STUDY WITH US

NEW IM Qbank+

Question

A 54-year-old man presents to the clinic for evaluation of recurrent episodes of syncope. He reports 4 syncopal episodes this summer, each lasting a few seconds and occurring during physical activity on a hot day. He denies chest pain, palpitations, or shortness of breath. His medical history is significant for hypertension and hyperlipidemia. He does not smoke and consumes alcohol occasionally. Medications include lisinopril and atorvastatin.

Vital signs include T 37.0°C (98.6°F), BP 140/90 mmHg, HR 52 bpm, and RR 16 breaths/minute. On physical examination, cardiac auscultation reveals a harsh systolic murmur at the 3rd left intercostal space that becomes louder with Valsalva. Carotid upstroke is brisk. The lungs are clear, and there is no peripheral edema.

Laboratory findings include a normal CBC, normal basic metabolic panel, and troponin I of 0.03 ng/mL (normal < 0.04 ng/mL). ECG result is shown (Figure).

Which of the following is the primary pathophysiological mechanism for this patient’s condition?

A. Neurocardiogenic response to increased venous return

B. Obstruction to left ventricular outflow

C. Impaired chronotropy

D. Impaired cardiac filling

E. Acute drop in systemic vascular resistance

🛑 Before scrolling to the answer 🛑

Dredge up everything you know about cardiology, and try to formulate the correct response.

This study method is called "effortful recall" and is crucial in making long-lasting memories that are accessible when you need them. 

Answer and Explanation

Answer

B. Obstruction to left ventricular outflow

Explanation

The patient’s syncope is most likely due to obstruction to left ventricular outflow caused by subvalvular obstruction from obstructive hypertrophic cardiomyopathy (HCM). The murmur with accentuation on Valsalva along with brisk carotid pulses is suggestive of HCM. In HCM, a thickened ventricular septum causes left ventricular outflow tract (LVOT) obstruction, often with symptoms initially manifesting only intermittently during physical activity, when dehydrated, or in a situation of vasodilation (e.g., using a hot tub or sauna). The LVOT obstruction leads to a decrease in cardiac output and cerebral perfusion, resulting in syncope. HCM is also associated with ventricular arrhythmias that can cause syncope and sudden cardiac death (SCD).

Neurocardiogenic response to increased venous return is a mechanism more consistent with vasovagal syncope, which leads to bradycardia, vasodilation, and reduced cerebral perfusion. It usually occurs at rest or in response to emotional or pain stimuli, not during physical activity, as in this patient’s case. Exertional syncope, on the other hand, points to a cardiac etiology.

Syncope from impaired chronotropy may be caused by atrioventricular block or other bradycardic rhythms. While this patient does have bradycardia, the rhythm is a sinus rhythm and not heart block The presence of anterolateral T-wave inversion on ECG is suggestive of HCM, as is the patient’s cardiac examination. Thus, a structural cardiac cause is a more likely etiology of his syncope.

Impaired cardiac filling is the cause of syncope in ventricular arrhythmias, as well as pericardial disease and restrictive cardiomyopathy. In tachyarrhythmias, there is not enough diastolic filling time to generate adequate cardiac output, and syncope and SCD can occur. While syncope in HCM may be caused by ventricular arrhythmias, this patient denies palpitations prior to syncope and his symptoms occur with exertion on hot days, which suggests a state of low preload that exacerbates LVOT obstruction.

Acute drop in systemic vascular resistance may occur due to vasodilator medications. This patient’s BP is not significantly low while taking lisinopril, an angiotensin-converting enzyme inhibitor (ACEI). When taken chronically, ACEIs do not typically cause an acute drop in systemic vascular resistance sufficient to result in syncope.

Board Testing Point

Understand that cardiac syncope can be caused by various pathophysiological mechanisms, including decreased cerebral perfusion due to left ventricular outflow tract (LVOT) obstruction in the setting of mitral valve disease, which can lead to syncope, especially during physical activity. It is necessary to understand the underlying pathophysiology to determine the appropriate diagnostic and management strategies.

medstudy app in hand

Ready to see the rest of the new Qbank+?

Refine your Internal Medicine knowledge with over 1,700 rigorously-crafted internal medicine board questions, strategically designed to address the most likely to be tested points in the latest ABIM exam blueprint.

GET STARTED