Inotropes for the cardiac surgical patient

Enhancing the cardiac contractility is a part of the "management encompassing resuscitation, initial and ongoing monitoring and supportive treatment" for "Cardiac surgery: including sternotomy for bypass grafting, valve surgery and aortic surgery", a Level 1 topic from Section 2.1.18 in the second edition of the CICM Syllabus for the Second Part Examination.

Luckily, there are only a few to chose from:

• Noradrenaline
• Adrenaline
• Dobutamine
• Milrinone
• Levosimendan

These links point to the primary exam section of this site where dense pharmacology information is explored, and the modern CICM Second Part Exam candidate can rest easy, knowing that the times of them having to draw up "compare and contrast" tables to demonstrate their understanding of these drugs is probably behind them. The question of "which inotrope" has been explored in numerous past CICM Fellowship exam SAQs, but never in the context of cardiac surgery, and mostly prior to 2008, when this material migrated to the First Part exam. The reason we have not seen this subsequently is because there is so little to write about that even this famously verbose author gets writer's block. There's not enough here even for a grey box summary.  Butterworth (1993), the equally dated Gillies et al (2004) and the more recent Chen et al (2021) would have to be the most authoritative source for the evidence in this topic, but because the data are mostly of poor methodological quality, it does not matter which of these you read. New drug names have appeared, but the choice of drug is still guided mostly by vibes.

When to start, or stop, the inotropes after cardiac surgery

That pulmonary artery catheterization is handsomely rewarded by Australian Medicare should seem like insufficient reason to insert these things, and yet even in this highly enlightened socialised health care system we find ourselves in an environment where they are deployed routinely in some centres. Whatever one's bias, the presence of such a device in the cardiac surgical patient does, genuinely, seem to help remove some of the guesswork from the assessment of their circulation. The hint that inotropes are indicated comes from the knowledge that, even in the absence of vasodilation and with good volume replacement, the cardiac index remains depressed. 

Even in the absence of a cardiac output monitor, the likelihood is that the contractility will have been well assessed in theatre via a TOE. In the vast majority of situations, the patient's inotropes will have been started at this stage, at the point at which the anaesthetist first determined that the contractility was impaired. The specific choice of inotrope was in this case theirs, and the challenge for the ICU team is therefore:

• Do you stop the inotrope, and when?
• Do you change the inotrope, and to which?
• and if there was none before, when do you start an inotrope?

The latter question falls more into the approach to the haemodynamically unstable cardiac surgical patient and will not be discussed any further here, as the topic of this chapter is the predictable monotony of the routine. These routine patients are of course all going to do reasonably well and none of the minor fiddling with their inotropes is going to make much difference for their outcome, which means that clinical trials looking at "hard" patient-centric endpoints will always produce negative results or be underpowered. Therefore, for the immediate post-op care of the patient on what seems to be a homeopathic dose of dobutamine or adrenaline, there is no evidence-based instructions in the literature, and the bedside junior in the night must submit to the brutal tyranny of the senior nursing staff and manage inotropes according to The Way We Do Things Around Here. 

That aside, what sensible recommendations can be made?

• Keep it going until after extubation. The inotrope, whatever it may be, is likely doing no significant harm, particularly where its dose is so low that one might question the judgment of the person who started it. One rationale for leaving it untouched is the known delayed nadir in contractility which is typically  at its worst at about six hours after the separation from bypass, i.e. exactly around the time EAST recommend we should be extubating the patient. From this, it follows that it would be counterproductive to withdraw contractility support from the patient at the time when they need it most, and then challenge them with the stress of extubation. 
• Try to stop it within 24 hours. The highest risk for AF is roughly 24-48 hrs following surgery, and one would not wish for the inotropes to be contributing to this risk; and the post-bypass dysfunction should have settled by 24 hrs or so. 
• Replace adrenaline with dobutamine, if you can. The main reason for this is the fact that to be able to trust the lactate is extremely helpful and adrenaline makes this impossible. With that caveat, adrenaline is perfectly fine as an inotrope and is the drug of choice for some units, for mainly cultural or economic reasons. 
• Add milrinone if the right heart is the main problem. Milrinone as a pulmonary artery vasodilator can make a big difference in RV function, as the RV is extremely sensitive to afterload. The caveat to the use of this agent is the accumulation in renal failure.
• If you are adding milrinone, why not give levosimendan instead, is a legitimate question considering Chen et al (2021) found it was the best studied of all the agents (unfairly, because marketing). On the other hand, with the heart now revascularised and the depressant effect of cardiopulmonary bypass so short-lived, one might argue that an inotrope with an effective duration of action measured in weeks is overkill.
• Start an inotrope when:
  • You are satisfied that the patient is now well-filled,
  • and not excessively vasodilated,
  • and you still have reason to believe that their cardiac output is insufficient
  • or you have produced some kind of objective assessment of their contractility, and the assessment is disappointing.
• Dobutamine is fine if you're confused. If, on the basis of whichever haemodynamic voodoo you believe, the need for an inotrope is established, then the choice of inotrope comes down to The Way We Do Things Around Here; but if the oracles of that church are not available or looking the other way, dobutamine is a safe initial choice for the beginner, mostly because its effect is rather shortlived, and if it becomes apparent that it was a terrible mistake, one's disgrace will be quickly forgotten. Pölönen et al (2000) used a fairly large dose of it (15 μg/kg/min!) on what appears to have been a relatively unselected group of 196 patients who came off bypass with an SvO₂ less than 70% and a lactate higher than 2, i.e without thinking too hard about whether they were shocked or not. That these patients did not appear to come to any specific harm is highly encouraging, even though many would have had right heart pathology and/or pulmonary hypertension (that might otherwise have called for something like milrinone or levo). Obviously throwing dobutamine randomly at an ill-defined pile of failing ventricles is inelegant, and to routinely resort to this will produce grumbling monologues from professorial seniors, but these people should be invited to instead invest their energies in gardening, or maybe actually training their junior staff to understand inotropes better.