Recent case reports described permanent injury from global cerebral ischemia in a beach chair position.1,2 Follow-up discussion in the APSF Newsletter did not result in consensus on safe limits of arterial blood pressure during anesthesia in the sitting position, how the blood pressure should be measured during head-up tilt, and the beta-blocker's role in these complications.3,4
Cases of cerebral ischemia in a beach chair position mandate the revision of postural cerebral perfusion management. Perfusion pressure is the difference between the inflow Pi and outflow pressure Po, measured at the organ level: CPP=MAP-CVP or CPP=MAP-ICP if ICP>CVP. While measuring pressure in the intercommunicating vessels, we have to account for the hydrostatic pressure difference (ρgh), where h is the difference in height between 2 measurement points and ρ is the density of blood. Because of the energy conservation law, heart work against gravity is zero (blood flows in a circular fashion as described by Harvey and potential energy remains the same upon completion of the circle).5 Therefore the site of CPP measurement could be anywhere, as long as the hydrostatic gradient from the measurement site to the organ level ρ remains the same for inflow and outflow pressures and there is no significant flow related pressure drop between the measurement site and the organ level.4 Simple addition of hydrostatic column from the measurement level to the organ level does not change CPP value: (MAP + ρgh) - (CVP + ρgh) = MAP - CVP. And yet so many neuroanesthesiologists continue to zero the arterial pressure transducer at the level of the external acoustic meatus.3
Several considerations come here into play:
Venous outflow depends not only on the outflow pressure, but also on the venous resistance. Veins tend to collapse when external pressure exceeds intraluminal pressure, and venous resistance correspondingly increases. Venous resistance becomes infinitely high during occlusion. This phenomenon can interchangeably be described by the nonlinear venous outflow resistance or the change in effective venous outflow pressure (Starling resistor). Starling resistor is implied in the classic definition of cerebral perfusion pressure (mean arterial pressure minus intracranial or venous pressure, whichever comes higher): CPP = MAP - ICP, when ICP > CVP, and CPP = MAP - CVP when CVP > ICP.4 Jugular veins are exposed to atmospheric pressure and collapse with the head-up position.6 This collapse can be directly observed when jugular vein distention (JVD - external jugular vein collapse point) moves with the body tilt. Complete cessation of flow in both jugular veins was observed in 2/23 healthy volunteers at 15° and in 9/23 at 90° head-up tilt.7
Pressure in jugular veins may become negative due to subtraction of the hydrostatic gradient ρgh from CVP. Therefore CPP = MAP - Patm (0), whenever CVP - ρgh < 0 and ICP < 0. Global brain ischemia during controlled hypotension in a beach chair position is a particular case of the "cerebral venous steal."8 Cerebral ischemia develops because of exhausted cerebral autoregulation (beta blockade) and is exacerbated by the jugular venous collapse in the sitting position, which leads to a further reduction of CBF (cardiac output diversion or "steal" from the brain similar to the blood flow diversion toward dependent portions of pulmonary circulation). This phenomenon occurs in the sitting position during craniotomy, when CVP - ρgh < 0 (Patm = ICP = 0 with open cranium) and can be accompanied by a venous air embolism if the non-collapsible venous sinus is injured. Cerebral venous steal due to jugular collapse can also occur in patients with intact cranium, when ICP ≤ 0 and CVP - ρgh << 0. Although the vertebral venous plexus becomes the predominant outflow pathway during jugular compression in the sitting position,7 flow through it is impeded during head rotation/tilt, especially in patients with cervical stenosis. Thus the practice of CPP measurement site adjustment to the skull base level, whenever patient position is changed and CVP - ρgh < 0, is justified. If jugular bulb pressure can be measured directly, pressure transducer level adjustments do not affect CPP calculation, as long as both the arterial and venous transducers stay at the same level.9
Given the above considerations, we propose generalizing the CPP formula to account for the effect of atmospheric pressure on the jugular veins. In a sitting position the atmospheric pressure (Patm = 0) will become an effective outflow pressure whenever it exceeds venous pressure.
(whichever results in the smallest difference).
If measurements are done at a different level than the skull base or the head position is changed, the hydrostatic pressure gradient (ρgh) has to be subtracted from all the terms of the CPP equation except from the atmospheric pressure, as atmospheric pressure does not change when adjusting the measurement level.
To minimize risk of unrecognized global cerebral ischemia in the sitting position we propose several simple considerations: