Removal Of Positive End-expiratory Pressure Research Articles

Measuring Expiratory Diaphragm Activity: An Electrifying Tool to Guide Positive End-Expiratory Pressure Strategy in Critically Ill Children?

Measuring Expiratory Diaphragm Activity: An Electrifying Tool to Guide Positive End-Expiratory Pressure Strategy in Critically Ill Children?

Positive end-expiratory pressure-induced increase in external jugular venous pressure does not predict fluid responsiveness in laparoscopic prostatectomy.

Dynamic change in central venous pressure (CVP) was associated with fluid responsiveness. External jugular venous pressure (EJVP) may reliably estimate CVP and have the advantages of being less invasive. We investigated whether increase in EJVP induced by positive end-expiratory pressure (PEEP) could be a reliable predictor of fluid responsiveness in patients undergoing robot-assisted laparoscopic prostatectomy (RALP). Fifty patients who underwent RALP with steep Trendelenburg position were enrolled. PEEP of 10cmH2O was applied for 5min and then 300ml of colloid was administered. EJVP, stroke volume variation (SVV), and cardiac index calculated by pulse contour method were measured before and after the PEEP challenge and colloid administration. Increase in cardiac index>10% was used to define the fluid responsiveness. Twenty-six patients were fluid responders. Neither the increase in EJVP after the initial PEEP nor SVV was significantly different between responders and non-responders. They were not significantly correlated with an increase in cardiac index. The areas under the receiver operating characteristic curve (AUC) of these two variables were not significantly greater than 0.5. However, a post hoc analysis revealed that AUC of a decrease in EJVP after removal of PEEP was significantly greater than 0.50. Our study results suggested that SVV and increase in EJVP after applying PEEP were not accurate predictors of fluid responsiveness during RALP. Further studies are required to find an adequate preload index in robot-assisted urologic surgery with steep Trendelenburg position.

Lung Stress and Strain During Mechanical Ventilation

Tidal volume (VT) and volume of gas caused by positive end-expiratory pressure (VPEEP) generate dynamic and static lung strains, respectively. Our aim was to clarify whether different combinations of dynamic and static strains, resulting in the same large global strain, constantly produce lung edema. Laboratory investigation. Animal unit. Twenty-eight healthy pigs. After lung computed tomography, 20 animals were ventilated for 54 hours at a global strain of 2.5, either entirely dynamic (VT 100% and VPEEP 0%), partly dynamic and partly static (VT 75-50% and VPEEP 25-50%), or mainly static (VT 25% and VPEEP 75%) and then killed. In eight other pigs (VT 25% and VPEEP 75%), VPEEP was abruptly zeroed after 36-54 hours and ventilation continued for 3 hours. Edema was diagnosed when final lung weight (balance) exceeded the initial weight (computed tomography). Mortality, lung mechanics, gas exchange, pulmonary histology, and inflammation were evaluated. All animals ventilated with entirely dynamic strain (VT 825±424 mL) developed pulmonary edema (lung weight from 334±38 to 658±99 g, p<0.01), whereas none of those ventilated with mainly static strain (VT 237±21 mL and VPEEP 906±114 mL, corresponding to 19±1 cm H2O of positive end-expiratory pressure) did (from 314±55 to 277±46 g, p=0.65). Animals ventilated with intermediate combinations finally had normal or largely increased lung weight. Smaller dynamic and larger static strains lowered mortality (p<0.01), derangement of lung mechanics (p<0.01), and arterial oxygenation (p<0.01), histological injury score (p=0.03), and bronchoalveolar interleukin-6 concentration (p<0.01). Removal of positive end-expiratory pressure did not result in abrupt increase in lung weight (from 336±36 to 351±77 g, p=0.51). Lung edema forms (possibly as an all-or-none response) depending not only on global strain but also on its components. Large static are less harmful than large dynamic strains, but not because the former merely counteracts fluid extravasation.

