Eumorfia Kondili

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

Proportional assist ventilation with load-adjustable gain factors in critically ill patients: comparison with pressure support.

ObjectivesIt is not known if proportional assist ventilation with load-adjustable gain factors (PAV+) may be used as a mode of support in critically ill patients. The aim of this study was to examine the effectiveness of sustained use of PAV+ in critically ill patients and compare it with pressure support ventilation (PS).Design and settingRandomized study in the intensive care unit of a university hospital.MethodsA total of 208 critically ill patients mechanically ventilated on controlled modes for at least 36 h and meeting certain criteria were randomized to receive either PS (n = 100) or PAV+ (n = 108). Specific written algorithms were used to adjust the ventilator settings in each mode. PAV+ or PS was continued for 48 h unless the patients met pre-defined criteria either for switching to controlled modes (failure criteria) or for breathing without ventilator assistance.ResultsFailure rate was significantly lower in PAV+ than that in PS (11.1 vs. 22.0%, P = 0.040, OR 0.443, 95% CI 0.206–0.952). The proportion of patients exhibiting major patient–ventilator dyssynchronies at least during one occasion and after adjusting the initial ventilator settings, was significantly lower in PAV+ than in PS (5.6 vs. 29.0%, P < 0.001, OR 0.1, 95% CI 0.06–0.4). The proportion of patients meeting criteria for unassisted breathing did not differ between modes.ConclusionsPAV+ may be used as a useful mode of support in critically ill patients. Compared to PS, PAV+ increases the probability of remaining on spontaneous breathing, while it considerably reduces the incidence of patient–ventilator asynchronies.

Akt2 Deficiency Protects from Acute Lung Injury via Alternative Macrophage Activation and miR-146a Induction in Mice

Acute respiratory distress syndrome (ARDS) is a major cause of respiratory failure, with limited effective treatments available. Alveolar macrophages participate in the pathogenesis of ARDS. To investigate the role of macrophage activation in aseptic lung injury and identify molecular mediators with therapeutic potential, lung injury was induced in wild-type (WT) and Akt2−/− mice by hydrochloric acid aspiration. Acid-induced lung injury in WT mice was characterized by decreased lung compliance and increased protein and cytokine concentration in bronchoalveolar lavage fluid. Alveolar macrophages acquired a classical activation (M1) phenotype. Acid-induced lung injury was less severe in Akt2−/− mice compared with WT mice. Alveolar macrophages from acid-injured Akt2−/− mice demonstrated the alternative activation phenotype (M2). Although M2 polarization suppressed aseptic lung injury, it resulted in increased lung bacterial load when Akt2−/− mice were infected with Pseudomonas aeruginosa. miR-146a, an anti-inflammatory microRNA targeting TLR4 signaling, was induced during the late phase of lung injury in WT mice, whereas it was increased early in Akt2−/− mice. Indeed, miR-146a overexpression in WT macrophages suppressed LPS-induced inducible NO synthase (iNOS) and promoted M2 polarization, whereas miR-146a inhibition in Akt2−/− macrophages restored iNOS expression. Furthermore, miR-146a delivery or Akt2 silencing in WT mice exposed to acid resulted in suppression of iNOS in alveolar macrophages. In conclusion, Akt2 suppression and miR-146a induction promote the M2 macrophage phenotype, resulting in amelioration of acid-induced lung injury. In vivo modulation of macrophage phenotype through Akt2 or miR-146a could provide a potential therapeutic approach for aseptic ARDS; however, it may be deleterious in septic ARDS because of impaired bacterial clearance.

Effects of respiratory rate on ventilator-induced lung injury at a constant Paco2 in a mouse model of normal lung

