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Ann Thorac Surg 2001;71:1428-1432
© 2001 The Society of Thoracic Surgeons

Original article: cardiovascular

Risk factors for post-cardiopulmonary bypass vasoplegia in patients with preserved left ventricular function

Armand Mekontso-Dessap, MDa, Rémi Houël, MDa, Céline Soustelle, MCSa, Matthias Kirsch, MDa, Dominique Thébert, MDa, Daniel Y. Loisance, MDa

a Service de Chirurgie Thoracique et Cardiovasculaire, CNRS UPRES-A 7053, Association Claude Bernard, Centre Hospitalo-Universitaire Henri Mondor, Créteil, France

Accepted for publication January 24, 2001.

Address reprint requests to Dr Houël, Centre Hospitalo-Universitaire Henri Mondor, 51, avenue du Maréchal de Lattre de Tassigny, 94010 Créteil Cédex, France
e-mail: maurette{at}univ-paris12.fr


   Abstract
Top
 Abstract
Introduction
 Patients and methods
 Results
 Comment
 References
 
Background. Although vasodilatory shock (VS) is one of the main complications of cardiopulmonary bypass (CPB), its pathophysiologic basis remains unclear. The aim of this study was to identify predisposing factors for the development of VS after CPB independent of ventricular function.

Methods. Thirty-six patients undergoing coronary artery bypass grafting who developed VS were compared with 72 control patients without post-CPB cardiogenic or vasoplegic shock, in a 2:1 case control study. Patients and controls underwent the same anesthetic protocol and were matched by age, sex, operation date, and left ventricle ejection fraction.

Results. Preoperative and intraoperative patient characteristics were not significantly different between the two groups. Preoperative use of angiotensin-converting enzyme inhibitors and intravenous heparin were independent predictors for post-CPB VS by multivariate analysis (relative risk of 2.26 and 2.78, respectively). Intensive care unit stay and hospital stay were significantly longer in VS cases than controls, without any difference in early postoperative mortality.

Conclusions. The only independent risk factors for postoperative VS identified were preoperative use of angiotensin-converting enzyme inhibitors and intravenous heparin. These risk factors were independent of age, gender, anesthetic protocol, and left ventricle ejection fraction.


   Introduction
Top
 Abstract
 Introduction
Patients and methods
 Results
 Comment
 References
 
Since the introduction of cardiopulmonary bypass (CPB) in cardiac operations, numerous adverse effects have been described, known collectively as postperfusion syndrome. A dilution of clotting factors and platelet dysfunction can result in coagulopathy. A release of proinflammatory cytokines can cause a systemic inflammatory response [1–3], contributing to myocardial reperfusion damage, lung injury, and a generalized profound vasodilation. This vasoplegic syndrome (VS), occurring in the early postoperative period of cardiac operation using CPB, is characterized by a severe hypotension, with decreased systemic vascular resistance, decreased arteriolar reactivity, and increased requirements for filling volume and vasopressive agents despite adequate cardiac output. From the literature, VS has been closely associated with low left ventricle ejection fraction (EF) and heart failure syndrome [4, 5]. However, this post-CPB morbid event also occurs in patients with normal ventricular function. Thus, it is important to prevent its onset in such patients. The present study examines preoperative and intraoperative predisposing factors for VS after coronary artery bypass grafting (CABG) in patients with normal ventricular function.


   Patients and methods
Top
 Abstract
 Introduction
 Patients and methods
Results
 Comment
 References
 
From January 1997 to January 2000, 1,413 patients underwent CABG under CPB without any associated procedure at Henri Mondor University Hospital (Créteil, France).

Cases
Vasodilatory shock was defined as a severe and persistent hypotension (mean arterial pressure less than 70 mm Hg), occurring in the early postoperative period (within the 6 hours after weaning from CPB), characterized by decreased systemic vascular resistance (indexed SVR less than 1,400 dynes-s · cm-5 · m-2), with normal or increased cardiac output (cardiac index more than 2.5 L · min-1 · m-2) or needing pharmacologic support by dopamine (more than 10 µg · kg-1 · min-1) or norepinephrine. All patients exhibiting features of cardiogenic (cardiac index less than or equal to 2.5 L · min-1 · m-2) or mixed (cardiogenic and vasoplegic) shock or receiving dobutamine or epinephrine were excluded from the analysis. Preoperative EF was determined using transthoracic echocardiography or angiography. Left ventricular EF was defined as normal when more than 0.50 and moderately reduced when between 0.35 and 0.50. Patients with EF lower than 0.35 were excluded from the study. Thus, the study population comprised 36 patients who developed isolated VS, for an overall incidence of 2.5%.

