ICU Webinar

As for any IABP insertion, the risk of occlusion of the left subclavian/left carotid artery exists if the balloon is inserted too far away towards the aortic arch. To avoid this malposition, we should guide the insertion and positioning of the balloon either by RX fluoroscopy, either by TEE (see lecture from Dr P Menon during the webinar), whether or not there is an inserted VA-ECMO.
If the VA-ECMO is placed centrally (using the CPB-cannulas) and if the IABP is placed correctly (cf supra), the risk of compromising the upper circulation seems to me quite low. If the ECMO is placed peripherally, based on the available literature, we know that:
-Yang et al. J Translational Medicine 2014, 12: 106. Postcardiotomy shock patients. If the heart is producing a pulsatile pressure gradient > 10mmHg, the addition of IABP to peripheral VA ECMO will significantly increase the cerebral blood flow compared to VA-ECMO alone. If the heart is not generating a pulsatile pressure > 10mmHg, the cerebral blood flow will be higher in the group receiving just the VA-ECMO.
-Chen et al. Ann Intensive Care 2019; 9:16. Postcardiotomy shock patients, retrospective study. In the group receiving IABP + VA-ECMO, there were less CRRT, less neurological complications, but more thrombosis complications. In this study, the association of IABP + VA-ECMO was an independent protective factor for in-hospital mortality.

I do not have any experience with the use of intratracheal milrinone. The group of A.Denault (Montreal) published about this use in case of acute RV dysfunction (JCVA 2017;31:489) and according to them, it is very powerful and easy to use. However, it is an emergent action helping to avoid RV failure during or just after weaning of CPB. It should be followed by the use of pulmonary vasodilator agents, preferably inhaled to avoid systemic vasoplegia, like inhaled NO or inhaled milrinone. Some colleagues told me that they already tested it in post-cardiotomy acute RV dysfunction, and confirmed that it was very efficient.

Yes, of course. The use of cathecholergic inotropes (Dobutamine, milrinone, epinephrine) is exhausting the ATP reserves of the cardiac muscle, which is the fuel of the myocardium. GIK, through the Krebs cycle, is restoring the ATP reserves. On a theoretical point of view, the association of levosimendan with GIK could be less useful, as levosimendan is supposed to avoid ATP consumption.

Based on the available literature, I may not recommend it as standard care, as there are no multicenter RCT confirming its usefulness in term of benefit on the survival rate. However, the side’s effects that we can induce with GIK are hypo-or hyperglycaemia/ hypo-or hyperkalemia. Glycaemia and K are parameters that are regularly checked by experienced teams during and after cardiac surgery and we are familiar with those corrections. Therefore, I do not consider those side’s effects as an issue. On a clinical point of view and to be pragmatic, I would suggest that every patient operated with CPB and known to have reduced LV EF with signs of elevated end-diastolic pressures, every patient operated in emergency, every patient operated because of acute myocardial ischemia, every patient for whom a prolonged CPB time is expected, may benefit from GIK. The main problem is that it exists as many GIK protocol as published studies.

First of all, we should keep in mind that those data, published by the Danish group, are retrospective data. In this retrospective study, those patients who received milrinone were older, with lower preoperative ejection fraction, higher EuroSCORE, longer time on cardiopulmonary bypass, and having more complex surgery; in other words they were probably more “sick”. Some hypotheses were addressed by this group to try to explain what they observed. 1) Milrinone is a more powerful vasodilator agent than dobutamine, and significant hypotension after cardiac surgery can induce hypoperfusion of coronary, renal and mesenteric arteries, which can be deleterious. 2) Milrinone in nonsurgical acute exacerbation of chronic heart failure (OPTIME-CHF study, J Am Coll Cardiol. 2003;41:997–1003) was shown to be harmful in patients with ischemic heart failure with LVEF < 40%.

There are, in the literature, as many GIK protocol as published data. This explains maybe why it is so difficult to find strong conclusive data in the literature about GIK. The historical formula was: a maximal glucose disposal rate of 400 mg/M2/min with an insulin infusion rate at 1,200 mU/ M2/min and KCI supplement rate at 0.08 mEq/M2/min. The formula proposed by the group of Geneva is 50ml G40% + Actrapid 20UI + 10 mEq KCl over 60min at the time of induction of anaesthesia. When I use it in the ICU after difficult cardiac surgery, I give 500ml G50% in 24h + insulin started at the infusion rate of 0.1U/Kg; the nurses are controlling every 30min glycaemia and K to adapt the infusion rate of insulin and K. Generally, a steady state is reached after +/- 2h. In the toxicologic literature (B-Blocker or Ca channel Blocker intoxication), you can find very high regime of insulin bolus, like 1 U/kg insulin bolus followed by a 1-10 U/kg/h continuous infusion (Clin Toxicol (Phila). 2011 Apr;49(4):277-83).