Care of Patients with Cardiac Problems

Chapter 37 Care of Patients with Cardiac Problems




Learning Outcomes



Safe and Effective Care Environment



Health Promotion and Maintenance



Psychosocial Integrity



Physiological Integrity



image


http://evolve.elsevier.com/Iggy/


Animation: Congestive Heart Failure


Animation: Pericardial Tamponade


Answers to NCLEX Examination Challenges and Decision-Making Challenges


Audio Glossary


Audio Key Points


Concept Map Creator


Review Questions for the NCLEX® Examination


This chapter focuses on heart failure and its common causes in the adult population; coronary artery disease is discussed in Chapter 40. Heart failure is the most common reason for hospital stays in patients older than 65 years in the United States. When the heart is diseased, it cannot effectively pump an adequate amount of arterial blood to the rest of the body. Arterial blood carries oxygen and nutrients to vital organs, such as the kidneys and brain, and peripheral tissues. When these organs and other body tissues are not adequately perfused, they may not function properly.



Heart Failure


Heart failure, sometimes referred to as pump failure, is a general term for the inability of the heart to work effectively as a pump. It results from a number of acute and chronic cardiovascular problems that are discussed later in this chapter and elsewhere in the cardiovascular unit.




Pathophysiology


Heart failure (HF) is a common chronic health problem, with acute episodes often causing hospitalization. Acute coronary disease and other structural or functional problems of the heart can lead to acute heart failure. Both acute and chronic HF can be life threatening if they are not adequately treated or if the patient does not respond to treatment.



Types of Heart Failure


The major types of heart failure are:



Because the two ventricles of the heart represent two separate pumping systems, it is possible for one to fail by itself for a short period. Most heart failure begins with failure of the left ventricle and progresses to failure of both ventricles. Typical causes of left-sided heart (ventricular) failure include hypertension, coronary artery disease, and valvular disease involving the mitral or aortic valve. Decreased tissue perfusion from poor cardiac output and pulmonary congestion from increased pressure in the pulmonary vessels indicate left ventricular failure (LVF).


Left-sided heart failure was formerly referred to as congestive heart failure (CHF); however, not all cases of LVF involve fluid accumulation. In the clinical setting, though, the term CHF is still commonly used. Left-sided failure may be acute or chronic and mild to severe. It can be further divided into two subtypes: systolic heart failure and diastolic heart failure.


Systolic heart failure (systolic ventricular dysfunction) results when the heart cannot contract forcefully enough during systole to eject adequate amounts of blood into the circulation. Preload increases with decreased contractility, and afterload increases as a result of increased peripheral resistance (e.g., hypertension) (McCance et al., 2010). The ejection fraction (the percentage of blood ejected from the heart during systole) drops from a normal of 50% to 70% to below 40% with ventricular dilation. As it decreases, tissue perfusion diminishes and blood accumulates in the pulmonary vessels. Manifestations of systolic dysfunction may include symptoms of inadequate tissue perfusion or pulmonary and systemic congestion. Systolic heart failure is often called “forward failure” because cardiac output is decreased and fluid backs up into the pulmonary system. Because these patients are at high risk for sudden cardiac death, patients with an ejection fraction of less than 30% are considered candidates for an implantable cardioverter/defibrillator (ICD; also known as an internal cardioverter/defibrillator) (see Chapter 36).


In contrast, diastolic heart failure (heart failure with preserved left ventricular function) occurs when the left ventricle cannot relax adequately during diastole. Inadequate relaxation or “stiffening” prevents the ventricle from filling with sufficient blood to ensure an adequate cardiac output. Although ejection fraction is more than 40%, the ventricle becomes less compliant over time because more pressure is needed to move the same amount of volume as compared with a healthy heart. Diastolic failure represents about 20% to 40% of all heart failure, primarily in older adults and in women who have chronic hypertension and undetected coronary artery disease. Clinical manifestations and management of diastolic failure are similar to those of systolic dysfunction (McCance et al., 2010).


