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Effects of mild hypothermia on hemodynamics in cardiac arrest survivors and isolated failing human myocardium.

ABSTRACT: Post-cardiac arrest myocardial dysfunction is a common phenomenon after return of spontaneous circulation (ROSC) and contributes to hemodynamic instability and low survival rates after cardiac arrest. Mild hypothermia for 24 h after ROSC has been shown to significantly improve neurologic recovery and survival rates. In the present study we investigate the influence of therapeutic hypothermia on hemodynamic parameters in resuscitated patients and on contractility in failing human myocardium. We analyzed hemodynamic data from 200 cardiac arrest survivors during the hypothermia period. The initial LVEF was 32.6 +/- 1.2% indicating a significantly impaired LV function. During hypothermia induction, the infusion rate of epinephrine could be significantly reduced from 9.1 +/- 1.3 microg/min [arrival intensive care unit (ICU) 35.4 degrees C] to 4.6 +/- 1.0 microg/min (34 degrees C) and 2.8 +/- 0.5 microg/min (33 degrees C). The dobutamine and norepinephrine application rates were not changed significantly. The mean arterial blood pressure remained stable. The mean heart rate significantly decreased from 91.8 +/- 1.7 bpm (arrival ICU) to 77.3 +/- 1.5 bpm (34 degrees C) and 70.3 +/- 1.4 bpm (33 degrees C). In vitro we investigated the effect of hypothermia on isolated ventricular muscle strips from explanted failing human hearts. With decreasing temperature, the contractility increased to a maximum of 168 +/- 23% at 27 degrees C (n = 16, P < 0.05). Positive inotropic response to hypothermia was accompanied by moderately increased rapid cooling contractures as a measure of sarcoplasmic reticulum (SR) Ca(2+) content, but can be elicited even when the SR Ca(2+) release is blocked in the presence of ryanodine. Contraction and relaxation kinetics are prolonged with hypothermia, indicating increased Ca(2+) sensitivity as the main mechanism responsible for inotropy. In conclusion, mild hypothermia stabilizes hemodynamics in cardiac arrest survivors which might contribute to improved survival rates in these patients. Mechanistically, we demonstrate that hypothermia improves contractility in failing human myocardium most likely by increasing Ca(2+)-sensitivity.

SUBMITTER: Jacobshagen C

PROVIDER: S-EPMC2858797 | biostudies-literature | 2010 May

REPOSITORIES: biostudies-literature

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Effects of mild hypothermia on hemodynamics in cardiac arrest survivors and isolated failing human myocardium.

Jacobshagen Claudius C Pelster Theresa T Pax Anja A Horn Wiebke W Schmidt-Schweda Stephan S Unsöld Bernhard W BW Seidler Tim T Wagner Stephan S Hasenfuss Gerd G Maier Lars S LS

Clinical research in cardiology : official journal of the German Cardiac Society 20100204 5

Post-cardiac arrest myocardial dysfunction is a common phenomenon after return of spontaneous circulation (ROSC) and contributes to hemodynamic instability and low survival rates after cardiac arrest. Mild hypothermia for 24 h after ROSC has been shown to significantly improve neurologic recovery and survival rates. In the present study we investigate the influence of therapeutic hypothermia on hemodynamic parameters in resuscitated patients and on contractility in failing human myocardium. We a ...[more]

