Total Positive End-expiratory Pressure Research Articles

Mechanical ventilation in severe asthma

In their review on mechanical ventilation in severe asthma, Stather and Stewart [1] raise a concern that use of external positive end-expiratory pressure (PEEP) will result in increased total PEEP and worsened gas trapping [1]. Of critical importance to our understanding of whether application of external PEEP will be beneficial is assessment of the presence or absence of expiratory flow limitation [2,3]. When the severity of airflow obstruction is such that flow limitation is present, application of PEEP will not influence expiratory flow or upstream pressures. At the bedside, one can examine for this by noting the effect of applied external PEEP on the inflation pressure of subsequent breaths. In the absence of flow limitation, increased external PEEP will be transmitted upstream, causing parallel increases in alveolar pressure, peak airway pressure, and end-inspiratory pressure. The associated increase in lung volume will tend to moderate this rise in airway pressure. When flow limitation is present, upstream pressures are 'protected' from increases in downstream pressure (or PEEP). In this situation, inflation pressures are independent of external PEEP. Occasionally, inflation pressure may actually decrease with external PEEP. Here, the external PEEP may act to 'stent open' the central airways and allow reduction in gas trapping and reduction in end-expiratory lung volumes [4]. Examination of the effect of increasing external PEEP on inflation pressure may allow identification of those patients who might benefit from administration of external PEEP.

Effects of Short-term Pressure-Controlled Ventilation on Gas Exchange, Airway Pressures, and Gas Distribution in Patients with Acute Lung Injury/ARDS: Comparison With Volume-Controlled Ventilation

The potential clinical benefits of pressure-controlled ventilation (PCV) over volume-controlled ventilation (VCV) in patients with acute lung injury (ALI) or ARDS still remain debated. We compared PCV with VCV in patients with ALI/ARDS with respect to the following physiologic end points: (1) gas exchange and airway pressures, and (2) CT scan intrapulmonary gas distribution at end-expiration. Prospective, observational study. A multidisciplinary ICU in a nonuniversity, acute-care hospital. Ten patients with ALI or ARDS (9 men and 1 woman; age range, 17 to 80 years). Sequential ventilation in PCV and VCV with a constant inspiratory/expiratory ratio, tidal volume, respiratory rate, and total positive end-expiratory pressure; measurement of gas exchange and airway pressures; and achievement of CT sections at lung base, hilum, and apex for the quantitative analysis of lung densities and of aerated vs nonaerated zones. PaO(2), PaCO(2), and PaO(2)/fraction of inspired oxygen ratio levels did not differ between PCV and VCV. Peak airway pressure (Ppeak) was significantly lower in PCV compared with VCV (26 +/- 2 cm H(2)O vs 31 +/- 2 cm H(2)O; p < 0.001; mean +/- SEM). The surface areas of the nonaerated zones as well as the total areas at each section level were unchanged in PCV compared with VCV, except at the apex level, where there was a significantly greater nonaerated area in VCV (11 +/- 2 cm(2) vs 9 +/- 2 cm(2); p < 0.05). The total mean CT number of each lung (20 lungs from 10 patients) was similar in the two modes, as were the density values at the basal and apical levels; the hilum mean CT number was - 442 +/- 28 Hounsfield units (HU) in VCV and - 430 +/- 26 HU in PCV (p < 0.005). These data show that PCV allows the generation of lower Ppeaks through the precise titration of the lung distending pressure, and might be applied to avoid regional overdistension by means of a more homogeneous gas distribution.

Effects of positive end-expiratory pressure on gas exchange and expiratory flow limitation in adult respiratory distress syndrome.

