Heart failure (HF) occurs when the heart is unable to pump sufficient blood to meet the metabolic needs of the body. The result of inadequate cardiac output (CO) is poor organ perfusion and vascular congestion in the pulmonary or systemic circulation. In the United States, heart failure is the fastest-growing cardiac disorder and it affects 2% of the population. Almost 1 million hospital admissions occur each year for acute decompensated heart failure, and the rehospitalization rates during the 6 months following discharge are as much as 50%. In spite of recent advances in the treatment of heart failure, the 5-year estimated mortality rate is almost 50%.
Heart failure may be described as backward or forward failure, high- or low-output failure, or right- or left-sided failure. In backward failure, the ventricle fails to eject its contents, which results in pulmonary edema on the left side of the heart and systemic congestion on the right. In forward failure, an inadequate CO leads to decreased organ perfusion. High-output failure is the inability of the heart to meet the increased metabolic demands of the body despite a normal or high CO. Low-output failure occurs when the ventricle is unable to generate enough CO to meet the metabolic demands of the body. This type of failure consists of impaired peripheral circulation and compensatory vasoconstriction. Right-sided failure occurs when the right ventricle is unable to maintain an adequate cardiac output, and systemic congestion occurs. When the left ventricle is unable to produce a CO sufficient to prevent pulmonary congestion, left-sided failure occurs. Complications of heart failure include pulmonary edema, renal failure, cerebral insufficiency, myocardial infarction, and cardiac dysrhythmias.
Heart Failure may result from a number of causes that affect preload (venous return), afterload (impedance the heart has to overcome to eject its volume), or contractility. Elevated preload can be caused by incompetent valves, renal failure, volume overload, or a congenital left-to-right shunt. Elevated afterload occurs when the ventricles have to generate higher pressures in order to overcome impedance and eject their volume. This disorder may also be referred to as an abnormal pressure load. An elevation in afterload also may be caused by hypertension, valvular stenosis, or hypertrophic cardiomyopathy. Abnormal muscle conditions may diminish contractility and cause a decrease in the ability of the heart muscle to act as a pump. Some common causes of diminished contractility include cardiomyopathy, coronary artery disease, acute myocardial infarction, myocarditis, amyloidosis, sarcoidosis, hypocalcemia, hypomagnesemia, or iatrogenic myocardial damage caused by drugs (adriamycin or disopyramide) or radiation therapy for mediastinal tumors or Hodgkin’s disease.
Nursing care plan assessment and physical examination
Patients with heart failure typically have a history of a precipitating factor such as myocardial infarction, recent open heart surgery, dysrhythmias, or hypertension. Symptoms vary based on the type and severity of failure. Ask patients if they have experienced any of the following: anxiety, irritability, fatigue, weakness, lethargy, mild shortness of breath with exertion or at rest, orthopnea that requires two or more pillows to sleep, nocturnal dyspnea, cough with frothy sputum, nocturia, weight gain, anorexia, or nausea and vomiting. Take a complete medication history, and determine if the patient has been on any dietary restrictions. Determine if the patient regularly participates in a planned exercise program.
The New York Heart Association has developed a commonly used classification system that links the relationship between symptoms and the amount of effort required to provoke the symptoms:
Class I: No limitations. No symptoms (fatigue, dyspnea, or palpitations) with ordinary activity.
Class II: Slight mild limitation of physical activity. Comfortable at rest or mild exertion but more than ordinary exertion leads to fatigue, palpitations, dyspnea, or angina.
Class III: Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity leads to fatigue, dyspnea, palpitations, or angina.
Class IV: Symptomatic at rest; discomfort increases with any physical activity; confined to bed or chair.
Observe the patient for mental confusion, anxiety, or irritability caused by hypoxia. Pale or cyanotic, cool, clammy skin is a result of poor perfusion. In rightsided heart failure, the jugular veins may become engorged and distended. If the pulsations in the jugular veins are visible 4.5 cm or more above the sternal notch with the patient at a 45-degree angle, jugular venous distension is present. The liver may also become engorged, and pressure on the abdomen increases pressure in the jugular veins, causing a rise in the top of the blood column.
This positive finding for heart failure is known as hepatojugular reflux (HJR). The patient may also have peripheral edema in the ankles and feet, in the sacral area, or throughout the body. Ascites may occur as a result of passive liver congestion. With auscultation, inspiratory crackles or expiratory wheezes (a result of pulmonary edema in left-sided failure) are heard in the patient’s lungs. The patient’s vital signs may demonstrate tachypnea or tachycardia, which occur in an attempt to compensate for the hypoxia and decreased CO. Gallop rhythms such as an S3 or an S4, while considered a normal finding in children and young adults, are considered pathological in the presence of heart failure and occur as a result of early rapid ventricular filling and increased resistance to ventricular filling after atrial contraction, respectively. Murmurs may also be present if the origin of the failure is a stenotic or incompetent valve.
