THORACIC AORTA: ESMOLOL FOR INTRAOPERATIVE .... repair of aortic rupture, showing their relation to aortic cross-clamping and to the infusions of esmolol.
British Journal of Anaesthesia 1991; 67: 483-^87
REPAIR OF TRAUMATIC TRANSECTION OF THE THORACIC AORTA: ESMOLOL FOR INTRAOPERATIVE CONTROL OF ARTERIAL PRESSURE S. G. FENNER, A. MAHONEY AND J. N. CASHMAN
The patient was transferred to this Regional Cardiothoracic Unit for investigation and manWe report the intraoperative use of esmolol for agement of suspected intrathoracic aortic injury. control of arterial pressure during repair of a On his arrival, assessment revealed a conscious of 110/70 mm traumatic transection of the descending thoracic patient with an arterial pressure 1 Hg, heart rate 100 beat min" , normal peripheral aorta. A mean infusion rate of esmolol 50.5 fig 1 1 pulses and good urine output. A subsequent arch kg' min~ resulted in a decrease in mean arterial pressure to 63 mm Hg and heart rate to 99 beat aortogram revealed a leak of contrast just distal to min'1 and was associated with excellent surgical the left subclavian artery, consistent with tranconditions. The infusion rate of esmolol was section of the descending thoracic aorta. The titrated easily against mean arterial pressure, patient was transferred immediately to the operatwhich increased rapidly on discontinuing its ing theatre for repair of this defect via a left infusion. Control of arterial pressure with esmolol thoracotomy. In the anaesthetic room, the right radial and was comparable to that achieved with sodium nitroprusside, but without the reflex tachycardia posterior tibial arteries were cannulated for or decrease in ?aOl associated with the latter measurement of proximal and distal arterial pressures during aortic cross-clamping. A 7agent. French gauge thermodilution pulmonary artery catheter (American Edwards Laboratories) was KEY WORDS placed via the right internal jugular vein. In the Anaesthetic techniques: induced hypotension. Arterial pressure: esmolol. sodium nitroprusside. Surgery: aortic tranoperating theatre full invasive haemodynamic section. monitoring was commenced during preoxygenation. Anaesthesia was induced with diamorphine 200 ug kg"1 i.v. followed by thiopentone 2 mg CASE REPORT kg"1 i.v. Suxamethonium l.Smgkg" 1 i.v. was A previously healthy 20-yr-old man was admitted administered to facilitate intubation with a 37to hospital following a road traffic accident. French gauge left-sided double-lumen endoClinical and radiological examinations at the bronchial tube. Further increments of dia-1 referring hospital had revealed multiple fractures, morphine were given to a total dose of 400 ug kg" central abdominal peritonism, but no evidence of significant head or chest injury. After resuscitation with i.v. fluids, laparotomy was performed S. G. FENNER*, B.SC., M.B., B.S., F.C.ANAES. ; A. MAHONEY-|-, and damaged small bowel and mesentery were M.B., B.S., F.C.ANAES.; J. N . CASHMAN, B.SC., M.B., B.S., F.C.ANAES. ; Department of Anaesthesia, St George's Hospital, resected, his fractured right elbow was stabilized Blackshaw Road, London SW17 0QT. Accepted for Publiin plaster of Paris and a right distal tibial traction cation: March 11, 1991. pin was inserted. On the first day after operation Present addresses: •Department of Anaesthesia, St Helier Hospital, Wrythe the patient complained of central chest pain and Carshalton, Surrey SM5 1AA. another chest x-ray revealed widening of the Lane, fDepartment of Anaesthetics, Charing Cross Hospital, superior mediastinum. A provisional diagnosis of Fulham Palace Road, London W6 8RF. intrathoracic aortic transection was made. Correspondence to S.G. F. SUMMARY
BRITISH JOURNAL OF ANAESTHESIA
484
r 140
140
115
o X E E 90 •
5 x o 65 -
40 4 -30
90
120
150
180
210
300
Time from induction (min) FIG. 1. Heart rate ( • ) and proximal MAP ( • ) changes during anaesthesia for repair of aortic rupture, showing their relation to aortic cross-clamping and to the infusions of esmolol and SNP.
