Global and regional differences in cerebral blood flow after asphyxial versus ventricular fibrillation cardiac arrest in rats using ASL-MRI

Abstract

Both ventricular fibrillation cardiac arrest (VFCA) and asphyxial cardiac arrest (ACA) are frequent causes of CA. However, only isolated reports compared cerebral blood flow (CBF) reperfusion patterns after different types of CA, and even fewer reports used methods that allow serial and regional assessment of CBF. We hypothesized that the reperfusion patterns of CBF will differ between individual types of experimental CA. In a prospective block-randomized study, fentanyl-anesthetized adult rats were subjected to 8 min VFCA or ACA. Rats were then resuscitated with epinephrine, bicarbonate, manual chest compressions and mechanical ventilation. After the return of spontaneous circulation, CBF was then serially assessed via arterial spin-labeling magnetic resonance imaging (ASL-MRI) in cortex, thalamus, hippocampus and amygdala/piriform complex over 1 h resuscitation time (RT). Both ACA and VFCA produced significant temporal and regional differences in CBF. All regions in both models showed significant changes over time (p<0.01), with early hyperperfusion and delayed hypoperfusion. ACA resulted in early hyperperfusion in cortex and thalamus (both p<0.05 vs. amygdala/piriform complex). In contrast, VFCA induced early hyperperfusion only in cortex (p<0.05 vs. other regions). Hyperperfusion was prolonged after ACA, peaking at 7 min RT (RT7; 199% vs. BL, Baseline, in cortex and 201% in thalamus, p<0.05), then returning close to BL at ~ RT15. In contrast, VFCA model induced mild hyperemia, peaking at RT7, (141% vs. BL in cortex). Both ACA and VFCA showed delayed hypoperfusion (ACA, ~30% below BL in hippocampus and amygdala/piriform complex, p<0.05; VFCA, 34–41% below BL in hippocampus and amygdala/piriform complex, p<0.05). In conclusion, both ACA and VFCA in adult rats produced significant regional and temporal differences in CBF. In ACA, hyperperfusion was most pronounced in cortex and thalamus. In VFCA, the changes were more modest, with hyperperfusion seen only in cortex. Both insults resulted in delayed hypoperfusion in all regions. Both early hyperperfusion and delayed hypoperfusion may be important therapeutic targets. This study was approved by the University of Pittsburgh IACUC 1008816-1.

Asphyxial cardiac arrest from drowning: Giving E-CPR the cold shoulder

“…The recent studies building on the classic work of Vaagenes et al support this notion and identify phenotype-specific pathophysiology after cardiac arrest. 12,15,16 Another interesting finding in this report is that one of the primary variables associated with 24 h survival was temperature <26 • C. Surprisingly that is in direct contrast to the work of Youn et al 7 of drowning victims resuscitated without E-CPR. It maybe that moderate hypothermia or deeper levels are protective in the specific setting of extracorporeal support.…”

Cerebral blood flow is decoupled from blood pressure and linked to EEG bursting after resuscitation from cardiac arrest

“…2(E)-2(I)), due to our system's relatively high temporal resolution (~seconds). Previous studies have not been able to identify the exact time and magnitude of the hyperemic peak and stabilized hypoperfusion post-ROSC due to the relatively poor temporal resolution (~5-30min) [7,10,23]. Interestingly, in a pediatric model of asphyxial CA, Manole et al [9] and Shaik et al [24] both did not observe a hyperemic peak in cortical CBF using MRI and LSI, respectively.…”

“…Many clinical and preclinical studies have investigated the dynamics of brain physiology.These studies have used a multitude of techniques to examine cerebral blood flow and electrophysiology following CA, such as Doppler techniques [4][5][6], positron emission tomography (PET) [7,8], magnetic resonance imaging (MRI) [9,10], and electroencephalography (EEG) [11][12][13][14]. CBF studies have reported a hyperemic phase, followed by a stabilized hypoperfusion phase, before CBF steadily increases toward baseline over 24h [15].…”

The pathophysiologies of asphyxial vs dysrhythmic cardiac arrest: implications for resuscitation and post-event management

“…Drabek et al [46] tested the hypothesis that CBF reperfusion patterns would differ between resuscitated asphyxial and dysrhythmic CA. The investigators concluded that regional differences exist between the 2 conditions, especially in the early post-ROSC cerebral hyperperfusion, and suggested early cerebral hyperperfusion and delayed hypoperfusion as potential therapeutic targets.…”

“…While the fibrillating myocardium continues to perform work, CO 2 is produced, but not removed, as coronary flow has ceased, resulting in an intramyocardial increase of CO 2 concentration that impairs contractility. [46] 2014 Rat model Equal duration (8 min) Regional and temporal differences in postresuscitation CBF between ACA and VFCA, measured using ASL-MRI. More pronounced early cerebral hyperperfusion in the cortex and thalamus after ACA ACA, asphyxial CA; VFCA, ventricular fibrillation-induced CA; ASL-MRI, arterial spin-labeling magnetic resonance imaging.…”