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Cerebral Blood Flow in Polytrauma: Transcranial Doppler Analysis in a Nonhuman Primate Shock Model.
Journal of Surgical Research 2018 December
BACKGROUND: In combat-related trauma, resuscitation goals are to attenuate tissue hypoxia and maintain circulation. During hemorrhagic shock, compensatory and autoregulatory mechanisms are activated to preserve cerebral blood flow. Transcranial Doppler (TCD) ultrasonography may be an ideal noninvasive modality to monitor cerebral hemodynamics. Using a nonhuman primate (NHP) model, we attempted to characterize cerebral hemodynamics during polytraumatic hemorrhagic shock using TCD ultrasonography.
MATERIALS AND METHODS: The ophthalmic artery was insonated at multiple time points during varying stages of shock. Hemorrhage was controlled and pressure targeted to 20 mmHg to initiate and maintain the shock period. Mean flow velocity (MFV), peak systolic velocity (PSV), end diastolic velocity (EDV), pulsatility index (PI), and resistance index (RI) were recorded. Results represent mean ± standard deviation; statistical significance is P < 0.05; n = 12.
RESULTS: Compared to baseline, MFV, PSV, EDV, and RI show significant changes after 60 min of hemorrhagic shock, (9.81 ± 3.60 cm/s; P < 0.01), (21.15 ± 8.59 cm/s; P < 0.01), (5.15 ± 0.21 cm/s; P < 0.01), (0.70 ± 0.11; P < 0.05), respectively. PI did not change during hemorrhagic shock. At end of prehospital care (T30), cerebral flow recovers for MFV, PSV, and RI while EDV remained decreased at T30 (6.15 ± 1.13 cm/s; P < 0.01) and 1 h of simulated transport (T90) (5.87 ± 0.62 cm/s; P < 0.01). Changes in PI at T30 and T90 were not significant. MFV diminished (16.45 ± 3.85 cm/s; P < 0.05) at T90.
CONCLUSIONS: This study establishes baseline and hemorrhagic shock values for NHP cerebral blood flow velocities and cerebrovascular indices. TCD ultrasonography may represent an important area of research for targeted resuscitation investigations using a hemorrhagic shock model in NHPs.
MATERIALS AND METHODS: The ophthalmic artery was insonated at multiple time points during varying stages of shock. Hemorrhage was controlled and pressure targeted to 20 mmHg to initiate and maintain the shock period. Mean flow velocity (MFV), peak systolic velocity (PSV), end diastolic velocity (EDV), pulsatility index (PI), and resistance index (RI) were recorded. Results represent mean ± standard deviation; statistical significance is P < 0.05; n = 12.
RESULTS: Compared to baseline, MFV, PSV, EDV, and RI show significant changes after 60 min of hemorrhagic shock, (9.81 ± 3.60 cm/s; P < 0.01), (21.15 ± 8.59 cm/s; P < 0.01), (5.15 ± 0.21 cm/s; P < 0.01), (0.70 ± 0.11; P < 0.05), respectively. PI did not change during hemorrhagic shock. At end of prehospital care (T30), cerebral flow recovers for MFV, PSV, and RI while EDV remained decreased at T30 (6.15 ± 1.13 cm/s; P < 0.01) and 1 h of simulated transport (T90) (5.87 ± 0.62 cm/s; P < 0.01). Changes in PI at T30 and T90 were not significant. MFV diminished (16.45 ± 3.85 cm/s; P < 0.05) at T90.
CONCLUSIONS: This study establishes baseline and hemorrhagic shock values for NHP cerebral blood flow velocities and cerebrovascular indices. TCD ultrasonography may represent an important area of research for targeted resuscitation investigations using a hemorrhagic shock model in NHPs.
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