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. However, the heart still is capable of functioning adequately unless there is underlying cardiac disease (see the Lifespan Considerations box). According to the American Heart Association (2020), all adults over the age of 20 should have their cholesterol levels checked once every 4 to 6 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 (CDC, 2020).
Lifespan ConsiderationsOlder 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 often are prescribed at lower doses than for younger adults. Even with lower doses of medications, observe the older adult closely for signs of toxicity, because 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
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, 2017b).
Cultural and ethnic considerations
Heart disease is the leading cause of death for African Americans, American Indians, Native Alaskans, and Caucasians (CDC, 2019). Between 1999 and 2017, twice as many African Americans died of heart disease than Asians or Pacific Islanders (CDC, 2019) and out of those patients diagnosed with high blood pressure, African Americans are 40% more likely to have uncontrolled hypertension (HHS, 2020).
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 causes tachycardia, hypertension, and vasoconstriction of the peripheral arteries. This increases the workload of the heart, thus reducing the amount of available oxygen to the heart muscle. The other chemicals in cigarettes, including tar and carbon monoxide, also contribute to heart disease. These chemicals cause atherosclerosis because of the buildup of fatty plaque in the vessels. Fibrinogen levels also rise as a result of these chemicals, leading to clot formation, which can cause MI or stroke (Texas Heart Institute, n.d.).
With the increased use of marijuana because of legalization in some states, studies are being conducted regarding the potential harm to various organs. A recent study estimates that the explosion in the use of marijuana will add significantly to the cardiovascular disease burden as already events such as sudden cardiac death, arrythmias, and stress cardiomyopathy have been documented in healthy patients with no cardiac risk factors (Singh, Saluja, Kumar et al., 2018).
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 (see Box 48.1).
- • 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 48.1).
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 the 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 often are 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 atorvastatin (Lipitor), simvastatin (Zocor), pravastatin (Pravachol), and rosuvastatin (Crestor); (4) fibric acid derivatives such as gemfibrozil (Lopid) and probucol; (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 now is allowed by the US 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. In 2017, the American College of Cardiology published definitions for high blood pressure and eliminated the prehypertension stage. New guidelines have normal blood pressure at less than 120/80 mm Hg; elevated blood pressure is a systolic of 120 to 129 mm Hg and a diastolic of less than 80 mm Hg; hypertension stage 1 occurs at systolic 130 to 139 mm Hg or diastolic 80 to 89 mm Hg; and hypertension stage 2 occurs at systolic equal to or greater than 140 mm Hg or diastolic equal to or greater than 90 mm Hg (CDC, 2020a).
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 levels of bad cholesterol and low levels of good cholesterol. This is known as diabetic dyslipidemia. Other contributing risk factors include poorly managed diabetes, high blood pressure, obesity, lack of physical activity, and smoking. According to the CDC (2020b), patients with diabetes are twice as likely to develop heart disease and the chances of heart disease due to diabetes increases based on the number of years since diagnosis. These risks can be mitigated with an active lifestyle and exercise, diet and weight control, managing stress, and keeping blood pressure under 140/90 mm Hg. It is also important to manage cholesterol levels and to stop smoking (CDC, 2020b).
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 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) occurs when there is a change in the electrical conduction of the heart that affects the heart rate, rhythm of the heart, or both. To understand dysrhythmias, it is important to first understand the heart’s normal electrophysiology. The normal electrophysiology of the heart causes a person to be in what is described as normal sinus rhythm. In a normal sinus rhythm, the primary functioning pacemaker of the heart is the sinus or SA node which depolarizes and send out depolarizing signals via the internodal system to affect the contraction of
myocardial cells of the atrium. The SA node depolarizes at a regular rate and rhythm after which the electrical impulse follows the normal conduction system of going to the AV node, bundle of his, down the left/right bundle branch, and into the Purkinje fibers to then cause ventricular muscle contraction. When the SA node paces the heart at a regular rate and rhythm, the following characteristics are evident:
- • Rate: 60 to 100 bpm
- • P waves (caused by atrial depolarization): Precede each QRS complex, are upright, and have a consistent shape and size
- • P-R interval: Time between the start of atrial contraction to the beginning of ventricular contraction; normal interval is between 0.12 and 0.2 seconds
- • QRS complex: represents the time from the beginning of ventricular contraction to the end of ventricular contraction; normal interval is less than 0.12 seconds
- • 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 the following: heartbeat of 100 to 120 bpm; P wave precedes each QRS complex though it may not be seen as it may be buried in the T wave; 1 P-wave for every QRS complex; PR interval is 0.12 to 0.2 seconds. Essentially, the only variable from normal sinus rhythm is an increase in rate above 100 bpm.
