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Ann Thorac Surg 2011;92:812-819. doi:10.1016/j.athoracsur.2011.04.020
© 2011 The Society of Thoracic Surgeons
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Original Articles: Adult Cardiac

Transfusion Increases the Risk for Vasoplegia After Cardiac Operations

Andrej Alfirevic, MDa,*, Meng Xu, MSb, Douglas Johnston, MDc, Priscilla Figueroa, MDd, Colleen G. Koch, MDa

a Department of Cardiothoracic Anesthesiology (Anesthesiology Institute), Cleveland Clinic, Cleveland, Ohio
b Department of Quantitative Health Sciences (Research Institute), Cleveland Clinic, Cleveland, Ohio
c Department of Thoracic and Cardiovascular Surgery (Heart and Vascular Institute), Cleveland Clinic, Cleveland, Ohio
d Institute of Pathology and Laboratory Medicine, Cleveland Clinic, Cleveland, Ohio

Accepted for publication April 4, 2011.

* Address correspondence to Dr Alfirevic, Department of Cardiothoracic Anesthesiology-J4, Cleveland Clinic, 9500 Euclid Ave, Cleveland, OH 44195 (Email: alfirea{at}ccf.org).


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 References
 
Background: Perioperative vasoplegia is associated with increased morbidity. Red blood cell (RBC) transfusion increases plasma concentrations of inflammatory mediators, possibly contributing to the development of vasoplegia. We investigated the prevalence of mild and profound postoperative vasoplegia, identified factors associated with its development, and examined the role of RBC and component transfusion on the occurrence of postoperative vasoplegia.

Methods: Between January 1, 2000, and January 1, 2007, 25,960 patients underwent on-bypass cardiac surgical procedures. The incidence of vasoplegia was defined as (1) mild vasoplegia requiring norepinephrine infusion for blood pressure support on the day of operation and postoperative day 1, and (2) profound vasoplegia requiring vasopressin, with or without concomitant norepinephrine infusion, on the day of operation and postoperative day 1. Separate logistic regression models were used to model risk factors for development of mild and profound vasoplegia.

Results: RBC transfusion increased risk-adjusted odd ratios (ORs) of developing mild vasoplegia (1.07 [95% confidence limits (CL), 1.05, 1.10]; p < 0.001) and profound vasoplegia (1.38 [1.31, 1.46] p < 0.001). The risk-adjusted ORs (95% CL) for mild vasoplegia and profound vasoplegia were similarly increased by fresh-frozen plasma (OR, 1.24 [1.10, 1.41], p < 0.001; and OR, 1.20 [1.13, 1.29], p < 0.001) and platelet transfusion (OR, 1.39 [1.25, 1.54], p < 0.001; and OR, 1.22 [1.14, 1.31], p < 0.001), respectively.

Conclusions: Red blood cells, fresh-frozen plasma, and platelet transfusion increased the prevalence of vasoplegia. RBC transfusion exhibited a dose-dependent response for developing vasoplegia with each RBC unit transfused. Further investigation is necessary to determine whether prophylactic use of vasopressor support in the setting of transfusion can ameliorate risk and effect outcomes.


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Results
 Comment
 References
 
Approximately 10% to 27% of cardiac surgical patients will exhibit mild to profound degrees of vasoplegia after cardiopulmonary bypass (CPB) [1–5]. The incidence varies depending on how vasoplegia is defined as well as by the surgical procedure performed [6–8]. Vasoplegia is characterized by significant reductions in blood pressure and is frequently associated with normal or hyperdynamic cardiac function. Although intravenous fluid administration is commonly the initial management strategy, pharmacologic support is often necessary to maintain adequate hemodynamics [1–3, 9–13]. Vasoplegia has been associated with increased patient morbidity, including delayed extubation and prolonged intensive care unit (ICU) stay [4, 5, 8], a higher incidence of renal failure [5], greater transfusion requirements [5], and increased death [4, 9–11, 13].

The vasoplegia has multiple causes, with some investigators reporting an increased prevalence with specific perioperative factors such as use of angiotensin-converting enzyme (ACE) inhibitors, reduced ejection fraction (EF < 0.35), longer duration of CPB, low mean arterial pressure before CPB, and lower hematocrit [1, 4, 5, 10, 11]. Some have attributed development of vasoplegia to the systemic inflammatory response related to CPB exposure [14, 15], accompanied by the release of inflammatory mediators [16] and injury to the vascular endothelium [1, 9, 17–20]. Perioperative factors, such as red blood cell (RBC) transfusion, have been found to influence inflammatory mediator release by increasing plasma concentrations of inflammatory mediators as well as by enhancing the inflammatory response to the operation [21].

