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T Vassilakopoulos

Publications and source records attributed to T Vassilakopoulos.

35 records · Page 2Linked to original sources
PubMed2000

Expiratory flow limitation and intrinsic positive end-expiratory pressure at zero positive end-expiratory pressure in patients with adult respiratory distress syndrome.

It has been suggested that in patients with adult respiratory distress syndrome (ARDS), intrinsic positive end-expiratory pressure (PEEPi) is generated by a disproportionate increase in expiratory flow resistance. Using the negative expiratory pressure (NEP) technique, we assessed whether expiratory flow limitation (EFL) and PEEPi were present at zero PEEP in 10 semirecumbent, mechanically ventilated ARDS patients. Because bronchodilators may decrease airway resistance, we also investigated the effect of nebulized salbutamol on EFL, PEEPi, and respiratory mechanics in these patients, and in seven patients we measured the latter variables in the supine position as well. In the semirecumbent position, eight of the 10 ARDS patients exhibited tidal EFL, ranging from 5 to 37% of the control tidal volume (VT), whereas PEEPi was present in all 10 subjects, ranging from 0.4 cm H(2)O to 7.7 cm H(2)O. The onset of EFL was heralded by a distinct inflection point on the expiratory flow-volume curve, which probably reflected small-airway closure. Administration of salbutamol had no statistically significant effect on PEEPi, EFL (as %VT), or respiratory mechanics. EFL (%VT) and PEEPi were significantly higher in the supine position than in the semirecumbent position, whereas the other respiratory variables did not change. Our results suggest that in the absence of externally applied PEEP, most ARDS patients exhibit EFL associated with small-airway closure and a concomitant PEEPi.

Adult↗
PubMed2000

Contribution of expiratory muscle pressure to dynamic intrinsic positive end-expiratory pressure: validation using the Campbell diagram.

In spontaneously breathing (SB) patients expiratory muscle contraction leads to an overestimation of dynamic intrinsic PEEP (PEEP(i),dyn). To quantify this overestimation, PEEP(i),dyn measured with the esophageal balloon technique was corrected for the increase in Pga over the course of expiration (Pga,exp rise), for the whole decay of Pga during inspiration (Pga,total decay) or for the part of Pga decay restricted between the onset of inspiratory effort and the point of zero flow (Pga,zf decay). Corrections were compared with the reference PEEP(i),dyn (PEEP(i),dyn ref ), calculated by using the Campbell diagram. In 15 ventilator-dependent, SB, and actively expiring patients, we found that the difference PEEP(i),dyn - Pga, total decay (mean +/- SD, 5.7 +/- 1.9 cm H(2)O) was quite similar to PEEP(i),dyn ref (5.3 +/- 1.9 cm H(2)O). Their mean difference was 0. 37 cm H(2)O with limits of agreement -0.09 to 0.83 cm H(2)O, indicating strong agreement between these methods. PEEP(i),dyn - Pga, exp rise (6.0 +/- 2.1 cm H(2)O) was also similar to PEEP(i),dyn ref. Their mean difference was 0.72 cm H(2)O with limits of agreement -1. 69 to 3.13 cm H(2)O, indicating good agreement. In contrast, mean difference of PEEP(i),dyn - Pga,zf decay and PEEP(i),dyn ref was 3. 14 cm H(2)O with limits of agreement -0.46 to 6.74 cm H(2)O, indicating lack of agreement. The error in measurement due to the subtraction of Pga,zf decay from PEEP(i),dyn (i.e., [PEEP(i),dyn - Pga,zf decay] - PEEP(i),dyn ref ) was proportional to the intensity of expiratory muscle contraction, as expressed by the Pga,exp rise (r = 0.903, p < 0.001). We conclude that in actively expiring patients an adequate correction of PEEP(i),dyn for the overestimation caused by expiratory muscle contraction can be made by subtracting either Pga,total decay or Pga,exp rise from PEEP(i), dyn, the former achieving the best performance.

Abdomen↗
PubMed1999

Weaning from mechanical ventilation.

For most mechanically ventilated patients, weaning can be accomplished quickly and easily. However, there is a smaller group of ventilated patients who fail to wean and remain ventilator-dependent. These patients account for a significant amount of health care costs and pose a great challenge for clinicians. Detailed knowledge of the etiology and pathophysiology of weaning failure is very important for the "treatment" of difficult to wean patients, and is thoroughly presented in this article. Based on this physiological background, strategies and techniques are proposed that are useful for the gradual transition to spontaneous ventilation.

Humans↗
PubMed1999

Strenuous resistive breathing induces proinflammatory cytokines and stimulates the HPA axis in humans.

Interleukin-1beta (IL-1beta) and interleukin-6 (IL-6), powerful stimulants of the hypothalamic-pituitary-adrenal (HPA) axis, increase in response to whole body exercise. Strenuous inspiratory resistive breathing (IRB), a form of clinically relevant "exercise" for the respiratory muscles, produces beta-endorphin through a largely unknown mechanism. We investigated (in 11 healthy humans) whether strenuous IRB produces proinflammatory cytokines and beta-endorphin in parallel with stimulation of the HPA axis, assessed by concurrent measurement of ACTH. Subjects underwent either severe [at 75% of maximal inspiratory pressure (P(m) (max))] or moderate (at 35% of P(m) (max)) IRB. Plasma cytokines, beta-endorphin, and ACTH were measured at rest (point R), at the point at which the resistive load could not be sustained (point F), and at exhaustion [15 min later (point E)]. During severe IRB, IL-1beta increased from 0.83 +/- 0.12 pg/ml at point R to 1.88 +/- 0. 53 and 4.06 +/- 1.27 pg/ml at points F and E, respectively (P < 0. 01). IL-6 increased from 5.30 +/- 1.02 to 10.33 +/- 2.14 and 11.66 +/- 2.29 pg/ml at points F and E, respectively (P = 0.02). ACTH and beta-endorphin fluctuated from 20.87 +/- 5.49 and 25.03 +/- 3.97 pg/ml at point R to 22.97 +/- 4.41 and 26.32 +/- 3.93 pg/ml, respectively, at point F and increased to 46.96 +/- 8.55 and 40.32 +/- 5.94 pg/ml, respectively, at point E (P < 0.01, point E vs. point F). There was a positive correlation between the IL-6 at point F and the ACTH and beta-endorphin at point E (r = 0.88 and 0.94, respectively; P < 0.01) as well as between the increase in IL-6 (between points R and F) and the increases in ACTH and beta-endorphin (between points F and E, r = 0.91 and 0.92, respectively; P < 0.01). Moderate IRB did not produce any change. We conclude that severe IRB produces proinflammatory cytokines and stimulates the HPA axis in humans secondary to the production of cytokines (especially IL-6).

Adrenocorticotropic Hormone↗
PubMed1999

Effects of different expiratory maneuvers on inspiratory muscle force output.

We assessed the effects of two different expiratory maneuvers (fast [F] or slow [S]) on the ability of normal subjects (n = 12, age 35 +/- 6 yr) to generate maximal inspiratory pressures and maximal inspiratory flows near residual volume (RV). With the F maneuver, the subject exhaled rapidly to RV and immediately performed a maximal inspiratory effort, whereas with the S maneuver the subject exhaled slowly to RV, paused for 4 to 6 s at RV, and then inspired forcefully. Maximal static inspiratory pressure against an occluded airway (PImax), and maximal dynamic inspiratory pressure (PIdyn) and maximal inspiratory flow (V Imax) with no added resistance, as well as the electromyographic activity of the parasternal muscles, were measured during each maneuver. Both maneuvers were initiated from TLC and were performed randomly. In comparison with the S maneuver, the F maneuver yielded values of higher (mean +/- SE) PImax (148 +/- 5 cm H2O versus 135 +/- 7 cm H2O, p < 0.05), PIdyn (33 +/- 2 cm H2O versus 28 +/- 2 cm H2O, p < 0.05), and V Imax (12.3 +/- 0.4 L/s versus 11.4 +/- 0.6 L/s, p < 0.05). In addition, the rate of rise of PImax, the rate of rise of PIdyn, and the integrated peak electromyographic activity of the parasternal muscles were significantly greater with the F than with the S maneuver, suggesting greater inspiratory muscle (IM) activation. The enhanced IM activation may be related to a specific inspiratory-expiratory muscle interaction similar to the agonist-antagonist interactions described for a pair of skeletal muscles.