Causes of sinus tachycardia include exercise, anxiety, fever, shock, medications, HF, excessive caffeine, recreational drugs, sympathetic influence on the SA node, and tobacco use. Patient maybe asymptomatic or manifest symptoms such as palpitations, hypotension, dizziness, anxiety, headaches, shortness of breath, and chest pain. Treatment goals include slowing the heart rate when it occurs, figuring out the underlying cause and treating it, and preventing future episodes. The heart rate can be slowed down by doing vagal maneuvers which involves coughing, bearing down as if having a bowel movement, or placing an ice pack on the face. All of these actions stimulate the vagus nerve which stimulates the parasympathetic system and slows the heart rate. If vagal maneuvers are unsuccessful, anti-arrhythmic medications such as adenosine (Adenocard) is administered intravenously followed by the potential use of synchronized cardioversion. Future episodes of sinus tachycardia can be prevented by treating the underlying cause. Sometimes, sinus tachycardia occurs without an identifiable cause. In these situations, a catheter ablation may be conducted which ablates a part of the sinus node thus decreasing the conduction of electrical impulses.
Sinus bradycardia
Sinus bradycardia is a slower than normal rhythm originating in the SA node. It is characterized by: a pulse rate of less than 60 bpm; ventricular and atrial rhythms occur at regular frequencies; P wave is preceded by a QRS complex; the PR interval is 0.12 to 0.2 seconds; and P to QRS complex ratio is 1:1. Essentially, the only difference between sinus rhythm and sinus bradycardia is the rate is slower than 60 bpm.
Causes of sinus bradycardia include lower metabolic rate, advancing age, inflammatory heart conditions, increased intracranial pressure, vagal nerve stimulation, carotid sinus massage, idiopathic sinus node dysfunction, athletic training, hypothyroidism, myocardial infarct, and medication (especially overuse of digitalis, beta-adrenergic blockers, or calcium channel blockers). Patients such as athletes in training may have sinus bradycardia without symptoms. In these patients, conditioning causes more efficient heart contractions such that the cardiac output is unchanged at lower heart rates. Symptomatic patients experience fainting, dizziness, shortness of breath, fatigue, activity intolerance, and chest pain. Treatments for sinus bradycardia include treating the underlying medical condition, changing medications, and preventing future episodes. If medication induced, a change in medication management is warranted. Patients stimulating the vagal nerve are taught to avoid bearing down during defecation. Hypothyroidism is treated with levothyroxine (Synthroid) and maintained at therapeutic levels. Patients experiencing hemodynamic instability with sinus bradycardia can be administered 0.5 mg of atropine IV every 3 to 5 minutes with a maximum dose of 3 mg. If this fails, a transcutaneous pacemaker is instituted with surgery scheduled for a permanent pacemaker. A pacemaker is a battery-operated device which contains 2 leads, one implanted in the atrium and one in the ventricle, that serves as the primary
pacemaker of the heart (Figs. 48.8 and 48.9.). A prescribed heart rate is set which serves as the rate at which a patient’s heart beats.
Supraventricular tachycardia
Supraventricular tachycardia (SVT) is the onset of a heart rate greater than 100 bpm that originates either from the atria or from the AV node which is above the ventricles hence the name SVT. SVT originating from the atria is known is atrial tachycardia and is the less common form of SVT, usually manifests in children, and begins slowly with a gradual heart rate increase of more than 100 bpm. SVT originating from the AV node is called atrioventricular nodal reentry tachycardia (AVNRT) and is the most common form of SVT (Mayo Clinic, 2019). Since AVNRT is most common it is the subject of discussion here and will be referred to as SVT as is common practice.
SVT occurs due to an accessory pathway located in or near the AV node. This accessory pathway sends electrical impulses to the AV node that causes the impulse to be rerouted back to the AV node again and again at a very fast rate. Each time the impulse is rerouted to the AV node, it causes the AV node to propagate the impulse down the bundle of His, into right and left bundle branches, and to the Purkinjie fibers which causes fast ventricular myocardial contraction.
SVT has an abrupt onset and an abrupt cessation. It is characterized by an atrial rate of 150 to 250 bpm; ventricular rate of 120 to 200 bpm; regular rhythm of P and R waves; P wave that may be seen but is mostly hidden in the T wave (ventricular repolarization); and a P to QRS complex ratio of 1:1 or 2:1.
