Diaphragm-protective mechanical ventilation

Mechanical ventilation injures not only the lungs but also the diaphragm, resulting in dysfunction associated with poor outcomes. The chief mechanisms of ventilator-induced diaphragm dysfunction are : disuse atrophy due to insufficient contraction and excessive ventilatory support ; concentric load-induced injury due to excessive contraction and insufficient ventilatory support ; eccentric load-induced injury due to contraction during the expiratory phase ; and longitudinal atrophy caused by high positive end-expiratory pressure. To protect the diaphragm during mechanical ventilation, maintaining proper levels of diaphragm contraction is paramount ; thus, monitoring of respiratory effort and finely tuned ventilator settings are necessary. Furthermore, maintaining of synchronization between the patient and the ventilator is also important. As diaphragm dysfunction is more likely to occur in critically ill patients, diaphragm-protective mechanical ventilation strategies are essential to reduce the mortality rate of intensive care unit patients. This review outlines clinical evidence of ventilator-induced diaphragm dysfunction and its underlying mechanisms, and strategies to facilitate diaphragm-protective mechanical ventilation

人工呼吸戦略up to date

In the second half of the 20th century, the polio epidemic led to dramatic advances in positive pressure mechanical ventilation. However, it has become known that mechanical ventilation itself exacerbates lung injury and increase mortality （ventilator-induced lung injury, VILI）. Over the past 20 years, numerous studies have been conducted to minimize the risk of VILI, and lung protective ventilation strategies consisting of low tidal volume, low plateau and driving pressure, and the use of appropriate end-expiratory positive pressure, became standard of care for acute respiratory distress syndrome （ARDS）. Furthermore, in recent years, it has revealed that excessive respiratory effort exacerbates lung injury （patient self-inflicted lung injury, P-SILI）, and the importance of controlling excessive respiratory effort has been recognized. However, strong suppression of respiratory effort leads to diaphragm atrophy, which may affect patient outcomes. Therefore, lung- and diaphragm-protective ventilation, which consists of monitoring respiratory effort closely and maintaining the effort at an appropriate level, has been proposed as a concept to avoid diaphragm atrophy while preventing P-SILI. Nevertheless, the mortality rate of ARDS is still high. Today, there is a need to move away from standardized treatment and to tailor ventilatory management to the individual risk of each patient

Reverse triggering induced by endotracheal tube leak in lightly sedated ARDS patient

Reverse triggering is respiratory entrainment triggered by the ventilator especially seen among heavily sedated patients. We confirmed reverse triggering induced by auto-triggering in lightly sedated patient through an esophageal pressure monitoring. The reverse triggering frequently caused breath stacking with increased tidal volume. Physicians should be aware, even at an optimal level of sedation, that reverse triggering can develop, possibly caused by auto-triggering

Change in diaphragm and intercostal muscle thickness in mechanically ventilated patients : a prospective observational ultrasonography study

Background: Diaphragm atrophy is observed in mechanically ventilated patients. However, the atrophy is not investigated in other respiratory muscles. Therefore, we conducted a two-center prospective observational study to evaluate changes in diaphragm and intercostal muscle thickness in mechanically ventilated patients. Methods: Consecutive adult patients who were expected to be mechanically ventilated longer than 48 h in the ICU were enrolled. Diaphragm and intercostal muscle thickness were measured on days 1, 3, 5, and 7 with ultrasonography. The primary outcome was the direction of change in muscle thickness, and the secondary outcomes were the relationship of changes in muscle thickness with patient characteristics. Results: Eighty patients (54 males and 26 females; mean age, 68 ± 14 years) were enrolled. Diaphragm muscle thickness decreased, increased, and remained unchanged in 50 (63%), 15 (19%), and 15 (19%) patients, respectively. Intercostal muscle thickness decreased, increased, and remained unchanged in 48 (60%), 15 (19%), and 17 (21%) patients, respectively. Decreased diaphragm or intercostal muscle thickness was associated with prolonged mechanical ventilation (median difference (MD), 3 days; 95% CI (confidence interval), 1–7 and MD, 3 days; 95% CI, 1–7, respectively) and length of ICU stay (MD, 3 days; 95% CI, 1–7 and MD, 3 days; 95% CI, 1–7, respectively) compared with the unchanged group. After adjusting for sex, age, and APACHE II score, they were still associated with prolonged mechanical ventilation (hazard ratio (HR), 4.19; 95% CI, 2.14–7.93 and HR, 2.87; 95% CI, 1.53–5.21, respectively) and length of ICU stay (HR, 3.44; 95% CI, 1.77–6.45 and HR, 2.58; 95% CI, 1.39–4.63, respectively) compared with the unchanged group. Conclusions: Decreased diaphragm and intercostal muscle thickness were frequently seen in patients under mechanical ventilation. They were associated with prolonged mechanical ventilation and length of ICU stay

