Thoracic ultrasound use in hospitalized and ambulatory adult patients: a quantitative picture.

INTRODUCTION AND OBJECTIVES: Thoracic ultrasound (TUS) has been established as a powerful diagnostic and monitoring tool in the Intensive Care Unit (ICU). However, studies outside the critical care setting are scarce. The aim of this study was to investigate the value of TUS for hospitalized or ambulatory community patients. MATERIALS AND METHODS: This was a retrospective study conducted from 2016 to 2020 in the TUS clinic at Heraklion University Hospital. TUS examination was performed using a standard ultrasound machine (EUB HITACHI 8500), and a high-frequency microconvex probe (5-8 MHz). Patients had been referred by their primary physician to address a range of different questions. The various respiratory system entities were characterised according to internationally established criteria. RESULTS: 762 TUS studies were performed on 526 patients due to underlying malignancy (n = 376), unexplained symptoms/signs (n = 53), pregnancy related issues (n = 42), evaluation of abnormal findings in X-ray (n = 165), recent surgery/trauma (n = 23), recent onset respiratory failure (n = 12), acute respiratory infection (n = 66) and underlying non-malignant disease (n = 25). Pleural effusion was the commonest pathologic entity (n = 610), followed by consolidation (n = 269), diaphragmatic dysfunction/paradox (n = 174) and interstitial syndrome (n = 53). Discrepancies between chest X-ray and ultrasonographic findings were demonstrated in 96 cases. The TUS findings guided invasive therapeutic management in 448 cases and non-invasive management in 43 cases, while follow-up monitoring was decided in 271 cases. CONCLUSIONS: This study showed that TUS can identify the most common respiratory pathologic entities encountered in hospitalized and community ambulatory patients, and is especially useful in guiding the decision making process in a diverse group of patients.

Sleep quality in survivors of critical illness.

PURPOSE: There is limited data regarding the sleep quality in survivors of critical illness, while the time course of the sleep abnormalities observed after ICU discharge is not known. The aim of this study was to assess sleep quality and the time course of sleep abnormalities in survivors of critical illness. METHODS: Eligible survivors of critical illness without hypercapnia and hypoxemia were evaluated within 10 days (1st evaluation, n = 36) and at 6 months after hospital discharge (2nd evaluation, n = 29). At each visit, all patients underwent an overnight full polysomnography and completed health-related quality of life questionnaires (HRQL). Lung function and electro-diagnostic tests (ED) were performed in 24 and 11 patients, respectively. RESULTS: At 1st evaluation, sleep quality and HRQL were poor. Sleep was characterised by high percentages of N1, low of N3 and REM stages, and high apnea-hypopnea index (AHI, events/h). Twenty-two out of 36 patients (61%) exhibited AHI ≥ 15 (21 obstructive, 1 central). None of the patients' characteristics, including HRQL and lung function, predicted the occurrence of AHI ≥ 15. At 6 months, although sleep quality remained poor (high percentages of N1 and low of REM), sleep architecture had improved as indicated by the significant increase in N3 [4.2% (0-12.5) vs. 9.8% (3.0-20.4)] and decrease in AHI [21.5 (6.5-29.4) vs. 12.8 (4.7-20.4)]. HRQL improved slightly but significantly at 6 months. Neither the changes in HRQL nor in lung function tests were related to these of sleep architecture. Six out of eight patients with abnormal ED at 1st evaluation continued to exhibit abnormal results at 6 months. CONCLUSIONS: Survivors of critical illness exhibited a high prevalence of obstructive sleep-disordered breathing and poor sleep architecture at hospital discharge, which slightly improved 6 months later, indicating that reversible factors are partly responsible for these abnormalities.

Patient-ventilator synchrony and sleep quality with proportional assist and pressure support ventilation.

