Secondary Logo

Journal Logo

Original Papers

Monitoring of respiratory function before and after cardiopulmonary bypass using side-stream spirometry

Bund, M.*; Seitz, W.*; Uthoff, K.; Krieg, P.; Strüber, M.; Piepenbrock, S.*

Author Information
European Journal of Anaesthesiology: January 1998 - Volume 15 - Issue 1 - p 44-49



Induction of general anaesthesia alters the shape and motion of the chest wall and diaphragm, resulting in a reduction in functional residual capacity (FRC) of the lung and an increase in alveolar-arterial oxygen tension difference [1-3]. Cardiac surgery requires prolonged general anaesthesia, extensive intrathoracic surgical manipulation and institution of cardiopulmonary bypass (CPB). It has been shown that changes in lung function after cardiac surgery are more pronounced compared with those after other types of major surgery [4]. Pulmonary dysfunction after CPB has been described in terms of a reduction in lung volumes[5], altered lung and chest wall mechanics [6,7], an increase in extravascular lung water content [8,9], ventilation-perfusion mismatch [10], a decrease in pulmonary surfactant activity [11] and changes in the fine structure of the lungs [12,13].

Investigations to assess these aspects of lung dysfunction are technically demanding and are not suitable for routine clinical use. Therefore, in the present study, we have investigated whether our routine respiratory monitoring, i.e. blood gas analysis and side-stream spirometry, can detect differences in pulmonary function before and after CPB.



Eighteen patients undergoing elective coronary artery bypass grafting (n = 12) or aortic valve replacement (n = 6) were studied. The study was approved by the local ethics committee and informed consent was obtained from each patient. The patients were free from pulmonary disease and had normal standard chest radiographs. Patients with depressed left ventricular function (ejection fraction <50%) were excluded.


All patients were premedicated orally with flunitrazepam 2 mg. Anaesthesia was induced with fentanyl 15 μg kg−1, etomidate 0.25 mg kg−1 and pancuronium 0.1 mg kg−1, and maintained with fentanyl, midazolam and pancuronium, as appropriate. After tracheal intubation, the patients' lungs were ventilated mechanically at FIO2 1.0 throughout the whole study. A time-cycled volume-constant anaesthesia ventilator (AV1, Dräger, Lübeck, Germany) was set to deliver a tidal volume of 12 mL kg−1 at an inspiratory-to-expiratory ratio of 1:2 and zero endexpiratory pressure. The ventilator was adjusted for 8-12 breaths min−1 in order to maintain the end-tidal CO2 tension between 4.5 and 5 kPa. All other ventilator settings were kept constant throughout the study.

Cardiopulmonary bypass

Extracorporeal circulation was instituted with catheters placed into the ascending aorta and right atrium (two-stage single cannula) after administration of heparin 300 IU kg−1. Priming volume consisted of 2000 mL of Ringer's solution. Cardiopulmonary bypass flow rates were kept at 2.2-2.5 L min−1 m−2 and mean arterial pressure was maintained at 50-60 mmHg. Body core temperature decreased to 28.4 ± 1.4°C. During bypass, the lungs were nonventilated and deflated. Prior to separation from CPB, the lungs were reinflated and ventilation was restored. Ventilatory settings before and after CPB were exactly the same. After separation from CPB, protamine chloride 3 mg kg−1 was administered to neutralize heparin.


Respiratory function was measured using side-stream spirometry. The flow sensor (D-Lite™, Datex Instr. Corp., Helsinki, Finland) was placed between the Y-piece and the endotracheal tube. The construction of the D-lite sensor is symmetrical with two opposite facing pitot tube-type pressure sensing ports. A double-lumen tube conducts the pressures to two differential pressure sensors located inside the monitor. One sensor measures airway pressure compared with ambient pressure. Pressure difference between the two pressure ports inside the D-lite is used to calculate inspiratory and expiratory gas flows, and to compute tidal and minute volumes during both inspiration and expiration[14]. This working principle means that there is no gas flow inside the double lumen tube. A multigas monitor analyses respiratory gases(e.g. O2, CO2, N2O and anaesthetic agents) to compensate for the effect of different gas compositions on tidal volume measurement.