Objective:The aim of this study was to evaluate the effects of respiratory rate (RR) at a constant Paco2 and conventional tidal volume (VT) on the development of ventilator-induced lung injury in normal lungs. Design:Prospective, randomized, experimental study. Setting:University research laboratory. Subjects:Adult male C57BL/6 mice. Interventions:Four groups of anesthetized mice were exposed to mechanical ventilation with different RRs and VTs. Three groups were assigned to one of three RRs (80, 120, and 160 breaths/min), and VT was set to 12, 10, and 8 mL/kg, respectively (RR80VT12, RR120VT10, and RR160VT8), to achieve normal Paco2. A fourth group was ventilated at 160 breaths/min and VT of 10 mL/kg (RR160VT10) with adjustment of dead space. All animals were ventilated for 120 mins with a positive end-expiratory pressure of 1.5 cm H2O and Fio2 of 1. Nonventilated animals were also studied. Measurements and Main Results:Arterial blood gases and static pressure–volume curves were not different among groups at the end of the experiment. Independent of ventilator settings, mechanical ventilation was associated with increased bronchoalveolar lavage protein and increased bronchoalveolar lavage and serum interleukin-6. Total bronchoalveolar lavage protein and interleukin-6 were significantly lower in RR80VT12 and RR160VT8 compared with RR120VT10 and RR160VT10. In all experimental conditions, mechanical ventilation was associated with activation of AKT and ERK1/2 kinases, known to be activated on stretch. Phosphorylation both of AKT and ERK1/2 was lower in RR80VT12 compared with other groups of ventilated animals. Histologic injury did not differ among nonventilated, RR80VT12, and RR160VT8 animals; however, it increased significantly and progressively in RR120VT10 and RR160VT10 animals. Conclusions:Mechanical ventilation with conventional VT induces lung injury in normal lungs, even without alteration in lung mechanics. Reduction of RR and VT ameliorates lung inflammation and injury.

Effects of dexmedetomidine on sleep quality in critically ill patients: a pilot study.

Background:Dexmedetomidine, a potent &agr;-2-adrenergic agonist, is widely used as sedative in critically ill patients. This pilot study was designed to assess the effect of dexmedetomidine administration on sleep quality in critically ill patients. Methods:Polysomnography was performed on hemodynamically stable critically ill patients for 57 consecutive hours, divided into three night-time (9:00 PM to 6:00 AM) and two daytime (6:00 AM to 9:00 PM) periods. On the second night, dexmedetomidine was given by a continuous infusion targeting a sedation level −1 to −2 on the Richmond Agitation Sedation Scale. Other sedatives were not permitted. Results:Thirteen patients were studied. Dexmedetomidine was given in a dose of 0.6 &mgr;g kg−1 h−1 (0.4 to 0.7) (median [interquartile range]). Compared to first and third nights (without dexmedetomidine), sleep efficiency was significantly higher during the second night (first: 9.7% [1.6 to 45.1], second: 64.8% [51.4 to 79.9], third: 6.9% [0.0 to 17.1], P < 0.002). Without dexmedetomidine, night-time sleep fragmentation index (7.6 events per hour [4.8 to 14.2]) and stage 1 of sleep (48.0% [30.1 to 66.4]) were significantly higher (P = 0.023 and P = 0.006, respectively), and stage 2 (47.0% [27.5 to 61.2]) showed values lower (P = 0.006) than the corresponding values (2.7 events per hour [1.6 to 4.9], 13.1% [6.2 to 23.6], 80.2% [68.9 to 92.8]) observed with dexmedetomidine. Without sedation, sleep was equally distributed between day and night, a pattern that was modified significantly (P = 0.032) by night-time dexmedetomidine infusion, with more than three quarters of sleep occurring during the night (79% [66 to 87]). Conclusion:In highly selected critically ill patients, dexmedetomidine infusion during the night to achieve light sedation improves sleep by increasing sleep efficiency and stage 2 and modifies the 24-h sleep pattern by shifting sleep mainly to the night.

Bronchodilator delivery with metered-dose inhaler during mechanical ventilation

The delivery of bronchodilators with metered-dose inhaler (MDI) in mechanically ventilated patients has attracted considerable interest in recent years. This is because the use of the MDI has several advantages over the nebulizer, such as reduced cost, ease of administration, less personnel time, reliability of dosing and a lower risk of contamination. A spacer device is fundamental in order to demonstrate the efficacy of the bronchodilatory therapy delivered by MDI. Provided that the technique of administration is appropriate, MDIs are as effective as nebulizers, despite a significantly lower dose of bronchodilator given by the MDI.

Short-term cardiorespiratory effects of proportional assist and pressure-support ventilation in patients with acute lung injury/acute respiratory distress syndrome

