Pressure Support Mechanical Ventilation Research Articles

Ventilatory changes during the use of heat and moisture exchangers in patients submitted to mechanical ventilation with support pressure and adjustments in ventilation parameters to compensate for these possible changes: a self-controlled intervention study in humans.

ObjectiveTo evaluate the possible changes in tidal volume, minute volume and respiratory rate caused by the use of a heat and moisture exchanger in patients receiving pressure support mechanical ventilation and to quantify the variation in pressure support required to compensate for the effect caused by the heat and moisture exchanger.MethodsPatients under invasive mechanical ventilation in pressure support mode were evaluated using heated humidifiers and heat and moisture exchangers. If the volume found using the heat and moisture exchangers was lower than that found with the heated humidifier, an increase in pressure support was initiated during the use of the heat and moisture exchanger until a pressure support value was obtained that enabled the patient to generate a value close to the initial tidal volume obtained with the heated humidifier. The analysis was performed by means of the paired t test, and incremental values were expressed as percentages of increase required.ResultsA total of 26 patients were evaluated. The use of heat and moisture exchangers increased the respiratory rate and reduced the tidal and minute volumes compared with the use of the heated humidifier. Patients required a 38.13% increase in pressure support to maintain previous volumes when using the heat and moisture exchanger.ConclusionThe heat and moisture exchanger changed the tidal and minute volumes and respiratory rate parameters. Pressure support was increased to compensate for these changes.

Model-based decision support for pressure support mechanical ventilation - implementation of physiological and clinical preference models

The paper presents modifications of the INVENT decision support system for providing decision support in pressure support mechanical ventilation. Physiological models of interstitial fluid and tissue buffering and metabolism, cerebrospinal fluid acid-base status, and central and peripheral chemoreflex respiratory drive were integrated with existing models of the system and methods were implemented for learning effect of changes in pressure support on tidal volume, metabolism, anatomical dead space and muscle response. Preference models were implemented describing risk of muscle atrophy and stress in relation to pressure support level. The system was evaluated retrospectively in three patients responding differently to changes in pressure support. The system was able to describe patients' changes in tidal volume, respiratory rate and alveolar ventilation and adapt decision support appropriately when patient responses were different from that expected from measurements at baseline level.

Coherence analysis overestimates the role of baroreflex in governing the interactions between heart period and systolic arterial pressure variabilities during general anesthesia

During general anesthesia positive pressure mechanical ventilation (MV) profoundly affects intrathoracic pressure and venous return, thus soliciting cardiopulmonary reflexes and modifying stroke volume. As a consequence heart period, approximated as the temporal distance between two consecutive R peaks on the ECG (RR), and systolic arterial pressure (SAP) variability series are usually highly correlated at the MV frequency (MVF) and this significant correlation is commonly taken as an indication of an active baroreflex. In this study the involvement of baroreflex was tested according to a time-domain linear Granger causality approach accounting explicitly for MV in two experimental protocols. In the first protocol volatile (VA) or intravenous (IA) anesthetic was administered in humans during pressure controlled MV (PCMV). In the second protocol IA was administered in pigs during PCMV or pressure support MV (PSMV). Causality analysis was contrasted with RR-SAP squared coherence. Significant coherence values at MVF were always found in both protocols. On the contrary, a significant causal link from SAP to RR was less frequently found in humans independently of the anesthesiological strategy and in animals during PCMV. PSMV was superior to PCMV in animals because it was able to better preserve a link from SAP to RR. During general anesthesia the involvement of baroreflex in governing RR-SAP variability interactions is largely overestimated by RR-SAP squared coherence and causality analysis can be exploited to rank anesthesiological strategies and MV modes according to the ability of preserving a working baroreflex.

Impact of prolonged mechanical ventilation on diaphragmatic protein synthesis

Mechanical ventilation (MV) is a life‐saving intervention in patients suffering from respiratory failure. Unfortunately, prolonged MV promotes the rapid development of diaphragmatic atrophy due to increased proteolysis and decreased protein synthesis. These experiments investigated the influence of two different modes of MV on rat diaphragm protein synthesis. Specifically, we examined the mixed protein synthesis rate of diaphragm muscle proteins during controlled MV (CMV) which causes complete diaphragmatic inactivity and pressure support MV (PSV) which permits partial activity of the diaphragm. Our results reveal that compared to spontaneously breathing animals, diaphragm protein synthesis rates are not depressed during the first 6‐hours of PSV but are significantly decreased in animals exposed to CMV. However, the rates of diaphragm protein synthesis are depressed at similar levels in both CMV and PSV animals during 6–12 hours of MV. We conclude that while PSV can initially delay the MV‐induced decreases in diaphragm protein synthesis, this protective effect is rapidly lost after the first 6 hours of MV. NIH RO1 HL087839 (SKP)

Hemodynamics and Blood Oxygen-Transport Function under Combined Anesthesia with Preserved Spontaneous Respiration

