A Successful Computerized Protocol for Clinical Management of Pressute Control Inverse Ratio Ventilation in ARDS Patients* Thomas D. East, Ph.D.; Stephan H. Bbhm; C. Jane Wallace, B.S.N.; Terry E Clemmer; M.D., F.C.C.E; LindeU K. Weaver; M.D.; James F. Orme [r., M.D.; and Alan H. Morris, M.D., F.C.C.R

We have developed a computerized protocol that provides a systematic approach for management of pressure controlinverse ratio ventilation (PCIRV). The protocols were used for 1,466 h in ten around-the-clock PCIRV evaluations on seven patients with severe adult respiratory distress syndrome (ARDS). Patient therapy was controlled by protocol 95 percent of the time (1,396 of 1,466 h) and 90 percent of the protocol instructions (1,937 of 2,158) were followed by the clinical staff. Of the 221 protocol instructions, 88 (39 percent) not followed were due to invalid PEEPi measurements. Compared with preceding values during CPPV, the expired minute ventilation was reduced by 27 percent during PCIRV while maintaining a pH that was not clinically different (mean difference in pH = 0.02). There was no difference in the PaOZ, PEEPi, or the Flos between pcmv and CPPV. The PEEP setting was reduced by 33 percent from 9±0.05 to 6±0.6 and the I:E ratio increased from 0.64 ± 0.04 to 2.3 ± 0.10. Peale airway pressure was reduced by 24 percent (from 59± 1.5 to 45±0.6) and mean airway pressure increased by 27 percent (from 22±0.8 to 28±0.6) in PCtRV. Right atrial and pulmonary artery pressures were higher and cardiac output lower in pcmv but blood pressure was unchanged. The success of this protocol has demonstrated the feasibility of using PEEPi as a primary

T contributes here is evidence that positive pressure ventilation to the lung damage in adult respiratory

distress syndrome (ARDS) patients. Barotrauma (pneumomediastinum, pneumothorax, subcutaneous and interstitial emphysema, and cystic altera' ~ ons of *From the Pulmonary and Critical Care Divisions, Department of Internal Medicine, LDS Hospital, the Department of Bioengineering, University of Utah, and the Department of Anesthesiology, University of Utah Medical Center, Salt Lake City {Dr. East}. Mr. Bohm is visiting research predoctoral fellow from the Department of Physiology, Rheinisch-Westflilische Hochschule Aachen, Aachen, Cermany Special Acknowledgment: We gratefully acknowledge the contribution of the following critical care physicians who participated in the clinical evaluations of the protocol logic: Nathan Dean, MD; Brad Rasmussen, MD; and James Pearl, MD. We also recognize Lisheng Peng, MEBE, for doing most of the software development; Barbara H. Hoffmann for her contributions during the clinical evaluation, as well as Susan Henderson, B.A., who did a majority of the database management, and Nathan L. Pace, M.D., who provided the statistical analysis, The helpful comments and cooperation of Polly Bailey and all the nurses and respiratory therapists of the Shock TraumalIntermountain Respiratory ICU at the LDS Hospital were sincerely appreciated. Manuscript received February 11; revision accepted July 3. Reprint requests: Dr. East, Pulmonary Division, LDS Hospital, 8th Avenue and C Street, Salt Lake City 84143

