Atropine in Inferior STEMI with Bradycardia and Wide Pulse Pressure Hypertension: a Case of Heart Rate-Mediated Systolic Decline and Diastolic Rise

Background Atropine sulfate is first-line therapy for symptomatic bradycardia in acute coronary syndromes. Its primary vagolytic effect aims to increase heart rate and cardiac output. We present a case that demonstrates the drug's distinct and sequential effects, where an initial rise in diastolic pressure is followed by a fall in systolic pressure .This underscores a potential hemodynamic risk in preload-dependent states. Case Presentation: A 69-year-old male with hypertension and chronic coronary syndrome presented with an inferior ST-elevation myocardial infarction (STEMI). Upon ICU admission, he had persistent chest pain with symptomatic bradycardia (52–56 bpm) and significant hypertension with a widened pulse pressure (187/75 mmHg). Intravenous atropine (0.5 mg) was administered. The hemodynamic response followed a definitive sequence: first, heart rate increased to 68–70 bpm. Subsequently, diastolic blood pressure rose to 91 mmHg, while systolic pressure fell to 148 mmHg, thereby narrowing the pulse pressure. Conclusion This response demonstrates atropine's dual hemodynamic actions. The increase in heart rate likely shortened diastolic filling time, reducing left ventricular preload and stroke volume, which consequently decreased systolic pressure. This case highlights that in patients with inferior STEMI and hypertension, atropine's efficacy for bradycardia may be accompanied by a reduction in systolic pressure, a consequence of reduced preload rather than vasodilation. Clinicians should be aware of this mechanism, especially in patients who may be preload-dependent.