Heart Failure HF is the inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients. In the past, HF was often referred to as congestive heart failure (CHEF), because many patients experience pulmonary of peripheral congestion. Currently HF is recognized as a clin- ical syndrome characterized by signs and symptoms of fluidoverload or of inadequate tissue perfusion. Eluid overload and decreased tissue-perfusion result when the heart can- not generate a CO sufficient to meet the body’s demands. The term HF indicates myocardial disease in which there is a problem with contraction of the heart (systolic dysfunc- tion) or filling of the heart (diastolic dysfunction) that may or may not cause pulmonary or systemic congestion. Some cases of HF are reversible, depending on the cause. Most often, HF is a progressive, life-long diagnosis that is man-_ aged_with lifestyle changes and medications to prevent acute congestive episodes.Chronic Heart Failure Aswith coronary artery disease, the incidence of HF increases with age. At least 5 million people in the United States have HF, and 550,000 new cases are diagnosed each year (American Heart Association [AHA], 2004). Although HF can affect people of all ages, the prevalence in people older than 75 years of age is about 10%, and as the U.S. popula- tion ages, HF has become an epidemic that challenges the country’s health care resources (AHA, 2004), HF is the most common reason for hospitalization of people older than 65 years of age and the second most common reason for vis- its to a physician’s office. The rate of hospital readmission remains staggeringly high. The economic burden caused by HF is estimated to be more than $25 billion in direct and indirect costs and is expected to increase (AHA, 2004). The increase in the incidence of HF reflects the increased number of elderly people and improvements in treatment of cardiac diseases, resulting in increased survival rates. Many hospitalizations could be prevented by appropriate outpatient care. Prevention and early intervention to arrest the progression of HF are major health initiatives in the United States.There are two types of HF, which are identified by assess- ment of left ventricular functioning, usually by echocardio- gram. The more common type is an alteration in ventricular contraction called systolic heart failure, which is charac- terized by a weakened heart muscte-The less common alter- ation is diastolic heart faline rice is characterized by a stiffand noncompliant heart muscle, making it difficult for the ventricle to fill. An assessment of the ejection fraction (EF) is performed to assist in determining the type of HF. EF, an indication of the volume of blood ejected with each contraction, is calculated by subtracting the amount of blood wat the end of systole from the amount at the end of diastole and calculating the tcentage of blood that is ejected. A nor- mal EF is 55% 10 6S Bot the ventricular volume; the ventri- cle does not completely empty between contractions. The EF is normal in diastolic HF but severely reduced in systolic HF. Although ad is a hallmark » the severity of HE is frequently Hotlied seem eee symptoms. The New York Heart Association (NYHA) Classification is described in Table 30-1, and the causes are explained in subsequent sections of this chapter. The American College of Cardiology and the American Heart Association (ACC/ AHA) have proposed a new HF classification system (Insti- tute for Clinical Systems Improvement {ICSI}, 2004). This system (Table 30-2) takes into consideration the naturalPathophysiology HF results from a variety of cardiovascular conditions, in- cluding chronic hypertension, coronary artery disease, and valvular disease. These conditions can result in decreased caute HOR Coatsle decreased filling (diastole), or both. Significant myocardial dysfunction most often occurs before the patient copetiences Signs anid gns and symptoms of HF such as Sere ea edema, or fatigue. develops, the body activates neurohormonal com- pensatory mechanisms. These mechanisms represent thebody's attempt to cope with the HF and are responsible for the signs and symptoms that eventually develop. Under- standing these mechanisms is important because the treat- ment of HF is aimed at relieving them. Systolic HF results in decreased blood volume being ejected from the ventricle. icular stretch is-sensed_by baroreceptors in the aortic and carotid bodie (Piano & Prasun, 2003). The sympathetic nervous system is then stimulated to i i eph- rine (Fig. 30-2). The purpose of this initial response is to igcrease-heart rate and contractility and support the failing myocardium, but the continued response has multiple nega- tive effects. Sympathetic stimulation causes vasoconstriction of the skin, gastrointestinal tract, and kidneys. A decrease in renal perfusion due to low CO and vasoconstriction then causes the r in_by the kidney. Renin promotes the formation of angiotensin I, a benign, inactive substance. Angiotensin-converting enzyme (ACE) in the lumen of pul- monary blood vessels converts angiotensin I to angiotensin Il, a potent vasoconstrictor, which then increases the blood pressure and afterload. Angiotensin II also stimulates the release of aldosterone from the adrenal cortex, resulting in sodium and fluid retention by the renal tubules and stimu- lating the thirst center. This leads to the fluid volume over- load commonly seen in HF. Angiotensin, aldosterone, and other neurohormones (eg, endothelin, prostacyclin) lead to an increase in preload and afterload, which increases stress on the ventricular wall, causing an inc in the workload of the heart. A counterregulatory mechanism is attempted through the release of natriuretic peptides. Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) are re- leased from the overdistended cardiac chambers, These sub- stances promote vasodilation and diuresis. However, their effect is usually not strong enough to overcome the negative effects of the other mechanisms.As the heart's wor increases, contractility of the myo- ventricle aca os =diastol < blood volume in the ieitased > Nursing Process Assessment The nursing assessment for the patient with HF fo- cuses on observing for effectiveness of therapy and for the patient’s ability to understand and implement self- management strategies. Signs and symptoms of pul- monary and systemic fluid overload are recorded and reported immediately so that adjustments can be made in therapy. The nurse also explores the patient’s emotional response to the diagnosis of HF, a chronic and often progressive condition. | Health History The health history focuses on the signs and symptoms of HF, such as dyspnea,shortness of breath, andcough. Sleep disturbances, particularly sleep suddenly interrupted by shortness of breath, may be reported. The nurse also asks about the number of pillows needed for sleep (an indication of orthopnea), edema, abdominal symptoms, altered mental status, activities of daily living, and the activities that cause fatigue. The nurse explores the patient's understanding of HF, self-management strategies, and the desire to adhere to those strategies. The nurse helps patients identify the impact the illness has had on their quality of life and successful coping skills that they have used. Family and significant others are often included in these discussions. Physical Examination The lungs are auscultated to detect crackles and wheezes. Crackles, which are produced by the sudden opening of edematous small airways and alveoli that have adhered together by exudate, may be heard at the end of inspiration and are not cleared with coughing. Wheezing may also be heard in some patients. The rate and depth of respirations are also documented. The heart is auscultated for an S; heart sound, a sign that the heart is beginning to fail and that increased blood volume fills the ventricle with each beat. HR and rhythm are also documented. When the heart rate is rapid, the SV. decreases because the ventricle has less time to fill. This in turn produces increased pressure in the atria and eventually in the pulmonary vascular bed." JVD is also assessed; distention greater than 3 cm above the sternal angle is considered abnormal, This is an estimate, not a precise measurement, of central venous pressure. Sensorium and level of consciousness must be eval- uated. As the volume of blood ejected by the heart de- creases, so does the amount of oxygen transported to the brain. The nurse assesses dependent parts of the patient's body for perfusion and edema. With significant de- creases in SV, there is a decrease in perfusion to the periphery, causing the skin to feel cool and appear pale or cyanotic. If the patient is sitting upright, the feet and lower legs are examined for edema; if the patient is supine in bed, the sacrum and back are also assessed for edema. Fingers and hands may also be- come edematous. The liver is assessed for hepatojugular reflux. The patient is asked to breathe normally while manual pressure is applied over the right upper quadrant of the abdomen for 30 to 60 seconds. If neck vein disten- tion increases more than 1 cm, the finding is positive for increased venous pressure. If the patient is hospitalized, the nurse measures h output carefully to establish a baseline against whic to assess the effectiveness of diuretic therapy. Intake and output records are rigorously maintained. It S important to know whether the patient has ingen more fluid than he or she has excreted (positive u balance), which is then correlated with a gain a weight. The patient must be monitored for oligu™(diminished urine output, less than 400 mL/24 hours) or anuria (urine output less than 50 mL/24 hours). The patient is weighed daily in the hospital or at home, at the same time of day, with the same type of clothing, and on the same scale. If there is a signifi- cant change in weight (ie, 2- to 3-Ib increase in a day or 5-lb increase in a week), the patient is instructed to notify the physician or to adjust the medications (eg, increase the diuretic dose) Diagnosis Nursing Diagnoses Based on the assessment data, major nursing diagnoses for the patient with HF may include the following: ¢ Activity intolerance and fatigue related to imbal- ance between oxygen supply and demand because of decreased CO * Excess fluid volume related to excess fluid or sodium intake, and retention of fluid related to the HF syndrome * Anxiety related to breathlessness and restlessness from inadequate oxygenation * Powerlessness related to inability to perform role responsibilities because of chronic illness and hospitalizations * Noncompliance related to lack of knowledge Collaborative Problems, Potential Complications Based on the assessment data, potential complications that may develop include the following: * Cardiogenic shock (see also Chapter 15) * Dysrhythmias (see Chapter 27) * Thromboembolism (see Chapter 31) * Pericardial effusion and cardiac tamponade (see Chapter 29)Planning and Goals Major goals for the patient may include promoting ac- tivity and reducing fatigue, relieving fluid overload symptoms, decreasing the incidence of anxiety or in- creasing the patient's ability to manage anxiety, en- couraging the patient to verbalize his or her ability to make decisions and influence outco mes, and teaching the patient about the self-care program. 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