OBJECTIVE: To examine patient-ventilator asynchrony and sleep quality in non-sedated critically ill patients ventilated with proportional assist ventilation with load adjustable gain factors (PAV+) and pressure support (PSV). METHODS: This was a randomized crossover physiological study conducted in an adult ICU at a tertiary hospital. Patients who exhibited patient-ventilator asynchrony on PSV were selected. Polysomnography was performed in these patients over 24 h, during which respiratory variables were continuously recorded. During the study period, each patient was randomized to receive alternating 4-h periods of PSV and PAV+ equally distributed during the day and night. Sleep architecture was analyzed manually using predetermined criteria. Patient-ventilator asynchrony was evaluated breath by breath using the flow-time and airway pressure-time waveforms. RESULTS: Fourteen patients were studied. The majority (85.7 %) had either acute exacerbation of COPD as admission diagnosis or COPD as comorbidity. During sleep, compared to PSV, PAV+ significantly reduced the patient-ventilator asynchrony events per hour of sleep [5 (1-17) vs. 40 (4-443), p = 0.02, median (25-75th interquartile range)]. Compared to PSV, PAV+ was associated with slightly but significantly greater sleep fragmentation [18.8 (13.1-33.1) versus 18.1 (7.0-22.8) events/h, p = 0.01] and less REM sleep [0.0 % (0.0-8.4) vs. 5.8 % (0.0-21.9), p = 0.02). CONCLUSIONS: PAV+ failed to improve sleep in mechanically ventilated patients despite the fact that this mode was associated with better synchrony between the patient and ventilator. These results do not support the hypothesis that patient-ventilator synchrony plays a central role in determining sleep quality in this group of patients.

Sleep during proportional-assist ventilation with load-adjustable gain factors in critically ill patients.

BACKGROUND: Proportional-assist ventilation with load-adjustable gain factors (PAV+) automatically adjusts the flow and volume assist to represent constant fractions of resistance and elastance of the respiratory system, respectively. Resistance and elastance are calculated at random intervals of 4-10 breaths, by applying a 300 ms pause maneuver at the end of selected inspirations. OBJECTIVES: To determine whether the large number of end-inspiratory occlusions during PAV+ operation influences sleep quality in critically ill patients who exhibited good patient-ventilator synchrony during pressure support (PS, baseline). METHODS: One and two nights' polysomnography was performed in sedated (protocol A, n=11) and non-sedated (protocol B, n=9) patients, respectively, while respiratory variables were continuously recorded. In each protocol the patients were ventilated with PAV+ and PS at two levels of assist (baseline and high). RESULTS: In both protocols sleep quality did not differ between the modes of support or the assist levels. In sedated patients sleep efficiency was slightly but significantly higher with PAV+ than with high PS, while it did not differ between modes in non-sedated patients. The two modes of support had comparable effects on respiratory variables. Independent of the mode of support and particularly at high assist, a significant proportion of patients developed periodic breathing during sleep (27% in protocol A and 44% in protocol B). CONCLUSION: In patients exhibiting good patient-ventilator synchrony during PS, the large number of short-term end-inspiratory occlusions with PAV+ operation did not adversely influence sleep quality. With both modes high assist may cause unstable breathing during sleep.

Influence of respiratory efforts on b2-agonist induced bronchodilation in mechanically ventilated COPD patients: a prospective clinical study.

BACKGROUND: Several in vitro studies have shown that at similar tidal volume (VT), bronchodilator delivery to target sites is significantly lower during controlled mechanical ventilation (CMV) than that during simulated spontaneous breathing. However, the influence of active respiratory efforts on the magnitude of b2-agonist induced bronchodilation in mechanically ventilated patients has not been examined. OBJECTIVE: To examine the influence of controlled and assisted modes of ventilatory support on the bronchodilative effect induced by b2-agonists administered with a metered dose inhaler (MDI) and a spacer device in a homogeneous group of mechanically ventilated patients with acute exacerbation of chronic obstructive pulmonary disease (COPD). METHODS: Prospective clinical study. Ten mechanically ventilated patients with acute exacerbation of COPD were prospectively randomized to receive 4 puffs of salbutamol (S, 100 micro g/puff) either with volume-controlled (VC) or pressure-support (PS) ventilation. On PS the pressure level was such that VT was comparable between ventilatory modes. After a 6-h washout period, patients were crossed-over to receive the drug by the alternative mode of ventilation. Static and dynamic airway pressures, minimum (R(int)) and maximum (R(rs)) inspiratory resistance, the difference between R(rs) and R(int) (DeltaR), end-inspiratory static compliance of the respiratory system (C(rs)), intrinsic positive end-expiratory pressure (PEEP(i)) and heart rate (HR) were measured before and at 15, 30, 60, 120, 180 and 240 min after S administration. RESULTS: S caused a significant decrease in dynamic and static airway pressures, PEEP(i), R(int) and R(rs). These changes were not influenced by the ventilatory mode and were evident at 15, 30, 60 and 120 min after S. HR, C(rs) and DeltaR did not change after S administration. CONCLUSIONS: Considering the use of propofol with its presumed bronchodilative properties as a shortcoming of our study, it is concluded that the magnitude of bronchodilation induced by salbutamol delivered by an MDI and a spacer device in mechanically ventilated COPD patients is not affected by the presence or absence of active respiratory efforts.

