Effects of Mild Therapeutic Hypothermia on Hemodynamic Support in Cardiogenic Shock After Acute Myocardial Infarction

TL;DR

This study examines how mild cooling affects the need for heart medications in patients with heart failure after a heart attack.

Contribution

The study introduces new insights into the impact of mild therapeutic hypothermia on vasopressor and inotrope use in cardiogenic shock.

Findings

MTH reduced norepinephrine requirements at multiple time points compared to the control group.

Dobutamine doses were higher at 10 hours but lower at 14 hours in the MTH group.

Arterial lactate levels initially increased with MTH but later decreased.

Abstract

Background: Acute myocardial infarction (AMI) is a prevalent etiology of cardiogenic shock (CS). Microcirculatory dysfunction may continue even when hemodynamic factors improve in CS because the condition is hemodynamically diverse. Patients with CS associated with AMI have been advised to utilize vasopressors and inotropic medications. The study aims to assess the effects of mild therapeutic hypothermia (MTH) on vasopressors and inotropes in patients with CS due to AMI.

Methods: The study was carried out on a cohort of 60 individuals who had CS after AMI. CS was operationally defined as the condition characterized by a systolic blood pressure below 90 mm Hg for a duration beyond 30 minutes or the presence of inotropes required to sustain a systolic blood pressure over 90 mm Hg without any indications of hypovolemia. Vasopressor and inotrope use were guided by cardiac specialists using a predefined hemodynamic protocol. Cardiogenic shock was defined by hypotension or inotrope dependence with evidence of hypoperfusion. Mean arterial blood pressure (MAP) and lactate levels were monitored every two hours for 30 hours to ensure treatment was based on objective criteria.

Results: Norepinephrine (NE) was significantly lower at four, six, eight, 10, 12, 14, 16, 18, and 20 hours in group I than in group II (p-value < 0.001) and was insignificantly different at 0, two, 22, 24, 26, 28, and 30 hours between both groups. The dobutamine dose was significantly higher at 10 hours in group I than in group II (p-value = 0.002) and was significantly lower at 14 hours in group I than in group II (p-value = 0.036) and was insignificantly different at 0, two, four, six, eight, 12, 16, 18, 20, 22, 24, 26, 28, and 30 hours between both groups.

Conclusions: Patients treated with MTH to 33°C for 24 to 36 hours were associated with reduced NE requirements and higher MAP, along with increased dobutamine doses, compared to those without MTH. Arterial lactate rose initially with MTH but later declined. However, complications, clinical outcomes, and 30-day mortality were comparable.

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