PMID: 20130890

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Project description:BackgroundLung injury is common in post-cardiac arrest syndrome, and is associated with increased morbidity and mortality. The aim of this study was to evaluate the effect of mild hypothermia on lung injury after cardiac arrest in swine based on lung ultrasound.MethodsTwenty-three male domestic swine weighing 36?±?2?kg were randomly assigned to three groups: therapeutic hypothermia (TH, n?=?9), normothermia (NT, n?=?9), and sham control (control, n?=?5) groups. Sham animals only underwent surgical preparation. The animal model was established with 8?min of ventricular fibrillation followed by 5?min of cardiopulmonary resuscitation. Therapeutic hypothermia was induced and maintained until 24?h post-resuscitation in the TH group by surface blanket cooling, followed by rewarming at a rate of 1?°C/h for 5?h. The extravascular lung water index (ELWI), pulmonary vascular permeability index (PVPI), PO2/FiO2, and lung ultrasound score (LUS) were measured at baseline and at 1, 3, 6, 12, 24, and 30?h after resuscitation. After euthanizing the swine, their lung tissues were quickly obtained to evaluate inflammation.ResultsAfter resuscitation, ELWI and PVPI in the NT group were higher, and PO2/FiO2 was lower, than in the sham group. However, those measures were significantly better in the TH group than the NT group. The LUS was higher in the NT group than in the sham group at 1, 3, 6, 12, 24, and 30?h after resuscitation. The LUS was significantly better in the TH group compared to the NT group. The lung tissue biopsy revealed that lung injury was more severe in the NT group than in the TH group. Increases in LUS were highly correlated with increases in ELWI (r?=?0.613; p?<?0.001) and PVPI (r?=?0.683; p?<?0.001), and decreases in PO2/FiO2 (r?=?-?0.468; p?<?0.001).ConclusionsMild hypothermia protected against post-resuscitation lung injury in a swine model of cardiac arrest. Lung ultrasound was useful to dynamically evaluate the role of TH in lung protection.

Project description:ImportanceComatose survivors of out-of-hospital cardiac arrest experience high rates of death and severe neurologic injury. Current guidelines recommend targeted temperature management at 32 °C to 36 °C for 24 hours. However, small studies suggest a potential benefit of targeting lower body temperatures.ObjectiveTo determine whether moderate hypothermia (31 °C), compared with mild hypothermia (34 °C), improves clinical outcomes in comatose survivors of out-of-hospital cardiac arrest.Design, setting, and participantsSingle-center, double-blind, randomized, clinical superiority trial carried out in a tertiary cardiac care center in eastern Ontario, Canada. A total of 389 patients with out-of-hospital cardiac arrest were enrolled between August 4, 2013, and March 20, 2020, with final follow-up on October 15, 2020.InterventionsPatients were randomly assigned to temperature management with a target body temperature of 31 °C (n = 193) or 34 °C (n = 196) for a period of 24 hours.Main outcomes and measuresThe primary outcome was all-cause mortality or poor neurologic outcome at 180 days. Neurologic outcome was assessed using the Disability Rating Scale, with poor neurologic outcome defined as a score greater than 5 (range, 0-29, with 29 being the worst outcome [vegetative state]). There were 19 secondary outcomes, including mortality at 180 days and length of stay in the intensive care unit.ResultsAmong 367 patients included in the primary analysis (mean age, 61 years; 69 women [19%]), 366 (99.7%) completed the trial. The primary outcome occurred in 89 of 184 patients (48.4%) in the 31 °C group and in 83 of 183 patients (45.4%) in the 34 °C group (risk difference, 3.0% [95% CI, 7.2%-13.2%]; relative risk, 1.07 [95% CI, 0.86-1.33]; P = .56). Of the 19 secondary outcomes, 18 were not statistically significant. Mortality at 180 days was 43.5% and 41.0% in patients treated with a target temperature of 31 °C and 34 °C, respectively (P = .63). The median length of stay in the intensive care unit was longer in the 31 °C group (10 vs 7 days; P = .004). Among adverse events in the 31 °C group vs the 34 °C group, deep vein thrombosis occurred in 11.4% vs 10.9% and thrombus in the inferior vena cava occurred in 3.8% and 7.7%, respectively.Conclusions and relevanceIn comatose survivors of out-of-hospital cardiac arrest, a target temperature of 31 °C did not significantly reduce the rate of death or poor neurologic outcome at 180 days compared with a target temperature of 34 °C. However, the study may have been underpowered to detect a clinically important difference.Trial registrationClinicalTrials.gov Identifier: NCT02011568.

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Effects of mild hypothermia on hemodynamics in cardiac arrest survivors and isolated failing human myocardium.

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Effects of mild hypothermia on hemodynamics in cardiac arrest survivors and isolated failing human myocardium.

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