Physiologic Changes During Bronchoscopy in Mechanically Ventilated Patients

Background : Bronchoscopy in patients on mechanical ventilation is being performed much more frequently. However, there is little data on the changes in physiologic parameters and no established mechanical ventilation protocol during bronchoscopy. A decreasing or the removal of positive end-expiratory pressure (PEEP) during bronchoscopy may precipitate severe hypoxemia and/or derecruitment. Methods : Our standardized mechanical ventilation protocol, without changing the PEEP level, was used during bronchoscopy. The physiological parameters were measured during the bronchoscopic procedure. Results : During bronchoscopy, respiratory acidosis, elevation of peak pressure, elevation of heart rate and auto-PEEP were developed, but were reversible changes. Procedure-related gross barotraumas or other severe complications did not developed. Conclusion : No serious complications developed during bronchoscopy under our standardized mechanical ventilation protocol when the PEEP level remained unchanged. The procedure time should be kept to a minimum to decrease the exposure time to undesirable physiological changes.

Effects of PEEP on Residual Vascularization in Oesophageal Substitution Gastroplasty by Surface Oximetry-Capnometry and Photoplethysmography

Objective: To evaluate the effects of positive end-expiratory pressure (PEEP) on residual vascularization in gastric tubes for oesophageal replacement. Design: Experimental open study. Materials: Eleven mongrel dogs. Methods: Intestinal parietal blood flow was evaluated by photoplethysmography (PPG) and measurement of surface oxygen (PsO₂) and carbon dioxide (PsCO₂) tensions under basal conditions. After Akiyama’s tubular gastroplasty, three levels of PEEP were administered. At each level, fluids were infused to counter the drop in cardiac output. PPG, surface gas tensions, arterial pressure, cardiac output and arterial blood gas tensions were monitored. Control sections of the bowel were also monitored by PPG. Results: Cardiac output dropped for each level of PEEP and returned to basal levels on volume restabilization and on removal of PEEP. Central venous pressure and pulmonary arterial and capillary pressures increased for each level of PEEP and only returned to basal levels on removal of PEEP. PsO₂ values dropped for each level of PEEP and returned to basal levels on volume restabilization and on removal of PEEP. PsCO₂ levels rose, and PPG wave amplitude dropped, for each level of PEEP; these two variables only returned to basal levels on removal of PEEP. PPG values for the control sections reflected those of the anastomotic area. Conclusions: PEEP affects surface oxygen values at the level of the gastroplasty by means of its effect on cardiac output. PEEP also creates a venous return compromise and PPG wave amplitude and surface carbon dioxide values are related to this compromise. All three variables could be significant in anastomotic wound healing.

Exposing guinea pigs to ozone for 1 wk enhances responsiveness of rapidly adapting receptors.

Acute exposure to ozone causes changes in breathing pattern and lung function which may be caused in part by stimulation of rapidly adapting receptors (RARs). The consequences of repeated daily ozone exposure on RAR responsiveness are unknown, although ozone-induced changes in pulmonary function diminish with repeated exposure. Accordingly, we investigated whether repeated daily ozone exposure diminishes the general responsiveness of RARs. Guinea pigs (n = 30) were exposed to 0.5 parts/million ozone or filtered air (8 h/day for 7 days). The animals were then anesthetized, and RAR impulse activity, dynamic compliance (Cdyn), and lung resistance were recorded at baseline and in response to four stimuli: substance P, methacholine, hyperinflation, and removal of positive end-expiratory pressure. Repeated daily ozone exposure exaggerated RAR responses to substance P, methacholine, and hyperinflation without causing physiologically relevant effects on baseline or substance P- and methacholine-induced changes in Cdyn and lung resistance. Because agonist-evoked changes in RAR activity preceded Cdyn changes, the data suggest that repeated daily ozone exposure enhances RAR responsiveness via a mechanism other than changes in Cdyn.

