Guidelines for specialized nutritional and metabolic support in the critically-ill patient. Update. Consensus SEMICYUC-SENPE: Cardiac patient

Recomendaciones para el soporte nutricional y metabólico especializado del paciente crítico. Actualización. Consenso SEMICYUC-SENPE: Paciente cardíaco

F. J. Jiménez Jiménez^a, M. Cervera Montes^b and A. L. Blesa Malpica^c

^aHospital Universitario Virgen del Rocío. Sevilla. Spain.
^bHospital Arnau de Vilanova. Valencia. Spain.
^cHospital Clínico San Carlos. Madrid. Spain.

ABSTRACT

Patients with cardiac disease can develop two types of malnutrition: cardiac cachexia, which appears in chronic congestive heart failure, and malnutrition due to the complications of cardiac surgery or any other type of surgery in patients with heart disease.
Early enteral nutrition should be attempted if the oral route cannot be used. When cardiac function is severely compromised, enteral nutrition is feasible, but supplementation with parenteral nutrition is sometimes required.
Sustained hyperglycemia in the first 24 hours in patients admitted for acute coronary syndrome, whether diabetic or not, is a poor prognostic factor for 30-day mortality. In critically-ill cardiac patients with stable hemodynamic failure, nutritional support of 20-25 kcal/kg/day is effective in maintaining adequate nutritional status.
Protein intake should be 1.2-1.5 g/kg/day. Routine polymeric or high protein formulae should be used, according to the patient's prior nutritional status, with sodium and volume restriction according to the patient's clinical situation.
The major energy source for myocytes is glutamine, through conversion to glutamate, which also protects the myocardial cell from ischemia in critical situations. Administration of 1 g/day of omega-3 (EPA+DHA) in the form of fish oil can prevent sudden death in the treatment of acute coronary syndrome and can also help to reduce hospital admission for cardiovascular events in patients with chronic heart failure.

Key words: Critically-ill cardiac patient. Cardiac cachexia. Omega-3 fatty acids. Hyperglycemia.

El paciente con patología cardíaca puede presentar 2 tipos de desnutrición: la caquexia cardíaca, que aparece en situaciones de insuficiencia cardíaca congestiva crónica, y una malnutrición secundaria a complicaciones de la cirugía cardíaca o de cualquier cirugía mayor realizada en pacientes con cardiopatía.
Se debe intentar una nutrición enteral precoz si no se puede utilizar la vía oral. Cuando la función cardíaca esté profundamente comprometida la nutrición enteral es posible, pero a veces precisará suplementación con nutrición parenteral.
La hiperglucemia aguda sostenida en las primeras 24 h en pacientes ingresados por síndrome coronario agudo, sean o no diabéticos, es un factor de mal pronóstico en términos de mortalidad a los 30 días. En el paciente crítico cardíaco con fallo hemodinámico en situación estable, un soporte nutricional de 20-25 kcal/kg/día es eficaz para mantener un estado nutricional adecuado.
El aporte proteico debe ser de 1,2-1,5 g/kg/día. Se administrarán fórmulas poliméricas o hiperproteicas habituales, según la situación nutricional previa del paciente, con restricción de sodio y volumen según su situación clínica.
La glutamina es la mayor fuente de energía para el miocito, vía conversión a glutamato, protegiendo además a la célula miocárdica de la isquemia en situaciones críticas. La administración de 1 g/día de ω-3 (EpA+DHA), en forma de aceite de pescado, puede prevenir la muerte súbita en el tratamiento del síndrome coronario agudo y también puede contribuir a una disminución de los ingresos hospitalarios, por eventos cardiovasculares, en la insuficiencia cardíaca crónica.

Palabras clave: Paciente crítico cardíaco. Caquexia cardíaca. Ácidos grasos omega-3. Hiperglucemia.

