Anesth Analg 2000;91:1134-1136
© 2000 International Anesthesia Research Society
CARDIOVASCULAR ANESTHESIA
An Unusual Presentation of Atrial Septal Defect in a Patient Undergoing Total Hip Arthroplasty
Barbara A. Marak, MD*,
Denise J. Wedel, MD*, and
Naser M. Ammash, MD
Departments of
*Anesthesiology and
Internal Medicine, Mayo Clinic, Rochester, Minnesota
Address correspondence and reprint requests to Denise J. Wedel, MD, Department of Anesthesiology, Mayo Clinic, 200 First St. SW, Rochester, MN 55905. Address e-mail to wedel.denise{at}mayo.edu
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Abstract
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Implications: Atrial septal defect is usually diagnosed and surgically repaired in childhood. We present a case of previously asymptomatic atrial septal defect that presented during total hip arthroplasty during general anesthesia in a 72-yr-old woman. Intraoperative transesophageal echocardiography assisted in the diagnosis and in determining the appropriate treatment.
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Introduction
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Atrial septal defect (ASD) is the second most common adult congenital heart defect after bicuspid aortic valve. It accounts for approximately 25% of all lesions seen in this population (1). Although most lesions are diagnosed and often repaired in childhood, ASD can remain unrecognized until adulthood. Morbidity and mortality of uncorrected defects increase with advancing age (2). Previous studies by Fahmy and Schiavone (3) and Hamilton et al. (4) have demonstrated that, by age 40 yr, 35%–60% of patients with ASD have a murmur or are symptomatic. Presenting symptoms are usually dyspnea on exertion and, less commonly, fatigue, atrial arrhythmias, or paradoxical emboli. We report an asymptomatic 72-yr-old woman with initial presentation of acute oxygen desaturation reversed by vasopressor treatment during routine total hip arthroplasty under general anesthesia. Diagnosis of ASD with bidirectional shunt was made intraoperatively with transesophageal echocardiography (TEE).
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Case Report
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A 72-yr-old woman with a history of untreated hypertension and two previous remote (1990 and 1993) transient ischemic attacks with amaurosis fugax (right eye), one with associated with left face and arm numbness, presented with degenerative joint disease requiring left total hip arthroplasty. Medications included aspirin, ranitidine, and gemfibrozil. Preoperative blood pressure (BP) was 162/98 mm Hg with a heart rate of 72 bpm. The remainder of her cardiovascular examination was unremarkable. Specifically, no murmur was heard. The preoperative electrocardiogram showed an unusual p axis, with possible ectopic atrial rhythm, but was otherwise normal. Chest radiograph revealed mild cardiac enlargement with a prominent left ventricle. Electrolytes and hemoglobin were normal. The patient refused regional anesthesia. Because of a symptomatic hiatal hernia, a rapid sequence IV induction technique with etomidate, fentanyl, and succinylcholine was chosen. The trachea was intubated without difficulty, and a radial arterial catheter was placed to monitor BP. Maintenance anesthesia included isoflurane, 70% N2O in oxygen, and oxymorphone. Her preanesthetic BP of 167/81 mm Hg decreased to 92/55 mm Hg after the induction. After ephedrine 10 mg IV, the BP was maintained between 118–145 and 70–85 mm Hg and SpO2 between 96% and 99%. At the surgeon’s request and considering her penicillin allergy, gentamicin and vancomycin were given. The patient was placed in the right lateral decubitus position. Approximately 1 h after incision, before reaming the femoral shaft, her systolic BP decreased from 128 to 110 mm Hg, and her SpO2 to 93%–96%. Blood loss measured approximately 300 mL, and 1500 mL of lactated Ringer’s solution had been infused. Delivered oxygen was increased to 100% and Hetastarch 500 mL was started. Hemoglobin level was 12.2 g/dL, and arterial blood gas analysis revealed a pH 7.40, PaO2 58 mm Hg, PaCO2 39 mm Hg, SpO2 90%. Immediately after the sample was drawn, the patient suddenly became increasingly hypoxemic with SpO2 values in the 80% range. Her BP remained stable between 115 and 120 mm Hg systolic. SpO2 decreased to the 60% range; mechanical ventilation was discontinued, and manual ventilation was initiated. Auscultation confirmed bilateral breath sounds. The endotracheal tube was suctioned; no fluid or mucus plug was found. Bronchoscopy by the consultant anesthesiologist was nondiagnostic. A second arterial blood gas analysis 10 min after the first revealed a pH of 7.49, PaO2 46 mm Hg, PaCO2 31 mm Hg, SpO2 85%. A tentative diagnosis of pulmonary embolus was considered, and a phenylephrine drip was begun to sustain BP. Emergency intraoperative TEE was requested. During the equipment setup, BP increased to more than 200 mm Hg systolic and SpO2 immediately increased to 100%. The TEE revealed a 1.0-cm secundum ASD with a bidirectional shunt, inferior wall hypokinesis that resolved at the end of the study, but overall preserved systolic function (Figure 1). As the phenylephrine was gradually decreased, a dopamine drip was started and filters placed on all IV infusion devices. At the completion of surgery, the patient was taken to the recovery room, tracheally extubated, and given oxygen by mask. Pharmacologic support to maintain adequate BP was gradually decreased over the next several hours, and supplemental oxygen withdrawn over two days. Neurology and cardiology consultation revealed no evidence of new stroke and recommended transcatheter closure of her ASD. Postoperative echocardiography two days after surgery showed a left-to-right shunt at rest, increased right ventricular systolic pressure (59 mm Hg) and mild-to-moderate tricuspid regurgitation. After 21/2 mo of anticoagulation with coumadin, the patient returned for ASD closure with an atrial septal occluder device by catheter technique. Postprocedure echocardiography revealed no residual shunt.
