Comparative Study between Different Modes of Ventilation during Cardiopulmonary Bypass and its Effect on Postoperative Pulmonary Dysfunction.

BACKGROUND: Postoperative pulmonary dysfunction is a prevalent complication after cardiac surgery; it has many contributing considerations due to either the surgery itself, anomalies to gas exchange or maybe as a result of alterations in lung mechanics. The aim of this study was to compare pressure-controlled ventilation versus volume-controlled ventilation in the presence of no ventilation group as a control group during cardiopulmonary bypass and its effect on postoperative pulmonary dysfunction. PATIENTS AND METHODS: Sixty-six patients going through open-heart surgeries were included in the study. They divided into three groups (Group P: Pressure-controlled ventilation, Group V: Volume-controlled ventilation, and Group C: Control group with no ventilation) in accordance with the mode of ventilation. Patients studied for chest X-ray, lung ultrasound, arterial oxygen partial pressure to fractional inspired oxygen ratio, alveolar-arterial oxygen gradient, static lung compliance, and dynamic lung compliance, taken after induction of anesthesia, 1-h post-CPB, and 1 h after arrival to cardiac surgical unit.
RESULTS: There was no significant difference regarding the chest X-ray and lung ultrasonography results among the three groups of the study. Regarding arterial oxygen partial pressure to fractional inspired oxygen ratio, alveolar-arterial oxygen gradient, static lung compliance, and dynamic lung compliance, the results showed lower values in the postbypass period, and the postoperative period compared to the postinduction period among the three groups of the study with no significant difference.
CONCLUSIONS: The evidence of clear benefits of maintaining ventilation alone during cardiopulmonary bypass is inconsistent. More studies are required to determine the precise role of different lung protective strategies during cardiopulmonary bypass.

INTRODUCTION

Postoperative pulmonary dysfunction (PPD) is considered to be a common postcardiac surgery's complication.[1] Forty percent of patients readmitted to the intensive care units present with respiratory failure and the adequate therapeutic management that might reduce the incidence is still unknown.[2] PPD pathophysiology is complex, and its mechanism is not clear. There are many surgical related factors that predispose cardiac surgical patients to the postoperative pulmonary complications such as the effects of general anesthesia combined with the effects of median sternotomy, cardiopulmonary bypass (CPB), internal mammary artery dissection, and the use of topical cooling for myocardial protection.[3] There are other contributing factors that predispose to PPD such as anomalies in the gas exchange, widening of the alveolar–arterial oxygen gradient, increased microvascular permeability in the lung, raised pulmonary vascular resistance, elevated pulmonary shunt fraction, and intrapulmonary aggregation of leukocytes and platelets.[4] Variations in lung mechanics also have an impact on PPD.

Atelectasis, pleural effusion, and postoperative hypoxemia without clinical symptoms in addition to acute respiratory distress syndrome which has a low incidence but high mortality are considered to be the main clinical manifestations of PPD.[5] The PPD is influenced by two main factors; the mechanical stress and trauma induced by mechanical ventilation and the exaggerated systemic inflammatory response to the cardiac surgery and its associated factors.[6]

Nonventilation during CPB has been practiced by most of the physicians. However, this nonventilation is associated with regional atelectasis, retained bronchial secretions, increased physiological arterial–venous shunts, pulmonary edema, poor compliance, and a higher incidence of infection.[7] Apnea during CPB has also been suggested to promote activation of lysosomal enzymes in the pulmonary circulation.[8]

It has been hypothesized that applying some maneuvers, such as the intermittent/continuous ventilation or continuous positive airway pressure (CPAP) and vital capacity maneuver (i.e. a peak airway pressure of 40 cmH2O with a fraction of inspired oxygen of 0.4 for about 15 s) during CPB might limit postbypass lung dysfunction.[9] Moreover, for the lungs that are totally dependent on oxygen supply from the bronchial arteries during the period of cardiac arrest, an additional contribution to lung tissue oxygenation through gas diffusion by continuous ventilation may be considered as a worthy measure.[10]

The aim of our study was to compare different ventilation modalities during CPB and its effect on PPD. As volume-controlled ventilation and pressure-controlled ventilation are considered to be the most common modes of ventilation used during anesthesia, so we preferred to compare for possibility of any benefit effect over no ventilation during CPB period.

