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#overdrive #ventilation improved #oxygenation in this #COVID #ARDS patient today by 10% #SpO2 w/o any change an #FiO2 or #PEEP. Ask me how or take a stab yourself with these hints. #MICU #PPCM
OK, here it is. Serious students of #respiratory #physiology know that acidosis is a potent stimulant of #respiration and conversely, alkalosis (metabolic & resp) is a potent inhibitor of respiratory drive. Hence my fascination with static apnea shallow water #breathhold #diving
Thus if you have a patient with severe air hunger, as evidenced by many signs including a "dip" in the pressure/time tracing (see photo), you may abrogate it by creating a mild alkalosis. One way is a concentrated #bicarbonate infusion (1 amp per hour for 12+ hours).
I target a serum bicarbonate of about 32, basically converting an acute respiratory acidosis (from, say, #ARDS) into a chronic respiratory acidosis. But bicarbonate is in short supply, and it discomfits some folks to give all that #sodium #bicarbonate, so.....
The alternative is to increase minute ventilation enough that a pH above the patient's "set point" for breathing is exceeded. Often this is just a couple of breaths above the patient's spontaneous rate, in this case 32; it was increased to 35. The tidal volume was also increased
From 380 (6cc/kg) to 400 (6.25cc/kg). That doesn't sound like much, but at 6cc/kg you are close to dead space ventilation in many patients. Vd/Vt approaches 100% as Vt approaches Vd. So small increases in Vt that would be negligible at higher Vt are significant at low Vt
If Vd/Vt is 50%; .380*32=12.16 liters*50%=6 liters VA (alveolar ventilation). Increasing Vt to 400cc at a rate of 35 we get .400*35=14 liters*50% = 7 liters VA. That's just a 15% increase in VA, but it *completely* abolished the respiratory efforts on the P/t trace sans paralysis
Several things result. 1st, as #alveolarventilation improves, there is a small improvement in oxygenation via the #alveolargasequation. This small improvement matters if you begin with SpO2 86% as in this patient because you're on the steep portion of O2-Hgb dissociation curve
2nd, the abrogation of respiratory efforts can significantly reduce O2 consumption and CO2 production. Tobin's Textbook of Mechanical Ventilation references a study showing that with severe #respiratorydistress, respiratory muscles can use 50% of oxygen consumption
The reduction in CO2 production will amplify the effect of the increased VA on PaCO2; and the reduction in #oxygenconsumption will reduce the #extractionratio and SvO2 will rise. The higher #mixedvenoussaturation reduces the effect of #venousadmixture on #shunt
Better stated, the effect of high #shuntfraction on arterial oxygenation is worse when the mixed venous saturation is low, and it improves when O2 consumption falls. This is *part* of the reason oxygenation improves with paralysis, independent of lung compliance/mechanics
All of these small effects are sufficient to cause a significant augmentation in SpO2, especially when you start on the steep section of the sigmoidal #oxyhemoglobin dissociation curve. There is no such thing as a free lunch, but this comes pretty close
