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

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.