Introduction

Malnutrition is present in 50% of patients with chronic congestive heart failure. Heart failure is associated with neurohormonal and immune changes that contribute to a hypercatabolic state, with intestinal malabsorption induced by different factors¹. Patients with heart disease may present 2 different types of malnutrition: classical heart cachexia, appearing in situations of chronic congestive heart failure (CHF), and a form of malnutrition secondary to complications of cardiac surgery or any major surgery in patients with heart disease². The incidence of cardiac cachexia has been estimated in 12-15% of patients with NYHA grades IIIII heart failure. This incidence increases to 10% per year if the grade of heart failure is III-IV^3,4 (IV).

What are the indications of nutritional support in critically-ill cardiac patients?

- CHF. These patients have chronic heart failure (HF) and chronic systemic inflammatory response syndrome (SIRS). Vasoconstriction and stimulation of the sympathetic nervous system are compensatory mechanisms of heart failure, which influences the inadequate use of nutrients⁴ (IV).

- Cardiac cachexia. It has been defined as a body mass loss of 27% or decrease of 80-85% from the ideal weight, but the most widely accepted meaning is defined as patients with CHF starting at least 6 months before and a weight loss in the past 6 months of at least 6% from the previous weight. Mortality is very high in cachectic patients, 18% at 3 months, 29% at 6 months, and 50% at 18 months⁵ (IV). Factors contributing to that mortality include: a deficient diet, the associated malabsorption syndrome, loss of nutrients through the intestinal and renal tract and imbalance in supply and losses in a hypermetabolism state⁶.

- Patients following cardiac surgery and patients with acute heart disease, such as evolution complication of another condition (SIRS, sepsis, etc.). These patients end up behaving as critically-ill patients for nosocomial superinfection, HF refractory to treatment, cardiogenic shock or enlarged cardiomyopathy pending heart transplant.

- Acute coronary syndrome (ACS). These patients usually require oral nutrition, and only enteral nutrition (EN) would be indicated in the course of complications inherent to their condition⁷. Patients in a cardiogenic shock condition on mechanical ventilation, balloon counterpulsation or external ventricular assistance, behave as a chronic critical illness requiring long-term artificial nutritional support⁸ (III).

What is the most adequate administration route?

Oral supply is the most appropriate, and if intake is very limited, it may be complemented with nutritional supplements. An early EN should be attempted if the oral route cannot be used. When heart function is severely affected (intraaortic contrapulsation balloon, ventricular assistance, etc.), EN can be performed, but will usually require supplementation with parenteral nutrition (PN) and its start, as a cautionary measure because of the risk of intestinal ischemia, is usually delayed beyond 24-48 hours after admission.

Patient instability, volume limitations, and the frequent changes in bowel function may require establishing total parenteral nutrition (TPN) or, sometimes, complementary parenteral nutrition (CPN)⁵ (IV). EN in these type of patients, with the appropriate caution and monitoring, is feasible and beneficial⁹ (III).

What amount and type of energy substrates are required?

The classical Harris-Benedict equation is acceptable for energy calculation, though easiest approaches have been shown to be useful, such as scheduling 20-25 kcal/kg/day within the first 48 hours and progress to 25-30 kcal/kg/day if required^12,13. The supplies are often limited for the total volume restriction, and energetic concentrated nutrients should be used (1.5-2 kcal/ml)¹⁴.

There are no specific recommendations related to the percentage of energy substrates that must be contained in the diet of critically-ill cardiac patients. The ratio kcal/g N₂ will be maintained at 100-150/1, decreasing it based on the degree of protein depletion or increase of metabolic stress¹⁵.

Carbohydrate supply

Glucose supply should be adjusted to obtain blood glucose levels < 150 mg/dL, and even in narrower limits postoperatively following heart surgery. Glycemia should be accurately monitored in critically-ill cardiac patients. Acute hyperglycemia is evidenced in 50% of ACS in non-diabetic patients and in 25% of diabetics. It has been proven that sustained hyperglycemia in the first 24 hours in patients admitted for ACS, whether diabetic or not, is a factor of poor prognosis in terms of mortality at 30 days^16,17 (IIb).

