The Out-of-Hospital Management of Acute Heart Failure

Marvin A. Wayne

Vincent N. Mosesso Jr.

Introduction

Acute heart failure (AHF) is one of only two cardiovascular diseases with an increasing prevalence; the other is atrial fibrillation. Five million Americans have the disease, and more than 500,000 are newly diagnosed each year. AHF is a major disease of our aging population¹ because most hospitalizations for AHF are of patients older than 65 years.² Heart failure (HF) results in more than 2 million hospitalizations annually and accounts for about 3% of the national health care budget.¹ Further, it is Medicare’s largest single disease expenditure. Approximately 300,000 deaths are annually related to HF.³

Heart failure, and its acute presentation, AHF, is a complex disease that includes at least four clinical syndromes: exacerbation of chronic HF, hypertensive crisis, acute pulmonary edema (APE), and cardiogenic shock.⁴ Of these four syndromes, APE and cardiogenic shock are the two most serious. Although the major clinical manifestations in both are a combination of decreased peripheral perfusion and pulmonary congestion, they differ in pathophysiology and hemodynamic changes. Accordingly, these syndromes require different therapeutic approaches.

APE, the most common clinical manifestation of AHF,⁵ is a life-threatening respiratory emergency usually occurring in the out-of-hospital setting. The overall prehospital mortality rate for APE in a retrospective Italian study has been reported to be 8%.⁶ Although similar data for the United States are not readily available, a favorable outcome for AHF is dependent on rapid assessment and treatment initiated in the out-of-hospital setting.

Pathogenesis of Ape

APE can be of a cardiogenic or noncardiogenic etiology. In the former, pulmonary edema results from increased microvascular hydrostatic pressure, whereas in the latter edema arises from increased pulmonary capillary
permeability. The end result is identical in both cases: an excessive accumulation of extravascular lung fluid.⁷ The primary cause of cardiogenic APE is cardiac dysfunction (Table 2-1). Noncardiogenic APE may be caused by several diverse events or diseases, which include systemic or pulmonary infection, trauma, septic shock, toxic inhalation, or aspiration of gastric contents.⁸ Because both types of APE have the same clinical manifestations—dyspnea, diaphoresis, decreased lung compliance, anxiety, and increased shunt fraction—distinguishing between the two can be extremely difficult.⁷

TABLE 2-1 Precipitating Causes of Acute Cardiogenic Pulmonary Edema (APE)

Cause	Incidence (%)
Worsening heart failure	26
Coronary insufficiency	21
Subendocardial infarction	16
Transmural infarction	10
Acute dysrhythmia	9
Medication noncompliance	7
Dietary indiscretion	3
Valvular insufficiency	3
Other	5
From Marx J, Hockberger R, Walls R. Rosen’s emergency medicine: concepts and clinical practice, 5th ed. Saint Louis: Mosby, 2002, with permission.

APE is often difficult to distinguish clinically from an exacerbation of chronic obstructive pulmonary disease (COPD) or other acute pulmonary disorders. The misdiagnosis of AHF in the out-of-hospital setting has been documented to be 23% in one study⁹ and as high as 32% in another.¹⁰ The need for the correct identification of precipitating events, and the rapid initiation of appropriate treatment, is critical to achieve a positive outcome. Inappropriate therapy, as a result of misdiagnosis, may result in harm to the patient. Hoffman and Reynolds⁹ reported that adverse effects were more common in misdiagnosed patients. Untoward effects included (a) respiratory depression in patients receiving morphine, (b) hypotension and bradycardia in patients receiving both morphine and nitroglycerin, and (c) arrhythmia associated with hypokalemia in patients receiving furosemide.