i.v. Anaesthesia during the 5-h procedure was maintained by intermittent positive pressure ventilation with 25—50 % nitrous oxide and enflurane in oxygen with intermittent boluses of fentanyl (total lS^gkg" 1 i.v.) and pancuronium (total 250 jig kg"1 i.v.). It was decided to use an i.v. infusion of esmolol (Brevibloc-Dupont Pharmaceuticals) to control systemic arterial pressure during aortic dissection, before aortic crossclamping. The authors were interested also to compare the cardiovascular conditions provided by esmolol with those provided by sodium nitroprusside (SNP) (currently our preferred agent for the intraoperative control of arterial pressure). Therefore, after 1 h the infusion of esmolol was changed to an i.v. infusion of SNP. During the course of surgery cardiac output, pulmonary artery pressures, pulmonary capillary wedge pressures (PCWP) and arterial blood-gas measurements were recorded at intervals in addition to the usual variables recorded during an intrathoracic vascular procedure. After induction of anaesthesia, arterial pressure stabilized at 80/55 mm Hg with a heart rate of 110-120 beat min"1. However, within 15 min of the commencement of surgery, arterial pressure and heart rate had
increased to 130/60 mm Hg and 140 beat min"1, respectively. At this point an infusion of esmolol 150 |ig kg"1 min"1 was commenced without a bolus loading dose. This produced a rapid decrease in heart rate and arterial pressure to 95 beat min"1 and 80/45 mm Hg, respectively (figs 1, 2). During the next 60 min of one lung-ventilation, before aortic cross-clamping, the infusion of esmolol was adjusted to maintain mean arterial pressure (MAP) at an average of 63 mm Hg, with an average heart rate of 99 beat min"1 (fig. 1). After esmolol was discontinued, MAP was controlled for the remaining 20 min before application of the aortic cross-clamps with an infusion of SNP which was commenced at a rate of 1.5 ug kg"1 min"1 (fig. 1). This produced a rapid decrease in arterial pressure to 72/44 mm Hg (fig. 2), but was associated with an increase in heart rate to 125 beat min"1 (fig. 1). There was an increase in cardiac index during infusion of SNP compared with values obtained both before induction and during the infusion of esmolol. Arterial blood-gas measurements revealed a decrease in P&ot from 10 kPa before infusion of SNP to 7.7 kPa during infusion of SNP, despite unchanged ventilation and inspired oxygen concentration.
ESMOLOL FOR THORACIC AORTIC TRANSECTION
485 200
200 -i
150 CD
E
E
E a. 100 < a ~a
E
x o
X
o 50
|SNP infusionl -30
—i—
30
300 90 120 150 180 210 240 270 Time from induction (min) FIG. 2. Proximal systolic (SAP) (O) and diastolic (DAP) ( • ) arterial pressures during anaesthesia for repair of aortic rupture, showing their relation to aortic cross-clamping and to the infusions of esmolol and SNP.
TABLE I. Proximal mean arterial pressures {MAP), pulmonary capillary wedge pressures (PCWP), cardiac indices and systemic arterial oxygen partial pressures (Pa o ,) ' " relation to intraoperative events and drug infusions during repair of transected thoracic aorta. OLV = One lung ventilation; x-clamp = aortic cross-clamps applied; n/a = not available
(mmHg)
PCWP (mmHg)
Cardiac index (litre min"1 m"1)
Arterial ft»o, (kPa)
-5
77
n/a
4.50
n/a
Nil
Before induction
75
^4
11
3.21
10.00
Esmolol 60 |ig kg"1 min"1
OLV
135 175 285
70 118 56
12 12 6
5.90 4.94 5.12
12.40
Nil Nil SNP
OLV + x-clamp OLV + x-clamp
Time (min)
MAP
Cardiac index measurements, arterial Pa0%, MAP and PCWP obtained before induction, during the infusion of esmolol, during aortic cross-clamping and during the infusion of SNP are shown in table I. The aortic cross-clamps were applied for 75 min, during which time the 95% transection of the descending aorta was repaired with a 16-mm Gelseal (Vascutek) graft whilst distal perfusion pressure (measured at the right posterior tibial
n/a
7.70
Drug infusions
1.2 ugkg"1 min"1
Events
OLV
artery) was maintained with a 7-mm Gout shunt (Argyle). At the surgeon's request, SNP was discontinued after aortic cross-clamping in order to maintain distal arterial pressure, which had decreased rapidly after the application of the cross-clamps. Distal MAP stabilized at 50 mm Hg after stopping SNP; proximal MAP was 117 mmHg. The infusion of SNP was recommenced just before the aortic cross-clamps were released and was adjusted to achieve a proximal
486
MAP of 60-70 mm Hg. Unfortunately, this was associated with an increase in heart rate from an average of 123 beat min"1 during aortic crossclamping to 132 beat min"1 after the cross-clamps had been released. A reduction in this heart rate was achieved before the end of surgery by administration of three increments of labetalol 10 mg i.v. After operation the lungs were ventilated mechanically for 48 h and the patient sedated with an i.v. infusion of papaveretum and intermittent i.v. bolus doses of diazepam. Arterial pressure was controlled with i.v. infusions of labetalol and SNP. During this period the patient underwent a 12-h orthopaedic operation for internal fixation of his fractured long bones. The patient was discharged eventually back to the referring hospital 4 days after the aortic repair.
