A 44-year-old man is brought to the hospital 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; 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 to touch and there is 1+ peripheral edema. Laboratory results are as follows: Which of the following is likely to be present in this patient compared to the normal state?

Question

A 44-year-old man is brought to the hospital 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; 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 to touch and there is 1+ peripheral edema.  Laboratory results are as follows:  Which of the following is likely to be present in this patient compared to the normal state?

Quizplus · Accepted Answer

11ec160b_3b5a_f226_9249_c1e5c07c88f0_MD0001_00 This patient with a recent upper respiratory infection has developed dyspnea, lower extremity edema, and an S3 on cardiac exam; this presentation suggests dilated cardiomyopathy with decompensated heart failure (CHF), likely from viral myocarditis. Renal decompensation (acute kidney injury or chronic kidney disease) occurs in up to 60% of patients with CHF and is often due to a complex syndrome known as cardiorenal syndrome. The pathophysiology of cardiorenal syndrome is multifactorial and includes both hemodynamic alterations related to the low output state and resultant neurohormonal changes. Decreased cardiac output results in renal hypoperfusion, which triggers the following adaptations: In the short-term, these adaptions increase the effective arterial blood volume and maintain systemic perfusion, allowing for a relatively normal glomerular filtration rate. However, over time, widespread vasoconstriction increases the afterload (ie, the resistance the heart must pump against) and ventricular overfilling leads to decreased pump efficiency, lowering cardiac output and furthering renal hypoperfusion. At a certain point, the decrease in cardiac output becomes overwhelming and glomerular filtration rate begins to drop. Characteristic laboratory findings in cardiorenal syndrome reflect activation of the RAAS and indicate a prerenal etiology, with low urine sodium and fractionated excretion of sodium (<1%). Urea is passively reabsorbed following sodium 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 normal responses to elevated extracellular fluid volume. In patients with CHF, the low cardiac output leads to activation of the RAAS which inhibits these actions. (Choices C and F) CHF is associated with decreased renal blood flow (due to low cardiac output/vasoconstriction) and increased renal venous pressure (due to volume overload), both of which act to reduce glomerular filtration rate. Elevated renal venous pressure is thought to reduce the glomerular filtration rate by increasing renal interstitial pressure and restricting blood flow through the afferent arteriole. Educational objective: Cardiorenal syndrome is due to hemodynamic alterations related to a low cardiac output state and maladaptive neurohormonal changes. Low cardiac output results in renal hypoperfusion, leading to activation of the renin-angiotensin-aldosterone system, antidiuretic hormone release, and increased sympathetic nervous system activity. The resultant increase in sodium and water reabsorption and systemic vasoconstriction have detrimental effects on left ventricular systolic function, further worsening cardiac output and renal perfusion.

A 44-Year-Old Man Is Brought to the Hospital with Fatigue