Controls
During the same period, patients who underwent CABG and did not exhibit VS or cardiogenic shock were selected as controls. We did a 2:1 case control study. For each case, 2 control patients were matched as follows: same age (± 5 years), same gender (male or female), same operation date (± 1 week), and same left ventricular EF (normal or moderately reduced).

Data collection
Hospital records were reviewed retrospectively. Operative comorbidity was defined as follows. Obesity was defined as a body weight greater than 20% of normal weight estimated by the Lorentz formula. Diabetes was defined as the need for insulin or any oral antidiabetic medication. Preoperative renal insufficiency was determined by serum creatinine levels higher than 1.5 mg/dL (130 µmol/L). Recorded life-threatening complications and postoperative morbidity were deep sternal infection, pneumonia, septicemia, reexploration for bleeding, intraoperative and postoperative myocardial infarction, tamponade, cardiac arrest, gastrointestinal complication, permanent stroke, renal failure, and occurrence of multiple organ dysfunction.

Anesthesia and cardiopulmonary bypass
Anesthetic protocol was identical in all patients, using intravenous (IV) midazolam hydrochloride, propofol, pancuronium bromide, and fentanyl or sulfentanyl citrate. Cardiopulmonary bypass was conducted under moderate systemic hypothermia (28°C to 32°C), with nonpulsatile, filtered arterial flow and gravity venous drainage. A hollow-fiber membrane oxygenator was used. Myocardial protection was achieved using antegrade, cold, crystalloid cardioplegia.

Statistical analysis
Statistical analysis was performed using SPSS Base 9.0 statistical software (SPSS Inc, Chicago, IL). Continuous variables were expressed as mean ± standard deviation and were compared using an unpaired two-tailed t test. Categorical variables, expressed as percentages, were analyzed with a {chi}2 test or a Fisher exact test. To identify risk factors for VS, univariate analysis of preoperative and intraoperative variables was performed by comparing cases and controls. To evaluate independent risk factors for VS, significant or marginally significant (p value <= 0.2) univariate risk factors were examined using forward stepwise logistic regression analysis. Coefficients were computed by the method of maximum likelihood. A two-tailed p value of less than 0.05 was used to indicate statistical significance.


   Results
Top
 Abstract
 Introduction
 Patients and methods
 Results
Comment
 References
 
Preoperative factors
Table 1 shows demographic characteristics and preoperative associated comorbidity of the two groups of patients. As expected, age and sex were identical for the 36 cases and 72 controls. Prevalence of smoking, diabetes, obesity, renal failure, dyslipidemia, stroke, peripheral vascular disease, and chronic obstructive pulmonary disease were not significantly different between the two groups. However, there was a trend toward an increased prevalence of hemodialysis for renal failure among cases when compared with controls, but this difference failed to achieve statistical significance. Prevalence of hypertension was lower in the VS group than in controls, but the difference did not reach statistical significance (p = 0.06).


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  		Table 1. Demographic Characteristics and Patient Comorbidities

 
Details of the preoperative cardiac status are presented in Table 2. Mean left ventricular EF was not different between the two groups. No difference was found between the two groups concerning New York Heart Association functional class. There was a trend toward an increased prevalence of myocardial infarction history among the cases in comparison with controls, but with no statistical significance. The prevalence of angina, cardiogenic shock, arrhythmia, atrioventricular block, coronary angioplasty, and previous cardiac operation was similar between the two groups.


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  		Table 2. Preoperative Characteristics

 
Table 3 shows preoperative medications of the two groups of patients. Use of IV heparin and angiotensin-converting enzyme (ACE) inhibitors was significantly more frequent in the VS group when compared with controls (p = 0.01 and p = 0.04, respectively). Preoperative use of nitrates was not statistically different between the two groups.


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  		Table 3. Preoperative Medications

 
Intraoperative factors
Intraoperative variables are listed in Table 4. There were no significant differences between the two groups concerning CPB time, aortic cross-clamping time, hypothermia, cardioplegia infused volume, hemofiltration use, filling volume requirements, minimal systemic vascular resistances (during CPB), and diuresis.


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  		Table 4. Intraoperative Factors

 
Postoperative factors
Early postoperative variables are displayed in Table 5. Early mortality was similar in both groups. Twenty-four (66.7%) patients in the VS group required autologous blood transfusion versus 34 (47.2%) patients in the control group (p = 0.06). There was a trend toward an increased prevalence of postoperative complications among the cases when compared with controls, but without statistical significance. The intensive care unit stay and the hospital stay were significantly longer in the VS group when compared with controls (p = 0.008 and p = 0.04, respectively), but extubation delay was similar in both groups.