Studies such as the DIGAMI (diabetes mellitus, insulin-glucose infusion in acute myocardial infarction)¹⁸ analyzed the metabolism/mortality ratio in ACS. The purpose was to obtain an accurate control of glycemia with high doses of insulin and decrease mortality by 25% at 3 months and by 52% at one year. Although the results were encouraging, they were not significant. The ECLA¹⁹ study reported a mortality reduction of two-thirds when glucose-insulin-potassium were perfused versus placebo, but in subsequent randomized studies, both DIGAMI-2²⁰ and CREATE-ECLA²¹, these objectives were not reached, though it was confirmed that hyperglycemia is an independent predictor of mortality (Ib).

Fat supply

The adverse effects of lipid emulsions on cardiac inotropism only occur when perfusion exceeds 5 mg/kg/min. At the standard doses, without exceeding 2 g/kg/day, all commercial solutions are useful, though emphasis is made on the value of ω-3 fatty acids²² (IV).

What are the protein needs and characteristics of their supply?

Protein supply should be 1.2-1.5 g/kg/day. In EN, proteins should provide 16-20% of the total energy supply in order to mantain a positive nitrogen balance. The regular polymeric or hyperprotein formulae will be administered, with sodium and volume restriction, according to the previous clinical and nutritional status of the patient²³ (IV).

What is the most advisable type of formula? Are specific nutrients required?

The most advisable type of formula must be modified based on the nutritional status of patients and their needs. Some amino acid may be necessary or useful in cardiac patients, while others have shown a myocardial depressant effect, such as homocysteine, since their values are a risk factor and are frequently increased in patients with HF. They are closely related to the decreased plasma levels of vitamins B₆, B₉ and B₁₂, required for their degradation²⁴ (IV).

Carnitine

It promotes fat entry in the mitochondria and indirectly activates pyruvate dehydrogenase, that improves glucose oxidation. Carnitine deficiency is associated with myocardiopathy and skeletal muscle dysfunction. Myocardial failure is generally associated with a marked depletion of carnitine of up to 50%. Carnitine administration (3-6 g in divided doses) may lead to improving hemodynamic status and myocardial dysfunction^23,25 (IV).

Glutamine

Experimental studies have shown that its administration, after myocardial ischemia, induces an earlier myocardial recovery, improve cardiac output and restoring ATP/ADP ratio. Glutamine has been shown to increase the synthesis of heat shock protein²⁶ which is also the greatest source of energy for the myocyte, by conversion to glutamate, also protecting the myocardial cell from ischemia in critical situations^27,28 (IV).

As a precursor of nitric oxide, it plays a major role in regulating cardiovascular function, particularly in diabetic patients. Intravenous doses of 3-5 g reduce blood pressure and platelet aggregation. Arginine prevents cardiovascular dysfunction, as it restores nitric oxide synthesis, reduces production of free radicals, and inhibits leukocyte adherence to the endothelium, though in mesenteric ischemic conditions bowel mucosa function may be worsened²⁹ (IV).

Taurine

It is a non-essential amino acid that contributes to control intracellular calcium values, and therefore appears to be useful to improve myocardial function²⁵ (IV).

ω-3 fatty acids

They have been shown to have some antiarrhythmogenic potential and could prevent malignant arrhythmia and reduce the incidence of sudden death, acting mainly to prevent it^30,31. The presence of ω-3 in myocardial cells stabilizes electrically membranes and prolongs the refractory period. They decrease the synthesis of inflammatory prostanoids and modulate the inflammatory response by reducing arachidonic acid catabolytes, preserving endothelial integrity and acting favourably on platelet activity. On the contrary, an excessive supply of ω-6 can increase platelet aggregation and promote chronic inflammation predisposing to plaque unstability³².

In randomized studies it has been recommended to provide a supplement of 1 g/day of ω-3 (EPA + DHA) as fish oil, for primary prophylaxis of sudden death in the treatment of ACS and for reducing hospital admissions for cardiovascular episodes in CHF^33,34 (Ib), though subsequent studies did not obtain the same results³⁵ (Ib).

