Abstract
Background'Stone heart' resulting from ischemic contracture of the myocardium, precludes successful resuscitation from ventricular fibrillation (VF). We hypothesized that mild hypothermia might slow the progression to stone heart.MethodsFourteen swine (27 ± 1 kg) were randomized to normothermia (group I; n = 6) or hypothermia groups (group II; n = 8). Mild hypothermia (34 ± 2°C) was induced with ice packs prior to VF induction. The LV and right ventricular (RV) cross-sectional areas were followed by cardiovascular magnetic resonance until the development of stone heart. A commercial 1.5T GE Signa NV-CV/i scanner was used. Complete anatomic coverage of the heart was acquired using a steady-state free precession (SSFP) pulse sequence gated at baseline prior to VF onset. Un-gated SSFP images were obtained serially after VF induction. The ventricular endocardium was manually traced and LV and RV volumes were calculated at each time point.ResultsIn group I, the LV was dilated compared to baseline at 5 minutes after VF and this remained for 20 minutes. Stone heart, arbitrarily defined as LV volume <1/3 of baseline at the onset of VF, occurred at 29 ± 3 minutes. In group II, there was less early dilation of the LV (p < 0.05) and the development of stone heart was delayed to 52 ± 4 minutes after onset of VF (P < 0.001).ConclusionsIn this closed-chest swine model of prolonged untreated VF, hypothermia reduced the early LV dilatation and importantly, delayed the onset of stone heart thereby extending a known, morphologic limit of resuscitability.
Highlights
Therapeutic hypothermia has been used since the 1950 s to mitigate neurological injury from cardiac arrest
It was demonstrated that mild hypothermia was able to significantly improve defibrillation success and resuscitative outcomes after 8 minutes of sustained ventricular fibrillation (VF) [8]
There was no difference in the LV and right ventricular (RV) volumes at baseline (Table 1; time 0)
Summary
Therapeutic hypothermia has been used since the 1950 s to mitigate neurological injury from cardiac arrest. Most of these investigations focused on moderate hypothermia (28°C-32°C), deep hypothermia (< 28°C), and profound hypothermia (< 15°C) for neuro-protection [1,2]. These deep levels of hypothermia have been used to provide safer open-heart surgery, presumably because of substantial reduction in neuronal and myocardial oxygen ischemia and ischemia-reperfusion insults have focused on neuro-protection [1,2,6,7]. The cardio-protective benefits of induced mild hypothermia are less well studied. The mechanisms of this benefit were not explained, it was shown not to be dependent on coronary artery perfusion pressure
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