Approximately 5 million Americans have heart failure (HF) and at least 550,000 more are newly diagnosed each year. HF is the most common Medicare diagnosis-related group. In 2006, direct costs associated with the condition reached nearly $30 billion.
Although HF incidence hasn’t declined in the past 20 years, overall survival has improved. Better risk factor identification, early intervention, and appropriate long-term care management have contributed to improved survival.
Heart failure defined
HF is a progressive syndrome diagnosed from both clinical findings and structural and functional cardiac changes. Most people with symptomatic HF have some degree of left ventricular dysfunction, as from hypertension, myocardial infarction, myocardial infection, or genetic abnormalities.
Left ventricular ejection fraction (LVEF) is the percentage of blood pumped by the left ventricle with each heart beat. The Heart Failure Society of America (HFSA) describes two broad types of HF—one with reduced LVEF and one with preserved LVEF. Measured by echocardiography, ejection fraction (EF) normally is 55% or higher. Patients with an EF of 35% or lower may not have HF signs and symptoms right away and at times may compensate fairly well. In the past, the term congestive heart failure (CHF) was used to denote EF below 35%.
In systolic HF, EF typically is below 35%. But in diastolic failure, EF may be normal even if the right ventricle is enlarged or has abnormal filling. Thus, because signs and symptoms may be unrelated to fluid volume overload, the term CHF isn’t preferred unless the patient has decompensation symptoms.
Acute decompensated heart failure (ADHF) occurs when cardiac output fails to meet the body’s metabolic needs. Sometimes termed fluid volume overload, this unstable condition requires immediate treatment because it impairs perfusion to systemic organs, jeopardizing their function. ADHF results in prolonged hospital stays and increased illnesses and deaths. (See Chronic vs. acute decompensated heart failure in pdf format by clicking the download now button.)
In ADHF, both systolic and diastolic dysfunction may occur. The acute phase is preceded by heart damage—for instance, from cardiac ischemia, a valvular disorder, exposure to toxins, viral infection, hypertension, or diabetes mellitus. These conditions can affect the heart in many ways, influencing both cardiac preload and after load and causing coronary artery vasculature changes.
Decreased cardiac output activates the renin-angiotensin-aldosterone system, which regulates blood pressure and fluid balance. Continuous activation eventually leads to exacerbation of HF, as the heart must work harder to pump adequate blood. Over time, the myocardium starts to enlarge; this causes cellular dysfunction and potential functional loss. LVEF then declines, signs and symptoms of fluid volume overload arise, and HF worsens. (See Neurohormonal response in heart failure in pdf format by clicking the download now button.)
Assessment and diagnosis
ADHF diagnosis hinges largely on clinical and diagnostic findings. (See ADHF signs and symptoms in pdf format by clicking the download now button.) Diagnostic studies may include chest X-ray, electrocardiography, and laboratory tests, particularly B-natriuretic peptide (BNP). Cardiac cells release BNP when stretched; this triggers vasodilation, which improves cardiac preload and afterload. Normally, BNP measures less than 100 pg/mL; higher levels typically signal fluid volume overload. BNP levels are particularly useful in patients with a history of chronic obstructive pulmonary disease, as chest X-rays don’t always show pulmonary congestion in these patients.
Staging and classifying HF
Several classification systems are used for HF. The system developed by the American College of Cardiology (ACC) and American Heart Association (AHA) has four stages, based on the patient’s predisposing conditions and degree of illness. (See Stages of heart failure in pdf format by clicking the download now button.)
The New York Heart Association (NYHA) system was developed to evaluate the patient’s signs and symptoms and response to therapy; it’s based on functional status. Unlike the ACC/AHA system, it recognizes that signs and symptoms may vary from day to day and may get better or worse. Certain device-based therapies hinge on correlating a patient’s NYHA functional classification with his ACC/AHA stage. (See New York Heart Association classification in pdf format by clicking the download now button.)
The immediate management goal for patients with ADHF is to improve symptoms and hemodynamic parameters. Treatment guidelines from the ACC, AHA, and HFSA differentiate ADHF management from chronic HF management.
For patients with ADHF, treatment depends largely on fluid volume and perfusion status. Understanding the four basic hemodynamic subtypes of HF helps guide management. (See Hemodynamic subtypes of heart failure in pdf format by clicking the download now button.)
A patient with adequate perfusion (warm and dry or warm and wet) should receive beta blockers (metoprolol or carvedilol), diuretics (furosemide or torsemide), and vasodilators. If blood pressure is stable, the physician may consider an angiotensin-converting enzyme (ACE) inhibitor if the patient isn’t already taking one. Appropriate vasodilators for HF patients may include I.V. nesiritide, I.V. nitroglycerin, and I.V. nitroprusside. Keep in mind that those receiving I.V. nitroglycerin or nitroprusside need close blood pressure monitoring; depending on facility policy, they may require admission to a critical care setting.
In contrast, patients with poor perfusion (cold and dry or cold and wet) should receive diuretics and inotropic drugs to improve perfusion status. Even patients with low blood pressure should receive diuretics, such as furosemide or torsemide. Initially, those with compromised perfusion need gentle diuresis, with drugs given by intermittent I.V. injection or continuous I.V. infusion. Some experts believe continuous I.V. infusion causes less renal damage because it doesn’t trigger the hormone surge that can come from intermittent I.V. dosing.
Inotropic drugs, such as dobutamine or milrinone, may help stabilize patients in the short term. (Prolonged use increases mortality.) Patients who need these drugs may not tolerate beta-blocker therapy initially. Once perfusion is adequate, as shown by sufficient urine output and stable blood pressure, beta-blocker therapy should begin.