With regard to enteral immunomodulatory diets enriched with arginine, nucleotides, and fish oil, in a randomized, prospective study conducted in 50 patients with poor ventricular function, who were to undergo cardiac surgery, oral supplements of these nutrients were provided during the 5 days prior to surgery, obtaining a lower infection rate, a reduction in the need for positive inotropes and a better preservation of renal function³⁶ (IIa).

What micronutrient and vitamin requirements are needed?

Serious forms of HF have been described in patients with thiamine³⁸ or selenium deficiency. In patients with ischemic heart disease, after reperfusion processes, supplying antioxidants (vitamin A, C, E and selenium) helps limit myocardial damage³⁹. Glutathione peroxidase and tocoferol reduction has been seen experimentally in patients with cardiomyopathy. Therefore, supplements of antioxidants in patients with heart failure, particularly vitamin E (400 IU), may contribute to improve cardiac function⁴⁰ (IV).

Severe selenium deficit may cause cardiomyopathy and is characterized by multiple fibrosis foci in the left ventricle. Zinc deficiency is common in patients with CHF and, therefore, the requirements established for these patients must be administred² (IV).

Recommendations

- In critically-ill cardiac patients with hemodynamic failure in stable condition, a nutritional support of 20-25 kcal/kg/day is effective for maintaining an adequate nutritional status (B).

- Nutritional formulae recommended in other critically-ill patients will be supplied according to the previous nutritional status, with sodium and volume restriction, in relation to the clinical condition of the patient (C).

- Parenteral nutrition would be indicated for cardiac cachexia, in case of intolerance to enteral nutrition or as complementary nutrition, particularly in patients with cardiovascular surgery (C).

- Hyperglycemia should be closely monitored in patients with acute coronary syndrome and after cardiac surgery, whether or not known diabetics, maintaining values < 150 mg/dL (B).

- Glutamine supply may be beneficial for patients with myocardial ischemia in a critical situation (C).

- Supplements with vitamin A, C, B complex, vitamin E, and selenium are recommended to improve heart function (C).

Conflict of interests

The authors declare that they have participated in activities funded by the pharmaceutical industry for marketing of nutritional products (clinical studies, educational programmes and attendance to scientific events). No pharmaceutical industry has participated in the preparation, discussion, writing, and establishing of evidences in any phase of this article.

References

1. Von Haehling S, Doehner W, Anker SD. Nutrition, metabolism, and the complex pathophysiology of cachexia in chronic heart failure. Cardiovasc Res 2007; 73: 298-309.         [ Links ]

2. Sandek A, Doehner W, Anker SD, Von Haehling S. Nutrition in heart failure: an update. Curr Opin Clin Nutr Metab Care 2009; 12: 384-91.         [ Links ]

3. Anker SD, John M, Pedersen PU, Raguso C, Cicoira M, Dardai E et al; DGEM (German Society for Nutritional Medicine); ESPEN (European Society for Parenteral and Enteral Nutrition). ESPEN Guidelines on Enteral Nutrition: Cardiology and Pulmonology. Clin Nutr 2006; 25: 311-8.         [ Links ]

4. Berry C, Clark AL. Catabolism in chronic heart failure. Eur Heart J 2000; 21: 521-32.         [ Links ]

5. Anker SD, Laviano A, Filippatos G, John M, Paccagnella A, Ponikowski P et al; ESPEN Guidelines on parenteral Nutrition: cardiology and pneumology. Clin Nutr 2009; 28: 455-60.         [ Links ]

6. Azhar G, Wei JY. Nutrition and cardiac cachexia. Curr Opin Clin Nutr Metab Care 2006; 9: 18-23.         [ Links ]

7. Meltzer JS, Moitra VK. The nutritional and metabolic support of heart failure in the intensive care unit. Curr Opin Clin Nutr Metab Care 2008; 11: 140-6.         [ Links ]

8. Berger MM, Revelly JP, Cayeux MC, Chiolero RL. Enteral nutrition in critically ill patients with severe hemodynamic failure after cardiopulmonary bypass. Clin Nutr 2005; 24: 124- 32.         [ Links ]

