Cardiovascular Responses to PEEP and CPAP Following Repair of Complicated Congenital Heart Defects

Cardiovascular Responses to PEEP and CPAP Followiig Repair of Complicated Congenital Heart Defects James M. Levett, M.D., Walter S. Culpepper, M.D., C. Y. Lin, M.D., Rene A. Arcilla, M.D., and Robert L. Replogle, M.D. ABSTRACT Fourteen infants and children ranging in age from 7 months to 8 years were studied in a hernodynamically stable condition following repair of various heart defects. Changes in cardiac index, stroke index, heart rate, systemic vascular resistance, mean arterial pressure, and central venous pressure were evaluated at levels of 0 , 5 , and 10 cm H 2 0 using positive end-expiratory pressure (PEEP) in 14 patients and continuous positive airway pressure (CPAP) in 3 patients. No significant changes were found in any of the measurements taken at the different levels.

The benefits of positive end-expiratory pressure (PEEP) and continuous positive airway pressure (CPAP) in the treatment of arterial hypoxemia unresponsive to increasing levels of the inspired oxygen concentration ( F I O ~ )are well established. Various clinical and experimental studies have been done correlating levels of PEEP with changes in pulmonary compliance, functional residual lung capacity, cardiac output (CO), left and right atrial pressures, pulmonary artery pressures, and blood gas determinations [l-61. Most clinical studies utilizing actual CO measurements have been done in adults, however, and little is known about the cardiovascular effects of PEEP and CPAP in infants and children. We report our studies of these effects in 14 infants and children after open-heart procedures. Patients and Methods Fourteen infants and children ranging in age from 7 months to 8 years were studied between From the Departments of Surgery, Anesthesiology, and Pediatrics, The Pritzker School of Medicine, University of Chicago, Chicago, IL. Accepted for publication Nov 9, 1982. Address reprint requests to Dr. Levett, Department of Surgery, 950 E 59th St, Chicago, IL 60637.

411

September, 1975, and November, 1980. The types of lesions involved and associated data are listed in Table 1. Seven patients underwent complete repair of the cardiac defect performed with standard techniques of cardiopulmonary bypass, and 7 patients underwent repair procedures using deep hypothermia and circulatory arrest at temperatures of 18" to 20°C as described in a previous report [7]. Following termination of bypass, a 3F Kimray thermistor wire+ was inserted into the pulmonary artery and secured with a small pursestring suture. A central venous pressure catheter was placed in the right atrium and its position verified at operation. All patients were studied during the first 24 hours after operation at a time when the condition of each was stable. Cardiac output was determined by the thermodilution technique using a Kimray Model 3500 thermodilution CO computer* attached to a strip-chart recorder. The techniques described in this article had been validated previously in canine laboratory experiments in which thermodilution CO determinations were compared with those obtained using an electromagnetic flowmeter; an r value of 0.98 was obtained by linear regression in comparing the two methods [8]. The quality of thermodilution curves was assessed on the recorder, and poor curves were discarded. Three milliliters of a solution of 5% dextrose in water at room temperature was injected into the right atrial catheter for each determination, and a total of three to five measurements was averaged for each CO data point. These measurements were begun with the patient on 0 cm H 2 0 of end-expiratory pressure and repeated after PEEP or CPAP was increased to 5 or 10 cm H 2 0 for 20 to 30 minutes. All patients were intubated and mechanically 'Kimray Medical Associates, Oklahoma City, OK.

412 The Annals of Thoracic Surgery Vol36 No 4 October 1983

Table 1. Clinical Characteristics of Study Patients Patient No. Age

Weight (kg) Diagnosis Operation

9mo 16mo 15mo 18mo 10mo 10mo 8mo

5.9

7mo

4.2

AV canal AV canal AV canal AV canal AV canal AV canal AV canal AV canal

18mo

9.7

VSD

10

10 mo

4.5

ASD, VSD

11

12 mo

7.6

ASD,

12

8 yr

23.0

VSD VSD

13

32 mo

12.2

Tetralogy

Complete repair Complete repair Complete repair Complete repair Complete repair Complete repair Complete repair Complete repair Patch closure of VSD Closure of ASD and VSD Closure of ASD and VSD Patch closure of VSD Complete repair

14

4 yr

15.7

Tetralogy

Complete repair

1 2

3 4

5 6 7 8 9

7.6 5.6

7.7 5.4 5.5

4.5

of Fallot

of Fallot

AV = atrioventricular; VSD ASD = atrial septal defect.