Causes of SVT include heart failure, thyroid disease, smoking, caffeine, drugs such as amphetamines and cocaine, surgery, anxiety and emotional stress, and pregnancy. Some patients may experience SVT with no identifiable cause. Clinical symptoms experienced vary depending on the rate, duration of occurrence, and the patient’s underlying conditions. SVT is usually of short duration and causes palpitations. Other symptoms experienced include a fluttering in the chest, rapid heartbeat, shortness of breath, lightheadedness, sweating, syncope, and a pounding sensation in the neck (Mayo Clinic, 2019a).
Medical management first looks at how well the patient tolerates the dysrhythmia and at the overall clinical picture. Patients with minimum symptoms and quick termination of SVT may require no treatment and just be self-monitored and treated. Patients experiencing significant symptoms requiring emergency room visits to terminate SVT are treated with a focus of preventing future episodes (Hinkle and Cheever, 2018). In the immediacy, SVT is terminated using vagal maneuvers, one or more doses of adenosine with a calcium channel blocker, or cardioversion. Catheter ablation is the treatment of choice as it destroys the tissue in the AV node that allows for rerouting of the impulse back into the AV node.
Atrial fibrillation
Atrial fibrillation is one of the most common types of heart arrythmias occurring in the United States with one in four people over the age of 40 at risk for being diagnosed with atrial fibrillation (Xie, Yu, Ambale-Venkatesh et al., 2020). It occurs when structural or electrophysiological abnormalities alter atrial tissue and then the altered atrial tissue forms abnormal impulses resulting in rapid and uncoordinated twitching of the atria (Hinkle and Cheever, 2018). The atria quiver or fibrillate instead of all the myocardial cells of the atria contracting as a unit. This disorganized quivering can be likened to a disorganized orchestra where the cacophony of sounds created produce a broken piece of music and in the case of the atria loss of coordinated contraction of all myocardial cells in the left and right atrium. Since the atria quiver rather than contract, the atrial kick is lost which results in decreased cardiac output. In addition, the quivering atria are no longer moving blood along and thus this allows blood to stagnate within the atria making the blood susceptible to clots. These clots can break off, flow into the ventricles, and then be pumped into pulmonary and systemic circulation causing pulmonary embolism or stroke. In normal heartbeats, atrial contraction is followed by ventricular contraction. In atrial fibrillation, atrial and ventricular contraction do not follow each other and are out of sync. The ventricles contract irregularly which decreases ventricular filling time and further decreases the cardiac output. Atrial fibrillation is characterized by atrial rate of 300 to 600
bpm; ventricular rate of 120 to 200 bpm; a highly irregular atrial and ventricular rhythm; no discernible P waves but irregular and undulating waves that vary in amplitude and shape; the PR interval is unmeasurable; and the P to QRS complex ratio is many to 1.
Causes of atrial fibrillation include advancing age, high blood pressure, drinking alcohol, sleep apnea, any chronic condition such as diabetes, asthma, and hyperthyroidism, and underlying heart disease such as high blood pressure, valvular disease, cardiomyopathy, MI and cardiac surgery. Other not-so-obvious causes of atrial fibrillation can be energy drinks, high ingestion of caffeine, over-the-counter medications for colds such as Actifed, Sudafed, or Contact, and even some herbs, such as St. John’s wort, which can interfere with clotting. In addition, atrial fibrillation can increase the risk of heart disease. This occurs in part due to the fact that the heart is contracting irregularly and faster which decreases the amount of time the heart spends in diastole. As a result, blood and oxygen supply to the coronary arteries is reduced leading to a risk for myocardial ischemia.
Patients with atrial fibrillation may be asymptomatic despite the loss in atrial kick and incomplete ventricular filling resulting in decreased cardiac output. Other patients may experience clinical symptoms such as palpitations, hypotension, shortness of breath, dyspnea on exertion, fatigue, syncope, chest pain, and a pulse deficit. Patients may also have signs and symptoms of emboli which vary based on the site of the embolization. Risk of stroke increases fivefold with atrial fibrillation. Risk of stroke is even higher in patients who have structural heart disease and hypertension and are over 65 years of age.
