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Patient-ventilator interaction during acute hypercapnia:pressure-support vs. proportional-assist ventilation

V. MARCO RANIERI, ROCCO GIULIANI, LUCIANA MASCIA,SALVATORE GRASSO, VITO PETRUZZELLI, NUCCIA PUNTILLO,GAETANO PERCHIAZZI, TOMMASO FIORE, AND ANTONIO BRIENZAIstituto di Anestesiologia e Rianimaxione, OspedalePoliclinico, Universith di Bari, 70100 Bari, Italy

Ranieri, V. Marco, Rocco Giuliani, Luciana Mascia,Salvatore Grasso, Vito Petruzzelli, Nuccia Puntillo,Gaetano Perchiazzi, Tommaso Fiore, and AntonioBrienza. Patient-ventilator interaction during acute hyper-capnia: pressure-support vs . proportional-assist ventilation.J. Appl. Physiol. 81(l): 426-436, 1996.-The objective of thisstudy was to compare patient-ventilator interaction duringpressure-support ventilation (PSV) and proportional-assistventilation (PAV) in the course of increased ventila tory re-quirement obtained by adding a dead space in 12 patients onweaning from mechanical ventilation. With PSV, the level ofunloading was provided by setting the inspiratory pressure at20 and 10 cmHzO, whereas with PAV the level of unloadingwas at 80 and 40% of the elastic and resistive load. Hypercap-nia increased (P < 0.001) tidal swing of esophageal pressureand pressure-time product per breath at both levels of PSVand PAV During PSV, application of dead space increasedventilation (VE) during PSV (67 t 4 and 145 t 5% during 20and 10 cmHsO PSV, respective ly, P < 0.001). This was due to arelevant increase in respiratory rate (48 t 4 and 103 t 5%during 20 and 10 cmHzO PSV, respect ively, P < O.OOl>,whereas the increase in tidal volume (VT) played a small role(13 t 1 and 21 t_ 2% during 20 and 10 cmHzO PSV,respect ively, P < 0.001). With PAV, the increase in irEconsequent to hypercapnia (27 IL 3 and 64 t 4% during 80and 40% PAV, respective ly, P < 0.001) was related to theincrease in VT (32 t 1 and 66 t 2% during 80 and 40% PAV,respect ively, P < O.OOl), respiratory rate remaining un-changed. The increase in pressure-time product per minuteand per liter consequent to acute hypercapnia and the senseof breathlessness were significantly (P < 0.001) higher duringPSV than during PAY Our data show that, after hypercapnicstimulation of the respiratory drive, the capability to increaseVE through changes in VT modulated by variations in inspira-tory muscle effort is preserved only during PAV, the compen-satory strategy used to increase VE during PSV requiresgreater muscle effort and causes more pronounced patientdiscomfor t than during PAVcarbon dioxide stimulation; weaning

ASANALTERNATIVETOSTANDARD volume-controlledmodesof mechanical ventilation, considerable interest hasrecently developed in partial ventilatory-support tech-niques. Their purpose is to assist each spontaneousbreath by providing positive pressure at the airwayopening (Pao) during spontaneous inspiration. Pressure-support ventilation (PSV) is the standard form ofpartial ventilatory support that can be used in sponta-neously breathing patients, both in the early phase ofacute respiratory failure (ARF) or during weaning frommechanical ventilation (6, 7, 17). During PSV, each