9. Berger MM, Chiolero RL. Enteral nutrition and cardiovascular failure: from myths to clinical practice. JPEN J Parenter Enteral Nutr 2009; 33: 702-9.         [ Links ]

10. Heymsfield SB, Casper K. Congestive heart failure: clinical management by use of continuous nasoenteric feeding. Am J Clin Nutr 1989; 50: 539-44.         [ Links ]

11. Rapp-Kesek D, Joachimsson PO, Karlsson T. Splanchnic blood flow and oxygen consumption: effects of enteral nutrition and dopexamine in the elderly cardiac surgery patient. Acta Anaesthesiol Scand 2007; 51: 570-6.         [ Links ]

12. McClave SA, Martindale RG, Vanek VW, McCarthy M, Roberts P, Taylor B et al; ASPEN, Board of Directors; American College of Critical Care Medicine; Society of Critical Care Medicine. Guidelines for the Provision and Assessment of Nutrition Support Therapy in the Adult Critically Ill Patient: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (ASPEN). JPEN J Parenter Enteral Nutr 2009; 33:277-316.         [ Links ]

13. Scurlock C, Raikhelkar J, Mechanick JI. Impact of new technologies on metabolic care in the intensive care unit. Curr Opin Clin Nutr Metab Care 2009; 12: 196-200.         [ Links ]

14. Mijan de la Torre A, Mateo-Sillera B, Pérez-García AM. Nutrición y enfermedad cardiaca. En: Gil-Hernandez A, editor. Tratado de Nutrición. Madrid: Acción Médica; 2005, pp. 599-629.         [ Links ]

15. Inzucchi SE. Clinical practice. Management of hyperglycemia in the hospital setting. N Engl J Med 2006; 355: 1903-11.         [ Links ]

16. Zarich SW, Nesto RW. Implications and treatment of acute hyperglycemia in the setting of acute myocardial infarction. Circulation 2007; 115: e436-9.         [ Links ]

17. Dziewierz A, Giszterowicz D, Siudak Z, Rakowski T, Mielecki W, Suska M et al. Impact of admission glucose level and presence of diabetes mellitus on mortality in patients with non-St segment elevation acute coronary syndrome treated conservatively. Am J Cardiol 2009; 103: 954-8.         [ Links ]

18. Malmberg K. Prospective randomised study of intensive insulin treatment on long term survival after acute myocardial infarction in patients with diabetes mellitus: DIGAMI (Diabetes Mellitus, Insulin Glucose Infusión in Acute Myocardial Infarction). Study group. BMJ 1997; 314: 1512-5.         [ Links ]

19. Díaz R, Paolasso EA, Piegas LS, Tajer CD, Moreno MG, Corvalan R et al. Metabolic modulation of acute myocardial infarction. The ECLA (Estudios Cardiologicos Latinoamerica) Collaborative Group. Circulation 1998; 98: 2227-34.         [ Links ]

20. Malmberg K, Ryden L, Wedel H, Birkeland K, Bootsma A, Dickestein K et al; DIGAMI-2 Investigators. Intense metabolic control by means of insulin in patients with diabetes mellitus and acute myocardial infarction (DIGAMI-2): effects on mortality and morbidity. Eur Heart J 2005; 26: 650-61.         [ Links ]

21. Mehta SR, Yusuf S, Díaz R, Zhu J, Pais P, Xavier D et al; CREATEECLA Trial Group Investigators. Effect of glucoseinsulin-potassium infusion on mortality in patients with acute ST-segment elevation myocardial infarction: the CREATEECLA randomized controlled trial. JAMA 2005; 293: 437-46.         [ Links ]

22. Von Haehling S, Lainscak M, Springer J, Anker SD. Cardiac cachexia: a systematic overview. Pharmacol Ther 2009; 121: 227-52.         [ Links ]

