Markedly improved pulmonary function after open heart surgery in infancy utilizing surface cooling, profound hypothermia, and circulatory arrest

Markedly improved pulmonary function after open heart surgery in infancy utilizing surface cooling, profound hypothermia, and circulatory arrest

Markedly Improved Pulmonary Function after Open Heart Surgery in Infancy Utilizing Surface Cooling, Profound Hypothermia, and Circulatory Arrest Paul ...

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Markedly Improved Pulmonary Function after Open Heart Surgery in Infancy Utilizing Surface Cooling, Profound Hypothermia, and Circulatory Arrest Paul G. Barash, MD, New Haven, Connecticut Michael A. Berman, MD, New Haven, Connecticut H. C. Stansel, Jr, MD, New Haven, Connecticut Norman S. Taker, MD, New Haven, Connecticut Leslie H. Cronau, MD, PhD, New Haven, Connecticut

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Methods Twenty-eight consecutive patients requiring open heart surgery were entered into a protocol for surfaceinduced profound hypothermia with circulatory arrest. The patients’ ages ranged from one day to forty-two months (mean, 15.2 months) and weight from 3.3 to 13 kg (mean, 7.6 kg). Diagnoses in the group included fourteen patients with ventricular septal defect, seven with tetralogy of Fallot, three with transposition of the great arteries, two with pulmonary valvular stenosis, one with total anomalous pulmonary venous return, and one with double outlet right ventricle. Preoperative digoxin and diuretics were required in seventeen patients (61 per cent). Five patients (19 per cent) had previous cardiac procedures (3, balloon atria1 septostomy; 1, ligation of a patent ductus arteriosus; 1, resection of coarctation of the aorta).

From the Yale University School of Medicine, New Haven, Connecticut. Reprint requests should be addressed to Paul G. Barash, MD, Department of Anesthesiology, Yale University School of Medicine, 333 Cedar Street, New Haven, Connecticut 06510. Presented at the Fifty-Sixth Annual Meeting of the New England Surgical Society, Portsmouth, New Hampshire, September 25-27, 1975.

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131. April 1978

In general, premeditation consisted of secobarbital (4 mg/kg) and morphine sulfate (0.1 mg/kg) intramuscularly 1 hour before induction of general anesthesia (atropine was administered during induction). Warming lights and a warming blanket were used to maintain the temperature at 37’C until the hypothermic process was begun. Induction was accomplished with 1 to 2 per cent halothane in oxygen. Intubation was facilitated with the use of succinylcholine (1 mg/kg) intravenously. Anesthesia was maintained with nitrous oxide in oxygen and 1 per cent halothane as tolerated. To prevent shivering and as an adjunct to the anesthetic, a muscle relaxant, pancuronium 1 mg, was administered intravenously. Intra-arterial and intravenous catheters were then placed. Maintenance intravenous solution was 10 per cent dextrose in 0.2 normal saline. Surface cooling was begun by application of ice packs. (Figure 1.) Temperature was monitored via tympanic, esophageal, and rectal probes. At a rectal temperature of 28%, the ice was removed and the operation was begun. After appropriate aortic and atria1 cannulation, cardiopulmonary bypass was used to decrease the temperature to its desired level (16 to 20°C rectal). The pump prime consisted of 1,500 cc fresh whole blood, 0.5 gm/kg mannitol, 44.6 mEq sodium bicarbonate, 2 mEq potassium chloride, 6,000 units heparin, and 1.5 gm calcium chloride. Anesthesia during cardiopulmonary bypass was maintained with halothane in 97 per cent oxygen and 3 per cent carbon dioxide. At the desired temperature (16 to 22OC rectal), a bolus of succinylcholine (4 mg/kg) intravenously was given to prevent movement during circulatory arrest. The patient was exsanguinated via the atria1 cannula. The surgical correction was then performed and air evacuation was achieved with subsequent rewarming (35 to 37°C rectal) on cardiopulmonary bypass. Protamine (2 mg/lOO units of heparin), platelet concentrate, and fresh frozen plasma were then administered. After the procedure, evaluation was made for extubation (see Comments). Monitoring for the operation consisted of arterial and venous pressure, electrocardiogram, electroencephalogram, temperature (esophageal, tympanic, and rectal), urine volume, arterial blood gases and pH, blood sugar level, and serum potassium level.