Right-sided heart (ventricular) failure may be caused by left ventricular failure, right ventricular myocardial infarction (MI), or pulmonary hypertension. In this type of heart failure (HF), the right ventricle cannot empty completely. Increased volume and pressure develop in the venous system, and peripheral edema results.


High-output heart failure can occur when cardiac output remains normal or above normal, unlike left- and right-sided heart failure, which are typically low-output states. High-output failure is caused by increased metabolic needs or hyperkinetic conditions, such as septicemia, high fever, anemia, and hyperthyroidism. This type of heart failure is not as common as other types.




Compensatory Mechanisms


When cardiac output is insufficient to meet the demands of the body, compensatory mechanisms work to improve cardiac output (Fig. 37-1). Although these mechanisms may initially increase cardiac output, they eventually have a damaging effect on pump function. Major compensatory mechanisms include:





Stimulation of the Sympathetic Nervous System

In heart failure (HF), stimulation of the sympathetic nervous system (i.e., increasing catecholamines) as a result of tissue hypoxia represents the most immediate compensatory mechanism. Stimulation of the adrenergic receptors causes an increase in heart rate (beta adrenergic) and blood pressure from vasoconstriction (alpha adrenergic).


Because cardiac output (CO) is the product of heart rate (HR) and stroke volume (SV), an increase in HR results in an immediate increase in cardiac output. The HR is limited, though, in its ability to compensate for decreased CO. If it becomes too rapid, diastolic filling time is limited and CO may start to decline. An increase in HR also significantly increases oxygen demand by the myocardium. If the heart is poorly perfused because of arteriosclerosis, HF may worsen.


Stroke volume (SV) is also improved by sympathetic stimulation. Sympathetic stimulation increases venous return to the heart, which further stretches the myocardial fibers causing dilation. According to Starling’s law, increased myocardial stretch results in more forceful contraction. More forceful contractions increase SV and CO. After a critical point is reached within the cardiac muscle, further volume and stretch reduce the force of contraction and cardiac output.


Sympathetic stimulation also results in arterial vasoconstriction. Vasoconstriction has the benefit of maintaining blood pressure and improving tissue perfusion in low-output states. However, constriction of the arteries increases afterload, the resistance against which the heart must pump. Afterload is the major determinant of myocardial oxygen requirements. As it increases, the left ventricle requires more energy to eject its contents and SV may decline.






Etiology


Heart failure (HF) is caused by systemic hypertension in most cases. About a third of patients experiencing myocardial infarction (MI, “heart attack”) also develop HF. The next most common cause is structural heart changes, such as valvular dysfunction, particularly pulmonic or aortic stenosis, which leads to pressure or volume overload on the heart. Common direct causes and risk factors for HF are listed in Table 37-1.


TABLE 37-1 COMMON CAUSES AND RISK FACTORS FOR HEART FAILURE










Right-sided HF in the absence of left-sided HF is usually the result of pulmonary problems such as chronic obstructive pulmonary disease (COPD) or pulmonary hypertension. Acute respiratory distress syndrome (ARDS) may also cause right-sided HF. These problems are discussed elsewhere in the cardiac unit.



Incidence/Prevalence


Over five million people in the United States have HF, causing about 875,000 hospitalizations each year. HF is the most common reason for hospital admission for people over 65 years of age. African Americans are affected more often than Euro-Americans, probably because they have more risk factors that can lead to HF. The disease is a major cause of disability and death after MI, often due to nonadherence to the treatment plan and recommended lifestyle changes.




Patient-Centered Collaborative Care



Assessment



History


When obtaining a history, keep in mind the many conditions that can lead to HF. Carefully question the patient about his or her medical history, including hypertension, angina (cardiac pain), MI, rheumatic heart disease, valvular disorders, endocarditis, and pericarditis. Ask about the patient’s perception of his or her activity tolerance, breathing pattern, sleeping pattern, urinary pattern, and fluid volume status, as well as his or her knowledge about HF.