PATIENTS AND METHODS

This prospective, randomized, double-blind study was conducted in cardiothoracic department at Ain Shams university hospitals After obtaining the approval of the ethical committee board, written informed consent was taken from the patients (males or females) scheduled for open-heart surgery (valve surgeries or on pump coronary artery bypass grafting surgeries) over 1 year (from January 2017 to March 2018). This study is registered in ClinicalTrials.com ID NCT03824301.

After exclusion of emergency cases, off-pump surgeries, patients with chronic lung diseases with forced expiratory volume in the first second (FEV1) or forced vital capacity (FVC) <40% of the predicted value, massive blood transfusion during surgery, complicated surgeries, redo surgeries, and patients with decompensated heart failure prior to surgery and patients refusal, 66 patients remained for the study.

Based on a computer-generated randomization list, patients were divided into three groups (Group P, Group V, and Group C) of 22 patients each. Group P included patients ventilated by pressure-controlled mode during CPB period, while Group V comprised patients ventilated by volume-controlled mode during CPB period and Group C or control group, in which patients are disconnected from the anesthesia machine during CPB period.

Perioperative anesthetic management was standardized for all patients. Preoperative investigations included pulmonary function tests, arterial blood gases (ABG), chest X-ray, and lung ultrasonography. On arrival to the operating room, patients were connected to the monitor (Aisys; Datex-Ohmeda, Inc., Wisconsin, USA), which included 5-lead electrocardiogram and oxygen saturation [SPO2]), and noninvasive blood pressure. Temperature is controlled through a heating-cooling unit and measured continuously through the oropharyngeal and rectal probes.

Patients received 0.04 mg.kg-1 midazolam i.v. (Midazolam Labesfal, 15 mg/3 mL) through the peripheral cannula 20 G that was inserted in the station before arriving to the operating room. Just before induction of anesthesia, a radial artery cannula inserted mostly in nondependent hand. After performing Allen's test, the skin was sterilized with chlorhexidine 2% in 70% alcohol swab stick and lidocaine 1 mL 2% infiltrated at the site of insertion, then the cannula inserted, checked, and connected to a pressure transducer (Aisys; Datex-Ohmeda, Inc., a General Electric Company, doing business as GE Healthcare, Madison, Wisconsin, USA) for continuous monitoring of invasive blood pressure. The pressure transducer was referenced to the mid-axillary level, and a baseline arterial SaO2 was recorded.

A central venous catheter (REF CS-14703 Multi-Lumen Central Venous Catheterization Set with Blue FlexTip Catheter ARROW, USA) inserted in the right internal jugular vein, under complete aseptic technique, using a portable ultrasound machine (Sonosite, M-Turbo Ultrasound System, FUJIFILM Sonosite, Inc. USA), a baseline ScvO2 was taken.

After preoxygenation for 3 min, anesthesia induced by fentanyl 5–10 μg/kg (50 μg/mL, 2 mL) and atracurium 0.5 mg.kg-1 (5 mL, 10 mg/mL). Three minutes later, patients intubated with cuffed endotracheal tube, the cuff pressure maintained at 20 cmH2O, the position of the endotracheal tube was checked by chest auscultation and end-tidal CO2 once the patient is connected to the anesthesia machine. The lungs were mechanically ventilated with 100% oxygen which was minimized gradually according to the ABG to 50% oxygen in air. The patient ventilated with volume-controlled mode, tidal volume (Vt) 6–8 mL.kg-1, respiratory rate (RR) 12–14/min, and the ventilation settings were adjusted to maintain end-tidal CO2 between 35 and 40 mmHg. Anesthesia was maintained by 0.5%–1% end-tidal sevoflurane in 50% oxygen in air flow, atracurium infusion at a rate 0.3 mg.kg-1 h-1 (2 ampoules 100 mg/10 mL, 20 mL syringe, with concentration 5 mg/mL), fentanyl infusion at a rate of 1–3 ug.kg-1 h-1 (500 μg/10 mL ampoule, diluted in 40 mL normal saline 0.9%, and concentration 10 μg/mL), and lactated Ringer solution at a rate of 8–10 mL.kg-1 h-1

