Bilevel Ventilation

Running head: BILEVEL VENTILATION 1

BiLevel Ventilation

Jason DubervilleCollin College Respiratory Care Program

Fall 2011

BILEVEL VENTILATION 2

Abstract

Shunting, cardiac output, and ventilator associated pneumonia, are three aspects of patient care

that can benefit from BiLevel ventilation. This paper will cover the basic technical aspects of the

BiLevel mode, followed by highlights from three clinical articles in which the mode was used to

improve patient outcomes. Finally, a brief reader's critique will end the paper.


Technical Aspects of BiLevel Ventilation

BiLevel is a trademarked term used to describe a mode of ventilation in the Puritan

Bennett 840 ventilator. According to documentation from Puritan Bennett, the mode is designed

for two ventilating strategies; Airway Pressure Release Ventilation (APRV) and Biphasic. From

the pressure-time scalar below, it is possible to see the elements of these two strategies, and how

they are related and similar. (Covidien 2011)

Figure 1: Components of a Biphasic wave form. (Covidien 2011)

Above is a Biphasic wave form, where inspiration is supported at a high pressure level (PEEPH)

and exhalations occurs at a lower level (PEEPL.) The factor which differentiates Biphasic

ventilation from APRV ventilation is the inspiration and expiration time. In Biphasic mode,

exhalation time (Etime) is long enough for spontaneous breaths to occur relatively frequently,

whereas in APRV mode, Etimes are very short, typically less than 1 second. APRV typically has

4 second inspiration times (Itime), with 1 second Etimes. This is commonly called an inverse I:E

ratio.


In addition to the basic function above, BiLevel is designed to further provide pressure

support to spontaneous breaths of the patient. From the chart below we can see how the

spontaneous breath support works. (Covidien 2011)

The purpose of this feature is to allow easier patient weaning from the APRV mode of

ventilation. Figure 2 shows weaning from the APRV mode can take the form of both reducing

the PEEPH level, and, increasing the Etime. In this way a smooth transition from APRV, through

Biphasic, to pressure supported spontaneous breathing, is made. The technical aspects of how

each of these settings can be implemented on the actual Puritan Bennett 840 ventilator are listed

in appendix A. Overall, spontaneous breathing of the patient is never unsupported. A default

level of 1.5 cmH2O of pressure support is given to spontaneous breaths above both PEEPH and

PEEPL levels respectively. Throughout the remainder of the paper BiLevel and APRV will be

used interchangeably, as well as the combined term BiLevel APRV. This serves to bridge the

gap between proprietary branding and clinical research in the area of APRV ventilation.


Shunting and BiLevel APRV

To understand the value of using BiLevel ventilation it helps to look at cases where the

mode was successful. Hirani, Marik, and Plante (2009) published two such clinical cases, in

Respiratory Care, that demonstrated successful outcomes in two pregnant patients with acute

respiratory distress syndrome (ARDS.)

The first case involved a 19-year-old patient at 30 weeks gestation, transferred to Thomas

Jefferson University Hospital, after a week stay in a regional hospital for cough, fever, and

shortness of breath. Upon arrival her PaO2/FiO2 ratio was 87, and she was receiving

ceftriaxone, ampicillin, and azithromycin. She had bilateral infiltrates. Bronchoalveolar lavage

(BAL) was performed and it was discovered Enterobacter cloacae was the source of her

pneumonia. (Hirani et. al. 2009)

The patient was given a tracheostomy, and, after no improvement for a two week period,

the decision was made to go from conventional ventilation to BiLevel APRV. Before the mode

change her FiO2 was at 0.9, with PEEP of 10cmH2O on assist control ventilation (A/C.) (Hirani

et. al. 2009) Table 2, below, shows the pre and post ventilation changes.

Table 2: Case #1.(Modified from Hirani et. al. 2009)

A/CVt 8ml/kg IBWPEEP 10cmH2O

FiO2 0.90

(1hr prior to APRV)

BiLevel APRVHiPEEP

28cmH20LPEEP 8cmH2OTimeLow 1.0 sec.

FiO2 0.90(6hr after APRV)

pH 7.45 7.47PaO2 torr 79 131Pco2 torr 40 36

PaO2/FiO2 87 145RR 20 121

Mean arterial Pressure torr 76 91Paw cm H2O 16.62 24

Paw torr 12 17.64PAO2 torr 602.5 612.57Pa/PA ratio 13% 21%

Estimated Shunt 87% 79%Expected PaO2 - 79.63

1 Set rate used as spontaneous breaths in APRV do not change Itimes or Etimes.2 Estimated PIP of 30 cmH2O, Itime 1, Etime 2 seconds.