Left-Sided Heart Failure

With left ventricular systolic dysfunction, cardiac output (CO) is diminished, leading to impaired tissue perfusion, anaerobic metabolism, and unusual fatigue. Assess activity tolerance by asking whether the patient can perform normal ADLs or climb flights of stairs without fatigue or dyspnea. Many patients with heart failure (HF) experience weakness or fatigue with activity or have a feeling of heaviness in their arms or legs. Ask about their ability to perform simultaneous arm and leg work (e.g., walking while carrying a bag of groceries). Such activity may place an unacceptable demand on the failing heart. Ask the patient to identify his or her most strenuous activity in the past week. Many people unconsciously limit their activities in response to fatigue or dyspnea and may not realize how limited they have become.


Perfusion to the myocardium is often impaired as a result of left ventricular failure, especially with cardiac hypertrophy. The patient may report chest discomfort or may describe palpitations, skipped beats, or a fast heartbeat.


As the amount of blood ejected from the left ventricle diminishes, hydrostatic pressure builds in the pulmonary venous system and results in fluid-filled alveoli and pulmonary congestion, which results in a cough. The patient in early HF describes the cough as irritating, nocturnal (at night), and usually nonproductive. As HF becomes very severe, he or she may begin expectorating frothy, pink-tinged sputum—a sign of life-threatening pulmonary edema.


Dyspnea also results from increasing pulmonary venous pressure and pulmonary congestion. Carefully question about the presence of dyspnea and when and how it developed. The patient may refer to dyspnea as “trouble in catching my breath,” “breathlessness,” or “difficulty in breathing.”


As exertional dyspnea develops (also called dyspnea upon or on exertion [DUE/DOE]), the patient often stops previously tolerated levels of activity because of shortness of breath. Dyspnea at rest in the recumbent (lying flat) position is known as orthopnea. Ask how many pillows are used to sleep or whether the patient sleeps in an upright position in a bed, recliner, or other type of chair.


Patients who describe sudden awakening with a feeling of breathlessness 2 to 5 hours after falling asleep have paroxysmal nocturnal dyspnea (PND). Sitting upright, dangling the feet, or walking usually relieves this condition.






Left-Sided Heart Failure

Left ventricular failure is associated with decreased cardiac output and elevated pulmonary venous pressure. It may appear clinically as:



Decreased blood flow to the major body organs can cause dysfunction, especially renal failure. Nocturia may occur when the patient is at rest.


The pulse may be tachycardic, or it may alternate in strength (pulsus alternans). Take the apical pulse for a full minute, noting any irregularity in heart rhythm. An irregular heart rhythm resulting from premature atrial contractions (PACs), premature ventricular contractions (PVCs), or atrial fibrillation (AF) is common in HF (see Chapter 36). The sudden development of an irregular rhythm may further compromise CO. Carefully monitor the patient’s respiratory rate, rhythm, and character, as well as oxygen saturation. The respiratory rate typically exceeds 20 breaths/min.


Assess whether the patient is oriented to person, place, and time. A short mental status examination may be used if there are concerns about orientation. Objective data are important because in daily conversation many people are skillful at covering up memory losses. Older adults are frequently disoriented or confused when the heart fails due to brain hypoxia (decreased oxygen).


Increased heart size is common with a displacement of the apical impulse to the left. A third heart sound, S3 gallop, is an early diastolic filling sound indicating an increase in left ventricular pressure. This sound is often the first sign of HF. A fourth heart sound (S4) also can occur; it is not a sign of failure but is a reflection of decreased ventricular compliance.


Auscultate for crackles and wheezes of the lungs. Late inspiratory crackles and fine profuse crackles that repeat themselves from breath to breath and do not diminish with coughing indicate HF. Crackles are produced by intra-alveolar fluid and are often noted first in the bases of the lungs and spread upward as the condition worsens. Wheezes indicate a narrowing of the bronchial lumen caused by engorged pulmonary vessels. Identify the precise location of crackles and wheezes and whether the wheezes are heard on inspiration, expiration, or both.





Laboratory Assessment


Electrolyte imbalance may occur from complications of HF or as side effects of drug therapy, especially diuretic therapy. Regular evaluations of a patient’s serum electrolytes, including sodium, potassium, magnesium, calcium, and chloride, are essential. Any impairment of renal function resulting from inadequate perfusion causes elevated blood urea nitrogen and serum creatinine and decreased creatinine clearance levels. Hemoglobin and hematocrit tests should be performed to identify HF resulting from anemia. If the patient has fluid volume excess, the hematocrit levels may be low as a result of hemodilution.