Routine continuous monitoring in the form of invasive blood pressure, heart rate, SPO2, end-tidal CO2, oropharyngeal and rectal temperature, urine output, sevoflurane, and air and oxygen were measured with gas analyzer. Arterial blood gases and venous blood gases were recorded on demand. During bypass time, fentanyl infusion at a rate of 1–3 ug.kg-1 h-1 was continued alone or in addition to 0.5%–1% end-tidal sevoflurane in 50% oxygen in airflow depending on the mode of ventilation during bypass.

Group P was ventilated with pressure-controlled mode, RR 6/min, peak inspiratory pressure 16–20 cmH2O (aiming to keep Vt around 4 mL/kg as possible), and positive end-expiratory pressure (PEEP) 4 cmH2O. Group V was ventilated with volume-controlled mode, VT 4 mL.kg-1, RR 6/min, and PEEP 4 cmH2O. Group C was disconnected from the anesthesia machine and received sevoflurane through the CPB pump.

In all groups, blood gas management during CPB was directed to keep the arterial carbon dioxide tension (PaCO2) at 35–40 mmHg. After starting rewarming, all patients were ventilated manually for 3 min after suction through the endotracheal tube and then shifted to the volume-controlled mode with VT 6–8 mL.kg-1, RR 12–14/min, and PEEP 5 cmH2O till the end of surgery.

After surgery, patients were transferred to the cardiac surgical unit (CSU) for postoperative care. Patients were ventilated by Maquet ventilator (Maquet, Servo I, Getinge Group, Maquet critical care, AB, Sweden). Settings were adjusted according to ABG which were withdrawn upon arrival to CSU then hourly till extubation. The patients ventilated with the following parameters: synchronized intermittent mandatory ventilation/pressure support mode, RR 12–14/min, Vt 6–8 mL/kg, PEEP 6 cmH2O, PS 12 cmH2O, and FiO2 50%. Continuous monitoring maintained in the form of; invasive blood pressure, SPO2, central venous pressure, urine output, and intercostal drains for bleeding. ABG measured on demand. Patients were covered by Bair Hugger warming blanket system (3M, USA) to keep body temperature above 36.6°C.

After the patient's stabilization, weaning from mechanical ventilation started, if successful spontaneous breathing trial for 30 min, patients were extubated. Following extubation, patients received nebulization with high flow oxygen 15 L/min in the form of ventolin and atrovent with normal saline and then Venturi mask 50% was applied.

Patients studied for the primary (subjective) outcome by chest X-ray and lung ultrasonography (portable sonosite, linear probe 10–5 mHZ) which was performed preoperatively, 1 h after arrival to CSU then on day 1 and day 2 to detect right and left lung collapse and pleural effusion. The secondary (objective) outcome contained P/F ratio (PaO2/FiO2), alveolar–arterial oxygen gradient (ΔA-aO2), static lung compliance (Cstat), and dynamic lung compliance (Cdyn) measured by the ventilator which were taken after induction of anesthesia, 1-h post-CPB and 1 h after arrival to CSU.

ΔA − aO2 was calculated as follows:

ΔA–aO2 = PAO2 − PaO2

PAO2 = PiO2−(PACO2/R)

PiO2 = FiO2 (PB − PH 2O)

or using common values:

PAO2 = FiO2 × (760–47)−PaCO2/0.8

where PAO2 = alveolar oxygen tension, PaO2 = partial arterial oxygen pressure, PiO2 = partial pressure of inspired oxygen, PACO2 = alveolar carbon dioxide tension (assumed to equal the partial arterial CO2 pressure due to the ease of exchange of CO2), R = respiratory quotient (assumed at 0.8), PB = barometric pressure (760 mmHg), PH 2O = water vapor pressure (47 mmHg, as inspired air is fully saturated at the level of the carina), and FiO2 = fractional concentration of inspired oxygen.

