Pressure-preset Ventilation

• review Pressure-preset Ventilation* Part 2: Mechanics and Safety Paul B. Blanch, B.A., R.R. T.; Michael Jones, R.R. T.; A. Joseph Layon, M.D., F.C.C.P.; and Neil Camnet; R.R . T. (Chest 1993; 104:904-12) APRV= airway pressure-release ventilation' ARDS = adult respiratory distress syndrome; Cr = total (lung-thorax) compliance' CPAP = continuous positive airway pressure' e = base for Datu: ~a~ loga~thm; .I:E = ins~iratory-to-expiratory ratio; IRDS = IdlOl!at~lc respiratory distress syndrome; IRV = inverse-ratio ventilation; PA= alveolar pressure above baseline; Paw = airway pressure; f'i!W =:= mean airway pressure; PCV = pressure-controll~ ventilation,. or pressure-control ventilation (a mode sel~~on on the. Siemens 900C ventilator); PEEP,=intrinsic positive e~d-expI~at0!1' pressure; PIFR = peak inspiratory Row rate; PIP - peak inOation pressure; Pp = preset pressure, controll.ed pressure, or constant pressure generated by the ventilatory apparatus; PPV = pressure-preset ventilation or controlled-pressure ventilation; PS = pressure support; PSV= p~ssure-sul?port ventilation; Raw = airways resistance; RE= al~ays. reS!Sta!1ce during expiration; 8J = airways resistance dunng IDSplration; SIMV synchronized intermittent manda!ory . ve~tilation ; T = time constant; TI = the time constant for l!1splrahon (RI x CT); TE = expiratory time; TI = inspiratory hme; VC-IRV = volume-controlled inverse-ratio ventilation· VCV =vol~me-controlled. ventilation; VONT=.ratio of dead space to tidal volume; VE= expiratory Row; VI= inspiratory Row; VL=volume change in the lung beginning at the endexpiratory volume ; VT=tidal volume.

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part 1 of this article discussed the historic development of pressure-preset ventilation (PPV). It was characterized as a simple system capable of generating a constant, predetermined amount of pressure. The clinical usefulness of PPV was not appreciated at first, and since delivered tidal volume (VT) depends on so many factors (requiring nearly continuous monitoring), ventilators capable of providing PPV eventually lost favor. Many of the following new ventilatory modes, however, are simple variations of pressure-preset ventilation: pressure-controlled ventilation (PCV), PCinverse-ratio ventilation (PC-IRV), airway pressurerelease ventilation (APRV), PC-synchronized intermittent mandatory ventilation (PC-SIMV), PC-SIMV + pressure support (PS), and even continuous flow, timecycled, pressure-limited ventilation. The fundamental difference between these new ventilatory modes and more conventional ones is that, by design, PPV attempts to apply and maintain a predetermined airway pressure (Paw) throughout inspiration. Pressure-preset ventilation is an extremely sophis*Fmm the .oe~tments .of Anesthesiology and Medicine (Dr. I.:ayon). U!?lver51ty ofFlonda College of Medicine; and Respiratory Care Services (Mr. Blanch. Jones, and Carnner), Shands Hospital at the University of Florida. Gainesville. 904

ticated version of pressure-limited ventilation. For example, simply changing inspiratory-to-expiratory time (I:E) during PPV will simultaneously alter the ventilator rate and PaW, which, in turn, may significantly alter VT, minute ventilation, and intrinsic positive end-expiratory pressure (PEEPJ Such complexity mandates that practitioners be familiar with PPV before instituting any form of it. Part 2 continues with the discussion of mechanical considerations and how they affect the safety of PPY, as well as conditions that may be beneficially affected by PPY. MECHANICAL CONSIDERATIONS

