I was gonna try and tackle these issues separately but since they're so interconnected, f it, let's just dive into everything. Hopefully it stays coherent.
As to the airway issue and choice of MAC vs. GA- let's assume the GI insists on doing the case prone. I think it is absolutely crucial to have an ETT in for this case, because we cannot allow the patient to hypoventilate and get hypercarbic and more hypoxemic. This isn't an in-and-out EGD, it's a complex ERCP with possible stenting. Let's do the patient, her heart, and ourselves a favor and optimize the respiratory situation.
Yes, you'd rather not instrument a bad COPDer's airway and put them on a vent if you don't have to. But I think you have to here. And she walked in (slowly) off the street- she didn't start in overt respiratory failure, so there is a better than even chance that she'll be extubatable at the end. If the airways get reactive and she doesn't declare herself ready when everything is done, you can vent temporarily in the PACU if necessary. I don't think the way you ventilate matters much for this short case, just make sure you don't breath stack and keep pressures reasonable and you'll be OK.
So on to the heart. When I say this right heart was massive, I mean it was truly enormous. As expected, there was flattening of the interventricular septum both is systole and diastole (pressure and volume overload), and the LV was small and D-shaped. One of those hearts where the RV has dilated into space normally occupied by the LV, decreasing the LVEDV and stroke volume.
The TR was a strong moderate, had i read the echo I would have called it mod-severe, which makes it necessary to take the read of "mild RV dysfunction" with a grain of salt- the RV has a low-pressure popoff to work with. Also, while the PASP by echo was "only" 2/3rds systemic, those estimates often underestimate the true RVSP. So I thought that I'd better treat this heart like one that is very capable of going down the pulmonary hypertension death spiral. Moreover, with all the PACs, the effective heart rate of perfusing beats was actually a fair bit lower than the EKG rate, which didn't help anything.
So as we all know, what makes pulmonary hypertension so dangerous is the death spiral of RV ischemia. The RV is normally perfused both is systole and diastole, unlike the LV (only in diastole). As PH and RVH progress, and pulmonary pressures approach systemic pressures, the RV starts losing that systolic perfusion, and only gets effective blood flow in diastole. If our BP goes down and the strained RV gets ischemic, its output drops (further decreasing BP and exacerbating ischemia) and it dilates, further reducing the LV chamber size (because of ventricular interdependence- only so much room in the pericardium) and decreasing the LV stroke volume- further decreasing BP and exacerbating ischemia. It's tough to bring patients with this physiology back from a code.
So our hemodynamic goals are: maintain diastolic perfusion (maintain SVR), while minimizing RV afterload (reduce PVR). We also want to maintain preload and avoid significant bradycardia. Fortunately there won't be fluid shifts during this nonsurgical case, so that's one less variable to deal with. And again, since hypoxia/hypercarbia will increase PVR, we want to control the ventilation to make sure those variables are optimized.
For those who have played with vasopressors in the heart room while you have a swan in, you've seen that with alpha agonists, the pulmonary pressures go up with every bolus. Usually this is OK, since systemic pressures should concomitantly rise, but this isn't always the case with sick patients. Norepi is better than phynelephrine IMO, since you the the RV a little beta bone.
Vasopressin is an ideal pressor for these patients. It has the desirable properties of raising the SVR (and therefore coronary perfusion pressure) without raising the PVR, optimizing RV perfusion. PA pressures should not change with boluses or infusions of vaso.
Other things to have around for patients like these- milrinone is in many ways a good drug for these folks. Increases RV contractility and decreases PA pressures. It does so at the cost of some SVR though, so important to have some pressor around to counteract that. Vaso again is ideal, but a little norepi is also good with milrinone.
Epi standing by if you really get into trouble, but keep it as a last resort- you hate to take a borderline ischemic RV and ask it to beat stronger and faster unless you really have to.
I'll stop there for now. All other comments welcome.
