Letter to the Editor

Modified Calculation of the Cerebral Perfusion Pressure in a Sitting Position: Jugular Starling Resistor and Related Clinical Implications

To the Editor:

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:

  1. Measuring arterial pressure alone does not define CPP. In the sitting position arterial pressure is different if measured at the head, torso, or calf level, while CPP is a pressure difference and remains the same. When the arterial pressure transducer drops on the floor, arterial hypertension can be falsely diagnosed. CPP = MAP - CVP would stay the same whether measured at the head, torso, or the floor level.
  2. The hydrostatic indifference level (HIL) is a point where pressure does not change during body tilt. Measuring MAP or (MAP - CVP) at this level should be indifferent to the body tilt. The only problem with this approach is that HIL has to be individually determined and HIL for venous and arterial systems was found to be different due to the difference in regional compliances.
  3. Even if we measure MAP and CVP simultaneously and eliminate the self-negating effect of hydrostatic column ρgh (25 cm water = 18 mmHg) from the brain to the measurement site, we can not reliably estimate CPP. Negative transmural pressure leads to jugular collapse with the head-up tilt. Directly measured jugular pressure above the thoracic inlet in the upright position stayed around 0 mmHg despite negative CVP in 8 healthy subjects with a gradient reaching 20 cm of water. No such gradient was observed in 2 patients with chronic cardiac tamponade.6
  4. Arterial pressure measured at the zero venous pressure level is arithmetically equivalent to cerebral perfusion pressure (CPP = MAP - 0). Skull base approximates zero venous pressure level when CVP - ρgh < 0, because jugular veins are exposed to the atmospheric pressure upon exiting the scull. This is the reason why we should adjust the site of arterial pressure measurement when sitting. That is why the skull base can be referred as zero venous pressure level for the cerebral perfusion pressure estimation, unless venous pressure is measured in the jugular bulb directly.
  5. Assessing CPP and adjusting the BP measurement level from the heart to the skull (about 20 mmHg) may not be important if MAP is maintained >70-100 mmHg (CPP >50-80), but it is critical if MAP is maintained at 50 mmHg (CPP 30 mmHg).

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.

Thus,

(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.

If CVP is maintained above 18 mmHg (ρgh), the classical CPP definition1,2 is valid and measurement level adjustments are not mandatory.

To minimize risk of unrecognized global cerebral ischemia in the sitting position we propose several simple considerations:

  1. Obtain baseline BP measurement in the sitting position and use it as a guide (measurement site is not critical as long as it does not change during the case and central blood pressure pulse wave propagation/reflection remains similar).
  2. Evaluate for signs of cervical stenosis; avoid cervical malpositioning which could impede blood outflow through the vertebral venous plexus.
  3. Document any patient position changes and changes in BP measurement site or technique.
  4. If patient position or BP monitoring site is changed, reassess the new CPP to account for the Starling resistor in the cervical veins (CPP = (MAP - ρgh) - max ((ICP - ρgh), (CVP - ρgh), Patm), whereas h is the height from skull base to BP measurement site, Patm=0.
  5. Visual assessment of the jugular vein column predicts if jugular veins will collapse in the sitting position.10
  6. Volume loading will counteract the effect of Patm on the jugular veins and will prevent their collapse once CVP > ρgh (about 18 mmHg).
  7. If the controlled hypotension is prolonged and exceeds diurnal minimum in the upright blood pressure, consider neuromonitoring (regional technique, maintaining verbal contact, near infrared cerebral oximetry, MCA Doppler, EEG, etc.).

Mindaugas Pranevicius, MD Osvaldas Pranevicius, MD, PhD Bronx, NY

References

  1. Cullen DJ, Kirby RR. Beach chair position may decrease cerebral perfusion; catastrophic outcomes have occurred. APSF Newsletter. 2007;22(2):25,27.
  2. Pohl A, Cullen DJ. Cerebral ischemia during shoulder surgery in the upright position: a case series. J Clin Anesth. 2005;17:463-9
  3. Cucchiara RF. Hazards of beach chair position explored. APSF Newsletter. 2008;22(4):81.
  4. Munis J. The problems of posture, pressure, and perfusion: cerebral perfusion pressure defined. APSF Newsletter. .2008; 22(4):82-3.
  5. Harvey W. On the motion of the heart and blood in animals. London: George Bell and Sons; 1889.
  6. Avasthey P. Venous pressure changes during orthostasis. Cardiovasc Res. 1972;6:657-63.
  7. Valdueza JM, von Munster T, Hoffman O, et al. Postural dependency of the cerebral venous outflow. Lancet. 2000;355:200-1.
  8. Pranevicius M, Pranevicius O. Cerebral venous steal: blood flow diversion with increased tissue pressure. Neurosurgery. 2002;51(5):1267,73; discussion 1273-4.
  9. Eckenhof JE, Enderby GE, Larson A, et al. Human cerebral circulation during deliberate hypotension and head-up tilt. J Appl Physiol. 1963;18:1130-8.
  10. Sinisalo J, Rapola J, Rossinen J, et al. Simplifying the estimation of jugular venous pressure. Am J Cardiol. 2007;100:1779-81.