Effects of Positive End-Expiratory Pressure on Hepatic Venous Oxygenation in Dogs

Background : Positive end-expiratory pressure(PEEP) ventilation causes reduction in cardiac output and increase of intra-thoracic pressure, hence reduction of hepatic blood flow. The purpose of this study is to evaluate the changes of hepatic venous oxygen saturation, tension and content during increase and removal of PEEP and to evaluate hemodynamic variable which has the greatest effect on hepatic oxygenation. Method : Eight dogs were anethetised with 1.0 vol% isoflurane and 100% oxygen. After 30 minutes of stabilization of vital signs, PEEP were increased from 0 cmH2O to 5 cmH2O and 10 cmH2O and lowered to 0 cmH2O again, and hemodynamic data (heart rate, arterial blood pressure, central venous pressure(CVP), pulmonary arterial pressure, pulmonary arterial occlusion pressure and cardiac output(CO)) and hepatic venous oxygenation data (hepatic venous oxygen saturation(ShvO2), tension(PhvO2) and content(ChvO2)) were measured at each step. Results : CO, ShvO2, PhvO2 and ChvO2 decreased significantly at 10 cmH2O PEEP compared to the baseline and 5 cmH2O PEEP and CO, ShvO2 and ChvO2 increased signicantly with removal of PEEP. CVP increased significantly at 10 cmH2O PEEP and decreased significantly with PEEP removal. PEEP showed close correlationship with CO and CVP considering all steps of PEEP and PEEP removal. ShvO2 and PhvO2 showed most close correlationship with CO considering all steps of PEEP and PEEP removal. Conclusion : ShvO2 with PEEP therapy is dependent upon CO. Therefore cardiac output maintenance is essential during PEEP therapy. For exact evaluation of hepatic oxygenation, it is valuable to monitor ShvO2. (Korean J Anesthesiol 1998; 35: 861∼869)

Transesophageal pulsed-doppler echocardiographic evaluation of transmitral and pulmonary venous flow during ventilation with positive end-expiratory pressure

During mechanical ventilation with high levels of positive end-expiratory pressure (PEEP) several hemodynamic changes occur, the mechanism of which has been the subject of various previous studies. The effects of increasing levels of PEEP during mechanical ventilation were measured on left atrial and left ventricular filling dynamics, as assessed by pulmonary venous and transmitral flow velocities, respectively. Using transesophageal echocardiography in 12 patients, Doppler flow velocities of pulmonary venous and transmitral flow were studied at baseline (0 cmH 2O PEEP) and at 5, 10, 15, and 20 cm H 2O with 10-minute intervals, and once more after removal of PEEP. In 2 of the 12 patients, PEEP could not be increased beyond 15 cmH 20, because cardiac index fell below 2.0 L/min/m 2. Pulmonary venous flow velocity and velocity time integral during systole significantly decreased from 48 ± 7 cm/s and 10.3 ± 2.2 cm at baseline to 35 ± 6 cm/s and 5.7 ± 2.5 cm at 20 cmH 2O PEEP, respectively ( P < 0.01). In contrast, early and late diastolic velocities and velocity time integrals did not change. In regard to transmitral flow, both early and late diastolic velocities significantly decreased from 51 ± 7 cm/s and 50 ± 9 cm/s at baseline to 38 ± 7 cm/s and 39 ± 7 cm/s at 20 cmH 2O PEEP, respectively ( P < 0.01). Early and late diastolic velocity time integrals decreased from 6.1 ± 1.8 cm and 4.7 ± 1.0 cm to 4.5 ± 1.0 cm (NS) and 3.4 ± 0.7 cm ( P < 0.05), respectively. Thus, at high levels of PEEP there is a reduction in both early and late diastolic left ventricular inflow through the mitral valve and a decrease in systolic left atrial filling through the pulmonary veins, while diastolic left atrial inflow does not change. Because systolic pulmonary venous flow is mainly affected by left atrial events, the observed change in pulmonary venous flow pattern suggests that high levels of PEEP principally influence left atrial function.