To assess the effects of different positive end-expiratory pressure (PEEP) levels (0, 5, 10, and 15 cm H2O) on tidal expiratory flow limitation (FL), regional intrinsic positive end-expiratory pressure (PEEPi) inhomogeneity, alveolar recruited volume (Vrec), respiratory mechanics, and arterial blood gases in mechanically ventilated patients with acute respiratory distress syndrome (ARDS). Prospective clinical study. Multidisciplinary intensive care unit of a university hospital. Thirteen sedated, mechanically ventilated patients during the first 2 days of ARDS. Detection of tidal FL and evaluation of total dynamic PEEP (PEEPt,dyn), total static PEEP (PEEPt,st), respiratory mechanics, and Vrec from pressure, flow, and volume traces provided by the ventilator. The average (+/-sd) tidal volume was 7.1 +/- 1.5 mL/kg, the total cycle duration was 2.9 +/- 0.45 secs, and the duty cycle was 0.35 +/- 0.05. Tidal FL was assessed using the negative expiratory pressure technique. Regional PEEPi inhomogeneity was assessed as the ratio of PEEPt,dyn to PEEPt,st (PEEPi inequality index), and Vrec was quantified as the difference in lung volume at the same airway pressure between quasi-static inflation volume-pressure curves on zero end-expiratory pressure (ZEEP) and PEEP. On ZEEP, seven patients exhibited FL amounting to 31 +/- 8% of tidal volume. They had higher PEEPt,st and PEEPi,st ( p<.001) and lower PEEPi inequality index ( p<.001) than the six nonflow-limited (NFL) patients. Two FL patients became NFL with PEEP of 5 cm H2O and five with PEEP of 10 cm H2O. In both groups, PaO2 increased progressively with PEEP. In the FL group, there was a significant correlation of PaO2 to PEEPi inequality index ( p=.002). For a given PEEP, Vrec was greater in NFL than FL patients, and a significant correlation of Pao to Vrec ( p<.001) was found only in the NFL group. We conclude that on ZEEP, tidal FL is common in ARDS patients and is associated with greater regional PEEPi inhomogeneity than in NFL patients. With PEEP of 10 cm H2O, flow limitation with concurrent cyclic dynamic airway compression and re-expansion and the risk of "low lung volume injury" were absent in all patients. In FL patients, PEEP induced a significant increase in PaO2, mainly because of the reduction of regional PEEPi inequality, whereas in the NFL group, arterial oxygenation was improved satisfactorily because of alveolar recruitment.

Increased Total Positive End-Expiratory Pressure Does Not Improve Hypoxemia during One-Lung Ventilation

In Reply:—On behalf of my co-authors I would like to thank Drs. Yokata and Sari for their correspondence and for sharing our interest in the pathophysiology of one-lung ventilation (OLV) as it applies to intraoperative management of patients during thoracic anesthesia. Their letter highlights three issues that arise out of our study of the interrelation of positive end-expiratory pressure (PEEP) and lung compliance with oxygenation during one-lung anesthesia:(1) Would it be more useful to use the inflection point derived from the expiratory limb of the pressure-volume (PV) curve of the ventilated lung, rather than the inspiratory lower inflection point (LIP), as a surrogate marker for the functional residual capacity (FRC) and the optimal endexpiratory lung volume? This is a possibility. As they mention, the expiratory inflection point has been demonstrated to be a useful guide for ventilatory management of patients with ARDS in the intensive care unit. Unfortunately, our experimental protocol did not allow for measurements on the expiratory portion of the PV curve. Although there are important differences in the respiratory mechanics between ARDS patients and those having intraoperative one-lung anesthesia, this would be a worthwhile question to study.(2) The level of auto-PEEP does not correlate with Pao2during one-lung ventilation (OLV). This is correct. A comparison of the PV curves of two patients with low levels of auto-PEEP in figure 2 and figure 3 of our manuscript demonstrates this point. 1The patient in figure 2 had an identifiable LIP, the application of PEEP raised the end-expiratory pressure closer to the LIP level and the patient had an improvement of Pao2with PEEP. The patient in figure 3 did not have a measurable LIP. Presumably this patient and others with similar PV patterns do not get down to the level of their FRC at end-expiration and are not helped by applied PEEP. So it is not merely the presence of auto-PEEP but also the underlying lung mechanics that determine whether a patient will benefit from PEEP during OLV.(3) Gravity and position may not be an important determinant of blood flow redistribution during OLV. The authors quote the study of Mure et al ., 2which was performed in closed-chest dogs to back up their point. While it is correct that we now appreciate that anatomic factors have a major contribution to the distribution of pulmonary blood flow, it is not clear how relevant this is to clinical OLV in the open-chest human. In fact, a recent report has confirmed the importance of operative position on oxygenation during OLV. A study by Watanabe et al ., 5demonstrated that there was a significant difference in oxygenation during OLV dependent on the patients position, with the mean Pao2in the lateral position exceeding that in the supine position by greater than 100 mmHg. Since the publication of our manuscript another study has been reported which validates our findings. Fujiwara et al . 3applied PEEP to the ventilated lung or continuous positive airway pressure (CPAP) to the nonventilated lung in a series of patients during OLV. They found that PEEP and CPAP were equivalent therapies and that both significantly increased Pao2during OLV. This is very different from the previous findings of Capan et al ., 4who showed that CPAP clearly increased mean Pao2during OLV while PEEP decreased mean Pao2. The difference between these two studies is in the patient populations. Capan studied patients with moderate or severe COPD having thoracotomies for lung cancer surgery. Fujiwara studied patients having OLV for esophageal surgery who are more likely to have normal pulmonary function. This supports our thesis that patients with normal or supra-normal lung elastic recoil (e.g . restrictive lung mechanics: pulmonary fibrosis, obesity) are the patients most likely to reach an end-expiratory lung volume below their FRC, and thus are the most likely to benefit from PEEP to the ventilated lung during OLV.

