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Case Reports  |   September 1995
Hemodynamic Responses to Electroconvulsive Therapy in a Patient 5 Years after Cardiac Transplantation
Author Notes
  • (Pargger, Kaufmann) Fellow in Anesthesia. Current position: Departement fur Anasthesie, Kantonsspital, Basel, Switzerland.
  • (Schouten, Welch) Instructor in Psychiatry.
  • (Drop) Associate Professor of Anaesthesia.
  • Received from the Departments of Anesthesia and Psychiatry, Massachusetts General Hospital, and Departments of Anaesthesia and Psychiatry, Harvard Medical School, Boston, Massachusetts. Submitted for publication January 18, 1995. Accepted for publication April 29, 1995.
  • Address correspondence to Dr. Drop: Department of Anesthesia, Massachusetts General Hospital, Boston, Massachusetts 02114. No reprints will be available.
Article Information
Case Reports
Case Reports   |   September 1995
Hemodynamic Responses to Electroconvulsive Therapy in a Patient 5 Years after Cardiac Transplantation
Anesthesiology 9 1995, Vol.83, 625-627.. doi:
Anesthesiology 9 1995, Vol.83, 625-627.. doi:
Key words: Blood pressure: hypertension. Electroconvulsive therapy. Heart: catecholamine supersensitivity; denervation.
CARDIAC transplantation leads to persistent denervation, with major consequences. Myocardial norepinephrine stores are depleted, [1] neuronal catecholamine uptake is lost, [2] and adaptation to stress and exercise is altered. The heart responds primarily by increasing stroke volume via the Frank-Starling mechanism, [3] whereas changes in heart rate (HR) are minimal. In the normally innervated heart, these responses occur simultaneously. [4] These alterations are of special interest in a cardiac recipient who presents for electroconvulsive therapy (ECT), which is associated with acute hemodynamic perturbations mediated by both the parasympathetic and sympathetic nervous systems. In a series of seven treatments, we documented the hemodynamic responses in a cardiac transplant recipient during and after ECT.
Case Report
A 62-yr-old man with a 6-month history of major depression was admitted for ECT. He was being treated with immunosuppressants including azathioprine, cyclosporine, and prednisone for cardiac transplantation 5 yr earlier. Other medical diagnoses included insulin-dependent diabetes mellitus; essential hypertension, which was treated with daily doses of hydralazine, clonidine, and atenolol; Parkinson's disease, treated with levodopa; and a cerebrovascular accident, which had resolved without residual motor disturbances. Four weeks previously, peritoneal dialysis was initiated for chronic renal failure, which was related to bilateral renovascular occlusive disease. However, because of small vessel disease, a revascularization procedure was ruled out. A magnetic resonance image of the brain showed lacunar infarcts and microangiopathy.
Because of severe motor retardation, exercise tolerance could not be assessed, but the patient denied precordial discomfort or angina. The electrocardiogram showed sinus tachycardia (124 beats/min) and nonspecific ST-T wave changes in AVR and V2. A transthoracic echocardiogram showed concentric LV hypertrophy but normal LV and RV size and function; ejection fraction was 59%. Right heart catheterization disclosed PA and RV pressures of 58/22 and 38/10 mmHg, respectively, and a cardiac index of 2.4 1 sup -1 *symbol* min sup -1 *symbol* m sup -2.
On each day of ECT, arterial blood pressure (BP) was monitored noninvasively (Dinamap, Critikon, Tampa, FL) every 1 min, and HR and leads II and V5 of the electrocardiogram were monitored immediately before and up to 15 min after application of ECT by a monitor (PC Express, Spacelabs, Redmond, WA) equipped with ST segment interpretation software. The electrocardiogram signal was calibrated at 10 mm for each 1 mV, with a frequency response of 0.01-100 Hz. All BP, HR, and ST-segment data were collected by a microcomputer, using a fast analog-to-digital converter and customized data acquisition software. This arrangement permitted simultaneous display (in real time) of all data, both in tabular form and as an X-Y graph (vs. time); 15 1-min divisions on the time axis spanned half the computer screen for detailed viewing. Simultaneously, all data were time-stamped and stored with clinical annotations in the order of their occurrence.
