aprv ventilation and cardiac output with infants

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Running Head: APRV VENTILATION AND CARDIAC OUTPUT WITH INFANTS 1 APRV Ventilation and Cardiac Output with Infants. Jason Duberville Collin College Respiratory Care Program Spring 2012

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Page 1: APRV Ventilation and Cardiac Output With Infants

Running Head: APRV VENTILATION AND CARDIAC OUTPUT WITH INFANTS 1

APRV Ventilation and Cardiac Output with Infants.

Jason Duberville

Collin College Respiratory Care Program

Spring 2012

Page 2: APRV Ventilation and Cardiac Output With Infants

APRV VENTILATION AND CARDIAC OUTPUT WITH INFANTS 2

Walsh, Merat, and La Rotta et.al. (2011) published an interesting study, in Critical Care

Medicine, that demonstrates higher positive end expiratory pressure (PEEP) can improve

pulmonary blood flow. This finding is contrary to the respiratory dogma, established by Counard

et. al. in 1948, that increasing PEEP reduces pulmonary blood flow via reduced venous return.

Walsh et. al. write.... “ higher mean airway pressure during APRV would tend to decrease

pulmonary blood flow, and hence the increased pulmonary blood flow seen during APRV, is all

the more significant.” (Walsh et. al. p. 2604)

The acronym APRV denotes “airway pressure release ventilation.” It is a ventilation

mode with long inspiratory times (Itime), at high PEEP levels. A typical pressure-time wave

form of APRV, as well as pressure control ventilation (PCV), is illustrated in figure 1. (Adapted

from Covidian.com 2012)

The design of the study

was a simple comparison of the

pulmonary blood flow between

the APRV mode, and, PCV

mode. Pulmonary blood flow

was measured before and after

muscle paralytics (e.g.

rocuronium) were removed for

both modes. The subjects were a

very specific group of patients:

neonates undergoing heart repair

surgery. Table 1 (below) shows the main findings of the study. The arrows show APRV

Page 3: APRV Ventilation and Cardiac Output With Infants

APRV VENTILATION AND CARDIAC OUTPUT WITH INFANTS 3

pulmonary circulation improved to 2.9L/min/m2, from 2.6L/min/m2, after muscle paralytics were

withheld. The PCV mode does not show a significant increase in pulmonary circulation when

muscle paralytics are removed.

The feature of the study that makes it outstanding is the explanation of mechanisms by

which increased PEEP levels might allow improved pulmonary circulation. The short answer is:

negative pressure generated in the thoracic space from spontaneous inspiration improves blood

flow. To demonstrate, Walsh et. al. (2011) recorded intrathoracic pressures with an esophageal

balloon, in two sample subjects, for both the APRV and PCV modes. A tracing from these

measurements is shown below in figure 2 (adapted from Walsh et. al. 2011.)

Table 1. Adapted from Walsh et. al. (2011.)

Page 4: APRV Ventilation and Cardiac Output With Infants

APRV VENTILATION AND CARDIAC OUTPUT WITH INFANTS 4

Figure 2. (Adapted fromWalsh et. al. 2011)

The tracings are recorded after muscle paralytics have been withdrawn. It can be seen

that in the APRV mode, periods of negative five centimeters of water pressure occur in the

thoracic space. These are shown at the “Intra Pleural Pressure” line-tracing of the APRV graph,

in figure 2. The PCV ventilation does not allow thoracic pressure to get into negative pressures.

The negative pressures in APRV are attributed to the chest expansion, as found in normal

physiological spontaneous breathing, from the respiratory drive. In other words, the respiratory

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APRV VENTILATION AND CARDIAC OUTPUT WITH INFANTS 5

rate continues during APRV to expand the chest. Expansion of the chest creates a negative

pressure, reducing afterload for the right ventricle, and increasing pulmonary blood flow.

The PCV mode does not receive negative pressures from spontaneous breaths, as Walsh

et. al. (2011) point out, because a mechanical inspiratory breath is triggered, creating positive

pressure in the alveoli, and then, the thoracic space (figure 1.)

Reader’s Critique

Walsh et. al. do a top notch job of collecting very difficult to obtain data, from a very

specialized group of patients. Not only do they report the main findings of pulmonary blood

flow improvement with APRV, they develop data to explain part of the mechanism of such

results. The paper is of moderate difficulty and made easier by good organization and simple

language.

Future areas of research are not explicitly stated by Walsh et. al., however one might

imagine questions that still need to be answered. For example: Is muscle fatigue an important

risk factor that should be tested with the APRV mode?

Looking at the 15 cm H2O positive pressure in the APRV mode, one might expect during

spontaneous exhalation esophageal pressures to rise to about 9 cm H2O (or 60%. of the 15 cm

H2O, based on calculations from Talmor et. al., 2008, see appendix a.) However, intrathoracic

pressures (esophageal) never get above 5 cm H2O. Does this suggest a constant inspiratory

effort between -4 cm H2O to -20 cm of H2O is being generated by the subjects? If muscle

fatigue develops, inspiratory effort could collapse, and gains in pulmonary blood flow might

quickly be lost, perhaps to less than PCV levels. PCV ventilation may have an advantage in the

long run over APRV due to the lower work of breathing required. This advantage would most

likely not show up in the limited 30 minute test periods used by Walsh and colleagues.

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APRV VENTILATION AND CARDIAC OUTPUT WITH INFANTS 6

Appendix A

Esophageal pressures appear to be about 60 percent of peak inspiratory pressure in adults,

as indicated with the arrows, and across different study conditions. Talmor et. al (2008), the

authors of the above table, note esophageal pressure variations due to disease states exist, but I

assume are likely to be larger in this ARDS patient population than in the neonatal subjects

studied by Walsh et. al. (2011.)

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APRV VENTILATION AND CARDIAC OUTPUT WITH INFANTS 7

References

Beck, J., Tucci, M., Emeriaud, G., Lacroix, J., Sinderby, C., (2004) Prolonged Neural Expiratory

Time Induced by Mechanical Ventilation in Infants. Pediatric Research 2004 Vol 55, No. 5

Cournand, A., Motley, H., Werko, L., Richards, D., (1948) Physiological Studies of the Effects

of Intermittent Positive Pressure Breathing on Cardiac Output in Man. American Journal

of Physiology 1948 152:162

Talmor, D., Sarge, T., Malhotra, A., O’Donnell, C., Ritz, R., Lisbon, A., Novack, V., Loring, S.

(2008) Mechanical Ventilation Guided by Esophageal Pressure in Acute Lung Injury. The

New Egland Journal of Medicine, November 13, 2008.

Walsh, M. A., Merat, M., La Rotta, G., Joshi, P., Joshi, V., Tran, T., Jarvis, S., Caldarone, C.,

Van Arsdell, G., Redington, A., Kavanagh, B., (2011) Airway Pressure Release

Ventilation Improves Pulmonary Blood Flow in Infants After Cardiac Surgery. Critical

Care Medicine. 2011 Dec;39(12) 2599-604