Translaryngeal tracheostomy in acute respiratory distress syndrome patients.

To prevent gas exchange deterioration during translaryngeal tracheostomy (TLT) in patients with acute respiratory distress syndrome (ARDS) ventilation is maintained through a small diameter endotracheal tube (ETT; 4.0 mm i.d.) advanced beyond the tracheostoma. We report on the feasibility of uninterrupted ventilation delivered through a high-resistance ETT in ARDS patients, and relevant ventilatory adjustments and monitoring. Prospective, observational clinical study in an eight-bed intensive care unit of a university hospital. Eight consecutive ARDS patients scheduled for tracheostomy. During TLT volume control ventilation was maintained through the 4.0-mm i.d. ETT. Tidal volume, respiratory rate, and inspiratory to expiratory ratio were kept constant. Fractional inspiratory oxygen was 1. Positive end expiratory pressure (PEEP) set on the ventilator (PEEP(vent)) was reduced to maintain total PEEP (PEEP(tot)) at baseline level according to the measured intrinsic PEEP (auto-PEEP). Data were collected before tracheostomy and while on mechanical ventilation with the 4.0-mm i.d. ETT. Neither PaCO(2) nor PaO(2) changed significantly (54.5+/-10.0 vs. 56.4+/-7.0 and 137+/-69 vs. 140+/-59 mmHg, respectively). Auto-PEEP increased from 0.6+/-1.1 to 9.8+/-6.5 cmH(2)O during ventilation with the 4.0-mm i.d. ETT. By decreasing PEEP(vent) we obtained a stable PEEP(tot) (11.4+/-4.3 vs. 11.8+/-4.3 cmH(2)O), and end-inspiratory occlusion pressure (26.7+/-7.4 vs. 28.0+/-6.6 cmH(2)O). Peak inspiratory pressure rose from 33.8+/-8.1 to 77.8+/-12.7 cmH(2)O. The high-resistance ETT allows ventilatory assistance during the whole TLT procedure. Assessment of stability in plateau pressure and PEEP(tot) by end-inspiratory and end-expiratory occlusions prevent hyperinflation and possibly barotrauma.

Influence of tidal volume on alveolar recruitment. Respective role of PEEP and a recruitment maneuver.

Both reduction in tidal volume (VT) and alveolar recruitment may be important to limit ventilator-associated lung injury during mechanical ventilation of patients with the acute respiratory distress syndrome (ARDS). The aim of this study was to assess the risk of alveolar derecruitment associated with VT reduction from 10 to 6 ml/kg. Whether this VT-related derecruitment could be reversed, either by a recruitment maneuver or by an increase in positive end-expiratory pressure (PEEP) level, was also investigated. Fifteen patients with ARDS were successively ventilated using conventional VT (CVT = 10 +/- 1 ml/kg) and low VT (LVT = 6 +/- 1 ml/ kg); total PEEP (PEEPtot) was individually set at the lower inflection point (Plip) of the pressure-volume curve (PEEPtot = 11 +/- 4 cm H(2)O). Pressure-volume curves were recorded from zero PEEP (ZEEP) and from PEEP, and recruited volume (Vrec) was calculated as the volume difference between the two curves for a given pressure. Despite a similar PEEPtot, Vrec was significantly lower with LVT than with CVT, indicating low VT-induced alveolar derecruitment. Reduction in VT was associated with a reduced Sa(O(2)). In 10 patients, Vrec was also measured before and after a recruitment maneuver (two sustained inflations at 45 cm H(2)O), and after an increase in PEEP (by 4 cm H(2)O). Low VT-induced derecruitment was reversed by a recruitment maneuver and by increasing PEEP. We conclude that a reduction in VT could be responsible for alveolar derecruitment, which may be transiently reversed by a reexpansion maneuver or prevented by a PEEP increase above Plip.

