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Ann Thorac Surg 2000;69:602-606
© 2000 The Society of Thoracic Surgeons

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Original Articles

Continuous pulmonary perfusion during cardiopulmonary bypass prevents lung injury in infants

^a Division of Cardiovascular Surgery, Tokyo Metropolitan Children’s Hospital, Tokyo, Japan

Address reprint requests to Dr Suzuki, Division of Cardiovascular Surgery, Tokyo Metropolitan Children’s Hospital, 1-3-1 Umezono, Kiyose-shi, Tokyo, 204-8567 Japan
e-mail: suzuki{at}chp.kiyose.tokyo.jp

	Abstract

Top Abstract Introduction Patients and methods Results Comment References

 
Background. Lung injury after cardiopulmonary bypass is a serious complication for infants with congenital heart disease and pulmonary hypertension. Excessive neutrophil sequestration in the lung occurring after reestablishment of pulmonary circulation implies that interaction between neutrophils and pulmonary endothelium is the major cause of lung injury.

Methods. Thirty infants with either ventricular septal defect or atrioventricular septal defect and with pulmonary hypertension were enrolled in this study. We performed continuous pulmonary perfusion during total cardiopulmonary bypass on 16 patients (perfused group) and conventional cardiopulmonary bypass on 14 patients (control group). PaO₂/FiO₂ and neutrophil counts were assessed from immediately before surgery to 24 hours after termination of cardiopulmonary bypass.

Results. PaO₂/FiO₂ was higher in the perfused group than in the control group, and the difference was significant throughout the study period. Neutrophil counts decreased below prebypass values in both groups at 30 minutes after aortic unclamping, and the difference was significant in the control group but was not in the perfused group. Duration of postoperative ventilatory support was significantly less in the perfused group.

Conclusions. Our study demonstrates that arrested pulmonary circulation during cardiopulmonary bypass is the major risk factor of lung injury and that continuous pulmonary perfusion is effective in preventing lung injury.

	Introduction

Top Abstract Introduction Patients and methods Results Comment References

 
Although technical refinements of cardiopulmonary bypass (CPB) have progressively improved the results of cardiac surgery, postoperative lung dysfunction remains as a serious complication that could lead to a life-threatening problem, particularly for infants with congenital heart disease and pulmonary hypertension [1]. Previous reports have demonstrated that direct contact of blood with the synthetic surface of the CPB circuit induces systemic inflammatory response [2] and progressive accumulation of neutrophils in the pulmonary circulatory system [3], which are presently known to result in tissue injury mediated by neutrophil-endothelium interaction and oxygen-derived free radicals [4, 5]. In addition, ischemic insult and reperfusion are known to induce the lung to be damaged. Because neutrophil sequestration usually occurs in the lung during CPB, particularly when the pulmonary circulation is reestablished after an arrest [6–8], it is highly probable that continued pulmonary circulation throughout the period of CPB will minimize ischemic insult and prevent lung injury. With these considerations in mind, we performed continuous pulmonary perfusion during total CPB and assessed its efficacy against the lung injury.

	Patients and methods

Top Abstract Introduction Patients and methods Results Comment References

 
Patients
Thirty infants with either ventricular septal defect (VSD) or atrioventricular septal defect (AVSD) and with pulmonary hypertension were enrolled in this study. Pulmonary hypertension was defined as pulmonary-to-systemic arterial systolic pressure ratio of greater than 0.5 (Pp/Ps > 0.5). The ages of the patients at the definitive surgical repair were limited to less than 1 year, so as to make their perioperative conditions uniform. Hence, their ages ranged from 1 to 11 months (mean 5.8 ± 0.5 months). There were 26 patients with VSD and 4 patients with complete form of AVSD. The patients were allocated to the perfused (n = 16) and the control (n = 14) groups at random before operation. The perfused group underwent continuous pulmonary perfusion during total CPB, whereas the control group underwent conventional CPB without corresponding pulmonary perfusion. Their data are depicted in Table 1. This study was approved by the Ethics Committee of Tokyo Metropolitan Children’s Hospital, and informed consent was obtained from all parents of the patients.

Cardiopulmonary bypass
The CPB circuit consisted of a roller pump (Stöckert Instrument GMBH, Munich, Germany) and a membrane oxygenator (VPCML; COBE Laboratories, Inc, Denver, CO; Capiox SX-10; Termo Corporation, Shizuoka, Japan). The circuit was primed with lactated Ringer’s solution, albumin, mannitol, and leukocyte-depleted whole blood to achieve and maintain the hematocrit value greater than 20%. Depletion of the leukocyte was achieved by leukocyte removal filter (Sepacell; Asahi Medical Co, Ltd, Tokyo, Japan). Anticoagulation was accomplished by intravenous administration of heparin sulfate (300 IU/kg), which was neutralized with protamine sulfate at the end of the operation. During CPB, nonpulsatile flow was maintained at 150 mL/kg/min. All patients were cooled with the perfusate to a moderate hypothermic state ranging from 28°C to 30°C. Cardiac arrest was accomplished by aortic cross-clamp and infusion of high-potassium (20 mEq/L) blood cardioplegia (20 mL/kg) into the aortic root. The same solution was repeatedly infused in 60-minute intervals (10 mL/kg) during aortic cross-clamp and immediately before unclamping. Blood gas management during CPB was directed toward maintenance of pH at 7.35 to 7.40 and arterial carbon dioxide tension (PaCO₂) at 35 to 40 mm Hg. Arterial oxygen tension (PaO₂) was maintained higher than 150 mm Hg. Blood gas management was conducted according to the principle of alpha-stat management, where temperature correction of the measured pH and PaCO₂ were not performed.