Tidal Volume Delivery Unlike volume-controlled ventilation (VCV), spontaneous breathing plays a fundamental role in determining VT during PPY. When a spontaneous breath coincides with a positive-pressure breath, the increased transpulmonary pressure (Paw minus pleural pressure) increases VT. Conversely, an asynchronous breath or an active attempt to exhale during mechanical inflation decreases VT. When asynchronous breathing becomes a problem, patients are generally sedated, relaxed by neuromuscular blockade, or both, particularly during the application of PC-IRY. When no spontaneous breathing occurs, the same physiologic factors influencing peak inRation pressure (PIP) during VCV (inspiratory time [TI], total lung compliance [CT], and airways resistance during inspiration [RID can alter VT during PPY. The most reliable and perhaps most effective way of ensuring an appropriate VTduring PPV is to use an TI that is at least three times the calculated TI. Momentto-moment changes in RI are therefore less likely to produce potentially dangerous variation in VT. Nevertheless, a sudden and dramatic change in CT may result in potentially dangerous changes in VT. Since such changes cannot be anticipated, exhaled VT must be monitored frequently, preferably continuously. Two techniques commonly used to determine an appropriate TI include (1) estimating TI at the bedside (TI = RI x CT), and (2) gradually prolonging TI while simultaneously measuring exhaled VT. The point at which further prolongation of TI produces no addiPrsssure-preset Ventilation. Part 2 (B/anch et a/)

tional increase in VTconstitutes the appropriate minimal inspiratory interval. During PPY, VT is directly proportional to the difference between end-inspiratory and end-expiratory alveolar pressure (PA) (VT= I1PA X Or). Therefore, as the end-expiratory PA (PEEPJ increases, whether inadvertently or by design, VT is progressively decreased. To preserve an advantageous VTand maintain gas exchange, it is often necessary to increase the preset pressure (Pp) on a one-for-one basis with the PEEP The combined data from two retrospective analyses of 50 patients who were switched from VCV to PCIRV suggest that a useful starting point for establishing PPV is to use a Pp of approximately 70 percent of the PIP required during VCV. I •2 The Pp is then increased or decreased to produce an advantageous VT. These two reports imply that PC·IRV improves Or in some patients. Some investigators believe that the beneficial effects of PC-IRY, including reduced PIP (improved Or) and improved oxygenation, result solely from intrinsic PEEP and not an increased mean Paw (Paw), decelerating VI pattern, or inverse I:E.3.4 A study of rabbits with idiopathic respiratory distress syndrome (IRDS), however, showed that PPV progressively improved Or as I:E was increased incrementally above 1:1 (Fig 1).5 Decreasing I:E incrementally below 1:1 had the opposite effect. Intrinsic PEEP was not a factor in this study. A flow transducer located at the proximal airway verified that exhalation was complete after each j•

CornplIence

breath, at each setting (except I:E of 4:1 and respiratory frequency of 60 breaths/min). Additional reports have offered indirect as well as direct evidence substantiating this finding.I.2.IH3 The classic work by Otis et al l4 offers one plausible explanation for this phenomenon. According to the theory, the lung is analogous to a parallel electrical circuit and is thus comprised of numerous duplicate pathways, each having a specific resistance and compliance. When exposed to a sinusoidal driving pressure , each alveolus fills in accordance to its operant time constant (TI). When the rate of breathing increases, or when disease (adult respiratory distress syndrome [ARDS], pneumonia) is present, gas distribution becomes increasingly unequal. This imbalance occurs primarily because of the expanding role that individual resistances play in overall pulmonary impedance. Pathways oflow resistance receive more flow (volume), and the effective Or decreases. 14 The respiratory system is not, however, always subjected to a sinusoidal driving pressure. This is particularly true during VCVwith a constant or square inspiratory flow (VI) waveform. 15 Under these circumstances, each alveolus initially fills at a rate primarily determined by, but inversely proportional to, the resistance of its specific conducting airway.15 After this initial curvilinear filling phase, a steady-state is achieved in which there is linear increase in both the pressure and volume within each alveolus. During the steady-state filling phase, each alveolus continues filling, only now the filling rate is directly proportional

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FIGURE 1. Relationship between inspiratory-toexpiratory ratio (I:E) and "relative" total (lungthorax)compliance (mean ± SE) at various breathing frequencies. At each frequency, compliance is expressed as a percentage of the compliance at an I:E of 1:1. (From Lachmann, Grossmann, Freyse, and

Bobertson.s)

CHEST I 104 I 3 I SEPTEMBER, 1993

1105

to its individual compliance. IS As a consequence of faster filling during the initial phase, alveoli connected to low-resistance pathways overinflate when compared with other alveoli with identical compliance but connected to highly resistant airways. Both PIP and the ratio of dead space to tidal volume (VDNT) may then increase.t" as alveoli associated with pathways of low resistance overinflate. Pressure-preset ventilation may prevent hyperinflation of alveoli because, once the Pp has heen reached, within any particular alveoli, flow into and expansion of that alveoli ceases. When an inverse I:E is also used, adequate time is allowed for gas to fiU alveoli with even the slowest filling rate, and both compliance and VDNT may, thus, improve.

