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Perioperative management of biventricular failure after closure of a long-standing massive arteriovenous fistula

[Le traitement périopératoire d'une défaillance biventriculaire suivant la fermeture d'une ancienne fistule artério-veineuse massive.]

From the Department of Anesthesiology and Reanimatology, Gunma University School of Medicine, Maebashi, Japan.

Address correspondence to: Dr. Takeshi Nara, Department of Anesthesiology, Gunma University School of Medicine, 3-39-22, Showa-machi, Maebashi, Gunma 371-8511, Japan. Phone: 027-220-8454; Fax: 027-220-8473; E-mail: narat{at}med.gunma-u.ac.jp

	Abstract

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Purpose: To report the perioperative management of arteriovenous fistula (AVF) closure in a patient with high-output heart failure and pulmonary hypertension.

Clinical features: In a 71-yr-old man, closure of a long-standing massive AVF between the right femoral artery and vein was performed. After closure of the AVF, his pulmonary artery pressure (PAP) increased from 52/21 mmHg to 68/26 mmHg, his cardiac index decreased from 5.27 L•min^–1•m^–2 to 3.18 L•min^–1•m^–2, and his pulmonary wedge pressure increased from 15 mmHg to 32 mmHg due to an acute increase in afterload. Co-administration of prostaglandin E₁ and a phosphodiesterase III inhibitor improved the cardiac index and the PAP.

Conclusions: Surgical closure of the fistula may not always lead to resolution of the high output cardiac failure. In this case, afterload management using arterial dilators (prostaglandin E₁, phosphodiesterase III inhibitor), use of inotropic drugs (phosphodiesterase III inhibitor), and close attention to volume status was crucial for a successful outcome after surgical AVF closure.

	Introduction

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LONG-STANDING massive arteriovenous fistulas (AVF) caused by trauma are infrequent, and surgical repair is even more infrequent.^1–5 The perioperative management of patients undergoing closure of large AVF is difficult, especially in those complicated by high output cardiac failure and/or pulmonary hypertension.⁶ In such patients, preoperative cardiac failure may not resolve immediately after closure of the AVF because the intervention induces an acute increase in afterload secondary to the sudden reduction of shunt flow. In this report, we describe the perioperative management of a patient with a large traumatic femoral artery to vein fistula. Administration of prostaglandin E₁ (PGE₁) and a phosphodiesterase III (PDE III) inhibitor significantly improved cardiac failure after closure of the AVF.

	Case report

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A 71-yr-old man, 53 kg in weight and 153 cm tall, had sustained a traumatic injury to his right groin 52 yr previously. He was first treated by compression of the bleeding site and later received blood transfusions. Otherwise, his history was unremarkable and he took no medication. Three months prior to his most recent hospitalization, he presented with a gradual onset of cold sensation and pain in the right leg. He was admitted to our hospital with mild exertional dyspnea, palpitations, and moderate swelling of the right lower limb. His blood pressure was 130/70 mmHg, heart rate 74 beats•min^–1, and respiratory rate 18 breaths•min^–1. A loud continuous murmur was audible upon auscultation and a strong thrill was palpated in the right groin. Both pedal pulses were palpable, but the pulse was weak on the right side. Auscultation of the heart revealed a prominent systolic murmur over the apex and over the second right intercostal space.

Angiography demonstrated a wide fistula between the right femoral artery and the circumflex vein, and there was no evidence of thrombosis in either vessel. The segment between the right external iliac artery and the femoral artery was tortuous. Both the femoral artery and vein were dilated. Chest radiography revealed cardiomegaly (cardiothoracic ratio: 64%), mild congestion of the lung fields, and calcification of the aorta. Left ventricular end-diastolic and end-systolic dimensions were 69 mm and 44 mm (normal range; 37–55 and 26–36 mm) respectively, and ejection fraction was 65% by echocardiography. The electrocardiogram (ECG) met voltage criteria for left ventricular hypertrophy.

