.

• Hispanics have a lower death rate from heart disease than do non-Hispanics.

• Major modifiable cardiovascular risk factors for Native Americans are obesity and diabetes mellitus.

Unstable angina is defined as an unpredictable and transient episode of severe and prolonged discomfort that appears at rest, has never been experienced before, or is considerably worse than previous episodes. It mimics an MI in that the discomfort it causes is often described as tightness or a crushing sensation in the chest, arms, back, neck, or jaw. For some patients, unstable angina is a red flag that an MI will occur.

Clinical Manifestations

Pain is the outstanding characteristic of angina pectoris (Figure 8-11). The patient usually describes the pain as a heaviness or tightness of the chest. At times it is thought to be indigestion. The pain is often substernal (below the sternum) or retrosternal (behind the sternum). Pain may radiate to other sites, or it may occur in only one site. The pain often radiates down the left inner arm to the little finger and also upward to the shoulder and jaw. Patients may also describe it as a pressure or a squeezing sensation, but usually not as a sharp pain. Sometimes a patient experiences posterior thoracic or jaw pain only. The chest pain may be accompanied by other signs and symptoms such as dyspnea, anxiety, apprehension, diaphoresis, and nausea. Symptoms of CAD in women vary and may be more subtle or generalized than in men. Women often report heaviness, squeezing, or pain in the left side of the chest, or pain in the abdomen, arm, mid-back, or scapular region. Women may also complain of palpitations and chest discomfort during rest, during sleep, or with exertion (American Heart Association, 2012a).

FIGURE 8-11 Sites to which ischemic myocardial pain may be referred. A, Upper chest. B, Beneath sternum, radiating to neck and jaw. C, Beneath sternum, radiating down left arm. D, Epigastric. E, Epigastric, radiating to neck, jaw, and arms. F, Neck and jaw. G, Left shoulder and inner aspect of both arms. H, Intrascapular. (From Lewis S, Dirksen SR, Heitkemper MM, et al.: Medical-surgical nursing: Assessment and management of clinical problems, ed 8, St. Louis, 2011, Mosby.)

The signs and symptoms of angina are often similar to those of MI. Anginal pain is believed to be caused by a temporary lack of oxygen and blood supply to the heart. It is often relieved by rest or medication such as nitroglycerin, which dilates the coronary arteries and increases the flow of oxygenated blood to the myocardium. Nitroglycerin administered sublingually usually relieves angina symptoms but does not relieve the pain from an MI. This is often used as a preliminary diagnostic tool to quickly differentiate angina from an MI.

Diabetes can cause nerve damage that can make the usual signs and symptoms of chest pain harder to detect. The patient may have no pain with an MI. Patients with diabetes are still cautioned to go to the emergency room if they experience chest discomfort, sweating, or nausea and/or vomiting (American Diabetes Association, 2009).