Fair enough, but let's assume that the patient is still viable. We could also assume that the patient is bradycardic with a rate of 30 or so rather than agonal. I don't have the luxury of pronouncing patients in the field. So, what's the least of the evils in increasing the heart rate?
The myocardium is already ischemic, and I agree that whatever interventions you do are going to increase oxygen demand even more, but the patient is going to die with a rate of 10 anyway so you (or at least I) would have to do something. Since this is a cardiac arrest patient I assume they are intubated and receiving 100% oxygen. This is all we can do to try to get the pyruvate that is causing the lactic acid production to be converted to acetyl CoA and enter the citric acid cycle and oxidative phosphorylation, right? I can't think of any other way to get those two pathways going, but my biochem is a little rusty. Also, if they're that acidotic, we can also think about bicarb.
I also found it interesting that you say that the myocardium gets most of its energy through fatty acid metabolism. I haven't had any physiology, so I don't doubt you, but that seems inefficient. Although fatty acid metabolism produces about twice as much ATP as glycolysis, it takes longer depending on the length of the aliphatic chain, and this energy would also have to be transported to the heart since it is (or...should be) deficient in fat. The heart will need ATP at a rate much faster than fatty acid metabolism could provide it whereas glycolysis is speedy and there is always glucose available in the blood. Oh well, such is life.
Anyway, back to how to increase heart rate: Although there is a risk for electrical damage, wouldn't TCP cause the smallest increase in oxygen demand since although the rate is increasing, which will increase demand, there are no drugs introduced that themselves cause an inherent increase in oxygen demand like the catecholamines epinephrine and dopamine. Also, I don't know what you mean by pacing being ineffective since all the myocardial cells that could fire were. I thought we used TCP as an external pacemaker to force the cells to fire faster when we don't have time for drugs to work, rather than using it to force some "inactive" cells to fire when they previously were not, or is it some of both?
Lastly, say you succeed in increasing vascular tone and force of contractility using a dopamine drip...is a heart rate of 10 really going to sustain them long enough for the rate to increase on its own? Also, dopamine itself is going to increase oxygen demand which you stated above would kill what remains of the hypoxic myocardium?