The following parameters were recorded: peak airway pressure (Ppeak), end-inspiratory plateau pressure (Pplat), end-expiratory pressure (Pexp), inspired tidal volume(Vt), expired volume and the volume expired in one second (V1.0). V1.0(%) represents the volume expired passively in the first second of expiration during mechanical ventilation. This parameter reflects changes in airway resistance. The resistance of the respiratory system (Rrs) is calculated as (Ppeak-Pplat) flow−1. The resistance of the respiratory system includes resistance of the airways and the endotracheal tube as well as tissue resistance [17]. The dynamic compliance of the respiratory system (Crs) is derived from Vt(PPlat-Pexp)−1.

Measurements were made at four stages:(1) before sternotomy; (2) after sternotomy, with the sternum retracted; (3) after termination of CPB and decannulation; and (4) after sternal closure.

Calibration of the flow sensor was performed using a calibration piston. Validation of the accuracy of tidal volume and compliance measurements with a BIO-TEK VT-2 ventilator tester(BIO-TEK Instruments Inc., Winooski, VT, USA) showed errors ranging from −4.5% to +4.8% for tidal volume and from −3.5% to +3.3% for compliance using different respirator settings [14].

Arterial blood samples were obtained from a radial artery cannula and analysed with a Corning 178 pH/blood gas analyser (Ciba Corning Diagnostics, Fernwald, Germany). The alveolar-arterial oxygen tension difference (AaDO2) was calculated using the alveolar gas equation with a respiratory quotient of 0.8. End-tidal PCO2 (PetCO2) was measured by infrared absorption (Ultima SV, Datex Instr. Corp., Helsinki, Finland) to calculate arterial to end-tidal CO2 tension difference and alveolar dead space fraction(VDalv/VTalv).

Statistical analysis

The mean of two consecutive values from all measurements was noted. Data are expressed as mean± SD. Values of the respiratory function before and after CPB were compared by means of the Wilcoxon matched-pairs test. The correlation of age, duration of CPB and PaO2 before operation with respiratory function after CPB was tested with the Spearman rank correlation coefficient. P<0.05 was considered significant.


The demographic data, and pre-operative myocardial and pulmonary function of the patients are summarized in Table 1. Determination of PaO2, vital capacity (VC) and 1-s forced expiratory volume(FEV1) 1-2 days before operation revealed normal lung function. Intraoperative variables are listed in Table 2. CPB was discontinued without positive inotropic support in all patients.

Table 1
Table 1:
Demographic data, and pre-operative myocardial and pulmonary function (mean ± SD)*
Table 2
Table 2:
Intra-operative data (mean ± SD)

Sternotomy was accompanied by a marked increase in dynamic compliance from 61.0 ± 10.2 to 78.6 ± 22.9 mL cmH2O−1. After CPB, the dynamic compliance of the respiratory system was significant lower(65.4 ± 22.4 mL cmH2O−1 with open chest and 51.1 ± 17.2 mL cmH2O−1 with closed chest) when compared with the corresponding values before CPB (Fig. 1). In contrast, Rrs and V1.0 showed no significant changes in relation to sternotomy or CPB (Table 3).

