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Ann Thorac Surg 1999;67:1006-1011
© 1999 The Society of Thoracic Surgeons

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Original Articles

Hemodynamic effects of methylprednisolone in patients undergoing cardiac operation and early extubation

^a Department of Anesthesiology Loyola University Medical Center, Foster G. McGaw Hospital, Maywood, Illinois, USA
^b Department of Thoracic and Cardiovascular Surgery, Loyola University Medical Center, Foster G. McGaw Hospital, Maywood, Illinois, USA

Accepted for publication September 17, 1998.

Address reprint requests to Dr Chaney, Department of Anesthesiology, Loyola University Medical Center, Foster G. McGaw Hospital, 2160 S First Ave, Maywood, IL 60153

Presented at the Twentieth Annual Meeting of the Society of Cardiovascular Anesthesiologists, Seattle, WA, April 25–29, 1998.

	Abstract

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Background. Whether or not methylprednisolone is beneficial during cardiac operation remains controversial. This study examines the effects of the drug on complement activation and hemodynamics in patients undergoing cardiac operation and early extubation.

Methods. Patients undergoing cardiac operation were randomized to receive either intravenous methylprednisolone (group MP) or intravenous placebo (group NS). Complement 3a (C3a) levels and hemodynamic parameters were obtained perioperatively. Extubation was accomplished at the earliest clinically appropriate time.

Results. Both groups exhibited equivalent increases in C3a levels after exposure to bypass. Group MP exhibited increased cardiac index, decreased systemic vascular resistance, and increased shunt flow when compared to group NS. More group MP patients required hemodynamic support and group MP patients had prolonged extubation times.

Conclusions. Methylprednisolone was unable to attenuate complement activation and led to hemodynamic alterations (primarily vasodilation) that may hinder early extubation in patients after cardiac operations.

	Introduction

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Cardiopulmonary bypass (CPB) exposes blood to large areas of synthetic materials, which triggers the production and release of various mediators that affect local and systemic vascular resistance and myocardial contractility. At the heart of this systemic inflammatory response is complement activation. These physiologic alterations can complicate the perioperative period by causing hemodynamic instability. Administration of methylprednisolone before CPB may [1–3] or may not [4–9] attenuate complement activation and may [10–14] or may not [3, 15–18] enhance hemodynamic stability.

Although a number of clinical studies suggest methylprednisolone may be beneficial in facilitating early extubation after cardiac operation, none have rigorously examined use of the drug in this setting. This prospective, randomized, double-blind, placebo-controlled clinical study examines the effects of methylprednisolone on complement activation and hemodynamics in patients undergoing coronary artery bypass grafting and early extubation.

	Material and methods

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After Institutional Review Board approval and informed consent, 60 patients scheduled for elective coronary ar-tery bypass grafting and early extubation were studied. We view all patients scheduled for elective coronary artery bypass grafting as early extubation candidates, including those having reoperations and those with decreased left ventricular function (ejection fraction <40%). Patients receiving preoperative steroids were excluded as were patients requiring preoperative intravenous inotropic or vasoactive drugs, intraaortic balloon support, supplemental oxygen, or mechanical ventilation.

Each patient was randomized to receive either intravenous methylprednisolone sodium succinate (A-Methapred; Abbott Laboratories, North Chicago, IL) (group MP) or intravenous normal saline (group NS). Group MP patients received methylprednisolone, 30 mg/kg during sternotomy and 30 mg/kg during initiation of CPB, whereas group NS patients received normal saline at the same two times. An Anesthesia Research Nurse performed the randomization and prepared the two syringes of blinded solution that were administered. All physicians and nursing staff caring for the patients perioperatively were unaware of treatment group.

The intraoperative anesthetic technique was standardized and consisted of intravenous fentanyl (20 µg/kg), midazolam (10 mg, total), and vecuronium. All of the fentanyl was administered before sternotomy. Regarding midazolam, 6 mg was administered before sternotomy, 2 mg during rewarming, and 2 mg during sternal closure. If required, inhaled isoflurane or intravenous nitroglycerin, or both drugs, were used before initiation of CPB. Hypothermic CPB (to a lowest temperature of 26°C) with a membrane oxygenator and crystalloid prime (2.0 L lactated Ringer’s solution, 50 mEq sodium bicarbonate, 12.5 g mannitol) was used in all. Nonpulsatile flows were maintained between 2.4 and 2.8 L · min^-1 · m^-2 and, if needed, isoflurane was used to maintain perfusion pressure between 50 and 70 mm Hg. Alpha-stat blood gas management was used in all. Separation from CPB was facilitated with intravenous dobutamine, norepinephrine, or nitroglycerin at the discretion of the anesthesiologist.

Blood samples were obtained five times: 10 minutes after intubation, 10 minutes after sternotomy, 20 minutes after CPB initiation, 10 minutes after sternal closure, and 60 minutes after intensive care unit (ICU) arrival. From each, complement 3a (C3a) levels were determined by methodology previously described [19] with radioimmunoassay kits purchased from Amersham Life Science Corporation (Arlington Heights, IL).