Estimating cardiac filling pressure in mechanically ventilated patients with hyperinflation.

When positive end-expiratory pressure (PEEP) is applied, the intracavitary left ventricular end-diastolic pressure (LVEDP) exceeds the LV filling pressure because pericardial pressure exceeds 0 at end-expiration. Under those conditions, the LV filling pressure is itself better reflected by the transmural LVEDP (tLVEDP) (LVEDP minus pericardial pressure). By extension, end-expiratory pulmonary artery occlusion pressure (eePAOP), as an estimate of end-expiratory LVEDP, overestimates LV filling pressure when pericardial pressure is >0, because it occurs when PEEP is present. We hypothesized that LV filling pressure could be measured from eePAOP by also knowing the proportional transmission of alveolar pressure to pulmonary vessels calculated as index of transmission = (end-inspiratory PAOP--eePAOP)/(plateau pressure--total PEEP). We calculated transmural pulmonary artery occlusion pressure (tPAOP) with this equation: tPAOP = eePAOP--(index of transmission x total PEEP). We compared tPAOP with airway disconnection nadir PAOP measured during rapid airway disconnection in subjects undergoing PEEP with and without evidence of dynamic pulmonary hyperinflation. Prospective study. Medical intensive care unit of a university hospital. We studied 107 patients mechanically ventilated with PEEP for acute respiratory failure. Patients without dynamic pulmonary hyperinflation (group A; n = 58) were analyzed separately from patients with dynamic pulmonary hyperinflation (group B; n = 49). Transient airway disconnection. In group A, tPAOP (8.5+/-6.0 mm Hg) and nadir PAOP (8.6+/-6.0 mm Hg) did not differ from each other but were lower than eePAOP (12.4+/-5.6 mm Hg; p < .05). The agreement between tPAOP and nadir PAOP was good (bias, 0.15 mm Hg; limits of agreement, -1.5-1.8 mm Hg). In group B, tPAOP (9.7+/-5.4 mm Hg) was lower than both nadir PAOP and eePAOP (12.1+/-5.4 and 13.9+/-5.2 mm Hg, respectively; p < .05 for both comparisons). The agreement between tPAOP and nadir PAOP was poor (bias, 2.3 mm Hg; limits of agreement, -0.2-4.8 mm Hg). Indexing the transmission of proportional alveolar pressure to PAOP in the estimation of LV filling pressure is equivalent to the nadir method in patients without dynamic pulmonary hyperinflation and may be more reliable than the nadir PAOP method in patients with dynamic pulmonary hyperinflation.

The effect of mode, inspiratory time, and positive end-expiratory pressure on partial liquid ventilation.

