Ventilation Failure In Patients Research Articles

The role of electrical impedance tomography in predicting the failure of non-invasive ventilation in patients with COVID-19-associated hypoxemic acute respiratory failure: a prospective observational study

INTRODUCTION: Data on prediction of the failure of non-invasive lung ventilation (NIV) in patients with respiratory failure associated with COVID-19, based on electrical impedance tomography (EIT) patterns are limited. OBJECTIVE: To identify predictors of non-invasive lung ventilation failure in patients with respiratory insufficiency associated with COVID-19, using electrical impedance tomography data. MATERIALS AND METHODS: A monocenter prospective cohort observational study was conducted in patients with moderate-to-severe COVID-19-associated acute respiratory failure, who underwent NIV in the ICU (n = 43). EIT was used to measure the actual ventilation area (SVENT), hyperinflation area (SHYPER), ventilation delay zone (SRVD), and calculate the proportion of ventilated lungs (AVENT), proportion of hyperinflation area (ZHYPER), proportion of RVD area (ZRVD), as well as the duration of hyperinflation during one respiratory cycle (THYPER), and the ratio of hyperinflation time to inhalation time. RESULTS: The study included 43 patients admitted 15 (10–22) days after the onset of COVID-19. Patients with NIV failure (n = 34) had higher ZHYPER values on the first day (19.5 (16.3–30.5) in the NIV success group and 35.2 (25.0–45.0) in the failure group, AUROC 0.80, p = 0.004, Cut-off 39.7, Se 85 %, Sp 89 %) and the last day (20.6 (10.4–28.5) in the success group and 32.7 (26.4–43.3) in the failure group, AUROC 0.92, p = 0.003, Cut-off 32.7, Se 50 %, Sp 100 %), as well as a higher THYPER/TINSP ratio on the last day of NIV (37.5 (31.0–47.9) in the success group and 65.3 (43.7–88.4) in the failure group, AUROC 0.87, p = 0.001, Cut-off 52.7, Se 71 %, Sp 100 %). AVENT, ZRVD, and inhalation time did not show prognostic significance. CONCLUSIONS: EIT can predict the NIV failure in moderate-to-severe ARDS associated with COVID-19, based on the assessment of alveolar overdistention zones. Further research are needed to investigate this theory.

Longitudinal Assessment of ROX and HACOR Scores to Predict Non-Invasive Ventilation Failure in Patients with SARS-CoV-2 Pneumonia

Longitudinal Assessment of ROX and HACOR Scores to Predict Non-Invasive Ventilation Failure in Patients with SARS-CoV-2 Pneumonia

The Neutrophil/Lymphocyte Ratio Could Predict Noninvasive Mechanical Ventilation Failure in Patients with Acute Exacerbation of Chronic Obstructive Pulmonary Disease: A Retrospective Observational Study.

PurposeTo determine the effectiveness of neutrophil/lymphocyte ratio (NLR), compared to traditional inflammatory markers, for predicting noninvasive mechanical ventilation (NIMV) failure in acute exacerbation of chronic obstructive pulmonary disease (AECOPD) patients.Patients and MethodsWe conducted this retrospective observational study including 212 AECOPD patients who required NIMV during hospitalization from January 2015 to December 2020 in the department of respiratory and critical care medicine of Beijing Chao-Yang Hospital (west campus). We reviewed the medical record to determine if NIMV succeeded or failed for each patient, and compared NLR with traditional markers (leukocyte, C-reactive protein [CRP] and procalcitonin [PCT]) between NIMV failure and NIMV success group. Receiver-operating characteristic (ROC) curve and multivariate logistic regression analysis were used to assess the accuracy of these markers for predicting NIMV failure.ResultsA total of 38 (17.9%) patients experienced NIMV failure. NLR was a more sensitive biomarker to predict NIMV failure (AUC, 0.858; 95% CI 0.785–0.931) than leukocyte counts (AUC, 0.723; 95% CI 0.623–0.823), CRP (AUC, 0.670; 95% CI 0.567–0.773) and PCT (AUC, 0.719; 95% CI 0.615–0.823). There was statistically positive correlation between NLR and leukocytes count (r=0.35, p<0.001), between NLR and CRP (r=0.258, p<0.001), between NLR and PCT (r=0.306, p<0.001). The cutoff value of NLR to predict NIMV failure was 8.9 with sensitivity 0.688, specificity 0.886 and diagnostic accuracy 0.868. NLR>8.9 (odds ratio, 10.783; 95% CI, 2.069–56.194; P=0.05) was an independent predictor of NIMV failure in the multivariate logistic regression model.ConclusionNLR may be an effective marker for predicting NIMV failure in AECOPD patients, and the patients with NLR>8.9 should be handled with caution since they are at higher risk of NIMV failure and require intubation. Further study with a larger sample size and with more data is necessary to confirm our study.