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  		Table 5. Postoperative Course

 
Multivariate analysis
Logistic regression analysis identified only preoperative use of IV heparin and ACE inhibitors as independent risk factors for postoperative VS (Table 6).


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  		Table 6. Risk Factors for Vasoplegic Syndrome

 

   Comment
Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
References
 
Arteriolar tone is a major determinant of SVR, regulated by the neurohormonal system and endothelial function. An increase in SVR is usually observed after CPB. This vasoconstriction may be related to a transient increase in several vasoactive hormones, including catecholamines, serotonin [6, 7], and arginine vasopressin [8].

On the contrary, some patients exhibit a clinical VS with profoundly low SVRs and decreased vascular reactivity up to 6 hours after CPB. This feature may be related to the release of vasodilatory inflammatory mediators observed after CPB [2, 3]. Arginine-vasopressin system impairment, endothelial dysfunction, and a decreased myogenic reactivity to catecholamines despite enhanced catecholamine release may also participate [9].

Argenziano and coworkers [4] found, in a prospective study of 145 patients undergoing CPB, low left ventricular EF (less than 0.35) as an independent risk factor for vasodilatory shock (relative risk of 9.1). These results could be explained by the impact of CPB on an already activated inflammatory state observed in patients with heart failure or severe cardiac dysfunction [10]. Nevertheless, VS does also occur in patients with adequate ventricular function. The precise pathophysiologic mechanism for its development in these patients remains unclear. In our study, controls were matched to the cases by not only age, sex, and operation date, but also by left ventricle EF. Thus we could look for other risk factors for VS, independently of preoperative heart failure.

Many reports have associated preoperative use of ACE inhibitors with hypotension and decreased vasoreactivity occurring after separation from CPB [11]. Actually, the renin-angiotensin system may play an important role in vascular tone changes during the postoperative period [12–14]. Inhibition of ACE results in a decrease in angiotensin II (one of the most potent endogenous vasopressor agents) and an increase in vasodilator bradykinin plasma levels. Cardiopulmonary bypass completely excludes the lung, the major site of bradykinin catabolism, and thus increases bradykinin plasma levels [15]. Furthermore, long-term use of ACE inhibitors leads to its accumulation in tissues especially when using recent long-acting molecules. Sufficient levels of ACE inhibitors may remain in tissues after CPB, contributing to a decrease in SVR in the postoperative period. In our study, preoperative use of ACE inhibitors was an independent predictor of VS. This finding agrees with that of a prospective study that identified preoperative use of ACE inhibitors, congestive heart failure, poor left ventricular function, duration of CPB, reoperation, age, and opioid anesthesia as independent risk factors for requiring two or more vasoconstrictor infusions after CPB [16].

In our study, preoperative IV heparin use appears to be an independent risk factor for VS. Anticoagulation using IV heparin was introduced preoperatively in patients with unstable angina or recent myocardial infarction (less than 21 days). Our result may correspond to a statistical confounding risk factor associated with an emergent procedure such as unstable angina or recent myocardial infarction. These conditions are often responsible for a marked stress response with subsequent elevated plasma catecholamines that could be depleted by CPB, leading to a diminished vascular tone and reactivity. The use of nitrates was not associated with an increased risk of VS, but this medication was not given exclusively to coronary unstable patients.

Interestingly, we found a trend toward lower prevalence of hypertension among cases compared with controls, but the difference was without statistical significance. Morbid hypertension has been variously associated with post-CPB systemic hyper- or normotensive profiles [17–19].

Some studies have found VS more frequent after extended CPB for complex operations [5]. In our study, all patients underwent an identical surgical procedure (coronary bypass graft operation) and CPB time was similar between cases and controls.

VS often is associated with coagulation disorders, is responsible for oozing and diffuse bleeding, and therefore patients often require transfusions of blood cells and blood products [20]. In our study, patients with VS tended to require more blood cell transfusions and to exhibit more complications than those in the control group, although these differences were not statistically significant. Operative morbidity is increased by the occurrence of post-CPB VS, with a consequent increased risk for the patient in the early postoperative period [20]. We found a significantly longer intensive care unit and hospital stay among patients with VS when compared with controls. However there was no intergroup difference on early mortality.

In summary, this study demonstrates that preoperative ACE inhibitor and IV heparin use are independent risk factors for the development of post-CPB VS in patients with normal ventricular function. Further studies will be necessary to determine the precise mechanism of this syndrome, with special emphasis on renin-angiotensin system activation and arteriolar catecholamine reactivity before CPB.