spontaneous breath is assisted by a constant positivepressure applied in the ventilator circuit during theduration of inspiration. Breathing frequency is deter-mined by the patient because no controlled cycle isdelivered. Tidal volume (VT) depends on the combinedaction of the pressure generated by the respiratorymuscles (Pmus), the ventilator (Pappl), and the totalimpedance of the respiratory system (6, 7, 17). Propor-tional-assist ventilation (PAV) is an alternative mode ofpartial ventilatory support recently proposed (32, 35),in which the ventilator generates pressure in propor-tion to patient effort; the more the patient pulls, themore pressure the machine generates. The ventilatoramplifies patient effort without imposing any ventila-tory or pressure targets.The main theoretical difference between PSV andPAV is the function that Pappl is designed to followduring inspiration (33). With PSV, the ventilator causesPappl to rise to a preset level and remain at that leveluntil the cycle-off criterion is reached. The amount ofPappl should not therefore be affected by the effort ofthe patient (6, 7, 17). By contrast, with PAV, the timecourse of Pappl is linked to the time course of the effortof the patient. Pappl rises as long as inspiratory-muscleeffort is produced by the patient. What is preset is not atarget pressure but the proportion between Pao andinspiratory-muscle effort, i.e., how much Pappl will risefor a given increase in Pmus during inspiration (32,35).On the basis of these theoretical distinctions, substan-tial differences in patient-ventilator interaction areexpected to occur between PSV and PAV during varia-tions in ventilatory requirement. The aim of this studywas therefore to assess hese differences and evaluatetheir physiological relevance in mechanically venti-lated patients during the weaning period during acutevariations in ventilatory requirement. We investigatedthe hypothesis that, whereas during PSV the increasein minute ventilation (VE) consequent to hypercapnicchemoreceptor stimulation would primarily be accom-plished by an increase in respiratory rate, with PAVthis would occur through an increase in VT with feweffects on respiratory rate. We expected this compensa-tory strategy to result in greater patient comfort andlower work of breathing.METHODS

Twelve patients admitted to the intensive care unit o f thePoliclinico Hospital (University of Bari) were studied. Theywere nasotracheally intubated (Portex cuffed endotrachealtube with an inner diameter varying from 7 to 8 mm) andmechanically ventilated for the management of ARF. Etiolo-

426 0161-7567/96 $5.00 Copyright o 1996 the American Physio logical Society

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EFFECTS OF CHANGES IN RESPIRATORY DRIVE: PSV VS. PAV 427gies of ARF included multiple trauma (5), myocardial infarc-tion (3), pneumonia (2), and sepsis (2). Entry criteria includedclinical and hemodynamic stabili ty and a maximal inspira-tory pressure of at least -20 cmHsO. During the study, nopositive end-expiratory pressure (PEEP) was applied. All patientswere in the weaning process, as prescribed by their attendingphysician. The investigative protocol was approved b y the localethics committee, and written informed consent was obtainedfrom each patient. A physician not involved in the studyprotocol was always present to provide for patient care.

Flow rate (V) was measured with a heated pneumotacho-graph (Fleisch no. 2; Fleisch, Lausanne, Switzerland) con-nected to a differential pressure transducer (MP-45, t2cmHzO; Validyne, Northridge, CA), which was inserted be-tween the Y piece of the ventilator circuit and the endotra-cheal tube. The pneumotachograph was linear over theexperimental range of V. Equipment dead space (not includ-ing the endotracheal tube) was 70 ml. Pao was measuredproximal to the endotracheal tube with a pressure transducer(Validyne, MP-45, 5100 cmH20). Changes in pleural pres-sure were estimated from changes in esophageal pressure(Pes) measured by using a double-lumen nasogastric tube(1.4-Fr, 127 cm; Mallinckrodt, Argyle, NY) with a thin-walledvinyl balloon (10 cm long, 3.8 cm circumference) incorporatedin the lower midportion of the tube and connected to adifferential pressure transducer (Validyne, MP-45, t 100cmHz0). The esophageal balloon was filled with l-l.5 ml ofair and positioned as previously described (2). All the abovevariables were displayed on an eight-channel strip-chartrecorder (7718A, Hewlett-Packard, Cupertino, CA) and col-lected on a personal computer through a 12-bit analog-to-digital converter at a sample rate of 100 Hz. Subsequent dataanalysis was performed by using the software package Ana-dat (RHT-InfoDat, Montreal, Quebec). VT was computedby the digital integration of the V signal.End-expiratory CO2 tension (PETIT > was continuouslymonitored between the pneumotachograph and the endotra-cheal tube with an infrared side-stream capnograph (Cap-nomac Ultima, Datex, Helsinki, Finland). A 20-gauge Tefloncatheter was inserted percutaneously for arterial blood sam-pling and measurement of blood gases (IL 1303, Instrumenta-tion Laboratories, Lexington, MA).

