do you fight a V/Q mismatch

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somthing clinical for a change:

I have recently read about the phenomena that exsits where patients in a (lateral recumbent position) for example will have a v/q mismatch. I qualify this with the explination that due to gravity , perfussion will prefer the dependant lung while ventilation would prefer the independant lung do to the increased tone of muscles of expiration which causes greater recoil of the lung thus increasing the compliance of the independant alveoli compared to that of the dependant lung alveoli.

now. what if I had to drop a lung? then what. what if i have an open chest which would only amplify the mismatch do the the increased distensbility of the independant lung. I am in awe as to how anesthesia providers blance these physiologic problems. I am sure we'll learn more down the road but due to my impatients I want an answer. how do you deal with a mismatch like this. what if one lung is sick.. yeesh... it just gets more and more complicated. :rolleyes:

It is only if there is a need in the presence of V/Q mismatch. is this correct? the case i had went smoothly with no significant drops in O2 sats. so we didnt need to do any of these interventions, i just want to make sure i didnt miss something of importance.

Actually, there WILL be a V/Q mismatch whether you see it or not. In the lateral position the normal blood flow to each lung is 60% to the dependent lung and 40% to the nondependent lung. The shunt flow is 10% divided equally between the 2 lungs (5% in each lung). So the non dependent lung has 35% of total cardiac output participating in gas exchange and the dependent lung has 55%. Once the nondependent lung is deflated, all blood flowing thru that lung is shunt flow and without HPV, 35% would need to be added to the 10% of usual shunt flow equalling 45% of cardiac output having a V/Q ratio that is closer to 0. HOWEVER, since HPV is assumed to shunt 50% of the nondependent lung's flow to the dependent ventilated flow, 17.5% (35%/2) plus the usual 5% shunt is therefore directed to the dependent lung. Now add in the 5% shunt from that lung and the total is assumed to be 27.5% shunt flow and 72.5% participates in gas exchange. A maximum PaO2 of 150 on an FiO2 of 1.0 is the usual maximum attainable. So, while not always clinically apparent, a V/Q mismatch does occur. Therefore one needs to avoid inhibiting HPV. Avoid SNP, NTG, Hydralazine, high MACs of volatile agents. Nitric Oxide reverses HPV so I'n not sure why that would help when you want HPV (Tenesma) Any other drugs I haven't mentioned??

BTW, I had board questions revolving around these concepts, so study hard if you are near the big quiz.

nitric oxide will improve your V/Q mismatch... don't worry about HPV so much... just use what makes sense physiologically, and by the way TNG would be fine as well...

I love these discussions! Thanks guys!

nitric oxide will improve your V/Q mismatch... don't worry about HPV so much... just use what makes sense physiologically, and by the way TNG would be fine as well...

Can you explain how the vasodilating properties of NO helps in the face of OLV? I'm not saying it doesn't work. I've never used it in the OR, we did use a lot in the ICU for patients with poor lung function and high PA pressures, worked like a dream. But I can't figure out the physiology in the face of needing HPV. O2 sats can be so bad (as you know) that the PA must be ligated or clamped early in the pneumonectomy to eliminate that shunt flow entirely so I can't get my pea-brain wrapped around the benifits of NO or NO producing drugs in this scenerio. Tenesma?

For all the newbies yet to be in school, could you please expand on what HPV (i'm assuming the "V" stands for ventilation) and TNG stand for? Thanks.

now let's say for some reason you can't oxygenate the collapsed lung and for some reason the surgeon can't clamp the PA feeding the collapsed lung - what are the things that will improve V/Q in the dependent lung?

the only way around it is to cheat a tiny bit.... Nitric oxide creates vasodilation in the ventilated part of the lung, so now you are shunting more blood towards your ventilated lung and therefore get better V/Q... sounds simple... and it works... I don't use it very often in the OR though - cause it is so ridiculously expensive - and therefore use it only if the patients life is in danger - but at least it is an extra card up your sleeve. I use it a lot more often for people with acute pulmonary hypertension or especially for heart transplants into recipients with long-standing pulmonary hypertension that hasn't responded to chronic milrinone or nesitiride (natrecor).

now let's say for some reason you can't oxygenate the collapsed lung and for some reason the surgeon can't clamp the PA feeding the collapsed lung - what are the things that will improve V/Q in the dependent lung?

the only way around it is to cheat a tiny bit.... Nitric oxide creates vasodilation in the ventilated part of the lung, so now you are shunting more blood towards your ventilated lung and therefore get better V/Q... sounds simple... and it works... I don't use it very often in the OR though - cause it is so ridiculously expensive - and therefore use it only if the patients life is in danger - but at least it is an extra card up your sleeve. I use it a lot more often for people with acute pulmonary hypertension or especially for heart transplants into recipients with long-standing pulmonary hypertension that hasn't responded to chronic milrinone or nesitiride (natrecor).

Thanks Tenesma, for KAT, HPV = hypoxic pulmonary vasoconstriction, the tendancy for areas of the lung that are hypoxic to shunt blood to areas with better oxygenation. TNG = Nitroglycerine. OLV = one lung ventilation.

we havent studied this yet but i read a research article on this at one time. speaking of NO, are you talking nitric oxide as in liquid ventilation, i read of this in the treatment of ARDS (acute resp. distress syndrome)?

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So am I right in interpreting your response to mean that NO only causes vasodilation in the ventilated parts of the lung? Otherwise, I would be concerned in increasing blood flow to the deflated lung as well, which might wosen your V/Q match even more. After all, perfusion is not the issue in the ventilated lung.

But...perhaps the increase in perfusion is enough to increase your oxygenation.

While we're on this topic... what do you all think the effect of a Neosynephrine gtt would be on your HPV. (perhaps only theoretically) I had an instructor state that this could worsen your HPV, but I'm questioning this logic just a little bit.

As long as you are ventilating the good lung, it is HPV after all, that's assisting your oxygenation. The blood flow is shunted to those parts of the lung that are being ventilated instead of the defalted lung. If this were not so, your shunt would be even greater.

that's right... NO only causes vasodilation in ventilated lung

Interesting stuff. How much systemic effect do you get from your NO?

well theoretically there are systemic effects, but we don't really see them...

of interest, you will soon be seeing nebulized or IV Viagra to augment the effects of NO on the lungs... i am serious..

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