Partial liquid ventilation (PLV) has been shown to be an effective means of improving oxygenation in the injured lung. However, little is known about how approach to ventilation during PLV affects gas exchange and pulmonary mechanics. We hypothesized that gas exchange and pulmonary mechanics would be best with positive end-expiratory pressure (PEEP) set above the lower inflection point (LIP) of the pressure-volume (P-V) curve regardless of mode of ventilation or inspiratory to expiratory time (I:E) ratio and that the efficiency of ventilation would be greatest with volume-controlled ventilation (VCV) compared with pressure-controlled ventilation (PCV) and with long inspiratory time as compared with short inspiratory time. Lung injury was induced in 14 sheep by lavage, 10 of which were studied. Sheep were then assigned to high-PEEP (Group H, n = 5) and low-PEEP (Group L, n = 5) groups. In Group H applied PEEP was set at the LIP and in Group L applied PEEP was set at 5 cm H2O after the lung was filled with perflubron (PFB). We randomly compared VCV and PCV with I:E ratios of 1:2, 1:1, and 2:1. Peak inspiratory pressure and VT were adjusted to maintain a constant end-inspiratory plateau pressure (Pplat) of about 25 cm H2O in both groups and a constant total PEEP of about 5 cm H2O in Group L and about 12 cm H2O in Group H. There were no differences in oxygenation among modes in Group H. In Group L VCV 2:1 and all of the PCV modes in Group L had a lower PaO2 than VCV 1:1 (p < 0.05). PaCO2 and VD/VT were significantly different (p < 0.05) among modes. VD/VT was highest during PCV 1:2 with PEEP of 5 cm H2O (p < 0.05). Quasi-static compliance in Group H was higher than in Group L (p < 0.05). We conclude that during low PEEP gas exchange deteriorated in VCV with long inspiratory time and in PCV. Oxygenation was enhanced during VCV 1:1 when compared with VCV at longer I:E ratios or PCV at any I:E ratio. With PEEP set at the LIP, adequate gas exchange and improved lung mechanics could be obtained in all modes assessed.

Expiratory phase tracheal gas insufflation and pressure control in sheep with permissive hypercapnia.

Tracheal gas insufflation (TGI) has been shown to be a useful adjunct to mechanical ventilation, decreasing PaCO2 during permissive hypercapnia. While TGI can be used either with pressure (PCV) or volume-controlled ventilation and continuously or only during the expiratory phase (Ex-TGI), there are no controlled studies evaluating the effects of Ex-TGI with PCV in acute lung injury when the direction of the insufflated flow or the inspiratory:expiratory (I:E) ratio are varied. We evaluated the effect that Ex-TGI with PCV would have on CO2 removal during both direct and reverse insufflated flow direction with varied I:E ratios when peak airway pressure, total positive end-expiratory pressure (PEEP), and tidal volume (VT) were kept constant. In addition we examined the effect that insufflation flow directed toward the mouth (reverse flow) would have on the generation of PEEP compared with flow directed toward the carina (direct flow). After saline lavage, nine sheep were ventilated with PCV to a baseline PaCO2 of 80 mm Hg. Ex-TGI (10 L/min) was then randomly applied in the reverse and direct direction with I:E set at 1:2 or 2:1. During 1:2 I:E PaCO2 decreased from 78 +/- 4 mm Hg to 60 +/- 7 mm Hg (23.5 +/- 8.9%) with direct flow and to 64 +/- 5 mm Hg (18.5 +/- 5.5%) with reverse flow (p < 0.05), whereas during 2:1 I:E PaCO2 decreased from 80 +/- 4 mm Hg to 69 +/- 8 mm Hg (13.7 +/- 9.2%) with direct flow and to 66 +/- 4 mm Hg (17.2 +/- 4.4%) with reverse flow (p < 0.05). Greater PEEP was developed with direct flow (2.8 cm H2O I:E 1:2 and 4.0 cm H2O I:E 2:1) than with reverse flow (-0.9 cm H2O I:E 1:2 and -0.4 cm H2O I:E 2:1), p < 0.05. There was no difference in the PaCO2 change between I:E with reverse flow, but the PaCO2 decrease was greater (p < 0.05) during 1:2 versus 2:1 I:E with direct flow. CO2 removal during PCV and Ex-TGI is more consistent with reverse flow than with direct flow and PEEP level is less affected by TGI with reverse flow than with direct flow.

