Hemodynamic and Catecholamine Responses Associated with Extracorporeal Shock Wave Lithotripsy Rahim Behnia, MD, PhD,* Jonathan Moss, MD, PhD,“f John B. Graham, MD,+ Harry W. Linde, PhD,§ Michael F. Roizen, MD_F Departments Medical

of’ Anesthesia

School,

and

and

Surgery,

the Department

*Associate Professor 01 Clinical Anesthesia, Northwestern University Medical School

University of Chicago, Chicago, 1L.

TProfessor University

Patients undergoing

of Anesthesia of Chicago

SProfessor of Urology, versity Medical School

and Critical

Northwestern

Care,

Uni-

of Anesthesia, Medical School

extracorporeal shock wave lithotripsy {ESWL) for nephroli-

hypothesized that those problems were a result of adrenal medulla9 Northwestern

Presented in part at the Fourth Annual Symposium on Shock Wave Lithotripsy: State of the Art, Indianapolis, March 1987, and at the Annual Meeting of the American Society of Anesthesiologists, San Francisco, October 1988. Received for publication July 19, 1989; revised manuscript accepted for publication December 20, 1989,

variables and circulating epinephrine and norepinephrine

levels in nine patients

End-tidal carbon dioxide (CO,) was maintained at 34 + 2 mmHg. Cardiac output (CO) und mean arterial pressure (MAP) resistance (TPR)

were measured, and total peripheral

was calculated at the following

time points: (1) after immersion

prior to shock wave therapy (control); (2) after 300 shocks; (3) after 800 shocks; and (4) 5 minutes after the completion of ESWL with the patient still immersed. Circulating epinephrine and norepinephrine concentrations were determined at the above times as well as before and after induction of anesthesia but prior to immersion. There was a statistically signaficant (p < 0.05) decrease in CO and un increase (p < 0.05) in MAP and TPR with ESWL treatment. These va1ue.s returned to baseline levels when treatment was stopped. Plasma epinephrine and norepinephrine values did not change significantly throughout the study period. It was concluded that these ESWL-associated hemodynamic changes were probably not mediated via epinephmne or norepinephrine.

Keywords: Extracorporeal shock wave lithotripsy; epinephrine; norepinephrine; hemodynamics; anesthetics, volatile; isoflurane.

0 1990 Butterworth-Heinemann

,J. Clin. Anesth.,

release of

Therefore, the effects of ESWL on cardiovascular

anesthetized with 1 .I% isojlurune in 50% nitrous oxide and oxygen were studied.

Address reprint requests to Dr. Behnia at the Department of Anesthesia, Northwestern University Medical School, Ward Building 12-203,303 E. Chicago Avenue, Chicago, IL 6061 l-3008. USA.

158

University

and Critical Care,

thiusis are anesthetized and immersed in water iu a semasitting position. Hypertension and tachycardia have been reported to accompany ESWL, and it was epinephrine or norepinephrine.

OProfessor University

Northwestern

of’Anesthesia

vol. 2, Mayilune

1990

Hemodynamic

Introduction Extracorporeal shock wave lithotripsy (ESWL) using the Dornier HM3 lithotripter (Munich, West Germany) has rapidly changed the management of upper urinary tract calculi. Since the first human trials began in Munich in February 1980, approximately 500,000 patients have been treated worldwide. Technological advances in ESWL have produced newer generations of lithotripters and increased their use. By 1988, more than 250 lithotripters had been distributed in 28 countries.’ While some of the newer lithotripters do not require anesthesia, many older ones, such as the Dornier HM3, do. Shock wave technology also has been used to treat cholelithiasis.” Treatment of urinary tract calculi using the Dornier HM3 lithotripter with the original generator and ellipsoidal reflector (15.6 cm) is sufficiently painful that the administration of regional or general anesthesia is required.J-” Patients are anesthetized and immersed in water in a semisitting position while highenergy shock waves travel through the body. This combination of anesthesia, immersion in water, and ESWL can affect the cardiovascular system and kidneys.“m5 Serious adverse effects of this procedure associated with cardiac complications, and even death from cardiovascular causes, have been reported.7.n ESWL-induced cardiovascular changes” may be caused by nociceptive stimulation or by the effects of shock waves on the adrenal medulla (releasing catecholamines) or the kidney (releasing renin, prostaglandins, and so on). Dissociation between neural and hormonal sympathetic responses can occur.” In this study, the effects of ESWL on cardiovascular variables and circulating epinephrine and norepinephrine levels in nine patients receiving general anesthesia for ESWL were determined.