Note that experts have found that the physiological measures of heart failure (such as ejection fraction) do not always predict how active, vigorous, or positive a patient feels about his or her health; rather, a person’s view of health is based on many factors such as social support, level of activity, and outlook on life.
Nursing care plan primary nursing diagnosis: Decreased cardiac output related to an ineffective ventricular pump.
Nursing care plan intervention and treatment
Initial management of the patient with heart failure depends on severity of heart failure, seriousness of symptoms, etiology, presence of other illnesses, and precipitating factors. Medication management is paramount in patients with heart failure. The general principles for management are treatment of any precipitating causes, control of fluid and sodium retention, increasing myocardial contractility, decreasing cardiac workload, and reducing pulmonary and systemic venous congestion. The physician may also prescribe fluid and sodium restriction in an attempt to reduce volume and thereby reduce preload.
If the elevated preload is caused by valvular regurgitation, the patient may require corrective surgery. Corrective surgery may also be warranted if the elevated afterload is caused by a stenotic valve. Another measure that may be taken to reduce afterload is an intra-aortic balloon pump (IABP). This is generally used as a bridge to surgery or in cardiogenic shock after acute myocardial infarction. It involves a balloon catheter placed in the descending aorta that inflates during diastole and deflates during systole. The balloon augments filling of the coronary arteries during diastole and decreases afterload during systole. IABP is used with caution because there are several possible complications, including dissection of the aortoiliac arteries, ischemic changes in the legs, and migration of the balloon up or down the aorta.
Other measures the physician may use include supplemental oxygen, thrombolytic therapy, percutaneous transluminal coronary angioplasty, directional coronary atherectomy, placement of a coronary stent, or coronary artery bypass surgery to improve oxygen flow to the myocardium. Finally, a cardiac transplant may be considered if other measures fail, if all other organ systems are viable, if there is no history of other pulmonary diseases, and if the patient does not smoke or use alcohol, is generally under 60 years of age, and is psychologically stable.
To conserve her or his energy and to maximize the oxygen that is available for body processes, encourage the patient to rest. Elevation of the head of the bed to 30 to 45 degrees may alleviate some of the dyspnea by lowering the pressure on the diaphragm that is caused by the contents of the abdomen and by decreasing venous return, thereby decreasing preload. The patient may need assistance with activities of daily living, even eating, if the heart failure is at end stage and the least bit of activity causes fatigue and shortness of breath. To assess the patient’s response to activity, check the blood pressure and heart rate, as well as the patient’s subjective response both before and after any increase in activity level. Prolonged periods of little or no activity can be very difficult to reverse; therefore, maintaining some level of activity is highly encouraged.
To control symptoms, provide ongoing monitoring throughout the acute phases of the patient’s disease. Monitor the patient for signs and symptoms of fluid overload, impaired gas exchange, and activity intolerance. Routine assessment of the cardiovascular and pulmonary systems is imperative in the early detection of exacerbation. Monitor daily intake and output, as well as daily weight, and conduct cardiopulmonary assessment.
Education of the patient and family is important for preventing exacerbations and frequent hospital visits. HF is clearly a condition that can be managed on an outpatient basis. A clear explanation of the disease process helps the patient understand the need for the prescribed medications, activity restrictions, diet, fluid restrictions, and lifestyle changes. Written material should be provided for the patient to take home and use as a reference. The patient may no longer be able to live alone or support himself or herself. Fear, anxiety, and grief can all stimulate the sympathetic nervous system, leading to catecholamine release and additional stress on an already compromised heart. Helping the patient work through and verbalize these feelings may improve psychological well-being and CO.
Nursing care plan discharge and home health care guidelines
To prevent exacerbations, teach the patient and family to monitor for an increase in shortness of breath or edema. Tell the patient to restrict fluid intake to 2 to 2.5 L per day and restrict sodium intake as prescribed. Teach the patient to monitor daily weights and report weight gain of more than 4 pounds in 2 days. Be sure the patient and family understand all medications, including effect, dosage, route, adverse effects, and the need for routine laboratory monitoring for drugs such as digoxin. Tell the patient to call for emergency assistance for acute shortness of breath or chest discomfort that is not alleviated with rest.