Adult↗
PubMed1999

Correcting static intrinsic positive end-expiratory pressure for expiratory muscle contraction. Validation of a new method.

We have recently shown (Eur. Respir. J. 1997;10:522-529) that in spontaneously breathing and actively expiring patients, static intrinsic positive end-expiratory pressure (PEEPi,st) can be corrected for expiratory muscle contraction by subtracting the average expiratory rise in gastric pressure (Pga,exp rise), calculated from three breaths just prior to an airway occlusion, from the end-expiratory airway pressure (Paw) of the first occluded inspiratory effort (PEEPi,st avg). However, since in some patients there is substantial variability in the intensity of expiratory muscle activity and hence in Pga,exp rise, this method may be inaccurate because the Pga,exp rise of breaths preceding airway occlusion may differ from that of the first postocclusion breath. In the present study, we introduced a new method consisting of synchronous subtraction of Pga,exp rise from Paw, both occurring during airway occlusion (PEEPi,st sub). PEEPi,st sub and PEEPi,st avg were each compared with the reference PEEPi,st (PEEPi,st ref), which was obtained during muscular paralysis and simulation of the spontaneous breathing pattern by the ventilator. We found that, in 25 critically ill patients, PEEPi,st sub (mean +/- SD, 5.3 +/- 2.6 cm H(2)O) was nearly identical to PEEPi,st ref (5.4 +/- 2.4 cm H(2)O). Their mean difference was -0.06 cm H(2)O with limits of agreement -0.96 to 0.84 cm H(2)O, indicating a strong agreement between these methods. In contrast, mean difference of PEEPi,st avg and PEEPi,st ref was 0.73 cm H(2)O with limits of agreement -3.97 to 5.43 cm H(2)O, indicating lack of agreement. Coefficient of variation of Pga,exp rise was 14.3 +/- 7.2% (range, 5.2 to 28.3%). There was a good correlation between the coefficient of variation of Pga,exp rise and the difference between PEEPi,st avg and PEEPi,st ref (r = 0.909; p < 0.001). We conclude that PEEPi,st can be accurately measured in spontaneously breathing patients by synchronous subtraction of Pga,exp rise from Paw during airway occlusion.

Abdominal Muscles↗
PubMed1999

Respiratory muscles in heart failure.

This paper reviews respiratory muscle performance in patients suffering from congestive heart failure. Respiratory muscle dysfunction is well documented in these patients, and is thoroughly discussed. The mechanisms underlying its development and the potential consequences are also presented.

Dyspnea↗
PubMed1998

The tension-time index and the frequency/tidal volume ratio are the major pathophysiologic determinants of weaning failure and success.

We have previously shown (Am. J. Respir. Crit. Care Med. 1995;152:1248-1255) that in patients needing mechanical ventilation, the load imposed on the inspiratory muscles is excessive relative to their neuromuscular capacity. We have therefore hypothesized that weaning failure may occur because at the time of the trial of spontaneous breathing there is insufficient reduction of the inspiratory load. We therefore prospectively studied patients who initially had failed to wean from mechanical ventilation (F) but had successful weaning (S) on a later occasion. Compared with S, during F patients had greater intrinsic positive end-expiratory pressure (6. 10 +/- 2.45 versus 3.83 +/- 2.69 cm H2O), dynamic hyperinflation (327 +/- 180 versus 213 +/- 175 ml), total resistance (Rmax, 14.14 +/- 4.95 versus 11.19 +/- 4.01 cm H2O/L/s), ratio of mean to maximum inspiratory pressure (0.46 +/- 0.1 versus 0.31 +/- 0.08), tension time index (TTI, 0.162 +/- 0.032 versus 0.102 +/- 0.023) and power (315 +/- 153 versus 215 +/- 75 cm H2O x L/min), less maximum inspiratory pressure (42.3 +/- 12.7 versus 53.8 +/- 15.1 cm H2O), and a breathing pattern that was more rapid and shallow (ratio of frequency to tidal volume, f/VT 98 +/- 38 versus 62 +/- 21 breaths/min/L). To clarify on pathophysiologic grounds what determines inability to wean from mechanical ventilation, we performed multiple logistic regression analysis with the weaning outcome as the dependent variable. The TTI and the f/VT ratio were the only significant variables in the model. We conclude that the TTI and the f/VT are the major pathophysiologic determinants underlying the transition from weaning failure to weaning success.