After at least one control measurement of BP and several measurements of HR, anesthesia was induced with sodium methohexital and succinylcholine (both 0.75 mg/kg), and the lungs were ventilated with oxygen via face mask. Taking the absence of a foot sole reflex as evidence of adequate muscular relaxation, a unilateral brief pulse square wave stimulus was delivered by a monitored ECT apparatus. Data collection continued until spontaneous ventilation resumed.
In all treatments, awake systolic and diastolic BP values ranged from 150 to 165 mmHg and from 88 to 92 mmHg, respectively, and HR from 124 to 133 beats/min. To protect against the possibility of supersensitivity of the heart to catecholamines, in the first treatment, we administered 100 mg esmolol immediately before induction of anesthesia. One minute later, the ECT stimulus was applied (Figure 1, top). Given the moderate responses, beta-blocker pretreatment was withheld in the subsequent ECT treatments. The hemodynamic responses observed during subsequent ECTs were remarkably uniform (Figure 1, bottom). Relatively small changes in BP and HR were observed. Changes in ST segments were minimal in all treatments.
Figure 1. (Top) Hemodynamic variables and ST segment data obtained during the first electroconvulsive therapy (ECT) treatment. After 100 mg esmolol, the ECT stimulus was followed by a transient decrease in systolic (triangles pointing up) and diastolic (triangles pointing down) blood pressure and heart rate. These variables returned to their control values within about 5 min. (Bottom) Hemodynamic variables and ST segment data obtained without esmolol pretreatment, during and after the second ECT treatment. The pattern of changes seen during all subsequent treatments was nearly identical to that seen here. The transient changes in blood pressure were modest; heart rate remained unchanged. In all treatments, deviations of ST segments from baseline were minimal. ST-II and ST-V = ST segment data in electrocardiogram leads II and V, respectively. Both panels show real-time recordings of data.
Figure 1. (Top) Hemodynamic variables and ST segment data obtained during the first electroconvulsive therapy (ECT) treatment. After 100 mg esmolol, the ECT stimulus was followed by a transient decrease in systolic (triangles pointing up) and diastolic (triangles pointing down) blood pressure and heart rate. These variables returned to their control values within about 5 min. (Bottom) Hemodynamic variables and ST segment data obtained without esmolol pretreatment, during and after the second ECT treatment. The pattern of changes seen during all subsequent treatments was nearly identical to that seen here. The transient changes in blood pressure were modest; heart rate remained unchanged. In all treatments, deviations of ST segments from baseline were minimal. ST-II and ST-V = ST segment data in electrocardiogram leads II and V, respectively. Both panels show real-time recordings of data.
Figure 1. (Top) Hemodynamic variables and ST segment data obtained during the first electroconvulsive therapy (ECT) treatment. After 100 mg esmolol, the ECT stimulus was followed by a transient decrease in systolic (triangles pointing up) and diastolic (triangles pointing down) blood pressure and heart rate. These variables returned to their control values within about 5 min. (Bottom) Hemodynamic variables and ST segment data obtained without esmolol pretreatment, during and after the second ECT treatment. The pattern of changes seen during all subsequent treatments was nearly identical to that seen here. The transient changes in blood pressure were modest; heart rate remained unchanged. In all treatments, deviations of ST segments from baseline were minimal. ST-II and ST-V = ST segment data in electrocardiogram leads II and V, respectively. Both panels show real-time recordings of data.
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Discussion
In this patient with essential hypertension, severe vascular occlusive disease in three major vascular beds, and cardiac denervation, a clinically significant hypertensive response was anticipated after ECT. Short-acting beta-adrenergic blocking drugs may be used for attenuation. [5] However, in this long-term cardiac recipient, several considerations relating to the combined effects of beta blockers and cardiac denervation were important. First, an increase in stroke volume is the principal cardiac response to stress after cardiac transplantation. [3] Second, there is a sustained reduction in myocardial content of norepinephrine, which is the physiologic adrenergic transmitter at the end-organ synapse. [2] Nevertheless, in the absence of rejection, contractility of the transplanted heart is not compromised, as measured by the slope of the end-systolic pressure versus dimension relation. [6] In addition, arterial hypertension in cardiac recipients is common, and beta-adrenergic blocking drugs may be part of their treatment. [6] Third, because termination of catecholamine action is determined primarily by neuronal norepinephrine uptake, [2] the greatest proportion of endogenously released norepinephrine is removed locally within the heart. Because this mechanism for norepinephrine removal disappears after cardiac denervation, for a given catecholamine secretion, responses may be exaggerated. In the denervated dog heart, this was shown by a fourfold increase in peak LV dP/dt after a given norepinephrine infusion rate as compared to the nondenervated heart. [7] However, these experimental data cannot be immediately applied clinically because, in human cardiac transplant recipients, only modest enhancements of inotropic responses to norepinephrine have been documented [8,9] and only modestly heightened chronotropic responses to epinephrine were observed. [10] Epinephrine is not a cardiac neurotransmitter in humans. Thus, patient data to support clinically significant denervation supersensitivity to catecholamines are lacking. [11] .