Cycling Mechanism Although each variant of PPV is a form of pressurelimited ventilation, PPV should not be confused with pressure-cycled ventilation. With the exception of pressure support ventilation (PSV), which is flowcycled, the principal cycling mechanism guiding PPV is time, not pressure. When the selected TI exceeds the interval required to inflate the lungs, flow ceases, but the exhalation valve remains closed. This situation produces an inspiratory plateau that differs from the end-inspiratory pause commonly used during VCV. \blume-Controlled ~ntilation and the End-Inspiratory lbuse: As gas flows from any positive pressure source (ventilator) into a patient's lungs, the driving pressure (Paw) is a function of the pressure required to elastically expand the lung and overcome the resistance to airflow through the conducting airways. Mathematically: P=VI1CT+ RawV

(1)

where P (or Paw) and VL is the volume change in the lung beginning at the end-expiratory volume. At the onset of a volume-controlled end-inspiratory pause, flow from the mechanical ventilator is abruptly terminated, but the exhalation valve remains closed. The cessation of gas flow eliminates resistive pressure, and Paw equilibrates to, and reflects, the elastic recoil pressure (VI1CT) of the respiratory system . When airways resistance (Raw) is high, the eventual elastic recoil pressure is significantly lower than PIP. In theory, an end-inspiratory pause should allow adequate time for the delivered VTto evenly distribute (or redistribute) throughout the lungs and, thereby, should improve the efficiency of ventilation. Redistribution at the alveolar level is known as "pendelluft." That is, gas moves from hyperinflated alveoli to underinflated alveoli (Fig 2).17 In several studies, an end-inspiratory pause may have improved gas distribution (VDNT) and the removal of CO 2 but did not improve oxygenation reliably.12.IB.19 There are several possible reasons for this variable response. For in908

stance, leaks in the breathing circuit, around the endotracheal tube cuff, or through a bronchopleural fistula prevent stabilization of Paw and an end-inspiratory pause never transpires. Meier and Baum'" offered another explanation: redistributed gas (pendelluft) may have already participated in gas exchange and therefore would have the composition of expiratory gas. As such, pendelluft would not improve oxygenation in the hypoventilated area, where pendelluft arrives during an end-inspiratory pause. Meier and Baum'" proved this hypothesis with an elegant experiment, which also demonstrated that if fresh gas, such as that compressed into the breathing circuit during a positive pressure breath, is available, it will discharge into the lungs during an end-inspiratory pause and thereby reduce pendelluft and improve oxygenation. lTessure-lTesent ~ntilation and the Inspiratory Plateau: In contrast, during a Pp inspiratory plateau, PIP (Pp) and elastic recoil are identical because VI has already decelerated to zero before the onset of the

a

b

c

FIGURE 2. In theory, an end-inspiratory pause improves the distribution of gas throughout the lungs by prolonging the time that delivered tidal volume remains in the lungs. A, Regional differences In alveolar volume are common in hyaline membrane disease or adult respiratory distress syndrome. B, Conventional volumecontrolled, positive-pressure breaths tend to be distributed to more compliant alveoli or those alveoli at the end of low resistance pathways, which results in hyperinOation and elevated peak inspiratory pressure while other alveoli receive little or no ventilation. C, Maintenance of the delivered gas within the lungs for a longer time allows redistribution of some gas from hyperinflated alveoli to underinflated alveoli (pendeUuft), which should reduce dead space volume and improve the overall ventilation/perfusion ratio . (From Kirby.'') ~

VenlIIalIon. FlIrt 2 (Blanch et tJI)

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A

c

FIGURE 3. An inflation hold during pressure-eontrolled inverse-ratio ventilation (PC-IRY) produces its effect by preventing alveolar hyperinflation and eliminating pendelluft. A. Regional differences in alveolar volume common in hyaline membrane disease or adult respiratory distress syndrome. B. During PC-IRY, alveolar inflation ceases when PA equilibrates with preset pressure. which prevents hyperinflation and elevated peak inspiratory pressure (PIP). C. During an inflation hold . a fresh flow of gas is provided from the ventilator as alveoli with long time constants gradually inflate or as atelectatic alveoli are recruited. This characteristic reduces dead space volume . lowers PIp, and improves the overall ventilation! perfusion ratio. (Adapted from Ktrby,")

