Evaluation of the Hemodynamic and Respiratory Effects of Inverse Ratio Ventilation with a Right Ventricular Ejection Fraction Catheter

Evaluation of the Hemodynamic and Respiratory Effects of Inverse Ratio Ventilation with a Right Ventricular Ejection Fraction Catheter* jan I. Poelaert, M.D.; Dirk P. Vogelaers, M.D.; and Francis A. Colardyn, M.D.

Pc-IRV has been shown to have respiratory advantages, compared with CPPV. However, the hemodynamic effects of this ventilation mode have not yet been fully elucidated. We used a REF catheter to monitor the hemodynamic changes in the RV. Fifteen ARDS patients were included in the study. The respiratory data showed a 35 percent decrease of PIP and a 32 percent decrease of Vri and VTe with Pc-IRV 4:1 compared with CPPV. Hemodynamic parameters showed a significant increase in CI (17 percent) in Pc-IRV 4:1, without change in REF. Observing in retrospect the pressure-volume relationship of the RV, we could differentiate a preload (group 1) and an afterload dependent group of patients (group 2), CI was significantly different in the two groups as it rose only in the preloaddependent patients. RVEDVI showed a significant change in group 1, whereas this was absent in the second group. REF was maintained in switching ventilation from CPPV to Pc-IRV with increasing I:E ratio. Pc-IRV appears to be a good alternative ventilatory mode in comparison with

CPPV in a selected group of patients with preload dependency (responders); in these patients with respiratory insufficiency, close hemodynamic monitoring is required to optimize ventilation, especially in relation to the hemodynamic effects. (Chest 1991; 99:1444-50)

since its description by Ashbaugh et al, 1•2 the persistently high mortality rate of ARDS has not improved . Until now, stabilization of ARDS with optimal ventilation seems to be the only valuable solution in clinical practice. Pressure-controlled inverse ratio ventilation (Pc-IRV) has been used experimentally in acute respiratory insufficiency in the adult for a few years. Some retrospective studies have shown that Pc-IRV ameliorates oxygenation.3-8 However, no extensive data on the hemodynamic alterations were obtained . Hemodynamic changes are likely to have considerable effects on oxygen transport and delivery. Because of the possible benefits of this ventilation mode in ARDS, it is important to extend our knowledge of its hemodynamic effects. Expecting changes in right ventricular (RV) preload and afterload, we used a RV ejection fraction catheter, which has been shown to give accurate data on RV ejection fraction by measuring stroke volume (SV) and RV end-diastolic volume (RVEDV). 9 · 10 Therefore, positive end-expiratory pressure (PEEP) ventilation and Pc-IRV with

different I:E ratios were compared in a prospective study.

*From the Department of Intensive Care, University Hospital, Ghent, Belgium. Manuscript received June 15; revision accepted November 6. Reprint requests: Dr. Poelaert, Department of Intensive Care, University Hospital Ghent, De Pintelaan 115, Ghent, Belgium B9000

1444

CI =cardiac index; CPPV =continuous positive pressure ventilation; Do.= oxygen delivery; I:E = inspiration:expiration ratio; LVSWI=Ieft ventricular stroke work index; MAP=mean artery pressure; PAP= mean pulmonary artery pressurei PAW= mean airway pressure; Pc-IRV =pressure controlled inverse ratio ventilation; PetC01 =end-tidal partial C01 pressure; PIP= peak inspiratory airway pressure; PVR =pulmonary vascular resistance; RAP= right atrial pressure; REF= right ventricuJar ejection fraction· RV =right ventricle; RVEDVI = right ventricular end-diastofk volume index; RVESVI =right ventricular end-systolic volume index; RVSWI = ridtt ventricular stroke work index; SVI ::=stroke volume inJex; SVR = systemic vascular resistance; VE =expiratory minute volume; VTe =expiratory tidal volume; VTi =inspiratory tidal volume

METHODS

lbtient Selection The following criteria were accepted for inclusion: (1) arterial hypoxemia with a Pa02 <70 mm Hg, ventilating with a Flo, of >0.6 in combination with 10 em H 2 0 PEEP; (2) bilateral diffuse infiltrates on chest roentgenogram; and (3) a pulmonary capillary artery wedge pressure < 18 mm Hg. Patients were excluded when craniocerebral trauma was associated with increased intracranial pressure (measured by a ventriculostomy) or in the presence of dysrhythmias or hemodynamic instability. Patients with intracardiac shunts, tricuspid insufficiency, or left ventricular regional wall motion abnormalities were also excluded from the study; the latter was verified by transesophageal echocardiography before starting. Cooperation in the study was agreed to by a member of the family, and the study was approved by the Local Ethics Committee.

