Brtsh Journal of Anaesthesa 1997; 79: 306 310 Comparson of volume controlled wth pressure controlled ventlaton durng one-lung anaesthesa M. TUĞRUL, E. ÇAMCI, H. K ARADENI Z, M. ŞENTÜRK, K. PEMBECI AND K. AKPIR Summary Pressure controlled ventlaton (PCV) s an alternatve mode of ventlaton whch s used wdely n severe respratory falure. In ths study, PCV was used for one-lung anaesthesa and ts effects on arway pressures, arteral oxygenaton and haemodynamc state were compared wth volume controlled ventlaton (VCV). We studed 48 patents undergong thoracotomy. After two-lung ventlaton wth VCV, patents were allocated randomly to one of two groups. In the frst group (n 4), onelung ventlaton was started by VCV and the ventlaton mode was then swtched to PCV. Ventlaton modes were performed n the opposte order n the second group (n 4). We observed that peak arway pressure (P 0.000001), plateau pressure (P 0.01) and pulmonary shunt (P 0.03) were sgnfcantly hgher durng VCV, whereas arteral oxygen tenson (P 0.0) was sgnfcantly hgher durng PCV. Peak arway pressure (Paw) decreased consstently durng PCV n every patent and the percentage reducton n Paw was 4 35% (mean 16.1 (SD 8.4) %). Arteral oxygen tenson ncreased n 31 patents usng PCV and the mprovement n arteral oxygenaton durng PCV correlated nversely wth preoperatve respratory functon tests. We conclude that PCV appeared to be an alternatve to VCV n patents requrng onelung anaesthesa and may be superor to VCV n patents wth respratory dsease. (Br. J. Anaesth. 1997; 79: 306 310). Key words Ventlaton, one-lung. Ventlaton, volume controlled. Ventlaton, pressure controlled. Durng one-lung anaesthesa, arteral hypoxaema s a major concern. 1 Volume controlled ventlaton (VCV) s the tradtonal method of performng onelung anaesthesa n patents undergong thoracc surgery and an ncrease n arway pressure s usually observed. If the method of ventlaton nvolves excessve amounts of arway pressure, vascular resstance of the dependent lung may be ncreased because of compresson of ntra-alveolar vessels. Thus hgh arway pressures of the dependent lung may counteract hypoxc pulmonary vasoconstrcton n the non-dependent lung by dvertng blood flow away from the ventlated lung, thereby ncreasng pulmonary shunt fracton. 3 One-lung ventlaton mples delverng the entre tdal volume nto one lung, whch may result n barotrauma of the dependent lung. In order to avod hgh arway pressures, anaesthetsts may ventlate the dependent lung wth lower tdal volumes and hgher ventlatory frequences durng one-lung anaesthesa. However, lower tdal volumes have been demonstrated to predspose the dependent lung to atelectass and worsen arteral oxygenaton. 4 5 Pressure controlled ventlaton (PCV) s an alternatve mode of ventlaton whch s used wdely n severe respratory falure. PCV has been shown to mprove arteral oxygenaton and decrease peak arway pressure because of ts deceleratng nspratory flow. 6 Unform dstrbuton of nspred gas wth PCV s the major cause of better arteral oxygenaton n patents wth respratory falure. 7 10 We appled PCV to one-lung anaesthesa and examned ts use as a tool to mprove ventlatory management of patents undergong thoracc surgery. In our study, PCV was used for one-lung anaesthesa and ts effects on arway pressure, arteral oxygenaton and haemodynamc state were compared wth those produced by VCV. Patents and methods The study was approved by the Unversty of Istanbul Ethcs Commttee and all patents gave nformed consent. We studed 48 patents, ASA I III, undergong thoracotomy requrng one-lung ventlaton. On the evenng before surgery, sprometry (forced vtal capacty (FVC) and forced expratory volume n 1 s (FEV 1 )) was performed n the sttng poston. An arteral blood-gas sample was also obtaned wth the patent breathng ar. Patents were excluded f they had a hstory of cardac, hepatc or renal dsease. All patents were premedcated wth dazepam 0.15 mg kg 1 orally, 1 h before arrval n the operatng room. On admsson to the operatng room,.v. MEHMET TUĞRUL*, MD, EMRE ÇAMCI, MD, HAKAN KARADENİZ, MD, MERT ŞENTÜRK, MD, KAMIL PEMBECİ, MD, KUTAY AKPİR, MD, Department of Anaesthesology and Intensve Care, Unversty of Istanbul, Istanbul Medcal Faculty, Türkye. Accepted for publcaton: Aprl 5, 1997. *Address for correspondence: I.Ü. Istanbul Tp Fakültes, Anestezyoloj Anablm Dal, 34390, Çapa, Istanbul, Türkye.