plateau. Furthermore, if, during the plateau phase, Paw decreases because of leaks or alveolar recruitment, the pressure differential that redevelops between the ventilator and alveoli produces an almost instantaneous VI at a rate high enough to maintain the plateau (preset) pressure. This type of end-inspiratory plateau may improve the efficiency of ventilation by several possible mechanisms. First, reliably maintain ing the plateau pressure increases Paw and eventually recruits more alveoli. Furthermore, lung inflation with PPV limits hyperinflation and virtually eliminates pendelluft. Finally, when alveoli are recruited, the inflow of fresh gas improves oxygenation by a mechanism similar to that proposed by Meier and Baum (Fig 3).17 In addition to improvements based on waveform, the differences between the end-inspiratory pause and the inspiratory plateau may partially explain why PCIRV often improves both oxygenation and ventilation,I.2.&II.21-29 whereas inverse I:E from reduced VI combined with an end-inspiratory pause during vol-

ume-controlled ventilation [VCV] (VC-IRV) fails to reliably improve oxygenation and reduces VONT less dramatically.18.30-32 Other Differences Between VC-fRVand PC-fRY: A related and common misconception is that VCV can be manipulated so that VC-IRV mimics PC-IRV precisely. In addition to the mechanical and functional differences during inspiratory plateau phases, it is extremely unlikely that the inherent or preprogrammed rate of deceleration of a volume-controlled ventilator would precisely match the needs imposed by pulmonary mechanics. Also, most volume-controlled ventilators do not decelerate to zero flow. If the rate of deceleration does not meet the needs of the patient, the inhalation phase during VCV would either prolong inhalation needlessly or produce a PIP that is higher than that during ppv. Furthermore, some ventilators limit operator manipulation of I:E during Vcv. For example, the Puritan-Bennett 7200ae allows a maximum I:E of approximately 3: I, regardless of the settings for VI and end-inspiratory pause .33 For these reasons, we believe that VC-IRV and PC-IRV should be considered separately, and that the distinction helps to explain the difference in opinions concerning IRV among authors investigating VCIRVI8.3G-32.34 or PC-IRV.I.2.~.2.-29 Exhalation

Exhalation during PPV should be passive, completely unimpeded, and determined solely by the patient's existing pulmonary mechanics . A bench test revealed that this is not the case (authors original data). Under identical conditions, VE was lower and the expiratory phase longer with the Puritan-Bennett 7200ae than with either the Siemens OOOC or the Hamilton Veolar. These findings clearly corroborate the previous work of authors investigating the function of different exhalation valves.~·36 Marini et al~ reported that during passive exhalation, a scissors-type exhalation valve, such as in the Siemens OOOC, lowered resistance to flow more than an inflatable diaphragm or mushroom valve ofthe type in the Puritan-Bennett 7200ae. Banner36 reported that, of all the ventilator/ exhalation valve combinations he tested, the Hamilton Veolar produced the lowest resistance to flow. These findings may have important clinical ramifications. Specifically,because limiting exhalation and creating PEEP. is often a therapeutic goal of PC-IRV,··6,R,37 any unexpected impedance to exhalation might make precise control of PEEP, difficult. Furthermore, additional resistive impedance during exhalation reduces the range of functional combinations of mechanical ventilatory breathing rate and I:E that will not develop PEEP, (that is, for those circumstances when PEEP, is unwanted). In the past, few authors realized that the gas trapped CHEST /104 / 3 / SEPTEMBER, 1993