These considerations pose a dilemma when a heart transplant recipient presents for ECT. If there were cardiac supersensitivity to catecholamines, a short-acting injectable beta-adrenergic blocking drug would be expected to be useful, especially in view of the major catecholamine surge characteristically associated with ECT. Anton et al. [12] found a 15-fold increase in plasma epinephrine levels and a threefold increase in norepinephrine levels after ECT. On the other hand, because the denervated heart depends on circulating catecholamines, a short-acting beta-blocking drug could produce a dramatic decrease in myocardial contractility. Because normal ventricular size and function had been established in this patient and because atenolol was part of the antihypertensive regimen before ECT, it seemed reasonable to administer intravenous esmolol at the time of the first ECT. In view of the decreased BP and HR that gradually returned to their control values within 3 min, esmolol was withheld in the subsequent ECT sessions, and changes in BP were less than 50% of predicted by data obtained in patients without cardiac denervation. [13] Hence, it is unlikely that cardiac supersensitivity was present. It is recognized that this patient presented with symptoms suggestive of multiorgan consequences of severe cardiovascular disease and that he was treated with antihypertensive drugs that act centrally and peripherally. It is possible, therefore, that responses recorded in this patient might not be representative for all cardiac transplant recipients presenting for general anesthesia during ECT. However, treatment with antihypertensives in cardiac transplant recipients is not the exception, but the rule, as shown by a previous study. [6] Of 34 cardiac transplant recipients, 31 were treated with beta-adrenergic blocking drugs, calcium channel blocking drugs, converting enzyme inhibiting drugs, or a combination of these. [6] .
The modest BP responses recorded in this patient are in accord with the view that supersensitivity to catecholamines after orthotopic cardiac transplantation is not of practical concern. This view is based on results obtained in the setting of a cardiac catheterization laboratory [8,9] and in the setting of clinical anesthesia in large heart transplant centers. [11] .
In this patient, the decrease in BP immediately after ECT was unexpected. One possible explanation is that it occurred secondary to methohexital, with a delay in appearance of pressor effects, typically seen after ECT. The persistence of denervation nearly 5 yr after cardiac transplant was confirmed by the absence of bradycardia after ECT. This is in agreement with human studies showing that bradycardia did not occur in heart transplant recipients after administration of methoxamine, whereas it could be demonstrated in age-matched control subjects. [14] Finally, because accelerated post-transplant coronary atherosclerosis frequently is observed by the third year after transplant, [15] cardiac transplant recipients are at increased risk for myocardial ischemic events. However, anginal pain is often absent after cardiac denervation. Therefore, close monitoring of ST segment trends is especially important.
The authors thank Len Firestone, M.D., for critical review of the manuscript and suggestions. They also thank E. Larsen, SpaceLabs Inc. (Redmond, WA), for the use of the SpaceLabs PCExpress patient monitor.
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Goldstein DS, Brush JE, Eisenhofer G, Stull R, Esler M: In vivo measurement of neuronal uptake of norepinephrine in the human heart. Circulation 78:41-48, 1988.
Clark DA, Schroeder JS, Griepp RB, Stinson EB, Dong E, Shumway NE, Harrison DC: Cardiac transplantation in man: Review of first three year's experience. Am J Med 54:563-576, 1973.
Savin WM, Haskell WL, Schroeder JS, Stinson EB: Cardiorespiratory responses of cardiac transplant patients to graded, symptom-limited exercise. Circulation 62:55-60, 1980.
Kovac AL, Goto H, Pardo MP, Arakawa K: Comparison of two esmolol bolus doses on the hemodynamic response and seizure duration during electroconvulsive therapy. Can J Anaesth 38:204-209, 1991.