Statistical analysis

Data were analyzed using SPSS 20 (IBM, Armonk, NY, USA). Analysis of variance was used to compare the three groups for quantitative parametric data with posthoc Tukey's test, performed if there was a significant difference among the groups, Chi-square test was used for comparison of qualitative data. Continuous parametric data were presented as mean ± standard deviation, and categorical data was presented as number of patients. P < 0.05 was considered statistically significant.

RESULTS

A total of 66 patients were enrolled in this study; no patients were excluded throughout the course of the study. There was no significant difference as regards demographic data as regard age, sex, and type of surgery [Table 1].

Table 1

Demographic data in the three groups of the study P group (pressure-controlled ventilation), V group (volume-controlled ventilation), and C group (control group)

	Group P (n=22)	Group V (n=22)	Group C (n=22)
Age (years)	58.86±4.3	59.64±6.8	60.9±4.8
Sex (male/female)	16/6	16/6	15/7
Type of surgery
Valve surgery	7	3	4
CABG	15	19	18

Data were expressed as mean±SD or number of patients. P>0.05 is statistically nonsignificant. CABG=Coronary artery bypass graft, SD=Standard deviation

As regards the PaO2 [Table 2], there was no significant difference between the 3 groups of the study at the post-induction period, Group P (176.64 ± 9.9), Group V (176.77 ± 7.6) and Group C (175.57 ± 8.96). In post – bypass period our results showed no significant difference between the 3 groups of the study although it was lower in the 3 groups in comparison to the post-induction period, Group P (176.45 ± 9.01), Group V (176.14 ± 8.89) and Group C (175.6 ± 8.99). The PaO2 remain the same in 1h post-operative as in post-bypass period but lower than the post-induction period with no significant difference between the 3 groups of the study, Group P (174.09 ± 9.68), Group V(175.86 ± 9.33) and Group C (173.6 ± 8.99).

Table 2

Changes of PaO2 in the three groups of the study P group (pressure-controlled ventilation), V group (volume-controlled ventilation), and C group (control group)

	Group P (n=22)	Group V (n=22)	Group C (n=22)
Postinduction	176.64±9.9	176.77±7.6	175.57±8.96
Postbypass	176.45±9.01	176.14±8.89	175.6±8.99
1-h postoperative	174.09±9.68	175.86±9.33	173.6±8.99

Data were expressed as mean±SD. P>0.05 is statistically nonsignificant. SD=Standard deviation

Regarding the PaCO2 [Table 3], there was no significant difference between the 3 groups of the study, at the post-induction period, in Group P (37.05 ± 1.2), in Group V (37.27 ± 1.03), and in Group C (37.24 ± 1.04). In post – bypass period our results showed no significant difference between the 3 groups of the study, and the same in the 3 groups in comparison to the post-induction period, in Group P (37.82 ± 2.53), in Group V (37.18±1.14) and in Group C (37.3 ± 1.09). The PaCO2 remain the same in 1h post-operative as in post-bypass period with no significant difference between the 3 groups of the study, in Group P (37.27 ± 0.99), in Group V (37.32 ± 0.95) and in Group C (37.1 ± 1.22).

Table 3

Changes of PaCO2 in the three groups of the study P group (pressure-controlled ventilation), V group (volume-controlled ventilation), and C group (control group)

	Group P (n=22)	Group V (n=22)	Group C (n=22)
Postinduction	37.05±1.2	37.27±1.03	37.24±1.04
Postbypass	37.82±2.53	37.18±1.14	37.3±1.09
1-h postoperative	37.27±0.99	37.32±0.95	37.1±1.22

Data were expressed as mean±SD. P>0.05 is statistically nonsignificant. SD=Standard deviation

As regards the static compliance the values in the post -bypass period were lower in the 3 groups of the study than the values in post-induction period, in the ventilated Groups P and V the values were higher than in Group C with no significance, Group P in post- induction (36.27±5.39), Group P in Post-bypass (35.6 ± 5.6), Group V in post-induction (36.27±6), Group V in post-bypass (35.32 ± 6.4), Group C in post-induction (34.9±5.61), Group C in post-bypass (34.6 ± 6.5). In 1h post-operative the values were lower in the 3 groups in comparison to the post-bypass period, in the ventilated group higher than the Group C, but with no significance, Group P (34.91± 6.14), Group V (33.18±7.31) and Group C (33.33±5.08) [Table 4].

