Metabolic and nutritional support in acute cardiac failure.
OBJECTIVE
Cardiovascular disease is one of the most important causes of morbidity and mortality in western countries, generating an increasing number of admissions to intensive care units. Cardiac failure has long been associated with nutritional disorders, malnutrition and cachexia being frequent during the late phases of congestive heart failure: undernutrition is also a determinant of outcome, even after cardiac transplantation.


RESULTS
It has been shown that early metabolic support can improve the recovery of the ischaemic heart. This paper reviews recent findings on substrates that can support the failing myocardium, which are mainly glucose-insulin, glutamine, taurine, selenium, thiamine, folic acid, and omega-3 fatty acids. Ischaemia-reperfusion generates tissue lesions that can be partly prevented through substrate manipulation.


CONCLUSIONS
Shifting the substrate metabolism from lipids to carbohydrates and reinforcing the antioxidant status reduces the deleterious biological and clinical consequences of acute ischaemic events. The use of the glucose-insulin-potassium infusion has become widespread with the re-discovery of its value in modulating cellular metabolism and accelerating recovery of the ischaemic myocardium. Antioxidants have gained acceptance in the perioperative phase, as well as in chronic heart failure. This constitutes another piece of evidence in favour of early metabolic and nutritional intervention. There also appears to be room for the prevention of acute deterioration of cardiac function after surgery with the preoperative administration of oral supplements containing omega-3 fatty acids.
Berger
Mette M
MM
Intensive Care Unit and Burns Centre, University Hospital, Lausanne, Switzerland. mette.berger@chuv.hospvd.ch
Mustafa
Iqbal
I
D000208:Acute Disease; D002318:Cardiovascular Diseases / Q000378:metabolism* / Q000628:therapy*; D005947:Glucose / Q000378:metabolism; D006333:Heart Failure / Q000378:metabolism / Q000628:therapy; D006801:Humans; D007328:Insulin / Q000378:metabolism; D017202:Myocardial Ischemia / Q000378:metabolism / Q000628:therapy; D009206:Myocardium / Q000378:metabolism*; D009752:Nutritional Status; D018529:Nutritional Support; D011188:Potassium / Q000378:metabolism
D007328:Insulin; D005947:Glucose; D011188:Potassium