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Figure 1. infant undergoing induction of hypothermia with application of ice packs. TABLE

I

Duration

of Various

Procedure Cardiopulmonary bypass Circulatory arrest Operation Anesthesia

Procedures Range (min)

Mean (min)

16 16 65 125

28.2 31.0 197.5 379.5

to to to to

61 50 400 445

Results Twenty-eight infants with congenital heart disease were entered into this protocol. In three instances, the defects encountered were considered uncorrectable. Three other infants died postoperatively of low cardiac output that was unresponsive to resuscitative measures and will not be considered further. The remaining twenty-two infants are long-term survivors with follow-up to eighteen months. The duration of various parts of the procedure are listed in Table I. Of the twenty-two survivors, eleven (50 per cent) were extubated in the operating room and five other children (23 per cent) in the recovery room within 70 minutes. Only five of twenty-two patients (23 per cent) required mechanical ventilation. Four of the five who required mechanical ventilation were extubated within 24 hours (mean, 19.05 hours). One patient, intubated preoperatively with a history of meconium aspiration as a newborn, required tracheostomy and prolonged ventilatory support. He was successfully extubated on day 13. Three of the patients requiring mechanical ventilation also had positive end expiratory pressure instituted. The follow-up of the twenty-two survivors revealed no evidence of subglottic stenosis or further pulmonary problems. Complications included postcardi-

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otomy syndrome (2 patients, sternal dehiscence (l), seizure secondary to hypocalcemia (l), and reintubation (1). These were treated early and without sequelae. The patient who required reintubation deserves special attention. She was a six month old, 7 kg infant with transposition of the great arteries who underwent a Mustard procedure and required mechanical ventilation for 18 hours before she met our criteria for extubation. Right middle lobe atelectasis developed 36 hours after extubation and the patient required endotracheal suction under direct vision. The next day she sustained lobar collapse again and required mechanical ventilation for 48 hours. After extubation on two separate occasions during her hospitalization, she again suffered lobar collapse and required endotracheal suction under direct vision. After these two episodes, her postoperative course was uneventful and she sustained no further cardiac or pulmonary complications. Comments A review of the literature suggests that mechanical ventilation is widely used in the postoperative support of infants and children undergoing cardiac surgery [1,2]. whereas some clinics use elective postoperative ventilation for 24 hours, mechanical ventilation can also be a liability. The improvement of pulmonary function; which decreases the need for mechanical ventilation, also helps to prevent iatrogenic complications. Downes et al [1] noted four deaths directly related to ventilatory treatment in a series of infants undergoing cardiac surgery. Stewart et al [2] have reported that occasionally pulmonary dysfunction either persisted or worsened with mechanical ventilation. In another series of fifty pediatric patients requiring longterm nasotracheal intubation, 14 per cent required tracheostomy for laryngeal edema, obstruction, or ulceration [3]. Not only are airway problems of concern, but another important risk factor is infection. Verhoog-Bloembergen and Leader 143 reported a 71 per cent infection rate in infants after nasotracheal intubation 11 per cent of whom died due to pneumonia. Battersby and Glover [5] state: “Changes are continuing to take place in this field but ventilatory support is likely to become of increasing importance as the age of corrective surgery is lowered.” Our clinical experience indicates that as the patient’s age at surgery decreases, postoperative pulmonary function can be improved as a result of improved technics in cardiac surgery and anesthe-

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improved Postoperative Pulmonary.Function

sia, and the need for mechanical ventilation postoperatively should be diminished. Recent experience indicates that intracardiac surgery can be safely performed in neonates and infants with the use of surface-induced profound hypothermia and circulatory arrest in conjunction with limited cardiopulmonary bypass [6-B]. The advantages of this technic include improved visualization of the defect, minimization of metabolic disturbances during cooling and rewarming, and decrease in perfusion time. An added benefit of this technic appears to be the lack of pulmonary complications in a group that is at higher morbidity and mortality risk. [I]. Not only are the pulmonary complications minimal, but this group of patients appears to have a decreased need for mechanical ventilation postoperatively. Certain features in our protocol deserve special attention in regard to the maintenance and subseimprovement quent of pulmonary function throughout the perioperative period. First, an inhalational agent, halothane, is used as a primary anesthetic. The advantage of this agent is that it allows relatively rapid excretion of the anesthetic at termination of the procedure. Intravenous agents require metabolic breakdown for their ultimate elimination and since we are managing neonates who have immature metabolic pathways and older infants whose metabolic pathways can be altered by the hypothermic process, it seems reasonable to avoid the prolonged respiratory depressant effect of these agents. Also, we can modulate the cardiovascular responses in an enriched oxygen atmosphere [9]. The vasodilation caused by halothane helps to achieve hypothermia. Finally, halothane is a potent bronchodilator, which can serve as an aid to intraoperative pulmonary toilet [IO]. Increased oxygen consumption due to hypothermia can cause further cardiopulmonary decompensation in the unanesthetized patient. Even with mild levels of hypothermia (35 to 36’C) oxygen consumption can be doubled in anesthetized infants who weigh less than 12 kg [II]. Thus, throughout the entire period of induction of anesthesia and until ice packs are placed, warming lights and a warming blanket are used to maintain the body temperature at 37’C. In addition, a muscle relaxant, pancuronium, is administered to prevent shivering. Intraoperative correction of metabolic acidosis with sodium bicarbonate is kept to a minimum to prevent postoperative-metabolic alkalosis. In this series, the initial metabolic acidosis decreased after rewarming on cardiopulmonary