Experimental procedure. Patients were studied in thesemirecumbent position. Maximal inspiratory pressure wasmeasured as the most negative airway pressure generatedwithin the first 20 s of total airway occlusion at end-expiratorylung volume (19). A one-way valve was used in the expiratoryline to ensure that efforts began from a lung volume less thanor equal to the equilibrium volume of the chest. All patientswere responsive and were instructed to make forceful effortsduring this manuever; they did not usually need the fullallotted time to reach a peak value. Before the study, allpatients were on PSV (Siemens Servo Ventilator 9OOC,Siemens Elema, Berlin, Germany) ranging between 10 and 18cmHZO [12.90 t 0.87 (SE) cmHaO].

Static elastance (Est,rs) and total resistance of the respira-tory system (RT,rs) were obtained by using the rapid airway-occlusion technique (10) during a period of respiratory muscleinac tivi ty obtained by injection of a short-acting hypnoticagent (propofol, 0.3 mgekg-l=rnin-l for 5 min) and controlledmechanical ventilation (VT of 10 ml/kg, constant inspiratoryV of 1 l/s, and respiratory rate of 12 breaths/min). Briefly, anend-expiratory airway occlusion was performed by pressingthe end-expiratory hold knob on the Siemens 9OOC vent ilator.Static intrinsic PEEP (PEEPi,t) was measured as the plateaupressure during the end-expiratorv airway occlusion on the

Pao signal. At the end of the following breath, an end-inspiratoryocclusion (EIO) was performed by pressing the end-inspiratoryhold knob on the ventilator. After EIO, the Pao signal exhibited aninitial drop [maximum pressure (P,,,) - pressure after firs tdrop], followed by a slow decline to an apparent plateaupressure (10). The corresponding pressure value at 3-5 safter EIO was taken as the static end-inspiratory recoilpressure of the respiratory system (Pst,rs) (10). Est,rs wascomputed by dividing the values of (Pst,rs - PEEPist) byVT. RT,rs was calculated by dividing (P,, - Pst,rs) byV immediately preceding the occlusion (10).Twenty to thirty minutes after static respiratory mechan-ics measurements, when respiratory muscle act ivi ty wasregained (judged to have occurred when negative swings inPes developed during inspiration), and patients awoke, theSiemens 9OOC was replaced by a Winnipeg venti lator (Univer-si ty of Manitoba, Winnipeg, Manitoba). This is an experimen-tal prototype designed to provide PAV but can also deliver allconventional modes of ventilation. The design and operationof this unit are similar to those previously described (32, 35).The gas-delivery system consists of a freely moving pistonreciprocating within a chamber. The electronics control amotor that moves a piston toward the patient. As the patientbreathes in, the piston moves freely into the cylinder, provid-ing an initial flow and volume; when the velocity of the pistonmovement (i.e., inspiratory flow) reaches a preset thresholdvalue, the motor starts to assist the movement of the piston.The flow level required to trigger the motor is variable, and inthe present study was set at 0.05 l/s (35). When the piston isactivated, it creates pressure in the piston chamber, and theforward movement of the piston produces airflow. This air isdirected to the patient through a one-way valve, the inspira-tory line, and the humidifier. The difference between thechamber pressure and the proximal airway pressure creates atrigger or assist signal. This signal, in turn, switches thethree-way solenoid valve connecting the pump pressure to theexhalation valve line and causes the exhalation valve to close.Gas transfer is terminated when the patient stops inspiratoryflow. This creates positive pressure with respect to thechamber pressure. When patient pressure exceeds chamberpressure, the trigger signal goes of f, causing the exhalationvalve line to open. This allows passive deflation through theexhalation valve. The piston returns to the starting position,intaking gas from the ventilator input as it moves backward.An external-demand blended-gas sys tem is attached to theinput opening. When the piston has returned to the startingposition, the machine resets and is ready for the nextinspiration. PEEP can be applied by adding a PEEP valve onthe exhalation line of the ventilator circuit. The motor appliesforce to the piston according to different command signalsregulated by the operating ventila tory mode. During PSV, thecontrol denotes the level of pressure assistance for a patient-initiated breath. The changeover from inspiration to expira-tion can be set as different absolute flow values or as differentpercentage values of the initial peak flow. In this study,cycl ing between inspiration and expiration occurs when theflow rate falls to 5 l/min. During PAV, the command signalsare instantaneous inspired flow (derived f rom the rate offorward motion of the piston) and instantaneous inspiredvolume (derived from piston displacement since the onset ofinspiration). Once flow begins, pressure in the chamber risesin proportion to ongoing flow and volume, thereby augment-ing the pressure gradient for chest expansion. The amount ofassistance for both flow and volume can be set as varyingpercent values of RT,rs and Est,rs through external controls.When this percentage is set below natient resistance