Medical management of atrial fibrillation is based on multiple factors including duration of the dysrhythmia and symptoms experienced by the patient. Patients with time identified new onset atrial fibrillation are treated with the goal of restoring normal sinus rhythm as soon as possible. When atrial fibrillation is identified within 24 to 48 hours of onset, the restoration to normal sinus rhythm may be achieved with administration of anti-rhythmics such as flecainide, dofetilide, propafenone, amiodarone, and IV ibutilide. If anti-arrhythmic medications are unsuccessful at converting atrial fibrillation to normal sinus rhythm, then synchronized cardioversion is used to convert the patient to normal sinus rhythm. If atrial fibrillation is discovered post 48 hours of onset or the duration is unknown, a transesophageal echocardiogram (TEE) is performed to determine the presence of thrombus in the atria prior to attempting conversion to a normal sinus rhythm. If no thrombi are present, conversion can be attempted either with medications or via electrical cardioversion. If the TEE images show thrombus in the atria, then anticoagulant therapy is initiated first as conversion to normal sinus will dislodge clots from the atria and cause embolic events. Immediate anticoagulant therapy used includes use of low molecular weight heparin and IV heparin. Symptomatic patients are managed with beta blockers or calcium channel blockers to help decrease the heart rate to below 80 bpm. When anti-arrhythmic medications and electrical cardioversion are unsuccessful, catheter ablation is considered. Catheter ablation destroys the cells in the atria that are giving rise to abnormal electrical impulses. Maze or mini-maze procedures are used for patients with refractory atrial fibrillation and only conducted if patients are already scheduled for other cardiac surgeries (Hinkle and Cheever, 2018).
In some patients, atrial fibrillation occurs with other comorbid conditions or comorbid conditions do not allow the patient to undergo more invasive treatment options. In these cases, the atrial fibrillation is considered to be “permanent” and the patient is managed symptomatically. These patients take beta blockers, calcium channel blockers, and anticoagulants to control symptoms and prevent the risks of emboli.
Anticoagulant therapy used to occur with warfarin, but it required monitoring of PT/INR and is susceptible to vitamin K ingestion in diet. Novel oral anticoagulants (NOACs) such as dabigatran, rivaroxaban, and apixaban are now commonly prescribed for patients with atrial fibrillation. The NOACs do not require laboratory monitoring, have fewer drug-drug interactions, have a rapid onset and offset and do not require bridging therapy, and are better at reducing the risk of thromboembolic events. In addition, as of 2018 (Harvard Health Publishing), rivaroxaban and apixaban effects can be reversed by the antidote andexanet alfa and dabigatran can be reversed with the administration of idarucizumab.
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 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 low, often between 30 and 40 bpm.
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 Fig. 48.8).
Premature ventricular contractions
Premature ventricular contractions (PVCs) are abnormal heartbeats that arise from the right or left ventricle and cause ventricular contraction before the next normal sinus impulse. PVCs are early ventricular beats that occur in conjunction with the underlying rhythm, which is unchanged except for the PVC itself. PVC occurrences can be random or occur in patterns of bigeminy, trigeminy, or quadrigeminy meaning every other ventricular beat is a PVC, every third is a PVC, or every fourth is a PVC, respectively.
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 cause of PVCs such as eliminating caffeine or alcohol, managing stress, and correcting electrolyte imbalances. Symptomatic PVCs can be treated with beta-adrenergic blockers such as carvedilol, antianginals, propranolol (Inderal), and anti-dysrhythmics such as procainamide and amiodarone.
Ventricular tachycardia
VT is a heart rhythm that originates from the ventricles itself. It is most commonly caused by ischemic heart disease. Heart ischemia results in electrolyte derangement in myocardial cells, in this case potassium, which partially depolarizes the myocardial cells. This partial depolarization creates currents between infarcted tissue and healthy myocardium which triggers spontaneous electrical impulses causing the ventricles to contract. Other causes of VT include hypertrophic cardiomyopathy, long QT syndrome, and congenital coronary artery anomalies, cocaine, drugs, and digitalis toxicity (Foth, Gangwani, and Alvey, 2020). VT is distinguished from PVCs as VT is defined as the occurrence of three or more PVCs in a row occurring at a rate exceeding 100 bpm. It is further characterized by ventricular rate of 100 to 200 bpm; QRS complex duration 0.12 seconds or greater of bizarre or abnormal shape; PR interval and P to QRS ratio cannot be determined. It is further classified as non-sustained (occurring for less than 30 seconds and causing no symptoms) and sustained (occurring for 30 or more seconds or causing hemodynamic instability in less than 30 seconds). VT is also classified based on the shape of the QRS complex: monomorphic as QRS morphology is stable and polymorphic where each QRS complex from beat to beat looks different. These classifications are important as they guide treatment decisions.
