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A 70-year-old man presents with chest pain and the ECG shown below. On initial evaluation his blood pressure is 90/50mmHg. Exam reveals a regular heart rhythm with no murmurs, clear lungs, and jugular venous pressure of 12mmHg (normal <8). He is administered sublingual nitroglycerine for ongoing chest pain. After receiving the drug he complains of dizziness and headache. Blood pressure decreases to 70/30mmHg.
- A. Hypersensitivity to nitroglycerine
- B. Right ventricular infarction
- C. Papillary muscle rupture
- D. Ventricular septal defect
- E. Left ventricular free wall rupture
This patient has chest pain and ECG findings of ST-segment elevation in the inferior leads (II, III, aVF). This is consistent with inferior wall myocardial infarction. Most myocardial infarctions affect only the left ventricle (when we say the “inferior wall” we mean the inferior wall of the left ventricle). However, about 30% of inferior myocardial infarctions can lead to right ventricular (RV) infarction (answer B) since branches of the right coronary artery supply the right ventricle.
The classic presentation of RV infarction is inferior ischemia on ECG associated with hypotension and distended neck veins (pathophysiology explanation below). RV infarction can be confirmed on ECG by demonstrating ST elevations in leads in special locations on the right side of the chest (normally chest leads are placed to the left of the sternum). These “right sided leads” are often used in the setting of inferior ST-segment elevations to evaluate for RV infarction.
To understand the hemodynamic consequences of RV infarction, think of the right ventricle as a “preload generating” chamber. Its major role is to pump blood to the left heart to be used to fill the left ventricle (i.e. blood that becomes preload). When RV contraction is lost due to RV infarction, cardiac output drops from low preload. In addition, signs of right heart failure such as increased jugular venous pressure can be seen.
Nitroglycerine administration in the setting of RV infarction as described in the question can be life-threatening. Nitroglycerine dilates veins and lowers preload. Doing so in a patient with RV infarction can cause hemodynamic collapse.
The major side effects of nitroglycerine are hypotension (from decreased preload), headache (from meningeal vasodilation) and reflex tachycardia (physiologic response to hypotension). Hypersensitivity reactions (answer A) are uncommon.
Mechanical complications of acute myocardial infarction include papillary muscle rupture (answer C), ventricular septal defect (answer D) and free wall rupture (answer E). These typically occur 5 to 10 days after infarction. These complications require the rupture of dead, necrotic heart tissue which takes time to evolve.