"Rox Index as Predictor of Ventilatory Failure in Patients Admitted to ICU July 2020 to January 2021"

The use of the ROX index in COVID 19 patients allows evaluating those with high risk of ventilatory failure...

Factors associated with non-invasive mechanical ventilation failure in patients with hematological neoplasia and their association with outcomes

BackgroundThe usefulness of non-invasive mechanical ventilation (NIMV) in oncohematological patients is still a matter of debate.AimTo analyze the rate of noninvasive ventilation failure and the main characteristics associated with this endpoint in oncohematological patients with acute respiratory failure (ARF).MethodsA ventilatory support protocol was developed and implemented before the onset of the study. According to the PaO2/FiO2 (P/F) ratio and clinical judgment, patients received supplementary oxygen therapy, NIMV, or invasive mechanical ventilation (IMV).ResultsEighty-two patients were included, average age between 52.1 ± 16 years old; 44 (53.6%) were male. The tested protocol was followed in 95.1% of cases. Six patients (7.3%) received IMV, 59 (89.7%) received NIMV, and 17 (20.7%) received oxygen therapy. ICU mortality rates were significantly higher in the IMV (83.3%) than in the NIMV (49.2%) and oxygen therapy (5.9%) groups (P < 0.001). Among the 59 patients who initially received NIMV, 30 (50.8%) had to eventually be intubated. Higher SOFA score at baseline (1.35 [95% CI = 1.12–2.10], P = 0.007), higher respiratory rate (RR) (1.10 [95% CI = 1.00–1.22], P = 0.048), and sepsis on admission (16.9 [95% CI = 1.93–149.26], P = 0.011) were independently associated with the need of orotracheal intubation among patients initially treated with NIMV. Moreover, NIMV failure was independently associated with ICU (P < 0.001) and hospital mortality (P = 0.049), and mortality between 6 months and 1 year (P < 0.001).ConclusionThe implementation of a NIMV protocol is feasible in patients with hematological neoplasia admitted to the ICU, even though its benefits still remain to be demonstrated. NIMV failure was associated with higher SOFA and RR and more frequent sepsis, and it was also related to poor prognosis.

Is immunosuppression status a risk factor for noninvasive ventilation failure in patients with acute hypoxemic respiratory failure? A post hoc matched analysis

BackgroundRecent European/American guidelines recommend noninvasive ventilation (NIV) as a first-line therapy to manage acute hypoxemic respiratory failure in immunocompromised patients. By contrast, NIV may have deleterious effects in nonimmunocompromised patients and experts have been unable to offer a recommendation. Immunocompromised patients have particularly high mortality rates when they require intubation. However, it is not clear whether immunosuppression status is a risk factor for NIV failure. We assessed the impact of immunosuppression status on NIV failure in a post hoc analysis pooling two studies including patients with de novo acute hypoxemic respiratory failure treated with NIV. Patients with hypercapnia, acute exacerbation of chronic lung disease, cardiogenic pulmonary edema, or with do-not-intubate order were excluded.ResultsAmong the 208 patients included in the analysis, 71 (34%) were immunocompromised. They had higher severity scores upon ICU admission, higher pressure-support levels, and minute ventilation under NIV, and were more likely to have bilateral lung infiltrates than nonimmunocompromised patients. Intubation and in-ICU mortality rates were higher in immunocompromised than in nonimmunocompromised patients: 61% vs. 43% (p = 0.02) and 38% vs. 15% (p < 0.001), respectively. After adjustment or using a propensity score-matched analysis, immunosuppression was not associated with intubation, whereas it remained independently associated with ICU mortality with an adjusted odds ratio of 2.64 (95% CI 1.24–5.67, p = 0.01).ConclusionsImmunosuppression status may directly influence mortality but does not seem to be associated with an increased risk of intubation in patients with de novo acute hypoxemic respiratory failure treated with NIV. Studies in this specific population are needed.