907

during PC-IRV generated a quantifiable pressure (PEEPJ, and most simply neglected to measure it. This was an unfortunate oversight, as knowing the precise moment to terminate exhalation may be a crucial factor in the success ofPC-IRY. Because PEEP, is a direct measure of the volume of trapped gas (V= PEEP, X CT), this is a useful and reproducible way of determining the precise moment to terminate exhalation. For example, if exhalation ends too quickly, the resulting high levels ofPEEP, create an immediate potential for cardiovascular stress. In addition, high levels of PEEP, reduce the pressure gradient between the ventilator and the alveoli at the onset of inspiration. This condition reduces VTand may lead to pronounced hypercarbia. On the other hand, if expiration lasts too long, PEEP, may be too low to effect the anticipated improvement in oxygenation. Without measurements of PEEP" it could be very difficult to duplicate accurately, for any particular patient, the beneficial effects noted for another. Certainly, it is not unreasonable to wonder if an I:E of 4:1 produces its benefit because the VI pattern is decelerating, PaW increases, and pendelluft decreases, or because the I:E occasionally provides a crude standard for determining the appropriate level of PEEP,. The PEEP, was discovered during conventional mechanical ventilation with PEEP at high ventilatory rates.38-40 Under these conditions, undetected PEEP, adversely affected hemodynamic stability and the process of ventilatory weaning.38 •41-43 Citing this literature, some investigators have suggested that PEEP, and externally applied conventional PEEP are identical and that ventilatory strategies likely to produce PEEP, therefore should be avoided in favor of techniques relying upon the more manageable conventional PEEp'3,4 Despite such unsubstantiated claims, it is at least plausible that, under some conditions, PEEP, produces measurably different effects and occasionally might be more therapeutic than externally applied PEEP. This area needs further investigation. The theory of IRV suggests that prolonged inspiration helps recruit alveoli with a long TI. 5 One author noted that if PC-IRV did not improve CT, the mode would be unsuccessful in that particular patient.7,28 This viewpoint implies that alveolar units with a long TI are the target of PC-IRY. The use of externally applied PEEP also targets slowly filling alveolar units. 44 The amount of externally applied PEEP required to expand such alveoli, however, may overexpand other, more compliant areas. As a result, lung volume increases, but the hyperinBated areas can increase VDNT and decrease cardiac output. By reducing or eliminating the amount of externally applied PEEP and relying on PEEP" end-expiratory pressure will be trapped in specific regions of the 908

lungs. The remaining sections of the lung (those having short TI) are not exposed to any significant intrinsic or externally applied PEEP. Since these alveoli are allowed to empty completely during exhalation, they may receive a regional increase in blood Bow. An interesting ramification of this theory involves the level of PEEP. within the targeted alveoli. Consider, for example, a measured PEEP, of 10 em H20. Hypothetically, if the alveoli were divided equally into those with long and those with short TI, then during exhalation, rapidly filling units would immediately deflate to a pressure near ambient. A PEEP, of 20 cm H20 would be required in the long-r alveoli to produce an average intrinsic PEEP of 10 em H20. Higher or lower values for PEEP, might exist in the target alveoli, as defined by the specific ratio of rapidly-toslowly filling units in each particular patient. Furthermore , this example demonstrates why applied PEEP (which transmits pressure equally to all alveoli regardless of individual time constants) cannot reliably duplicate the effect of PEEP•. The complete or nearly complete deBation of parts of the lungs in the presence of PEEP. may help explain how some patients tolerate PC-IRV and PEEP, (up to 23 cm H20) without the hemodynamic compromise common with conventional PEEp'6,7,25,28,45 At least one case report has documented a therapeutic substitution of PEEPI for conventional PEEp'46In practice though, the systematic substitution of PEEP, for conventional PEEP is complex and, up to now, generally involved a trial-and error manipulation of expiratory time (TE): each adjustment of Te required that PEEP, be measured because PA decays exponentially during exhalation as shown: PA = dPmax (e-Tl'frE) (2) where e = the base for the natural logarithms . Thus, PA could not be accurately predicted by a simple linear equation or ratio. In an effort to simplify the therapeutic application of PEEP" we developed a single, composite-function, logarithmic equation that predicts the requisite TE for any particular (desired) PEEP, level." With this equation, only an initial measurement of PEEP, is required, and the number of subsequent measurements required to adjust the ventilator is reduced. Even after PEEP. is successfully adjusted, however, alterations in CT and Raw may in turn affect PEEP, over time . These effects may occur either within specific regions of the lung or globally. Such complexity makes the true natures and roles of both types of PEEP conjectural until laboratory and clinical studies clarify the specific physiologic variables and conditions that each impact. Respiratory and Hemodynamic Monitoring During