B-type natriuretic peptide (BNP) is used for diagnosing HF (in particular, diastolic HF) in patients with acute dyspnea. As discussed earlier, it is part of the body’s response to decreased cardiac output from either left or right ventricular dysfunction. An increase in BNP, in conjunction with history and physical, best differentiates between the dyspnea of HF and that associated with lung dysfunction (Wexler et al., 2009). However, patients with renal disease may also have elevated BNP levels (Chen et al., 2010).


Urinalysis may reveal proteinuria and high specific gravity. Microalbuminuria is an early indicator of decreased compliance of the heart and occurs before the BNP rises. It serves as an “early warning detector” that lets the health care provider know that the heart is experiencing early signs of decreased compliance, long before symptoms occur.



Arterial blood gas (ABG) values often reveal hypoxemia (low blood oxygen level) because oxygen does not diffuse easily through fluid-filled alveoli. Respiratory alkalosis may occur because of hyperventilation; respiratory acidosis may occur because of carbon dioxide retention. Metabolic acidosis may indicate an accumulation of lactic acid.








Improving Cardiac Output




Interventions

Collaborative care begins with nonsurgical interventions, but the patient may need surgery if these are not successful in meeting optimal outcomes.



Nonsurgical Management

Nonsurgical management relies primarily on a variety of drugs (Table 37-3). If drug therapy is ineffective, other nonsurgical options are available.


TABLE 37-3 COMMONLY USED DRUG CLASSIFICATIONS FOR PATIENTS WITH SYSTOLIC HEART FAILURE







Drugs to improve stroke volume include those that reduce afterload, reduce preload, and improve cardiac muscle contractility. A major role of the nurse is to give medications as prescribed, monitor for their therapeutic and adverse effects, and teach the patient and family about drug therapy. A variety of classes of drugs that reduce afterload and preload are used to manage heart failure (see Table 37-3).



Drugs That Reduce Afterload


By relaxing the arterioles, arterial vasodilators can reduce the resistance to left ventricular ejection (afterload) and improve CO. These drugs do not cause excessive vasodilation but reverse some of the inappropriate or excessive vasoconstriction common in HF.



Angiotensin-Converting Enzyme Inhibitors (ACEIs) and Angiotensin-Receptor Blockers (ARBs)


Patients with even mild heart failure (HF) resulting from left ventricular dysfunction are given a trial of ACE inhibitors or ARBs. Both ACE inhibitors (e.g., enalapril [Vasotec] and fosinopril [Monopril]) and ARBs (e.g., valsartan [Diovan], irbesartan [Avapro], and losartan [Cozaar]) improve function and quality of life for patients with HF. ACE inhibitors are the first-line drug of choice, but some health care providers prefer to start the patient on an ARB because ACE inhibitors can cause a nagging, dry cough. For patients with acute HF, the health care provider may prescribe an IV-push ACE inhibitor such as Vasotec IV.


The ACE inhibitors and ARBs suppress the renin-angiotensin system (RAS), which is activated in response to decreased renal blood flow. ACE inhibitors prevent conversion of angiotensin I to angiotensin II, resulting in arterial dilation and increased stroke volume. ARBs block the effect of angiotensin II receptors and thus decrease arterial resistance and arterial dilation. In addition, these drugs block aldosterone, which prevents sodium and water retention, thus decreasing fluid overload. Both ACEIs and ARBs work more effectively for Euro-Americans than for African-American populations. Volume-depleted patients should receive a low starting dose, or the fluid volume should be restored before beginning the prescribed drug. Monitor for hyperkalemia, a potential adverse drug effect in patients who have renal dysfunction.



Assess for orthostatic hypotension, acute confusion, poor peripheral perfusion, and reduced urine output in patients with low systolic blood pressure. Monitor serum potassium and creatinine levels to determine renal dysfunction. Additional nursing implications for selected ACE inhibitor/ARB drugs are described in Chapter 38 on p. 783 in the Drug Therapy section.




