DRG Category: 292
Mean LOS: 4.3 days
Description MEDICAL: Heart Failure and Shock With CC
Nursing Type Primary: acute care
Nursing Type Secondary: critical care
System Primary: cardiovascular
System Secondary: not applicable
Heart failure (HF) occurs when the heart is unable to pump sufficient blood to meet the metabolic needs of the body. It is the most common nonfatal consequence of cardiovascular disorders and is the only major heart disease that is increasing significantly throughout the world. The American Heart Association (AHA) estimates that as many as 6.5 million people in the United States have HF, and in the next 15 years, it anticipates an increase of 46% in HF prevalence. Almost 1 million hospital admissions occur each year for acute decompensated HF, and the rehospitalization rates during the 6 months following discharge are as much as 50%. In spite of recent advances in the treatment of HF, the 5-year estimated mortality rate is almost 50%.
In HF, the result of inadequate cardiac output (CO) is poor organ perfusion and vascular congestion in the pulmonary or systemic circulation. HF 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 CO, and systemic congestion occurs. When the left ventricle is unable to produce a CO sufficient to prevent pulmonary congestion, left-sided failure occurs.
Several pathophysiological mechanism are involved in HF. Local angiotensin II production increases the heart's workload because of sodium and water retention, promotes progressive loss of myocardial function, and increases myocardial mass. As the heart fails, myocytes (heart muscle cells) enlarge, go through apoptosis (cellular death), and the heart muscle is remodeled and becomes maladaptive. Both systolic and diastolic failure occurs, and atrial natriuretic peptide and beta-type natriuretic peptide promote vasodilation and sodium loss. Complications of HF include pulmonary edema, renal failure, cerebral insufficiency, myocardial infarction, and cardiac dysrhythmias.
HF 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 (doxorubicin or disopyramide) or radiation therapy for mediastinal tumors or Hodgkin disease. Some clinical experts classify the causes as underlying causes (acquired or congenital structural abnormalities), fundamental causes (biochemical or physiological mechanisms), precipitating causes (valvular conditions, medications, radiation), and genetic causes (see next section). Risk factors include myopathy, previous myocardial infarction, valvular heart disease, alcohol use, substance abuse, hypertension, diabetes mellitus, dyslipidemia, sleep disorders, thyroid disease, and chemotherapy/radiotherapy.
HF is a complex disease combining the actions of numerous genes with environmental factors. Many HF risk factors have genetic causes or are associated with genetic predispositions. These include hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM), coronary heart disease, myocardial infarction, and hypertension. Genetic polymorphisms of the renin-angiotensin-aldosterone system (RAAS) and sympathetic system have also been associated with susceptibility to and/or mitigation of HF. Gene variants in the ADRA2C adrenoceptor and the ADRB1 adrenoceptor have been associated with a higher risk of HF among African Americans.
HF may occur at any age and in both genders as a result of congenital defects, hypertension, valve disease, coronary artery disease, or autoimmune disorders. Elderly people, however, are much more prone to the condition because of chronic hypertension, coronary artery disease, myocardial infarction, chronic ischemia, or valve disease, all of which occur more frequently in the elderly population. As compared with white/European American people, the incidence and prevalence of HF are higher in black/African American people and people of Hispanic/Latino and Native American backgrounds. Although men and women have similar rates of HF, women tend to have the condition later in life than men, and they survive longer with heart failure than their male counterparts.
HF occurs in all regions of the globe, but the cause of HF varies by the resources available in the region. In developing regions, such as South and Central America, Chagas disease, an infection that generally occurs in the tropics by a protozoan parasite, plays an important role. Valvular cardiomyopathy is also more common in developing regions, and HF occurs at earlier ages than in developed regions. Outcomes in patients from developing countries are worse than in developed countries, likely because of a shortage of healthcare resources in developing countries. In developed parts of the world such as North America and Western Europe, HF is most often caused by ischemic heart disease and ischemic cardiomyopathy. Compared with people living in North American and Western European, recent immigrants from developing nations and the former Soviet republics have a higher prevalence of HF.
Patients with HF typically have a history of a precipitating factor such as myocardial infarction, recent open heart surgery, dysrhythmias, alcohol/substance abuse, or hypertension. Symptoms vary depending 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:
The most common symptom of heart failure is shortness of breath, which may occur with exertion (exertional dyspnea) or at night (orthopnea and paroxysmal nocturnal dyspnea). Dyspnea at rest may occur. 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 right-sided HF, 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 distention 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 HF 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 HF 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 HF (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. HF is often accompanied by depression or anxiety.