=

ventricular septal defect;

ventilated with a Bennett MA-1 volume-cycled respirator at a tidal volume of 10 to 15 cc per kilogram and F I O ~of 0.35 to 0.6. Positive endexpiratory pressure was instituted using the standard respirator setting for increasing endexpiratory pressure. Patients on CPAP were placed on a Bourns CPAP device at F102 of 0.35 to 0.6. No changes were made in F1OZ for any patient during the experimental period, and drug infusions also remained constant during this time. Blood gas determinations were done within five minutes of collection using a Radiometer Model ABC 1 micro-blood gas analyzer (Radiometer, The London Co., Cleveland, OH) and corrected for the patient’s temperature. Pressures were measured with Statham P23 Db or Ailtech pressure transducers calibrated to a mercury standard with the level of the right atrium used as the zero reference point in all calibrations. Calculations were made according to the following formulas. Cardiac index (CI), expressed

in liters per minute per square meter of body surface area (BSA), was obtained by dividing the CO by the BSA. Stroke index (SI), expressed in milliliters per square meter of BSA, was obtained by dividing the CI by the heart rate. Finally, systemic vascular resistance (SVR) in dynes sec cmp5/m2 was determined by this formula: SVR

=

[(MAP - CVP) 79.9]/CI

where MAP is the mean systemic arterial pressure and CVP is the mean central venous pressure.

Results The results are shown in Tables 2 and 3, which represent separate experiments for levels of PEEP and CPAP, respectively, in different groups of the 14 patients. Each patient served as his or her own control, and PEEP and CPAP were not compared against each other. Results for PEEP are expressed as mean values ? standard error of the mean. There were no significant differences in any of the measured values at 0,5, and 10 cm H 2 0 of PEEP when analyzed using the Student paired t test. The small number of patients who were studied using CPAP prevents any statistical analysis, and the data are therefore presented as obtained. Comment The concept of using PEEP to improve blood oxygenation was introduced into the clinical setting over 10 years ago. Early reports showed clearly that arterial oxygen tension and saturation were improved with an increase in functional residual lung capacity and a decrease in intrapulmonary shunting [9, lo]. Clinical studies in adults and experimental studies in animals have examined the effect of PEEP on CO and various filling pressures of the heart. Early studies by Cournand and associates [ll],in 1948, demonstrated decreased CO associated with decreased net right ventricular filling pressures in human beings receiving intermittent positive-pressure breathing by mask with PEEP. Later reports by Lutch and Murray [12], Qvist and colleagues [13], and Sykes and

413 Levett et al: Cardiovascular Responses to PEEP and CPAP

Table 2. Changes in Cardiovascular Variables with Varying Levels of PEEPalb Level of PEEP Experiment 1 (N Variable

0 cm H 2 0

30.07

Experiment 2 (N

12)

5 cm H 2 0

3.76 t 0.44

Cardiac index (L/min/m*) Stroke index (ml/m2) Heart rate (beatdmin) Systemic vascular resistance (dynes sec ~ m - ~ / m ~ ) Mean arterial pressure (mm Hg) Central venous pressure (mm Hg) PaOz (mm Hg) PaC02 (mm Hg)

=

0 cm H 2 0

3.79 t 0.34

=

14)

10 cm H 2 0

3.65 t 0.33

3.54 t 0.29

2.77

29.89 t 3.27

29.8

4.03

30.98 2 3.67

218.3 t 4.09

126.7 t 3.99

123.3 t 4.98

122.2 t 4.58

1,411

1,364 t 259

1,411 t 237

1,241 t 89

?