LV filling pressure during PEEP measured by nadir wedge pressure after airway disconnection.

Pulmonary arterial occlusion pressure (Ppao) may not accurately reflect left ventricular filling pressure (LVFP) during ventilation with positive end-expiratory pressure (PEEP) because increases in pleural pressure (Ppl) increase measured intrathoracic vascular and cardiac chamber pressures relative to atmospheric while decreasing LVFP by decreasing venous return. Steady-state values of Ppao off PEEP are not useful in understanding the hemodynamics on PEEP because of changes in blood volume distribution and ventricular afterload associated with the removal of PEEP. We hypothesized that changes in Ppao immediately after abrupt airway disconnection from PEEP selectively reflect removal of PEEP-associated Ppl changes prior to other physiological changes. In pentobarbital-anesthetized closed-chest dogs, we compared absolute left atrial pressure and left atrial pressure relative to Ppl (Platm) prior to abrupt disconnection from 15 cmH2O PEEP (on-PEEP), with Ppao at its nadir (nadir Ppao) following airway disconnection in three sequential conditions: control (normal), after propranolol-induced acute ventricular failure, and after oleic acid-induced lung injury. For all conditions at low LVFP (less than 9 Torr), nadir Ppao reflects Platm better than on-PEEP Ppao, while at higher LVFP (greater than 9 Torr), on-PEEP Ppao better reflects Platm than nadir Ppao (P less than 0.05). Accurate predictions of on-PEEP Platm can be made using both on-PEEP and nadir Ppao values in a multiple regression equation.

Biventricular Volumes and Function in Patients with Adult Respiratory Distress Syndrome Ventilated with PEEP

The ventricular volume and function changes induced by the addition of 12 cm H2O of positive end-expiratory pressure (PEEP) during mechanical ventilation were studied in 11 patients with the adult respiratory distress syndrome. Cardiac output was measured by thermodilution and ventricular ejection fraction by the multiple gated equilibrated cardiac blood pool scintigraphy. Right and left end-diastolic volumes were then calculated by dividing stroke volume by ejection fraction. The PEEP caused a 14 percent decrease of the cardiac output secondary to a decrease in stroke volume. On the basis of the relationship between stroke volume and ventricular end-diastolic volume, we conclude that reduction in preload was the major component of the decrease in cardiac output. After removal of PEEP, we observed a rebound phenomenon characterized by higher values for stroke volume and cardiac output than before the application of PEEP.

Time course and mechanisms of lung-volume increase with PEEP in acute pulmonary failure.

To determine the effects of a step change in end-expiratory pressure on functional residual capacity (FRC) and lung-thorax compliance (CLT), 10 cm H2O positive end-expiratory pressure (PEEP) was applied in eight patients who needed mechanical ventilation for acute pulmonary failure. Of the total change in FRC, 66 +/- 5.3 per cent (mean +/- SEM) was complete within the next breath, and 90 per cent change was achieved in 4.6 +/- 1.4 breaths (24 +/- 6.4 sec). There was no statistically significant difference between times to 90 per cent FRC change with application and with removal of PEEP. In another 13 patients, PEEP was increased in 5 cm H2O steps from 3 to 18 cm H2O. Mean FRC at 3 cm H2O PEEP was 1.51 +/- 0.20 1 (55 +/- 7.0 per cent predicted supine value). Mean CLT did not change significantly until 18 cm H2O PEEP was reached, at which point it decreased (P < 0.005). The static compliance derived from change in FRC (deltaFRC/deltaPEEP) increased with increments of PEEP (P < 0.05) compared with the initial level. At PEEP levels of 8 and 13 cm H2O, mean FRC was larger than would be predicted from mean CLT (P < 0.005), but it was not significantly different at 3 cm H2O PEEP. The lung component accounted for 62 +/- 3.7 per cent of the lung-thorax compliance difference. These data define a time-dependent increase in lung volume that resembles pressure-volume hysteresis in normal man. Possible mechanisms include surface tension changes, recruitment of nonventilated lung, and stress relaxation of lung and chest wall. This study may explain the greater efficiency of PEEP compared with large tidal-volume ventilation in increasing PaO2 in patients with acute pulmonary failure.