Methods All patients had to receive sedation with Fentanyl (1.5 1-LWJ0.6, I:E 1:1 (without pause time), 10 em H 2 0 PEEP, and a respiratory rate of 14 (Servo 900C, Siemens Elema, Sweden). As a second step, pressure-controlled ventilation with an I:E ratio of 1:1 (50 percent inspiratory time fraction) without PEEP and without pause time but with the same VE was started. Then, the I:E ratio was finally Effects of lnwrse Ratio Ventilation with Right Ventricular Catheter (Poelaert)

upgraded to 2:1 (67 percent inspiratory time fraction) and to 4:1 (80 percent inspiratory time fraction). A total of four ventilatory steps were thus studied; in the whole ventilatory protocol, respiratory frequency was not changed. None of the patients received inotropic support. There was a 30-minute stabilization period before measurements. The following hemodynamic data were obtained: HR, MAP, PCWP, RAP, PAP, CO, CI, REF, SVI, RVEDVI , and RVESVI. The RV parameters were calculated by a REF-1 cardiac output computer (Edwards Laboratory, CA, USA). Cardiac output measurements were performed by making five (.'Om parable estimates with (.'Old 5 percent dextrose in water," measured at the beginning of the ventilatory cycle. 10 The following respiratory parameters were measured: VE, VTe and VTi, PIP, and mean airway pressure (paw), SaO,, and PetCO,. PEEP, was measured after a 2-s expiratory hold. Extrinsic PEEP was turned off in the Pc-ventilation mode. The following data were measured by the laboratory: arterial, mixed venous, and capillary blood gases and hemoglobin (.'()ncentration (Corning 2500 CO-oximeter). The following data were calculated: SVR, PVR, LVSWI, RVSWI, CaO, and CvO,, Do,, and Vo,.

Statistical Analysis Overall statistical analysis was performed using ANOVA. The Wilcoxon matched pair signed rank test or the Mann-Whitney U test was used for subgroup analysis. Significance was accepted if p<0.05.

Table 1-Primary Patlwwgic Findings on Admission in the ICU Retrospectively Divided in Two Groups* Patient No./ Age, yr/Sex Croup 1 l/16/M

Pathologic Finding Polytrauma Polytrauma Burns (70 percent), including trachea CMV-positive renal transplant Postoperatively after hip prosthesis (rheumatoid arthritis) Polytrauma Polytrauma Viral pneumonia with negative bacteriology and serology

2135/M 3/64/F

4133/M 5/21/F 6147/M 7/32/M

8130/M Croup2

Polytrauma Polytrauma CMV-positive renal transplant Polytrauma

l/351M

2/61/M 3156/F 4151/F

Excluded as described in the text l/79/M 2/69/M 3/67/F

COLD with pneumonia Hypothermia Hypothermia

*See text. RESULTS

Fifteen patients with acute respiratory failure were assessed for the protocol. Primary pathologic findings at the time of admission to the ICU are shown in Table 1. Three patients were excluded by the presence of left ventricular wall motion abnormalities demonstrated by transesophageal echocardiography. Table 2 shows the overall respiratory data obtained in the different ventilation modes: a significant decrease in PIP was observed, from 37 ± 7 em H 20 to 24 ± 7 em H 20, whereas paw varied with (extrinsic or intrinsic) PEEP. All ventilatory volumes were reduced in switching PEEP ventilation to Pc-IRV. Table 3 shows the overall hemodynamic parameters. An increase in HR (from 106 ± 11 beats per minute [BPM] to 114 ± 13 BPM), MAP (109 ± 16 mm Hg to 114 ± 11 mm Hg), and expecially CI (4 .73 ± 1.27 Umiwm 2 to 5.55 ± 1.66 Umin·m 2) could be observed. REF remained constant (0.37). On the contrary, RVEDVI initially rose from 113 ±52 mVm 2 with 10 em H 20 PEEP ventilation to 157 ± 100 mVm 2 with Pc-IRV 2:1, whereafter a decrease in RVEDVI was observed to 130±59 mVm 2 • However, neither of the mentioned parameters changed significantly, with the exception of the Cl. According to the trend ofhemodynamic parameters, a clearly different hemodynamic behavior of the RV was observed in upgrading the pressure-controlled ventilation (Table 4); a significantly different initial PAP, due to pulmonary hypertension, could be correlated with a significant difference in Pa0 2 (131 mm Hg in group 1 [n = 8] compared with 78 mm Hg in