23. Mijan A, Martin E, De Mateo B. Cardiac cachexia. Nutr Hosp 2006; 21 (Suppl. 3): 84-93.         [ Links ]

24. Herrmann M, Taban-Shomal O, Hubner U, Bohm M, Herrmann W. A review of homocysteine and heart failure. Eur J Heart Fail 2006; 8: 571-6.         [ Links ]

25. Soukoulis V, Dihu JB, Sole M, Anker SD, Cleland J, Fonarow GC et al. Micronutrient deficiencies an unmet need in heart failure. J Am Coll Cardiol 2009; 54: 1660-73.         [ Links ]

26. Novak F, Heyland DK, Avenell A, Drover JW, Su X. Glutamine supplementation in serious illness: a systematic review of the evidence. Crit Care Med 2002; 30: 2022-9.         [ Links ]

27. Khogali SE, Pringle SD, Weryk BK, Rennie MJ. Is glutamine beneficial in ischemic heart disease? Nutrition 2002; 18: 123-26.         [ Links ]

28. Kelly D, Wischmeyer PE. Role of L-glutamine in critical illness: new insights. Curr Opin Clin Nutr Metab Care 2003; 6: 217-22.         [ Links ]

29. Böger RH. L-arginine therapy in cardiovascular pathologies: beneficial or dangerous? Curr Opin Clin Nutr Metab Care 2008; 11: 55-61.         [ Links ]

30. Leaf A, Kang JX, Xiao YF, Billman GE. Clinical prevention of sudden cardiac death by n-3 polyunsaturade fatty acids and mechanism of prevention of arrhytmias by n-3 fish oils. Circulation 2003; 107: 2646-52.         [ Links ]

31. Schrepf R, Limmert T, Claus Weber P, Theisen K, Sellmayer A. Immediate effects of n-3 fatty acid infusion on the induction of sustained ventricular tachycardia. Lancet 2004; 363: 1441-2.         [ Links ]

32. Harris WS, Poston CW, Haddock C. Tissue n-3 and n-6 fatty acids and risk for coronary heart disease events. Atherosclerosis 2007; 193: 1-10.         [ Links ]

33. Marchioli R, Barzi F, Bomba E, Chieffo C, Di Gregorio D, Di Mascio R et al; GISSI-prevenzione Investigators. Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico (GISSI)-prevenzione. Circulation 2002; 105: 1897-903.         [ Links ]

34. Tavazzi L, Maggioni AP, Marchioli R, Barlera S, Franzosi MG, Latini R et al; Gissi-HF Investigators. Effect of n-3 polyunsaturated fatty acids in patients with chronic heart failure (the GISSIHF trial): a randomised, double-blind, placebo-controlled trial. Lancet 2008; 372: 1223-30.         [ Links ]

35. Kromhout D, Giltay EJ, Geleijnse JM; Alpha Omega Trial Group. n-3 fatty acids and cardiovascular events after myocardial infarction. N Engl J Med 2010; 363: 2015-26.         [ Links ]

36. Tepaske R, Velthuis H, Oudemans-van Straaten HM, Heisterkamp SH, Van Deventer SJ, Ince C et al. Effect of preoperative oral immune-enhancing nutritional supplement on patients at high risk of infection after cardiac surgery: a randomised placebocontrolled trial. Lancet 2001; 358: 696-701.         [ Links ]

37. Alsafwah S, Laguardia SP, Arroyo M, Dockery BK, Bhattacharya SK, Ahokas RA et al. Congestive heart failure is a systemic illness: a role for minerals and micronutrients. Clin Med Res 2007; 5: 238-43.         [ Links ]

38. Darcel F, Roussin C, Vallat JM, Charlin C, Tournebize P, Doussiet E. Polyneuropathies in vitamin B1 deficiency in Reunion and Mayotte islands in 70 patients of Maori and Comorian descent. Bull Soc Pathol Exot 2009; 102: 167-72.         [ Links ]

Correspondence:
F. J. Jiménez Jiménez.
Hospital Universitario Virgen del Rocío.
Sevilla. Spain. ]]> E-mail: fjavierjimenez@telefonica.net