Continuous positive-pressure ventilation decreases right and left ventricular end-diastolic volumes in the dog.

We investigated the mechanism(s) responsible for the decreased cardiac output during continuous positive-pressure ventilation (CPPV). Seven dogs were anesthetized with chloralose-urethane, intubated, and ventilated using a volume ventilator. We measured heart rate, stroke volume, and the determinants of stroke volume: left and right ventricular end-diastolic volumes, isovolumic and ejection phase indices of myocardial contractility, and pulmonary and systemic arterial pressures. Myocardial blood flow was estimated using radioactive microspheres. Variables were measured during a control period of intermittent positive-pressure ventilation (IPPV), 8-20 minutes after the initiation of CPPV using 12 cm H2O positive end-expiratory pressure (PEEP), and 8-20 minutes after the removal of PEEP. CPPV decreased cardiac output but did not affect total or regional myocardial blood flow or the ratio of subendocardial to subepicardial blood flow. Isovolumic and ejection phase indices of myocardial cointractility, heart rate, and systemic arterial pressure did not change during CPPV. Right and left ventricular end-diastolic and end-systolic volumes decreased markedly during CPPV. We conclude that CPPV decreases cardiac output in accordance with Starling's law by decreasing preload.

Humorally Mediated Alterations in Cardiac Performance as a Consequence of Positive End-Expiratory Pressure

Two experimental designs were used to study the mechanism of the decreased cardiac output associated with the use of positive end-expiratory pressure (PEEP). In the first study of nine dogs the application of 15 cm H2O PEEP led to a decrease in cardiac output (CO) from 2.68 +/- 1.05 to 2.01 +/- 1.26 liters/min (+/- SD) (p less than 0.05) concomitant with an increase in transmural central venous pressure of 5.2 +/- 0.9 to 8.4 +/- 2.7 mm Hg (p less than 0.05) and a slight increase in transmural left atrial pressure of 6.8 +/- 3.3 to 7.3 +/- 3.6 mm Hg (p less than 0.1). These data are consistent with altered ventricular performance. In a second study nine pairs of dogs were cross-circulated. Application of 15 cm H2O PEEP to one member of the experimental pair led to a decrease in the CO of the other member from 2.71 +/- 0.98 to 2.21 +/- 0.81 liters/min (p less than 0.001). This decrease returned toward baseline with the removal of PEEP (p less than 0.02). Results indicate that one mechanism whereby PEEP reduces the cardiac output is through the action of a humoral agent.

Positive end‐expiratory pressure

Changes induced in arterial oxygenation by positive end-expiratory pressure (PEEP) were analysed in twenty-nine instances in seven patients with chronic obstructive airway disease and acute respiratory failure, who were receiving IPPV. A significant decrease in mean PaO2 was found 4 hours after the removal of PEEP (P smaller than 0-01), but after its addition during the same period the PaO2 change was not significant. PaCO2 values were not modified by PEEP. The slight increase in mean PaO2 (20-9 mmHg) encountered during controlled ventilation with PEEP seems of doubtful clinical value. Alveolar-arterial oxygen gradient, while breathing oxygen 100%, was found to be elevated with a mean value of 276 mmHg. It appears from our results that PEEP is of little or no value in the routine ventilatory treatment of patients with chronic obstructive airway disease unless hypoxaemia is believed to be caused by a large intrapulmonary shunt.