Effect of controlled ventilation on diaphragm

Background : Since diaphragm passivity induces oxidative stress that leads to rapid atrophy of diaphragm, we investigated the effect of controlled ventilation on diaphragm thickness during assist-control ventilation (ACV). Methods : Previously, we measured end-expiratory diaphragm thickness (Tdiee) of patients mechanically ventilated for more than 48 hours on days 1, 3, 5 and 7 after the start of ventilation. We retrospectively investigated the proportion of controlled ventilation during the initial 48-hour ACV (CV48%). Patients were classified according to CV48% : Low group, less than 25% ; High group, higher than 25%. Results : Of 56 patients under pressure-control ACV, Tdiee increased more than 10% in 6 patients (11%), unchanged in 8 patients (14%) and decreased more than 10% in 42 patients (75%). During the first week of ventilation, Tdiee decreased in both groups : Low (difference, -7.4% ; 95% confidence interval [CI], -10.1% to -4.6% ; p < 0.001) and High group (difference, -5.2% ; 95% CI, -8.5% to -2.0% ; p = 0.049). Maximum Tdiee variation from baseline did not differ between Low (-15.8% ; interquartile range [IQR], -22.3 to -1.5) and High group (-16.7% ; IQR, -22.6 to -11.1, p = 0.676). Conclusions : During ACV, maximum variation in Tdiee was not associated with proportion of controlled ventilation higher than 25%

Monitoring of muscle mass in critically ill patients : comparison of ultrasound and two bioelectrical impedance analysis devices

Background: Skeletal muscle atrophy commonly occurs in critically ill patients, and decreased muscle mass is associated with worse clinical outcomes. Muscle mass can be assessed using various tools, including ultrasound and bioelectrical impedance analysis (BIA). However, the effectiveness of muscle mass monitoring is unclear in critically ill patients. This study was conducted to compare ultrasound and BIA for the monitoring of muscle mass in critically ill patients. Methods: We recruited adult patients who were expected to undergo mechanical ventilation for > 48 h and to remain in the intensive care unit (ICU) for > 5 days. On days 1, 3, 5, 7, and 10, muscle mass was evaluated using an ultrasound and two BIA devices (Bioscan: Malton International, England; Physion: Nippon Shooter, Japan). The influence of fluid balance was also evaluated between each measurement day. Results: We analyzed 93 images in 21 patients. The age of the patients was 69 (interquartile range, IQR, 59–74) years, with 16 men and 5 women. The length of ICU stay was 11 days (IQR, 9–25 days). The muscle mass, monitored by ultrasound, decreased progressively by 9.2% (95% confidence interval (CI), 5.9–12.5%), 12.7% (95% CI, 9.3–16.1%), 18.2% (95% CI, 14.7–21.6%), and 21.8% (95% CI, 17.9–25.7%) on days 3, 5, 7, and 10 (p < 0.01), respectively, with no influence of fluid balance (r = 0.04, p = 0.74). The muscle mass did not decrease significantly in both the BIA devices (Bioscan, p = 0.14; Physion, p = 0.60), and an influence of fluid balance was observed (Bioscan, r = 0.37, p < 0.01; Physion, r = 0.51, p < 0.01). The muscle mass assessment at one point between ultrasound and BIA was moderately correlated (Bioscan, r = 0.51, p < 0.01; Physion, r = 0.37, p < 0.01), but the change of muscle mass in the same patient did not correlate between these two devices (Bioscan, r = − 0.05, p = 0.69; Physion, r = 0.23, p = 0.07). Conclusions: Ultrasound is suitable for sequential monitoring of muscle atrophy in critically ill patients. Monitoring by BIA should be carefully interpreted owing to the influence of fluid change

Electrical muscle stimulation on upper and lower limb muscles in critically ill patients

Objectives: Electrical muscle stimulation (EMS) is widely used to enhance lower limb mobilization. Although upper limb muscle atrophy is common in critically ill patients, EMS application for the upper limbs has been rarely reported. The purpose of this study was to investigate whether EMS prevents upper and lower limb muscle atrophy and improves physical function. Design: Randomized controlled trial. Setting: Two-center, mixed medical/surgical intensive care unit (ICU). Patients: Adult patients who were expected to be mechanically ventilated for >48 h and stay in the ICU for >5 days. Interventions: Forty-two patients were randomly assigned to the EMS (n = 17) or control group (n = 19). Measurements and Main Results: Primary outcomes were change in muscle thickness and cross-sectional area of the biceps brachii and rectus femoris from day 1 to 5. Secondary outcomes included incidence of ICU-acquired weakness (ICU-AW), ICU mobility scale (IMS), length of hospitalization, and amino acid levels. The change in biceps brachii muscle thickness was −1.9% vs. −11.2% in the EMS and control (p = 0.007) groups, and the change in cross-sectional area was −2.7% vs. −10.0% (p = 0.03). The change in rectus femoris muscle thickness was −0.9% vs. −14.7% (p = 0.003) and cross-sectional area was −1.7% vs. −10.4% (p = 0.04). No significant difference was found in ICU-AW (13% vs. 40%; p = 0.20) and IMS (3 vs. 2; p = 0.42) between the groups. The length of hospitalization was shorter in the EMS group (23 [19–34] vs. 40 [26–64] days) (p = 0.04). On day 3, the change in the branched-chain amino acid level was lower in the EMS group (40.5% vs. 71.5%; p = 0.04). Conclusion: In critically ill patients, EMS prevented upper and lower limb muscle atrophy and attenuated proteolysis and decreased the length of hospitalization