Our objectives were to (1) investigate the prevalence of mild and profound postoperative vasoplegia, (2) identify risk factors associated with development of vasoplegia, and (3) examine the role of intraoperative RBC and component transfusion on the development of vasoplegia.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 References
 
Patient Population
The patient population consisted of 25,960 patients who underwent cardiac surgical procedures requiring CPB from January 1, 2000, to January 1, 2007. Perioperative variables were prospectively collected and entered into the Cardiothoracic Anesthesia Registry by trained database management personnel. The Cardiovascular Information Registry was also accessed for additional perioperative information. The databases have been approved by our Institutional Review Board, with individual patient consent waived.

We defined two outcomes for vasoplegia:

1 Patients who were considered to have mild vasoplegia requiring use of norepinephrine infusion for blood pressure support on the day of operation and postoperative day 1.
2 Patients who were considered to have profound vasoplegia requiring use of vasopressin, with or without concomitant use of norepinephrine, on the day of operation and postoperative day 1.

In our clinical practice, Neo-Synephrine (Bayer HealthCare, Leverkeusen, Germany) is used for transient episodes of intraoperative hypotension. If a patient fails to respond to repeated boluses of Neo-Synephrine, a norepinephrine infusion is administered to maintain blood pressure after adequate volume status and cardiac output have been achieved. When patients become refractory to norepinephrine, a vasopressin infusion is added for blood pressure support.

Statistical Methods
Baseline univariate comparisons were made between patients with and without the diagnosis of vasoplegia. Continuous variables were described with median and 25th and 75th percentiles, with p values from the Wilcoxon rank sum test for tests of differences between patients with and without mild and profound vasoplegia. Categoric variables were described with frequencies and percents, with p values from {chi}2 tests for testing differences between patients with and without mild and profound vasoplegia.

Separate logistic regression models were used to model risk factors for probability of developing mild and profound vasoplegia. To adjust for differences in confounding variables between the groups, potential risk factors were selected using logistic regression with stepwise variable selection procedure on 1000 bootstrap resamples for patients with mild vasoplegia (norepinephrine infusion only) and profound vasoplegia (vasopressin with or without concomitant norepinephrine infusion). A bagging algorithm was used to summarize the results. Entry criterion and stay criteria for stepwise selection processes were p = 0.07 and p = 0.05, respectively. Final logistic regression models on mild and profound vasoplegia outcomes were built by using risk factors that appeared in 50% of all models from the bootstrap resamples. All analyses were performed with SAS 9.2 software (SAS Institute, Cary, NC).


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 References
 
Mild Vasoplegia
There were 7437 patients (28.6%) who exhibited mild vasoplegia requiring norepinephrine on the day of operation and POD 1. Use of intraoperative RBC and component therapy differed among patients with and without mild vasoplegia: patients who received a RBC transfusion had higher prevalence of mild vasoplegia vs patients who did not receive a transfusion. Similarly, the prevalence that mild vasoplegia would develop was significantly higher in patients who received fresh frozen plasma (FFP), cryoprecipitate, and platelet concentrates. Baseline demographics, laboratory values, and comorbidity differed among patients with and without mild vasoplegia, as well as preoperative ACE inhibitor and antiarrhythmic use. Longer duration of CPB was associated with more vasoplegia (Table 1).


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  		Table 1 Baseline Characteristics Among Patients With and Without Mild Vasoplegia
 
Profound Vasoplegia
Overall, profound vasoplegia developed in 754 (2.9%) patients and required the use of vasopressin on the day of operation and POD 1. Profound vasoplegia developed more commonly in patients who received intraoperative RBC transfusion and component therapy. Distribution of demographics, comorbidity, and perioperative factors differed among groups. Profound vasoplegia was more common in patients who received therapy with ACE inhibitors and antiarrhythmic agents, whereas it was less common in those who received β-blockers and calcium channel blockers. Longer CPB duration and cross-lamp times resulted in more profound vasoplegia (Table 2).