?

237

?

64.27 t 2.01

67.25 t 2.57

64.8 t 3.08

68.3 t 3.49

11.35 +- 1.15

11.23 t 1.15

13.8 t 1.08

15.9 t 1.15

113 t 14.5

125.3 t 11.8

107.3 t 15.9

29.5 t 3.09

27.0 t 4.88

28.1 t 3.26

127.6

rt

12.3

32.3 t 3.0

"Values shown are mean 2 standard error of the mean. b T ~ different o experiments were conducted in the same group of patients. PEEP = positive end-expiratory pressure; Pa02 = partial pressure of arterial oxygen; PaC02 = partial pressure of arterial carbon dioxide.

Table 3 . Changes in Cardiovascular Variables at Varying Levels of CPAP in 3 Patients Level of CPAP Patient 6

Cardiac index (L/min/m2) Stroke index (ml/m2) Heart rate (beatdmin) Systemic vascular resistance (dynes sec cmP5/m2) Mean arterial pressure (mm Hg) Central venous pressure (mm Hg) Pa02 (mm Hg) PaC02 (mm Hg)

Patient 8 10cm

Patient 9

Ocm H20

5cm H20

H20

Ocm H20

5cm H20

10cm H20

Ocm H20

5cm H20

10cm HI0

2.80

3.04

2.93

5.28

6.09

6.69

3.11

3.20

4.0

26.2

27.9

28.5

44.74

52.95

57.67

31.1

30.7

40.0

107

109

103

118

115

116

100

104

100

999

737

927

529

524

550

1,875

1,701

1,258

53

48

52

50

53

52

85

81

83

18

20

18

15

13

6

12

13

20

240 28

175 19

200 25

36 28

40 32

53 24

69 36

73 43

67 47

CPAP = continuous positive airway pressure; PaOz arterial carbon dioxide.

=

partial pressure of arterial oxygen; PaCOZ = partial pressure of

414 The Annals of Thoracic Surgery Vol 36

No 4 October 1983

co-workers [14] confirmed these observations and suggested that CO would be better maintained with higher CVP when PEEP is used. Decreases in CO with PEEP were found by Powers and associates [15] to be associated with increases in pulmonary vascular resistance; there was no depression of CO with PEEP in half of their series. Sugerman and colleagues [16] reported on 8 patients with diffuse interstitial pulmonary edema and found no appreciable effect of PEEP on CO, SVR, or pulmonary vascular resistance. Kumar and co-workers [lo] noted normal or greater than normal CI with PEEP in 8 patients with acute respiratory failure, and Harken and associates [17] found improvement in CO with PEEP following cardiac operations in patients with a higher left ventricular end-diastolic pressure (LVEDP)(12.9 5 1.1 mm Hg) compared with those who had a lower LVEDP (7.6 2 1.1 mm Hg). Kirby and colleagues [ 181 studied patients given large amounts of PEEP and reported no adverse effect on CO at levels up to 4.4 cm H20. The use of mechanical ventilation in infants and children with respiratory failure following cardiac operations has been routine since the late 1960s and is well summarized in the comprehensive article by Downes and co-workers [19] published in 1970. Pick and associates [20] demonstrated an increase in functional residual lung capacity associated with an increase in arterial oxygenation in 10 children who were put on mechanical ventilation with PEEP after open-heart operations. The use of PEEP in infants and children decreased largely because of the interest engendered in the use of CPAP, reported by Gregory and colleagues 1211 in 1971 as a treatment for newborn idiopathic respiratory distress syndrome. Many studies of CPAP soon followed, including several reports showing the efficacy of this method in managing infants and children following open-heart procedures [22, 23, 241. Hatch and co-workers [25] showed the benefit derived from CPAP used after openheart operations in infants with preoperative pulmonary venous obstruction and low postoperative compliance. In 1975, Gregory and associates [26] found low functional residual lung capacity following cardiac procedures in infants less than 3 months of age and demonstrated

