Low Cardiac Output Syndrome in congenital cardiac surgery

In my opinion, the lack of strong evidence for the prevention of LCOS using milrinone is a downside of the actual requirement to use "big data" in order to make recommendadtions, pooling together heterogeneous populations and diseases. When used in selected groups of patients, Milrinone is a very useful drug and the perfect fit between the pathophysiology of LCOS in very young patients (systemic and pulmonary vasoconstriction) and the inodilatatory properties of Milrinone makes it a drug of choice for prevention and treatment of LCOS in young patients. Howevere, its efficacy in older patients is lower, probably because the mechanism of LCOS in older patients is different (vasoplegic shock, most of the time). Therefore, it should not be used in all patients but probably in the youngest ones. After all, no big data was published before the use of epinephrine for resuscitation has become common practice ...

It is likely that a good understanding of the underlying pathophysiologic mechanism responsible of LCOS in each cardiac disease is one of the most important elements. Second, we have to use monitoring tools which allow us to act in real time, and probably repeated echocardiographic assessment, together with multisite NIRS monitoring and/or monitoring of venous saturation are very helpful. I also believe that the experience of the physician is a major factor, and I strongly encourage pediatric cardiac anesthesiologhists to train in large centers, which allow them to increase the number and complexity of the patients they see and handle during their training.

GUCH patients often have diastolic dysfunction of their right ventricle. Levosimendan has lusitropic effect and is a strong pulmonary vasodilator. It is, therefore, very likely that it has the potential to improve RV function in these patients. A retrospective analysis in GUCH patients receiving either levosimendan or milrinone hase been recently published by the team in Bordeaux, showing shorter ventilation durations in patients receiving levosimendan, and lower vasoactive-inotropic scores. These results need to be confirmed in prospective trials.

Ventricular dysfunction is quite common after VSD repair and usually recover between 1 and 6 months post-op. True incidence of LCOS after VSD repair is unsual, especially in a patient with normal preop. function and short bypass run. Most unexpected LCOS are associated to poor myocardial protection. Carefull administration of cardioplegia is crucial to decrease the risk LCOS.

My apologies if my presentation was not clear. Hydrocortisone should be administered in the context of vasopressor resistant shock. Methylprednisolone is sometimes used and has been studied for the prevention of SIRS and associated complications.

PICCO is an interesting technology, but its use in childen undergoing cardiac surgery is challenging. Due to the number of artefact during the intraoperative period, PICCO is usually not relevant. In the postoperative period, PICCO was thought to be a promising technology but remains rarely used. In the cardiac ICU, most programs have an easy access to echocardiography that remains the primary option to look at heart function and cardiac output in the context of LCOS.

I agree. LA lines are used in some specific cases to guide postoperative management.

Patients with Einsenmengers reaction per definition do no not react on selective pulmonal vasodilators any more due to fibrotic pulmonary vascular tissue. That causes a shunt reversal from R-L together with increasing cyanosis. The basic problem in most patients is that the left ventricle lacks of volume because the right one is not able to bring its blood to the left side. In those patients, the treatment of LCOS is often an act of desperation. One can discuss with the cardiac surgeon to establish a Potts shunt operatively. This will not cure the underlying disease but helps the right ventricle to shunt blood to the systemic circulation and may increase cardiac output but it will worsen the cyanosis over time.

Do you focus on acute right ventricular failure due to pulmonary hypertonic crisis? If this is the case I would suggest to use a selective pulmonary vasodilator like NO. Preserve the preload because a chronic overload right heart needs preload. Perform echocardiography and look at the ventricular septal movement. If the septum is shifted towards the LV and has paradox movement I would use a vasopressor with a dose that is sufficient to shift back the septum to the right to re-shape the right and mostly augment the left ventricle. In all cases I did norepinephrine was sufficient to reach that therapeutic goal. I have not enough experience with the use of terlipressin in those cases. In patients with chronic failure the data are not supporting the chronic use of terlipressin or vasopressin in patients with pulmonary hypertension

We are talking about treatment of children with a congenital heart defect and LCOS. That makes our world a lot more difficult because before therapy we need to have a diagnosis. I mean we need to know which part of the heart is failing and why. For example, patients with aortic coarctation or aortic valve stenosis will have a significant hypertrophy of the left myocardium. If we decrease the systemic vascular resistance in those patients, we might decrease the myocardial coronary blood flow and creating myocardial ischemia. In those patients a low dose vasopressor (i.e. norepinephrine 0,05 ug/kg/min) might be a very good idea. If we have a LV failure together with elevated LA pressure, reduced ejection fraction and signs of beginning ischemia, (i.e. ST-elevation) one might consider using an inodilator like milrinone together with an inotrope like adrenaline. I called that “LV systolic“ failure in one of my last slides. Patients with a decreased systemic vascular resistance like the one with sepsis highly benefit from a vasopressor therapy. I called this LV diastolic failure.

A very interesting question and mean too! It’s hard to find the right moment to go on ECMO and sometimes the decision is more team dependent than following objective parameters. I would say as soon as you start to think that ECMO will be the last option. Another hint is when you need to increase your inotropes step by step in order to maintain systemic perfusion. I am sorry that I cannot give you a better answer than that.

The same limitation to the use of NIRS postoperatively apply intraoperatively: size of the patient, lack of evidence/validdation of NIRS in diagnosing LCO. Larger prospecctive studies with accurate definition of LCO and defined outcomes are needed.

Being a noninvasive and continuous monitor, NIRS has the potential to be used as a tool for diagnosis and management of LCOS. However, as it currently stands, it is not useful by itself but in combination with other parameters such as lactate, physical exam, vital signs, echocardiography and the experince of the clinicians. In a recent study, the combination of NIRS and BP was predictive of LCO and mortality.

Hb and Hb O2 impacts oxygen supply and hence the value of NIRS. As mentionned in the talk, the NIRS measurement is not a direct measure of oxygen supplly and demand but a weighted value based on the arterioles, venules and capillaries in the area when near-infrared is reflected. I agree that knowing the Hb of the patient will help in troubleshooting when the NIRS is low.