Septic Shock in Low-Cardiac-Output Patients With Heart and Lung Transplantation: Diagnosis and Management Dilemma

Abstract

LOW-CARDIAC-OUTPUT SYNDROME (LCOS) commonly is encountered after heart, heart-lung, and lung transplantation. Several reasons can be ascribed to LCOS after thoracic organ transplantation, namely suboptimal donor, poor donor management, poor organ preservation, prolong ischemia time, high baseline pulmonary artery pressure in the recipient, old age, comorbid illnesses, and long cardiopulmonary bypass time. 1 Leeman M. Van C.M. Vachiery J.L. et al. Determinants of right ventricular failure after heart transplantation. Acta Cardiol. 1996; 51: 441-449 PubMed Google Scholar , 2 Luckraz H. Goddard M. Charman S.C. et al. Early mortality after cardiac transplantation: Should we do better?. J Heart Lung Transplant. 2005; 24: 401-405 Abstract Full Text Full Text PDF PubMed Scopus (33) Google Scholar , 3 Trulock E.P. Christie J.D. Edwards L.B. et al. Registry of the International Society for Heart and Lung Transplantation: Twenty-second official adult heart transplant report—2005. J Heart Lung Transplant. 2005; 24: 945-955 Abstract Full Text Full Text PDF PubMed Scopus (275) Google Scholar , 4 Segovia J. Pulpon L.A. Sanmartin M. et al. Primary graft failure in heart transplantation: A multivariate analysis. Transplant Proc. 1998; 30: 1932 Abstract Full Text Full Text PDF PubMed Scopus (42) Google Scholar , 5 Lima B. Rajagopal K. Petersen R.P. et al. Marginal cardiac allografts do not have increased primary graft dysfunction in alternate list transplantation. Circulation. 2006; 114: I27-I32 Crossref PubMed Scopus (126) Google Scholar , 6 Wittwer T. Wahlers T. Marginal donor grafts in heart transplantation: Lessons learned from 25 years of experience. Transpl Int. 2008; 21: 113-125 Crossref PubMed Scopus (90) Google Scholar LCOS prolongs the postoperative recovery, requires higher doses of inotropes, and compromises end-organ perfusion. International Society for Heart and Lung Transplantation data suggest that 50% of cardiac complications and nearly 19% of early deaths after heart transplantation are due to right ventricular (RV) dysfunction. 7 Hosenpud J.D. Bennett L.E. Keck B.M. et al. The Registry of the International Society for Heart and Lung Transplantation: Seventeenth official report. J Heart Lung Transplant. 2000; 19: 909-931 Abstract Full Text Full Text PDF PubMed Scopus (432) Google Scholar Several studies have established the relationship between elevated pulmonary vascular resistance (PVR) and the risk of death due to acute RV failure after heart transplantation. 8 Griepp R. Stinson E. Dong E. et al. Determinants of operative risk in human heart transplantation. Am J Surg. 1971; 122: 192-197 Abstract Full Text PDF PubMed Scopus (91) Google Scholar , 9 Kirklin J.K. Naftel D.C. McGiffin D.C. et al. Analysis of morbid events and risk factors for death after cardiac transplantation. J Am Coll Cardiol. 1988; 11: 917-924 Crossref PubMed Scopus (137) Google Scholar , 10 Kirklin J.K. Naftel D.C. Kirklin J.W. et al. Pulmonary vascular resistance and the risk of heart transplantation. J Heart Lung Transplant. 1988; 7: 331-336 Google Scholar , 11 Erickson K.W. Constanzo-Nordin M.R. O’Sullivan E.J. et al. Influence of preoperative transpulmonary gradient on late mortality after orthotopic heart transplantation. J Heart Transplant. 1990; 9: 526-527 PubMed Google Scholar Elevated PVR and pulmonary artery pressure hinder RV-pulmonary artery coupling, and ischemia and reperfusion injury exacerbate the RV failure. Poor left ventricular (LV) filling and LCOS arise due to an interventricular septal shift and reduced pulmonary artery flow in RV dysfunction. Similarly, delayed recovery of PVR and pulmonary artery pressure could contribute to RV dysfunction after single-lung transplantation. In addition, graft rejection and reperfusion injury may further aggravate the pre-existing high pulmonary artery pressure. LCOS has a deleterious effect on the heart itself and exacerbates biventricular dysfunction. Furthermore, it delays endotracheal extubation and predisposes patients to ventilator-associated pneumonia. Multiorgan perfusion defect and dysfunction coupled with increased risk of ventilator-associated pneumonia in an immunocompromised state provide fertile ground for superimposition of sepsis. Complications due to infections and sepsis are the most common cause of morbidity and mortality at all time points after lung transplantation. 12 Miller L.W. Naftel D.C. Bourge R.C. et al. Infection after heart transplantation: A multi institutional study. Cardiac Transplant Research Database Group. J Heart Lung Transplant. 1994; 13: 381-392 PubMed Google Scholar , 13 Brooks R.G. Hofflin J.M. Jamieson S.W. et al. Infectious complications in heart-lung transplant recipients. 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Semin Respir Infect. 1993; 8: 207-215 PubMed Google Scholar The incidence of infectious complications is nearly twice as high in lung transplantation patients compared to heart transplantation patients. Infectious complications are responsible for at least half of the deaths that occur after lung transplantation. 19 Chaparro C. Maurer J.R. Chamberlain D. et al. Causes of death in lung transplant recipients. J Heart Lung Transplant. 1994; 13: 758-766 PubMed Google Scholar Sepsis exerts its effect either by inducing myocardial dysfunction or by its effect on cardiovascular function. 20 Waisbren B.A. Bacteremia due to gram-negative bacilli other than the Salmonella; a clinical and therapeutic study. AMA Arch Intern Med. 1951; 88: 467-488 Crossref PubMed Scopus (102) Google Scholar , 21 Bone R.C. Gram-negative sepsis: Background, clinical features, and intervention. Chest. 1991; 100: 802-808 Abstract Full Text Full Text PDF PubMed Scopus (149) Google Scholar Reductions in ejection fraction and stroke volume despite normal cardiac output also have been described. 22 Parker M.M. Shelhamer J.H. Bacharach S.L. et al. Profound but reversible myocardial depression in patients with septic shock. Ann Intern Med. 1984; 100: 483-490 Crossref PubMed Scopus (1012) Google Scholar Superimposed cardiovascular dysfunction in sepsis has been observed to increase mortality from 20% to 90%. 23 Parrillo J.E. Parker M.M. Natanson C. et al. Septic shock in humans: Advances in the understanding of pathogenesis, cardiovascular dysfunction, and therapy. Ann Intern Med. 1990; 113: 227-242 Crossref PubMed Scopus (1035) Google Scholar In this case series, the authors evaluated the consequences of septic shock in 4 patients experiencing LCOS after heart and lung transplantation.