Ann Thorac Surg 1997;64:1046-1049
© 1997 The Society of Thoracic Surgeons
Original Article: Cardiovascular
Hemodynamic Advantages of Left Atrial Epinephrine Administration in Open Heart Operations
Atilla Aral, MD,
Mehmet O
uz, MD,
Haldun Özberrak, MD,
Ye
im Batislam, MD,
Tümer Çorapçiolu, MD,
Neyyir T. Eren, MD,
Refik Taöz, MD,
Hakki Akalin, MD
Departments of Cardiovascular Surgery and Anesthesiology, Faculty of Medicine, University of Ankara, Ankara, Turkey
Accepted for publication April 6, 1997.
 |
Abstract
|
|---|
Background. It is often necessary to administer a catecholamine to patients who have undergone cardiac operations. However, there are some potential disadvantages to using the central venous circulation, a routine route for catecholamine infusion. The advantages of the left atrial infusion of epinephrine were investigated in 21 patients.
Methods. The first group received epinephrine through the central venous route (central venous group), and the second group received adrenaline through the left atrial route (left atrial group). Hemodynamic studies were performed in all patients before and after the infusions. Blood samples were also taken from the radial and pulmonary arteries to determine the epinephrine concentrations.
Results. The average pulmonary arterial pressure and pulmonary vascular resistance were higher in the central venous group, whereas higher cardiac indices and average blood pressures were noted in the left atrial group (p < 0.05). There was a statistically significant difference in the epinephrine concentrations in the pulmonary arterial and radial arterial samples between the two groups.
Conclusions. We conclude that epinephrine infusion through the left atrial route is associated with greater hemodynamic advantages than infusion through the central venous route.
|
Introduction
|
|---|
See also page 1049.
Patients undergoing open heart operations may require inotropic agents, particularly epinephrine, during the perioperative period [1]. It is generally our practice to administer the epinephrine infusion after the discontinuation of cardiopulmonary bypass through the central venous route if there is low ventricular performance after the cessation of cardiopulmonary bypass.
Use of the central venous route has some potential disadvantages, however. Because of the dysequilibrium dilution effect and pulmonary elimination, lower concentrations of the inotropic agent reach the heart and systemic circulation [2]. Furthermore, when administered through the central venous route, epinephrine may trigger pulmonary vasoconstriction, resulting in increased pulmonary arterial pressure and pulmonary vascular resistance, which in turn may lead to an extensive right ventricular afterload resulting in right heart failure. These disadvantages may be avoided by infusing the epinephrine into the left atrium.
In the present study, we attempted to identify the relative hemodynamic advantages of epinephrine infusion through the left atrium rather than through the central venous route and to determine the systemic and pulmonary circulation concentrations of the agent after infusion using either route.
|
Material and Methods
|
|---|
The study population consisted of 21 patients who underwent coronary artery bypass grafting and needed an epinephrine infusion because of low ventricular performance after the cessation of cardiopulmonary bypass. The patients had all been admitted to our clinic for elective coronary artery bypass grafting, and all had normal renal, respiratory, and endocrine functions.
Patients were divided into two groups. The first group consisted of 14 randomly selected patients who received a central venous epinephrine infusion for 15 minutes (0.06 µg • kg-1 • min-1) immediately after the cessation of cardiopulmonary bypass, and the remaining 7 patients received an epinephrine infusion at the same dose and rate and for the same length of time through the left atrium. The average preoperative left ventricular ejection fraction in the central venous group was calculated to be 0.38 ± 0.41, whereas it was 0.35 ± 0.54 in the left atrial group. Total revascularization was performed in all the patients, using the left internal mammary artery to revascularize the left anterior descending coronary artery and reversed saphenous veins to revascularize other stenosed or occluded coronary arteries. Characteristics of the central venous and left atrial groups are summarized in Table 1
. There were no statistically significant differences between the two groups in terms of the preoperative and operative characteristics. Our standard anesthetic techniques were used in both groups.
Nonpulsatile-flow, membrane oxygenators, medium hypothermy, and cold crystalloid cardioplegia were used in all operations.