Fig. 1
Fig. 1:
Dynamic compliance (mean ± SD): (a) before sternotomy; (b) after sternotomy, with the sternum retracted; (c) after termination of cardiopulmonary bypass (CPB); and (d) after sternal closure.*P<0.05 compared with the corresponding values before CPB (c/b and d/a).
Table 3
Table 3:
Resistance of the respiratory system (Rrs) and volume expired in 1 s (V1.0) (mean ± SD) before and after cardiopulmonary bypass (CPB)

The mean AaDO2 increased from 33.0± 10.6 kPa before CPB to 36.1 ± 12.5 kPa after CPB (not significant). Arterial to end-tidal CO2 tension difference showed a non-significant increase(0.67 ± 0.39 kPa before vs. 0.79 ± 0.54 kPa after CPB), corresponding with an elevation of alveolar dead space fraction from 15.3 ± 6.9% to 17.6± 10.3% (not significant). There were no correlations between age, PaO2 before operation or duration of CPB, and AaDO2 or dynamic compliance after CPB.


Respiratory abnormalities following cardiac surgery with the use of extracorporeal circulation are well-documented [5,15-17]. Pulmonary dysfunction after cardiac surgery may be attributable to surgical manipulations including sternotomy [6], harvesting of the internal mammary artery [18,19] and pleurotomy [20]. Possible pulmonary sequelae of CPB are accumulation of extravascular lung water [8], loss of surfactant [11], sequestration of polymorphonuclear leucocytes in the alveolar microcirculation [13] and activation of various mediators as a result of the exposure of blood to non-endothelial surfaces [21]. The extent of negative effects on the lung is dependent on duration and technique of bypass [12,22]. The present study investigates changes in pulmonary function as a result of uncomplicated cardiac surgery using standard respiratory monitoring, i.e. blood gas analysis and sidestream spirometry.

We observed significant changes in the dynamic compliance of the respiratory system related to sternotomy and CPB with this method. As a result of altered chest wall compliance, sternotomy was accompanied by an increase (+28.9%) in Crs, whereas sternal closure caused a decrease (−21.9%). To elucidate the effect of extracorporeal circulation on pulmonary compliance, only the corresponding values before and after CPB were compared. After CPB, these data showed the same decrease in dynamic compliance with open (−16.8%) or closed (−16.2%) chest. Hence, this reduction in compliance can be explained by a restrictive pulmonary impairment.

These findings are in accordance with earlier experimental studies. A progressive decrease in pulmonary compliance and in pulmonary surface activity has been reported during CPB in dogs [11]. The reduction in pulmonary compliance was 15% after 2 h of bypass and 45% after 4 h. Stanley [23] observed a 20% decrease in static pulmonary compliance 30 min after CPB compared with pre-operative values in calves that were not ventilated during CPB. A significant decrease in total lung capacity, vital capacity and functional residual capacity has been described by other investigators [5,18,19,24], but these studies have been undertaken on extubated patients 2 days to 6 weeks after surgery.

We observed no significant change in airway resistance in relation to sternotomy or CPB in our patients. An increase in airway resistance is associated with a reduction in the volume expired in 1 s, but the V1.0 values were similar before and after CPB. Resistance of the whole respiratory system (Rrs) also did not change significantly throughout the study period. The resistance values measured before and after CPB in our patients were in the normal range, whereas values above 12 cmH2O L−1 s have been observed in patients with cardiogenic or non-cardiogenic pulmonary oedema[25].

In our patients, we found no significant change in alveolar-arterial oxygen difference related to CPB. A substantial increase in AaDO2 following cardiac surgery has been reported by other investigators and has been attributed to an increase in pulmonary shunt fraction [15,26,27]. Pre-operative assessment of our patients showed no severely depressed ventricular function (EF>50%). Our study was designed to use standard haemodynamic and respiratory monitoring equipment. Therefore, a pulmonary artery catheter was not inserted. Hence, we were not able to discern whether a small increase in AaDO2 observed in some patients was related to intrapulmonary right-to-left shunting or haemodynamic (decrease in cardiac out-put) and metabolic(elevated oxygen consumption) changes. Boldt and colleagues [28] demonstrated that PaO2 and shunt fraction remained unchanged after CPB when monoatrial cannulation with partial bypass was employed throughout the CPB period. Short duration CPB and use of this cannulation technique may explain the very small effect on AaDO2 in our patients. On the other hand, a moderate ventilation-perfusion mismatch might be present in the results presented here, since AaDO2 should not be influenced by the lack of homogeneity in V˙/Q˙ at FIO2 1.0.