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  		Table 2 Baseline Characteristics Among Patients With and Without Profound Vasoplegia
 
Risk Adjustment
Mild vasoplegia
Red blood cell transfusion significantly increased risk-adjusted odds for developing mild vasoplegia in a dose-dependent manner. Each RBC unit transfused increased the odds of developing mild vasoplegia by 1.07 (95% confidence limits [CL], 1.05, 1.10; p < 0.001). Intraoperative use of FFP also significantly increased the odds for developing mild vasoplegia (OR, 1.24; 95% CL, 1.10, 1.40; p < 0.001) as did platelet transfusion (OR, 1.39; 95% CL, 1.25, 1.54; p < 0.001; Fig 1 and 2A-B Go). A number of traditionally reported risk factors significantly increased development of mild vasoplegia. Preoperative ACE inhibitor therapy also increased the risk for developing mild vasoplegia, whereas a higher preoperative hematocrit reduced the odds for developing mild vasoplegia (Table 3).


Figure 1
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  		Fig 1. Variables significantly related to odds for developing mild vasoplegia. (ACE = angiotensin-converting enzyme; Afib = atrial fibrillation; CI = confidence interval; CPB = cardiopulmonary bypass; FFP = fresh-frozen plasma; HCT = hematocrit (%); LVF* = left ventricular function—normal-mild vs moderate-severe; OR = odds ratio).

 

Figure 2
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  		Fig 2. (A) Probability in unadjusted odds ratios (OR) of developing mild vasoplegia by number of red blood cells (RBC) transfused. (B) Risk-adjusted probability in odds ratios (OR) of developing mild vasoplegia by number of red blood cell (RBC) units transfused in an intermediate risk patient as calculated for a 70-year-old man with diabetes, history of atrial fibrillation and myocardial infarction, no hypertension, no endocarditis, moderate-severe left ventricular function on preoperative angiotensin-converting enzyme inhibitors, no calcium channel blockers, creatinine (1.4 mg/dL), cardiopulmonary bypass duration of 90 minutes, hematocrit of 30, who receives a transfusion of fresh frozen plasma and platelets.

 

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  		Table 3 Risk Factors for Mild Vasoplegia From Multivariable Logistic Regression Model
 
Profound vasoplegia
We found significant interaction terms between RBC and component therapy in the model on profound vasoplegia (Table 4). Risk increased in a dose-dependent manner per unit increase in RBC transfusion. Use of intraoperative cryoprecipitate similarly increased the odds that profound vasoplegia would develop (Fig 3 , Fig 4A and B).


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  		Table 4 Risk Factors for Profound Vasoplegia From Multivariable Logistic Regression Model
 

Figure 3
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  		Fig 3. Perioperative variables significantly related to the odds of developing profound vasoplegia. (Afib = atrial fibrillation; CI = confidence interval; CPB = cardiopulmonary bypass; FFP = fresh frozen plasma; HCT = hematocrit (%); LVF* = left ventricular function—normal-mild vs moderate-severe; OR = odds ratio; RBC = red blood cells.)

 

Figure 4
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  		Fig 4. (A) Probability in unadjusted odds ratios (OR) of developing profound vasoplegia by number of red blood cell (RBC) units transfused. (B) Risk-adjusted probability in odds ratios (OR) of developing profound vasoplegia by number of red blood cell (RBC) units transfused in an intermediate risk patient.

 
Other risk factors for the development of profound vasoplegia included male sex and a number of comorbidities, as did valve procedures and longer CPB duration. Preoperative medications, such as β-blockers and calcium channel blockers reduced the risk, and preoperative ACE inhibitors were not a risk factor for development of profound vasoplegia (Table 4).


   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
References
 
Red blood cells, FFP, and platelet transfusion significantly increased the unadjusted and risk-adjusted odds for developing vasoplegia necessitating pharmacologic support. An interesting finding was that RBC transfusion exhibited a dose-dependent increase for developing both mild and profound vasoplegia with each RBC unit transfused. For example, a transfusion of 3 RBC units would increase the odds of developing mild and profound vasoplegia by 3.24 and 3.39, respectively; an effect greater than all other risk factors for the development of vasoplegia. Although transfusion is necessary for select patients, its use has been associated with more complications after cardiac operations [22–25]. Our results demonstrate an additional complication related to transfusion, one that places the patient a higher reported risk for morbidity [4, 9, 10, 11, 13].

Our findings of a higher incidence of vasoplegia with transfusion are partly supported by Fransen and colleagues [21], who demonstrated that RBC transfusion directly increases levels of circulating inflammatory mediators and potentiates an inflammatory mediator release in response to the surgical procedure. Investigators have previously linked hemodynamic instability observed with vasoplegia to the release of inflammatory mediators, such as interleukin-6 and interleukin-8 [26].

