Cardiology Clinical Case / MCQS / Uworld for Usmle step 2 / case 2

Cardiology Clinical Case  / MCQS / Uworld for Usmle step 2 / case 2 with answer and explanation and references and Educational objective

A 68-year-old man comes to the emergency department with a 3-week history of progressive dyspnea, orthopnea, and lower extremity edema. His past medical history is significant for hypertension, type 2 diabetes mellitus, myocardial infarction 8 years ago, and congestive heart failure. Current medications include metoprolol, digoxin, enalapril, furosemide, spironolactone, and aspirin. His blood pressure is 135/80 mm Hg, and pulse is 75/min and regular. Symmetric 2+ pitting edema of the lower extremities is present. Point of maximal impulse is displaced to the left and a soft holosystolic murmur is heard at the apex. Bilateral crackles are present over the lower lobes. Laboratory results are as follows:

·        Complete blood count

Hemoglobin 11 g/dL

Platelets 300,000/µL

Leukocytes 7,500/µL

·        Serum chemistry

Sodium 128 mEq/L

Potassium 5.3 mEq/L

Creatinine 1.9 mg/dL

Calcium 9 mg/dl

Phosphorus 4 mg/dL

Electrocardiogram shows normal sinus rhythm and no acute ischemic changes. Which of the following is most likely accurate regarding this patient's condition ?

A. Hyponatremia indicates severe heart failure . B. Increasing sodium intake will help to control the electrolyte abnormalities. C. Increasing the dose of digoxin may be indicated . D. Serum norepinephrine level is low . E. The combination of furosemide and enalapril is the cause of  hyperkalemia .

Answer : A

Explanation :

Poor prognostic factors in systolic heart failure
Clinical	·        Higher NYHA functional class ·        Resting tachycardia ·        Presence of S3 gallop ·        Elevated jugular venous pressure ·        Low blood pressure (< 100/60 mm Hg( ·        Moderate to severe mitral regurgitation ·        Low maximal oxygen consumption (peak VO2)
Laboratory	·        Hyponatremia ·        Elevated pro-BNP levels ·        Renal insufficiency
Electrocardiography	·        QRS duration >120 msec ·        Left bundle branch block pattern
Echocardiography	·        Severe LV dysfunction ·        Concomitant diastolic dysfunction ·        Reduced right ventricular function ·        Pulmonary hypertension
Associated conditions	·        Anemia ·        Atrial fibrillation ·        Diabetes mellitus

LV = left ventricular;  NYHA =New York Heart Association;  Pro-BNP= N-terminal pro-brain natriuretic peptide;  VO2= oxygen consumption.

This patient's clinical features - dyspnea, orthopnea, lower extremity edema, displaced apical impulse, and bilateral lung crackles - are consistent with decompensated congestive heart failure (CHF) due to left ventricular (LV) systolic dysfunction. Hyponatremia in patients with CHF usually parallels the severity of heart failure and is an independent predictor of adverse clinical outcomes.

In patients with CHF, low cardiac output, along with decreased perfusion pressure at the baroreceptors and renal afferent arterioles, leads to neurohumoral activation with the release of renin, norepinephrine (Choice D), and secretion of antidiuretic hormone  (ADH). ADH (vasopressin) binds to V2 receptors in the renal collecting ducts and promotes water reabsorption. while renin (via angiotensin Il) and norepinephrine increase

proximal sodium and water reabsorption and limit water delivery to the distal tubules. These actions promote free water retention and lead to dilutional hyponatremia.

(Choice B) Restriction of water intake is the initial therapy for hyponatremia in patients with CHF. Salt tablets (in addition to fluid restriction) can be used in patients with hyponatremia due to syndrome of inappropriate antidiuretic hormone secretion (SIADH), but should not be used in edematous patients with volume overload.

(Choice C) Patients with higher digoxin levels have increased risk of toxicity with no evidence of improvement in symptoms or outcomes for those with decompensated CHF.

(Choice E) Low distal sodium and water delivery in CHF leads to reduced potassium excretion and subsequent hyperkalemia. Furosemide enhances potassium excretion,  and the combination of angiotensin-converting enzyme inhibitors and loop diuretics improves cardiac output and may correct electrolyte abnormalities.

Educational objective:

Hyponatremia in patients with congestive heart failure parallels the severity of heart failure and is an independent predictor of adverse clinical outcomes. It is caused by increased levels of renin, norepinephrine and antidiuretic hormone. Treatment involves fluid restriction, angiotensin-converting enzyme inhibitors, and loop diuretics.

 

References: 1.   Hyponatremia in congestive heart failure. Another link : Hyponatremia in congestive heart failure.

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