Table 4

Changes of compliance in the three groups of the study P group (pressure-controlled ventilation), V group (volume-controlled ventilation) and C group (control group)

	Group P (n=22)	Group V (n=22)	Group C (n=22)
Static compliance
Postinduction	36.27±5.39	36.27±6	34.9±5.61
Postbypass	35.6±5.6	35.32±6.4	34.6±6.5
1-h postoperative	34.91±6.14	33.18±7.31	33.33±5.08
Dynamic compliance
Postinduction	41.73±5.889	40.91±6.6	37.9±4.88
Postbypass	40.18±6.04	39.45±6.07	37.71±6.24
1-h postoperative	36.23±5.60	36.27±7.34	36.76±5.85

Data were expressed as mean±SD. P>0.05 is statistically nonsignificant. SD=Standard deviation

Regarding the dynamic compliance, the post-induction results showed no significant difference between the 3 groups of the study, Group P (41.73±5.889), Group V (40.91±6.6), and Group C (37.9±4.88). The post-bypass period showed lower levels in the 3 groups more than the post-induction levels but Group P is higher than Group V and Group C with no significance. In 1h post-operative the values were lower in the 3 groups than the post-bypass period [Table 4].

As regards the PaO2/FiO2 ratio [Table 5], the post-induction period results showed no significant difference between the 3 groups of the study Group P (364.81 ± 18.56), Group V (363.33 ± 16.83), and Group C (355.14 ± 17.03). Regarding the post-bypass period, which was lower than the post-induction period in the 3 groups of the study, Group P (362.73 ± 18.98), Group V (363.27 ± 19.33) and Group C (354.64 ± 17.54). In 1h postoperative, the results showed decrease in the values of PaO2/FiO2 ratio among the 3 groups of the study compared to the post-bypass period with no significant difference Group P (348.68 ± 19.27) Group V (348.68± 19.27) and Group C (347 ± 19.46).

Table 5

Changes of PaO2/FiO2 ratio in the three groups of the study P group (pressure-controlled ventilation), V group (volume-controlled ventilation), and C group (control group)

	Group P (n=22)	Group V (n=22)	Group C (n=22)
Postinduction	364.81±18.56	363.33±16.83	355.14±17.03
Postbypass	362.73±18.98	363.27±19.33	354.64±17.54
1-h postoperative	347.64±19.16	348.68±19.27	347±19.46

Data were expressed as mean±SD. P>0.05 is statistically nonsignificant. SD=Standard deviation

As regards the Δ A-a O2, our results showed [Table 6] an increase in the values in the post-bypass period Group P (17.6 ± 1.26), Group V (17.5 ± 1.2), Group C (17.9 ± 1.3) and in 1h post-operative Group P (18.05± 1.28), Group V (18.2± 1.24), Group C (18.23± 1.27) in comparison to the post-induction period in the 3 groups of the study with no significant difference Group P (17.2±1.25), Group V (17.1±1.13) and Group C (17.5±1.25).

Table 6

Changes of A-a gradient (KPa) in the three groups of the study; P group (pressure-controlled ventilation), V group (volume-controlled ventilation), and C group (control group)

	Group P (n=22)	Group V (n=22)	Group C (n=22)
Postinduction	17.2±1.25	17.1±1.13	17.5±1.25
Postbypass	17.6±1.26	17.5±1.2	17.9±1.3
1-h postoperative	18.05±1.28	18.2±1.24	18.23±1.27

Data were expressed as mean±SD. P>0.05 is statistically nonsignificant. SD=Standard deviation

The chest X-ray and lung ultrasound taken on 1-h postoperative, day 1 and 2, showed no significant differences between the three groups of the study [Tables 7 and 8].