Swan-Ganz and radial arterial catheters were placed in all patients before the induction of anesthesia. Immediately after the discontinuation of cardiopulmonary bypass and completion of the epinephrine infusion, blood samples were obtained from the radial artery and the pulmonary artery through the Swan-Ganz catheter and the adrenaline levels measured (Packard Auto-Gamma Scintillation 5320 instrument) (normal range, 14 to 111 ng/L).
Hemodynamic studies were performed at the times when the blood samples were collected for determination of the epinephrine concentrations. The cardiac indices, average blood pressures, average pulmonary arterial pressures, and systemic and pulmonary vascular resistance values were evaluated.
Left atrial pressures were measured in both groups before and after the epinephrine infusion. The left atrial pressures in the central venous group were measured through a 22-gauge needle placed in the left atrium and connected to a transducer. Triple-lumen catheters placed in the right superior pulmonary vein were used in the left atrial group.
All data were expressed as the mean ± standard deviation. The results were evaluated statistically using Student's t test and the test for two proportions from independent groups. Our institution's ethics committee authorized the study, and all the attendants were informed about this study.
|
Results
|
|---|
All patients completed the protocol without any problems that would compromise the study results, such as the administration of an epinephrine infusion before operation, the need to restart cardiopulmonary bypass, and the administration of a drug that could alter the epinephrine concentration in the blood.
All patients required an epinephrine infusion after the cessation of cardiopulmonary bypass because of low ventricular performance. There were no significant differences between the two groups in terms of the hemodynamic variables before the start of the epinephrine infusion. However, after completion of the epinephrine infusion, the average arterial pressures and cardiac indices in the left atrial group were higher than those in the central venous group. The difference was statistically significant at (p < 0.05). In addition, the pulmonary arterial pressures and pulmonary vascular resistances were higher in the central venous group than in the left atrial group, with the difference statistically significant (p < 0.01 to 0.05). There was no significant difference between the two groups in the left atrial pressures and systemic vascular resistances (p > 0.5). All hemodynamic results are given in Table 2.
Immediately after the discontinuation of cardiopulmonary bypass, there was no statistically significant difference between the two groups (p > 0.05) in the epinephrine concentrations in the blood samples taken from the radial and pulmonary arteries. However, the epinephrine concentrations in the blood samples taken from the radial artery after the completion of epinephrine infusion were significantly higher (p < 0.01) in the left atrial group than in the central venous group, whereas the concentrations in the samples originating from the pulmonary artery were significantly lower (p < 0.01) in the left atrial group than in the central venous group. The epinephrine concentrations are given in Table 3.
Upon completion of the infusion and the gathering of hemodynamic data and blood samples, the left atrial catheters were removed. No complications attributable to the use of the left atrial catheters were encountered among our patients.
|
Comment
|
|---|
The average blood pressures and cardiac indices were increased in both groups of patients after the epinephrine infusion. Nevertheless, the increases were greater in the left atrial group than in the central venous group, and the difference was statistically significant (p < 0.05).
Cathecol O-methyltransferase and monoamine oxidase in the lung, liver, kidney, and intestinal surfaces play an important role in the biotransformation of epinephrine [3–5]. Our measurements of the epinephrine concentration showed that less epinephrine reaches the heart when infused through the central venous route as a result of pulmonary elimination and the dysequilibrium dilution effect. This results in a decreased inotropic effect. On the other hand, epinephrine infused through the left atrium provides a much higher degree of inotropic support, because this ensures direct infusion to the heart.
Significant increases in the systemic vascular resistance were not encountered in either group after the epinephrine infusion. It can therefore be inferred that the rise in the blood pressure stems from the increase in cardiac output. However, it is known that the infusion of increased amounts of epinephrine will lead to higher systemic vascular resistance [6]. Although it has been shown that epinephrine can display the characteristics of a systemic vasoconstrictor at higher doses, a systemic vasoconstrictor effect was also not noted for the doses used in this study.