During total CPB, the perfused group underwent continuous pulmonary perfusion with the oxygenated blood at the flow rate of 30 mL/kg/min. The perfusate was infused into the pulmonary arterial trunk through an 18-gauge pediatric cardioplegia cannula (DLP, Inc, Grand Rapids, MI) and was drained away from the left atrium through a vent circuit to secure a bloodless field. The continuous pulmonary perfusion was continued until unclamping of the aorta. By contrast, the pulmonary artery was not perfused in the control group, so that the forwarded pulmonary blood flow was arrested during total CPB. The mechanical ventilation was arrested in both groups with positive endexpiratory pressure at 5 cm H₂O.

Lung function
Arterial blood gas analysis was performed with the samples obtained from the peripheral systemic artery (Blood Gas System 288; Ciba Corning, Medfield, MA). The ratio of arterial oxygen tension to inspired oxygen fraction (PaO₂/FiO₂ ratio) was used as the parameter of the pulmonary function and was measured before the operation and at 3, 6, 12, and 24 hours after the termination of CPB. All patients were kept sedated with continuous intravenous infusion of morphine sulfate and were ventilated mechanically for at least 24 hours after termination of CPB.

Leukocyte counting
Blood samples were obtained from the peripheral systemic artery as well as blood gas analysis, and the neutrophils were counted before the operation, at 30 minutes after removal of the aortic cross-clamp, and immediately after termination of CPB. Measurements were made by Coulter counter (SE-9000; Sysmex Corporation, Kobe, Japan) and the values were corrected for the hematocrit values at the respective sampling points.

Statistical analysis
Statistical analysis was performed with StatView software (Abacus Concepts, Inc, Berkeley, CA). Data were expressed as mean plus or minus standard error of the mean. An unpaired t test was used to determine differences between the groups. One-way repeated-measures analysis of variance (ANOVA) followed by the multiple comparison method was used to detect differences among the sampling points within each group. Two-way repeated-measures ANOVA was used to determine differences between the groups over time of the study. A p value less than 0.05 was considered statistically significant.

	Results

Top Abstract Introduction Patients and methods Results Comment References

 
There were no significant differences between groups with respect to age, body weight, duration of CPB, duration of the aortic cross-clamp, preoperative pulmonary-to-systemic arterial systolic pressure ratio, pulmonary-to-systemic flow ratio, and pulmonary-to-systemic vascular resistance ratio (Table 1). Pulmonary-to-systemic arterial systolic pressure ratio at the termination of CPB revealed no significant difference between the groups (0.35 ± 0.03 vs 0.33 ± 0.02, p = 0.5083).

Lung function
In both groups, the PaO₂/FiO₂ ratio decreased gradually during the period from 3 to 12 hours after termination of CPB and showed the nadir at 12 hours. Then, the values increased by 24 hours and approached near to the prebypass value in the perfused group, but stayed less than that in the control group (Fig 1). At each measuring point, the PaO₂/FiO₂ ratio of the perfused group was significantly higher than that of the control group. Namely, the mean values of the perfused vs the control group at 3, 6, 12 and 24 hours after the termination of CPB were: 384.4 ± 24.9 vs 281.2 ± 31.9 mm Hg (p = 0.0155), 347.8 ± 30.1 vs 217.5 ± 28.6 mm Hg (p = 0.0043), 295.3 ± 17.4 vs 165.8 ± 16.2 mm Hg (p < 0.0001), and 336.1 ± 21.1 vs 257.1 ± 26.2 mm Hg (p = 0.0248), respectively (Fig 1). When compared with the prebypass value, the postbypass values of the control group were significantly less throughout the postbypass period, namely at 3 hours (p = 0.0053), 6 hours (p < 0.0001), 12 hours (p < 0.0001), and 24 hours (p = 0.0007). By contrast, only 12 hours after the termination of CPB was the value significantly lower than prebypass value in the perfused group (p = 0.0083) (Fig 1). Moreover, the trend of the PaO₂/FiO₂ ratio revealed a significant difference between the groups by two-way repeated-measures ANOVA (p = 0.0031).

View larger version (16K): [in this window] [in a new window]   Fig 1. Postoperative trends of PaO2/FiO2 ratio in the perfused (n = 16) and control (n = 14) groups. Data are presented as mean ± SEM. p < 0.01 when compared with prebypass value within each group for both groups; *p < 0.05, perfused group vs control group; **p < 0.01, perfused group vs control group.

View larger version (20K): [in this window] [in a new window]   Fig 2. Neutrophil counts before, during, and at the end of CPB. Values are corrected for hematocrit. Data are presented as mean ± SEM. p < 0.05 when compared with prebypass value within each group.