A2A and 5‐HT Receptors are Differentially Required for Respiratory Plasticity Over the Course of Motor Neuron Loss in Intrapleurally CTB‐SAP Treated Rats

Loss of respiratory (e.g., phrenic) motor neurons leads to ventilatory failure in patients with neuromuscular diseases, but there are currently no treatments to maintain ventilation or to significantly and consistently preserve/restore ventilatory capacity in these patients. Genetic models have been used to study the impact of motor neuron loss; however, the rate and amount of motor neuron death cannot be controlled in these models, and degeneration is not limited to only respiratory motor neurons making it difficult to study treatment modalities to improve ventilation. Thus, we have developed a novel model of controlled respiratory motor neuron death using intrapleural injection of cholera toxin B conjugated to saporin (CTB‐SAP), in which we find that eupneic ventilation is maintained despite deficits in maximal ventilatory capacity. Our previous results demonstrated that respiratory plasticity is not only observed 7 days (d) after CTB‐SAP delivery, but that it is actually enhanced compared to control treatments. At 28d, however, respiratory plasticity is comparable to control levels, suggesting that the underlying mechanisms of plasticity at both time points may differ. Further, we suggest that neuroplasticity mechanisms contribute to maintain ventilation in the face of respiratory motor neuron loss. Although multiple cellular pathways give rise to respiratory plasticity, this study will focus on serotonin (5‐HT) and adenosine 2A (A2A) receptors based on our preliminary receptor expression data. Our preliminary data indicate that A2A receptor expression is increased in 7d, not 28d, CTB‐SAP treated rats, whereas 5‐HT receptor expression decreases at 7d and recovers to control levels in 28d CTB‐SAP treated rats. Thus, we hypothesize that distinct mechanisms (A2A receptor‐dependent at 7d, 5‐HT receptor‐dependent at 28d) enable respiratory plasticity and maintain eupneic ventilation in CTB‐SAP‐induced neuropathology. Using anesthetized, paralyzed and ventilated CTB‐SAP treated adult Sprague Dawley rats, we studied acute intermittent hypoxia (AIH; 3, 5 min bouts of 10.5% O2) induced phrenic long‐term facilitation (pLTF) following intrathecal C4 delivery of either the A2A receptor antagonist (10 μM MSX‐3) or the 5‐HT receptor antagonist (20 mM methysergide) to rats that received bilateral, intrapleural injections of: 1) CTB‐SAP (25μg), or 2) un‐conjugated CTB and SAP (control) in rats treated 7d or 28d prior. Our preliminary results indicate that pLTF is abolished after MSX‐3 at 7d and methysergide at 28d vs. controls and vehicle treated CTB‐SAP rats. These observations suggest that A2A receptors are necessary for respiratory plasticity early (7d), but 5‐HT receptors are required late (28d). Studies are underway to assess whether these receptors are required to maintain eupneic ventilation using whole‐body plethysmography. Results from this project will increase our understanding of how respiratory plasticity is initiated and how eupneic ventilation is maintained over the course of neuropathology, and will have broad implications for potential therapies to preserve/restore ventilatory function in disorders in which respiratory motor neuron death is associated.Support or Funding InformationNIH R00 HL119606 and SCIDRPThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Noninvasive ventilation failure in patients with hypoxemic respiratory failure: the role of sepsis and septic shock.

Background:Sepsis and septic shock are common in noninvasive ventilation (NIV) patients. However, studies on the association between sepsis and NIV failure are lacking.Methods:A prospective multi-center observational study was performed in 16 Chinese intensive care units (ICUs). Patients who used NIV due to hypoxemic respiratory failure were enrolled. Sepsis and septic shock were diagnosed according to the guideline of sepsis-3.Results:A total of 519 patients were enrolled. Sepsis developed in 365 patients (70%) and septic shock developed in 79 patients (15%). However, 75 patients (14%) had no sepsis. NIV failure was 23%, 38%, and 61% in patients, with no sepsis, sepsis, and septic shock, respectively. Multivariate analysis found that sepsis [odds ratio (OR) = 1.95, 95% confidence interval (CI): 1.06–3.61] and septic shock (OR = 2.47, 95% CI: 1.12–5.45) were independently associated with NIV failure. In sepsis and septic shock population, the NIV failure was 13%, 31%, 37%, 53%, and 67% in patients with sequential organ failure assessment (SOFA) scores of ⩽2, 3–4, 5–6, 7–8, and ⩾9, respectively. Patients with nonpulmonary induced sepsis had similar NIV failure rate compared with those with pulmonary induced sepsis, but had higher proportion of septic shock (37% versus 10%, p ⩽ 0.01) and lower ICU mortality (10% versus 22%, p ⩽ 0.01).Conclusions:Sepsis was associated with NIV failure in patients with hypoxemic respiratory failure, and the association was stronger in septic shock patients. NIV failure increased with the increase of organ dysfunction caused by sepsis.The reviews of this paper are available via the supplemental material section.

Risk factors for noninvasive ventilation failure in patients with post-extubation acute respiratory failure after cardiac surgery.

