Relationship between cardiac output and cerebral blood flow in patients with intact and with impaired autoregulation

Abstract

Intravascular volume expansion has been successfully employed to promote blood flow in ischemic brain regions. This effect has been attributed to both decreased blood viscosity and increased cardiac output resulting from volume expansion. The physiological mechanism by which changes in cardiac output would affect cerebral blood flow (CBF), independent of blood pressure variations, is unclear, but impaired cerebral autoregulation is believed to play a role. In order to evaluate the relationship between cardiac output and CBF when autoregulation is either intact or defective, 135 simultaneous measurements of cardiac output (thermodilution method) and CBF (by the 133Xe inhalation or intravenous injection method) were performed in 35 severely head-injured patients. In 81 instances, these measurements were performed after manipulation of blood pressure with phenylephrine or Arfonad (trimethaphan camsylate), or manipulation of blood viscosity with mannitol. Autoregulation was found to be intact in 55 of these cases and defective in 26. A wide range of changes in cardiac output occurred after administration of each drug. No correlation existed between the changes in cardiac output and the changes in CBF, regardless of the status of blood pressure autoregulation. A significant (40%) increase in CBF was found after administration of mannitol when autoregulation was defective. These data support the hypothesis that, within broad limits, CBF is not related to cardiac output, even when autoregulation is impaired. Thus, the effect of intravascular volume expansion appears to be mediated by decreased blood viscosity rather than cardiac output augmentation.

Lack of association between carotid artery volume blood flow and cardiac output.

“…Some authors described a passive association between HMV and CBF in primates 6,21 ; others failed to show a correlation in humans. 7 The disappointing results of an Austrian hemodilution stroke trial 22 should be discussed in this context. Despite some restrictions due to methodological assumptions of the ultrasonographic technique and derivation of parameter values through calculation, quantitative flow volume rate determination in the carotid arteries allows direct comparison with cardiac output parameters.…”

“…2 A review of the literature suggests that the impact of cardiac output on CBF is uncertain, with conflicting data in animals, healthy volunteers, and neurosurgical or cardiologic patients. [3][4][5][6][7][8] In addition, methodological differences to define CBF enhance difficulties with interpreting these studies. Cerebral blood flow was assessed by means of singlephoton emission computed tomography (SPECT) 3,6,7 or blood flow velocity of the middle cerebral artery.…”

“…[3][4][5][6][7][8] In addition, methodological differences to define CBF enhance difficulties with interpreting these studies. Cerebral blood flow was assessed by means of singlephoton emission computed tomography (SPECT) 3,6,7 or blood flow velocity of the middle cerebral artery. 9 These methods are difficult, because they either require radioactive tracers (SPECT) C Article ing results: some authors described an almost linear correlation of the methods, 10,11 whereas others found a mismatch, 12 indicating relevant changes of the diameter in the basal cerebral arteries.…”

Persistent low cerebral blood flow velocity following profound hypothermic circulatory arrest in infants

“…Bouma et al found no correlation between changes in cardiac output and changes in cerebral blood flow in head-injured patients, even in the absence of autoregulation. 24 Cerebral perfusion pressures and inotropic interventions were similar in both groups. Although no comment earl be made about the actual cardiac output, the cerebral perfusion pressures were similar in both groups so it is unlikely that it accounted for the observed differences in mCBFV.…”

Cerebrovascular Connexin Expression: Effects of Traumatic Brain Injury

“…Autoregulation, cerebral vasodilation or vasoconstriction in response to decreases or increases in systemic arterial blood pressure, respectively, is significantly reduced locally (Lewelt et al, 1980), regionally, and globally after fluid-percussion (DeWitt et al, 1992), as well as other models of experimental traumatic brain injury (TBI; Armstead et al, 2011;Engelborghs et al, 2000;Nawashiro et al, 1995). Cerebral autoregulation is also impaired after head injury in patients (Bouma and Muizelaar, 1990). Although impaired cerebral vascular reactivity after TBI may be the result of a pathological imbalance in the myriad cerebral vasoconstrictors (Armstead, 1999) or vasodilators (Gulbenkian et al, 2001), the underlying causes of cerebral vascular dysfunction after TBI are not well understood.…”