Treatment

Although improving signs and symptoms are the principal immediate goals, successful inpatient therapy for worsening HF involves a comprehensive care plan. Treatment to relieve symptoms should be applied in a way that limits side effects and reduces the risk of cardiac and renal injury. Precipitating factors must be identified and chronic oral therapy optimized during the patient's hospitalization. Patients who could potentially benefit from revascularization should be identified. Education must be provided concerning dietary sodium restriction, self-assessment of volume status and principal cardiac medications. Optimizing inpatient care is critical to achieve symptom relief and low readmission rates within an acceptable period of hospitalization.

Symptom Relief. Symptoms in patients hospitalized for HF typically arise from 2 distinct causes: pulmonary or systemic congestion and poor end-organ function from inadequate cardiac output. Data from several studies demonstrate that volume expansion and congestion are far more common than symptoms arising from low cardiac output.37 Dyspnea often improves significantly within the first few hours from diuretic and vasodilator therapy even though volume loss may not be substantial. Several additional days of hospitalization are often necessary to return the patient to a volume status that makes discharge acceptable.

Adverse Effects of Therapy. High-dose diuretic therapy is a marker for increased mortality during hospitalization for HF, as it is in chronic HF.38,39 Whether this is a direct adverse effect of diuretics or a reflection of the severity of the HF is unclear. However, complications of diuretic therapy that could result in poor outcomes include electrolyte disturbance, hypotension, volume depletion, and worsening renal function. Treatments that effectively relieve symptoms in patients with ADHF, such as diuretics, morphine, vasodilators, and inodilators, can be associated with significant short- and even long-term adverse effects on renal function.

Troponin release has been documented during hospitalization for ADHF.40 These findings suggest that myocyte loss from necrosis and apoptosis may be accelerated in patients admitted with ADHF. Mechanisms potentially accounting for cell death are still being determined but may include neurohormonal activation and pharmacologic therapy. Medications that increase myocardial oxygen demand have the potential to induce ischemia and may damage hibernating but viable myocardium, especially in patients with ischemic heart disease. Experimental data indicate that dobutamine can cause necrosis in hibernating myocardium.41 One outcome study comparing dobutamine to levosimendan suggested greater risk in patients randomized to dobutamine.42

Precipitating Factors. Many episodes of worsening HF requiring hospitalization are triggered by comorbid conditions and may not be due to progressive cardiac dysfunction. Poor medication adherence, inability to maintain a restricted sodium diet, or unwillingness to follow the care plan may be the primary cause of many admissions. Not surprisingly, these factors predispose to high rates of readmission following hospital discharge.

Optimization of Oral Pharmacologic Therapy. Hospitalization for ADHF presents an excellent opportunity to restructure the patient's chronic oral medication regimen. The inpatient period is especially useful in adjusting oral therapies in patients with low blood pressure, reduced heart rate and impaired renal function, circumstances which typically make dose adjustment problematic on an outpatient basis. The need for potassium and magnesium supplementation can also be addressed.

Device Therapy. Evaluate the patient for implantable cardioverter defibrillator (ICD) or biventricular pacing therapy (see Section 9).

Education. Hospitalization provides the opportunity to enhance patients' understanding of their HF. Although retention of knowledge imparted during an admission may be limited, introduction of key concepts, including the seriousness of HF, important aspects of therapy, and monitoring volume status, sets the stage for additional education in the follow-up period. See Section 8 for additional information on patient education.

Disease Management. Referral to a disease management program for HF can be facilitated by resources in the hospital and is often a key to reducing the risk of readmission. Patients with frequent hospitalization are readily identifiable as candidates for this approach. See Section 8 of this guideline for a full discussion of disease management approaches in HF.

The value of specific clinical assessments to monitor the response of patients admitted with ADHF has not been evaluated in controlled studies. However, there is sufficient consensus of expert opinion to support the utility of serial evaluation of specific data obtained from the history, physical examination, and laboratory findings during hospitalization.

Tracking Volume Status. Evidence that congestion is resolving should be carefully documented during hospitalization by monitoring reduction in symptoms (orthopnea, dyspnea, paroxysmal nocturnal dyspnea [PND], abdominal bloating, and edema) and signs (jugular venous pressure [JVP], rales, peripheral edema, ascites) of volume overload. Daily weights and determination of intake and output are not always accurate indicators of volume status, but still are critical in this assessment, as long as they are correlated with changes in symptoms and physical signs of fluid overload.

Blood Pressure. Blood pressure may decline significantly during hospitalization due to multiple factors including diuretic and vasodilator therapy, bed rest, and a more limited sodium intake. Although declines in blood pressure are typically well tolerated, symptomatic hypotension is an important adverse event in patients admitted with decompensated HF. Excessive or overly rapid diuresis (or overly rapid fluid removal with ultrafiltration), or excessive vasodilator therapy, even when fluid overload is still present, may produce symptomatic hypotension. Documentation of orthostatic blood pressure change on admission and after therapy may help reduce the likelihood of this side effect.

Laboratory Assessment. Serial determinations of electrolytes (especially sodium, potassium, and magnesium) and renal function (blood urea nitrogen [BUN] and serum creatinine) are necessary during diuresis. Patients may become hypokalemic and require supplemental potassium. Measurement of serum potassium and renal function should be performed more frequently in patients experiencing substantial diuresis (more than 2 L/day) or in patients with abnormalities in serum potassium concentration or renal function before the initiation of diuretic therapy.

*See background section for additional recommendations on laboratory evaluations.

Deterioration of renal function during diuresis is a poor prognostic sign and may occur even before achieving euvolemic status. Studies indicate that increasing serum creatinine is associated with an increase in morbidity and mortality in patients with ADHF.28,29,31,32,38-45 A major dilemma occurs when creatinine rises in the face of continued signs and symptoms of congestion. Few data are available to guide clinicians to the best response to a decline in renal function in this setting. Most physicians continue diuresis as long as the increase in creatinine is modest, since failure to relieve ongoing congestion often leaves the patient symptomatic and at risk for a poor outcome. If increasing creatinine is thought to reflect intravascular volume depletion, either relative or absolute, then reduction or temporary discontinuation of diuretic or vasodilator therapy should be considered, with a reduction in the rate of diuresis to prevent a rapid depletion of intravascular volume. Adjunctive use of inotropic therapy should be considered. If substantial fluid excess persists and diuresis cannot be achieved without an unacceptable degree of azotemia, then dialysis should be considered.

The prognostic significance of worsening renal function in the setting of drug therapy is more difficult to determine. Outpatient initiation of ACE inhibitor therapy commonly increases serum creatinine, especially in severe HF. In chronic HF, modest increases have been associated with long-term reductions in mortality and hospital admissions.46,47 Routine and frequent laboratory tests recommended in ADHF are shown in Table 12.5.

Electrolytes, BUN, creatinine. and troponin have been discussed. A complete blood count will exclude anemia. Determination of oxygen saturation will define the need for supplemental oxygen. Arterial blood gases may detect unsuspected carbon dioxide retention and suggest a comorbid pulmonary problem. Liver function tests may be elevated when there is poor hepatic perfusion or congestion or may indicate a comorbid hepatic problem. Urinalysis will exclude urinary tract infections and will help exclude acute tubular necrosis if there has been a hypotensive episode and the creatinine is rising.