PPV

Monitoring VT: Monitoring VT is particularly imPressure-preset Ventilation, Part 2 (Blsnch et 81)

portant to safely apply PPY. Because VTis not directly controlled by the ventilator and may partly depend on Cr and Raw; a sudden change in either of these physiologic variables may instantaneously change VT. Unexpected decreases in VT are not immediately hazardous and are usually detected in ample time by an exhaled minute volume alarm. A notable exception occurs when the Siemens 900C is used for patientassisted PCY. Because the 900C does not have alarms for low VT or high respiratory rate (other ventilators capable of PCV have either one or both of these alarms), a decreased VT may go undetected if respiratory rate increases concurrently such that minute ventilation is unchanged. Sudden and dramatic increases in VT are a completely different matter. Barotrauma is theoretically possible with even one excessive VT, and, unfortunately, currently available ventilators that can generate PPV are not equipped to limit VT. Such a safety feature is urgently needed, because significant and sometimes dramatic improvements in Or, and thus, VT are common during PPY, particularly during PC_IRy'1,2·6-11.13 A safety feature limiting VT might function in a manner analogous to the pressure-limiting controls and alarms found on virtually all mechanical ventilators. Most ventilators equipped with a PPV mode are guided by microprocessor, and this characteristic should facilitate development of a Vr-limitmg mechanism. For example, it is conceivable that software changes might allow the VTcontrol that is now unused in the PPV mode to serve two functions . During PPY, the VT control would allow the operator to select a maximal safe VT. Any breath violating this threshold would be terminated and audible and visual alarms would be activated. Another possibility would be that a "smart" PPV mode could be developed. Software changes might allow the operator to select a particular VT and TI. The microprocessor then would vary the Pp (up or down) automatically to keep VT at the set level. Apparently, a limited version of such a system, called pressure-regulated VCV is being developed by Siemens." Monitoring PEEPl: Inadvertently or intentionally inducing PEEP. during PC-IRV creates yet another monitoring dilemma. For reproducibility as well as patient safety, monitoring and controlling PEEP. is essential. Unfortunately, no reliable method of accurately measuring PEEP. now exists. Nevertheless, several measurement techniques are widely used . 1. In the absence of spontaneous ventilation, a pressure transducer and pneumotachograph can be placed at the proximal portion of the airway. Intrinsic PEEP is taken as the pressure at the opening of the airway at the onset of VI.41 2. Another less reproducible method of determining PEEP. involves an appropriately timed maneuver

referred to as an "expiratory hold." The operator occludes both the inspiratory limb and the exhalation valve either manually or automatically (by button) at the precise moment the next controlled breath is scheduled to eommence.P Intrinsic PEEP is taken as the pressure at the proximal airway once it equilibrates. A number of circumstances can render an expiratory hold inaccurate, however. If the ventilator does not have an expiratory hold button, the clinician must precisely time the application of the hold. The breathing circuit and endotracheal tube cuff must not leak. Furthermore, the patient must not attempt a spontaneous breath during the maneuver. Even if all other forms of potential error are eliminated, the loss of gas from the lungs into the breathing circuit during equilibration produces an erroneously low value . Although the use of breathing circuits with a low compressible volume could minimize this type of error, such circuitry is not always practical. 3. The volume of gas remaining in the thorax at the end of exhalation can be directly monitored. 32 •49 Although this method (respiratory inductive plethysmography) is as accurate as the expiratory-hold maneuver.'" thoracic gas volume is an indirect measurement and therefore subject to error. Furthermore, the necessary equipment is not commonly available and may not be practical for routine use in the intensive care unit. On occasion, externally applied PEEP and PEEP. will coexist. When this occurs, measurement techniques will not estimate the PEEP., but instead estimate the absolute end-expiratory PA or the total PEEP: total PEEP = PEEP. + external PEEP. The actual PEEP. in this situation becomes the difference between total and external PEEP. Further complicating the quantification of PEEP. with the first two methods is that neither one measures or estimates the amount of gas trapped behind prematurely collapsed airways. The problem of measuring PEEP. may ultimately be resolved mathematically. It may be possible to calculate PEEP. accurately based on measurements of RI and airways resistance during expiration (RE), Pp, TI, and I:E.SO Hemodynamic Monitoring: There is a very real possibility of hemodynamic depression during the use of PPY, particularly in conjunction with inverse I:E (PC-IRY, APRV). This mode often dramatically increases PaW and can generate PEEPh both of which can decrease venous return or cardiac output. Before instituting either of these modes, clinicians should make provisions to continuously monitor cardiovascular variables. In addition, therapists using PPV should cautiously adjust all available ventilatory alarms. These alarms may vary among ventilator types but generally include alarms for high and low exhaled minute volume, high and low respiratory rates, low CHEST 1104 I 3 I SEPTEMBER, 1993

