Observation Unit—Treatment Protocols

J. Douglas Kirk

Introduction

Although there are guidelines from various sources about the management of patients with heart failure, most pertain to chronic management.¹ Limited data are available from randomized controlled trials of acute decompensated heart failure (ADHF) patients in the emergency department (ED), much less the observation unit (OU). As a result, little consensus exists regarding their management, adding to the inconsistent care. This chapter focuses on therapeutic management, with respect to general supportive measures, pharmacologic therapy, and, most important, specific treatment protocols or algorithms that can be implemented in your institution.

General Support

The majority of patients admitted to the OU with ADHF have a chief complaint of dyspnea, and supplemental oxygen should be administered initially in essentially all patients. Pulse oximetry should be used to measure the effectiveness, with a target of maintaining an oxygen saturation of 95% or greater. This may require high-flow oxygen by facemask in some patients, whereas others may need oxygen only by nasal cannula.

Patients with severe dyspnea or hypoxia, typically seen in cases of flash pulmonary edema from severe hypertension and diastolic dysfunction (a unique syndrome more related to “hemodynamic mismatch”² than true “cardiac failure”), may require more aggressive airway maneuvers. In such cases, endotracheal intubation may be warranted or inevitable, but every attempt should be made to avoid intubation because of its associated morbidity in these patients. Obviously, patients this ill are not good candidates for OU care. However, the use of aggressive airway adjuncts such as noninvasive ventilation (NIV) may assist in avoiding the need for intubation while maintaining adequate oxygenation and ventilation. NIV should not be considered a substitute for intubation or, more importantly, other pharmacologic management but rather as a bridge to therapies
directed at reducing filling pressures and pulmonary congestion. Further, brief periods of NIV should not exclude patients from the OU by definition, especially in patients with acute pulmonary edema from hemodynamic mismatch.

Initial Management of Acute Pulmonary Edema

Although many patients with acute pulmonary edema are too sick for subsequent OU management, a number will turn around quickly with aggressive ED treatment, particularly those with hemodynamic mismatch. Concurrent with the previously mentioned airway maneuvers, all efforts should be directed at reducing pulmonary congestion. The most rapid improvement will be achieved with potent vasodilators such as nitroglycerin, nesiritide, or nitroprusside. Although each is quite effective, their immediate intravenous use often requires too much time to set up, a luxury these patients may not have. Initiation of sublingual nitroglycerin therapy, in doses larger than those typically used for chest pain (two to six 0.4-mg tablets or sprays) can be quite effective.³ One can achieve significant reductions in pulmonary capillary wedge pressure and blood pressure (afterload) with an improvement in respiratory symptoms, often within minutes. Patients can then be transitioned to one of the aforementioned intravenous vasodilators and typically are reasonable candidates for the OU.

The addition of an intravenous diuretic to this strategy is common and makes some practical sense because it will result in significant diuresis and hence a drop in preload, although probably not immediately. However, a number of these patients do not suffer necessarily as much from total fluid overload as from maldistribution of fluid into the pulmonary bed. By limiting diuretic use in these patients, important deleterious effects may be avoided, confirming the primary role of vasodilators in this population (Table 6-1). Although the data are limited in the use of any of these agents in the setting of acute pulmonary edema and respiratory distress, there appears to be an immediate benefit from rapid administration of sublingual nitroglycerin with or without an intravenous loop diuretic. Further recommendations on the use of these agents cannot be made until further research elucidates the utility and safety of such an approach.

Pharmacologic Therapy

Although general supportive measures such as maintaining adequate oxygenation are critical, the mainstay of therapy is pharmacologic. The primary goal is to decrease filling pressures. An additional important goal is improving cardiac output through a reduction in afterload or improvement in contractility. In patients with diastolic dysfunction, improving the ventricle’s ability to fill with blood is key, through efforts to improve myocardial relaxation.

TABLE 6-1 Untoward Effects of Therapeutic Agents for ADHF

Diuretics	Vasodilators	Inotropes
Decreased renal perfusion	Tachycardia (NTG, NTP)	Increased mortality
Volume depletion	Tachyphylaxis (NTG)	Proarrhythmic
Electrolyte abnormalities (K⁺, Ca⁺², Mg⁺²)	Neurohormonal activation (NTG, NTP)	Tachycardia
Neurohormonal activation:	Thiocyanate toxicity (NTP)	Neurohormonal activation
↑ renin-angiotensin aldosterone	Need for titration (NTG, NTP)
↑ sympathetic nervous system	Need for invasive monitoring (NTP, ± NTG)
ADHF, acute decompensated heart failure; NTG, nitroglycerin; NTP, nitroprusside. Adapted from Kirk JD, Diercks DB. Acute decompensated heart failure. In: Aghababian RV, ed. Essentials of emergency medicine. Sudbury, MA: Jones & Bartlett, 2006: 117–124.

