Systolic left ventricular function is preserved during therapeutic hypothermia, also during increases in heart rate with impaired diastolic filling

Abstract

BackgroundSystolic left ventricular function during therapeutic hypothermia is found both to improve and to decline. We hypothesized that this discrepancy would depend on the heart rate and the variables used to assess systolic function.MethodsIn 16 pigs, cardiac performance was assessed by measurements of invasive pressures and thermodilution cardiac output and with 2D strain echocardiography. Left ventricle (LV) volumes, ejection fraction (EF), transmitral flow, and circumferential and longitudinal systolic strain were measured. Miniaturized ultrasonic transducers were attached to the epicardium of the LV to obtain M-mode images, systolic thickening, and diastolic thinning velocities and to determine LV pressure-wall dimension relationships. Preload recruitable stroke work (PRSW) was calculated. Measurements were performed at 38 and 33°C at spontaneous and paced heart rates, successively increased in steps of 20 up to the toleration limit. Effects of temperature and heart rate were compared in a mixed model analysis.ResultsHypothermia reduced heart rate from 87 ± 10 (SD) to 76 ± 11 beats/min without any changes in LV stroke volume, end-diastolic volume, EF, strain values, or PRSW. Systolic wall thickening velocity (S′) and early diastolic wall thinning velocity decreased by approximately 30%, making systolic duration longer through a prolonged and slow contraction and changing the diastolic filling pattern from predominantly early towards late. Pacing reduced diastolic duration much more during hypo- than during normothermia, and combined with slow myocardial relaxation, incomplete relaxation occurred with all pacing rates. Pacing did not affect S′ or PRSW at physiological heart rates, but stroke volume, end-diastolic volume, and strain were reduced as a consequence of reduced diastolic filling and much more accentuated during hypothermia. At the ultimate tolerable heart rate during hypothermia, S′ decreased, probably as a consequence of myocardial hypoperfusion due to sustained ventricular contraction throughout a very short diastole.ConclusionsSystolic function was maintained at physiological heart rates during therapeutic hypothermia. Reduced tolerance to increases in heart rate was caused by lack of ventricular filling due to diastolic dysfunction and shorter diastolic duration.

Does therapeutic hypothermia during extracorporeal cardiopulmonary resuscitation preserve cardiac function?

“…The increased dobutamine requirements observed during HT may be related to altered pharmacologic properties of dobutamine with a reduced effect [34] as supported by the similar requirements in the two groups after rewarming. HT also affects LV function, causing slower LV contraction and relaxation velocities [35], and may thus increase the need for inotropic stimulation to reach preset targets. The optimal MAP target during HT is not known, and could possibly differ from MAP target at normothermia, but for comparison, they were set at the same level.…”

Changes in Left Ventricular Electromechanical Relations During Targeted Hypothermia

“…The experiment was performed in an open chest porcine model. Data for the present study were collected from experiment series published in two previous articles [6,24]. The open model facilitated recording of high quality echocardiographic images needed for the study, otherwise di cult to obtain in the pigs.…”

“…When the protocol was nished, the animals were euthanatized by bolus infusion of 80 mmol potassium chloride and 1000 mg pentobarbital. The animals were mechanically ventilated via a tracheostomy tube by a fraction of air/oxygen (FiO 2 0.4), with tidal volumes of 10 to 15 ml/kg and surgically prepared with sternotomy as previously reported [6,24]. Threelead ECG was obtained by surface leads.…”

“…Hemodynamic data regarding systolic and diastolic function obtained from the experiment has been published [6,24], but is included as background data in the current manuscript. All data presented concerning the electromechanical relations, has been analysed for this study.…”

New Developments in the Treatment of Acute Myocardial Infarction Associated with Out-of-Hospital Cardiac Arrest. A Review

“…Induced mild hypothermia after global cerebral hypoxia is associated with improved outcomes as a consequence of the neuroprotective effect, via suppressing different path-ways of cell death, decreasing cerebral oxygen consumption and reducing the release of stimulatory amino acids and free radicals. [34][35][36][37] Over the last decade, therapeutic hypothermia has become standard care for comatose patients after OHCA with a shockable rhythm, but an analysis of the current studies on therapeutic hypothermia in patients with non-shockable rhythm indicates that controversy still exists.…”