bypass. Thus, the base deficit after induction of anesthesia averaged 7.1 mEq/L. The base deficit decreased to 3.2 mEq/L 30 minutes after the cessation of cardiopulmonary bypass and rewarming. This agrees with the observation of Johnston et al [12] and further confirms the earlier work of Ballinger et al [13] that showed maintenance of hepatic function on rewarming can facilitate the correction of the metabolic acidosis which results from hypothermia. After the sternum is closed, mechanical ventilation is discontinued and the anesthesiologist assists ventilation. Thus, by the time the skin incision is closed the patient can have an excellent tidal volume. The tracheobronchial tree is then irrigated with normal saline and suctioned until there is no longer any secretions. At this point, the patient is evaluated for extubation. Criteria for extubation include: (1) cardiovascular and pulmonary stability; (2) adequate level of consciousness; (3) tidal volume greater than 6 cc/kg; (4) vital capacity (if possible) 12 to 18 cc/kg; (5) negative inspiratory force greater then -20 cmHz0 [14]; and (6) satisfactory arterial blood gases during spontaneous ventilation. If all criteria are met, the patient is extubated. For the next 5 minutes, while the patient is breathing 100 per cent oxygen via face mask, repeat arterial blood gases are analyzed. If these are satisfactory, the patient is moved to the pediatric cardiovascular recovery unit. On arrival, intermittent positive pressure breathing with racemic epinephrine (Vaponephrinea) is administered in a 1:8 dilution for prophylactic therapy of post-intubation laryngeal edema [15]. After this, two consecutive treatments are made with the dronchodilator isoetharine (BronkosoP). These drugs are used to form the foundation of active pulmonary therapy on the part of our nursing and respiratory therapy staff. (Figure 2.) As an adjunct to clinical judgment, adherence to this protocol has resulted in only one infant requiring mechanical ventilation for more than 24 hours. If the patient has not met our criteria for early extubation, mechanical ventilation is instituted. Coordination of the patient with mechanical ventilation is achieved by neuromuscular blockade with intermittent infusion of pancuronium. Sedation is maintained by administration of morphine (0.05 to 0.1 mg/kg) as needed. When cardiopulmonary stability is achieved, the weaning process is begun. The patient is then extubated after the previously described criteria are met. (Figure 3.)

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Summary

The use of surface-induced profound hypothermia with limited cardiopulmonary bypass and circulatory arrest markedly diminished the need for mechanical ventilation for patients undergoing cardiac surgery. Eleven of twenty-two patients were extubated in the operating room and five more patients within 70 minutes postoperatively. Five patients required mechanical ventilation. Four of the five were extubated within 24 hours (mean, 19.05 hours); only one patient required mechanical ventilation greater than 24 hours. This experience would indicate that as the age of surgery is decreased, in conjunction with improved technics of cardiac surgery and anesthesia, the need for mechanical ventilation should be diminished.

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Figure 2. Physiologic data obtained in a fourteen month old, 7.1 kg infant with a ventricular septal defect. This patient’s data represent the typical case of extubatton in the operating room. Blood gas and pH values are corrected to the patient’s temperature. (FIo2 = fractional concentration of oxygen In the inspired gas.)

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Figure 3. Physiologic data of a twenty-one month old, 10.5 kg Infant with a ventricular septal defect and anomalous right ventricular muscle bundle. This is an exampte of the short-term (less than 24 hours) mechanical ventl/at/on required in four of the patients. Note the dramatic response to positive end expkatory pressure and its early discontinuance with maintenance of excellent arterial blood gases. Blood gas and pH values are corrected to the patient’s temperature.