Midazolam (2 mg) was injected intramuscularly 30 min before induction of anesthesia. Radial and pulmonary artery catheters were inserted under local anesthesia. An epidural catheter was inserted via the second lumbar interspace. After a successful test dose (1% mepivacaine 2 ml), anesthesia was established with 1.5% mepivacaine (10 ml every 90 min). Thirty minutes after the initial dose of 1.5% mepivacaine, anesthesia to cold sensation was obtained between Th6–S2 dermatome. Before surgery, the cardiac index (CI) was increased and pulmonary hypertension was also present. The systemic vascular resistance index (SVRI) was very low preoperatively. All perioperative hemodynamic data are shown in the Table. After clamping the right external iliac artery, systemic arterial pressure (SAP), pulmonary artery pressure (PAP), and SVRI increased immediately. The CI decreased to 3.18 L•min^–1•m^–2, and the pulmonary wedge pressure (PCWP) increased to 32 mmHg. The height of the v-wave on the PCWP tracing wave did not change and ECG showed no remarkable change. These data suggested acute left ventricular dysfunction and, therefore, a continuous infusion of PGE₁ (0.05 µg•kg^–1•min^–1) was initiated in order to decrease SVR and PVR. The SAP, PAP, and SVRI decreased and the CI increased 15 min after the administration of PGE₁. After closure of the AVF and release of the iliac artery clamp, the PAP decreased to 28/14 mmHg, while the SVRI remained within normal limits. PGE₁ administration (0.025 to 0.05 µg•kg^–1•min^–1) was continued until the end of the operation. The patient received 700 ml crystalloid during the operation. Total blood loss was 400 g, and urine output was 800 ml, for an estimated intraoperative fluid balance of -500 ml.

	Discussion

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This report documents a marked decline in cardiac function after closure of an AVF in a patient with a high output state from long-standing and massive shunting through the fistula. The patient presented with mild exertional dyspnea and palpitations. Chest radiography revealed cardiomegaly with mild pulmonary vascular congestion. These clinical data suggest that the patient had high output heart failure and volume overload preoperatively. Contrary to a previous report showing rapid reversibility of heart failure with closure of an AVF,⁷ our patient exhibited significant cardiac depression and pulmonary edema after the closure of his fistula.

High output cardiac failure due to arteriovenous shunting is a complication seen in elderly patients with large, chronic fistulas, and is frequently accompanied by other cardiac abnormalities.⁸ In such patients, cardiac failure may not resolve after closure of the fistula.⁹ In our patient, the SVRI increased (2.6 fold) and the CI decreased (0.6 fold) following clamping of the iliac artery, and the PCWP increased from 15 to 32 mmHg. The patient had no chest pain and ECG showed no ST-T change. In addition, an increase in the height of the v-wave was not observed. These data ruled out ischemic left ventricular failure and mitral regurgitation, and suggested that the sudden increase in afterload resulted in acute left ventricular dysfunction. Subsequent administration of PGE₁ decreased the afterload of both the left and right ventricle¹⁰ and improved cardiac function.

Volume overload is frequently seen in patients with high output cardiac failure.¹¹ Although the patient's intraoperative fluid balance was negative, he developed pulmonary edema postoperatively. Sudden termination of the PGE₁ infusion increased the afterload of both ventricles and this may have led to the second episode of cardiac failure. In addition, return of a normal peripheral vascular resistance, as the effect of the epidural anesthetic receded may have also facilitated congestive heart failure and pulmonary edema. Use of PGE₁, a PDE III inhibitor, and a diuretic were very effective. The PDE III inhibitor amrinone produces pulmonary and systemic vasodilation due to an increase in cyclic nucleosides in vascular smooth muscle, or a decrease in calcium entry and positive inotropic effects.¹²

Ingram et al.⁶ reported similar findings in a patient with a hemodialysis fistula. The patient suffered progressive depression of left ventricular function. He was extremely sensitive to such afterload reducing agents such as nifedipine and captopril. Patients with high output cardiac failure and a chronically low SVRI may be very sensitive both to increases in afterload and to vasodilators.

Epidural blockade is frequently used for vascular surgery. In general, patients undergoing vascular surgery potentially benefit from epidural anesthesia, because the associated sympathetic blockade enhances blood flow to the lower limbs. In patients with AVF, since SVR is low preoperatively, sympathetic blockade further decreases SVR and may induce hemodynamic instability. On the other hand, volume overload is frequently seen in patients with high output cardiac failure, and epidural blockade may be safely induced in these patients. Since AVF may be accompanied by epidural venous engorgement, it is essential for the anesthesiologist to minimize the possibility of accidental intravascular puncture. In addition, the majority of these patients are receiving anticoagulation therapy preoperatively to prevent thrombosis. During surgery heparin is also usually given prior to arterial cross-clamping. Furthermore, in many cases, anticoagulation therapy is continued in the immediate postoperative period. Decisions to use epidural anesthesia with anticoagulation therapy should be made on a case-by-case basis after careful evaluation of the possible risks and benefits.

Surgical closure of an AVF with massive shunting may not always lead to immediate resolution of the high output cardiac failure and may result in a marked decline of cardiac function postoperatively. Afterload management using arterial dilators, "inodilators", and close attention to volume status may be required to achieve a successful outcome after surgical closure of such AVF.

Revision received February 7, 2001. Accepted for publication October 24, 2000.

	References

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