Anesth Analg 2003;97:339-340
© 2003 International Anesthesia Research Society
CARDIOVASCULAR ANESTHESIA
Intentional Circulatory Arrest to Facilitate Surgical Repair of a Massively Bleeding Artery
Lothar A. Schwarte, MD, and
Matthias Hartmann, MD
Department of Anesthesiology, Heinrich-Heine-University, Duesseldorf, Germany
Address correspondence and reprint requests to Matthias Hartmann, MD, Department of Anesthesiology, Heinrich-Heine-University, Moorenstrasse 5, D-40225 Duesseldorf, Germany. Address e-mail to Matthias.Hartmann{at}uni-duesseldorf.de
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Abstract
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IMPLICATIONS: Cardiocirculatory arrest can be induced by adenosine and maintained over several minutes by application of high positive end-expiratory pressure to allow surgical control of a near hemorrhage from a large ruptured artery.
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Introduction
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Massive arterial bleeding may prevent the visualization of the surgical site and preclude the otherwise feasible repair of an injured vessel. We present a case in which the intentional induction of a short cardiocirculatory arrest using adenosine and positive end-expiratory pressure (PEEP) enabled surgical control of near-fatal arterial hemorrhage.
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Case Report
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A 66-yr-old patient (ASA physical status III, New York Heart Association class II, and Canadian Cardiovascular Society class I) was admitted for elective resection of a thoracoabdominal aortic aneurysm (Crawford type I). Preoperative evaluation revealed that the left subclavian artery derived from the aneurysm’s neck. A transposition of the origin of the left subclavian artery from the aorta to the left carotid artery was performed as the first operation to allow adequate aortic cross-clamping.
During anesthesia, arterial blood pressure (right radial artery), electrocardiogram (ECG), and arterial oxygen saturation (pulse oximetry) were continuously monitored. After cervical incision, the subclavian artery was dissected down to the aorta and divided near the aortic arch. The proximal subclavian artery stump was oversewn. Before implantation of the distal subclavian artery into the common carotid artery, massive bleeding (2 L) occurred from the proximal subclavian artery stump, which had ruptured near the weakened aortic wall.
Controlled hypotension was induced by hypovolemia, blood loss was conserved with a cell saver, and the rupture was controlled by the surgeon’s finger. A mean arterial blood pressure of 40 mm Hg was maintained by application of lactated Ringer’s solution (1.5 L) and epinephrine (25 ng · kg-1 · min-1). After close inspection, the surgeon decided that the rupture was untreatable, even under the condition of controlled hypotension, because massive bleeding prevented adequate visualization. At our suggestion, however, the surgeon agreed that the repair would be possible with a blood-free field within a short time. Therefore, we planned a transient controlled cardiac arrest. Infusion of epinephrine was stopped, and adenosine was administered as a bolus (48 mg IV) to induce blockade of the atrioventricular node and a cardiac arrest that lasted 35 s (Fig. 1). Thereafter, sinus rhythm returned, but the repair was not completed, and we inflated the lungs with a PEEP of 30 cm H2O to prolong circulatory arrest. This maneuver maintained arterial blood pressure at 20 mm Hg and completely blocked arterial pressure pulsations, whereas the ECG showed sinus rhythm. The visualization of the surgical site was adequate, and the vascular repair was finished in 3 min. Thereafter, PEEP was released, and the arterial blood pressure increased rapidly. Correction of hypovolemia (1.5 L of lactated Ringer’s solution and processed cell saver blood) and the administration of epinephrine (50 ng · kg-1 · min-1) normalized the hemodynamic situation. The further course of the operation was uncomplicated, and the patient recovered without signs of neurological deficit.
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Figure 1. Time course of heart rate (derived from electrocardiogram), pulse rate (derived from pulse oximeter), and arterial blood pressures (systolic, mean, and diastolic) as derived from the trend registration. During hemorrhage, hypotension was induced by hypovolemia. Adenosine (ADO; 48 mg) induced a cardiac arrest with a 35-s duration (measured by a stopwatch). Extension of circulatory arrest was achieved by application of positive end-expiratory pressure (PEEP) (30 cm H2O). Release of PEEP and the administration of epinephrine and crystalloids normalized arterial blood pressure after completion of the vessel repair.