group 2 [n = 4] with pulmonary hypertension). The RVEDVI in group 1 showedaclearvariation: switching ventilation from CPPV to Pc-IRV 2:1 resulted in a significant increase of RVEDVI from llO to 145 mV m2 , whereafter a steady decrease was seen towards 128 mVm 2 with Pc-IRV 4:1. A continuous increase in CI from 4.5 Umin·m 2 with CPPV to 5.8 Umin·m 2 with Pc-IRV 4:1 was found in this group. With the higher PAP (group 2), no significant changes in RVEDVI or CI were found during upgrading from CPPV (139 mVm 2) to Pc-ventilation 1:1 (127 mVm 2). CI remained constant (from 5.3 towards 5.1 Umin·m 2) . In neither of the patient groups did REF change significantly (in the first group from 0.40 in CPPV to 0.42 in Pc-IRV 4:1 and in the second group from 0.39 in CPPV to 0 .44 in Pc-IRV 2:1 ). RVSWI was significantly higher in the second group compared with Table 2-Respiratory Parameters in Pc-IRV Compared with CPPV in ARDS* Ventilation

VTi

VTe

PIP

Paw

PEEP

CPPV 1:1 2:1 4:1 CPPV

889±214 851 ±243 756±205 606± 160 870±201

848±240 829±268 732± 194 575± 175t 859± 199

37±7 24±7t 25±8t 24±8t 35±6

19±3 12±4t 17±6 19±7 20±4

lO 3:j: 6:j: lO:j: 10

*Due to the pressure preset ventilation, PIP is markedly increased albeit Paw does not show the same pattern. tp<0.05 in comparison to baseline measurements. CPPV: 10 em H,O PEEP-ventilation; 1:1: Pc-IRV 1:1; 2:1: Pc-IRV 2:1 (see text for more details); 4:1: Pc-IRV 4:1. :j:PEEP. CHEST I 99 I 6 I JUNE. 1991

1445

Table 3-Henwdynamic Parameters (n=l2; mean±SD)

10 em H,O PEEP PC 1:E 1:1 PC 1:E 2:1 PC 1:E 4:1 10 em H,O PEEP

HR

MAP

CVD

PAP

CI

LVSWI

REF

RVEDVI

RVSWI

PVR

106± 11 110± 14 109± 12 114 ± 13 109± 11

109± 16 101 ±34 106± 15 115± 15 110± 17

9±4 9±5 8±4 9±5 9±5

33±8 34±9 34±8 38±9 32±8

4.73± 1.27 5.20± 1.66 5.14± 1.55 5.56± 1.66* 4.90± 1.35

59.6±23.5 63.3±26.4 59.4 ± 21.9 65.8± 17.8 58.9±20. 1

.37± .11 .37±.07 .38± .08 .38± . 16 .36± .90

119±55 130±64 147±84* 129±57 120±57

15.5±9.3 16.6±9.8 16.8±8.8 19.4± 10.3 16.1 ±8.5

178±86 149±82 156±86 173±92 180±91

*p<0.05.

Table 4-Hemodynamic Parameters in Pc-lRV (Mean±SD) Group 2 (n = 4)

Group 1 (n = 8)