There were no significant changes in the left atrial pressures in either group after the adrenaline infusion. However, patients in the central venous group showed significantly higher average pulmonary arterial pressures and pulmonary vascular resistance values than did the patients in the left atrial group. We can infer from this that the vasoconstriction triggered in the pulmonary artery by the epinephrine was directly responsible for causing the higher average pulmonary arterial pressures and pulmonary vascular resistance values in the central venous group. However, the epinephrine concentrations measured showed that less epinephrine reached the pulmonary artery in the left atrial group because of systemic elimination and the dysequilibrium dilution effect. No significant increase in the pulmonary arterial pressure and pulmonary vascular resistance was noted in the left atrial group.
There are reports in the literature regarding epinephrine infusion through the left atrial route [7–9]. Some investigators even maintain that the infusion of a prostaglandin E1 through the pulmonary artery concurrent with the administration of epinephrine into the systemic circulation through the left atrium yields better results [10, 11]. However, those studies did not examine the epinephrine concentrations in the systemic and pulmonary circulation.
Continuous left atrial infusion may lead to air embolization and hemorrhage after withdrawal of the catheter in the postoperative period. In our study therefore, the left atrial catheters were introduced with extreme care to prevent such air embolization. After data collection, the left atrial catheters were removed and the pledgetted mattress suture was tied and checked to make sure that there was no bleeding. We did not encounter any bleeding or embolization problems in our study. Removing the catheters under direct vision reduces the probability of such complications to an almost infinitesimally male risk.
We conclude that epinephrine infusion through the left atrium is associated with much greater hemodynamic advantages than infusion through the central venous route. For this reason, we believe that left atrial epinephrine infusion is a worthwhile practice in those patients showing low ventricular performance and pulmonary hypertension after the discontinuation of cardiopulmonary bypass in open heart operations.
|
Footnotes
|
|---|
Address reprint requests to Dr Aral, Oyak Sitesi 2, Blok No 38, 06610 Cankaya, Ankara, Turkey.
|
References
|
|---|
- Kapur PA. Potent inotropes are the drugs of choice after cardiopulmonary bypass: an opposing view. J Cardiothorac Anesth 1987;1:256–8.[Medline]
- Comroe JH. Nonrespiratory functions of the lungs and circulation. In: Physiology of respiration. 2nd ed. Chicago: Year Book, 1974:285–92.
- Axelrod J. Metabolism of epinephrine and other sympathomimetic amines. Physiol Rev 1959;39:751–76.[Free Full Text]
- Laverty R. Catecholamines: role in health and disease. Drugs 1978;16:418–25.[Medline]
- Reves JG. Vasoactive drugs and when to use them. In: Thomas SJ, ed. Manual of cardiac anesthesia. New York: Churchill Livingstone, 1984:35–54.
- Weiner N. Norepinephrine, epinephrine and the sympathomimetic amines. In: Goodman GA, Goodman LS, Rall TW, et al, eds. The pharmacological basis of therapeutics. 7th ed. New York: Macmillan, 1985:145–67.
- Pearl RG, Maze M, Rosenthal MH. Pulmonary and systemic hemodynamic effects of central venous and left atrial sympathomimetic drug administration in the dog. J Cardiothorac Anesth 1987;1:29–35.[Medline]
- Haider W, Zwolfer W, Hiesmayr M, et al. Improved cardiac performance and reduced pulmonary vascular constriction by epinephrine administration via a left atrial catheter in cardiac surgical patients. J Cardiothorac Vasc Anesth 1993;7:684–7.[Medline]
- Fullerton DA, St. Cyr JA, Albert JD, Grover FL. Hemodynamic advantage of left atrial epinephrine administration after cardiac operations. Ann Thorac Surg 1993;56:1263–6.[Abstract]
- Whitman GJR, Martel D, Weiss M, et al. Reversal of protamine-induced catastrophic pulmonary vasoconstriction by prostaglandin E1. Ann Thorac Surg 1990;50:303–5.[Abstract]
- D'Ambra MN, LaRaia PJ, Philbin DM, Watkins WD, Hilgengerg AD, Buckley MJ. Prostaglandin E1: a new therapy for refractory right heart failure and pulmonary hypertension after mitral valve replacement. J Thorac Cardivasc Surg 1985;89:567–72.[Abstract]
Top
Abstract
Introduction
