The PaCO2 is almost irrelevant to cerebral blood flow; the extracellular pH determines the caliber of the arterioles. However, since CO2 moves immediately across the blood-brain and blood-CSF barriers, and anions like bicarbonate move very slowly (six hours to correct the pH back down to 7.3, the normal CSF pH, following the induction of hyperventilation in a normal host), cerebral blood flow does change with abrupt changed in the PaCO2. With a systemic metabolic acidosis, though the choroid plexus should be even more efficient at exporting bicarbonate from the CSF into the systemic venous circulation, so that the initial cerebral vasoconstriction should be fairly quickly ameliorated. The real problem in cerebral blood flow will come when the systemic tonicity falls; the brain may start to swell, compromising blood flow. –Tom Bleck
(Brit J Anaes 2001;86(6):859)
reduced venous return can paradoxically cause vasovagal response with bradycardia and hypotension
Ephedrine makes the most sense as an antidote
Don’t know if this is either simple or lucid but; assuming the pressure within the left ventricle (LV) is a constant, the application of a positive intra-thoracic pressure reduces the LV transmural pressure, that is, the LV doesn’t need to develop as much wall tension to produce the same intraventricular pressure. Less wall tension, less work, less oxygen consumption, less afterload. Michael Thanks. That’s what I had previously assumed, but Pinsky made it sound like there was a significant increase in CO & fall in PW. A decrease in tension would primarily reduce myocardial O2 demand. That may translate to better haemodynamics in patients with critical coronary artery stenosis, but he made it sound like it happened in many clinical situations, not only those with significant on going IHD.
Yes, I think he is correct. It benefits more than just those with known/active IHD. If the mean arterial pressure (MAP) is 70 mmHg (and the mean LV pressure is the same) the application of 10 cmH2O of CPAP will reduce LV transmural pressure and afterload by 13% (approx), this may be the difference between adequate pulmonary function and pulmonary oedema. I look after a lot of ancient crumbling octogenarians with clapped-out hearts. When they appear ready to be extubated (OK on 5 cmH2O PEEP and 5 cm H2O Pressure Support), their haemodynamics may still be habituated to the afterload reducing effects of positive intrathoracic pressure. Removing this may be enough to put them into pulmonary oedema. In these patients, I try to avoid post-extubation hypertension so that this doesn’t exacerbate the removal of PEEP. The obverse situation also occurs. That is pulmonary oedema due to upper airway obstruction. Big negative intrathoracic pressures increase LV afterload and produce forward and backward LV failure. I’ve seen this in fit, healthy 20 year olds subjected to botched airway management during elective surgery.
Yes, I think he is correct. I’m sure he’s correct. FWIW, I asked him this after the talk but he had to rush for some other session. He mentioned that it had something to do with reflex sympathetic vasodilation & was lost in animal models whose baroreceptors were removed. However, he was whisked off before any further elaboration & I’m sure there is more to it than this. If the mean arterial pressure (MAP) is 70 mmHg (and the mean LV pressure is the same) the application of 10 cmH2O of CPAP will reduce LV transmural pressure and afterload by 13% (approx) Please elaborate. Does the CPAP selectively increase the LVEDP. Why doesn’t it also affect the aortic pressure.The aorta too is intrathoracic. Granted the LVEDP is lower that the aortic diastolic pressure. If that is the case, this CPAP effect should essentially kick in when the CPAP is the same or higher than the LVEDP. Is this the case. The obverse situation also occurs. That is pulmonary oedema due to upper airway obstruction. Big negative intrathoracic pressures increase LV afterload and produce forward and backward LV failure. Pinsky also mentioned this in his talk. I earlier thought it was a simple Starling forces effect. Positive pressure in pulmonary cappillary & massive negative intraalveolar pressure. Big gradient & hence increase transudation of fluid across the membrane.
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