Dissociation of Cerebral Blood Flow and Femoral Artery Blood Pressure Pulsatility After Cardiac Arrest and Resuscitation in a Rodent Model: Implications for Neurological Recovery

Figures

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  Figure 1. Pulsatile cerebral blood flow (CBF) and arterial blood pressure (ABP) dynamics after resuscitation from asphyxial cardiac arrest (ACA). A, Relative CBF (rCBF) (green; top) and ABP (purple; bottom) time courses during a representative ACA and resuscitation experiment. B through F, Representative 1.5‐second periods of rCBF data from phases labeled in A (top). The y axis is rescaled for each figure (B through F) to show the same CBF range. B, Baseline pulsatile CBF. C, Cardiac arrest (CA) pulsatile CBF. D, Hyperemia pulsatile CBF. E, Early hypoperfusion pulsatile CBF. F, Late hypoperfusion pulsatile CBF. G through K, Representative 1.5 seconds of ABP data from phases labeled in A (bottom). The y axis is rescaled for each figure (G through K) to show the same blood pressure range. G, Baseline pulsatile ABP. H, CA pulsatile ABP. I, Hyperemia pulsatile ABP. J, Early hypoperfusion phase of pulsatile ABP. K, Late hypoperfusion phase of pulsatile ABP. CPR indicates cardiopulmonary resuscitation.

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  Figure 2. Heart rate calculations from cerebral blood flow (CBF) data agree well with those from arterial blood pressure (ABP) data during all experimental phases. A, Time courses from each of the 11 subjects that compare ABP and CBF heart rate (HR) calculations. Data from laser speckle imaging to measure CBF are in green, and data from peripheral ABP are in purple. B, Comparison of ABP and CBF HR calculations from all experiments (n=11) during asphyxial (n=358; R 2=0.80; left), nonasphyxial (n=4615; R 2=0.93; middle), and all experimental time points (n=4973; R 2=0.94; right).

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  Figure 3. Resuscitation after asphyxial cardiac arrest (ACA) leads to deficits in cerebral blood flow (CBF) pulsatility, whereas arterial blood pressure (ABP) pulsatility minimally changes. Combined 5‐ and 7‐minute ACA comparison between CBF (green, circle) pulsatility and ABP (purple, square) pulsatility (n=11) using normalized peak‐to‐trough metric (A) and normalized peak power metric (B). Experimental phases are baseline (B), cardiac arrest (CA), hyperemia (H), early hypoperfusion (EH), and late hypoperfusion (LH). *P<0.05, **P<0.01, and ***P<0.001.

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  Figure 4. Longer asphyxial duration leads to higher arterial blood pressure (ABP) pulsatility, but does not significantly influence deficits in cerebral blood flow (CBF) pulsatility. A and B, Two methods to calculate CBF pulsatility (normalized peak to trough and peak power) demonstrate that there is no significant difference in CBF pulsatility between 5‐minute (n=6) and 7‐minute (n=5) asphyxial cardiac arrest (ACA) experiments during cardiac arrest (CA), hyperemia (H), early hypoperfusion (EH), and late hypoperfusion (LH). C and D, Two methods to calculate ABP pulsatility (normalized peak to trough and peak power) demonstrate that there is no significant difference between 5‐minute (n=6) and 7‐minute (n=5) ACA experiments during CA, H, and EH (P>0.05). During LH, 7‐minute ACA experiments have significantly greater pulsatility than 5‐minute experiments (P=0.03). Experimental phases are baseline (B), CA, H, EH, and LH. (*P<0.05).

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  Figure 5. Relative cerebrovascular resistance (rCVR) increases after resuscitation and is inversely correlated to cerebral blood flow (CBF) pulsatility but not arterial blood pressure (ABP) pulsatility. A, Representative experiment illustrating temporal changes in rCVR. B, Combined 5‐ and 7‐minute asphyxial cardiac arrest (ACA) shows rCVR is significantly elevated during cardiac arrest (CA) (P<0.001), early hypoperfusion (EH) (P=0.002), and late hypoperfusion (LH) (P<0.001), whereas rCVR remains at near baseline (B) levels during hyperemia (H) (P=0.17) (n=11). Experimental phases are B, CA, H, EH, and LH. C through E, Combined 5‐ and 7‐minute ACA comparison of CBF normalized peak‐to‐trough data and rCVR during H, EH, and LH (n=11). C, Comparison of CBF pulsatility and normalized rCVR during H (R=−0.68; P=0.025). D, Comparison of CBF pulsatility and normalized rCVR during EH (R=−0.42; P=0.20). E, Comparison of CBF pulsatility and normalized rCVR during LH (R=−0.78; P=0.007). F through H, Combined 5‐ and 7‐minute ACA comparison of ABP normalized peak‐to‐trough data and normalized rCVR during H, EH, and LH (n=11). F, Comparison of ABP pulsatility and normalized rCVR during H (R=0.04; P=0.92).…

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  Figure 6. Worse short‐term neuroelectrical recovery is associated with higher arterial blood pressure (ABP) pulsatility, whereas changes in cerebral blood flow (CBF) pulsatility are not associated with short‐term neuroelectrical recovery. A, Representative experiment that shows temporal changes in electroencephalographic (EEG) information quantity (IQ). B through D, Combined 5‐ and 7‐minute asphyxial cardiac arrest (ACA) comparisons of CBF normalized peak‐to‐trough data during hyperemia (H), early hypoperfusion (EH), and late hypoperfusion (LH) to EEG IQ 90 minutes after return of spontaneous circulation (ROSC) (n=10). Experimental phases are baseline, cardiac arrest, H, EH, and LH. B, Comparison of CBF pulsatility during H and EEG IQ 90 minutes after ROSC (R=−0.20; P=0.58). C, Comparison of CBF pulsatility during EH and EEG IQ 90 minutes after ROSC (R=0.21; P=0.56). D, Comparison of CBF pulsatility during LH and EEG IQ 90 minutes after ROSC (R=0.13; P=0.73). E through G, Combined 5‐ and 7‐minute ACA comparisons of ABP normalized peak‐to‐trough data during H, EH, and LH to EEG IQ 90 minutes after ROSC (n=10). E, Comparison of ABP pulsatility during H and EEG IQ 90 minutes after ROSC…