Reference5 1. Downes JJ, Nicodemus HD, Pierce WW, Waldhausen JA: Acute respiratory failure in infants following cardiovascular surgery. J Thorac Cardiovasc Surg 59: 21, 1970. 2. Stewart S, Edmunds LH, Kirklin JW, Allarde RR: Spontaneous breathing with continuous positive airway pressure after open intracardiac operations in children. J Thorac Cardiovasc Surg 65: 37, 1973. 3. McDonald IH, Stocks JG: Prolonged nasotracheal intubation. Br JAnaesthesiol37: 161. 1965. 4. Verhoog-Bloembergen MPJ. Leader GL: Long-term nasotracheal intubation. Int Anesthesiol C/in 12: 24 1, 1974. 5. Battersby EF, Glover WJ: Management of respiratory insufficiency in infants with congenital heart disease. ht Anssthesiol C/in 12: 141, 1974. 6. Barrat-Boyes BG, Simpson M, Neutze J: Intracardiac surgery in neonates and infants using deep hypothermia with surface cooling and limited cardiopulmonary bypass. Circu-

The American Journal of Surgery

Improved

lation 43: 25, 1971. 7. Venugopal P, Olszowka J, Wagner H, Vlad P, Lambert E, Subramanian S: Early correction of congenital heart disease with surface induced deep hypothermia and circulatory arrest. J Thorac Cardiovasc Sura 66: 375, 1972. 6. Mori A, Muraoka R, Yokota Y, Okamata Y, Ando F, Fukumasu H, Oku H, lkeda M, Shirotani H, Hikasa Y: Deep hypothermia combined with cardiopulmonary bypass for cardiac surgery in neonates and infants. J Thorac Cardiovasc Surg 64: 422. 1972. 9. Barash PG, Hobbins JC, Hook R, Stansel HC, Wittemore R, Hehre FW: Management of coarctation of the aorta. J Thorac Cardiovasc Surg 69: 76 1 I 1975. 10. Avaido DM: Regulation of bronchomotor tone during anesthesia. Anesthesiology 42: 66, 1975. 11. Hendren WH: Pediatric surgery. N Engl J Med 289: 456, 1973. 12. Johnston AE, Radde IC, Stewart DJ, Taylor J: Acid-base and electrolyte changes in infants undergoing profound hypothermia for surgical correction of congenital heart defects. Can Anaesth Sot J 2 1: 23, 1974. 13. Ballinger WF, Vollenvieder H, Templeton JY. Pierucci J: Acidosis of hypothermia. Ann Surg 154: 517, 1961. 14. Wescott DA, Bendixen HH: Neostigmine as a curare antagonist: a clinical study. Anesthesiology 23: 324, 1962. 15. Jordan WS, Graves CL, Elwyn RA: New therapy for post-intubation laryngeal edema and tracheitis in children. JAMA 212: 585, 1970.

Discussion Mortimer J. Buckley (Boston, MA): The group at New Haven have done an outstanding job in the management of infants with cardiovascular disease, and Doctor Stansel has shown an ever increasing success with his approach. The series reported today certainly outlines an excellent technic to reduce the need of prolonged ventilation in the postoperative period. We have found that other technics, however, have shown similar improvement with core cooling (cooling of the infant by perfusion) that we have the same average perfusion time since the pump is shut off during the correction. Our difficulties with respiratory complications postoperatively have been related to two factors. First,

volume 131, Aore

1976

Postoperative

Pulmonary

Function

the amount of hemodilution that was carried out in the infant younger than six months, and especially in the first month of life. This seems to he related to the dilution of protein and total osmdlarity with resulting increased permeability of the capillaries. As we have corrected this, there has been less edema formation in the infants. Second, we use spontaneous ventilation with expiratory resistance in the early postoperative period. This was suggested by Doctor Kirklin a number of years ago and we have found this extremely helpful. I would like to ask the authors two questions. How successful is their technic in the infant younger than six months and especially in the first months of life? Have they found any difference in the respiratory management of infants with decreased pulmonary blood flow as opposed to infants with increased pulmonary blood flow? Our problem has been predominantly with those infants in whom flooding of the lungs has developed after relief of pulmonic obstruction.

Paul G. Barash (closing): When we used the core cooling technic, pulmonary hemorrhage was a problem. However, since we began using the surface-induced profound hypothermia technic, no infant has had this complication. I think there are three reasons for the improvement. First, with operation on the infants at an early age, perhaps, the pulmonary changes are more easily reversed. Second, there is a decreased time on cardiopulmonary bypass. Third, we are using a non-narcotic anesthetic which does not commit our patient to prolonged mechanical ventilation postoperatively. Occasionally, young infants require mechanical ventilatory support. However, postoperatively, we rely primarily on neuromuscular blockade supplemented with a minimum dose of narcotics to achieve coordination of the patient with the ventilator. Thus, we are able to wean patients from the respirator earlier and we think we can prevent pulmonary and laryngeal complications.

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