DoesAirwayPressure Release Ventilation Alter LungFunction After AcuteLungInjury

Background: Duringairwaypressure release ventilation(APRV), tidal ventilation occurs between theincreased lungvolume established bytheapplication of continuous positive airway pressure (CPAP) andtherelaxation volume oftherespiratory system. Concern has beenexpressed that release ofCPAPmaycause unstablealveoli tocollapse andnotreinflate whenairway pressure isrestored. Objective: Tocompare pulmonary mechanics andoxygenation inanimals withacute lunginjury during CPAP withandwithout APRV. Design: Experimental, subject-controll ed, randomized crossover investigation. Setting: Anesthesiology research laboratory, University ofSouth Florida College ofMedicine Health Sciences Center. Subjects: Tenpigsofeither sex. Interventions: Acute lunginjury wasinduced withan intravenous infusion ofoleic acid (72,ug/kg) followed by randomly alternated 60-min trials ofCPAPwithand without APRV.Continuous positive airway pressure wastitrated toproduce anarterial oxyhemoglobin saturation ofatleast 95%(FIo2=0.21). Airway pressure release ventilation wasarbitrarily cycled toatmospheric pressure 10times perminute witharelease timetitrated tocoincide withattainment ofrespiratory system relaxation volume. Measurements: Cardiac output, arterial andmixed venous pH,blood gastensions, hemoglobin concentrationandoxyhemoglobin saturation, central venous pressure, pulmonary andsystemic artery pressures, pulmonary artery occlusion pressure, airway gasflow, airwaypressure, andpleural pressure weremeasured. Tidal volume (VT), dynamic lungcompliance, intrapulmonaryvenous admixture, pulmonary vascular resistance, systemic vascular resistance, oxygen delivery, oxygen consumption, andoxygen extraction ratio were calculated. Mainresults: Central venous infusion ofoleic acidreducedPaO2from94+4 mm Hg to52±9 mm Hg (mean ±1SD)(p<0.001) anddynamic lungcompliance from40±6mL/cmH20to20±6mL/cmH20(p=0.002) andincreased venousadmixture from13±3% to 32+7%(p<0.001) intenswineweighing 33.3+4.1 kg while they werespontaneously breathing roomair. Afterinduction oflunginjury, theswine received CPAP (14.7 ±3.3cmH2O) withorwithout APRVat10breaths perminute witharelease timeof1.1+0.2s.Although meantranspulmonary pressure wassignificantly greater during CPAP(11.7±3.3 cmH20)vsAPRV(9.4±3.8 cm H20)(p<O.OOl), there werenodifferences inhemodynamicvariables. PaCO2wasdecreased andpHawas increased during APRVvsCPAP(p=0.003 andp=0.005). PaO2declined from83±4mm Hgto79±4mm Hg (p=0.004) during APRV,butarterial oxyhemoglobin saturation (96.6 ±1.4%vs96.9±1.3%,) didnot.Intrapulmonary venous admixture (9+3% vs11±5%)and oxygen delivery (469 +67mL/minvs479±66mL/min) werenotaltered. After treatment periods andremoval ofCPAPfor60min, PaO2andintrapulmonary venous admixture returned tobaseline values. Discussion: Intrapulmonary venous admixture, arterial oxyhemoglobin saturation, andoxygen delivery were maintained byAPRVatlevels induced byCPAPdespite thepresence ofunstable alveoli. Decrease inPaO2was caused byincrease inpHaanddecrease inPaCO2, not bydeterioration ofpulmonary function. We conclude thatperiodic decrease ofairway pressure created by APRVdoesnotcausesignificant deterioration inoxygenation orlungmechanics. (Chest 1995; 107:805-08)