Immediate Management of the ADHF
Newly developed clinical practice guidelines for the management of ADHF exist, but management is still based largely on empirical evidence.12 Begin ADHF treatment in the ED with intravenous diuretics (unless contraindicated). A majority of ADHF patients will respond to diuretics alone.13 If the patient responds poorly to diuretics, the use of nesiritide in conjunction with diuretics has proven beneficial, as shown in the analysis of data from the ADHERE registry indicating that patients treated with intravenous nesiritide had a lower hospital mortality rate than patients treated with milrinone or dobutamine.14 Other options include ultrafiltration, an intervention that has been noted to reduce lengths of stay and rehospitalization rates in patients with ADHF.
Nesiritide is a recombinant form of BNP without direct inotropic effects but with venous, arterial, and coronary vasodilatory properties that can improve symptoms in ADHF.15 The recommended dosage for nesiritide is an IV bolus of 2 mcg per kg, followed by a continuous infusion of 0.01 mcg/kg/min. In the setting of hypotension with a systolic blood pressure less than 100 mm Hg, however, an initial IV bolus dose is not recommended; instead, the patient may start with a continuous infusion of 0.01 mcg/kg/min, or consider other therapies.
In hemodynamically unstable patients with a systolic blood pressure less than 90 mm Hg, or in those with evidence of end organ hypoperfusion (cardiogenic shock), inotropic support may be considered until the patient is stabilized. (See Table 3, p. 22.) Recognize that inotropic agents have adverse effects on the neurohormonal system and are not recommended routinely but may be essential for temporary stabilization. (For more on pharmacologic management of ADHF, see Table 4, p. 24.)
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Figure 2. Posteroanterior and lateral chest X-rays showing basilar infiltrates and an enlarged cardiac silhouette
Subacute Management of ADHF
Once acute decompensation has been reversed and an euvolemic state has been achieved, shift therapy to a combination of three classes of medications: diuretics, angiotensin-converting enzyme (ACE) inhibitors, and beta-blockers, unless contraindicated. The benefits of these drugs have been established by evidence from numerous large-scale clinical trials.3,12
Start ACE inhibitors in all patients with heart failure due to left ventricular systolic dysfunction (unless contraindicated or if the patient is intolerant).3 Give ACE-I to patients who have experienced a recent episode of ADHF, along with diuretics to maintain sodium balance and to prevent peripheral and pulmonary edema. ACE inhibitors are contraindicated for patients who are pregnant and for those with childbearing potential, as well as for individuals with a prior history of angioedema or renal failure after receiving the drug. Instruct patients to avoid any sudden change of position, as they may experience orthostatic hypotension while taking ACE inhibitors.
Some patients are intolerant of ACE inhibitors due to a persistent cough that occurs in approximately 5% to 10% of Caucasian patients and in up to 50% of Chinese patients.16 Angiotensin receptor blockers (ARBs) are an established alternative.17 Two ARBs (candesartan and valsartan) are recommended for treatment of heart failure based on evidence from controlled clinical trials.17,18 These drugs have demonstrated a reduction in hospitalizations, and candesartan, when used as an alternative to ACE-I, has been shown to reduce mortality. Additionally, in patients with evidence of left ventricular dysfunction after myocardial infarction, valsartan provided a benefit that was not inferior to ACE inhibitors.17
Initiate beta-blockers at very low doses and gradually increased as tolerated. Monitor patients closely for symptoms of hypotension, significant weight gain, fluid retention, bradycardia, and heart block. In addition, inform patients that they may experience generalized fatigue or weakness with the initiation of beta-blockers. In a cancer patient it is difficult to differentiate between fatigue caused by the disease and the side effects of therapy. Fatigue associated with beta-blocker therapy usually resolves spontaneously within a few days. Make every effort to achieve optimum target beta-blocker dose.