Patient 1:

This is an older man with moderate alcohol use who developed the clinical syndrome of heart failure. Echocardiography was unremarkable. He was noted to have a wide pulse pressure and Quincke’s pulse on exam, which led to the hypothesis of high output heart failure. Right heart catheterization confirmed the diagnosis, demonstrating a cardiac output of 12 L/min. Thiamine levels were severely low, consistent with the diagnosis of wet beriberi. With abstinence from alcohol and thiamine replacement therapy, the patient completely recovered without the need for diuretic therapy. Pulse pressure narrowed back to normal.

Patient 2:

This is a young man with a history of a congenital quadricuspid aortic valve and 16 years earlier had undergone a Ross procedure
(during which the aortic valve was replaced by a pulmonary autograft and the pulmonary valve was replaced by a pulmonary homograft), who developed endocarditis of the pulmonary autograft.

Video courtesy of NEJM: “Quincke’s Pulse”

Patient 3:

This is a middle-aged woman with end-stage renal disease who receives dialysis through a brachial arteriovenous fistula.

This patient also has a continuous bruit over the fistula.

Patient 4:

This patient has severe aortic regurgitation.

Patient 5:

This patient has severe aortic regurgitation.

Patient 6:

This patient has Quincke’s pulse related to the high output state of sepsis.

Patient 7:

This patient has severe aortic regurgitation.

Patient 8:

This is a middle-age man who was admitted to the hospital with cardiogenic shock of unclear etiology. He was discovered to have Corrigan’s pulse on exam, which led to the discovery of Quincke’s pulse, radial-femoral pulse delay, and discrepent blood pressures between the upper and lower extremities. He was subsequently diagnosed with coarctation of the aorta.

This patient also has Corrigan’s pulse, vigorous peripheral pulses in the upper extremities, radial-femoral pulse delay, and a systolic murmur.

Patient 9:

This is an older woman with NASH cirrhosis who was admitted to the hospital with hepatic encephalopathy. She was noted to have a wide pulse pressure and Quincke’s pulse on examination. There was no clinical evidence of heart failure, so this likely represents simple high-output physiology (not high-output heart failure).

Patient 10:

Older man with underlying cirrhosis and obesity who presents with the clinical syndrome of heart failure (exertional dyspnea, orthopnea, elevated JVP) and is found to have wide pulse pressure and Quincke’s pulse, raising the possibility of high-ouput heart failure.