George Prinianakis

Bedside waveforms interpretation as a tool to identify patient-ventilator asynchronies

ObjectiveDuring assisted modes of ventilatory support the ventilatory output is the final expression of the interaction between the ventilator and the patient’s controller of breathing. This interaction may lead to patient-ventilator asynchrony, preventing the ventilator from achieving its goals, and may cause patient harm. Flow, volume, and airway pressure signals are significantly affected by patient-ventilator interaction and may serve as a tool to guide the physician to take the appropriate action to improve the synchrony between patient and ventilator. This review discusses the basic waveforms during assisted mechanical ventilation and how their interpretation may influence the management of ventilated patients. The discussion is limited on waveform eye interpretation of the signals without using any intervention which may interrupt the process of mechanical ventilation.DiscussionFlow, volume, and airway pressure may be used to (a) identify the mode of ventilator assistance, triggering delay, ineffective efforts, and autotriggering, (b) estimate qualitatively patient’s respiratory efforts, and (c) recognize delayed and premature opening of exhalation valve. These signals may also serve as a tool for gross estimation of respiratory system mechanics and monitor the effects of disease progression and various therapeutic interventions.ConclusionsFlow, volume, and airway pressure waveforms are valuable real-time tools in identifying various aspects of patient-ventilator interaction

Metastatic liver disease and fulminant hepatic failure: presentation of a case and review of the literature.

Although liver metastases are commonly found in cancer patients, fulminant hepatic failure (FHF) secondary to diffuse liver infiltration is rare. Furthermore, clinical presentation and laboratory findings are obscure and far from being pathognomonic for the disease. We report a case of a patient who died in the intensive care unit of our hospital from multiple organ failure syndrome secondary to FHF, as a result of liver infiltration from poorly differentiated small cell lung carcinoma. We also present the current knowledge about the clinical picture, laboratory findings and physical history of neoplastic liver-metastasis-induced FHF.

Effect of the physical properties of isoflurane, sevoflurane, and desflurane on pulmonary resistance in a laboratory lung model.

Background:Airway resistance depends not only on an airway’s geometry but also on flow rate, and gas density and viscosity. A recent study showed that at clinically relevant concentrations, the mixtures of volatile agents with air and oxygen and oxygen–nitrogen affected the density of the mixture. The goal of the current study was to investigate the effect of different minimum alveolar concentrations (MACs) of three commonly used volatile agents, isoflurane, sevoflurane, and desflurane, on the measurements of airway resistance. Methods:A two-chamber fixed-resistance test lung was connected to an anesthesia machine using the volume control mode of ventilation. Pulmonary resistance was calculated at baseline (25% oxygen in air); at 1.0, 1.5, and 2.0 MAC; and also at the same concentrations, 1.2% and 4%, of isoflurane, sevoflurane, and desflurane mixtures with 25% oxygen in air. The analysis of variance test for repeated measures and probabilities for post hoc Tukey and least significant difference tests were used. Results:Isoflurane affected pulmonary resistance only at 2 MAC. Sevoflurane caused a significant increase of pulmonary resistance at 1.5 and 2 MAC, whereas desflurane caused the greatest increase in pulmonary resistance at all MAC values used. At 1.2% concentration, no difference from the baseline resistance was observed, whereas at 4%, the three agents produced similar increases of pulmonary resistance. Conclusion:High concentrations of volatile agents in 25% oxygen in air increased the density of the gas mixture and the calculated resistance of a test lung model with fixed resistance.

Physiologic comparison of neurally adjusted ventilator assist, proportional assist and pressure support ventilation in critically ill patients.

UNLABELLED To compare, in a group of difficult to wean critically ill patients, the short-term effects of neurally adjusted ventilator assist (NAVA), proportional assist (PAV+) and pressure support (PSV) ventilation on patient-ventilator interaction. METHODS Seventeen patients were studied during NAVA, PAV+ and PSV with and without artificial increase in ventilator demands (dead space in 10 and chest load in 7 patients). Prior to challenge addition the level of assist in each of the three modes tested was adjusted to get the same level of patients effort. RESULTS Compared to PSV, proportional modes favored tidal volume variability. Patient effort increase after dead space was comparable among the three modes. After chest load, patient effort increased significantly more with NAVA and PSV compared to PAV+. Triggering delay was significantly higher with PAV+. The linear correlation between tidal volume and inspiratory integral of transdiaphragmatic pressure (PTPdi) was weaker with NAVA than with PAV+ and PSV on account of a weaker inspiratory integral of the electrical activity of the diaphragm (∫EAdi)-PTPdi linear correlation during NAVA [median (interquartile range) of r(2), determination of coefficient, 16.2% (1.4-30.9%)]. CONCLUSION Compared to PSV, proportional modes favored tidal volume variability. The weak ∫EAdi-PTPdi linear relationship during NAVA and poor triggering function during PAV+ may limit the effectiveness of these modes to proportionally assist the inspiratory effort.