PCV as an alternatve mode of ventlaton for one-lung anaesthesa 307 and ntra-arteral cannulae were nserted under local anaesthesa and an ECG was attached. After preoxygenaton, anaesthesa was nduced wth fentanyl g kg 1 and propofol.5 mg kg 1 ; tracheal ntubaton was facltated wth vecuronum 0.1 mg kg 1. The trachea was ntubated wth an Unvent tracheal tube (Fuj Corp, Japan). The bronchal blocker of the Unvent tube was nserted nto the manstem bronchus of the operatve sde guded by a fbreoptc bronchoscope and separaton of the lungs was demonstrated by capnography. 11 Wth ths method, the tracng from the end-tdal carbon doxde analyser connected to the proxmal end of the bronchal blocker of the Unvent shows a typcal respratory waveform. As the bronchal blocker cuff s gradually nflated, a straght lne on the waveform ndcates that lung solaton has occurred. After nducton of anaesthesa a 7-F pulmonary artery catheter (Abbott, Crtcare Systems, USA) was nserted va the rght nternal jugular ven. Isoflurane 1 1.5%, fentanyl 0.05 0.1 g kg 1 mn 1 and vecuronum 0.03 mg kg 1 every 30 mn were used for mantenance of anaesthesa. Fentanyl bolus doses of 50 100 g and.v. fluds were admnstered to mantan systemc arteral pressure wthn 0% of pre-nducton values. Oesophageal temperature was montored throughout the procedure and mantaned greater than 36.5 C by a heatng blanket (Bçakçlar, Turkey) placed under the patent. Our study conssted of three steps. Two-lung ventlaton (TLV) wth VCV (TLV-VCV) was performed n the lateral decubtus poston n all patents (Servo 900C, Semens, Stockholm, Sweden). On ntaton of one-lung ventlaton, patents were allocated randomly to one of two groups. In the frst group (n 4), one-lung ventlaton was started by VCV (OLV-VCV) and the ventlaton mode was then changed to PCV (OLV-PCV). The modes of ventlaton were performed n the opposte order n the second group (n 4). Durng TLV-VCV and OLV-VCV, patents lungs were ventlated wth a tdal volume of 10 ml kg 1 and ventlatory frequency was adjusted to mantan arteral carbon doxde tenson ( P a CO ), at 4.5 6 kpa. PCV was ntated wth a peak arway pressure that provded a tdal volume of 10 ml kg 1. Ventlatory frequency was adjusted to mantan P a CO, at 4.5 6 kpa durng OLV-PCV. Wth both PCV and VCV, we used a 5% nspratory tme and a 10% pause tme. Inspratory oxygen concentraton ( F I O ) was adjusted to 0.5 n ar durng two-lung ventlaton and to 1.0 durng one-lung ventlaton. End-tdal concentratons of carbon doxde and soflurane were montored usng a Crtcare 1100 (Crtcare Inc, USA). In accordance wth data obtaned from prevous studes, 1 13 all measurements were made 30 mn after ntaton of the ventlaton mode. All operatons were performed by the same surgcal team and the study was completed before any pulmonary vessels were lgated. Measurements were completed durng the mnutes n whch the surgeons stopped compressng the operatve lung. The followng varables were measured and recorded at the end of each perod. Arteral and venous oxygen tensons and saturatons ( Pa O, S a O, - SV O ), Pa CO and haemoglobn (Hb) were analysed wthn 5 mn usng ABL 505 and OSM3 Hemoxmeter (Radometer, Copenhagen, Denmark). Heart rate (HR), mean arteral pressure (MAP), pulmonary artery pressure (MPAP), central venous pressure (CVP) and pulmonary artery occluson pressure (PAOP) were recorded from the Crtcare 1100 (Crtcare Inc, USA). Deltran II transducers (Utah Medcal, USA) were used to measure pulmonary arteral and systemc pressures. The zero reference was the md-chest level and vascular pressures were measured at end-expraton. Cardac output (CO) was measured by a thermodluton technque usng njecton of 10 ml of 0.9% salne at 0 C (Abbott Crtcare Systems, USA). The mean value of three measurements was obtaned. Pulmonary shunt (Qs/Qt) was calculated fr om standard formulae. 