Initiating events or conditions, including myocardial ischemia, hypertensive crisis, fluid excess, medication noncompliance, diet, and overexertion, may trigger AHF. Each may set in motion a vicious cycle of events that results in cardiogenic APE. The key components of this cycle, outlined in Figure 2-1, all involve left ventricular (LV) dysfunction.¹¹ A marked increase in systemic vascular resistance in conjunction with impaired myocardial
contractility, from either systolic or diastolic dysfunction, results in pulmonary edema. This increase in vascular resistance leads to an increase in LV diastolic pressure resulting in increased pulmonary venous pressure. This increases hydrostatic pressure, which then forces fluid to leak out of the pulmonary capillaries into the pulmonary interstitial space and alveoli, producing edema. As edema worsens, so does oxygen diffusion, and thus oxygen saturation drops and further compromises cardiac contractility, creating a positive feedback circuit.¹²

FIGURE 2-1 Processes involved in pulmonary edema. Cycle may begin at any point but once begun is self-perpetuating. (From Sacchetti AD, Harris RH. Acute cardiogenic pulmonary edema. What’s the latest in emergency treatment? Postgrad Med 1998;103:145–147, with permission.)

Field Assessment

Assessment begins with a rapid, focused history and physical examination of the patient. This includes patient history, recent illness, prescribed medications, medication compliance, and diet. Together this constitutes an important first step in the field diagnosis of AHF (Table 2-2). Critical elements of the physical examination include accurate determination of vital signs. AHF/APE is often associated with marked elevation in systolic blood pressure. Prehospital providers, even in the absence of peripheral edema, should strongly consider cardiogenic pulmonary edema in patients presenting with acute respiratory distress, hypoxemia, tachypnea, rales or wheezing, and marked hypertension. Such patients often have histories of poorly controlled hypertension and/or prior cardiac disease. Blood pressure of greater than 180/120 mm Hg is common in this setting and is a good sign of reversibility. In these patients, a rapid reduction in blood pressure often produces prompt relief of respiratory distress. Marked
hypertension associated with acute respiratory distress and wheezing, particularly in elderly patients without a history of asthma or pulmonary infection, is strongly suggestive of APE. Such a presumptive diagnosis may be supported by the presence of cardiovascular medications and the absence of respiratory medications, such as metered-dose inhalers. Even when these facts are present, out-of-hospital personnel should always consider alternate etiologies such as pulmonary embolism, pneumonia, asthma, and drug overdose before diagnosing patients as having APE. Although rhythm strips and standard 12-lead electrocardiograms (ECGs) are useful in identifying arrhythmia and/or acute coronary syndrome, they are insensitive and nonspecific for diagnosing AHF.¹³^,¹⁴ Furthermore, these ECGs and rhythm strip tracings may be prone to misinterpretation.¹⁵ Recently, a new type of ECG has been developed. This system uses an
acoustic sensor at leads V₃ and V₄ to diagnose the presence of S₃ and/or S₄ heart sounds (Audicor Inovice Medical Systems, Portland, OR). The presence of an S₃ in patients older than 45 years is highly specific for the presence of HF and may aid in the diagnosis of AHF.¹⁵^,¹⁶

TABLE 2-2 Diagnosis of Congestive Heart Failure

Prior history and comorbid states

Chronic heart failure
Hypertension
Ischemic heart disease
Valvular heart disease
Anemia
Dysrhythmias
Thyroid disease

Current situation

Medications (prescribed regimen and current compliance, other drug use)
Symptoms of acute coronary syndromes
Diet or exercise indiscretions in patients with known heart failure
Signs of pulmonary edema such as tachypnea, low oxygen saturation, rales, and peripheral edema
Signs of chronic obstructive pulmonary disease, asthma, or airway obstruction
Signs of pneumonia or sepsis, such as fever and purulent sputum

Tools

Pulse oximetry
End-tidal carbon dioxide trends
ECG rhythm and 12-lead if does not delay transport

Potential future diagnostic aids

B-type natriuretic peptide
Noninvasive cardiac output
Correlated audio electrocardiography

ECG, electrocardiogram.