The important number to note on Table 2 is the "Expected PaO2." Based on the patient's

level of shunt, 87%, on conventional ventilation, APRV generating PAO2 of 612.57torr should

produce PaO2 of 79.63 torr. In fact we see a better PaO2, of 131 torr, from APRV. Where did

this extra 51 of PaO2 come from? APRV pushed out some of the fluid in the lungs to gain more

working lung space. The BiLevel APRV mode pushed back 8% of the shunted area in 6 hours.

This is a key statistic to look at when explaining why APRV can be a good ventilation mode and

measuring therapeutic outcomes.

A similar story occurs in the second patient presented by Hirani et. al.(2009.) A 24-year-

old patient at 31 weeks presented with fever, shortness of breath, palpations and diarrhea. She

was given fluids, broad-spectrum antibiotics, and a chest x-ray revealed left lower lobe

pneumonia. The patient continued to decline and within 2 days intubation and mechanical

ventilation were required. Chest x-ray revealed lobar collapse and worsening consolidation.

Hypoxemia persisted despite PEEP of 14cmH2O and FiO2 of 1.0, with PaO2/Fio2 of 47mmHg.

At this point the decision was made to switch to APRV mode and within two hours significant

improvement in oxygenation and PaO2/FiO2 gains to 118mmHg occurred. Table 3, below,

provides a full account of the pre and post APRV ventilation.

Again, expected PaO2, based on almost identical FiO2 and Paw, is should be about 47

torr, and APRV is able to bring in an extra 71 torr of PaO2 by reducing the amount of the

shunting. The conventional ventilation had and almost 93% shunt, which reduced to 83% within

90 minutes of starting APRV. This is a significant improvement.


Table 3: Case #2.(Modified from Hirani et. al. 2009)

A/CVt 7.5ml/kg

IBWPEEP 14cmH2O

FiO2 1.0

(prior to APRV)

BiLevel APRVHiPEEP 33cmH20LPEEP 10cmH2OTimeLow 0.9 sec.

FiO2 0.90(1.5hr after

APRV)

pH 7.24 7.33PaO2 torr 47 118Pco2 torr 38 32

PaO2/FiO2 47 118RR 20 14

Mean arterial Pressure torr 67 77Paw cm H2O 213 28.0

Paw torr 15.44 20.58PAO2 torr 680.94 686Pa/PA ratio 6.9% 17.2%

Estimated Shunt 93% 83%Expected PaO2 -- 47.33

In conclusion, both mothers were able to deliver viable births while on ventilation. Both

were able to recover, wean from ventilation, and return home. Both the children returned home

within a period of weeks in good condition. In these cases, BiLevel APRV proved to be a tool

for use at critical oxygenation levels, allowing the mother to be ventilated while at the same time

the infant to remain in the womb until the 32 week mark, where surfactant production typically

begins. Had BiLevel APRV gains in oxygenation not been achieved, early delivery may have

been required.

3 PIP 35cmH2O, I:E ratio 1:2.


Cardiac Output and BiLevel APRV

Kaplan, Bailey, & Formosa (2001) produced a study for the journal Critical Care

demonstrating the benefit of BiLevel APRV ventilation on cardiac performance with acute lung

injury (ALI) and acute respiratory distress patients (ARDS.) The study looked at 12 patients

receiving pressure control ventilation (PCV), and noted changes in cardiac output and sedation

needs after change to BiLevel APRV. The initial settings of PCV were titrated to maintain

PaO2 above 60, with FiO2 at or below 60. In addition, PaCO2 target levels were between 35-45

torr. Table 4, below, shows PCV settings compared with APRV.

PCV APRVPawpk/PEEPH cmH2O 38+/- 3 25+/-3Pawmean cmH2O 18+/- 3 12+/-2Paralytics(% of patients)

74 4

Sedative use(% of PCV patients)

100 68

Pressors(% of patients)

92 45

Lactate mmol/l 2.2 +/- 0.4 1.8+/-0.3Cardiac Indexl/min/m2

3.2+/- 0.4 4.6+/-0.3

DO2ml/min

997+/- 108 1409+/-146

SvO2 (%) 72+/- 4 80+/-5(not significant)

CVPmmHg

18 +/- 4 12+/-5

Urine Outputcc/kg per h

0.83 +/- 0.2 0.96+/-0.3

Table 4: Median and % values. Modified from Kaplan et. al. 2001.

APRV PEEPH levels were initially set at 75% of PCV peak airway pressure (Pawpk) and titrated

after 30 minutes. The interesting aspect of table 3 is that BiLevel APRV was able to obtain the

same targeted PaO2 > 60 with a lower mean airway pressure (12cmH2O verses 18cmH2O with

P/C.) Unfortunately, the blood gas values and mean FiO2s are not reported in the data, so it is

difficult to see exactly how this result did occur.