Materials and Methods Hemodynamic and catecholamine responses associated with ESWL were measured in nine unpremedicated patients (Table l), two women and seven men with no history of cardiopulmonary or renal disTable

1.

Clinical Details of Patients

Number of patients Age (yr) Weight (kg) Height (cm) IV infusion (ml/kg/h) Body temperature (“C)

End-tidal CO, (mmHg)

9 45 + 14 85 ? 24 169 2 8 6 to 8

37 -+ 0.4 34 I+_2

and catecholamine

changes with ESWL:

Behnia et al.

eases. The experimental protocol was approved by the Institutional Review Board of Northwestern University, and each patient gave informed consent. The electrocardiogram (EKG) was monitored throughout the ESWL procedures, and the R wave was used to trigger the shock waves. A peripheral vein was cannulated to allow administration of 5% dextrose in lactated Ringer’s solution at a rate of 6 to 8 ml/kg/h. This rate of intravenous (IV) infusion was chosen to increase urine output to aid removal of pulverized stones from the urinary tract. Another catheter was placed in a radial artery to monitor systemic arterial blood pressure. The pressure transducer was adjusted to a zero point at the level of the left ventricle and electronically calibrated at the start of study. Two patients were placed on the lithotripsy chair before induction of anesthesia. Seven patients were anesthetized on a cystoscopy table, and their ureteral stones were pushed into the renal pelvis via a cystoscope before transfer to the lithotripsy chair. Anesthesia was induced in all patients with thiopental sodium 4 to 6 mg/kg, and muscle relaxation was provided with vecuronium 0.08 mg/kg IV. The trachea was intubated, and ventilation was controlled with a volume-cycled ventilator to maintain end-tidal CO, at 34 ? 2 mmHg (mean +- SD). Anesthesia was maintained with isoflurane 1.11% + 0.20% in 50% nitrous oxide and oxygen. Body temperature was monitored by an esophageal temperature probe (Datascope Corp., Paramus, NJ), and end-tidal concentrations of COP, 02, isoflurane, and nitrous oxide were measured via a mass spectrometer calibrated daily (Perkin-Elmer, Pompano, CA). The patients were strapped on the lithotripsy chair and immersed to the level of the clavicle in 37°C water. After immersion, the lithotripsy chair and the patients’ position were adjusted to focus the shock waves on the targeted stone as seen on the image intensifier screen. A transesophageal ultrasonic Doppler probe (Accucom, Datascope Corp., Paramus, NJ) was inserted into the esophagus to measure cardiac output (CO).1o,11 Although CO was measured continuously to enable comparisons between subjects, the reported mean * SD CO values were those obtained over 3 minutes during each of the following periods: (1) after immersion in the water bath, immediately before shock wave therapy (control); (2) after 300 shocks; (3) after 800 shocks; and (4) 5 minutes after the completion of ESWL treatment with the patient in the same position and still immersed in water. TPR was calculated from MAP and CO. Blood samples, drawn by syringe from the radial artery catheter, were obtained to measure circulating epinephrine and norepinephrine during each of the

J. Clin. Anesth.,

vol. 2, May/June

1990

159

Table

2.

~ietnod~nxnic

Changes

Assotided

with

ESW12q’

Control

HK (beats/minute) (mmHg) CO (Limin) TPR (dyne.sec.cnl

85

anesthetized

tSignificant

1,X7

;)

and immersed

(p < 0.05) changes

ESWI. = extracorporeal peripheral resistance.

x4

shock

z 242

t

IO

Xfi :t S

;(I

1%

!)-l -t Ifi’;

SL’? !,

3.8 2

O.i-iC

-t

0.3-i-

2.066 i- 4!)5f-

f

!I

I.(i z ().I, I Xi” 2 ?-,!I _____

control.

wave lithotripsy;

HK = heart

rate;

MAP

Plasma Epinephrine

Awake After induction of anesthesia Anesthesia and immersion in water 300 shocks 800 shocks Posttreatment (5 minutes) = extracorporeal

shock

J. Clin. Anesth., vol. 2, May/June 1990

= mean

wave lithotripsy.

arter-ial

prc$surc;

(I()

= c-ar-that output;

.l‘I’K = I