Arterial to end-tidal CO2 tension differences obtained before CPB in the present study are in accordance with the reports of other authors [29,30]. After CPB, mean PaCO2-PetCO2 and alveolar dead space fraction scarcely changed in our patients. Fletcher [30] also reported no significant changes in mean PaCO2-PetCO2 during coronary artery bypass grafting. In contrast, other investigators found a marked increase in arterial to end-tidal CO2 tension difference and alveolar dead space following CPB, which could be explained by the lack of pulmonary blood flow during CPB and pulmonary capillaries not fully reopening after CPB [27,29]. From this point of view, monoatrial cannulation with partial bypass seems to be advantageous.

In conclusion, pulmonary function as measured by alveolar gas exchange was not compromised after CPB for uncomplicated cardiac surgery. In contrast, the study demonstrates a substantial reduction in the dynamic compliance of the respiratory system, which can be identified with standard respiratory monitoring. Diminished lung compliance leads to an increased work of breathing which results in a higher oxygen consumption and an increased myocardial work [31]. Further studies are required to demonstrate if easily measured intra-operative variables can predict patients who are at risk for increased work of breathing and difficult weaning.


1 Finsterer U. Lungenfunktion unter Narkose. Anästh Intensivmed 1983; 24: 277-287.
2 Rehder K. Anaesthesia and the respiratory system. Can Anaesth Soc J 1979; 26: 451-462.
3 Westbrook PR, Stubbs SE, Sessler AD, Rehder K, Hyatt RE. Effects of anesthesia and muscle paralysis on respiratory mechanics in normal man. J Appl Physiol 1973; 34: 81-86.
4 Andersen NB, Ghia J. Pulmonary function, cardiac status, and postoperative course in relation to cardiopulmonary bypass. J Thorac Cardiovasc Surg 1970; 59: 474-483.
5 Van Belle AF, Wesseling GJ, Penn OCKM, Wouters EFM. Postoperative pulmonary function abnormalities after coronary bypass surgery. Respir Med 1992; 86: 195-199.
6 Locke TJ, Griffiths TL, Mould H, Gibson GJ. Rib cage mechanics after median sternotomy. Thorax 1990; 45: 465-468.
7 Zin WA, Caldeira MPR, Cardoso WV, Auler JOC, Saldiva PHN. Expiratory mechanics before and after uncomplicated heart surgery. Chest 1989; 95: 21-28.
8 Breckenridge IM, Digerness SB, Kirklin JW. Increased extracellular fluid after open intracardiac operation. Surg Gynecol Obstet 1970; 131: 53-56.
9 Byrick RJ, Kay JC, Noble WH. Extravascular lung water accumulation in patients following coronary artery surgery. Can Anaesth Soc J 1977; 24: 332-345.
10 Hachenberg T, Tenling A, Nyström SO, Tyden H, Hedenstierna G. Ventilation-perfusion inequality in patients undergoing cardiac surgery. Anesthesiology 1994; 80: 509-519.
11 Mandelbaum I, Giamonna ST. Extracorporeal circulation, pulmonary compliance and pulmonary surfactant. J Thorac Cardiovasc Surg 1964; 48: 881-889.
12Asada S, Yamaguchi M. Fine structural change in the lung following cardiopulmonary bypass. Chest 1971; 59: 478-483.
13Ratliff NB, Young WG, Hackel DB, Mikat E, Wilson JW. Pulmonary injury secondary to extracorporeal circulation. J Thorac Cardiovasc Surg 1973; 65: 425-432.