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 (taue) and effective deflation compliance (Crs(eff)) 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 taue/Crs(eff) 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 taue of the pure respiratory system (taue(rs)) was calculated as the product of Rrs and Crs(eff). At zero PEEP, taue(rs) 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.

Duration of salbutamol-induced bronchodilation delivered by metered-dose inhaler in mechanically ventilated COPD patients.

The delivery of bronchodilators with metered-dose inhaler (MDI) and a spacer in mechanically ventilated patients has become a widespread practice. However, the duration of action of bronchodilators delivered with this technique is not well established. The purpose of the study was to examine the duration of bronchodilation induced by short-term beta 2-agonists administered with an MDI and a spacer in a group of mechanically ventilated patients with exacerbation of chronic obstructive pulmonary disease (COPD). Ten patients with COPD, mechanically ventilated on volume-controlled mode, received 6 puffs of salbutamol (S, 100 micrograms/puff). S was administered with an MDI adapted to the inspiratory limb of the ventilator circuit using an aerosol cloud enhance spacer. Static and dynamic airway pressures, minimum (Rint) and maximum (Rrs) inspiratory resistance, the difference between Rrs and Rint (delta R), static end-inspiratory system compliance (Cst, rs), intrinsic positive end-expiratory pressure (PEEPi) and heart rate (HR) were measured before and at 15, 30, 60, 120, 180, 240, 300, 360 min after S. S caused a significant decrease in dynamic and static airway pressures, PEEPi, Rint and Rrs. These changes were evident at 15 minutes and remained significant for 2 hours after S. The duration of bronchodilation was highly variable and unpredictable among patients, lasting in some patients more than 4 hours while in others wearing off in less than 2 hours. We conclude that 6 puffs of S delivered with an MDI and a spacer device induces significant bronchodilation in mechanically ventilated patients with COPD, the duration of which is highly variable precluding guidelines regarding the time scheduled for dosing.

Acute effects of ventilator settings on respiratory motor output in patients with acute lung injury.

OBJECTIVE: During assisted mechanical ventilation, changes in ventilator settings may acutely affect the respiratory motor output via the mechanoreceptor reflex feedback system, thus interfering with patient management. This feedback system in mechanically ventilated patients with parenchymal lung injury remains largely unexplored. To investigate this, the early response of respiratory motor output to varying ventilator settings was determined in 13 sedated patients with acute lung injury. DESIGN: During assist/control and pressure support (PS) ventilation changes in (1) tidal volume (V(T)) at fixed inspiratory flow (V'(I)), (2) V'(I) at fixed V(T) and (3) PS level were employed and the response of respiratory motor output was followed for two breaths after the change. Respiratory motor output was assessed by total pressure generated by the respiratory muscles (Pmus), computed from esophageal pressure (Pes). RESULTS: Neural expiratory time increased with increasing V(T) and PS, while it remained constant with V'I changes. Neural inspiratory time (T(I)n) increased with decreasing V'(I) and PS, but was not affected by V(T) changes. None of the changes in ventilator settings influenced significantly the rate of rise of Pmus, used as an index of respiratory drive. The changes in respiratory timing resulted in significant changes in breathing frequency, which increased with decreasing V(T) and PS and increasing V'(I). The time integral of Pmus, an index of respiratory effort, increased with increasing T(I)n. These acute responses were not related to the severity of deterioration of respiratory system mechanics. CONCLUSIONS: We conclude that alterations in commonly used ventilator settings induce acute changes in respiratory timing, without affecting the respiratory drive. These changes, probably mediated via mechanoreceptor reflex feedback, are dependent on the type of the alteration in the ventilator settings.