increases in this variable of 33% and 35% in acyanotic and cyanotic infants, respectively, following administration of 5 mm Hg of CPAP. Although no clinical studies of CO in this age group are available, it has been shown experimentally in piglets that CPAP lowers both MAP and CO [27, 281. The present study was undertaken in an attempt to assess the cardiovascular effects of PEEP and CPAP following open-heart operations in children with congenital defects. Our results show that the increase in systemic arterial oxygenation is not accompanied by significant changes in CI, SI, heart rate, SVR, MAP, or CVP at levels of 5 and 10 cm H 2 0 of PEEP. Although not statistically significant because of the small number of patients, the data on CPAP would also suggest preservation or possibly even augmentation of CO at levels of 5 and 10 cm H 2 0 of CPAP. Despite the fact that CVPs relative to atmosphere were measured in this study instead of transmural pressures (since intrapleural pressures were not measured), the overall results for CVP and SVR were not affected. Several aspects of this study warrant discussion. Although the preoperative conditions of these children were variable and included differences in the degree of congestive heart failure as well as differences in pulmonary vascular resistance, all of the patients were studied in a stable hemodynamic condition postoperatively and were therefore comparable in that respect. Patients in an unstable condition might well have had different responses to our interventions. It would have been advantageous to measure pulmonary artery and left-sided pressures in order to calculate changes in pulmonary vascular resistance. Since this was not done in the study, no statement can be made about the effects of PEEP and CPAP upon pulmonary vascular resistance in these patients. Finally, it should be noted that samples were taken routinely from the superior vena cava and pulmonary artery following termination of cardiopulmonary bypass in the operating room in order to check for residual shunts; none were found in any of the study patients. If functional residual lung capacity is indeed depressed following open-heart procedures in

415 Levett et al: Cardiovascular Responses to PEEP and CPAP

infants as demonstrated by Gregory and colleagues [26], then the lack of effect on CO of PEEP and CPAP is not surprising. Suter and coworkers [29] have shown in adults with respiratory failure that low initial values of functional residual capacity are associated with the greatest benefit from PEEP and that maximum oxygen transport is achieved at levels of PEEP corresponding to maximum static compliance. It is possible that higher levels of PEEP or CPAP would have produced different results in our study; this was not tested, however, since such levels are rarely used clinically. Neither pulmonary compliance nor pulmonary vascular resistance was measured in this investigation. These would be of interest in future studies to assess the effect of preexisting pulmonary disease on response to PEEP and CPAP. Adults with emphysema have high levels of functional residual lung capacity and increased pulmonary vascular resistance, and such patients characteristically respond to PEEP by decreases in CO [30]. However, such correlations have not been demonstrated in infants and children. We conclude that levels of PEEP and CPAP up to 10 cm H 2 0 may be used in hemodynamically stable infants and children following repair of congenital heart defects and that no marked changes in cardiovascular measurements can be expected to occur. Supported in part by a grant (RR-305) from the General Clinical Research Centers Programs of the Division of Research Resources, National Institutes of Health.