Adult↗
PubMed1997

Pressure support ventilation in adult respiratory distress syndrome: short-term effects of a servocontrolled mode.

PURPOSE: To assess the short-term effects of pressure support ventilation in adult respiratory distress syndrome (ARDS), we studied 17 patients with moderate to severe ARDS using mandatory rate ventilation (MRV), a servocontrolled mode of PSV having respiratory rate as the targeted parameter. MATERIALS AND METHODS: Based on the duration of ARDS, the patients were divided into two groups: Group 1, early ARDS (duration up to 1 week), 10 patients; Group 2, intermediate ARDS (duration between 1 and 2 weeks). The patients were initially ventilated with assisted mechanical ventilation then with MRV, and finally with controlled mechanical ventilation. After a 20-minute period allowed for stabilization in each mode, ventilatory variables, gas exchange, hemodynamics, and patient's inspiratory effort were evaluated. RESULTS: During MRV blood gases, airway pressures and hemodynamic variables remained within acceptable limits in all patients. Compared with assisted mechanical ventilation, during MRV, patients of group 1 decreased their VT and V (from 0.64 +/- 0.04 to 0.42 +/- 0.03 L/sec) and increased their TI/TT (from 0.39 +/- 0.03 to 0.52 +/- 0.03). f did not change. PAO2 - PaO2 and QS/QT decreased (from 306 +/- 16 to 269 +/- 15 mm Hg, and from 20.2 +/- 1.4 to 17.5 +/- 1.1, respectively), while PaCO2 increased (from 44 +/- 3 to 50 +/- 3 mm Hg). On the contrary, patients of group 2 increased their VT (from 0.69 +/- 0.02 to 0.92 +/- 0.09 L), decreased their f (from 22.3 +/- 0.5 to 19.3 +/- 0.3 b/min), although they did not change their V and TI/TT. PAO2 - PaO2 and QS/QT remained stable. PaCO2 diminished (from 39 +/- 3 to 34 +/- 3 mm Hg). Pressure support level was higher in group 2 than in group 1 (29.4 +/- 3.0 v 19.8 +/- 2.9 cm H2O). CONCLUSIONS: We conclude that (1) PSV delivered by MRV may adequately ventilate patients with moderate to severe ARDS, preserving gas exchange and hemodynamics, at least for the short period tested; (2) early and intermediate ARDS respond in a different manner to MRV in terms of breathing pattern, gas exchange, and level of pressure assistance; and (3) patients with early ARDS are those who have an improvement in intrapulmonary oxygenation probably due, at least in part, to alveolar recruitment augmented by active diaphragmatic contraction.

Adult↗
PubMed1997

Inspiratory maneuver effects on peak expiratory flow. Role of lung elastic recoil and expiratory pressure.

We investigated the effects of two different inspiratory maneuvers (fast or slow) on the ability of normal subjects to generate peak expiratory flows (PEF) and maximal dynamic expiratory pressures (Pexp) during the performance of a forced vital capacity maneuver. During the fast maneuver (F), the subject inspired rapidly to total lung capacity (TLC) and immediately performed a maximal expiration, whereas in the slow maneuver (S) the subject inspired slowly to TLC, paused for 4-5 s at TLC and then performed a maximal expiration. Ten normal subjects performed a series of such maneuvers. In addition to PEF and Pexp, we measured EMG activity of abdominal (EMGabd) and rib cage muscles, and lung elastic recoil pressure (PesL). Overall, F yielded higher PEF values than S (by approximately 7%); in addition, PesL, Pexp, rate of rise of Pexp (dPexp/dt), and EMGabd were similarly higher with F than with S (p < 0.05 for all). Analysis of individual data showed that the intermaneuver differences in PEF were largely explained by differences in PesL, Pexp or dPexp/dt. Our data suggest that, in comparison with the slow maneuver, the fast maneuver induces a greater change in both the lung elastic recoil and expiratory muscle activation which account for differences in PEF between the two maneuvers. The enhanced expiratory muscle activation with the fast maneuver suggests a specific inspiratory-expiratory muscle interaction analogous to agonist-antagonist interactions described for skeletal muscles.