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428 EFFECTS OF CHANGES IN RESPIRATORY DRIVE: PSV VS. PAVand elastance, chamber pressure increases only if the patienteffort increases. When inspiratory effort decreases at end-inspiration, inspiratory flow decreases and then stops, caus-ing the integrator to reset and the assistance to terminate.Two levels of vent ilatory support were used during PSVand PAV Pressure levels of 10 and 20 cmHs0 were appliedduring PSV, whereas 40 and 80% of elastic and resistiveassistance were given during PAVTo induce acute hypercapnia with a consequent variationin patient ventilatory requirement, a fixed dead space of 150ml was applied between the pneumotachograph and the Ypiece of the venti lator circuit (30). Measurements were ob-tained before (dead space of f ) and afte r (dead space on)application of dead space. During dead space on, an increasein PET,,~ o f 30% of its baseline value was considered as thetarget value. The necessary time to obtain this resultamounted to 8-10 min (9.11 t 0.11 min). Ventilatory modes,levels of assistance, and dead space were randomly applied.Measurements were obtained from 20-25 breaths in eachexperimental condition once a stable breathing pattern wasobserved. During dead space on, arterial blood samples andmeasurements of PETIT were obtained 15-20 min (18.11 t0.18 min) after the target increase in PETIT had beenobtained and a stable PETE-, level was observed at both levelsof PSV and PAV The fractional inspired 02 concentrationremained constant throughout the study period.

Data analysis . Inspiratory time (TI), expiratory time (TE),and total breathing cycle time (TT) were determined from theV tracing. Tidal excursions of Pes (Apes) were also determined.During PSV and PAV, inspiratory pulmonary resistance(RL) and el as t ante (EL) were calculated by using the Meadand Wittenberger technique (21). Briefly, RL and EL werecalculated by fitting the equation of motion of a single-compartment model by using multilinear regression, as fol-lows

APL = RL.~&~~ + EL. AV (1)where APL is inspiratory change in transpulmonary pressure(calculated by subtracting Pes from Pao), AV is inspiratorychange in lung volume between end-expiratory lung volumeand VT, and Vpeak is peak inspiratory flow (14). The level ofintrinsic PEEP during different levels of PSV and PAV(PEEPidyn) was measured as the negative deflection in Pesfrom the onset of inspiratory effort to the point of zero V (13,22). This approach is based on the assumption that change in

Table 1. Patient characteristics

pleural pressure required for initiation of inspiratory V isequal to the opposing level of elastic recoil pressure present atend expiration and/or the cessation of expiratory effo rt (13,22).