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5. Cassidy SS, Robertson CH, Pierce AK, Johnson RL: Cardiovascular effects of positive endexpiratory pressure in dogs. J Appl Physiol 44:743, 1978 6. Liebman PR, Patten MT, Manny J, et al: The mechanism of depressed cardiac output on positive end-expiratory pressure (PEEP). Surgery 83:594, 1978 7. Lamberti JJ, Lin CY, Cutiletta A, et al: Surface cooling (20°C) and circulatory arrest in infants undergoing cardiac surgery. Arch Surg 113:822, 1978 8. Beyer J, Lamberti JJ, Replogle RL: Validity of thermodilution cardiac output determination: experimental studies with and without pulmonary insufficiency. J Surg Res 21:313, 1976 9. McIntyre RW, Laws AK, Ramachandran PR: Positive expiratory pressure plateau: improved gas exchange during mechanical ventilation. Can Anaesth SOC16:477, 1969 10. Kumar A, Falke JJ, Geffin B, et al: Continuous positive-pressure ventilation in acute respiratory failure: effects on hemodynamics and lung function. N Engl J Med 283:1430, 1970 11. Cournand A, Motley HL, Werko L, Richards DW: Physiological studies of the effects of intermittent positive pressure breathing on cardiac output in man. Am J Physiol 152:162, 1948 12. Lutch JS, Murray JF: Continuous positivepressure ventilation: effects on systemic oxygen transport and tissue oxygenation. Ann Intern Med 76:193, 1972 13. Qvist J, Pontoppidan H, Wilson RS, et al: Hemodynamic responses to mechanical ventilation with PEEP: the effect of hypervolemia. Anesthesiology 42:45, 1975 14. Sykes MK, Adams AP, Finlay WEI, et al: The effects of variations in end-expiratory inflation pressure on cardio-respiratory function in normo-, hypo-, and hypervolemic dogs. Br J Anaesth 42:669, 1970 15. Powers SR, Manna1 R, Neclerio M, et al: Physiologic consequences of positive end-expiratory pressure (PEEP) ventilation. Ann Surg 178:265, 1973 16. Sugerman JJ, Olofsson KB, Pollock TW, et al: Continuous positive end-expiratory pressure ventilation (PEEP) for the treatment of diffuse interstitial pulmonary edema. J Trauma 12:263, 1972 17. Harken AH, Brennan MF, Smith B, Barsamian EM: The hemodynamic response to positive endexpiratory ventilation in hypovolemic patients. Surgery 76:786, 1974 18. Kirby RR, Downs JB, Civetta JM, et al: High level positive end-expiratory pressure (PEEP) in acute respiratory insufficiency. Chest 67:156, 1975 19. Downes JJ, Nicodemus HF, Pierce WS, Waldhausen JA: Acute respiratory failure in infants

416 The Annals of Thoracic Surgery Vol36 No 4 October 1983

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25. Hatch DJ, Taylor BW, Glover WJ, et al: Continuous positive-airway pressure after open-heart operations in infancy. Lancet 2:469, 1973 26. Gregory GA, Edmunds LH, Kitterman JA, et al: Continuous positive airway pressure and pulmonary and circulatory function after cardiac surgery in infants less than three months of age. Anesthesiology 43:426, 1975 27. Schleman MM, Gootman N, Crane LA: Cardiovascular responses to continuous positive pressure breathing in the piglet. Pediatr Res 8:470, 1974 28. Mockrin L, Bancalari E, Rowe M: Hemodynamic effects of continuous positive and negative pressure breathing in newborn pigs. Pediatr Res 8:468, 1974 29. Suter PM, Fairley HB, Isenberg MD: Optimum end-expiratory airway pressure in patients with acute pulmonary failure. N Engl J Med 292:284, 1975 30. Ashbaugh DG, Petty TL: Positive end-expiratory pressure: physiology, indications and contraindications. J Thorac Cardiovasc Surg 65:165, 1973

Notice from the Southern Thoracic Surgical Association The Thirtieth Annual Meeting of the Southern Thoracic Surgical Association will be held at the Marriott’s Marco Island Beach Hotel in Marco Island, FL, November 3-5, 1983. There will be a $100 registration fee for nonmember physicians except for guest speakers, authors and coauthors on the program, and residents. There will be a $25 registration fee for attendees of the Postgraduate Course on Thursday, November 3. This meeting has been approved for Category I, 14 hours CME credit.

The Scientific Program appears at the end of this issue of The Annals of Thoracic Surgery (pp 370-372). Manuscripts of papers accepted for the program must be in a form suitable for publication in The Annals of Thoracic Surgery and submitted to the Secretary-Treasurer prior to presentation. Hotel reservations are sent to members. Guests may correspond with the Marriott’s Marco Beach Hotel & Villas, Marco Island, FL 33937; phone (813) 394-2511.