Diuretics

Diuretics are often first-line therapy in the OU management of patients with ADHF and as such have become a mainstay of many treatment protocols in the OU. The rationale is that patients are volume overloaded, and, although this may be true, more important than a total increase in volume is the acute elevation in filling pressures. Nonetheless, diuretics are effective in reducing preload and removing excess fluid. The loop diuretic furosemide is most commonly used, although other loop diuretics are equally effective. Suggested starting doses are 40 mg of intravenous furosemide in diuretic naive patients or an amount equivalent to the patient’s total usual daily dose given intravenously. Peak diuresis should occur within 30 to 60 minutes. Repeated doses, in some instances double the initial dose, are often used in patients who fail to respond. Doses greater than 160 mg of furosemide are likely to produce as many side effects as results and should be discouraged. In patients with diuretic resistance, use of an additional diuretic that works on the proximal tubule (e.g., metolazone) may produce an effective diuresis. Caution should be exercised with excessive diuretic use. In addition to the well-described electrolyte depletion (K⁺, Mg⁺²), recent literature demonstrates that diuretics result in decreased renal perfusion and neurohormonal activation by increasing renin and norepinepherine.⁴^,⁵ The short-term gains with diuretic therapy may be offset by the decrease in renal perfusion and resultant deleterious long-term effects (Table 6-1).

Vasodilators

A minority of patients have mild exacerbations of ADHF and therapy with oxygen and loop diuretics may be sufficient, especially if their visit is due to brief periods of medical or dietary noncompliance. However, this frequently
is not adequate and the addition of vasodilators becomes necessary, particularly in patients with severe hypertension and diastolic dysfunction. Most are well perfused and hence are best treated with vasodilators such as nitroglycerin, nesiritide, or nitroprusside. Some patients with mild ADHF may respond to sublingual, oral, topical, or intravenous nitrates, and several OU treatment protocols advocate this approach.³^,⁶ Others have promoted the use of sublingual angiotensin-converting enzyme inhibitors (ACEIs) in this setting, based largely on a small trial of 22 patients who showed symptomatic improvement after treatment with sublingual captopril.⁷

Data from ADHERE, a multicenter heart failure registry, suggest that patients treated with an intravenous vasodilator initiated in the ED versus later in the hospital or not at all had lower mortality (4.3% vs. 10.9%, unadjusted, p <0.0001) and shorter hospital lengths of stay (3 vs. 7 days, p <0.001).⁸ These data generate some enthusiasm that early goal-directed therapy initiated in the ED or OU may hold promise and further study is warranted.

Despite their widespread acceptance as standard therapy, surprisingly little clinical outcome data exist for the vasodilators nitroglycerin and nitroprusside to support their use in ADHF. Physician familiarity with nitroglycerin use in patients with chest pain makes the combination of nitroglycerin and diuretics frequent first-line therapy. Nitroprusside can also be particularly useful in patients with acute pulmonary edema associated with severe hypertension but its use is uncommon. However, there are several limitations to these therapies, including the deleterious effects of neurohormonal activation and the need for titration and hemodynamic monitoring (Table 6-1). The latter two characteristics make these agents ill-suited for use in the OU. This has led to a search for better therapeutic agents, ideally ones that improve acute symptoms and hemodynamics as well as mortality. Further, ease of use is an important consideration in choosing an agent to be used in the OU.

Natriuretic Peptides

Nesiritide is the only intravenous vasodilator studied to date in the OU environment. Approved by the Food and Drug Administration in 2001, it became the first commercially available natriuretic peptide used for the treatment of ADHF. It is identical to human endogenous B-type natriuretic peptide (BNP) and serves as an antagonist to pathologic neurohormonal activation that occurs in heart failure. This feature is common among heart failure pharmacologic agents with proven mortality benefit, including ACEIs and beta-blockers. Its most important effect is the general counterbalancing of vasoconstrictive neurohormones in patients with poor cardiac output.

Nesiritide produces significant reductions in pulmonary capillary wedge pressure, right atrial pressure, and systemic venous resistance within minutes and concomitant increases in stroke volume and cardiac output.⁹ In addition, it does not possess many of the untoward properties associated with diuretics, inotropes, or other vasodilators (Table 6-1). In the PRECEDENT
trial, a comparison of nesiritide with dobutamine, the investigators found fewer arrhythmias and no increase in heart rate with nesiritide.¹⁰ Data from the VMAC trial demonstrated that nesiritide decreased pulmonary capillary wedge pressure more than either nitroglycerin or standard therapy at 3 hours and more than nitroglycerin at 24 hours.¹¹ Dyspnea and global clinical status were improved compared with standard therapy and similar to that of nitroglycerin. In addition, nesiritide’s hemodynamic effects were longer lasting, without a need for up-titration, which was frequently necessary in the nitroglycerin group to maintain adequate reduction in wedge pressure.¹² To date nesiritide is the only therapy that has been shown in randomized controlled trials of ADHF to provide significant symptomatic and hemodynamic improvement compared with placebo plus standard care.¹¹ However, it has not been studied in a trial prospectively designed or adequately powered to evaluate its effect on mortality, and some have questioned its safety.¹³

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