The use of inotropic drugs in patients in coma after cardiac arrest and receiving target temperature management is debatable. The cardiac index may be 40-50% less in a patient who has reached a temperature of 33C. The patient may have a bradycardia as well. There is probably not much need to treat a pulse >40/min or a CI of 1.5L/min. Inotropic drugs will increase the work of the heart, and therefor the oxygen consumption. As most of these patients have experienced an ischemic cardiac event, using (high doses of) inotropic drugs may not be a good idea. In general avoid drugs, that cause tachycardia.

Blood pressure may be more important, as the auto-regulation of the brain may not function very well, and the cerebral blood flow may greatly depend on the blood pressure. So, norepinephrine may be the drug of choice for that.

Central or mixed venous oxygen saturation (ScvO2 or SvO2) could used to monitor supply and demand of oxygen; monitoring lactate may be less useful, as this is often increased during hypothermia.

We have to await RCT's looking into this problem. The TTM-trial, which will be published next week, will have data in secondary analysis looking into cardiovascular data, and may shed some light on this topic.

I agree with Dr. Kuiper that inotropic drugs should be avoided in therapeutic hypothermia because of the increased oxygen consumption especially in post-MI patients.

As recent studies have shown patients in cardiac shock treated with intropic agents had a higher mortality than patients not treated with introps. I dont think these results will change in hypothermic patients, but I also wait for more RCT to proof this theory. At the moment we use thermodilution method to measure cardiac output and vascular resistance. In my opinion monitoring oxygen consumption by mixed venous oxygen saturation has to many failure potential, What could be the conclusion of a high oxygen consumption ? CI to low? Hb to low? Pulmonal oxygenation to low ? and what about the microcirculation ? So there are lot of work to do to find the optimal treatment in this group,

Thank you very much for interesting comments! Does this mean that you will avoid using inotropic drugs even in patients were CI is severly reduced, compared to your average patient treated with therapeutic hypothermia?

Dear Sir

Vasoactive drugs may be administered after ROSC to support cardiac output, especially blood flow to the heart and brain. Drugs may be selected to improve heart rate (chronotropic effects), myocardial contractility (inotropic effects), or arterial

pressure (vasoconstrictive effects), or to reduce afterload (vasodilator effects). Unfortunately many adrenergic drugs are not selective and may increase or decrease heart rate and afterload, increase cardiac arrhythmias, and increase myocardial ischemia by creating a mismatch between myocardial oxygen demand and delivery. Myocardial ischemia, in turn, may further decrease heart function. Some agents may also have metabolic effects that increase blood glucose, lactate, and metabolic rate. There is a paucity of data about which vasoactive drug to select first, although providers should become familiar with the differing adverse effects associated with these drugs, which might make a particular agent more or less appropriate for a specific patient.

*2010 American Heart Association Guidelines for Cardiopulmonary

Resuscitation and Emergency Cardiovascular Care (Part 9: Post–Cardiac Arrest Care)