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Hemodynamic Responses to Electroconvulsive Therapy in a Hypertensive Patient with End-Stage Pulmonary Fibrosis

Viguera, A. MD; Welch, C. MD; Bigatello, L. MD; Drop, L. J. MD

doi: 10.1213/00000539-199809000-00050
Case Reports

Departments of (Viguera, Welch) Psychiatry and (Bigatello, Drop) Anesthesia and Critical Care, Massachusetts General Hospital, Boston, Massachusetts.

Accepted for publication June 9, 1998.

Address correspondence to L. J. Drop, Department of Anesthesia and Critical Care, Massachusetts General Hospital, Boston, MA 02114. Address e-mail to drop@helix.mgh.harvard.edu.

The autonomic nervous system contributes significantly to the control of pulmonary circulation, and both [alpha]- and beta-adrenoreceptors are distributed throughout the pulmonary vessels for effective stress responses [1]. Characteristic of stress is an increase in catecholamines locally released by sympathetic stimulation or reaching the pulmonary bed via the circulating blood [2]. In normal humans, the resulting increase in pulmonary vasomotor tone leads to only a very small increase in pulmonary artery (PA) pressure [1], even in the presence of large increases in blood flow. In contrast, the PA pressure may markedly increase in response to increased pulmonary blood flow when pulmonary hypertension preexists [3], with important consequences for right ventricular (RV) performance. This combination is of special interest when electroconvulsive therapy (ECT) is planned in a patient with pulmonary hypertension. ECT is characterized by a twofold increase in cardiac output [4], a 34% increase in arterial pressure [5], and a massive catecholamine surge [6]. Severe pulmonary hypertension is a hallmark of idiopathic pulmonary fibrosis (IPF) [7]. The consequences of this condition in combination with ECT, however, are unknown. In a series of seven treatments, we documented the hemodynamic responses to ECT in a patient with severe IPF.

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Case Report

A 89-yr-old man with IPF and a 25-yr history of major depression was admitted with recurrent unipolar illness of 6-mo duration. Prednisone treatment had been instituted 10 yr earlier for pulmonary fibrosis, and, to confirm that diagnosis, radiographs of the chest had shown diffuse bilateral reticular opacities and honeycombing, but no cardiomegaly was seen. Because of exacerbation of exertional dyspnea 4 mo previously, a transthoracic echocardiogram had been performed, revealing an estimated PA pressure of 75 mm Hg and RV dilation. At that time, prednisone had been increased to 60 mg/d, but tapering of this dose had begun 3 wk before the present admission. At home, the patient used continuous supplemental oxygen. He had given up smoking 35 yr ago. He also had cerebrovascular disease with multiple lacunar infarcts but without persistent neurological deficit. On physical examination, there was dyspnea at rest with a respiratory rate of 28-30 breaths/min, and the dyspnea became pronounced on walking a distance of <5 m. He denied angina or precordial discomfort. Wheezing was absent, and PaO2 was 89%-93% when breathing room air with supplemental oxygen at 2 L/min by nasal cannula. A transthoracic echocardiogram showed RV dilation and hypokinesis but normal left ventricular (LV) function; the estimated LV ejection fraction was 65%, and the estimated systolic PA pressure was 62 mm Hg. Pulmonary function tests showed a vital capacity of 3.13 L (73% of predicted) and a forced expiratory volume in 1 s of 71% (72% of predicted), which changed slightly with a bronchodilator. Systemic blood pressure was 180/100 mm Hg. An electrocardiogram (ECG) showed sinus arrhythmia with a heart rate of 88 bpm and unifocal atrial premature beats. The antidepressant drug regimen included paroxetine and trazodone, which were discontinued 4 days before the first ECT; other treatments included prednisone (as mentioned) and a stool softener. Because the two different antidepressants failed to bring about improvement, ECT was planned, as it had been effective 20 yr earlier.

For the first treatment with ECT, a radial artery and a central venous cannula was placed in the antecubital fossa for drug infusion; for technical reasons, venous pressure measurements were not obtained. Systemic arterial blood pressure was recorded on a multichannel direct-writing recorder via a calibrated pressure transducer. While the patient was breathing room air, arterial blood gas values were PaO2 75 mm Hg, PaCO2 49 mm Hg, and pHa 7.35. During the first ECT, systolic PA pressures were estimated by using a transthoracic echocardiogram using the velocities of tricuspid and pulmonary regurgitation flows and RV peak flow acceleration time. Such estimates are in close agreement with measurements obtained from direct catheterization throughout the pressure range of 30-90 mm Hg [8]. A close correspondence also applies to RV and mean PA pressure values [9,10]. We obtained concurrent systolic PA pressure estimates at control and at 2- to 4-min intervals up to 9 min after the application of ECT and later verified them from a magnetic tape recording. At bedside, the echocardiographer was unaware of the dose and timing of the drugs administered. The position of the ultrasound Doppler probe on the chest during a 45[degree sign] left lateral decubitus position was constant, and motion artifacts were minimized after muscular paralysis produced by succinylcholine. Systemic blood pressures and leads II and V5 of the ECG were recorded and data collected at the bedside by a microcomputer with customized software, allowing simultaneous real-time display and storage of all data. The sampling frequency of ECG data was every 7 s. Apparatus was ready for inhalation of appropriate concentrations of nitric oxide. During the second and later treatments, we recorded noninvasive arterial pressure measurements every 1 min, and only a large bore peripheral venous line was inserted.