Bradykinin causes vasodilation and is considered a mediator in hypotensive episodes associated with transfusion [27]. Before current prestorage leukoreduction procedures, cases of severe hypotension associated with transfusion were attributed to use of bedside leukocyte depletion filters. Negatively charged filter surfaces were reportedly capable of activating the contact system, ultimately generating large amounts of bradykinin. Concomitant use of ACE inhibitors and patients with reduced bradykinin metabolism were more susceptible to hypotensive reactions [28, 29]. Bradykinin is inactivated by a number of peptides, among which is ACE; hence, metabolism can be blocked in patients who take ACE inhibitors [27]. Shiba and colleagues [30] reported serum bradykinin levels were inversely related to the activity of ACE and were elevated in patients taking ACE inhibitors.

Arnold and colleagues [31] reported 2 patients with severe hypotension after transfusion who were receiving ACE inhibitor therapy and who also received prestorage leukoreduced products. One patient exhibited impaired degradation of des-Arg9-bradykinin (BK) and both patients had mildly impaired bradykinin degradation. Another investigation suggested prestorage leukocyte reduction of platelet concentrates, particularly in patients receiving ACE inhibitor therapy, was capable of contributing to hypotension after transfusion due to generation of high concentrations of bradykinin during storage [32]. Our RBC units were prestorage leukocyte-reduced per the US Food and Drug Administration's recommendation for use of prestorage leukoreduction [33]. In our investigation, the statistical interaction between transfusion and ACE inhibitor therapy was tested and was not significant.

We found a number of traditional risk factors for development of vasoplegia in our patient population. ACE inhibitors were associated with mild vasoplegia but not the development of profound vasoplegia. Continuation of ACE inhibitors on the day of the operation is somewhat controversial, with some reports noting an association with more complications after cardiac operations [1, 10, 11, 34, 35]. Medications such as ACE inhibitors modulate vasoconstrictive properties of neurohormones, such as arginine vasopressin, may potentiate vasodilation after CPB [36, 37] Hasija and colleagues [12] reported that preoperative continuation of ramipril was associated with hypotension on induction of anesthesia and after separation from CPB. Interestingly, they demonstrated prophylactic low-dose infusion of arginine vasopressin ameliorated that risk [12]. Of note, discontinuation of ACE inhibitors for at least 10 hours preoperatively has been associated with a reduced risk of hypotension after anesthesia induction [38].

In contrast, Licker and colleagues [39] reported no association between long-term ACE inhibitors and changes in hemodynamic stability in patients with preserved left ventricular function. We can speculate that preoperative use of ACE inhibitors does not increase the risk of profound vasoplegia per se, yet is associated with mild vasoplegia amenable to treatment with intravenous fluids and norepinephrine infusion.

Study Limitations
This was a cohort investigation in which unmeasured patient or processes-of-care variables could have influenced study results. Our study points toward a risk association rather than causation between RBC and component transfusion and the development of vasoplegia. Although we did not have measures of inflammatory markers, mild and profound vasoplegia may have been partly related to the systemic inflammatory response to CPB in addition to inflammation mediators related to transfusion. We did not have information on dose and duration of therapy for ACE inhibitors, only that patients were receiving ACE inhibitor therapy preoperatively. In general, we do not withhold ACE inhibitors preoperatively. We did not have data on cardiac output in patients experiencing vasoplegia, but from experience, these patients will have increased cardiac indices.

Our prospective cohort study design did not allow for two groups to be mutually exclusive because of the nature of progression of vasoplegia development and need for escalating doses of norepinephrine with the addition of vasopressin therapy. Nevertheless, the association with RBC and component transfusion and development of vasoplegia remained consistent and significant.

Conclusion
Our investigation examined two large patient groups by our clinical practice for vasopressor use. Transfusion of RBC and component therapy significantly increased the unadjusted and risk-adjusted odds for development of mild and profound vasoplegia. Although mild vasoplegia is more common and responsive to norepinephrine infusion, profound vasoplegia required escalating doses of pharmacologic support. Evidence suggests development of vasoplegia is related to an increased risk for morbidity and death [4, 9–11]. Further investigation is necessary to determine whether intraoperative prophylactic use of vasopressor support in the setting of transfusion can ameliorate risk.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 

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