Effect of inspiratory flow rate on beta2-agonist induced bronchodilation in mechanically ventilated COPD patients.

OBJECTIVES: To test the effect of two different inspiratory flow rates on the bronchodilation induced by beta2-agonists administered by metered dose inhaler (MDI). PATIENTS: Ten patients with acute exacerbation of chronic obstructive pulmonary disease and receiving mechanical ventilation with constant inspiratory flow (V'I). DESIGN: Patients received four puffs of salbutamol (100 microg/puff) with either low V'I (0.6 l/s) or high V'I (1.2 l/s) administered with an MDI adapted to inspiratory limb of the ventilator circuit using an aerosol cloud enhance spacer. After a 6-h washout patients were crossed-over to receive the drug by the alternative mode of administration. MEASUREMENTS AND RESULTS: Static and dynamic airway pressures, intrinsic positive end-expiratory pressure, and minimum and maximum inspiratory resistance values showed a significant decrease after salbutamol. These changes were not affected by the inspiratory flow rate and were evident 15, 30, and 60 min after administration. Heart rate, static end-inspiratory respiratory system compliance, and the difference between minimum and maximum inspiratory resistance were unchanged after salbutamol. CONCLUSIONS: Salbutamol delivered by MDI and spacer device induces significant bronchodilation in mechanically ventilated patients with chronic obstructive pulmonary disease, but the magnitude of the effect is not affected by the inspiratory flow rate. These results do not support flow rate manipulations when bronchodilators are administered during controlled mechanical ventilation.

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.

Bronchodilator delivery by metered-dose inhaler in mechanically ventilated COPD patients: influence of flow pattern.

In mechanically ventilated patients the flow pattern during bronchodilator delivery by metered-dose inhaler (MDI) could be a factor that might influence the effectiveness of this therapy. In order to test this the effect of two different inspiratory flow patterns on the bronchodilation induced by beta2-agonists administered via MDI and spacer in a group of mechanically ventilated patients with chronic obstructive pulmonary disease (COPD) was examined. Eighteen mechanically ventilated patients with COPD, were prospectively randomized to receive two (n=8, protocol A) or six (n=10 protocol B) puffs salbutamol (100 microg x puff(-1)) either under pressure control (decelerating flow pattern) or under volume control (square wave flow pattern). With both modes, tidal volume and inspiratory time were identical. Salbutamol was administered via an MDI adapted to the inspiratory limb of the ventilator circuit using an aerosol cloud-enhancer spacer. After a 6-h washout, patients were crossed over to receive the same dose of salbutamol (200 or 600 microg, respectively in protocols A and B) by the alternative mode of administration. Static and dynamic airway pressures, minimum (Rint) and maximum (Rrs) inspiratory resistance and the difference between Rrs and Rint (deltaR) were measured before and at 15, 30 and 60 min after salbutamol. Independent of the dose, salbutamol caused a significant decrease in dynamic and static airway pressures, Rint and Rrs. These changes were not influenced by the inspiratory flow pattern and were evident at 15, 30 and 60 min after salbutamol. It is concluded that salbutamol delivered via metered dose inhaler and spacer device, induces significant bronchodilation in mechanically ventilated patients with chronic obstructive pulmonary disease, the magnitude of which is not affected by the inspiratory flow/time profile.

How to set the ventilator in asthma.