Table 3 also shows that lower mean airway will increase cardiac output, by reducing

systemic vascular resistance on venous return and pulmonary capillary resistance in the lungs.

This factor is focused on by Kaplan et. al. and shows the potential value of BiLevel APRV in

many clinical situations where cardiac output is a priority issue for the patient. In ARDS patients

cardiac function itself is not the primary issue, rather fluid outs, driven by hydrostatic pressures,

is a closely monitored factor. In this sense the increase cardiac output provides necessary

support for the reduction of edema.

Because oxygenation is also an issue, CaO2 can be analyzed from the table using the

basic equation CIxCax10=DO2 and plugging in the numbers. Table 3 shows CaO2 for PVC

would be about 31.5 ml/dl, and APRV to be 30.63ml/dl. The normal CaO2 range is 15-24ml/dl,

however some slight polycythemia may be occurring due to diuretic therapy often used with

ARDS/ALI patients.

Finally, an important additional benefit of BiLevel APRV is decreased sedation

requirements, as well as decreased paralytics and pressor needs for the patients. Table 3 shows

improvement in these areas. In the study lorazapam and midazolam, titrated to 65-70 on the

BIS index (see appendix B), use was reduced. Also, vecuronium and cis-atracurium, the

paralytics used, were discontinued in almost all the patients on BiLevel APRV. Pressors were

titrated to achieve a MAP of 75torr or greater and Kaplan et. al. (2001) write... "Almost half the

patients were successfully weaned off pressors when transitioned to APRV. The probable

explanation for the enhanced cardiac performance with reduced pressors stems from reduced

peak and mean airway pressures." (p.224)


Ventilator Associated Pneumonia and BiLevel APRV

Walkey, Nair, and Papadopoulos, et. al. (2011) recently published a study showing

ventilator associated pneumonia (VAP) likelihood can be reduced using APRV. Specifically, in

pulmonary contusion situations, which carry a high VAP rate of 18.3 occurrences per 1000

ventilator days (verses 7.7/1000 non contusion patients), APRV was shown to significantly

reduce the patients chances of acquiring VAP. (Walkey et.al. 2011.) The amount of improved

patient outcomes can be seen in Figure 3.

Figure 3. (Walkey et. al. 2011.)

As the number of ventilator days increase, one can see a dramatic benefit to APRV ventilation

compared with conventional ventilation in regards to VAP.

This study was developed at the Boston Medical Center, a 629 bed, inner city, level 1

trauma center. The subjects were those patients with pulmonary contusions that required

mechanical ventilation for longer than 48 hours. The study was done during a period when the

VAP ventilator bundle was also being used, so results may be considered as above and beyond

what is gained by the VAP bundle. (Walkey et. al. 2011)


The two factors highlighted by Walkey et. al. contributing to the results are reduced

sedation needs, as measured by the Riker Sedation Agitation Scale, and improved PaO2/FiO2

ratios. The Riker Sedation Agitation Scale is a 7 point scale nursing used to assess the need for

sedation. A goal of 3-4 is typical being "calm and cooperative." A score of 7 is the worst:

"patient attempting to get ET tube." The full scale is listed in appendix C. For APRV patients,

72.2 percent of the time they were within the 3-4 range verses 47.2 percent of the time with

conventional ventilation. Walkey et. al. (2011) are careful to note..."there were no differences in

total dosage of sedative or narcotic medications" (p. 44) between APRV and conventional

ventilation. Median per ventilator day sedation and narcotic needs between the two groups are

listed below in table 5.

APRV (n = 31) Conventional (n = 33)Benzodiazepine 5.8 (0.74 - 24) 4.3 (0.85 - 19)Propofol 1212 (236 -2062 ) 1340 (226-2363)narcotic (mg fentanyl equivalents.) 2.5 (1.7-3.4) 2.3 (1.2 - 3.3)

Table 5.

No explanation for the discrepancy between the SAS scoring difference, but the same amount of

sedation given overall, is provided by the authors. There may be an answer to be found from an

experienced clinician, however, this information is outside the current scope of this paper.

Walkey et. al.(2011) also point out studies by Putensen et.al (2001) and Rathberger et. al. (1997)

have supported the notion APRV does reduce the overall amount of required sedation compared

with conventional ventilation.

PaO2/FiO2 ratio improvement with APRV can be readily explained by the astute

clinician, because the mean airway pressure (Paw) in APRV is likely to be significantly higher.

In short, APRV pumps up the PaO2 with what amounts to extra PEEP. Table 5, below, shows

the estimated median Paw for the APRV and conventional ventilation groups in this study.