14 Meriläinen P, Hänninen H, Tuomaala L. A novel sensor for routine continuous spirometry of intubated patients. J Clin Monit 1993; 9: 374-380.
15 Macnaughton PD, Braude S, Hunter DN, Denison DM, Evans TW. Changes in lung function and pulmonary capillary permeability after cardiopulmonary bypass. Crit Care Med 1992;20: 1289-1294.
16 Peters RM. Effects of cardiopulmonary bypass on lung function. In: Utley JR, ed. Pathophysiology and Technique of Cardiopulmonary Bypass. Baltimore, MD: Williams and Wilkins, 1983; 164-174.
17 Pezella AT, Asciotti A, Richardi P. Noncardiogenic pulmonary oedema following cardiopulmonary bypass: a report of two cases and review of the literature. Perfusion 1988; 3: 21-28.
18 Berrizbeitia LD, Tessler S, Jacobowitz IJ, Kaplan P, Budzilowicz L, Cunningham JN. Effect of sternotomy and coronary bypass surgery on postoperative pulmonary mechanics. Comparison of internal mammary and saphenous vein bypass grafts. Chest 1989; 96: 873-876.
19 Braun SR, Birnbaum ML, Chopra PS. Pre- and postoperative pulmonary function abnormalities in coronary artery revascularization surgery. Chest 1978; 73: 316-320.
20 Burgess GE, Cooper JR, Marino RJ, Peuler MJ, Mills NL, Ochsner JL. Pulmonary effect of pleurotomy during and after coronary artery bypass with internal mammary artery versus saphenous vein grafts. J Thorac Cardiovasc Surg 1978; 76: 230-234.
21Salama A, Hugo F, Heinrich D, Höge R, Müller R, Kiefel V, Mueller-Eckhardt C, Sucharit B. Deposition of terminal C5b-9 complement complexes on erythrocytes and leukocytes during cardiopulmonary bypass. N Engl J Med 1988; 318: 408-414.
22 Wisselink P, Feola M, Alfrey CP, Suzuki M, Ross JL, Kennedy JH. Prolonged partial cardiopulmonary bypass and the integrity of small blood vessels. J Thorac Cardiovasc Surg 1970; 60: 789-795.
23 Stanley TH, Liu WS, Gentry S. Effects of ventilatory techniques during cardiopulmonary bypass on postbypass and postoperative pulmonary compliance and shunt. Anesthesiology 1977; 46: 391-395.
24 Jenkins SC, Soutar SA, Forsyth A, Keates JRW, Moxham J. Lung function after coronary artery surgery using the internal mammary artery and the saphenous vein. Thorax 1989; 44: 209-211.
25 Mancebo J, Benito S. Pulmonary mechanics in acute respiratory failure. Intens Care World 1993; 10: 64-67.
26 Matthay MA, Wiener-Kronish JP. Respiratory management after cardiac surgery. Chest 1989; 95: 424-434.
27Parker DJ, Karp RB, Kirklin JW, Bedard P. Lung water and alveolary and capillary volumes after intracardiac surgery. Circulation 1972; (Suppl. 1) 45, 46: 139-146.
28 Boldt J, Zickmann B, Dapper F, Hempelmann G. Does the technique of cardiopulmonary bypass affect lung water content? Eur J Cardiothorac Surg 1991; 5: 22-26.
29 Bermudez J, Lichtiger M. Increases in arterial to end-tidal CO2 differences after cardiopulmonary bypass. Anesth Analg 1987; 66: 690-692.
30Fletcher R, Veintemilla F. Changes in the arterial to end-tidal PCO2 differences during coronary artery bypass grafting. Acta Anaesthesiol Scand 1989; 33: 656-659.
31 Wilson RS, Sullivan SF, Malm JR, Bowman FO. The oxygen cost of breathing following anesthesia and cardiac surgery. Anesthesiology 1973; 39: 387-393.

CARDIAC SURGERY, cardiopulmonary bypass; PULMONARY FUNCTION, spirometry

© 1998 European Academy of Anaesthesiology