14 Peak arway pressure (Paw) and mean arway pressure (Pmaw) were recorded durng each mode of ventlaton. Inspratory plateau was establshed by actvatng the nspratory hold on the Semens Servo 900C ventlator. Inspratory plateau pressure (Pplt) was measured durng the last 0.3 s of each hold manoeuvre. We studed P a O data n order to dentfy whch patents would beneft fr om OLV-PCV. The relatonshp between ndvdual P a O dfferences between OLV-PCV and OLV-VCV and respratory functon tests was studed by lnear r egr esson analyss. Data are presented as mean (SD). Pared Student s t test, ANOVA and ch-square test were used to test the sgnfcance of the dfferences between groups. Statstcal sgnfcance was assumed at P 0.05. Results Patent data are shown n table 1. Mean values for ventlaton, gas exchange and haemodynamc varables at each tme are presented n tables and 3. Durng one-lung ventlaton, arteral hypoxaema ( S a O 90%) requrng renflaton of the collapsed lung dd not occur n any patent. - Pa CO, Sa O, S V O, Hb, MAP, MPAP, PAOP, CVP and CO dd not dffer sgnfcantly between any of the ventlaton modes. Comparson of the OLV-VCV and OLV-PCV modes revealed sgnfcant dfferences n Paw, Pplt, Table 1 Patent data. FVC Forced vtal capacty, FEV 1 forced expratory volume n 1 s, P a O =arteral oxygen tenson, Pa CO arteral carbon doxde tenson (mean (SD) [range] or number) (n 48) Age (yr) 56.4 [30 78] Weght (kg) 70.3 (11.5) [46 95] Sex (M/F) 38/10 Rght-left-sded thoracotomy 8/0 Lobectomy/pneumonectomy 9/19 Preoperatve FVC (% predcted) 77.1 (15) [46 117] Preoperatve FEV 1 (% predcted) 76.8 (14) [43 11] Preoperatve P a CO (kpa) 5 (0.63) [3.95 6.7] Preoperatve P (kpa) 10. (1.1) [7.9 1.8] a O
308 Brtsh Journal of Anaesthesa Table Ventlaton and gas exchange data (mean (SD)). Paw Peak arway pressure, Pplt plateau pressure, Pmaw mean arway pressure, Pa O arteral oxygen tenson, Sa O arteral oxygen saturaton, Pa CO arteral carbon doxde tenson, SV O mxed venous oxygen saturaton, Qs/Qt ntrapulmonary shunt, TLV two-lung ventlaton, OLV one-lung ventlaton, PCV pressure controlled ventlaton, VCV volume controlled ventlaton. *P 0.05 compared wth OLV-VCV, ***P 0.001 compared wth OLV-VCV TLV-VCV OLV-VCV OLV-PCV Tdal volume (ml) 708 (11) 714 (111) 710 (114) Paw (cm H O) 1.4 (4.7) 8.3 (5.1) 3.65 (3.85)*** Pplot (cm H O) 15.7 (3.8) 18.5 (4.) 17.8 (3.7)* Pmaw (cm H O) 6.7 (1.4) 7.8 () 7.95 (1.55) P a O (kpa) 7.5 (7.9) 8.4 (15.6) 3.3 (14.4)* S a O (%) 99.1 (0.98) 98.3 (3.1) 98.7 (.1) P a CO (kpa) 4.8 (0.77) 5.06 (0.87) 5.05 (0.9) SV O (%) 80.7 (6.8) 81. (8.3) 81.4 (7.3) Qs/Qt (%) 16.7 (6.) 40. (10.1) 36. (10)* Fgure 1 Indvdual P a O dfference between PCV and VCV vs FVC (forced vtal capacty) (r 0.30, P 0.0) (y 168.6 1.8x). Table 3 Haemodynamc data (mean (SD)). HR Heart rate, MAP mean arteral pressure, MPAP mean pulmonary artery pressure, PAOP pulmonary artery occluson pressure, CVP central venous pressure, CO cardac output, TLV twolung ventlaton, OLV one-lung ventlaton, PCV pressure controlled ventlaton, VCV volume controlled ventlaton TLV-VCV OLV-VCV OLV-PCV HR (beat mn 1 ) 77.5 (11) 79.4 (9.8) 78.8 (10) MAP (mm Hg) 94 (14) 9 (11) 9.7 (1) MPAP (mm Hg) 18 (3.) 