The Effect of Pre-existing Pulmonary Vascular Disease on the Response to Mechanical Ventilation with PEEP Following Open-heart Surgery

The effects of mechanical ventilation with and without positive end-expiratory pressure (PEEP) on hemodynamic performance and blood-gas exchange were studied in ten patients following open-heart surgery. Ventilation at constant tidal volume (15 ml/kg body weight) with 10 cm H2O PEEP following aortic valve replacement (AVR) IN FIVE PATIENTs without pulmonary vascular disease was associated with the following significant changes: a rise in arterial Po2, a fall in the alveolar-arterial Po2 gradient when Fio2 = 1.0, decreases in calculated Qs/Qt and cardiac index. Using a similar pattern of ventilation following mitral valve replacement (MVR) in patients with elevated pulmonary vascular resistance, we found a significant decrease in cardiac index (but less than in the AVR group), a significant elevation of calculated physiologic deadspace (Vd/Vt) and no change in Qs/Qt. An hour after removal of PEEP, intravascular pressures, blood flow and blood-gas exchange values of all patients with AVR had returned to control levels; patients with MVR had persistently significantly low cardiac indices, while Vd/Vt returned to pre-PEEP values. These findings suggest that evaluation of responses to different ventilation patterns must take into account pre-existing V/Q abnormalities secondary to pulmonary vascular disease, particularly when these are secondary to chronic congestive heart failure. Following AVR, Qs/Qt changed in the same direction as cardiac index (CI) irrespective of ventilatory pattern: CI decreased and rose as CI increased. The authors conclude that with increasing severity of pulmonary vascular disease, changes in airway pressure will have an unpredictable effect on cardiac index unless the level of myocardial competence is taken into account. In the presence of ventricular failure, changes in pleural (and therefore transmural) pressures will be minimal compared with the high filling pressures and exert no influence on stroke volume. Although pulmonary venous hypertension was more pronounded in the MVR than in the AVR group, there was no significant difference between the postoperative values for Qs/Qt (Fio2 = 1.0), a condition probably fostered by marked differences in pre-existing V/Q.

Hemodynamic Responses to Mechanical Ventilation with PEEP

The hemodynamic effects of prolonged mechanical ventilation with positive end-expiratory pressure (PEEP), with and without blood volume augmentation, were studied in 18 beagles anesthetized with halothane (0.7 per cent end-tidal). Addition of 12 cm H2O PEEP during mechanical ventilation in normavolemic dogs was associated with reductions of transmural cardiac filling pressures, cardiac index and stroke index to 50 per cent of control values. Circulatory adaptation did not occur. Filling pressures and flow remained unchanged during the ensuing 8 hours when PEEP was maintained. They returned to control levels when PEEP was discontinued, except for the transmural right ventricular end-diastolic pressure, which remained elevated above control levels. Systemic vascular resistance was unchanged, but pulmonary vascular resistance doubled upon addition of PEEP. Following autologous whole blood transfusion (25 ml/kg) during mechanical ventilation with PEEP, cardiac index returned to, and remained at, control levels. After PEEP was discontinued, cardiac index increased acutely and remained elevated for the remainder of the study period (as long as 7 hours). Comparable transfusion during mechanical ventilation without PEEP elevated cardiac index only transiently. Right atrial, pulmonary capillary wedge, and right and left ventricular end-diastolic pressures showed marked increases relative to atmospheric with PEEP and after transfusion. Calculated transmural pressures demonstrated clear reductions with application of PEEP, followed by increases to control levels with transfusion and further increases to above control when PEEP was discontinued. Study of ventricular function curves revealed that changes in filling pressures and not to changes in ventricular contractility. Transmural pulmonary arterial diastolic pressure rose throughout the 12 hours of study, despite return of pulmonary vascular resistance to control level with removal of PEEP. Thus, acute decreases in cardiac filling pressure, cardiac index, and stroke index persist consequent to application of PEEP, and circulatory adaptation does not occur. The apparent hemodynamic deterioration may be reversed by blood volume augmentation, but when PEEP is discontinued, hypervolemia with consequent increases in filling pressures and a move along a ventricular function curve will occur. Changes in cardiac index will depend upon the overall state of right and left ventricular contractility.