control variable for oxygenation. This computerized PCIRV protocol should make the future use of PCIRV less mystifying, simpler, and more systematic. (Cheat 1992; 101:697-710) autoPEEP = difference between setPEEP and the actual endexpiratory lung pressure {em HsO~ C(a-v)O. = arterial-mixed venous oxygen content (mVdI); CPAP = continuous positive airway pressure ventilation; CPPV = controUed positive pressure ventilation; Cth = total thoracic compliance; DBP = diastolic arterial blood pressure (mm Hg); desired PEEPi = desired value for PEEPi (em 0.0); Do. = oxygen delivery (mllmln); ECCO.R = extracorporeal CO. removal; ECMO = emacorporeal membrane oxygenation; liE = inspiratory : expiratory ratio; IRV = inverse ratio· ventilation; MBP = mean arterial blood pressure (mm Hg); PAOP=puImonary artery occlusion pressure (mm Hg); PAP=mean pulmonary artery pressure (mm Hg); Paw=mean airway pressure (em H.O); PCIBV= pressure control inverse ratio ventilation; PEEPi = intridsic PEEP (end-expiratot-y lung pressure at the end of a 2-s endexpiratory hold) (em 0.0) in~ic PEEP=setPEEP+ autoPEEP; Ppeak=peak inspiratory pressure (em H.O); PRA = rigbt atrial pressure (mQlHg); QslQt = pulmonary shunt fraction; Qt = cardiac output (Umin); setPEEP = PEEP value set on the ventilator (em. UsO); TE = expiratory time (s); TI = inspiratory time (s); VA = alveolar ventilation (Urpin); VDNT= physiologic dead space to titLtI volume ratio; VE= expiratory minute ventilation (Umin); Vo. = oxygen consump: tion (mVmin); VB = ventilatory rate (breaths/min); VT= tidal volume (m1)

the lung) is a significant complication of positive pressure ventilation.P In lower mammals, high peak inspiratory pressure (Ppeak) has been shown to damage the lung. 3 ,4 Positive airway pressure has been associated with the development of bronchopulmonary dysplasiav" and with bronchiolectasis in adults. 6 Pressure control inverse ratio ventilation (PCIRV) is intended to reduce the likelihood of iatrogenic lung damage during positive pressure ventilation. During mechanical ventilation with PCIR~ Ppeak is constant and the inspiratory-expiratory (I:E) ratio is typically 1:1 to 4:1. The inspiratory flow decelerates as the airway pressure equilibrates at Ppeak during the relatively long inspiratory time. Since, the expiratory time (TE) is short relative to the time required for complete exhalation, alveolar pressure may not fall to the end-expiratory pressure level expected from the ventilator settings of positive end-expiratory pressure (PEEP). Thus, end-expiratory alveolar pressure (PEEPi) may be higher than the setPEEE This is well recognized"!' and known as autoPEEE The impact on CHEST I 101 I 3 I MARCH, 1992

697

Table I-A SummtJry ofthe Primary Impact ofVentUator AtljutJtmenta on (hygenation and Ventilation ift lbtientB without Significant Obaf1lCtive Lung Diaeaae* autoPEEP=O em IIsO

A

Common Mode of Mechanical Ventilation: CPPV when I:E is low and VB is not >30. Less Common Mode of Mechanical Ventilation: PCIRV when VB is 0 em 1Is0 Most CommoD Mode of Mechanical Ventilation: PCIRV when VR is > 10 or I:E is > 1.2. Less Common Mode of Mechanical Ventilation: CPPV when I:E is .... 1.0 or at high VB. B

Ventilator Adjustments

t Flo.

f setPEEP t I:E fVR f Ppeak

Ventilation

Oxygenation

t PAOli

~ (Ppeak - setPEEP) and f setPEEP-+ t PEEPi and f Paw ~ (TE)-+ t PEEPi and t Paw ~ (TE)-+ f PEEPi

t (Ppeak -

setPEEP)-+

t PEEPi and t Paw

~ (Ppeak - PEEPi)-+ ~ VT-+ ~ \FE ~ (Ppeak - PEEPi)-+ ~ VT-+ ~ \FE ~ (Ppeak- PEEPi)-+ ~ VT t VR and ~ VT-+?VE change t (Ppeak- PEEPi)-+ f VT-+ t \FE

*The effects with and without the presence of autoPEEP are shown. Secondary effects such as 80w patterns and distribution of ventilation are neglected in this comparison.