Adult↗
PubMed1997

Accurate measurement of intrinsic positive end-expiratory pressure: how to detect and correct for expiratory muscle activity.

It has been shown that expiratory muscle contraction leads to an overestimation of intrinsic positive end-expiratory pressure (PEEPi). To quantify this overestimation, we compared PEEPi, measured during spontaneous breathing (SB) by the end-expiratory airway occlusion technique (PEEPi,occl) with static PEEPi (PEEPi,st). PEEPi,st was measured using end-expiratory airway occlusion during simulation of SB by the ventilator with the patient relaxed, and was considered to represent the "gold standard" for PEEPi,occl. Twelve ventilator-dependent patients were studied during SB (pressure support 5-7 cmH2O). Full mechanical ventilation was resumed when they were unable to sustain SB. Subsequently, by manipulating the variables of the ventilator, we simulated the pattern of SB and measured PEEPi,st, corresponding to PEEPi,occl. On the basis of the presence or absence of expiratory rise in gastric pressure (Pga) (rapid drop of end-expiratory Pga at the beginning of inspiration, Pga,exp,rise), and abdominal muscle electromyographic (EMG) activity, patients were subdivided into those either actively (Group 1) or passively expiring (Group 2). In Group 1 (8 patients), PEEPi,occl was higher than PEEPi,st (13.3+/-2.0 vs 6.8+/-1.1 cmH2O; p<0.01). PEEPi,occl-Pga,exp,rise (6.9+/-1.1 cmH2O) was quite similar to PEEPi,st; their mean difference was 0.03 cmH2O with limits of agreement -0.48 to +0.53 cmH2O. In Group 2, PEEPi,occl was similar to PEEPi,st. We conclude that, in actively expiring patients, an accurate estimation of the actual PEEPi,st can be obtained by subtracting Pga,exp,rise from PEEPi,occl.

Abdominal Muscles↗
PubMed1996

Respiratory muscles and weaning failure.

Weaning failure is, unfortunately, a rather common phenomenon for mechanically-ventilated patients (especially those with chronic obstructive pulmonary disease (COPD)), and the respiratory muscles play a pivotal role in its development. Weaning fails whenever an imbalance exists between the ventilatory needs and the neurocardiorespiratory capacity. This can happen if there is an increase in the energy demands of the respiratory muscles, a decrease in the energy available, a decrease in neuromuscular competence, or if the respiratory muscles pose an impediment to the heart and blood flow. The imbalance created will lead to weaning failure through the development of respiratory muscle fatigue, hypercapnia, dyspnoea, anxiety and organ dysfunction.

Anxiety↗
PubMed1995

The load of inspiratory muscles in patients needing mechanical ventilation.

We studied 31 consecutive mechanically ventilated patients with acute respiratory failure in two stages: (1) During spontaneous breathing through the respirator, switching from full mechanical assistance to continuous positive airway pressure mode with 0 cm H2O pressure. We measured maximum inspiratory pressure and continuously monitored the pattern of breathing. After 8 to 25 min, none of the patients were able to sustain spontaneous breathing and mechanical ventilation was required to resume. (2) Subsequently, during mechanical ventilation, by manipulating the variables of the ventilator we simulated the pattern of spontaneous breathing the patients had just before the re-institution of mechanical ventilation. We assessed the respiratory mechanics by the constant flow end-inspiratory and end-expiratory occlusion method. Intrinsic positive end-expiratory pressure was present in 29 patients. The ratio of the mean inspiratory pressure per breath over the maximum inspiratory pressure (Pi/pimax), as well as Ppeak/pimax, had excessively high mean values, equal to 0.42 +/- 0.11 and 0.56 +/- 0.10, respectively. Pressure-time index was 0.14 +/- 0.04. When we plotted the Pi/Pimax and Ppeak/Pimax against the dynamic increase in FRC, we found that the Pi/Pimax of 13 patients (42%) and the Ppeak/Pimax of 25 of 31 patients (81%) were placed above a hypothetical critical line, representing the critical inspiratory pressures above which fatigue may occur. In addition, almost all patients were gathered around the critical line. We conclude that during discontinuation from mechanical ventilation (MV) almost all patients breathe against a high inspiratory load and their inspiratory muscles perform work that may lead to fatigue.

Adult↗