	Comment

Top Abstract Introduction Patients and methods Results Comment References

 
Despite the extensive investigations in relevance to CPB, postoperative dysfunction of the lung remains as a life-threatening problem, particularly among infants with congenital heart diseases revealing high pulmonary blood flow and pressure [1]. Previous studies have demonstrated that exposure of blood to the synthetic surface of the CPB circuit activates the complements, thereby provoking a systemic inflammatory response [2], and CPB elevates the values of the circulating inflammatory cytokines [9, 10], which exerts activating stimuli on the endothelial cells. The activated endothelial cells promote widespread expression of a variety of adhesion molecules, which play crucial roles in adhesion of the complement-activated neutrophils to the endothelial cell surface and also in the subsequent neutrophil migration into the extravascular space [11–13]. Once bound to the endothelium, the activated neutrophils release cytotoxic protease and oxygen-derived free radicals, which are responsible for the end-organ damage [4, 5]. According to this evidence, the neutrophil-mediated damaging effect has been considered the major contributing factor to lung injury seen after CPB.

In addition to the CPB-derived inflammatory response, ischemic insult and reperfusion are known to induce lung function to be damaged. Previous reports have demonstrated that reperfusion after an ischemic insult accelerates structural and functional abnormalities of the endothelial cells with an ensuing result of progressive organ injury, in which activated neutrophils play the crucial role as well [14–18]. During total CPB, the lung is perfused solely by the bronchial arterial system, so that the lung is exposed and at risk for the development of ischemic insult. An experimental study demonstrated that the regional blood flow and tissue adenosine triphosphate (ATP) in the lung decreased to 11% and 50% of the prebypass values, respectively, during total CPB. By contrast, during partial CPB, the regional blood flow decreased only to 41% of the prebypass value, and tissue ATP remained unchanged [19]. Other studies clarified the fact that lesser deprivation of pulmonary arterial blood flow during CPB provoked much less severe lung injury [20, 21]. Furthermore, neutrophil accumulation or extensive neutrophil sequestration in the lung is known to occur commonly when the pulmonary circulation is reestablished during CPB [6–8].

Based on this evidence, our study was conducted with the assumption that restored pulmonary arterial blood flow during total CPB may prevent the pulmonary ischemia and subsequent lung injury. In fact, a recent experimental study has revealed that low-flow lung perfusion during total CPB demonstrated better preservation of tissue ATP stores and arterial oxygen tension in the piglet model [22]. In our study, the fact that the perfused group showed well-preserved PaO₂/FiO₂ ratios and significantly less duration of ventilatory support in the early postoperative period suggests that continuous pulmonary perfusion during total CPB is an effective means to preventing the lung injury. As for the neutrophil counting analysis, our study provided evidence that the neutrophil sequestration in the lung is less severe in the perfused group. Neutrophils are sequestered according to intravascular pathologies such as neutrophil plugging in the alveolar capillaries and sticking to the pulmonary arterioles and venules, which were thought to be caused by mechanical hindrance and neutrophil-endothelial interaction mediated by adhesion molecules [23–25]. Our results imply that continuous pulmonary perfusion during total CPB minimized ischemic insult and inhibited neutrophil sequestration by minimizing mechanical hindrance and neutrophil-endothelial interaction in pulmonary microvessels. This study also suggests that ischemia-reperfusion injury is an augmenting factor of the lung injury. With respect to depletion of the neutrophils, as our study failed to disclose the difference of neutrophil counts between the right and left atrium, our results did not necessarily ascribe depletion of the neutrophils to the sequestration into the lung. However, previous studies clearly demonstrated neutrophil sequestration in the lung after reperfusion of the lung [3, 21]. In this context, the neutrophil depletion, which occurred in the systemic circulation after unclamping of the aorta, may imply that the neutrophils are sequestered mostly to the lung.

Normally, the bronchial blood flow is given a share of nearly 8% to 10% of the systemic blood flow. A recent study has shown that the pulmonary dysfunction and ultrastructural derangement of the lung tissue after CPB were less severe among the patients whose bronchial blood flow exceeded 25% of the systemic blood flow [26]. Another experimental work has also shown that the pulmonary blood flow of 35 mL/kg/min obviated the lung injury [22]. Although these studies failed to clarify the optimal flow rate of the bronchial arterial system during CPB, it is likely that more than normal bronchial blood flow is the prerequisite for protection of the lung during CPB. The flow rate of 30 mL/kg/min, which was employed in our study, constituted 20% of the total bypass flow and presumably amounted to 30% of the systemic blood flow. Because no experimental work has been performed in relevance to the physiologic pulmonary flow rate during total CPB, further investigative work is required to determine the optimal flow rate for the continuous pulmonary perfusion.

In conclusion, our results suggest that ischemia-reperfusion injury can be the augmenting factor of lung injury for infants with congenital heart disease and pulmonary hypertension, and that continuous pulmonary perfusion during total CPB is an effective means to preventing the lung injury that is derived from CPB.

	References

Top Abstract Introduction Patients and methods Results Comment References

 

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