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Biomedical subjects

S Zakynthinos

Publications and source records attributed to S Zakynthinos.

9 recordsLinked to original sources
PubMed1997

Changes in thoracopulmonary compliance and hemodynamic effects of positive end-expiratory pressure in patients with or without heart failure.

PURPOSE: The purpose of this study was to confirm that positive end-expiratory pressure (PEEP) has a different effect on cardiac index (CI) in patients with or without heart failure, even after controlling for differences in thoracopulmonary compliance (Ctp) and minimizing the secondary effects of PEEP related changes in oxygenation and breathing effort. MATERIALS AND METHODS: The hemodynamic effects of PEEP were evaluated in two groups of sedated and paralyzed patients with a low Ctp at 0 PEEP: 12 patients with normal pulmonary artery occlusion pressure (Ppao) and a CI > 2.5 L/min and 12 patients with a CI < 2.5 L/min and increased oxygen extraction ratio, despite a Ppao > 15 mm Hg. RESULTS: In patients with low CI and high Ppao, PEEP had no hemodynamic effect and Ctp remained low at all PEEP levels. However, PEEP-induced CI reduction in patients with normal cardiovascular function was associated with an increase in Ctp with incremental PEEP. Concerning PEEP-related hemodynamic effects, the significance between group differences persisted when data were analyzed after controlling for Ctp changes. However, Ctp changes with PEEP were the most significant correlators and discriminators of the magnitude and direction of PEEP-induced CI change. CONCLUSIONS: We conclude that (1) the observed different effect of PEEP on CI in patients with and without heart failure persists after the elimination of secondary effects due to underlying differences in Ctp, oxygenation, and breathing effort; and (2) PEEP-related changes in Ctp should be taken into consideration when dealing with the cardiovascular effects of PEEP. Our data support the hypothesis that, in addition to the transmission of PEEP to the pleural space, changes in lung volume are a significant determinant of PEEP-induced CI changes.

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↗
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↗
PubMed1993

Effect of diaphragmatic fatigue on control of respiratory muscles and ventilation during CO2 rebreathing.

We studied the influence of diaphragmatic fatigue on the control of ventilation and respiratory muscle contribution to pressure swings in six normal seated subjects. CO2 was rebreathed before and after diaphragmatic fatigue induced by breathing against an inspiratory resistance requiring 60% maximal transdiaphragmatic pressure with each breath until exhaustion. After diaphragmatic fatigue for a given level of end-tidal PCO2, we found that tidal volume, breathing frequency, minute ventilation, duty cycle, and mean inspiratory flow did not change; esophageal pressure swings were the same, but gastric and transdiaphragmatic pressure swings were decreased; and the slope of the transpulmonary pressure-gastric pressure relationship determined at zero flow points at end expiration and end inspiration was increased. End-expiratory transpulmonary pressure progressively decreased and end-expiratory gastric pressure progressively increased with increasing end-tidal PCO2 by the same magnitude before and after diaphragmatic fatigue. We conclude that diaphragmatic fatigue induces proportionately greater contributions of inspiratory rib cage muscles than of the diaphragm, which results in the preservation of ventilatory response to CO2 despite impaired diaphragmatic contractility.

Adult↗
PubMed1993

Effect of global inspiratory muscle fatigue on ventilatory and respiratory muscle responses to CO2.

We evaluated the effect of global inspiratory muscle fatigue on ventilation and respiratory muscle control during CO2 rebreathing in normal subjects. Fatigue was induced by breathing against a high inspiratory resistance until exhaustion. CO2 response curves were measured before and after fatigue. During CO2 rebreathing, global fatigue caused a decreased tidal volume (VT) and an increased breathing frequency but did not change minute ventilation, duty cycle, or mean inspiratory flow. Both esophageal and transdiaphragmatic pressure swings were significantly reduced after global fatigue, suggesting decreased contribution of both rib cage muscles and diaphragm to breathing. End-expiratory transpulmonary pressure for a given CO2 was lower after fatigue, indicating an additional decrease in end-expiratory lung volume due to expiratory muscle recruitment, which leads to a greater initial portion of inspiration being passive. This, combined with the reduction in VT, decreased the fraction of VT attributable to inspiratory muscle contribution; therefore the inspiratory muscle elastic work and power per breath were significantly reduced. We conclude that respiratory control mechanisms are plastic and that the respiratory centers alter their output in a manner appropriate to the contractile state of the respiratory muscles to conserve the ventilatory response to CO2.

Adult↗
PubMed1989

Effects of furosemide on pulmonary shunts.

In 23 mechanically ventilated anuric (six) or oliguric (17) patients (less than 16 ml/h of urine output) with severe gas exchange abnormality, we investigated the effect of furosemide on intrapulmonary shunt (Qs/QT). Before and after 0.5, 1, and 2 h of IV administration of 200 mg of furosemide, we assessed the intrapulmonary shunt and PaO2 while patients' hemodynamic measurements were monitored. Ventilatory parameters remained constant throughout the study. While the urine output was minimal and no alteration in hemodynamic values was found, the Qs/QT decreased from 27.7 +/- 2.3 percent (mean +/- SEM) at control to 24.3 +/- 2.1 percent (p less than 0.01) at 0.5 h, 21.7 +/- 2.1 percent (p less than 0.001) at 1 h, and 18.1 +/- 1.8 percent (p less than 0.001) at 2 h. The PaO2 showed no significant difference at 0.5 h but rose significantly from 96 +/- 14 to 105 +/- 14 mm Hg (p less than 0.05) and 111 +/- 14 mm Hg (p less than 0.01) at 1 and 2 h, respectively. Since we observed no changes in hemodynamics, we speculate a direct effect of furosemide in the pulmonary vasculature affecting the ventilation-perfusion mismatch and, therefore, the Qs/QT and PaO2.

Acute Kidney Injury↗