Stroke question

[sarcoid]

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So I came up with this question while studying for my path final this week (unit on the cns, & I rocked it!)

If you have an obese patient, w/ htn, will sleep position affect inter-cranial arterial pressure? Specifically, does sleeping in prone position have the same affect as say a valsalva maneuver? If it can be reasoned that it does, then does sleeping prone have implications on SAH from a berry aneurysm?

 

[typhoonegator]

Intra-abdominal pressure and intra-thoracic pressure do affect intracranial pressure through decreased venous return and resultant increased venous hydrostatic pressure. More blood in the head means higher ICP (Monroe-Kellie doctrine). This is why we don't like to run high PEEP on our head traumas, although it can turn into a compromise. It is also why we used to (and rarely still) do bedside laparotomies for refractory elevated ICP, and why pentobarb coma and cisatracurium are so effective in treating ICP spikes.

However, you must remember that these issues are most prevalent in people with impaired cerebral autoregulation, decreased compliance, and/or space-occupying lesions. Hence, we don't worry about 20cm of PEEP in an ARDS patient without an intracranial process, nor do we worry about the fact that your ICP is probably 60 while you're pooping. Cerebral autoregulation allows us to maintain steady cerebral perfusion pressures across a wide range of systemic arterial pressure.

Increased venous hydrostatic pressure, unless really severe, is not going to transmit back to the arterial circulation and manifest as increased arterial wall strain. You're more likely to see cerebral edema and venous hemorrhage.

Finally, arterial wall strain is more severe for wide pulse pressures (elastic modulus), which plays a dominant role in many models of aneurysm formation and rupture. Venous congestion would be (if anything) more likely to raise diastolic arterial pressure, thus reducing wall strain.

 

[danielmd06]

If you have an obese patient, w/ htn, will sleep position affect inter-cranial arterial pressure? Specifically, does sleeping in prone position have the same affect as say a valsalva maneuver?

All things being equal the short answer is "no." But there is a clinically relevant point here if you happen to have OSA. Since this seems to go along the lines of what you were asking...

Supine positioning usually worsens obstructive sleep apnea (from gravitational effect on the oropharyngeal soft tissues and from nocturnal fluid redistribution) and you can thus expect more sypathetic surges (involved in apnea termination) than you might get from sleeping in non-supine positions. The periodic activation of the sympathetic nervous system could thus put you at further increased risk of nocturnal (or daytime) ischemic or hemorrhagic stroke.

 

[sarcoid]

Intra-abdominal pressure and intra-thoracic pressure do affect intracranial pressure through decreased venous return and resultant increased venous hydrostatic pressure. More blood in the head means higher ICP (Monroe-Kellie doctrine). This is why we don't like to run high PEEP on our head traumas, although it can turn into a compromise. It is also why we used to (and rarely still) do bedside laparotomies for refractory elevated ICP, and why pentobarb coma and cisatracurium are so effective in treating ICP spikes.

However, you must remember that these issues are most prevalent in people with impaired cerebral autoregulation, decreased compliance, and/or space-occupying lesions. Hence, we don't worry about 20cm of PEEP in an ARDS patient without an intracranial process, nor do we worry about the fact that your ICP is probably 60 while you're pooping. Cerebral autoregulation allows us to maintain steady cerebral perfusion pressures across a wide range of systemic arterial pressure.

Increased venous hydrostatic pressure, unless really severe, is not going to transmit back to the arterial circulation and manifest as increased arterial wall strain. You're more likely to see cerebral edema and venous hemorrhage.

Finally, arterial wall strain is more severe for wide pulse pressures (elastic modulus), which plays a dominant role in many models of aneurysm formation and rupture. Venous congestion would be (if anything) more likely to raise diastolic arterial pressure, thus reducing wall strain.

Thanks for the response! Typhoon, you cleared up my misunderstanding of the mechanism of increased abdominal pressure effects. It makes sense to me now that venus pressure is affected more than arterial pressure by an increased intra-abdominal pressure such as valsalva or prone poitioning. And would thus have more effect on ICP than arterial press. I can see how increased PEEP would be a prob as well.

Your answer led me to another question, and one that may not have an answer. If so many ppl have htn, but only some develop cerebral bf autoreg deficiencies, isnt the autoregulation deficit more of a risk factor for hemorrhagic stroke than just htn w/ normal cerebral autoregulation?

I can see that if preexisting htn precipitates autoregulation deterioration, then the easiest preventable cause of stroke is maintaining good bp. But my thought is: is there were a way to study pt's with htn to determine if their htn has a greater propensity to lead to stroke than for other pt's with htn? Obviously many more people have htn than ever stroke out. Some seem more susceptible to do so and if there were a clinical way to determine susceptibility (other than FH) it might help prevention efforts. There might be a way and my ignorance is just showing, but my curiosity is peeked.

 

[sarcoid]

All things being equal the short answer is "no." But there is a clinically relevant point here if you happen to have OSA. Since this seems to go along the lines of what you were asking...

Supine positioning usually worsens obstructive sleep apnea (from gravitational effect on the oropharyngeal soft tissues and from nocturnal fluid redistribution) and you can thus expect more sypathetic surges (involved in apnea termination) than you might get from sleeping in non-supine positions. The periodic activation of the sympathetic nervous system could thus put you at further increased risk of nocturnal (or daytime) ischemic or hemorrhagic stroke.

Wow, the things they don't teach in med-school... If OSA PTS are waking up 100x an hr at night, that would be a huge amount of sns activity and possibly contribute to the morning fatigue (in addition to loss of rem). The cv problems from that amount of stimulation are obvious, I just never thought about it (we only focused on the sleep wave changes). thanks for the reply Danielmd.