Patient-Ventilator Interaction

Sharshar and coworkers designed a ventilator that adjusts airway pressure in proportion to the generation of transdiaphragmatic pressure during inspiration. The ventilator was evaluated in seven healthy subjects during normocapnia and with increases in carbon dioxide tension (PCO₂) of 3, 6, and 9 mm Hg. Each inflation cycle was triggered by either a preset increase in transdiaphragmatic pressure or preset inspiratory flow threshold, whichever occurred first (it was pressure in six subjects and flow in one subject). Untimely triggering or intense (or prolonged) triggering efforts were not seen at any level of hypercapnia. During servoventilator assistance, airway pressure increased in proportion to variation in transdiaphragmatic pressure. Both with and without the servoventilator, hypercapnia produced increases in tidal volume, respiratory rate, pressure–time product, and intrinsic PEEP. Pressure–time product was lower with the servoventilator than without it. The authors conclude that a servoventilator driven by transdiaphragmatic pressure delivers an increase in airway pressure in proportion to subject effort, and is effective in decreasing subject effort during normocapnia and hypercapnia without inducing untimely or excessive triggering attempts. An editorial commentary by Sinderby accompanies this article.

When mechanical ventilation is delivered under normocapnic conditions, its cessation is accompanied by central apneas. To determine whether increases in tidal volume or increases in respiratory rate are responsible for the change in respiratory rhythm, Rice and coworkers increased tidal volume (to 135–220% of eucapnic volume) and respiratory rate (1 or 3 breaths above eucapnic rate) in seven healthy subjects during NREM sleep. During controlled ventilation, an increase in tidal volume (by 65% or more of eucapnic volume) plus an increase in rate (of 1 breath per minute) eliminated transdiaphragmatic pressure. Cessation of controlled ventilation was accompanied by prolongation of expiratory time (by two to four times the control value); the increases in expiratory time were proportional to the increases in tidal volume during controlled ventilation but were independent of further increases in ventilator rate. During and after assist-control ventilation, increases in tidal volume (to 135 to 220% of eucapnic volume) were accompanied by decreases in transdiaphragmatic pressure in proportion to the increase in tidal volume; each ventilator inflation was actively triggered and the increase in expiratory time on cessation of mechanical ventilation was less than 20% of that seen after cessation of controlled ventilation. The authors conclude that both increases in ventilator rate and delivered volume during mechanical ventilation cause inhibition of respiratory motor output via nonchemical mechanisms (neuromechanical effects of repeated and augmented lung inflation), and that the resetting of respiratory rhythm is greater with additional increase in ventilator rate than with increase in delivered volume alone.

The ventilatory response to hypoxia in the presence of hypocapnia is controversial. Corne and coworkers used volume-cycled ventilation to measure the ventilatory response to hypoxia during eucapnia and hypocapnia. The response of respiratory muscle pressure to hypoxia (expressed as cm H₂O per percentage change in oxygen saturation) was 0.53 at eucapnia, 0.26 at end-tidal PCO₂ of 6 mm Hg below eucapnia, and 0.003 at PCO₂ of 12 mm Hg below eucapnia. Similar reductions were evident for respiratory rate (expressed as breaths per minute per percentage change in oxygen saturation): 0.17 at eucapnia, 0.11 at PCO₂ of 6 mm Hg below eucapnia, and 0.01 at PCO₂ of 12 mm Hg below eucapnia. The responses of respiratory muscle pressure and respiratory rate at a PCO₂ of 12 mm Hg below eucapnia were not significantly different from zero. The authors conclude that regardless of the strength of the hypoxic ventilatory response at eucapnia, the responses are lost when PCO₂ is reduced (in a stable manner) by 6 to 12 mm Hg below eucapnia.

To determine the prevalence of noise in the intensive care unit (ICU) and its effect on sleep, Gabor and coworkers did polysomnography on 7 mechanically ventilated patients and 6 healthy subjects over 24 hours in the ICU. Time-synchronized environmental monitoring was also performed. The average level of noise was 51 dB in the open ICU and 43 dB in an isolated single room (noise is 70 dB in a busy office, and 40 dB in a bedroom). In the patients, increases in sound occurred 37 times per hour of sleep and were responsible for 21% of all arousals and awakenings. Patient-care activities occurred 8 times per hour and were responsible for 7% of all arousals and awakenings. Compared with an open ICU, healthy subjects slept longer when placed in a single ICU room (9.5 versus 8.2 hours); sleep architecture was not altered. The authors conclude that noise and patient-care activities account for 28% of arousals and awakenings in critically ill patients receiving mechanical ventilation.

Arterial pulse pressure is known to increase during mechanical inflation and decrease during exhalation secondary to cyclic changes in left-ventricular stroke output. To determine whether the changes during inflation result from improvement in left-ventricular systolic function, Vieillard-Baron and coworkers did transesophageal echocardiography, Doppler studies, and arterial pressure measurements in 31 septic patients. Lung inflation produced a 16.6% increase in left-ventricular stroke volume, which was directly related to a 13.1% increase in left-ventricular diastolic volume and a 12.2% increase in left-ventricular ejection fraction. The authors conclude that the improvement in left-ventricular function during mechanical inflation is primarily the result of increased left-ventricular filling.

Citations 1-6 of 6 total displayed.

Ventilatory Assist Driven by Patient Demand

Christer Sinderby
Am. J. Respir. Crit. Care Med. 168: 729-730. [Full text]

Transdiaphragmatic Pressure Control of Airway Pressure Support in Healthy Subjects

Tarek Sharshar, Gilbert Desmarais, Bruno Louis, Gilles Macadou, Raphaël Porcher, Alain Harf, Jean-Claude Raphaël, Daniel Isabey, and Frédéric Lofaso
Am. J. Respir. Crit. Care Med. 168: 760 -769. First published online as doi:10.1164/rccm.200203-241OC [Abstract] [Full text]

Cyclic Changes in Arterial Pulse during Respiratory Support Revisited by Doppler Echocardiography

Antoine Vieillard-Baron, Karim Chergui, Roch Augarde, Sebastien Prin, Bernard Page, Alain Beauchet, and François Jardin
Am. J. Respir. Crit. Care Med. 168: 671 -676. First published online as doi:10.1164/rccm.200301-135OC [Abstract] [Full text]

Controlled versus Assisted Mechanical Ventilation Effects on Respiratory Motor Output in Sleeping Humans

Anthony J. Rice, Hideaki C. Nakayama, Hans C. Haverkamp, David F. Pegelow, James B. Skatrud, and Jerome A. Dempsey
Am. J. Respir. Crit. Care Med. 168: 92 -101. First published online as doi:10.1164/rccm.200207-675OC [Abstract] [Full text]

Hypoxic Respiratory Response during Acute Stable Hypocapnia

Stephen Corne, Kim Webster, and Magdy Younes
Am. J. Respir. Crit. Care Med. 167: 1193-1199. [Abstract] [Full text]

Contribution of the Intensive Care Unit Environment to Sleep Disruption in Mechanically Ventilated Patients and Healthy Subjects

Jonathan Y. Gabor, Andrew B. Cooper, Shelley A. Crombach, Bert Lee, Nisha Kadikar, Harald E. Bettger, and Patrick J. Hanly
Am. J. Respir. Crit. Care Med. 167: 708-715. [Abstract] [Full text]

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