18.6 (3) 19.1 (4.6) PAOP (mm Hg) 15.1 (.3) 15.5 (3.7) 15.7 (3.7) CVP (mm Hg) 10.8 (3.7) 11.4 (3.6) 11.6 (3.6) CO (ltre mn 1 ) 4.4 (0.9) 4.55 (0.8) 4.6 (0.87) P a O and Qs/Qt. Paw was sgnfcantly lower durng OLV-PCV than durng OLV-VCV (3.65 (3.85) cm H O vs 8.3 (5.1) cm H O) (P 0.000001). Compared wth OLV-VCV, Paw decreased consstently durng OLV-PCV n every patent, rangng from 1 to 13.5 cm H O. The percentage Paw dfference was 4 35% (mean 16.1 (8.4) %). Pplt was also sgnfcantly lower durng OLV-PCV than durng OLV-VCV (17.8 (3.7) vs 18.5 (4.) cm H O) (P 0.01). Mean P a O was sgnfcantly hgher durng OLV- PCV (3.3 (14.4) kpa vs 8.4 (15.6) kpa) (P 0.03) than durng OLV-VCV. Arteral oxygenaton mproved n 31 patents wth OLV-PCV and n 17 patents wth OLV-VCV (P 0.008). Twenty-three of 31 patents (74%) who had an mproved P a O value wth OLV-PCV had an FVC lower than 77%, whereas only sx of 17 (35%) patents who had an mproved P a O wth VCV had an FVC lower than 77% (P 0.0). Also, 19 of 31 patents (61%) whose P a O mproved wth OLV-PCV had an FEV 1 lower than 77%, whereas fve of 17 (30%) patents whose P a O mproved wth OLV-VCV had an FVC lower than 77% (P 0.07). On the bass of lnear regresson analyss ndvdual P a O dfference between OLV-PCV and OLV-VCV showed a sgnfcant correlaton wth FVC (r 0.30, P 0.0) (fg. 1), but no sgnfcant correlaton wth FEV 1 (r 0.4, P 0.09). Mean Qs/Qt was sgnfcantly hgher durng OLV- VCV (40. (10.1) vs 36. (10) %, P 0.0) than durng OLV-PCV. Qs/Qt was found to be hgher durng OLV-VCV n 3 patents, whereas OLV- PCV resulted n hgher Qs/Qt values n only 16 patents (P 0.00). Dscusson VCV s the common mode of ventlaton used n patents undergong one-lung anaesthesa. In our study, we performed pressure controlled ventlaton to overcome some of the problems observed wth one-lung anaesthesa. We planned to use almost the same tdal volumes to examne the effects of each mode on arway pressures, pulmonary shunt and arteral oxygenaton. As tdal volumes greater than 10 ml kg 1 were reported to ncrease arway pressure and pulmonary vascular resstance n the dependent lung, 5 15 16 we chose a tdal volume of 10 ml kg 1 for the dependent lung whch was reported to be least detrmental to arteral oxygenaton. 17 As t has been documented prevously that P a O tends to ncrease over 1 h after the onset of one-lung anesthesa, 18 we randomzed the order of PCV and VCV. Hgh arway pressures may lead to barotrauma of the dependent lung. 19 It has been reported that hgh peak nspratory pressure has some nfluence on the ncdence of barotrauma 0 and avodng hgh peak nspratory pressures seems to be a safe form of ventlaton. 1 In our study, peak nspratory pressures were consstently lower durng PCV. A reducton n peak nspratory pressure of 4 35% nduced by PCV s an advantage for one-lung anaesthesa. It has been demonstrated prevously that PCV s assocated wth sustaned reductons n peak nspratory pressure because of ts deceleratng flow profle. 7 8 In studes performed n patents wth respratory falure, peak nspratory pressure was shown to declne from 38 to 33 cm H O 9 and from 43 to 40 cm H O 10 by PCV. The benefcal effects of reduced peak nspratory pressures durng PCV n terms of mnmzng lung njury have been attrbuted to concomtant reductons n peak alveolar pressure and consequent decreases n alveolar dstenson. However, there are no studes comparng the
PCV as an alternatve mode of ventlaton for one-lung anaesthesa 309 ncdence of atrogenc lung njury usng PCV or VCV. It was postulated that the very rapd ntal flows wth PCV may cause dfferent effects on fllng patterns, and thus the rsk of barotrauma from shearng may be less usng pressure vs volume breaths. 3 There s a growng tendency to defne endnspratory plateau pressure as a more mportant determnant of barotrauma than peak arway pressure. 