   References
Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 

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  2. Downing S.W., Edmunds L.H. Release of vasoactive substances during cardiopulmonary bypass. Ann Thorac Surg 1992;54:1236-1243.[Abstract]
  3. Boyle E.M., Pohlman T.H., Johnson M.C., Verrier E.D. Endothelial cell injury in cardiovascular surgery: the systemic inflammatory response. Ann Thorac Surg 1997;63:277-284.[Abstract/Free Full Text]
  4. Argenziano M., Chen J.M., Choudhri A.F., et al. Management of vasodilatory shock after cardiac surgery: identification of predisposing factors and use of a novel pressor agent. J Thorac Cardiovasc Surg 1998;116:973-980.[Abstract/Free Full Text]
  5. Kirklin J.K. Prospects for understanding and eliminating the deleterious effects of cardiopulmonary bypass. Ann Thorac Surg 1991;51:529-531.[Medline]
  6. Tan C.K., Glisson S.N., El-Etr A.A., Ramakrishnaiah K.B. Levels of circulating norepinephrine and epinephrine before, during and after cardiopulmonary bypass in human. J Thorac Cardiovasc Surg 1976;71:928-931.[Abstract]
  7. Agnoletti G., Scotti C., Panzali A.F., et al. Plasma levels of atrial natriuretic factor (ANF) and urinary excretion of ANF, arginine vasopressin and catecholamines in children with congenital heart disease: effect of cardiac surgery. Eur J Cardiothorac Surg 1993;7:533-539.[Abstract]
  8. Feddersen K., Aurell M., Delin K., Haggendal J., Aren C., Radegran K. Effects of cardiopulmonary bypass and prostacyclin on plasma catecholamines, angiotensin II and arginine-vasopressin. Acta Anaesthesiol Scand 1985;29:224-230.[Medline]
  9. Wang S.Y., Stamler A., Li J., Johnson R.G., Sellke F.W. Decreased myogenic reactivity in skeletal muscle arterioles after hypothermic cardiopulmonary bypass. J Surg Res 1997;69:40-44.[Medline]
  10. Levine B., Kalman J., Mayer L., Fillit H.M., Packer M. Elevated circulating levels of tumor necrosis factor in severe chronic heart failure. N Engl J Med 1990;323:236-241.[Abstract]
  11. Thaker U., Geary V., Chalmers P., Sheikh F. Low systemic vascular resistance during cardiac surgery: case reports, brief review, and management with angiotensin II. J Cardiothorac Anesth 1990;4:360-363.[Medline]
  12. De Leeuw P.W., van der Starre P.J., Harinck-de Weerdt J.E., de Bos R., Tchang P.T., Birkenhager W.H. Humoral changes during and following coronary bypass surgery: relationship to postoperative blood pressure. J Hypertens Suppl 1983;1:52-54.[Medline]
  13. Taylor K.M., Bain W.H., Russel M., Brannan J.J., Morton I.J. Peripheral vascular resistance and angiotensin II levels during pulsatile and no-pulsatile cardiopulmonary bypass. Thorax 1979;34:594-598.[Abstract/Free Full Text]
  14. Hayase S., Shimizu T., Nakajima M. Role of sympathoadrenal and renin-angiotensin system in hemodynamic state after coronary artery bypass grafting. Nagoya J Med Sci 1987;49:1-15.[Medline]
  15. Cugno M., Nussberger J., Biglioli P., Giovagnoni M.G., Gardinali M., Agostoni A. Cardiopulmonary bypass increases plasma bradykinin concentrations. Immunopharmacology 1999;43:145-147.[Medline]
  16. Tuman K.J., McCarthy R.J., O’Connor C.J., Holm W.E., Ivankovich A.D. Angiotensin-converting enzyme inhibitors increase vasoconstrictor requirements after cardiopulmonary bypass. Anesth Analg 1995;80:473-479.[Abstract]
  17. Roberts A.J., Niarchos A.P., Subramanian V.A., et al. Systemic hypertension associated with coronary artery bypass surgery. Predisposing factors, hemodynamic characteristics, humoral profile, and treatment. J Thorac Cardiovasc Surg 1977;74:846-859.[Abstract]
  18. Estafanous F.G., Tarazi R.C., Viljoen J.F., el-Tawil M.Y. Systemic hypertension following myocardial revascularization. Am Heart J 1973;85:732-738.[Medline]
  19. Wallach R., Karp R.B., Reves J.G., Oparil S., Smith L.R., James T.N. Pathogenesis of paroxysmal hypertension developing during and after coronary bypass surgery: a study of hemodynamic and humoral factors. Am J Cardiol 1980;46:559-565.[Medline]
  20. Gomes W.J., Carvalho A.C., Palma J.H., et al. Vasoplegic syndrome after open heart surgery. J Cardiovasc Surg 1998;39:619-623.[Medline]



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