Table 7

Chest X-ray changes in the three groups of the study; P group (pressure-controlled ventilation), V group (volume-controlled ventilation), and C group (control group)

	Group P (n=22)	Group V (n=22)	Group C (n=22)
Preoperative
Lt lung collapse	0	0	0
Rt lung collapse	0	0	0
Lt pleural effusion	0	0	0
Rt pleural effusion	0	0	0
1-h postoperative
Lt lung collapse	1	2	1
Rt lung collapse	0	0	0
Lt pleural effusion	1	0	1
Rt pleural effusion	0	0	0
Day 1
Lt lung collapse	2	3	1
Rt lung collapse	0	0	0
Lt pleural effusion	1	2	1
Rt pleural effusion	1	1	1
Day 2
Lt lung collapse	3	3	2
Rt lung collapse	0	0	0
Lt pleural effusion	1	1	1
Rt pleural effusion	1	1	1

Data were presented as number of patients. P>0.05 is statistically nonsignificant. Rt=Right, Lt=Left

Table 8

Lung ultrasound changes in the three groups of the study; P group (pressure-controlled ventilation), V group (volume-controlled ventilation), and C group (control group)

	Group P (n=22)	Group V (n=22)	Group C (n=22)
Preoperative
Lt lung compliance	0	0	0
Rt lung compliance	0	0	0
Lt pleural effusion	1	0	1
Rt pleural effusion	0	0	0
1-h postoperative
Lt lung compliance	1	2	1
Rt lung compliance	0	0	0
Lt pleural effusion	1	0	1
Rt pleural effusion	0	0	0
Day 1
Lt lung compliance	2	3	1
Rt lung compliance	0	0	0
Lt pleural effusion	1	2	1
Rt pleural effusion	1	1	1
Day 2
Lt lung compliance	3	3	2
Rt lung compliance	0	0	0
Lt pleural effusion	1	1	1
Rt pleural effusion	1	1	1

Data were presented as number of patients. P>0.05 is statistically nonsignificant. Rt=Right, Lt=Left

In 1-h postoperative, one patient developed left lung collapse in Group P compared to two patients in Group V and one patient in Group C. No patients developed right lung collapse or pleural effusion in the three groups. One patient developed left pleural effusion in Group P and C and 0 patients in Group V.

On postoperative day 1, two patients developed left lung collapse in Group P compared to three patients in Group V and one patient in Group C. No patients developed right lung collapse in the three groups. One patient developed left pleural effusion in Group P compared to two patients in Group V and one patient in Group C. One patient developed right pleural effusion in each group.

On postoperative day 2, three patients developed left lung collapse in Groups P and V and two patients in Group C. No patients developed right lung collapse in the three groups. One patient developed left and right pleural effusion in the three groups of the study.

DISCUSSION

The incidence of postoperative pulmonary dysfunction is predominantly caused by stimulation of lysosomal enzymes in the pulmonary circulation which is provoked by apnea during CPB.[8] Hypoventilation during CPB is linked with the advancement of microatelectasis, hydrostatic pulmonary edema, poor compliance, and an increased incidence of infection.[11] Maintaining mechanical ventilation during CPB may reducing postoperative pulmonary complications.[7] Atelectasis is the preeminent determinant in lung exchange postoperatively and may perform a fundamental role in ventilatory abnormality after cardiac surgery than edema which arises as a result of increased permeability.[6]

The systemic inflammatory response to CPB plays a principal role for lung injury following bypass. Bypass primes and activates neutrophils both by their exposure to mechanical shear stress and artificial surfaces.[12] In addition, bypass results in the activation of the complement pathways and is also associated with the release of pro-inflammatory cytokines that lead to extravasation of fluids and activated leukocytes, with trapping and sequestration of these leukocytes in the interstitial lung tissues during their pulmonary vascular transit.[13]

CPB prompts induction of oxygen free radicals that mediate pulmonary endothelial damage as well. Lungs are exposed to ischemia during bypass, and postischemic reperfusion of lungs activates the inflammatory pathway. Thus, systemic inflammatory response and ischemic reperfusion during CPB establish a vicious cycle in the pathogenesis of post-CPB lung injury.[14]