4 In our study, plateau pressure was found to be sgnfcantly lower durng PCV. Furthermore, t s possble durng VCV for some alveol to receve hgher pressures durng nspraton than the endnspratory plateau pressure. In contrast, n no parts of the lung can the pressure be hgher than the preset pressure durng PCV. Because of the hgh peak nspratory pressures usually observed wth the ntaton of one-lung anaesthesa, most anaesthetsts tend to ventlate the dependent lung wth lower tdal volumes and hgher respratory frequences amng to protect the dependent lung from hypernflaton. However, lower tdal volumes have been demonstrated to predspose the dependent lung to develop atelectass, thereby worsenng arteral oxygenaton. 4 5 We assume that lower arway pressures obtaned wth PCV allow the use of hgher tdal volumes durng one-lung anaesthesa. Factors that play a role n the hypoxaema frequently seen durng one-lung anaesthesa nclude reducton n dependent lung volume caused by nducton of anaesthesa, abdomnal and medastnal compresson, suboptmal postonng, low ventlaton: perfuson ratos and atelectass because of a hgh F I O, and problems n removal of secretons. 5 Hypoxc pulmonary vasoconstrcton s an autoregulatory mechansm that dverts blood flow away from hypoxc, atelectatc lung towards the remanng normoxc, ventlated lung and t s very effectve n reducng hypoxc lung blood flow when the percentage hypoxc lung s ntermedate (30 70%), that s the amount of lung that s hypoxc durng one-lung anaesthesa. 6 Compresson of small ntra-alveolar vessels durng nflaton of alveol produces ncreased resstance to pulmonary blood flow n the dependent lung. Ths ncrease n vascular resstance may dvert blood flow to the non-ventlated alveol of the non-dependent lung. Further ncreases n tdal volume and arway pressure n the dependent lung are then unlkely to mprove oxygenaton and may make arteral oxygenaton worse by dvertng blood flow to the non-dependent lung. 4 16 17 Although not necessarly reflectng ntra-alveolar pressure, the hgh peak and plateau pressures observed wth VCV n our study may play a role n dvertng blood flow to the nondependent lung and produce a hgher pulmonary shunt. One of the ams of ths study was to nvestgate the effects of PCV on arteral oxygenaton durng onelung anaesthesa. It was demonstrated earler that mprovement n arteral oxygenaton by PCV was not related to varatons n mean arway pressure but resulted mostly from the benefcal effects of the deceleratng nspratory flow pattern produced by PCV on the dstrbuton of gas wthn the lung. 7 In dseased lungs wth dfferent tme constants, the deceleratng flow of PCV sustans alveolar pressure longer than the constant flow of VCV, thereby adng recrutment and mprovng homogenous dstrbuton of nspred gas. In our study, P a O mproved n most patents durng PCV and mean P a O was sgnfcantly hgher than that durng VCV. The mprovement n arteral oxygenaton durng PCV may be explaned by the flow profle of ths mode and also the lower pulmonary shunt obtaned wth PCV. To answer the queston whch patents benefted more from PCV we nvestgated the correlaton between ndvdual P a O dfferences between PCV and VCV, and respratory functon tests. We found that there was a sgnfcant correlaton between ndvdual P a O dfference between PCV and VCV, and FVC. Patents whose P a O mproved wth PCV generally had a poor FVC (fg. 1). Many of the studes demonstratng better arteral oxygenaton wth PCV compared wth VCV were performed n patents wth severe respratory falure. 7 9 As may be expected, those patents who had dependent lung pathology of varyng severty, especally patents wth restrctve dsease, benefted from the deceleratng flow pattern of PCV whch mproved dstrbuton of alveolar gas and arteral oxygenaton. Acknowledgements We thank Dr Smru Turnaoğlu for manuscrpt preparaton, Vldan Vural for secretaral help and Fügen Yavuz Pr for techncal assstance. References 1. Malmkvst G, Fletcher R, Nordström L, Werner O. Effects of lung surgery and one-lung ventlaton on pulmonary arteral pressure, venous admxture and mmedate postoperatve lung functon. Brtsh Journal of Anaesthesa 1989; 63: 696 701.. Benumof JL. 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