|Test||Normal Result||Abnormality With Condition||Explanation|
|Echocardiography (ECHO)||Normal heart size, structure, and cardiac output||Depressed cardiac output, evidence of cardiomegaly||Measures chamber size, valvular structure and function, ventricular wall motion, and an estimated ejection fraction|
|Multigated blood pool imaging||Normal cardiac output and ejection fraction||Alterations in cardiac output and ejection fraction, often decreased||Assesses cardiac volume during both systole and diastole; data are used to determine ejection fraction; values are depressed in low-output failure|
|B-type natriuretic peptide (BNP)||< 100 pg/dL: no HF||100–300 pg/dL: HF is present; 300+: mild HF; 600+: moderate HF; 900+: severe HF||Naturally formed polypeptide; major source of plasma BNP in the cardiac ventricles; BNP level increases when HF symptoms worsen and decreases when the condition stabilizes|
Cardiac Magnetic Resonance Imaging (cMRI): Has the ability to obtain information on structure and function with one noninvasive test. Electrocardiography: Reveals ventricular hypertrophy, ventricular dilatation, and axis deviation, although this test is not conclusive in itself and needs to be followed up with an ECHO. Chest X-ray: May show cardiomegaly, pulmonary vascular congestion, alveolar or interstitial edema, or pleural effusions. Other Tests: Tests include serum electrolytes, blood urea nitrogen, arterial blood gases, genetic testing, liver enzymes, prothrombin time, color flow mapping, and cardiac angiograms.
Diagnosis: Decreased cardiac output related to an ineffective ventricular pump as evidenced by dyspnea, tachycardia, and/or peripheral edeam
Outcomes: Cardiac pump: Effectiveness; Circulation status; Tissue perfusion: Abdominal organs and peripheral; Vital sign status; Electrolyte and acid-base balance; Endurance; Energy conservation; Fluid balance
Interventions: Cardiac care; Circulatory care: Mechanical assist device; Fluid/electrolyte management; Medication administration; Medication management; Oxygen therapy; Vital signs monitoring
MEDICAL. Initial management of the patient with HF depends on severity of HF, seriousness of symptoms, etiology, presence of other illnesses, and precipitating factors. Medication management is paramount in patients with HF. 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. Nonpharmacologic therapy includes nutrition, weight loss, and exercise. The physician may also prescribe fluid and sodium restriction in an attempt to reduce volume and thereby reduce preload.
SURGICAL. 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. Other measures the physician may use include supplemental oxygen, thrombolytic therapy, percutaneous transluminal coronary interventions, directional coronary atherectomy, placement of a coronary stent, or coronary artery bypass surgery to improve oxygen flow to the myocardium. Circulatory devices such as ventricular assist devices and total artificial hearts can serve as a bridge to transplantation. Intra-aortic balloon counterpulsation or extracorporeal membrane oxygenation may be used for organ underperfusion in emergency situations. 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.
|Medication or Drug Class||Dosage||Description||Rationale|
|Vasodilators||Varies by drug||Decrease arterial and venous vasoconstriction due to activation of adrenergic and renin-angiotensin systems; increase venous capacitance; drugs such as nitroglycerin and angiotensin-converting enzyme inhibitors (ACEIs) such as captopril, enalapril, and lisinopril; angiotensin receptor blockers (ARSs) such as losartan, valsartan, candesartan||Reduce vasoconstriction, thereby reducing afterload and enhancing myocardial performance and decreasing preload and ventricular filling pressures|
|Diuretics||Varies by drug||Increase excretion of sodium and water with drugs such as furosemide (Lasix) and metolazone (Zaroxalyn)||Used for patients with volume overload|
|Digoxin||0.125–0.375 mg PO qd||Cardiotonic||Increases cardiac contractility and helps manage some atrial dysrhythmias; may increase myocardial oxygen demand|
Human B-Type Natriuretic Peptides: Dilates arteries and veins; used in case of serious HF. Dobutamine: Sympathomimetic, selective beta-1 stimulator that increases contractility, improves CO, decreases pulmonary capillary wedge pressure, and increases renal blood flow (as a result of improved CO). Dopamine: Low doses to stimulate dopaminergic receptors, causing renal vasodilation and improved renal function. Beta-Adrenergic Blocking Agents (Metoprolol, Carvedilol): Agents improve symptoms, exercise tolerance, cardiac hemodynamics, and left ventricular performance; they decrease mortality in HF patients, especially those with ischemic and idiopathic cardiomyopathy. Other Drugs: Antihypertensive agents (hydralazine, minoxidil) and, in severe cases of HF, nitroprusside may be used in an attempt to reduce afterload and improve CO. Norepinephrine is used for profound hypotension; phosphodiesterase inhibitors (milrinone, amrinone) cause increased contractility, decreased pulmonary vascular resistance, and decreased afterload. Anticoagulants may be used to decrease the risk of thromboembolism.
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 HF 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. The patient and family may need end-of-life care and a referral to hospice.
Dudley, N., Ritchie, C., Wallhagen, M., Covinsky, K., Cooper, B., Patel, K., . . . Chapman, S. (2017). Characteristics of older adults in primary care who may benefit from primary palliative care in the US. Journal of Pain and Symptom Management, 55(2), 217–225.
PREVENTION. 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.
MEDICATIONS. 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.
COMPLICATIONS OF HF. Tell the patient to call for emergency assistance for acute shortness of breath or chest discomfort that is not alleviated with rest.
Nursing Central is an award-winning, complete mobile solution for nurses and students. Look up information on diseases, tests, and procedures; then consult the database with 5,000+ drugs or refer to 65,000+ dictionary terms. Complete Product Information.