When caring for patients receiving inotropic drugs, monitor vital signs closely. Evaluate urine output, mental status, and oxygen saturation frequently; stay alert for sudden reductions, which could quickly lead to problems. Ask the physician about acceptable parameters for urine output, blood pressure, and oxygen saturation. According to the HFSA, patients with ADHF need invasive hemodynamic monitoring only if they don’t respond to treatment.
Intra-aortic balloon pump
Patients who don’t respond to drug therapy may be candidates for more invasive and aggressive therapy, such as an intra-aortic balloon pump (IABP). Used only in critical care settings, this device improves myocardial oxygenation and reduces cardiac workload.
If your patient has an IABP, monitor vital signs closely and evaluate invasive hemodynamic parameters frequently. Check urine output and level of consciousness every 30 minutes initially and then every hour. Also monitor the IABP itself, checking for blood in the tubing, appropriate waveforms, and helium volume in the tank (check every 4 hours). Evaluate the transducer level and zero it during every shift. Maintain the IABP catheter properly as indicated. Immobilize the affected extremity and assess its vascular status regularly.
Also assess for signs and symptoms of:
- inappropriate balloon placement, such as diminished pulses or sensation in the left arm, decreased urine output, and abdominal pain
- aortic dissection, such as decreased pulses; acute back, flank, or chest pain; reduced cardiac output; and increased heart rate.
Left ventricular assist device
Another invasive therapy is a left ventricular assist device (LVAD), which restores normal blood flow, thus easing dyspnea and other HF symptoms and resting the heart so it can recover normal function. LVADs are reserved for patients with end-stage HF. They can be used as a bridge to heart transplantation in patients with cardiomyopathy or as destination therapy for terminally ill patients not eligible for heart transplantation.
Additional drug therapy
Once your patient is stable and starts to show signs of improvement, perform a careful medication review. Current pharmacologic recommendations for HF patients include beta blockers, ACE inhibitors, or angiotensin II receptor blockers (ARBs) and/or an aldosterone antagonist before discharge.
Long-term therapy aims to relieve symptoms, increase exercise tolerance, maintain heart function, and prolong life. ACE inhibitor therapy should begin in the hospital once congestion resolves or should be started gradually at low dosages and titrated after inotropic therapy has been tapered. Be aware that in HF patients, ACE inhibitors block the renin-angiotensin cycle; if intolerance develops, marked by renal function changes or a dry hacking cough, ARBs should be attempted instead. By blocking the action of angiotensin II, ARBs reduce systemic vascular resistance and decrease aldosterone release. Some patients may receive epleronone, an aldosterone antagonist, which blocks activation of aldosterone and thus helps reduce vascular resistance.
Beta blockers, such as bisoprolol, carvedilol, or sustained-release metoprolol succinate, help decrease mortality in HF patients. They should be started in the hospital and titrated gradually until the optimal dosage is reached. Spironolactone, an aldosterone inhibitor, is a class I recommendation shown to help reduce mortality. If your patient is receiving it, watch closely for hyperkalemia from the drug’s potassium-sparing properties.
If HF signs and symptoms persist, the physician may prescribe digoxin. Although this drug isn’t a class I recommendation, patients who’ve been on it for several years can keep taking it, as no evidence-based contraindications for maintaining digoxin therapy exist.
Implantable cardiac defibrillators help prevent unexpected arrhythmia-related deaths in patients with LVEF of 30% or lower and NYHA class II through IV signs and symptoms. Cardiac resynchronization therapy (CRT) also can play a crucial role in preventing HF progression and improving functional class. CRT is recommended for patients with prolonged QRS complexes (more than 120 ms), LVEF of 35% or lower, and advanced signs and symptoms (NYHA class III or IV) while on optimal drug therapy.
Patients should start learning how to manage HF as soon as they’re admitted to the hospital. But this can pose a challenge because of the extent of the patient’s illness and the amount of information that must be covered. Insurance companies typically reimburse hospitals only for a 4-day stay for HF patients; yet the average stay exceeds 4 days.
Inform patients (and their families) that HF is a progressive disorder and can’t be cured. However, emphasize that dietary, lifestyle, and other behavioral modifications can help manage symptoms and reduce the need for hospital readmissions. Be sure to teach them about:
- factors that contribute to fluid volume overload (such as a diet high in sodium and excessive fluid intake)
- the need to restrict sodium intake to 2,000 mg/day and to restrict fluids to 64 oz/day
- the importance of taking prescribed medications consistently
- weighing themselves daily to detect fluid volume overload; inform them that a gain of 3 to 4 lb (1.4 to 1.8 kg) over 1 to 2 days most likely stems from fluid retention, not food
- when to notify their healthcare provider; for instance, when their weight changes, when they develop increased shortness of breath, or if urinary frequency occurs or urine output changes.
Knowledge brings hope
To manage ADHF effectively, you must understand how and why the condition develops, be able to recognize signs and symptoms, monitor patients closely, and know about treatment options. This knowledge is crucial in reducing patients’ hospital stay, minimizing readmissions, decreasing complications, and prolonging life.
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Both authors work at the Cleveland Clinic in Cleveland, Ohio. Maria L. Held is a Clinical Nurse Specialist and Marjorie Sturtz is a Certified Nurse Practitioner. The authors do not have any financial arrangements or affiliations with any corporations offering financial support or educational grants for continuing nursing education activities.