REF SVI RVEDVI RVESVI PAP CI LVSWI RVSWI

.40± . 12 42± 12 110±39 68±35 27±7§ 4.5± 1.7 62±21 12±5§

2:1

1:1

PEEP

.38± .16 48± 18* 145±92* 97±86* 28±8:j: 5.2± 1.8 60±24 14±6*

.40±.13 49± 16* 131 ±57* 82±49* 30±7* 5.1 ± 1.6* 57± 19 15±6t

PEEP

4:1

.41 ± .13 43±16 104±61 72±41 26±6§ 4.7±1.8 63±23 14±5§

.42± .12 52± 16t 128±40* 76±33 34±9* 5 .8 ± I.7t 66±19 19±6t

PEEP .39± . 10 50± 17 139±83 90±69 41 ±5§ 5.3± 1.5 71±29 22± 12§

2:1

1:1 .44± .11 51±20 127±82 76±65 41±5:j: 5.3± 1.5 71±33 14±5

.44± . 13 49±20 127±91 79±77 37±11 5.2± 1.8 65±28 19± 13

4:1

PEEP

.41± . 14 47±18 134±95 87±84 41± 11 5.1±1.7 65± 19 21 ± 17

.40± .12 50± 16 135±86 88±71 42±9 5.2± 1.7 66±24 20±15

PEEP= CPPV with 10 em H,O PEEP. 1:1 = Pc-IRV 1:1 (50 percent inspiration time, without pause time). 2:1 = Pc-IRV 2:1 (67 percent inspiration time, without pause time). 4:1 = Pc-IRV 4:1 (80 percent inspiration time, without pause time). *p<0.05, intragroup differences. tp
Table 5-0xygenation Parameters in Pc-lRV (mean±SD) Group 2 (n = 4)

Group 1 (n = 8) PEEP

1:1

2:1

4 :1

PEEP

PEEP

1:1

2:1

4:1

PEEP

78±24:j: 131 ±56:j: 79±27* 87±28 95±26 115±29 82±51 69±23 67±14 PaO, 74 ± 19t PaCO, 39±2 41±3 44±4 54± 12* 42±3 42±6 43±9 43±5 49±12 44±6 SvO, 70±7* 74±7 76±5 75±6 70±7 66± 12 74±6 65±9 69±8 68±10 Do, 1,187±301 1,315±466 1,320±381* 1,499±437t 1,265±411 1,746±810 1,642±887 1,632±873 1,596±809 1,649±788 Vo, 294±65 333± 110 294± 110 296±93 305±87 454± 182 395± 163 417±183 352±139 440± 156 PEEP= CPPV with 10 em H,O PEEP. 1:1 = Pc-IRV 1:1 (50 percent inspiration time). 2:1 = Pc-IRV 2:1 (67 percent inspiration time) (without pause time). 4:1 = Pc-IRV 4:1 (80 percent inspiration time). *p<0.05, intragroup differences. tp
group 1 (22 to 12 g·m/m 2 , respectively), but showed no change in switching the ventilation mode to PcIRV 4:1. On the contrary, the RVSWI rose in group 1 significantly from 12 towards 19 g·m/m 2 • Table 5 demonstrates the oxygenation parameters in the two groups. The Pa0 2 measurements differed significantly between the two groups (131 mm Hg in group 1 vs 78 mm Hg in group 2). With Pc-IRV 1:1, we observed a significant drop in Pa0 2 (from 131 to 79 mm Hg) and in Sv02 (from 74 to 70 percent) in group 1 but not in group2. In group 1, PaC0 2 increased significantly in the Pc-IRV 4:1 mode compared with 1446

the other modes (54 mm Hg vs 39 mm Hg). Do 2 rises significantly in group 1 (from 1187 ± 301 mVmin to 1499±437 mVmin) but not in group 2. Vo2 did not change in a significant way in either group. DISCUSSION

Pc-IRV was first introduced by Reynolds 12 in the late 1960s and was applied by Boros 13 • 14 in pediatric respiratory distress syndrome. In the beginning of the 1970s, volume-controlled ventilation was generally accepted as support of adults with respiratory insufficiency. However, pressure-controlled time-cycled inEffects of ln\lerse Ratio Ventilation with Right Ventricular Catheter (Poelaert)

verse ratio ventilation was promoted by very few authors5 • 12• 13 • 15 for this indication and thus remained controversial. For the last few years, some retrospective studies have suggested possible advantages of this technique:l-6·16 decrease of PIP with conserved PAW resulting in amelioration of the oxygenation. However, opponents of this ventilation mode could not demonstrate a single advantage compared with classic PEEP ventilation because of the possible dangers of increased end-expiratory alveolar pressure (PEEP1), which is commonly not measured. 17 Moreover, no extensive hemodynamic studies were performed, especially with respect to changes in the RV parameters. The mechanism of this ventilation mode seems to be related to the alveolar time constant that is known to be short in the healthy alveoli and long in diseased alveoli. By shortening the expiration time, a gastrapping effect is obtained, which creates a PEEP1, recruiting collapsed alveoli with long alveolar time constants. IK Changing the ventilator from volumecontrolled CPPV with an I:E 1:1 to a Pc-ventilation with I:E 1:1, 2:1, and 4:1, a totally different pressure waveform could be observed (Fig 1). In contrast to an increasing pressure pattern in the CPPV mode, a