Pressure-time product (PTP) per breath (PTP/b) for theinspiratory muscle was measured as the area under the Pessignal from the beginning of the inspiratory deflection to theend of inspiratory V relative to the Pes tracing obtainedduring the period of controlled mechanical venti lation andrespiratory muscle relaxation and assuming that elastance ofthe chest wall (CW) was linear within the VT range (27). Thestatic CW line was placed by assuming that the end-expiratory elastic recoil pressure of the CW was equivalent tothe end expiratory position of Pes during tidal breathing (12).This assumption was verified by occluding the airway at endexpiration during the four experimental conditions and dem-onstrating that the end-expiratory position of Pes underoccluded breaths was essentially identical to that duringunoccluded breaths. PTP per minute (PTP/min) was calcu-lated as PTP/b multiplied by respiratory rate. PTP per liter ofiTE (PTP/I) was calculated as PTP/min divided by i7E.

The level of dyspnea during the application of dead spacewas evaluated at both levels of PSV and PAV Patients wereinstructed to indicate any change in the sense of breathless-ness by pointing to a bidirectional ordinal scale (0 = no change;- l/+ 1 = very slight worsening/improvement; - 2/+ 2 = slightworsening/improvement; - 3/+ 3 = moderate worsening/im-provement; -4/+4 = marked worsening/improvement;-5/+5 = very marked worsening/improvement) (4,23).

StatisticaL anaZysis. Values are expressed as means t SE.Values obtained at different CO2 levels and with differentmodes of partial ventilation were compared by using theanalysis of variance for repeated measures. Regression analy-sis was performed with the least squares method. A value ofP < 0.05 was considered statist ically significant.

RESULTSCauses of ARF, sex, age, days of mechanical ventila-tion, and static respiratory mechanics during con-trolled mechanical ventilation obtained on the day ofthe study are shown in Table 1 for the individualpatients. Arterial O2 (Pao,) and CO2 (Paco2>pressuresand pH values just before the study are also indicated.

Patient Age, Paoz pace: *, MIP, Est,rsf, RT,rst, PEEPis, 7No. Sex yr Cause of ARF FIO, Torr Torr pH* cmH20 cmH20/l cmH20 - 1-l - st cmH20 Day1 F 372 F 623 M 414 F 285 F 216 M 517 M 678 M 499 F 5710 F 58

11 M 2512 M 38

SepsisPneumoniaSepsisMultiple traumaPancreatis, laparotomy, sepsisMultiple traumaPeritonitis, laparotomy, sepsisMultiple traumaPneumoniaPneumoniaMultiple traumaMultiple trauma

0.4 91 43 7.42 -30 25 14 0.55 40.4 98 44 7.41 -37 20 16 0.38 80.3 118 39 7.40 -41 30 13 0.37 40.4 115 41 7.41 -52 23 15 0.51 80.3 109 42 7.40 -41 20 15 1.12 90.4 110 41 7.40 -38 20 18 0.59 140.4 134 39 7.46 -37 18 17 3.31 100.3 105 38 7.41 -40 20 16 1.15 80.4 109 41 7.42 -42 22 18 0.87 80.3 108 35 7.43 -44 21 15 1.02 50.4 110 42 7.40 -31 23 12 1.02 110.4 98 39 7.43 -33 20 14 0.55 14

* Data obtained during pressure-support ventilation just before study; f data obtained during short trial of respiratory mus cle inactivity andcontrolled mech anical ventilation previous to experimental procedure. ARF, acute respiratory failure; FI+ fraction of inspired 02 mech anicalventilation; Pao,, arterial 02 tension; Pace,, arterial CO2 tension; MIP, maximal inspiratory pressure; Est,rs, static elastance of respiratorysystem; Rqrs, total resistance of respiratory system; PEEPi,t, s tatic intrinsic positive end-expiratory pressure.

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EFFECTS OF CHANGES IN RESPIRATORY DRIVE: PSV VS. PAV 429Table 2. Effects of dead space on Pace, and PETIT, dead space was applied at both levels of PAV, tidalat different levels of PSV and PAV excursions in Pes, VT, Pappl, and V markedly in-creased, whereas respiratory rate remained unchangedPace,, Torr PETIT,, Torr Pace, - PETITE, Torr (Fig. 2).

PSV 20 cmHz0 When dead space was applied, VE increased (P