A 44-year-old man is brought to the emergency department with fatigue, shortness of breath, and lethargy. The patient had a brief upper respiratory illness about a month ago but began experiencing progressive dyspnea on exertion 2 weeks ago. He has no significant medical history and takes no medications. Blood pressure is 100/70 mm Hg and pulse is 95/min and regular. The apical impulse is palpated in the sixth intercostal space along the left anterior axillary line. An S3 is heard on cardiac auscultation. Bibasilar crackles are present. Distal extremities are cold, and there is 1+ peripheral edema. Laboratory results are as follows:
| Blood urea nitrogen | 45 mg/dL |
| Serum creatinine | 1.8 mg/dL |
| Urine microscopy | |
| Red blood cells | 0/hpf |
| White blood cells | 0-1/hpf |
| Sediment | none |
Which of the following is most likely to be present in this patient compared to the normal state?
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This patient with a recent upper respiratory infection has dyspnea, lower extremity edema, and an S3; this presentation suggests decompensated heart failure (DHF), likely due to dilated cardiomyopathy from viral myocarditis. The pathophysiology of DHF involves reduced cardiac output leading to decreased renal blood flow, which triggers neurohormonal adaptations that perpetuate a cycle of decompensation (Choice F). These ultimately maladaptive neurohormonal changes include the following:
Renin-angiotensin-aldosterone system (RAAS) activation, leading to increased proximal tubular sodium reabsorption (direct effect of angiotensin II)
Antidiuretic hormone release, resulting in increased free water reabsorption in the collecting ducts
Sympathetic nervous system activation, resulting in systemic vasoconstriction
In the short term, these adaptions increase blood volume and maintain systemic perfusion, allowing for a relatively normal glomerular filtration rate (GFR). However, over time, vasoconstriction-induced increased afterload and ventricular overfilling lead to decreased pump efficiency and decompensated failure. Renal dysfunction (eg, acute kidney injury) occurs in up to 60% of patients with DHF; it is often due to cardiorenal syndrome, a complication of the vicious cycle of DHF.
In cardiorenal syndrome, back pressure from the failing heart increases central venous and renal venous pressure (Choice C) to the point that the glomerular capillary filtration gradient drops substantially (due to interstitial edema causing increased hydrostatic pressure in Bowman capsule) and GFR significantly decreases. Characteristic laboratory findings in cardiorenal syndrome reflect activation of the RAAS and indicate a prerenal etiology, with low urine sodium (ie, fractional excretion of sodium <1%) and bland urine sediment. Urea passively follows sodium reabsorption in the proximal tubule, leading to an elevated blood urea nitrogen/creatinine ratio (>20:1).
(Choices A, B, and D) Decreased sodium and urea reabsorption and increased free water excretion are the normal responses to volume overload. However, in DHF, the appropriate response to volume overload is disrupted as the kidneys misinterpret reduced renal perfusion as an indicator of volume depletion (rather than volume overload) and activate RAAS and other maladaptive systems in response.
Educational objective:
Decompensated heart failure involves a vicious cycle of hemodynamic alterations and maladaptive neurohormonal changes resulting from decreased renal perfusion. Cardiorenal syndrome is a complication of this cycle, in which back pressure from the failing heart increases renal venous pressure to the point that the glomerular filtration rate drops substantially.