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A 51-year-old African American man presents to the emergency department (ED) with a chief complaint of dyspnea and swelling. He has a history of hypertension (HTN) and non-insulin-dependent type 2 diabetes. He works as a long-haul truck driver and reports not having seen a physician in over 3 years due to his work schedule and is no longer taking any home medications. He is saturating 93% on room air, has a pulse rate of 80 bpm, a blood pressure of 194/92 mm Hg, and a temperature of 36.5°C. Examination is remarkable for distention of the jugular veins, diffuse rales on inspiration, and 2+ pitting edema to midthigh. Initial electrocardiogram (ECG) shows left ventricular hypertrophy (LVH) by voltage criteria and left-axis deviation. A chest x-ray shows diffuse interstitial edema. Initial bloodwork is notable for a sodium of 135 mEq/L, creatinine of 1.1 mg/dL, albumin of 3.6 g/dL, hemoglobin of 12.9 g/dL, and brain natriuretic peptide (BNP) of 456 pg/mL. The patient receives oral hydralazine and intravenous (IV) nitroglycerin while in the ED with improvement of his blood pressure to 146/85 mm Hg, but he remains dyspneic with minimal exertion. A transthoracic echocardiogram reveals a hypertrophied left ventricle with moderately depressed left ventricular ejection fraction (LVEF) of 35% to 40% and grade II diastolic dysfunction.


Acute congestion from volume overload is a major driver of hospitalization in heart failure (HF). Loop diuretics remain the cornerstone of decongestive therapy.1,2

Figure 27-1 illustrates the principle behind diuretic therapy in acute HF. An initial clinical evaluation of patients with suspected acute decompensated heart failure (ADHF) should focus on determining fluid status and excluding cardiogenic shock.1

Figure 27-1

The principle of diuretic therapy in acute decompensated heart failure (ADHF). The acutely failing heart is functioning in the flat portion of the Frank-Starling curve, where small increases in blood volume result in large increases in left ventricular end-diastolic pressure (LVEDP) without significantly increasing cardiac output (CO). Inversely, decreasing the intravascular volume can significantly decrease the LVEDP and thus relieve congestive symptoms without significantly decreasing CO.

In general, patients with cardiogenic shock should be adequately stabilized prior to diuretic therapy.1 Patients with pulmonary edema despite relatively normal volume status have hemodynamic congestion (eg, hypertensive emergency, acute valvular pathology) but may still benefit symptomatically from adjunctive diuretic therapy, which exhibits acute venodilatory effects.1 Those patients who are clearly volume overloaded should receive loop diuretics to improve symptoms and functional status. Diuretics should be given intravenously for more rapid onset of action and predictable bioavailability.1

The diuretic strategies discussed in this chapter apply to both heart failure with reduced ejection fraction (HFrEF) as well as heart failure with preserved ejection fraction (HFpEF).


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