oxygenation and ventilation of ventilator adjustments, with and without autoPEEP present, is summarized in Table 1. For the common controlled positive pressure ventilation (CPPV) support of ARDS when there is no autoPEE~ the adjustment of oxygenation and ventilation are simple and independent of one another (Table 1, part A). In contrast, for PCIRV support of ARDS, when autoPEEP is present, the adjustment of oxygenation and ventilation is much more complex and almost all adjustments of the ventilator result in changes in both oxygenation and ventilation (Table 1, part B). Often these changes are in opposite directions (ie, increasing I:E may increase oxygenation and decrease ventilation). These issues make PCIRV titration complex and confusing and underlie the trial and error approach commonly used with PCIRV in the intensive care unit (ICU). Although all conclude that Ppeak can be reduced by PCIRV and some have demonstrated decreased VDNT,7,12,13 increased C th,7,12,1" increased Pa02,12-15 and reduced QslQt,12,13 none of the published PCIRV studies are controlled prospective randomized clinical trials focusing on outcome variables such as mortality or morbidity23,24 (Table 2). The postulated mechanisms for the increased oxygenation efficiency include recruitment of alveoli13,1" combined with a more favorable ventilation:perfusion ratio. 13,19 Most of the authors did not find dramatic changes in hemodynamic parameters and oxygen delive~7,17,22 although some report problems.P-P We conclude from a review of the

techniques used previously to manage PCIRV (Table 2) that there is no standard approach to the management of PCIRV23 and that many articles lack the description or quantification of parameters such as PEEPi and ventilatory rate (VR) without which it is very difficult to define the conditions of the study A large part of the confusion that surrounds PCIRV u is the definition of ccPEEf This confusion has been propagated by a Hurry of names (CCPEE~" "intrinsic PEE~" "autoPEE~" "inadvertent PEE~u "end-expiratory lung pressure (EELP)," "volume encumbered expiratory pressure (VEEP),U "breath stacking," and "gas trapping') used to refer to the alveolar pressures generated during inverse ratio ventilation (IRV).25 These terms, while sometimes used interchangeably, have heen associated with different meanings and different measurement techniques in different publications. While air trapping has generally heen viewed as unfavorable, some have pointed out that what is important is the actual end-expiratory and mean pressures generated in the alveoli, not how they were established.26-28 They argue persuasively that PEEPi should he physiologically equivalent to setPEEP delivered by a mechanical device such as a PEEP valve or a water column. This assumes that changing distribution of PEEPi within the lung due to local time constant (T) variations is of secondary importance. The purpose of this work was to develop and clinically test the feasibility and acceptability of a Clinical Managementof ARDS Patients (East et 81)

Table I-A Summary ofPCIRV MontJgernent Techniquea Ulled in Pnmioualy PublUhed Stadia· Reference

Paol Flo1 inCPPV

PEEP CPPV

I:E

VB

TItration Method

PEEPi

10

3

15

Mentioned but no data

1.5

Adjusted to

I:E ratio focus study: I:E = 3 used for all I:E ratio focus study: I:E = 1.5 used for all

No.

N

7

5

54?

14

18

0

18

105

0 IfRR>20 then t setPEEP to 5-10 I:E ratio focus t I:E to maximize C.. and minimize Ppeak? I:E ratio focus I:E = 2.3 or 4, rationale unclear PEEPi focus start at I:E =2, adjust I:E and VB to maintain a desired PEEPi I:E ratio focus f I:E to 4 then t setPEEP to 4-8 PEEPi focus I:E = 2, adjust VB to keep PEEPi -- PEEP inCPPV I:E ratio focus t I:E to 3 then f Ppeak to a max of 40 then t I:E to 4

Ppeak

Decreased

A successful computerized protocol for clinical management of pressure control inverse ratio ventilation in ARDS patients.

We have developed a computerized protocol that provides a systematic approach for management of pressure control-inverse ratio ventilation (PCIRV). Th...
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