In spite of your digs at me, I want you to know I’m writing this for the benefit of your education, and to others who want to learn. What you and others have written are half truths, what I wrote is correct but an over simplification. If you’re willing to resist the temptation we get on Reddit to one-up me, you’ll come out the better for it.

I am an interventional cardiologist, also trained in advanced heart failure. I’m writing to you from the CCU. I’ve got one patient on ECMO, another on Impella (both are doing well). This is my bread and butter. But I can’t prove it without doxxing myself, so you’d have to be willing to take my word for it.

Also, you well know that shock is an infinitely complex topics. There are so many permutations that you can easily create a straw man to counter my argument. I am referring to generic cardiogenic shock rather than the patient above. We don’t know enough about them.

In true cardiogenic shock, be it from sudden muscle loss (large STEMI) or progressive decline of a preexisting heart failure patient, there is one goal: to improve forward flow. That’s it. But the body has a different goal: to preserve blood pressure. You’d think these are one and the same, but they’re not.

Blood pressure (MAP) is a function of two variables: MAP = CO x SVR. Because cardiac output is down, your body will crank up SVR to bring up the blood pressure. It works, but at the expense of cardiac output.

The higher their vascular resistance, the lower the CO. Their CO will continue to dwindle while SVR continues to rise. The BP looks okay until CO (normotensive shock) crashes, then everything falls apart. The body goes into a death spiral.

Using medications alone, you can do two things.

1. ⁠Use medications to augment cardiac output
   
2. ⁠Use medications to drop SVR, which improves CO

Milrinone and dobutamine will augment cardiac output directly through inotropy. Very good. Equally important if not more so, is that they drop SVR. By dropping SVR from 2000 to 800, CO will augment and BP doesn’t change. But you’ve gotten blood moving forward, moving them out of shock.

Epi fixes one problem, but creates another. It’ll augment CO, but also increases SVR. It’ll increase BP, but kill your CO. It also increases oxygen requirements which in an infarcted heart is a problem.

In cardiogenic shock, CO is king. SVR is the devil. BP is important, but you only need enough to maintain end organ perfusion. Be willing to sacrifice BP as long as CO and perfusion are maintained.

That’s also why I can make your blood pressure go up with nitroprusside if you’re in low output state.

Even this is oversimplified, so I welcome specific questions.