Background: Recent data indicate that assisted modes of mechanical ventilation improve pulmonary gas exchange in patients with acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Proportional assist ventilation (PAV) is a new mode of support that amplifies the ventilatory output of the patient effort and improves patient–ventilator synchrony. It is not known whether this mode may be used in patients with ALI/ARDS. The aim of this study was to compare the effects of PAV and pressure-support ventilation on breathing pattern, hemodynamics, and gas exchange in a homogenous group of patients with ALI/ARDS due to sepsis. Methods: Twelve mechanically ventilated patients with ALI/ARDS (mean ratio of partial pressure of arterial oxygen to fractional concentration of oxygen 190 ± 49 mmHg) were prospectively studied. Patients received pressure-support ventilation and PAV in random order for 30 min while maintaining mean airway pressure constant. With both modes, the level of applied positive end-expiratory pressure (7.1 ± 2.1 cm H2O) was kept unchanged throughout. At the end of each study period, cardiorespiratory data were obtained, and dead space to tidal volume ratio was measured. Results: With both modes, none of the patients exhibited clinical signs of distress. With PAV, breathing frequency and cardiac index were slightly but significantly higher than the corresponding values with pressure-support ventilation (24.5 ± 6.9 vs. 21.4 ± 6.9 breaths/min and 4.4 ± 1.6 vs. 4.1 ± 1.3 l · min−1 · m−2, respectively). None of the other parameters differ significantly between modes. Conclusions: In patients with ALI/ARDS due to sepsis, PAV and pressure-support ventilation both have clinically comparable short-term effects on gas exchange and hemodynamics.

Lung emptying in patients with acute respiratory distress syndrome: effects of positive end-expiratory pressure

The pattern of lung emptying was studied in 10 mechanically-ventilated patients with acute respiratory distress syndrome. At four levels of positive end-expiratory pressure (PEEP) (0, 5, 10 and 15 cmH2O) tracheal (Ptr) and airway pressures (Paw), flow (V′) and volume (V) were continuously recorded. Tidal volume was set between 0.5–0.6 L and V′/V curves during passive expiration were obtained. Expired volume was divided into five equal volume slices and the time constant (τe) and effective deflation compliance (Crseff) of each slice was calculated by regression analysis of V/V′ and postocclusion V/Ptr relationships, respectively. In each slice, the presence or absence of flow limitation was examined by comparing V′/V curves with and without decreasing Paw. For a given slice, total expiratory resistance (Rtot) (consisting of the respiratory system (Rrs), endotracheal tube (Rtube) and ventilator circuit (Rvent)) was calculated as the τe/Crseff ratio. In the absence of flow limitation Rrs was obtained by subtracting Rtube and Rvent from Rtot, while in the presence of flow limitation Rrs equaled Rtot. The τe of the pure respiratory system (τers) was calculated as the product of Rrs and Crseff. At zero PEEP, τers increased significantly towards the end of expiration (52±31%) due to a significant increase in Rrs (46±36%). Application of PEEP significantly decreased Rrs at the end of expiration and resulted in a faster and relatively constant rate of lung emptying. In conclusion, without positive end-expiratory pressure the respiratory system in patients with acute respiratory distress syndrome deflates with a rate that progressively decreases, due to a considerable increase in expiratory resistance at low lung volumes. Application of positive end-expiratory pressure decreases the expiratory resistance, probably by preventing airway closure, and as a result modifies the pattern of lung emptying.

Estimation of inspiratory muscle pressure in critically ill patients

BackgroundRecently, a new technology has been introduced aiming to monitor and improve patient ventilator interaction (PVI monitor). With the PVI monitor, a signal representing an estimation of the patient’s total inspiratory muscle pressure (PmusPVI) is calculated from the equation of motion, utilizing estimated values of resistance and elastance of the respiratory system.ObjectiveThe aim of the study was to prospectively examine the accuracy of PmusPVI to quantify inspiratory muscle pressure.Methods and interventionsEleven critically ill patients mechanically ventilated on proportional assist ventilation with load-adjustable gain factors were studied at three levels of assist (30, 50 and 70%). Airway, esophageal, gastric and transdiaphragmatic (Pdi) pressures, volume and flow were measured breath by breath, whereas the total inspiratory muscle pressure (Pmus) was calculated using the Campbell diagram.ResultsFor a given assist, PmusPVI throughout inspiration did not differ from the corresponding values calculated using the Pdi and Pmus signals. Inspiratory and expiratory time did not differ among the various methods of calculation. Inspiratory muscle pressure decreased with increasing assist, and the magnitude of this decrease did not differ among the various methods of pressure calculation.ConclusionsA signal generated from flow, volume and airway pressure may be used to provide breath-by-breath quantitative information of inspiratory muscle pressure.

Identifying and relieving asynchrony during mechanical ventilation

Patient–ventilator asynchrony refers to the uncoupling between the mechanically delivered breath and the patient’s respiratory effort. It is common during assisted mechanical ventilation and may affect the morbidity of critically ill patients. Close inspection of pressure, volume and flow waveforms – displayed by modern ventilators – may help the physician to recognize and act appropriately to minimize patient–ventilator asynchrony. During the last two decades new modes of assisted mechanical ventilation have been introduced, aiming to improve patient ventilator synchrony by modulating the triggering function and the variables that control the flow delivery and the cycling off.