In addition to these diagnostic tests, a number of other diagnostic aids have been developed to improve accuracy in the evaluation and diagnosis of AHF. Although not currently used in the prehospital environment, a rapid bedside assay of blood levels of B-type natriuretic peptide, a neurohormone secreted mainly by the cardiac ventricles in response to volume expansion and pressure overload, is useful in establishing or excluding the diagnosis of AHF in patients with acute dyspnea in the emergency department (ED).¹⁶^,¹⁷^,¹⁸^,¹⁹^,²⁰ and ²¹ Application of such testing in the out-of-hospital environment may be a logical extension and further aid in diagnosis. Currently, noninvasive cardiac output (NICO) devices, such as impedance cardiography,²² have also been suggested as diagnostic tools, but their complexities and cost have to date precluded their out-of-hospital use.

TABLE 2-3 Management of Acute Congestive Heart Failure: Overview

Identify CHF
Identify and treat specific etiology when possible
Provide oxygen and ventilatory support when needed
Reduce LV preload
Reduce LV afterload
Provide inotropic support when needed
Match receiving facility with needed resources

CHF, congestive heart failure; LV, left ventricular.

Management of Ape

Fluid accumulation in the lungs associated with APE, until recently, was attributed to excess accumulation of total body fluid. Accordingly, treatment of APE was aimed at removing excess fluid by promoting massive diuresis. However, this explanation did not reconcile with APE cases without an increase in total body water. The current explanation is that APE results from fluid redistribution within the body whereby a part of the intravascular volume is redistributed to the lungs as a consequence of increased intravascular pressure.¹² Primary objectives for the treatment of AHF and associated APE are to reduce pulmonary capillary pressure, to redistribute pulmonary fluid, and to improve forward flow.¹¹^,¹² These goals may be achieved by reducing LV preload and afterload, providing ventilatory and inotropic supports, and identifying and treating the underlying etiology of the syndrome (Table 2-3). It should be recognized that these treatment measures are intended for APE patients who are normotensive or
hypertensive and not those who are hypotensive. The latter comprises cardiogenic shock arising secondary to severe LV systolic dysfunction; these patients may need inotropic or mechanical cardiac support, and the treatment of these critically ill patients is beyond the scope of this review.

Reduction of LV Preload

The initial effort to reduce the pulmonary congestion in patients presenting with APE should be to reduce the pressure and volume of blood flow to the pulmonary vasculature. This may be accomplished by dilating the venous capacitance system. This will result in decreased blood return to the right ventricle (preload), hence reducing blood flow to the pulmonary vascular bed. The net result is a reduction in LV preload, which then allows the LV output to more closely match inflow from the pulmonary system.¹¹ Pharmacologic therapy to reduce LV preload includes the use of nitrates primarily and, to a more limited extent, morphine and loop diuretics such as furosemide.

Nitrates

Nitroglycerin and related drugs at low dosages are primarily venodilators effective in decreasing pulmonary artery pressure. Intracellularly, they react with and convert sulfhydryl groups to S-nitrosothiols and nitric oxide. These reactive groups then activate the enzyme guanylate cyclase, which catalyzes the formation of cyclic guanosine monophosphate (cGMP). This nucleotide induces the reentry of calcium back into the sarcoplasmic reticulum of vascular smooth muscle thereby causing its relaxation.²³

Nitroglycerin is currently the vasodilator agent of choice for the reduction of LV preload in the field. It is fast acting, efficient, and easy to administer.¹¹^,¹² Nitroglycerin’s effectiveness in reducing mortality in patients with APE in the prehospital setting has been demonstrated by Bertini (1997).⁶ In this study, even hypotensive patients (systolic blood pressure <100 mm Hg) were found to respond positively to nitroglycerin. Likewise, Hoffman and Reynolds⁹ compared a number of prehospital management protocols for APE and concluded that nitroglycerin was beneficial, whereas morphine and furosemide had no additive effect when combined with nitroglycerin and were occasionally deleterious. The beneficial hypotensive effect of nitroglycerin must be closely monitored so that the reduction in blood pressure does not deleteriously reduce LV preload and the ability to produce adequate cardiac output. Thus, a potential disadvantage of nitroglycerin is that it can lead to excessive hypotension,⁸ particularly in patients without adequate preload [e.g., hypovolemia and inferior wall myocardial infarction (MI) with significant right ventricular (RV) involvement].

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