Hemodynamic measurements were obtained four times: 10 minutes after intubation, 10 minutes after sternotomy, 10 minutes after sternal closure, and 60 minutes after ICU arrival. A pulmonary artery catheter (Swan-Ganz Thermodilution Paceport Catheter; Baxter Healthcare Corp, Irvine, CA) was used in all patients. Cardiac outputs were obtained at end-expiration in duplicate and averaged. Hemodynamic measurements included heart rate, mean arterial pressure (MAP), central venous pressure (CVP), mean pulmonary artery pressure, and pulmonary artery occlusive pressure. Cardiac index (CI), systemic vascular resistance (SVR), pulmonary vascular resistance (PVR), oxygen delivery index (ODI), oxygen consumption index (OCI), and shunt flow were calculated using standard equations (see Appendix). Mechanical ventilation parameters were standardized (respiratory rate, 8; tidal volume, 10 mL/kg, fractional concentration of oxygen, 1.0; positive end-expiratory pressure, +5; inspiratory to expiratory ratio, 1:3) for at least 10 minutes before each measurement.

Postoperative extubation was accomplished at the earliest clinically appropriate time. Criteria for extubation in our ICU include an appropriate sensorium, normothermia, hemodynamic stability, adequate pulmonary function (partial pressure of oxygen 60 mm Hg with fractional concentration of oxygen 0.4), adequate urine output, and minimal chest tube output. If a patient developed hypertension or tachycardia, or had excessive movement at a time when extubation was not yet appropriate (for any reason), the ICU nurse was free to administer intravenous midazolam. In patients who were not extubated within 24 hours of ICU arrival, the reason for prolonged intubation was ascertained.

Postoperative complications and treatments were recorded daily until hospital discharge. All patients had a creatine phosphokinase (CK) level assayed and an electrocardiogram recorded on the first postoperative day. If the total CK was more than 200 IU/L, CK-MB levels were assayed and the CK-MB index calculated (). If the initial total CK was more than 200 IU/L, two additional total CK and CK-MB levels were measured 6 and 12 hours later. Myocardial infarction was defined as a CK-MB index >3.0 or new Q waves or ST segment elevation.

Statistical analysis
Pearson’s ² or Fisher’s exact test was applied to categorical data. Student’s t test (two-tailed) was used to test the difference between means in the two groups regarding demographic and clinical characteristics of patients and intraoperative data. To account for repeated measurements, one-way repeated measures analysis of variance was used along with statistical construct to compare mean measurements 10 minutes after intubation and 60 minutes after ICU arrival. A p value less than 0.05 was considered statistically significant and p values are reported only when significance was found. Results are expressed as the mean ± one standard deviation, unless otherwise indicated.

	Results

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Thirty patients were randomized to each group. Demographic and clinical characteristics and intraoperative data are presented in Tables 1 and 2, respectively. Despite randomization, patients in group NS weighed more and therefore, received less intraoperative midazolam when calculated in micrograms per kilograms.

Postoperative atrial fibrillation occurred in 8 group MP patients and 9 group NS patients. Cardioversion was required in 2 patients in group MP and 1 in group NS. Postoperative ventricular tachycardia occurred in 2 group MP patients and 1 group NS patient. Of the 2 patients in group MP, 1 required defibrillation and both required insertion of an automatic implantable cardioverter defibrillator. The 1 patient in group NS required insertion of an automatic implantable cardioverter defibrillator. One patient in each group experienced myocardial infarction (both defined as a postoperative CK-MB Index >3.0). The group NS patient also demonstrated ST segment elevation. Both eventually died.

Three patients in group MP and 1 patient in group NS experienced postoperative cerebral infarction. All 4 patients were eventually discharged from the hospital to a chronic care facility.

One patient in group MP and 2 patients in group NS died. All three were initially extubated within 24 hours of ICU arrival. The group MP patient experienced myocardial infarction and intestinal ischemia (requiring operation) and died on postoperative day 7. One group NS patient developed a bleeding gastric ulcer (requiring operation) and died on postoperative day 45. The other group NS patient experienced myocardial infarction secondary to clotted vein grafts, which eventually led to emergent operation and death on postoperative day 2.

Fifty-seven of the 60 patients were discharged from the hospital. The mean duration of postoperative hospital stay in group MP (6.9 ± 4.1 days; range, 3 to 20 days) was no different than in group NS (8.3 ± 5.1 days; range, 4 to 27 days).

	Comment

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
This prospective, randomized, double-blind, placebo-controlled clinical study revealed that, when compared to patients receiving placebo, patients receiving methylprednisolone exhibited equivalent increases in C3a levels after exposure to CPB and exhibited increases in CI, decreases in SVR, and increases in shunt flow. Furthermore, patients receiving methylprednisolone were more likely to require hemodynamic support and had prolonged extubation times. We conclude that methylprednisolone, as used in this study, is unable to attenuate complement activation associated with CPB and initiates hemodynamic alterations (primarily vasodilation) that may hinder early extubation in patients after cardiac procedures.