Effect of propofol on breathing stability in adult ICU patients with brain damage.

The aim of the study was to investigate Propofols effect on breathing stability in brain damage patients, as quantified by the Loop Gain (LG) of the respiratory system (breathing stability increases with decreasing LG). In 11 stable brain damage patients full polysomnography was performed before, during and after propofol sedation, titrated to achieve stage 2 or slow wave sleep. During each period, patients were ventilated with proportional assist ventilation and the % assist was increased in steps, until either periodic breathing (PB) occurred or the highest assist (95%) was achieved. The tidal volume amplification factor (VT(AF)) at the highest assist level reached just before PB occurred was used to calculate LG (LG=1/VT(AF)). In all but one patient, PB was observed. With propofol, the assist level at which PB occurred (73 + or - 19%) was significantly higher, than that before (43 + or - 35%) and after propofol sedation (49 + or - 29%). As a result, with propofol LG (0.49 + or - 0.2) was significantly lower than that before (0.74 + or - 0.2) and after propofol sedation (0.69 + or - 0.2) (p<0.05). We conclude that Propofol decreases LG. Therefore it exerts an overall stabilizing effect on control of breathing.

Effect of voluntary respiratory efforts on breath-holding time

INTRODUCTION Near the end of a maximal voluntary breath-hold, re-inhalation of the expired gas allows an additional period of breath-holding, indicating that the breaking point does not depend solely on chemical drive. We hypothesized that afferents from respiratory muscle and/or chest wall are significant in breath-holding. METHODS Nineteen normal adults breathed room air through a mouthpiece connected to a pneumotachograph and were instructed to breath-hold with and without voluntary regular respiratory efforts against an occluded airway. RESULTS Fifty one trials with and 53 without respiratory efforts were analyzed. The mean number of efforts per minute was 19+/-2.3 and the mean lowest airway pressure (P(aw)) -16.6+/-5.4 cmH(2)O. Breath-holding time (BHT) did not differ without (33.0+/-18.2 s) and with (29.3+/-12.3 s) efforts. In five patients arterial blood gasses were measured before and at the end of breath-holding and they did not differ between trials without and with efforts, indicating similar chemical drive. Our results suggest that afferents from respiratory muscle and/or chest wall are not the major determinants of BHT.

Effect of Albuterol on Expiratory Resistance in Mechanically Ventilated Patients

BACKGROUND: In mechanically ventilated patients with COPD, the response of the expiratory resistance of the respiratory system (expiratory RRS) to bronchodilators is virtually unknown. OBJECTIVE: To examine the effect of inhaled albuterol on expiratory RRS, and the correlation of albuterol-induced changes in expiratory RRS with end-inspiratory resistance and the expiratory flow-volume relationship. METHODS: We studied 10 mechanically ventilated patients with COPD exacerbation, before and 30 min after administration of albuterol. We obtained flow-volume curves during passive expiration, divided the expired volume into 5 equal volume slices, and then calculated the time constant and dynamic effective deflation compliance of the respiratory system (effective deflation CRS) of each slice via regression analysis of the volume-flow and post-occlusion volume-tracheal pressure relationships, respectively. For each slice we calculated expiratory RRS as the time constant divided by the effective deflation CRS. RESULTS: Albuterol significantly decreased the expiratory RRS (mean expiratory RRS 42.68 ± 17.8 cm H2O/L/s vs 38.08 ± 16.1 cm H2O/L/s) and increased the rate of lung emptying toward the end of expiration (mean time constant 2.51 ± 1.2 s vs 2.21 ± 1.2 s). No correlation was found between the albuterol-induced changes in expiratory RRS and that of end-inspiratory resistance. Only at the end of expiration did albuterol-induced changes in the expiratory flow-volume relationship correlate with changes in expiratory RRS in all patients. CONCLUSIONS: In patients with COPD, albuterol significantly decreases expiratory resistance at the end of expiration. In mechanically ventilated patients, neither inspiratory resistance nor the whole expiratory flow-volume curve may be used to evaluate the bronchodilator response of expiratory resistance.