Patients with stable VT are monitored with ECG and given anti-arrhythmic medications such as procainamide or sotalol for monomorphic VT without acute MI or severe heart failure and IV amiodarone if cardiac function is impaired due to other heart disease (Hinkle and Cheever, 2018). Patients with no underlying heart disease are started on a beta blocker or a calcium channel blocker (Foth, Gangwani, and Alvey, 2020). Patients in monomorphic VT who are symptomatic are cardioverted. Patients with VT who are pulseless are defibrillated. Treatment for VT also considers the EF. Patients with an EF of less than 35% are candidates for the placement of an implantable cardioverter defibrillator while patients with EFs above 35% are managed with oral amiodarone. Catheter ablation is also a treatment of choice (Hinkle and Cheever, 2018). Ongoing VT suppression is obtained with oral beta-adrenergic blockers or calcium channel blockers.
Ventricular fibrillation
Ventricular fibrillation occurs when part of the ventricular myocardium depolarizes erratically in an uncoordinated fashion. The result is quivering of the ventricles rather than a coordinated forceful contraction. The quivering of ventricles constitutes a medical emergency as cardiac output is essentially nil to all organs of the body including the coronary arteries of the heart. A continuance in ventricular fibrillation will result in more myocardial ischemia and eventual death. Patients in ventricular fibrillation are always without a pulse, an audible heartbeat, and respirations. Ventricular fibrillation is also characterized by a ventricular rate greater than 300 bpm, extremely irregular rhythm, no discernible P waves or QRS complexes, and the presence of irregular undulating QRS waves with changing amplitudes (Hinkle and Cheever, 2018).
The most common cause of ventricular fibrillation is CAD resulting in a myocardial infarct. Other causes of ventricular fibrillation include untreated VT, previous ventricular fibrillation episodes, previous MI, cardiomyopathy, illegal drugs (Ludhwani, Goyal, and Jagtap, 2020), electrolyte imbalances, digitalis or quinidine toxicity, and hypothermia.
Most patients in ventricular fibrillation suffer sudden collapses due to cardiac arrest. Patients may demonstrate some signs previous to the occurrence of ventricular fibrillation that may avert this dysrhythmia. These signs include chest pain, shortness of breath, nausea, and vomiting. Patients with chronic cardiac issues may also experience worsening of symptoms prior to the onset of ventricular fibrillation.
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 amiodarone and epinephrine. Defibrillation is the most effective method of ending ventricular fibrillation and ideally should be performed within 15 to 20 seconds of onset to avoid brain damage from the lack of blood flow.
Assessment and Diagnostic Tests of All Cardiac Dysrhythmias
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, nausea, light headedness, vertigo, anxiety, dyspnea, fatigue, and chest discomfort.
Collection of objective data includes immediate visual observation of the patient. Signs may include syncope, irregular pulse, tachycardia, bradycardia, and tachypnea. Noting patient response to the dysrhythmia is essential as it guides treatment management.
Cardiac dysrhythmias are assessed by using electrocardiography. A 12 lead is preferred. Patients may also be diagnosed after wearing telemetry or Holter monitors for 24 hours or more. Laboratory work is also done to detect a medication toxicity.
Cardiac Dysrhythmias—Medical Management
Table 48.1 outlines medication treatments for various cardiac dysrhythmias.
Nursing Interventions and Patient Teaching for Cardiac Dysrhythmias
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 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.
Patient problems and interventions for the patient with a cardiac dysrhythmia include but are not limited to the following:
| Patient Problem | Nursing Interventions |
|---|---|
| Discomfort, related to ischemia | Administer medications as ordered |
| Teach relaxation techniques | |
| Institute position change and support | |
| Administer prescribed oxygen | |
| Insufficient Cardiac Output, related to cardiovascular disease | Monitor heart rate and rhythm |
| Reduce cardiac workload by encouraging bed rest | |
| Elevate head of bed 30–45 degrees for comfort | |
| Restrict activities as ordered; plan care to avoid fatigue | |
| Administer antidysrhythmic agents as ordered | |
| Monitor for signs of drug toxicity | |
| Impaired 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 VT, 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. 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).
| Generic Name | Action | Nursing Interventions |
|---|---|---|
| Anticoagulant | ||
| warfarin | 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
|
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, 2016b). 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 Figs. 48.8 and 48.9). A permanent pacemaker power source is placed subcutaneously, usually over the pectoral muscle on the patient’s nondominant side. 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.
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 EF and exercise tolerance. It improves the quality of life for patients with worsening HF (American Heart Association, 2016b).
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 weightlifting until given permission by the health care provider (American Heart Association, 2016b).
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. In the past patients had to avoid objects such as high-output electrical generators or large magnets such as a MRI scanner because these objects could cause interference resulting in the pacemaker going into a fixed mode. Because of the grade of titanium metals used, patients who have pacemakers placed in the past several years can have MRI testing without difficulty. The patient always should report the use of a pacemaker before having an MRI.
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.