Interventions That Reduce Preload


Ventricular fibers contract less forcefully when they are overstretched, such as in a failing heart. Interventions aimed at reducing preload attempt to decrease volume and pressure in the left ventricle, increasing ventricular muscle stretch and contraction. Preload reduction is appropriate for HF accompanied by congestion with total body sodium and water overload.




Drug Therapy


Common drugs prescribed to reduce preload are diuretics and venous vasodilators. Morphine sulfate is also given for patients in acute heart failure (HF) to reduce anxiety, decrease preload and afterload, slow respirations, and reduce the pain associated with a myocardial infarction (MI).


The health care provider adds diuretics to the regimen when diet and fluid restrictions have not been effective in managing the symptoms of HF. Diuretics are the first-line drug of choice in older adults with HF and fluid overload (Joseph et al., 2009). These drugs enhance the renal excretion of sodium and water by reducing circulating blood volume, decreasing preload, and reducing systemic and pulmonary congestion.


The type and dosage of diuretic prescribed depend on the severity of HF and renal function. High-ceiling (loop) diuretics, such as furosemide (Lasix, Furoside image, Novosemide image), torsemide (Demadex), and bumetanide (Bumex), are most effective for treating fluid volume overload.



For those patients with acute HF, Lasix or Bumex can be administered by IV push (IVP). Lasix can be given in doses of 20 to 40 mg IV and increased by 20 mg every 2 hours until the desired diuresis is obtained. The usual IV initial dose for Bumex is 1 to 2 mg once or twice daily, but it is more often given in a continuous infusion of 10 mg over 24 hours.


The practitioner may initially use a thiazide diuretic, such as hydrochlorothiazide (HCTZ) (HydroDIURIL, Urozide image) and metolazone (Zaroxolyn), for older adults with mild volume overload. Zaroxolyn is a long-acting agent and is therefore often given every second, third, or fourth day, depending on patient need and tolerance.


Unlike loop diuretics, the action of thiazides is self-limiting (i.e., diuresis decreases after edema fluid is lost). Therefore the dehydration that may occur with loop diuretics is not common with these drugs. Patients also prefer thiazides because of the gradual onset of diuresis.


As HF progresses, many patients develop diuretic resistance with refractory edema. The health care provider may choose to manage this problem by prescribing both types of diuretics.


Monitor for and prevent potassium deficiency (hypokalemia) from diuretic therapy. The primary signs of hypokalemia are nonspecific neurologic and muscular symptoms, such as generalized weakness, depressed reflexes, and irregular heart rate. A potassium supplement may be prescribed for some patients. Other practitioners prescribe a potassium-sparing diuretic, such as spironolactone (Aldactone), for patients at risk for dysrhythmias from hypokalemia. Although not as effective as other diuretics, Aldactone helps retain potassium and thus decrease the risk of ventricular dysrhythmias.


Patients being managed with ACE inhibitors or ARBs and diuretics at the same time may not experience hypokalemia. However, if their kidneys are not functioning well, they may develop hyperkalemia (elevated serum potassium level). Review the patient’s serum creatinine level. If the creatinine is greater than 1.8 mg/dL, notify the health care provider before administering supplemental potassium.


The health care provider may prescribe venous vasodilators (e.g., nitrates) for the patient with HF who has persistent dyspnea. Significant constriction of venous and arterial blood vessels occurs to compensate for reduced CO. Constriction reduces the volume of fluid that the vascular bed can hold and increases preload. Venous vasodilators may benefit by:



Nitrates may be administered IV, orally, or topically. IV nitrates are used most often for acute HF. These drugs cause primarily venous vasodilation but also a significant amount of arteriolar vasodilation. Monitor the patient’s blood pressure when starting nitrate therapy or increasing the dosage. Patients may initially report headache, but assure them that they will develop a tolerance to this effect and that the headache will cease or diminish. Acetaminophen (Tylenol, Exdol image) can be given to help relieve discomfort.