The interaction between applied peep and auto-peep during one-lung ventilation

Objective: To investigate the relationship between applied external positive end-expiratory pressure (PEEP) and auto-PEEP and the resultant total PEEP experienced by the patient during one-lung ventilation (OLV). Design: A prospective clinical study. Setting: A university hospital. Participants: Ten adult patients undergoing elective thoracotomies. Interventions: End-expiratory airway occlusion and measurement of plateau pressure during two-lung ventilation (TLV) and OLV with and without the application of 5 cm H 2O of external PEEP via the anesthetic ventilator. The effect of variation of the inspiratory-expiratory ratio on total PEEP with and without applied external PEEP was also studied. Main Results: The mean level (±SD) of auto-PEEP changing from two-lung to one-lung ventilation rose from 0.9 (±0.8) cm H 2O to 6.0 (±3.0) cm H 2O at an inspiratoryexpiratory ratio of 1: 2. The application of 5 cm H 2O external PEEP did not increase the total PEEP (7.3 ± 2.0 cm H 2O) significantly. The total PEEP increased significantly when the duration of expiration was decreased, and decreased when expiratory time increased. The change in total PEEP caused by the application of external PEEP during OLV correlated inversely with the preexisting level of auto-PEEP (r = −0.84). Conclusion: The change in end-expiratory pressure experienced by the ventilated lung during OLV when external PEEP is applied depends on the preexisting level of auto-PEEP. This may explain some of the inconsistencies in the clinical results of application of external PEEP during OLV. The total PEEP delivered to the patient should be measured whenever external PEEP is applied during OLV.

Experimental studies on lung mechanics, gas exchange and oxygen delivery under open lung conditions Mechanical ventilation with decelerating versus constant inspiratory flow

The treatment of patients with acute respiratory failure poses an ever‐present clinical challenge since conventional ventilation sometimes causes further impairment of lung function. Thus, it is important to identify characteristics of different ventilatory patterns and ventilatory strategies that affect airway pressures, lung volumes, pulmonary gas exchange and hemodynamics. In order to mimic acute respiratory failure in the patient, we have used an experimental animal injury model, characterized by highly unstable alveoli.The basic prerequisite for this thesis was a positive end‐expiratory pressure (PEEP) sufficient to keep the lung open throughout the whole ventilatory cycle. Different inspiratory flow patterns were studied by using a successful recruitment procedure together with ventilation performed using PEEP levels below, at, and above the inflection‐point pressure. To elucidate the effect of prolonged inspiration time, sufficient PEEP was supplied to prevent end‐expiratory collapse already during the reference mode with an inspiration/expiration ratio (I:E ratio) of 1:1. When an I:E ratio of 2:1 or above was used, both studies (one with mean airway pressure constant and the other with total PEEP constant) showed impaired hemodynamics, but displayed unaffected arterial oxygen tension. Decelerating inspiratory flow delivers the major part of the tidal volume during early inspiration under sustained constant inspiratory pressure. This reduces serial dead space and improves alveolar ventilation. In all studies, decelerating inspiratory flow showed increased carbon dioxide elimination, i.e. improved alveolar ventilation, but decelerating inspiratory flow was found to be no better for alveolar recruitment or in oxygenation.In an attempt to explain radiological observations when studying the relationship of pulmonary radiological appearance to end‐expiratory pressure, Staubs' concept of quantal alveolar behavior was used. This states that the individual alveolus fills essentially independently of its neighbors and has a propensity to be either air‐filled and expanded, or completely fluid‐filled and collapsed. Stepwise sequential deflation of the lung from full expansion, followed by stepwise inflation of the lung, produced a pressure/attenuation loop. This hysteresis phenomenon implies that the attenuation of the lung relates to the set PEEP, but also to the immediately preceding structural status. For identical end‐expiratory pressures the attenuation on the hysteresis down‐slope invariably had a higher value than that of the up‐slope. Thus, the pressure at which alveolar collapse takes place differs from that of expansion.In conclusion, ventilation with decelerating inspiratory flow revealed lower peak inspiratory and higher mean airway pressure than did constant inspiratory flow. No differences in end‐inspiratory pressure were seen. Decelerating inspiratory flow delivers the major part of the tidal volume during early inspiration, which reduces serial dead space and improves alveolar ventilation. The decelerating inspiratory flow was found to be no better than constant inspiratory flow for alveolar recruitment or oxygenation. When the lung was ventilated with PEEP sufficient to prevent end‐expiratory collapse, an inspiration‐to‐expiration ratio at and above 2:1 impaired hemodynamics. Our results suggest that, in order to obtain and maintain open lung conditions, the lung must be recruited and PEEP reduced to the level just above the alveolar collapse pressure.