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Figure 1. Transesophageal echocardiography short axis view at the level of the ascending aorta demonstrating the 1-cm secundum atrial septal defect (arrow). Ao = aorta, LA = left atrium, MPA = main pulmonary artery, RA = right atrium.
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Discussion
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Considered one of the most common congenital cardiac anomalies in adults, ASD is seldom diagnosed beyond age 70 years, but there are rare reported cases (5–8). The physiology of ASD involves a left-to-right shunt that develops early in infancy, after the fetal right ventricular hypertrophy and pulmonary vascular resistance decrease postnatally. As right heart ventricular volume overload develops, pulmonary blood flow increases enough to produce a murmur often diagnosed around age 2–3 years (9). An isolated ASD in adults most commonly presents with dyspnea, atrial arrhythmias, and as congestive heart failure (10), with the severity of shunting determined primarily by the size of the defect and the ratio of systemic to pulmonary vascular resistance. However, adults often lack both obvious murmurs or symptoms, making diagnosis more difficult than in children (1).
Although a left-to-right intracardiac shunt is the rule, any condition that upsets the relative pressure gradient across the ASD may change the shunt direction resulting in hypoxemia and possible paradoxical embolization. Significant hypertension, as in our patient, helps maintain the left-to-right intracardiac shunt. An uncorrected large (>2 cm) ASD can be complicated by pulmonary hypertension (6%–13%) with reversal or bidirectional shunt between pulmonary and systemic circulations, but this rarely presents intraoperatively (3). The etiology of our patient’s shunt reversal and hypoxemia was likely multifactorial. General anesthesia increases the PA-aO2 gradient and shunt (12). Mechanical ventilation also causes intraoperative right-to-left intracardiac shunting (11).
Relative systemic hypotension in a patient with poorly controlled hypertension, such as ours, could have been potentiated by isoflurane, infusion of vancomycin, and decreased vascular volume from blood loss and dehydration. The transient right ventricular hypokinesis seen on TEE may have increased right atrial pressures, contributing to the shunt. Flow across an ASD is dependent on the ratio of systemic to pulmonary vascular resistance. A decrease in systemic vascular resistance will favor right-to-left intracardiac shunting, whereas increasing systemic resistance will increase the right-to-left shunt. Pulmonary embolus as a cause for this finding cannot be definitively eliminated, although no embolus was seen on TEE. Hypoxemia may have been exacerbated by occult thromboembolism or fat embolism. Embolic events can accompany femoral shaft manipulation (which had not yet occurred in this case) but can also occur earlier in the procedure during surgical dissection and retraction. As the systolic BP increased, our patient’s relative pressure gradient changed back to left-to-right with resolution of her hypoxemia.
Intraoperative hypoxemia can have many etiologies. Described causes that must be eliminated include equipment failure, mainstem bronchial or esophageal intubation, aspiration of foreign material or airway obstruction, pneumothorax, bronchospasm, atelectasis, pulmonary edema, or pulmonary embolism from thrombus, fat, or air (12). Postoperative evaluation of the patient did not determine any other pathology, which could explain the intraoperative findings. The presence of a moderate-size ASD with bidirectional shunt and the temporal improvement in symptoms with an increase in BP supported the ASD as being the most likely etiologic factor. Reversal of an intracardiac shunt in an adult is unusual, but must be considered.
Postoperative management involves maintenance of the normal shunt by avoiding agents or procedures that could upset the existing balance. The risk of paradoxical emboli is significant and warrants evaluation. This was considered a probable etiology of our patient’s previous transient ischemic attacks, which involved at least two different cortical areas, resulting in the cardiologist’s decision to close her ASD without further evaluation.
Lack of obvious preoperative symptoms or murmur in an elderly patient made the intraoperative diagnosis of ASD and resultant hypoxemia more elusive in this case. TEE provided valuable information and a definitive diagnosis leading to prompt and appropriate perioperative management in this patient.
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References
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Accepted for publication July 10, 2000.
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Abstract
Introduction