Urinary titin as a biomarker for muscle atrophy

Objective: Although skeletal muscle atrophy is common in critically ill patients, biomarkers associated with muscle atrophy have not been identified reliably. Titin is a spring-like protein found in muscles and has become a measurable biomarker for muscle breakdown. We hypothesized that urinary titin is useful for monitoring muscle atrophy in critically ill patients. Therefore, we investigated urinary titin level and its association with muscle atrophy in critically ill patients. Design: Two-center, prospective observational study Setting: Mixed medical/surgical intensive care unit (ICU) in Japan Patients: Nonsurgical adult patients who were expected to remain in ICU for >5 days Interventions: None Methods: Urine samples were collected on days 1, 2, 3, 5, and 7 of ICU admission. To assess muscle atrophy, rectus femoris cross-sectional area and diaphragm thickness were measured with ultrasound on days 1, 3, 5, and 7. Secondary outcomes included its relationship with ICU-acquired weakness (ICU-AW), ICU Mobility Scale (IMS), and ICU mortality. Measurements and Main Results: Fifty-six patients and 232 urinary titin measurements were included. Urinary titin (normal range: 1–3 pmol/mg Cr) was 27.9 (16.8–59.6), 47.6 (23.5–82.4), 46.6 (24.4–97.6), 38.4 (23.6–83.0), and 49.3 (27.4–92.6) pmol/mg Cr on days 1, 2, 3, 5, and 7, respectively. Cumulative urinary titin level was significantly associated with rectus femoris muscle atrophy on days 3–7 (p < 0.03), although urinary titin level was not associated with change in diaphragm thickness (p = 0.31–0.45). Furthermore, cumulative urinary titin level was associated with incidence of ICU-AW (p = 0.01) and ICU mortality (p = 0.02) but not with IMS (p = 0.18). Conclusions: In nonsurgical critically ill patients, urinary titin level increased 10–30 times compared with the normal level. The increased urinary titin level was associated with lower limb muscle atrophy, incidence of ICU-AW, and ICU mortality

Dexmedetomidine and sleep during HFNC

Purpose : High-flow nasal cannula oxygen therapy (HFNC) is a new type of non-invasive respiratory support for acute respiratory failure patients. However, patients receiving HFNC often develop sleep disturbances. We therefore examined whether dexmedetomidine could preserve the sleep characteristics in patients who underwent HFNC. Patients and Methods : This was a pilot, randomized controlled study. We assigned critically ill patients treated with HFNC to receive dexmedetomidine (0.2 to 0.7 μg / kg / h, DEX group) or not (non-DEX group) at night (9:00 p.m. to 6:00 a.m.). Polysomnograms were monitored during the study period. The primary outcomes were total sleep time (TST), sleep efficiency and duration of stage 2 non-rapid eye movement (stage N2) sleep. Results : Of the 28 patients who underwent randomization, 24 were included in the final analysis (12 patients per group). Dexmedetomidine increased the TST (369 min vs. 119 min, p = 0.024) and sleep efficiency (68% vs. 22%, P = 0.024). The duration of stage N2 was increased in the DEX group compared with the non-DEX group, but this finding did not reach statistical significance. The incidences of respiratory depression and hemodynamic instability were similar between the two groups. Conclusions : In critically ill patients who underwent HFNC, dexmedetomidine may optimize the sleep quantity without any adverse events

免疫不全患者に対するHFNC

Background : Non-invasive positive pressure ventilation （NPPV） is highly recommended for immunocompromised patients with acute respiratory failure. In this population it remains uncertain, however, whether high flow nasal canula（HFNC）is as beneficial as NPPV. Methods : We retrospectively studied immunocompromised patients with acute respiratory failure admitted to our ICU from ２０１１ to ２０１８. The background and clinical outcomes of patients initially treated with HFNC and NPPV were compared. Results : Upon admission, １２ patients were treated with HFNC and １０ with NPPV. While the length of ICU stay was significantly shorter in HFNC group （HFNC４．６days vs. NPPV１３．８days, p=０．０２）, no intergroup difference was seen in ICU mortality （１６．７％ vs.３０．０％, p=０．４６）or intubation rate（３３．３％ vs.５０．０％, p=０．４３）. Conclusions : For immunocompromised patients with acute respiratory failure, HFNC may be an alternative to NPPV. Further prospective investigation is warranted