The static pressure–volume relationship of the respiratory systemdetermined with a computer‐controlled ventilator

The pressure-volume relationship of the respiratory system offers a guideline for setting of ventilators. The occlusion method for determination of the static elastic pressure-volume (Pel(st)/V) relationship is used as a reference and the aim of the study was to improve it with respect to time consumption and precision of recording and analysis. The inspiratory Pel(st)/V curve was determined with a computer-controlled ventilator using its pressure and flow sensors. During an automated procedure, an operator-defined volume history preceded each of a number of study breaths. These were interrupted at different volumes evenly distributed over a predefined volume interval. Total positive end-expiratory pressure (PEEP) was measured and could be separated into its components, external PEEP and auto-PEEP. The volume relationship between the curve and the current tidal volume was defined. An analytical method for definition of a linear segment of the Pel(st)/V curve and determination of its compliance is presented. In eight healthy human anaesthetized subjects duplicate Pel(st)/V curves were studied with respect to compliance and the position along the volume axis of the linear segment. The difference in compliance between measurements was 1.6 +/- 1.3 ml cmH2O(-1) or 1.2 +/- 0.9%. The position of the curve differed between measurements by 15 +/- 10 ml or by 1.1 +/- 0.9%. In a patient with acute lung injury the feasibility of applying a numerical method for a more detailed description of the Pel(st)/V curve was illustrated.

Controlled expiration in mechanically-ventilated patients with chronic obstructive pulmonary disease (COPD)

In patients with severe chronic obstructive pulmonary disease (COPD), lung emptying may be affected by flow limitation. We tested the hypothesis that the airway compression leading to flow limitation can be counteracted by controlling the expiratory flow. The effects of an external resistor on lung emptying were studied in six patients with COPD, who were mechanically ventilated whilst sedated and paralysed. Respiratory mechanics were obtained during ventilatory support with and without the resistor. Airway compression was assessed using the interruptor method. For the study, a turbulent resistor was applied with the highest resistance level that did not increase the end-expiratory lung volume. At this resistance level, external positive end-expiratory pressure (PEEP) was generated in all patients. As total PEEP levels remained unchanged at both settings during the controlled expiration, the levels of intrinsic PEEP were significantly decreased from 0.96+/-0.30 to 0.53+/-0.19 kPa (mean+/-SD). Comparison of the expiratory flow-volume curves at both settings revealed that, during the controlled expiration, the flows were significantly decreased during the first 40% of the expired volume and significantly increased during the last 60%. As the end-expiratory lung volumes remained unchanged during both settings, these increments in flow indicated a decrease in effective resistance. Airway compression was observed during unimpeded expirations in all patients using the interruptor method. During the application of the resistor, airway compression was no longer detectable. In patients with chronic obstructive pulmonary disease receiving ventilatory support, the application of an external resistor could decrease effective expiratory resistance by counteracting airway compression, without increments in end-expiratory lung volume.

Under open lung conditions inverse ratio ventilation causes intrinsic PEEP and hemodynamic impairment.

Inverse ratio ventilation (IRV) is commonly used in clinical practice. Several studies have used IRV in order to recruit collapsed alveoli. In a randomised trial in twelve surfactant depleted piglets, the lungs were ventilated with sufficient positive end-expiratory pressure (PEEP) to prevent end-expiratory collapse, and the effects of increased inspiration-to-expiration (I:E ratio) were evaluated. Pressure regulated ventilation (with I:E of 1:1, constant tidal volume and decelerating inspiratory flow) was used at 30 breaths per minute (bpm). I:E ratios of 1.5:1, 2.3:1 and 4:1 were applied sequentially. When the I:E ratio was increased, external PEEP had to be reduced in order to keep total PEEP constant. Functional residual capacity, airway pressures, gas exchange, extrathermal volume and hemodynamics were measured. With I:E ratios above 2:1 intrinsic PEEP was generated and with concomitant decrease in cardiac index. PaO2 was not affected, but oxygen delivery was reduced. It is concluded that I:E ratios of 2:1, or above, generate increased intrinsic PEEP with compromised hemodynamics.