Von Scheidt W, Neudert J, Erdmann E, Kemkes BM, Gokel JM, Autenrieth G: Contractility of the transplanted, denervated human heart. Am Heart J 121:1480-1488, 1991.
Vatner DE, Lavallee M, Amano J, Finizola A, Homcy CJ, Vatner SF: Mechanisms of supersensitivity to sympathomimetic amines in the chronically denervated heart of the conscious dog. Circ Res 57:55-64, 1985.
Leachman RD, Cokkinos DVP, Cabrera R, Leatherman LL, Rochelle DG: Response of the transplanted, denervated human heart to cardiovascular drugs. Am J Cardiol 27:272-276, 1971.
Cannom DS, Rider AK, Stinson EB, Harrison DC: Electrophysiological studies in the denervated transplanted human heart: Response to norepinephrine, isoproterenol and propranolol. Am J Cardiol 36:859-866, 1975.
Gilbert EM, Eiswirth CC, Mealey PC, Larrabee P, Herrick CM, Bristow MR: Beta adrenergic supersensitivity of the transplanted human heart is presynaptic in origin. Circulation 79:344-349, 1989.
Firestone L: Autonomic influences on cardiac function: Lessons from the transplanted (denervated) heart. Int Anesth Clin 27:283-291, 1989.
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Castelli I, Steiner LA, Kaufmann MA, Alfille PA, Schouten R, Welch CA, Drop LJ: Comparative effects of esmolol and labetalol to attenuate hyperdynamic states after electroconvulsive therapy. Anesth Analg 80:557-561, 1995.
Borow KM, Neumann A, Arensman FW, Yacoub MH: Left ventricular contractility and contractile reserve after cardiac transplantation. Circulation 71:866-872, 1985.
Firestone L, Firestone S: Organ transplantation, Anesthesia. 4th edition. Volume 2. Edited by Miller RD. New York, Churchill Livingstone, 1994, pp 1981-2009.
Figure 1. (Top) Hemodynamic variables and ST segment data obtained during the first electroconvulsive therapy (ECT) treatment. After 100 mg esmolol, the ECT stimulus was followed by a transient decrease in systolic (triangles pointing up) and diastolic (triangles pointing down) blood pressure and heart rate. These variables returned to their control values within about 5 min. (Bottom) Hemodynamic variables and ST segment data obtained without esmolol pretreatment, during and after the second ECT treatment. The pattern of changes seen during all subsequent treatments was nearly identical to that seen here. The transient changes in blood pressure were modest; heart rate remained unchanged. In all treatments, deviations of ST segments from baseline were minimal. ST-II and ST-V = ST segment data in electrocardiogram leads II and V, respectively. Both panels show real-time recordings of data.
Figure 1. (Top) Hemodynamic variables and ST segment data obtained during the first electroconvulsive therapy (ECT) treatment. After 100 mg esmolol, the ECT stimulus was followed by a transient decrease in systolic (triangles pointing up) and diastolic (triangles pointing down) blood pressure and heart rate. These variables returned to their control values within about 5 min. (Bottom) Hemodynamic variables and ST segment data obtained without esmolol pretreatment, during and after the second ECT treatment. The pattern of changes seen during all subsequent treatments was nearly identical to that seen here. The transient changes in blood pressure were modest; heart rate remained unchanged. In all treatments, deviations of ST segments from baseline were minimal. ST-II and ST-V = ST segment data in electrocardiogram leads II and V, respectively. Both panels show real-time recordings of data.
Figure 1. (Top) Hemodynamic variables and ST segment data obtained during the first electroconvulsive therapy (ECT) treatment. After 100 mg esmolol, the ECT stimulus was followed by a transient decrease in systolic (triangles pointing up) and diastolic (triangles pointing down) blood pressure and heart rate. These variables returned to their control values within about 5 min. (Bottom) Hemodynamic variables and ST segment data obtained without esmolol pretreatment, during and after the second ECT treatment. The pattern of changes seen during all subsequent treatments was nearly identical to that seen here. The transient changes in blood pressure were modest; heart rate remained unchanged. In all treatments, deviations of ST segments from baseline were minimal. ST-II and ST-V = ST segment data in electrocardiogram leads II and V, respectively. Both panels show real-time recordings of data.
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