Unfortunately, tolerance to the vasodilating effects develops when nitrates are given around-the-clock. To prevent this tolerance, the health care provider may prescribe at least one 12-hour nitrate-free period out of every 24 hours (usually overnight). Nitrates such as isosorbide (Imdur, ISMO) are prescribed to provide nitrate-free periods and reduce the problem of tolerance. Chapter 40 discusses nitrates in more detail.




Drugs That Enhance Contractility


Contractility of the heart can also be enhanced with drug therapy. Positive inotropic drugs are most commonly used, but vasodilators and beta-adrenergic blockers may also be administered. For chronic HF, low-dose beta blockers are most commonly used. Digoxin (Lanoxin) may be prescribed to improve symptoms, thereby decreasing dyspnea and improving functional activity. This older and long-used drug is not expensive. In some settings, nesiritide (Natrecor) may be administered for end-stage HF, although this drug is very expensive (see discussion of Natrecor for acute HF on p. 751).



Digoxin


Although not as commonly used today, digoxin (Lanoxin, Novodigoxin image), a cardiac glycoside, has been demonstrated to provide symptomatic benefits for patients in chronic heart failure (HF) with sinus rhythm and atrial fibrillation. Digoxin (sometimes called “dig”) therapy reduces exacerbations of HF and hospitalizations when added to a regimen of ACE inhibitors or ARBs, beta blockers, and diuretics. However, it may increase mortality due to drug toxicity, especially in older adults.


The potential benefits of digoxin include:



Digoxin is erratically absorbed from the GI tract. Many drugs, especially antacids, interfere with its absorption. It is eliminated primarily by renal excretion. Older patients should be maintained on lower doses of the drug than younger patients.



image Nursing Safety Priority


Drug Alert


Increased cardiac automaticity occurs with toxic digoxin levels or in the presence of hypokalemia, resulting in ectopic beats (e.g., premature ventricular contractions [PVCs]). Changes in potassium level, especially a decrease, causes patients to be more sensitive to the drug and cause toxicity.


The clinical manifestations of digoxin toxicity are often vague and nonspecific and include anorexia, fatigue, blurred vision, and changes in mental status, especially in older adults. Toxicity may cause nearly any dysrhythmia, but PVCs are most commonly noted. Assess for early signs of toxicity such as bradycardia and loss of the P wave on the ECG. Carefully monitor the apical pulse rate and heart rhythm of patients receiving digoxin.


The health care provider determines the desirable heart rate (HR) to achieve. Some health care providers prefer a rate less than 60 beats per minute. Report the development of either an irregular rhythm in a patient with a previously regular rhythm or a regular rhythm in a patient with a previously irregular one. Monitor serum digoxin and potassium levels (hypokalemia potentiates digoxin toxicity) to identify toxicity. Older adults are more likely than other patients to become toxic because of decreased renal excretion.


Any drug that increases the workload of the failing heart also increases its oxygen requirement. Be alert for the possibility that the patient may experience angina (chest pain) in response to digoxin.



Other Inotropic Drugs


Patients experiencing acute heart failure (HF) are candidates for IV drugs that increase contractility. For example, beta-adrenergic agonists, such as dobutamine (Dobutrex), are used for short-term treatment of acute episodes of HF. Dobutamine improves cardiac contractility and thus cardiac output and myocardial-systemic perfusion.


A more potent drug used for acute HF, milrinone (Primacor), functions as a vasodilator/inotropic medication with phosphodiesterase activity. Also known as a phosphodiesterase inhibitor, this drug increases cyclic adenosine monophosphate (cAMP), which enhances the entry of calcium into myocardial cells to increase contractile function. Like the beta-adrenergic agonists, Primacor is given IV.


Levosimendan (Simdax) is a calcium-sensitizing medication and a positive inotropic drug. It appears to bind to troponin C in the heart muscle and therefore increases the contraction of the heart. Simdax is used most often in patients who have had or are at high risk for myocardial infarction. Chapter 40 discusses inotropic drugs in more detail.


Stay updated, free articles. Join our Telegram channel

Jul 18, 2016 | Posted by in NURSING | Comments Off on Care of Patients with Cardiac Problems

Full access? Get Clinical Tree

Get Clinical Tree app for offline access