Hemodynamic responses to external counterbalancing of auto-positive end-expiratory pressure in mechanically ventilated patients with chronic obstructive pulmonary disease

To study the effect of positive end-expiratory pressure (PEEP) on right ventricular hemodynamics and ejection fraction in patients with chronic obstructive pulmonary disease and positive alveolar pressure throughout expiration by dynamic hyperinflation (auto-PEEP). Open, prospective, controlled trial. General intensive care unit of a community hospital. Ten patients sedated and paralyzed with an acute exacerbation of chronic obstructive pulmonary disease undergoing mechanical ventilation. Insertion of a pulmonary artery catheter modified with a rapid response thermistor and a radial arterial catheter. PEEP was then increased from 0 (PEEP 0) to auto-PEEP level (PEEP = auto-PEEP) and 5 cm H2O above that (PEEP = auto-PEEP +5). At each level of PEEP, airway pressures, flow and volume, hemodynamic variables (including right ventricular ejection fraction by thermodilution technique), and blood gas analyses were recorded. The mean auto-PEEP was 6.6 +/- 2.8 cm H2O and the total PEEP reached was 12.2 +/- 2.4 cm H2O. The degree of lung inflation induced by PEEP averaged 145 +/- 87 mL with PEEP = auto-PEEP and 495 +/- 133 mL with PEEP = auto-PEEP + 5. The PEEP = auto-PEEP caused a right ventricular end-diastolic pressure increase, but there was no other significant hemodynamic change. With PEEP = auto-PEEP + 5, there was a significant increase in intravascular pressures; this amount of PEEP reduced cardiac output (from 4.40 +/- 1.38 L/min at PEEP 0 to 4.13 +/- 1.48 L/min; p < .05). The cardiac output reduction induced by PEEP = auto-PEEP + 5 was > 10% in only five cases and this group of patients had significantly lower right ventricular volumes than the group with less cardiac output variation (right ventricular end-diastolic volume: 64 +/- 9 vs. 96 +/- 26 mL/m2; right ventricular end-systolic volume: 38 +/- 6 vs. 65 +/- 21 mL/m2; p < .05) without significant difference in the other variables that were measured. Neither right ventricular ejection fraction nor right ventricle volumes changed as PEEP increased, but there were marked interpatient differences and also pronounced changes in volume between stages in individual patients. In the study conditions, PEEP application up to values approaching auto-PEEP did not result in the impairment of right ventricular hemodynamics, while higher levels reduced cardiac output in selected patients.

Cardiorespiratory Effects of Pressure-controlled Ventilation With and Without Inverse Ratio in the Adult Respiratory Distress Syndrome

To assess the cardiorespiratory effects of pressure-controlled ventilation (PCV) and pressure-controlled inverse ratio ventilation (PC-IRV), we compared pressure-controlled ventilation with an inspiratory-to-expiratory time ratio (I/E) of 1/2 (PCV) and of 2/1 (PC-IRV) to volume-controlled ventilation (VCV) with an I/E of 1/2 in 10 patients suffering from the adult respiratory distress syndrome. In all modes, the inspiratory oxygen fraction, tidal volume, respiratory rate, and total positive end-expiratory pressure (PEEPt = applied PEEP + intrinsic PEEP) were kept constant. Each ventilatory mode was applied for 1 h in a randomized order. No significant differences in PaO2 were observed among the three modes. The PaCO2 was lower (p < 0.05) in PC-IRV (39 +/- 4 mm Hg) than in PCV (43 +/- 5 mm Hg) and in VCV (45 +/- 5 mm Hg). The peak airway pressure was significantly lower in PC-IRV than in PCV (p < 0.05) and in PCV than in VCV (p < 0.05), but plateau pressure was not different in the 3 modes. The mean airway pressure (mPaw) was significantly higher (p < 0.05) in PC-IRV (21.4 +/- 0.7 cm H2O) than in PCV (17.1 +/- 0.7 cm H2O) and VCV (16.4 +/- 0.5 cm H2O). As a consequence of this increased mPaw, PC-IRV induced a decrease in cardiac index (CI) (3.3 +/- 0.2 vs 3.7 +/- 0.2 L/min/m2 in VCV; p < 0.05) and hence in oxygen delivery (DO2) (424 +/- 28 vs 469 +/- 38 ml/min/m2 in VCV; p < 0.05). Our results suggest that neither PCV nor PC-IRV bring any benefit over VCV in terms of arterial oxygenation. Moreover, the increase in mPaw induced by PC-IRV may be deleterious to the CI and DO2.