All patients with bronchial asthma are at risk of developing severe episodes of airway narrowing that do not respond to the usual medical treatment, a life-threatening situation referred to as status asthmaticus. In some cases, ventilatory failure occurs, necessitating mechanical ventilation to support gas exchange and to unload the respiratory muscles, giving time for other therapeutic interventions to improve the functional status of the patient. Mechanical ventilatory support poses additional risks to the patients, due to interaction between the pathophysiology of the disease and the process of mechanical ventilation. Dynamic hyperinflation, a cardinal feature of the pathophysiology, may cause serious complications during mechanical ventilation. Setting the ventilator, such as to minimize the dynamic hyperinflation, is a key point in the management of mechanically ventilated patients with status asthmaticus. Strategies to reduce dynamic hyperinflation, such as hypoventilation (permissive hypercapnia), increase of expiratory time and promotion of patient-ventilator synchrony are mandatory and significantly decrease the morbidity and mortality of the disease. Continuous monitoring of the effectiveness of these strategies, as well as the functional status of the patient, is crucial in order to limit complications associated with mechanical ventilation and to identify the time that weaning can start.

Low flow inflation pressure-time curve in patients with acute respiratory distress syndrome.

OBJECTIVE: In mechanically ventilated patients with ARDS, determination of the lower (LIP) and upper (UIP) inflection points of the static pressure-volume curve (P-V) is crucial for planning ventilatory strategies. Recently, a simple new method was proposed for measuring the P-V curve by inflating the lung with constant low flow [14]. We hypothesized that during low flow inflation LIP and UIP might be determined using the pressure-time curve (P-T) instead of P-V. METHODS: Eleven paralyzed patients with ARDS were studied. During volume control ventilation the patients were allowed to reach passive functional residual capacity (FRC) and then ventilator frequency, inspiratory to total breath duration ratio and tidal volume (VT) were set to 5 breaths/ min, 80% and 500 or 1,500 ml, respectively. With these settings, constant inspiratory flow (V'I) was administered for 9.6 s and ranged, depending on VT, between 0.05 and 0.15 l/s. P-V and P-T were obtained at two levels of positive end-expiratory pressure (PEEP; 0 and 10 cm H2O), with V'I being achieved either fast (< 0.1 s, minimum delay) or slowly (0.4 s, maximum delay). RESULTS: With minimum flow delay for a given experimental condition, the shape of the P-T did not differ from that of P-V. In all cases P-T correctly identified the presence of LIP and UIP, which did not differ significantly between P-T and P-V. With maximum flow delay, compared to P-V, the initial part of P-T was significantly shifted to the left. P-T did not identify the presence of UIP and LIP in one and two cases, respectively. CONCLUSIONS: Provided that constant flow is given relatively fast, P-T accurately determines the shape of P-V, as well as the LIP and UIP. Flow delay causes a leftward shift of the initial part of P-T, masking the presence of LIP and UIP in some cases.

Response of respiratory motor output to varying pressure in mechanically ventilated patients.

It has been shown in mechanically ventilated patients that pressure support (PS) unloads the respiratory muscles in a graded fashion depending on the PS level. The downregulation of respiratory muscles could be mediated through chemical or load-related reflex feedback. To test this hypothesis, 8 patients with acute lung injury mechanically ventilated on PS mode (baseline PS) were studied. In Protocol A, PS was randomly decreased or increased by at least 5 cmH2O for two breaths. During this time, which is shorter than circulation delay, only changes in load-related reflex feedback were operating. Sixty trials where PS increased (high PS) for two breaths and 62 trials where PS decreased (low PS), also for two breaths were analysed. Thereafter, the patients were assigned randomly to baseline, low or high PS and ventilated in each level for 30 min (Protocol B). The last 2 min of each period were analysed. Respiratory motor output was assessed by total pressure generated by the respiratory muscles (Pmus), computed from oesophageal pressure (Poes). In Protocol A, alteration in PS caused significant changes in tidal volume (VT) without any effect on Pmus waveform except for neural expiratory time (ntE). ntE increased significantly with increasing PS. In Protocol B, Pmus was significantly down-regulated with increasing PS. Carbon dioxide tension in arterial blood (Pa,CO2) measured at the end of each period increased with decreasing PS. There was not any further alteration in ntE beyond that observed in Protocol A. These results indicate that the effect of load-related reflex on respiratory motor output is limited to timing. The downregulation of pressure generated by the respiratory muscles with steady-state increase in pressure support is due to a slow feedback system, which is probably chemical in nature.