For all treatments, general anesthesia was induced with methohexital (0.65 mg/kg) and succinylcholine (0.75 mg/kg), and these drug doses were constant for the series of treatments. The lungs were ventilated with 100% O2 via a face mask until spontaneous breathing resumed. Pulse oximeter readings were 100% throughout. ECT was administered by a unilateral brief pulse stimulus (average 55 Ws), which was followed by a seizure shown by slight movements of the feet, averaging 40 s. In the first treatment, a bolus dose of 250 mg of esmolol was administered IV within 2 s after application of the stimulus, and peak systolic arterial blood pressures were limited to 220/110 mm Hg (representing peak increases in systolic and diastolic pressures from control by 40 and 10 mm Hg, respectively) and heart rate to 120 bpm (Figure 1A). The echocardiogram showed RV dilation and hypokinesia both before and after ECT, but, on close comparison (preversus post-ECT), there was no change in the degree of RV dilation or hypokinesia. The highest systolic PA pressure estimate was 75 mm Hg (from a control value of 62 mm Hg) (Figure 2). The ST segment of the ECG remained unchanged throughout. The characteristic asystole immediately after the ECT stimulus was limited to 2.4 s (Figure 3).

Figure 1

Figure 1

Figure 2

Figure 2

Figure 3

Figure 3

During the second and subsequent treatments, we changed the timing and dose of esmolol administration so that an IV bolus of 300 mg of the drug immediately preceded the ECT stimulus. During these treatments, upward deviations of arterial pressure were <10 mm Hg from control, and heart rate did not exceed 88 bpm (Figure 1B). No pulmonary wheezing was present at any time. Rapid awakening followed each treatment. The patient was discharged in remission after a series of seven treatments.

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Discussion

This case report describes a successful course of ECT in a 89-yr-old man with severe pulmonary hypertension. Under experimental conditions, hypothalamic stimulation [8] and a catecholamine surge [6] are powerful stimuli, known to increase systolic PA pressure by as much as 50 mm Hg [1]; in addition, substantial increases in left atrial and aortic pressures and in cardiac output occur [1,4,11]. Markedly increased systolic PA pressure may be expected in patients with end-stage pulmonary fibrosis, as this condition is characterized by a reduced pulmonary vascular cross-sectional area. Because of decreased capillary recruitment [12], even moderate increases in cardiac output may produce very severe pulmonary hypertension. Death may be attributable to acute RV failure [13].

These considerations pose a difficult clinical dilemma. The respective degrees of acute systemic and pulmonary hypertensive responses to ECT were unpredictable, and the relative importance of each and their interaction could not be adequately assessed. For attenuation of systemic hypertensive responses to ECT, nitroso-vasodilators, including sodium nitroprusside and nitroglycerin, were considered, but the resulting tachycardia, especially in an octogenarian, may also require selective beta-adrenergic blockade. Although selective beta1-adrenergic blockers are very useful to attenuate both hypertension and tachycardia [5], in large doses, they may produce beta2-adrenergic blockade leading to bronchospasm when bronchospastic disease preexists. Consistent with this concern is that, because of a very intense sympathetic discharge typically associated with ECT, we infused 8-10 times the loading dose of esmolol recommended in standard pharmacology texts [14,15] for the management of a hypertensive crisis (0.5 mg/kg or 30 mg in a 60 kg person). In addition, beta-adrenergic blocking drugs may leave the pulmonary vascular [alpha]-receptors unopposed [1], thereby exaggerating pulmonary hypertension when a massive catecholamine surge occurs. The consensus was to address systemic and pulmonary responses specifically and separately. We would administer 250 mg of esmolol immediately after the stimulus so that this drug would offset the anticipated sharp increase in arterial pressure typically seen after ECT. The selected esmolol dose was followed by an increment of peak arterial pressure by 40 mm Hg to 220 mm Hg. In all six subsequent ECT sessions, the dose and timing of the esmolol bolus was changed to 300 mg infused immediately before ECT, and the systemic hypertensive response was abolished while tachycardia was minimized (Figure 1B). For attenuation of pulmonary hypertension, aerosolized prostacyclin was considered but not selected because, in the presence of pulmonary fibrosis, increased pulmonary shunting has been reported without improvement of pulmonary hypertension [16]. Instead, a system for the inhalation of the selective pulmonary vasodilator nitric oxide (NO) was ready at the bedside. Because this gas has the greatest therapeutic potential for pulmonary vasodilation when RV failure is present or pulmonary hypertension is extreme [17], the echocardiogram recorded during ECT was instrumental in guiding therapy. Because the highest recorded systolic PA pressure was limited to 75 mm Hg (Figure 2), which had been measured 4 mo previously during an exacerbation of pulmonary hypertension, NO inhalation seemed unnecessary. This relatively small change in systolic PA pressure cannot be readily explained by transient RV failure, because the degree of RV dilation and hypokinesis before ECT was indistinguishable on the echocardiogram from that after the combination of ECT and esmolol administration. The precise mechanism of action of esmolol is not known, although a decrease in sympathetic outflow, suppression of renin release, and blockade of adrenoreceptors have all been postulated. [15]. Even after a large dose of esmolol, no exaggerated asystolic period was observed (Figure 3). Finally, pulmonary wheezing did not appear after esmolol infusion, which is consistent with the absence of true bronchospastic disease.

In summary, this case report described successful anesthesia and ECT in a patient with documented severe pulmonary hypertension. With 100% oxygen inhalation and esmolol pretreatment, the observed changes in systolic PA pressure estimates after ECT were of a magnitude seen 4 mo earlier in this patient during an exacerbation of the pulmonary hypertension, and with the selection of an appropriate time interval between the esmolol infusion and ECT stimulus, the systemic pressor response to ECT was effectively attenuated.

We thank SpaceLabs Medical (Redmond, WA) for the loan of SpaceLabs PCExpress patient monitor, Datalogger, and two-channel printer. We also thank Dr. Mark Kaufmann (Basel, Switzerland) for use of the customized software allowing real-time physiological data display.

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