A 58-year-old man is brought to the emergency department due to severe chest pain that began an hour ago. The patient describes the pain as pressure-like in the center of his chest. He has also had nausea but no shortness of breath. Medical history is remarkable for hypertension and diet-controlled diabetes mellitus. Temperature is 37.6 C (99.7 F) , blood pressure is 94/62 mm Hg, and pulse is 64/min. On physical examination, the patient is diaphoretic. Cardiac auscultation reveals a normal S1 and S2 with no murmurs or extra heart sounds. The lungs are clear to auscultation. ECG shows ST-segment elevation in leads II, III, aVF, and V4R. Which of the following hemodynamic findings are most likely present in this patient?

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11ec25c8_d35f_a45c_bc81_056cb8241dcc_MD0003_00 This patient's severe, pressure-like chest pain and ST-segment elevation in ECG leads II, III, and aVF are diagnostic of inferior wall myocardial infarction, which commonly involves the right ventricle. ST-segment elevation in right-sided precordial ECG leads (eg, V4R) confirms right ventricular myocardial infarction (RVMI). Bradycardia in the setting of hypotension is another clue to RVMI because RVMI frequently involves ischemic disruption of the sinoatrial and/or atrioventricular node. right-sided precordial ECG RV ischemia causes an abrupt decrease in RV contractility, leading to increased RV end-diastolic volume (or preload), and increased pressure is transmitted backward to increase right atrial and central venous pressures and cause jugular venous distension. With impaired RV contractility, decreased blood is pumped through the pulmonary circulation to the left atrium, resulting in low pulmonary capillary wedge pressure (an estimate of left atrial pressure) and decreased left ventricular (LV) preload. Pulmonary edema is absent (ie, the lungs are clear to auscultation). With reduced LV filling, cardiac output drops to cause hypotension, and there is compensatory vasoconstriction to increase systemic vascular resistance and help maintain blood pressure (Choice B). Although RV preload is increased in RVMI, a gentle further increase in RV preload (ie, with intravenous normal saline) often assists the failing right ventricle in pumping blood through the pulmonary circulation, increasing LV preload and improving hypotension. (Choice A) Decreased SVR is the primary disturbance in septic shock, and there is a compensatory increase in heart rate and LV contractility to increase cardiac output. RV and LV preload are decreased, in part due to fluid leakage out of the vasculature. septic shock (Choice D) A marked reduction in SVR (eg, arteriovenous fistula) is the primary disturbance in high-output LV failure. Cardiac output is increased with blood rapidly returning to the right atrium, increasing both RV and LV preload and overloading the left ventricle. high-output LV failure (Choice E) LV contractile dysfunction is the primary disturbance in cardiogenic shock due to LV myocardial infarction (ie, low-output LV failure). LV preload is increased, and increased pressure is transmitted backward through the lungs to also increase RV preload. SVR is increased in response to reduced cardiac output. This patient's clear lungs and absence of shortness of breath are consistent with normal or low (but not increased) LV preload. low-output LV failure Educational objective: Right ventricular myocardial infarction is confirmed by ST-segment elevation in the right-sided precordial ECG leads (eg, V4R). Increased right ventricular preload, decreased left ventricular preload, and reduced cardiac output with hypotension and a compensatory increase in systemic vascular resistance are expected. References: Acute right ventricular myocardial infarction. (http://www.ncbi.nlm.nih.gov/pubmed/29902098)

A 58-Year-Old Man Is Brought to the Emergency Department Due