Targeted Temperature Management at 33°C Versus 36°C and Impact on Systemic Vascular Resistance and Myocardial Function After Out-of-Hospital Cardiac Arrest

Abstract

emodynamic instability with low cardiac output and low to normal filling pressures is frequent in survivors after out-of-hospital cardiac arrest (OHCA), but may not always be apparent at hospital admission. 1 The hemodynamic profile suggestive of myocardial stunning and vasodilation is part of the postcardiac arrest syndrome, characterized by impaired vasoregulation, reduced cardiac output, and hypotension, which all contribute to decreased organ perfusion.2 Although application of targeted temperature management (TTM) in comatose survivors after OHCA is an established part of postresuscitation care, its effects on central hemodynamics may pose additional challenges to the treating physicians. Our current knowledge of the hemodynamic implications of TTM is limited because most descriptive studies are small or used noninvasive methods for hemodynamic evaluation, 3,4 whereas other studies were primarily designed for evaluating outcome. 5,6 A recent large randomized study, the Target Temperature Management after Cardiac arrest trial (TTM Trial), compared the beneficial effects of a target temperature of 33°C compared with 36°C after OHCA. Both regimens were equally efficacious in terms of mortality (50% versus 48%; P=0.51) and unfavorable neurological outcome (54% versus 52%; P=0.78). 7This study reports the impact on central hemodynamics in survivors after OHCA randomized to a TTM at 33°C or 36°CBackground-Cardiovascular dysfunction is common after out-of-hospital cardiac arrest as part of the postcardiac arrest syndrome, and hypothermia may pose additional impact on hemodynamics. The aim was to investigate systemic vascular resistance index (SVRI), cardiac index, and myocardial performance at a targeted temperature management of 33°C (TTM33) versus 36°C (TTM36

Pulmonary Arterial Compliance in Acute Respiratory Distress Syndrome: Clinical Determinants and Association With Outcome From the Fluid and Catheter Treatment Trial Cohort*

“…While the clinical effect of this approach on RV afterload has not been demonstrated prospectively, our results confirm that these components of RV protection- including ventilator driving pressure and acidosis- are indeed associated with PVR and C PA , and that fluid balance also plays an important role. Our results suggest that optimization of heart rate in patients with arrhythmia, avoidance of hypothermia (suggested by our study and others to increase pulmonary vascular resistance (35)), and avoiding positive fluid balance should be assessed in future studies of RV protection in ARDS. Our findings could contribute to the design of an RV protective approach to mechanical ventilation that should be evaluated prospectively.…”

Reply to Letter: ‘Can therapeutic hypothermia of 33°C itself not modulate inflammatory response after out-of-hospital cardiac arrest?’

“…Thus, all patients were treated according to our department protocols with similar choice of sedative agents, pre-specified hemodynamic goals and standardized use of vasopressors and/or inotropic as described in the paper. 3 This is important to acknowledge when interpreting the results as the present single-center population may be more homogeneous regarding post-cardiac arrest management compared to the general TTM trial population. According to the TTM protocol all patients were treated according to local protocol with no differences between temperature allocation groups.…”

Improving Survival From Cardiac Arrest: A Review of Contemporary Practice and Challenges

“…Echocardiography often shows left ventricular systolic dysfunction, but echocardiographic abnormalities do not consistently predict vasopressor requirements or outcomes. 52,84 Inotropic agents should be reserved for patients with objective evidence of organ hypoperfusion coupled with low cardiac output or low central venous oxygen saturation; dobutamine is effective at low doses for reversal of myocardial dysfunction (Figure 4). 52,76 Bradycardia itself generally does not require specific treatment as long as perfusion is adequate.…”