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Case 8 Cardiology

Heart Failure

Work it one clue at a time. The diagnosis stays hidden until you reveal it.

Clue 1

A man presents to you with the clinical syndrome of heart failure (weight gain, orthopnea, elevated JVP, etc.). BP is 144/48 mm Hg.

This should generate a hypothesis. Yoo you look for other specific physical findings. What do you notice in this video?

Clue 2

Quincke’s pulse is consistent with your hypothesis, so you look for more evidence in his neck. And you have found it.

Clue 3

You then listen to the patient’s heart in anticipation of hearing a decrescendo diastolic murmur and confirming your suspicions.

But there is no decrescendo diastolic murmur. Further, his echocardiogram is totally normal. There is no aortic valve pathology. There is no systolic dysfunction.

Wide pulse pressure, Quincke’s pulse, and Corrigan’s pulse are not specific for aortic regurgitation. They are physical manifestations of a hyperkinetic state from ANY cause.

The combination of high-output physiology and HF should generate a new hypothesis. You test your hypothesis with right heart catheterization.

Clue 4

You have diagnosed the patient with high-output heart failure. What’s causing it?

Retrospective history reveals the consumption of 3-4 glasses of wine daily. Hypothesis-driven laboratory investigation is pursued.

Clue 5

You have now diagnosed the patient with high-output heart failure secondary to thiamine deficiency (wet beriberi).

Alcohol leads to thiamine deficiency through a variety of mechanisms, including poor diet and decreased absorption of thiamine in the GI tract.

Why is the diagnosis of wet beriberi so critical to make? It is curable. Take a look at BP and PP over time with alcohol cessation and thiamine replacement:

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