Objective: to improve the results of surgical treatment, by ruling out the negative effects of mechanical ventilation (MV) via combined anesthesia without myoplegia during operations on the lower abdomen. Subjects and methods. One hundred and twenty-one patients aged 20 to 64 years were examined. The patients were divided into 2 groups: 1) inhalation anesthesia under total myoplegia and continuous MV; 2) inhalation anesthesia without myoplegia and with preserved spontaneous respiration or pressure-support MV (PSMV). Results. The procedure of the latter allows combined anesthesia with preserved spontaneous respiration during operations on the lower abdomen and great vessels to have inadequate transport of oxygen under its relatively increased uptake in 98% of patients without any risk. MV made to prosthelytize external respiration function under combined anesthesia and total myoplegia causes a decrease in cardiac index (CI) by 40% or more (p<0.05) and increases in total peripheral vascular resistance (TPVR) by 50% or more (p<0.05) and intrapulmonary shunt by 3 times (p<0.05). Combined anesthesia without myoplegia and MV prevent induced changes in CI, TPVR, and Qs/Qt. The differences are significant throughout the follow-up (an intraoperative step and 9 postoperative hours). Conclusion. To rule out myoplegia and MV during combined anesthesia prevents MV-induced changes in CI, TPVR, and Qs/Qt. Key words: combined anesthesia, spontaneous respiration, hemodynamics, blood oxygen-transport function.

Commentary: Nemoto T et al. (1999). Automatic control of pressure support mechanical ventilation using fuzzy logic

AbstractThere is currently no universally accepted approach to weaning patients from mechanical ventilation, but there is clearly a feeling within the medical community that it may be possible to formulate the weaning process algorithmically in some manner. Fuzzy logic seems suited to this task because of the way it so naturally represents the subjective human notions employed in much of medical decision‐making. The purpose of the present study was to develop a fuzzy logic algorithm for controlling pressure support ventilation in patients in the intensive care unit, utilizing measurements of heart rate, tidal volume, breathing frequency and arterial oxygen saturation. In this report, we describe the fuzzy logic algorithm and demonstrate its use retrospectively in 13 patients with severe chronic obstructive pulmonary disease, by comparing the decisions made by the algorithm with what actually transpired. The fuzzy logic recommendation agreed with the status quo to within 2 cm H2O an average of 76% of the time, and to within 4 cm H2O an average of 88% of the time (although in most of these instances no medical decisions were taken as to whether or not to change the level of ventilatory support). We also compared the predictions of our algorithm with those cases in which changes in pressure support level were actually made by an attending physician, and found that the physicians tended to reduce the support level somewhat more aggressively than the algorithm did. We conclude that our fuzzy algorithm has the potential to control the level of pressure support ventilation from ongoing measurements of a patient’s vital signs. Abstract reprinted from the American Journal of Respiratory and Critical Care Medicine, volume 160, Nemoto T et al., ‘(1999) Automatic control of pressure support mechanical ventilation using fuzzy logic.’, pages 550–556. © 1999, reproduced with permission from The American Thoracic Society.

Influence of arterial O2 on the susceptibility to posthyperventilation apnea during sleep

To investigate the contribution of the peripheral chemoreceptors to the susceptibility to posthyperventilation apnea, we evaluated the time course and magnitude of hypocapnia required to produce apnea at different levels of peripheral chemoreceptor activation produced by exposure to three levels of inspired P(O2). We measured the apneic threshold and the apnea latency in nine normal sleeping subjects in response to augmented breaths during normoxia (room air), hypoxia (arterial O2 saturation = 78-80%), and hyperoxia (inspired O2 fraction = 50-52%). Pressure support mechanical ventilation in the assist mode was employed to introduce a single or multiple numbers of consecutive, sigh-like breaths to cause apnea. The apnea latency was measured from the end inspiration of the first augmented breath to the onset of apnea. It was 12.2 +/- 1.1 s during normoxia, which was similar to the lung-to-ear circulation delay of 11.7 s in these subjects. Hypoxia shortened the apnea latency (6.3 +/- 0.8 s; P < 0.05), whereas hyperoxia prolonged it (71.5 +/- 13.8 s; P < 0.01). The apneic threshold end-tidal P(CO2) (Pet(CO2)) was defined as the Pet(CO2)) at the onset of apnea. During hypoxia, the apneic threshold Pet(CO2) was higher (38.9 +/- 1.7 Torr; P < 0.01) compared with normoxia (35.8 +/- 1.1; Torr); during hyperoxia, it was lower (33.0 +/- 0.8 Torr; P < 0.05). Furthermore, the difference between the eupneic Pet(CO2) and apneic threshold Pet(CO2) was smaller during hypoxia (3.0 +/- 1.0 Torr P < 001) and greater during hyperoxia (10.6 +/- 0.8 Torr; P < 0.05) compared with normoxia (8.0 +/- 0.6 Torr). Correspondingly, the hypocapnic ventilatory response to CO2 below the eupneic Pet(CO2) was increased by hypoxia (3.44 +/- 0.63 l.min(-1).Torr(-1); P < 0.05) and decreased by hyperoxia (0.63 +/- 0.04 l.min(-1).Torr(-1); P < 0.05) compared with normoxia (0.79 +/- 0.05 l.min(-1).Torr(-1)). These findings indicate that posthyperventilation apnea is initiated by the peripheral chemoreceptors and that the varying susceptibility to apnea during hypoxia vs. hyperoxia is influenced by the relative activity of these receptors.

