The regulation of the cerebral arteriolar tone under different metabolic circumstances.
It is obvious that there are different systemic factors that may influence cerebral arteriolar tone by decreasing it through vasodilation (increases in PaCO2 levels, decreases in PaO2 levels) or vasoconstriction (hypocapnia or hyperoxia producing oxygen free radicals) that may frequently occur in critically ill patients. ADP may be an indicator of a decreased energy storage of the cells and therewith an important regulatory factor to increase local or systemic cerebral blood flow in critical conditions. Additionally this is the place where we have to mention the cerebral metabolic rate for oxygen (CMRO2). In some circumstances of ICU treatment CMRO2 may be increased, resulting in overproduction of CO2 and increased ADP concentration in the cells resulting in vasodilation of the arterioles (e.g., this is the case in hypermetabolic states, high fever and epileptic status). In contrast, CMRO2 may be decreased after administration of several sedato-hypnotic drugs or opiates used frequently during ICU treatment and also after the use of inhalational anesthetics. These changes in the cerebral arteriolar tone are most sensitively reflected by the pulsatility index that decreases during vasodilation and increases after vasoconstriction of the cerebral arterioles.
Most important indications and findings of transcranial Doppler monitoring in critical care settings
There are numerous critical care conditions in which TCD is regularly used as a monitoring tool. In some other critical care conditions, TCD is more an ancillary test or a method that helps in understanding the pathophysiological background of the systemic disease. Table 20.1 summarizes the typical alterations of mean blood flow velocities and pulsatility indices in different critical care conditions.
Critical care condition | MBFV | PI |
---|---|---|
TBI/elevated ICP | ↓ | ↑ |
Vasospasm | ↑ | ↓ |
Brainstem death | ↓ until 0-flow | ↑ |
Meningitis | ↑ | ↑ |
Loss of cerebral autoregulation upper threshold | ↑ | ↑ |
Loss of cerebral autoregulation lower threshold | ↓ | ↓ |
Severe preeclampsia/eclampsia | ↑ | – |
Severe sepsis, septic encephalopathy | ↓ | ↑ |
Fulminant hepatic failure | ↓ | ↑ |
Sickle cell anemia | ↑ | ↓ |
Decreased cardiac output | ↓ | ↑ |
Shock, above the threshold of autoregulation | ↓ | ↑ |
PaCO2↑ | ↑ | ↓ |
PaCO2↓ | ↓ | ↑ |
Hypothermia | ↓ | ↑ |
Rewarming after hypothermia | ↑ | ↓ |
Hypermetabolism/fever | ↑ | ↓ |
Anesthetic induction agents/sedato-hypnotics | ↓ | – |
Volatile anesthetic agents (MAC-dependent) | → or ↑ | → or ↓ |

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