To avoid this dysfunction, some maneuvers had been applied such as the intermittent ventilation or the application of CPAP during CPB.[15] CPAP application has been reported as an effective adjunct in some studies.[16] However, others noted either no difference or a nonsignificant difference lasting <4–8 h between patients treated CPAP compared to controls.[17] Maintaining ventilation at the same time with pulmonary artery perfusion during CPB has been suggested as another alternative to mitigate the post CPB deterioration of lung function.[18] In an experimental comparative study, Friedman et al. stated that ventilation with pulmonary artery perfusion during CPB might have advantages in conserving lung function by lessening platelet and neutrophil sequestration and debilitating the thromboxane B2 response after CPB.[19] Another experimental study by Serraf et al. showed no significant improvement in pulmonary vascular resistance, respiratory index, or oxygen tension with continuous ventilation with CPB.[20]

In the current study, there was nonsignificant decrease in static lung compliance, dynamic lung compliance, and PaO2/FiO2 ratio in the postbypass period, together with the nonsignificant increase of Δ (A-a) O2 in 1-h postoperative in the three groups of the study. The ventilated patients showed better values compared to the control group but still nonsignificant. Our results do not correlate completely with the results of Salama et al. who studied the effect of low Vt ventilation during CPB on postoperative lung injury in 60 patients scheduled for elective CABG.[14] The study showed that postbypass extravascular lung water (EVLW) was significantly less in mechanically ventilated group due to less extravasation in the interstitial lung tissues that was reflected as significant higher compliance and better gas exchange in the mechanically ventilated group. The postbypass PaO2/FiO2 ratio was significantly higher and Δ (A-a) O2 was significantly lower in the mechanically ventilated group when the lungs were continuously ventilated during CPB, reflecting better oxygenation. The better oxygenation could be explained by recruitment of the lungs and prevention of microatelectasis improving the gas exchange across the alveolar–capillary membrane with less extravasated fluid, in addition to maintaining the normal blood flow to the lung. The postoperative radiological complications, as atelectasis and effusion in the current study, showed nonsignificant difference between the three groups of the study, which correlate with Salama et al. study.[14]

Ventilation's effects during CPB have been examined in a number of studies. John and Ervine showed in their randomized study that combined ventilation during CPB by Vt of 5 mL.kg-1 resulted in significant smaller EVLW and a shorter extubation time.[21] Davoudi et al. ventilated the lungs with 3 mL.kg-1 Vt and PEEP of 5 cmH2O in one group and compared it with other group without ventilation or PEEP and found that postbypass PaO2 was significantly higher, and the decrease in postoperative FEV1 and FVC was significantly lower in the ventilated group.[22]

Zabeeda et al. studied 75 patients who were split into five groups receiving CPAP and high-frequency ventilation with either 21% or 100% inspired oxygen. The Δ (A-a) O2 was lower and the PaO2 was higher 5 min after bypass in patients receiving CPAP, but this difference disappeared on chest closure and postoperative.[23] Berry et al. studied 90 patients using range of CPAP, continuous ventilation and nonventilation techniques. There was an increase in EVLW in all groups with decrease in postoperative oxygenation being most pronounced in patients with high CPAP compared to those with low CPAP or controlled mechanical ventilation. No significant improvement compared with no ventilation was demonstrated.[17]

One of the limitations of the study is the nonestimation of the inflammatory mediators and another limitation is the noncompliance of surgeons to lung movement during the procedure. Other additional methods may contribute to further lung protection during CPB, such as pulmonary perfusion techniques and shift to modified CPB circuits.

CONCLUSIONS

To date, the evidence of clear benefits of maintaining ventilation alone during CPB is inconsistent with most studies showing nonsignificant preservation of lung function. A wide range of ventilator strategies have been attempted, no convincing clinical benefits for any of these strategies have been shown and thus ventilation on CPB cannot be supported as a strategy to improve postoperative lung function. More studies are required to determine the precise role of different lung protective strategies during CPB.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.