BRITISH JOURNAL OF ANAESTHESIA
ruption and haemorrhage [12]. Furthermore, it is important after application of the cross-clamps in order to prevent acute left ventricular failure [12]. Even at relatively low infusion rates, esmolol proved to be extremely effective in controlling this patient's arterial pressure before aortic crossclamping. The effect of esmolol on arterial pressure was adjusted easily because of its short elimination half-life. The negative chronotropic effect of esmolol in this patient was observed clearly when compared with SNP, which produced tachycardia. This effect of esmolol may be of considerable advantage in patients with ischaemic heart disease, in whom the tachycardia and reduced coronary artery perfusion pressure produced by SNP may impair the myocardial oxygen supply and demand relationship, which may in turn be associated with myocardial ischaemia [8, 13]. The negative chronotropic effect of esmolol may also be useful in younger DISCUSSION patients who usually exhibit marked compensaEsmolol is an ultra-short acting P-adrenoceptor tory tachycardia when controlled hypotension is antagonist. In normal subjects after i.v. ad- induced with an arteriolar dilating agent such as ministration, it has distribution and elimination SNP. Furthermore, SNP causes a much greater half-lives of only 2 min and 9 min [1], respect- decrease in diastolic arterial pressure than esmolol ively. Esmolol has a rapid onset of action: an [14]. This may have important implications for effect on heart rate is observed within 3 min [2]. It maintenance of coronary and renal artery peris metabolized rapidly, predominantly by eryth- fusion pressures. A further undesirable action of rocyte esterases, to an acid metabolite (a 1500-fold SNP is its effect on hypoxic pulmonary vasoless potent adrenoceptor antagonist than esmolol) constriction (HPV). Esmolol has no discernible and methanol. Plasma cholinesterases are not effect upon HPV, demonstrated by minimal involved in the metabolism and there is thus no changes in PCWP and Paot, as opposed to SNP significant effect on the inactivation of suxa- which causes decreases in both [14]. We were methonium [3,4]. Less than 1 % of an ad- interested to observe these differences between ministered dose of esmolol is recovered un- esmolol and SNP in our patient (table I). changed in the urine; more than 70% of the acid Esmolol is relatively contraindicated in patients metabolite is recovered from the urine [5]. with left ventricular dysfunction, as it may reduce Esmolol has been shown to be effective in cardiac output further. Sodium nitroprusside attenuating the hypertension and tachycardia usually causes an increase in cardiac output (as resulting from laryngoscopy and tracheal intu- seen here) and therefore may be the preferred bation [2, 6, 7], for the control of intraoperative agent in this situation [14]. Some of the dishypertension and tachycardia [7, 8] and has been advantages of using SNP may be attenuated by used effectively as part of the management of concomitant use of a p-adrenoceptor antagonist arterial pressure during resection of phaeochromo- such as propranolol or the mixed a- and Pcytoma [9]. In addition, esmolol has been used adrenoceptor antagonist, labetalol [12, 15]. Both successfully to control atrial tachyarrhythmia [10] of these agents have elimination half-lives which and in the management of angina pectoris [11]. are substantially longer than those of esmolol or The authors are unaware of any previous report SNP, making fine control of arterial pressure and of the use of esmolol to control arterial pressure heart rate during anaesthesia unpredictable and during surgery to repair transection of the thoracic difficult to achieve. Any deleterious effects of aorta. In such cases, control of arterial pressure is P-adrenoceptor antagonism, caused by esmolol, important before application of aortic cross- should resolve quickly and spontaneously as a clamps in order to prevent further aortic dis- result of its rapid metabolic breakdown. A more
ESMOLOL FOR THORACIC AORTIC TRANSECTION logical approach to control of arterial pressure during anaesthesia and surgery for cases such as this might be to use infusions of a short-acting vasodilating agent such as SNP in combination with an ultra-short acting [3-adrenoceptor antagonist such as esmolol.
7.
8. 9.
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