Carotid body denervation eliminates apnea in response to transient hypocapnia.

We determined the effects on breathing of transient ventilatory overshoots and concomitant hypocapnia, as produced by pressure support mechanical ventilation (PSV), in intact and carotid body chemoreceptor denervated (CBX) sleeping dogs. In the intact dog, PSV-induced transient increases in tidal volume and hypocapnia caused apnea within 10-11 s, followed by repetitive two-breath clusters separated by apneas, i.e., periodic breathing (PB). After CBX, significant expiratory time prolongation did not occur until after 30 s of PSV-induced hypocapnia, and PB never occurred. Average apneas of 8.4 +/- 1-s duration after a ventilatory overshoot required a decrease below eupnea of end-tidal Pco(2) 5.1 +/- 0.4 Torr below eupnea in the intact animal and 10.1 +/- 2 Torr in the CBX dog, where the former reflected peripheral and the latter central dynamic CO(2) chemoresponsiveness, as tested in the absence of peripheral chemoreceptor input. Hyperoxia when the dogs were intact shortened PSV-induced apneas and reduced PB but did not mimic the effects of CBX. We conclude that, during non-rapid eye movement sleep, carotid chemoreceptors are required to produce apneas that normally occur after a transient ventilatory overshoot and for PB.

Effect of ventilatory drive on carbon dioxide sensitivity below eupnea during sleep.

We determined the effects of changing ventilatory stimuli on the hypocapnia-induced apneic and hypopneic thresholds in sleeping dogs. End-tidal carbon dioxide pressure (PET(CO2)) was gradually reduced during non-rapid eye movement sleep by increasing tidal volume with pressure support mechanical ventilation, causing a reduction in diaphragm electromyogram amplitude until apnea/periodic breathing occurred. We used the reduction in PET(CO2) below spontaneous breathing required to produce apnea (DeltaPET(CO2)) as an index of the susceptibility to apnea. DeltaPET(CO2) was -5 mm Hg in control animals and changed in proportion to background ventilatory drive, increasing with metabolic acidosis (-6.7 mm Hg) and nonhypoxic peripheral chemoreceptor stimulation (almitrine; -5.9 mm Hg) and decreasing with metabolic alkalosis (-3.7 mm Hg). Hypoxia was the exception; DeltaPET(CO2) narrowed (-4.1 mm Hg) despite the accompanying hyperventilation. Thus, hyperventilation and hypocapnia, per se, widened the DeltaPET(CO2) thereby protecting against apnea and hypopnea, whereas reduced ventilatory drive and hypoventilation narrowed the DeltaPET(CO2) and increased the susceptibility to apnea. Hypoxia sensitized the ventilatory responsiveness to CO2 below eupnea and narrowed the DeltaPET(CO2); this effect of hypoxia was not attributable to an imbalance between peripheral and central chemoreceptor stimulation, per se. We conclude that the DeltaPET(CO2) and the ventilatory sensitivity to CO2 between eupnea and the apneic threshold are changeable in the face of variations in the magnitude, direction, and/or type of ventilatory stimulus, thereby altering the susceptibility for apnea, hypopnea, and periodic breathing in sleep.

Automatic control of pressure support mechanical ventilation using fuzzy logic.

There is currently no universally accepted approach to weaning patients from mechanical ventilation, but there is clearly a feeling within the medical community that it may be possible to formulate the weaning process algorithmically in some manner. Fuzzy logic seems suited this task because of the way it so naturally represents the subjective human notions employed in much of medical decision-making. The purpose of the present study was to develop a fuzzy logic algorithm for controlling pressure support ventilation in patients in the intensive care unit, utilizing measurements of heart rate, tidal volume, breathing frequency, and arterial oxygen saturation. In this report we describe the fuzzy logic algorithm, and demonstrate its use retrospectively in 13 patients with severe chronic obstructive pulmonary disease, by comparing the decisions made by the algorithm with what actually transpired. The fuzzy logic recommendations agreed with the status quo to within 2 cm H(2)O an average of 76% of the time, and to within 4 cm H(2)O an average of 88% of the time (although in most of these instances no medical decisions were taken as to whether or not to change the level of ventilatory support). We also compared the predictions of our algorithm with those cases in which changes in pressure support level were actually made by an attending physician, and found that the physicians tended to reduce the support level somewhat more aggressively than the algorithm did. We conclude that our fuzzy algorithm has the potential to control the level of pressure support ventilation from ongoing measurements of a patient's vital signs.