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Discussion
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Intentional induction of temporary circulatory arrest has been described for the testing of implantable cardioverter defibrillators (1), placement of endovascular aortic stents (2), and minimally invasive coronary surgery (3). In addition, few reports describe the treatment of penetrating cardiac injuries during temporary cardiac arrest (4,5). This case report, however, describes, for the first time, an intentionally induced circulatory arrest to allow surgical repair of a massively bleeding artery.
In general, electrical-induced ventricular fibrillation and application of adenosine are two methods typically used to induce circulatory arrest. The advantage of ventricular fibrillation is that the duration can be chosen as required. However, specialized equipment is necessary for both induction and reversal. In contrast, adenosine-induced circulatory arrest is easily achieved with bolus application of adenosine and is therefore practicable in emergency situations. Disadvantages of adenosine are the great interindividual variability of duration (6) and the requirement of circulation to deliver the drug to the heart. Thus, an extension of the circulatory arrest by repetition of the adenosine bolus is not possible.
In this case, we extended the adenosine-induced circulatory arrest by application of PEEP, which resulted in a prevention of venous return in the hypovolemic patient. This combined approach allowed control of the duration of the circulatory arrest. This aspect is of special importance because the duration of the surgical repair (three minutes) narrowed cerebral ischemia tolerance. Although the administration of PEEP is a simple technique to prolong circulatory arrest, there are several drawbacks. The effect of PEEP is critically dependent on intravascular volume, and the induction of a circulatory arrest will succeed only in severely hypovolemic patients. Furthermore, the method might not be applicable in thoracic surgery (inflation of the lungs) or neurosurgery (increase in cranial pressure).
In this case, the induction of a circulatory arrest was ultimately lifesaving. The risks of this procedure in emergency situations, however, are unknown. Because the induction of a circulatory arrest for the implantation of defibrillators and stents is a safe procedure, we think that the risks are acceptable under these different conditions (1,7). This case demonstrates that the intentional induction of circulatory arrest is a valuable option in vascular surgery for controlling massive arterial bleeding.
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References
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- Adams DC, Heyer EJ, Emerson RG, et al. Implantable cardioverter-defibrillator: evaluation of clinical neurologic outcome and electroencephalographic changes during implantation. J Thorac Cardiovasc Surg 1995; 109: 565–73.[Abstract/Free Full Text]
- Kahn RA, Marin ML, Hollier L, et al. Induction of ventricular fibrillation to facilitate endovascular stent graft repair of thoracic aortic aneurysms. Anesthesiology 1998; 88: 534–6.[ISI][Medline]
- Latham P, Joshi GP. Coronary revascularization without cardiopulmonary bypass: use of ischemic preconditioning and adenosine. Anesthesiology 1998; 88: 828–30.[ISI][Medline]
- Wada J. Electrically induced fibrillation in cardiac arrest and resuscitation. In: Stephenson HE Jr, ed. Cardiac arrest and resuscitation. St. Louis: CV Mosby Co, 1974: 783–95.
- Lim R, Gill IS, Temes RT, Smith CE. The use of adenosine for repair of penetrating cardiac injuries: a novel method. Ann Thorac Surg 2001; 71: 1714–5.[Abstract/Free Full Text]
- Hashimoto T, Young WL, Aagaard BD, et al. Adenosine-induced cardiac asystole to induce transient profound systemic hypotension. Anesthesiology 2000; 93: 998–1001.[ISI][Medline]
- Kahn RA, Moskowitz DM, Marin ML, et al. Safety and efficacy of high-dose adenosine-induced asystole during endovascular AAA repair. J Endovasc Ther 2000; 7: 292–6.[ISI][Medline]
Accepted for publication April 3, 2003.
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Abstract
Introduction