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VT, high Pa\Y, and high and low continuous positive airway pressure (CPAP). Until each of these monitoring dilemmas is resolved, PPV-and specifically PC-IRV and APRV-should be used cautiously. The PC-IRV or APRV will require almost continuous monitoring, particularly immediately after initiation of the mode. Ventilator management should be restricted to clinicians thoroughly familiar with the idiosyncrasies and ramifications of PPY. RESPIRATORY CONDmONS THAT BENEFIT FROM IRV Even among staunch proponents of the various forms of PPV (including APRV and PC-IRV), there is little disagreement that these modes are not effective for every patient. 1.6.28 The problem is determining who would benefit from PPV and who would not. This consideration applies to virtually all forms of mechanical ventilation but is particularly important for PPY. In light of existing monitoring dilemmas and insufficient safety mechanisms previously mentioned, patients not likely to benefit should not be exposed to the risks involved. In neonatology, regardless of pathophysiologic factors, almost all respiratory conditions requiring mechanical ventilation are managed with a variant of PPV-continuous 8o\Y, pressure-limited, time-cycled ventilation. Thus, the decision is much simpler: whether or not to use IRY. After Reynolds and Herman 21.22 first reported that IRV was useful in treating IRDS, IRV was frequently employed. Since then, this modality has fallen out of favor," Although the reason is not clear-cut, confusing and misleading symptoms resulting from undiagnosed PEEP may have shaken clinician confidence in the mode . Another possible reason was supplied by Reynolds himself, who suggested that IRVnot be applied during recovery from IRDS. During this phase, widespread and uneven airways obstruction is present, and a long inspiratory phase would almost certainly lead to circulatory embarrassment, gas trapping, or both." Determining the precise moment that recovery begins might well be impossible. Hence, the frequency with which these side effects occur during IRV may have created further disillusionment with the mode. For adult patients, treatment is complicated by the simple fact that PPV (PC-IRV, APRV) is seldom used. Furthermore, only certain ventilators offer these modes, and frequently, switching modes may involve switching ventilators as well. Most literature suggests that PC-IRV or APRV is of use in treating severe ARDS or acute respiratory failure,'·2.6.24.Z7.28.51.52 and one author reports having treated some patients with pneumonia." Each report describes slightly different criteria for initiating these modes. Some common criteria have been as follows: high PEEP (> 10 cm j

910

H 20), an inability to provide an acceptable level of oxygenation despite a fractional concentration of inspired O2 of 2=0.80, diffuse bilateral radiographic infiltrates, and elevated pulmonary capillary wedge pressure. Despite these criteria, a certain percentage of patients either do not improve with PC-IRV,··6 or worse, suffer immediate cardiovascular and hemodynamic eomplications.t-" An overlooked but potentially predictive factor useful as criteria for suitability of PC-IRV was proposed by Gattinoni et al.Z7 After a review of36 patients with severe ARDS who were treated with PC-IRV, the measurement of static CT emerged as a practical indicator for success. In this study, any patient who had static CT of less than 25 ml/cm H 20 failed to respond to PC-IRV and required low-frequency positive pressure ventilation with extracorporeal CO 2 removal (19 of 36 patients). Patients with static CT of 25 to 30 ml/cm H 20 improved dramatically during PC-IRV, and the mode in most cases was switched successfully to spontaneous CPAP within 48 h (12 of 27 patients). Once static CT was >30 ml/em H 20, treatment was switched successfully to spontaneous CPAP. Unfortunately, to our knowledge, this information has been ignored, and additional research investigating this concept or other predictive factors has not been published. Until such research is completed and published, the process of properly identifying which conditions to treat with PPV remains subject to error. CONCLUSIONS Pressure-preset ventilation is a complicated yet intriguing mode . Some interesting but preliminary reports have described a number of potential applications. Pressure-preset ventilation apparently functions by a number of theoretically advantageous characteristics such as an exponentially decelerating VI pattern, an elevated PaW, a static inspiratory plateau, and PEEP•. Unfortunately, lack of scientific evidence and criteria for applicability complicate its use . Furthermore, currently available mechanical ventilators capable of PPV are not equipped to ensure safety. Until additional scientific evidence is published and technical problems are resolved, PPV should be considered an unproven mode and used accordingly. In the meantime, potential users ofPPV should familiarize themselves with all the technical and physiologic characteristics associated with all the variants of the mode : PSv, APRV, PCv, PC-IRV, PC-SIMV, and PCSIMV + PS. ACKNOWLEDGMENTS: The authors wish to thank both Pauline Snider and Lynn Dirk for their patience and skillful editorial help in the preparation of the manuscript.

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