10

PEEP

square waveform appears with Pc-IRV 4:1: due to an abrupt increase of flow in the airways, recruitment of alveoli was observed nine years ago by Lachmann et al, 19 concomitant with an increase in compliance using Pc-IRV. The respiratory effects, found in our experiments, confirm the data in the literature .H A significant decrease in PIP was found (35 percent); a lower PIP is linked to a lower frequency of pneumothorax and pneumomediastinum .20 •21 A decline in PIP combined with a higher paw can lead to a significant amelioration of gas exchange that has been demonstrated by several investigators in animal studies,l 5 •22 •23 neonates, 24 and adults. 25 McCulloch et al, 26 suggested that recruitment of lung volume by raised PAW can reduce the extent of high PIP ventilation-induced lung injury. In our ARDS group of patients, we found a 36 percent decrease in PAW from CPPV to Pc-IRV 1:1 without PEEP; indeed, the intrinsic PEEP in the latter mode appeared to be significantly lower. However, the longterm follow-up of arterial oxygen saturation was not the aim of the study, as such data are available in the literature. 3-7 · 16 Cardiac dynamics during PEEP ventilation are

PC-1 RV

1=1

1. Respiratory parameters (example) with How, volume , and pressure curves in CPPV (10 em 11,0 PEEP) (50 percent inspiratory phase time), Pc-ventilation 1:1 (50 percent inspiratory phase time), Pc-IRV 2:1 (67 percent inspiratory phase time), and Pc-IRV 4:1 (80 percent inspiratory phase time) without pause time in each ventilation mode. Note that volume curves show increasingly exponential kinetit-s with upgrading l :E ratio. Flow curves demonstrate the decreasing Row pattern in Pc-ventilation in mntrast to CPPV. FIGURE

CHEST I 99 I 6 I JUNE, 1991

1447

complex27 •28 ; however, reduction in cardiac output during CPPV seems to be well correlated with a decrease in venous return and preload of the LV, concomitant with an increase in afterload of the RV. By equilibrium radionuclide angiography, it has been shown that the biventricular volume is reduced with PEEP, compatible with a decrease of venous return 29·30 and a change in ventricular configuration.30 Others have confirmed the importance of preload by other methods like transesophageal echocardiography. 31 We evaluated the hemodynamic effects of Pc-IRV compared with CPPV with a REF-catheter. With the technologic advance by the manufacturer of mounting a rapid-response thermistor, a beat-to-beat temperature change analysis created the possibility of calculating ventricular volumes. From the obtained RV volumes, REF can be calculated. This method is unaffected by arbitrarily and poorly reproducible zero points for pressure transducers since the on-line volume estimation depends only on the measurement of temperature differences. In addition, impedance of the pulmonary circulation seems to acquire more and more importance and plays a major role in RV performance in ARDS patients, whereas the calculated value of PVR is only a partial measure of it. 32 Whereas CI in our study population increases with about 17 percent in Pc-IRV 4:1, the highest RVEDVI is reached in Pc-IRV 2:1, suggesting optimal PEEP is obtained with this ventilation mode. This is also suggested by the VoJDo2 ratio, which decreases at an I:E of 4:1. The further rise of CI in the Pc-IRV 4:1 seems to be correlated with a sympathomimetic effect due to a 50 P A P(mmHg)

significant rise in PaC0 2 concomitant with an increase in HR and MAP. Indeed, in augmenting the I:E ratio, we did not increase the minute ventilation volume to correct PaC02 as this would implicate a hemodynamic change. The rise in CO could perhaps be rather falsely low as measurements started at the beginning of the inspiration phase: the longer the inspiration phase, the more the chance to measure in a period of ventilation when RV output would be mostly impaired . As we proposed earlier in post-CABG patients, a better parameter for considering RV compliance and afterload is RV wall tension, which can be derived from RVEDVI, whereas REF shows the overall function of the right system. 33 Pressure-volume curves of the LV can show shifts even without change in LV systolic performance.34 The same can also be stated about the RV. This was also mentioned by Martinet al35 in two ARDS patients. In the 12 patients studied, we observed a difference in CI and RVEDVI, so we could differentiate them into two groups: the first with augmenting RVEDVI with consequently increasing CI , thus with a preload dependency, and the second group with significantly higher PAP, without RVEDVI variability or CI change (Table 4). In Figure 2, we plotted RVEDVI vs PAP for the two groups. Achange in pressure-volume relationship, and thus change in RV function, can be observed. CI increases in group 1 in about 29 percent, whereas no change in CI can be demonstrated in group 2. The rise in PaC02 was significant with the 4:1 mode compared with the other ventilation modes and could partially explain the CI augmentation with the 4:1