PaO2 for pre and post APRV data is not reported in this study, nor is FiO2, making further

analysis difficult. However, it is reasonable to assume FiO2 was not significantly different in

both groups and merely a reporting oversight. Table 6 clearly shows APRV will improve

PaO2/FiO2 ratios simply based on higher alveolar air pressures.

APRV Conventional I:E estimation 4:1 1:3PIP cm H2O 25.8 25.4PEEP cm H2O

1.2 5.8

Paw cm H2O 20.88 10.7Table 6.

Walkey et. al. (2011) conclude, tentatively, that with this group of pulmonary contusion

patients, a reduced risk of VAP is likely the result of increased lung recruitment with APRV

ventilation.


Discussion and Reader's Critique

Three possible benefits of BiLevel ventilation have been demonstrated in this paper.

First, ARDS treatment with BiLevel APRV can gain precious PaO2 increments by reducing

shunt, while at the same time protecting lung tissue from repeated high peak pressures stresses

during inspiration. Second, BiLevel can be used to improve cardiac output by titrating PEEPH

significantly below peaks pressures of conventional ventilation, and thereby protecting blood

flow. Third, ventilator associated pneumonia is shown to be reduced with BiLevel APRV

ventilation in higher risk populations due to reduced sedation needs related to improved patient-

ventilator asynchrony, and lung recruitment.

Although each of these studies provided excellent data in regards to BiLevel ventilation,

some areas of improvement for future work should be noted. First, Hirani et. al. (2009)

neglected to put in the peak pressures for the conventional modes of ventilation for their patients.

A pre-read by a respiratory therapist in future might add this improvement to the excellent work

of these fine physicians. Second, Kaplan et. al. (2001) did not put the pre and post median blood

gas values for the move to BiLevel from pressure control ventilation. Hopefully future studies

will include this information. And third, Walkey et. al. (2011) might integrate a better metric

than the PaO2/FiO2 (P/F) ratio when comparing BiLevel APRV to conventional ventilation.

The P/F ratio does not take into account PEEP levels, and thus is an unclear gauge for comparing

one patient to another, or one group to another, in terms of better or worse from a respiratory

standpoint. It is acceptable for this study, but future work might incorporate the oxygen index

ratio, or the arterial to alveolar pressure (a/A) ratios.


ReferencesCovidien (2011) Puritanbennett.com, Retrieved from

http://www.puritanbennett.com/serv/TechSup.aspx

Hirani, A., Marik, P., Plante, L., (2009) Airway Pressure-Release Ventilation in Pregnant

Patients With Acute Respiratory Distress Syndrome: A Novel Strategy. Respiratory

Care, October 2009 Vol 54, No. 10

Kaplan, L., Bailey, H., Formosa, V., (2001) Airway Pressure Release Ventilation Increases

Cardiac Performance in Patients with Acute Lung Injury/Adult Respiratory Distress

Syndrome. Critical Care 2001, 5:221-226

Putensen, C., Zech, S., Wrigge, H. (2001) Long-Term Effects of Spontaneous Breathing during

Ventilatory Support in Patients with Acute Lunge Injury. American Journal of

Respiratory and Critical Care Medicine 2001, 164:43-49

Rathberger, J., Schorn, B., Falk, V., Kazmaier, S., Spiegel, T., Burchardi, H., (1997) The

Influence of Controlled Mandatory Ventilation (CMV), Intermittent mandatory

Ventilation, and Biphasic Intermittent Positive Airway Pressure (BIPAP) on Duration of

Intubation and Consumption of Analgesic and Sedatives. A Prospective Analysis in 596

Patients Following Adult Cardiac Surgery. European Journal of Anaesthesiology 1997;

14:576-582

Walkey, A., Nair, S., Papadopoulos, S., Agarwal, S., Reardon, C., (2011) Use of Airway

Pressure Release Ventilation is Associated with a Reduced Incidence of Ventilator-

Associated Pneumonia in Patients with Pulmonary Contusion. The Journal of TRAUMA

Injury, Infection, and Critical Care. 2011, Vol 70, No. 3


Appendix A(1)


Appendix A(2)

A.2A.2


Appendix B

The bispectral index (BIS) is measure of consciousness. It is based on electromyographic

waveforms generated by neuronal activity. Leads on the patient's frontal and parietal plates

generate the wave forms. The scale is a proprietary number, describing various states of

consciousness as listed in Figure 1. It is used to replace or supplement Guedel's classification

system for determining depth of anesthesia. (Images in from Google public image search.)

Figure 1: BIS descriptors. Figure 2: BIS leads.

Figure 3: BIS user interface.


Appendix C

Bilevel Ventilation

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