Patients undergoing cardiac operations experience an abnormal whole body inflammatory response after initiation of CPB. Although every arm of the inflammatory response is involved, at the heart is complement activation. The major detrimental physiologic effects are initiated by the terminal components C5a and the C5b-9 complex and C3a is a useful marker of in vivo complement activation. Early clinical studies revealed that complement activation was linked to postoperative cardiac, pulmonary, and renal morbidity [20]. More recently, inhibition of complement activation has been shown to decrease blood loss and time to extubation and improve hemodynamics [21–23].

Inhibition of detrimental CPB-induced physiologic effects is possible with corticosteroids. In the 1960s, methylprednisolone became the drug of choice because of its efficacy in shock and sepsis and its advantageous side effect profile [14]. The dose used, 30 mg/kg, was empirically chosen and remains the standard. However, a supplemental dose must be administered at initiation of CPB to maintain adequate plasma levels of drug into the postoperative period [16]. Besides decreased complement activation [1–3], potential clinical benefits include enhanced hemodynamic stability [10–14] and improved pulmonary function [7]. Morbidity [11] and mortality [17] may even be reduced.

Complement activation during cardiac operation is affected by numerous factors. Methylprednisolone may [1–3] or may not [4–9] reliably attenuate complement activation and these discrepancies may be explained by the small numbers of patients in most studies, the differing doses and timing of drug used, and the variable end points. Jansen and colleagues [6] found that methylprednisolone, 30 mg/kg administered after induction of anesthesia, was unable to attenuate complement activation (determined with blood C3a levels). We also found that methylprednisolone was unable to attenuate complement activation.

Whether or not administration of methylprednisolone before CPB enhances hemodynamic stability also remains controversial [3, 10–18]. However, the drug may increase CI [10, 13], decrease SVR [10, 12, 13], and decrease arrhythmias [11]. We found that methylprednisolone increased CI and decreased SVR and that these physiologic alterations led the two groups to be managed very differently postoperatively. To maintain equivalent MAPs, more group MP patients required dobutamine and more group NS patients required nitroglycerin 60 minutes after ICU arrival. Although we had no rigid protocol to dictate drug administration, it is common practice of the nurses in our ICU to administer dobutamine to increase MAP and nitroglycerin to decrease MAP. We found no link between complement activation and hemodynamic changes.

Although clinical studies suggest methylprednisolone may facilitate early extubation after cardiac operations, this study rigorously examines the use of the drug in this setting. One observational study found that patients administered 1.0 g of methylprednisolone immediately before CPB followed by four doses of dexamethasone (4.0 mg each) every 6 hours had prolonged extubation times when compared to control patients not receiving steroids (13.1 ± 2.3 hours versus 10.5 ± 1.0 hours, respectively) although the difference was not significant [1]. Another observational study found that patients administered 30 mg/kg methylprednisolone after induction of anesthesia had significantly prolonged respiratory support when compared to historical controls (85 ± 181 hours versus 27 ± 16 hours, respectively, p = 0.05) [18]. We found that methylprednisolone prolonged extubation time. Although group MP patients received more intraoperative midazolam, the difference was small and would not cause prolonged intubation. Furthermore, both groups received similar amounts of midazolam during the time period from ICU arrival to extubation, indicating that group MP patients did not experience excessive postoperative sedation. Although one cannot determine exactly what caused the difference in extubation time between groups, vasodilation induced by methylprednisolone may have contributed in two ways. First, the fact that more group MP patients required dobutamine to support MAP may have made the ICU nurses reluctant to initiate weaning from mechanical ventilation. Second, the increased shunt flow (induced by vasodilation) in group MP patients may have prolonged weaning from mechanical ventilation by causing oxygenation difficulties. Data presented elsewhere from this cohort revealed that patients in group MP exhibited higher mean postoperative alveolar–arterial oxygen gradient when compared to patients in group NS (420 ± 96 mm Hg versus 360 ± 104 mm Hg, respectively, p = 0.02) [24].

In conclusion, this prospective, randomized, double-blind, placebo-controlled clinical study revealed that methylprednisolone, 30 mg/kg during sternotomy and 30 mg/kg during initiation of CPB, was unable to attenuate complement activation and led to increases in CI, decreases in SVR, and increases in shunt flow. Furthermore, patients receiving the drug were more likely to require hemodynamic support and had prolonged extubation times. Thus, methylprednisolone, as used in this study, was unable to attenuate complement activation associated with CPB and initiated hemodynamic alterations (primarily vasodilation) that may hinder early extubation in patients after cardiac operation.

	Acknowledgments

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This study was supported by Department of Anesthesiology, Research Fund, Loyola University Medical Center.

	Appendix

 

where CcO₂ = end-capillary O₂ content; CaO₂ = arterial O₂ content; and CvO₂ = mixed venous O₂ content

	References

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 

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