,,..,1

lirw. z

40

30

20

10

0

50

100

200

300

50

100

200

2

RVEDVI(ml/m

)

300

FIGURE 2. Differences in behavior in the two different groups of ARDS patients. Left: group l preload dependent patients. Right: group 2 afterload dependent patients without changing Cl and RVEDVI. CPPV (10 em H 2 0 PEEP) shown as starting point; Pc-ventilation 1:1 (arrows); Pc-IRV 2:1 (squares); and Pc-IRV 4:1 (circles).

1448

Effects of Inverse Ratio Ventilation with Right Ventricular Catheter (Poelaert)

mode. In group 2, the same trend was found but this was not significant, probably due to the low number of patients. Considering the changing RV diastolic function reSected by a change in RVEDVI, the REF-catheter would be the first choice for bedside monitoring of a patient with respiratory insufficiency where invasive hemodynamic monitoring is indicated. Indeed, radionuclide angiography is not useful for repetitive bedside measurements and a classic pulmonary thermodilution catheter gives only a part of the information (no volume estimation); transesophageal echocardiography is more cumbersome and needs great expertise. If these data will be confirmed, a preload-dependent patient would benefit from Pc-IRV; despite an increase in RVSWI, apparently, the RV is not able to raise the CI, probably due to an already higher afterload, with the high initial PAP. As none of the patients studied received inotropic support, group 2 would perhaps benefit from inodilatory support relieving afterload (eg, with dobutamine). In conclusion, REF was preserved in these patients across the range ofCPPV towards augmented I:E ratio with pressure-controlled ventilation. From these data we were able to differentiate in retrospect-in relation to an increase of CI and RVEDVI-the patients into two groups as "responders" and "nonresponders" for this ventilatory mode. Finally, meticulous invasive hemodynamic monitoring must always be combined with respiratory monitoring to most effectively utilize this ventilatory mode .

20

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2

3

4

5

6

7

8

Ashbaugh DC, Bigelow DB, Petty TL. Acute respimtory distress in adults. Lancet 1967; 2:319-23 Ashbaugh DC, Petty TL, Bigelow DB, Harris TM. Continuous positive pressure breathing in adult respimtory distress syndrome. Thorac Cardiovasc Surg 1969; 57:31-41 Thamtt SR, Allen RP, Albertson TE . Pressure controlled inverse mtio ventilation in severe adult respimtory failure. Chest 1988; 94:755-62 Lain DC, DiBenedetto R, Morris SL, Van Nguyen A, Saulters R, Causey D . Pressure control inverse mtio ventilation as a method to reduce peak inspimtory pressure and provide adequate ventilation and oxygenation. Chest 1989; 95:1081-88 Andersen JB. Ventilatory stmtegy in catastrophic lung disease: inverse mtio ventilation (IRV) and combined high frequency ventilation (CHFV). Acta Anaesth Scand 1989; 33;S90:145-48 Lachmann B, Schairer W, Armbruster S, Van Daal GJ, Erdman W Improved arterial oxygenation and CO. elimination following changes from volume-genemted PEEP ventilation with inspiratory/expimtory (liE) mtio of 1:2 to pressure-generated ventilation with liE ratio of 4:1 in patients with severe adult respiratory distress syndrome (ARDS). Adv Exp Med Bioi 1989; 248:77986 Enderson BL, Farnham JW, Langdon JR. Inverse I:E ratio ventilation can improve oxygenation in adult respiratory distress syndrome. Crit Care Med 1989; Sl52 Gurevitch MJ, Van Dijke, Young ES, Jackson K. Improved oxygenation and lower peak airway pressure in severe adult

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14th National Conference on Pediatric/Adult Allergy and Clinical Immunology The State University of New York at Buffalo will present this conference July 19-21 at the Four Seasons Hotel, Toronto, Canada. For information, please contact Ms. Rayna Saville, Coordinator, Continuing Medical Education, 219 Bryant Street, Buffalo 14222 (716: 877-7965).

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Effects of lnwrse Ratio Ventilation with Right Ventricular Catheter (Poelaert)