3. Cerebral Blood flow

The brain weighs 2% of the human organism yet receives 15% of the cardiac output. The intracranial contents consist of brain tissue (approximately 1,400–1,500 g), blood (100–150 ml), CSF (110–120 ml) and extracellular fluid (<100 ml).

Normal cerebral blood flow (CBF): normal CBF is 50 ml 100 g-1 of brain tissue per minute, and is determined by the Cerebral perfusion pressure (CPP). The CPP = MAP – (CVP + ICP). The normal CPP is 70–80 mmHg. Blood flow to grey matter is more than twice that to white matter.

Over a wide range of MAP, typically between 50 and 150 mmHg, autoregulation maintains normal flow. The process is not instantaneous, and may take some seconds to complete. The classic cerebral autoregulation curve is an oversimplification; there is not a neat linear relationship between MAP and CBF at each end of the curve, and changes in perfusion pressure may be regional. Chronic hypertension shifts the autoregulatory curve to the right; drug-induced hypotension shifts it to the left (Figure 3.10). The mechanisms which underlie autoregulation are primarily myogenic, modulated by stretch receptors in vascular smooth muscle, and metabolic, in which hydrogen ions and substances such as nitric oxide and adenosine accumulate in the tissues at low flow and mediate vasodilatation.

PaCO2: there is a linear relationship between PaCO2 and CBF in the range of partial pressures from 3.5 to 10.0 kPa. Below 3.5 kPa, cerebral vasoconstriction leads to tissue hypoxia (with subsequent reflex vasodilatation); at around 10.0–12.0 kPa there is a ceiling at which blood flow is maximal (at around 120 ml 100 g1 min1)

: decreases in the partial pressure of oxygen below 8 kPa are associated with sharp increases in CBF up to around 110 ml 10 0 g1 min1. At 4.0 kPa, CBF is doubled. Hyperoxia is associated with decreases in CBF (Figure 3.12).

Changes in temperature are associated with altered requirements for cerebral oxygen (the cerebral metabolic rate for oxygen, CMRO2), Although the relationship is linear rather than exponential. Thus, while at 37C, a 1 C drop in temperature is accompanied by a fall in CMRO2 of 6–7%; at a brain temperature of 15 C (during deep hypothermic circulatory arrest, for example), a further 1 C drop results in a decrease in CMRO2 of only 1%.

CBF is linked to CMRO2 by a mechanism that has not yet been fully elucidated. There is a short lag time of 1–2 minutes.

Rheology: lower plasma viscosity is associated with enhanced capillary flow, although there is a balance between optimal rheology and oxygen delivery. A haematocrit above 50% risks intravascular sludging and a reduction in CBF, and a haematocrit below 30% is associated with decreased oxygen flux

Kety–Schmidt method: this is an application of the Fick principle, which states that flow is equal to the amount of a substance taken up or excreted by an organ, divided by the arteriovenous (AV) concentration difference itrous oxide is used as the diffusible tracer. The subject breathes 10% N2O for 10 minutes, during which time paired peripheral arterial and jugular venous bulb samples are taken

Transcranial Doppler ultrasonography: this gives a measure of the velocity of red cells flowing through large cerebral arteries, most commonly the middle cerebral, and can be used in clinical practice. The velocity can give an index of flow provided that the diameter of the artery is determined independently, and provided that this diameter changes little (as is the case with the major cerebral arteries).

Intravenous induction agents: all except for ketamine reduce CMRO2, and as a result CBF falls in tandem. Autoregulation is not affected. Ketamine increases MAP, which leads to a rise in blood flow

Volatile anaesthetic agents: these uncouple CBF and CMRO2. They reduce CMRO2 but are associated with a rise in CBF secondary to their capacity to vasodilate the cerebral circulation and abolish autoregulation. The response to changes in PaCO2 is unchanged. This action is dose-dependent but can partly be offset by the vasoconstrictor effect of hyperventilation. Autoregulation is abolished by 1.5 MAC of all the agents bar sevoflurane. This has only 30% of the vasodilatory potential of isoflurane and does not impair autoregulation. Nitrous oxide increases CBF by increasing the CMRO2, while also affecting autoregulatory mechanisms.

Opioids: opioids have little direct effect, but CBF will rise in response to CO2 retention should respiratory drive be depressed.

chronic hypertension shifts the autoregulatory curve to the right, while drug-induced hypotension shifts it to the left (Figure 3.10). If autoregulation is attenuated by the use of volatile anaesthetics, then CBF and ICP will rise in parallel with an increase in MAP.

Venous pressure: Any of the many factors which increase venous pressure, such as position, coughing, straining against a ventilator, impeded drainage from the head and neck, volume overload or the use of IPPV and PEEP, will decrease CPP and reduce CBF.

there will be focal areas of injured brain in which autoregulation is lost, whereas elsewhere it is retained. Cerebral vasodilatation may further compromise these areas by diverting blood away (‘cerebral steal’); conversely, the vasoconstriction associated with hyperventilation may divert blood from normal to damaged brain, where vasoconstrictor responses have been lost (‘inverse steal’).