The effect of noninvasive ventilation (NIV) in patients with acute respiratory failure (ARF) after cardiac surgery is controversial. This study identified the feasibility of NIV and assessed the risk factors of NIV failure in patients with ARF after cardiac surgery. We retrospectively reviewed data from 112 patients with ARF requiring NIV and categorized them into the NIV failure and success groups. Patient data were extracted for further analysis, the primary outcomes were the need for endotracheal intubation and NIV-related in-hospital mortality. The risk factors for NIV failure in patients with post-extubation ARF was analyzed. The median time from extubation to NIV was 11 hours. No difference in the EuroSCORE existed between the two groups. NIV failed in 38.4% of the patients. The NIV failure group had a higher in-hospital mortality and stay at the longer intensive care unit (ICU). Most cases of NIV failure occurred within 1-48 hours of the treatment. The main causes of early NIV failure were a weak cough reflex and/or excessive secretions and hemodynamic instability. A Sequential Organ Failure Assessment (SOFA) score ≥10.5, vasoactive-inotropic score ≥6, and pneumonia were predictors of NIV failure, whereas a body mass index (BMI) ≥25.0 kg/m2 predicted NIV success. NIV was effective in the study population. Multiple organ dysfunction, pneumonia, and significant inotropic drug support before NIV were associated with NIV failure, whereas a BMI ≥25 kg/m2 was a predictor of NIV success.

Outcomes and predictors of failure of non-invasive ventilation in patients with community acquired pneumonia in the ED

ObjectiveWe set out to describe the use and analyze the predictors of non-invasive ventilation failure in patients with community-acquired pneumonia who receive non-invasive ventilation as first line ventilatory therapy in the emergency department. MethodsA retrospective cohort study was conducted among consecutive patients with community acquired pneumonia requiring ventilator support presenting to two tertiary care university-affiliated emergency departments. Multivariable logistic regression analysis was used to determine predictors of non-invasive ventilation failure at initiation of non-invasive ventilation and at two hours of non-invasive ventilation use; ResultAfter excluding patients with a do not resuscitate order status, 163 (74.8%) patients with community acquired pneumonia were initially treated with non-invasive ventilation on initial presentation to the emergency department. Non-invasive ventilation failure occurred in 50% of patients and was found to be associated with the absence of chronic obstructive airway disease, APACHE II score, the need for hemodynamic support and the number of CXR quadrants involved. Two-hour physiological parameters associated with non-invasive ventilation failure included higher respiratory rate, lower serum pH and the ongoing need of hemodynamic support. ConclusionIn conclusion, the use of non-invasive ventilation to support patients presenting to the emergency department with respiratory failure and community acquired pneumonia is common and is associated with a significant failure rate. Hemodynamic support is a strong predictor of failure. The selection of the appropriate patient and monitoring of physiological parameters while on NIV is crucial to ensure successful treatment.

Risk factors for noninvasive ventilation failure in patients with acute cardiogenic pulmonary edema: A prospective, observational cohort study

PurposeWe identified risk factors for noninvasive ventilation (NIV) failure in patients with acute cardiogenic pulmonary edema (ACPE). Materials and methodsWe conducted an observational cohort study over a 3-year period in a 28-bed emergency intensive care unit (EICU) and prospectively included all consecutive patients in whom NIV was attempted as initial ventilatory support for ACPE. The primary outcome variables were NIV failure rate and risk factors for NIV failure. ResultsAmong the 118 patients in the study, NIV failed for 44 (37.3%) patients. Risk factors for NIV failure were Killip class IV (odds ratio [OR], 28.56; 95% confidence interval [CI], 2.17–375.73; p=0.011), left ventricular ejection fraction (LVEF) <30% (OR, 9.54; 95% CI, 1.01–90.55; p=0.050) and B-type natriuretic peptide (BNP) ≥3350pg/mL (OR, 39.63; 95% CI, 3.92–400.79; p=0.002) at baseline, and fluid balance ≥400mL within 24h after ACPE (OR, 13.19; 95% CI, 1.18–147.70; p=0.036). ConclusionsNIV failure occurred in 37.3% of ACPE patients in a real-world EICU. When patients had Killip class IV, a lower LVEF, a higher BNP, and a more positive fluid balance within 24h after ACPE, the risk of failure was higher. Trial registration ClinicalTrials.gov identifierNCT02653365.

Tonsillar cyst: an unusual cause of ventilatory failure

COPD is a common disease that places a considerable burden on society; estimates based on disability life-years (DALY) suggests that COPD will become the fifth leading cause of disability worldwide by 2020.1 The term ‘exacerbation of COPD’ describes an acute deterioration in the patient's baseline symptoms (notably dyspnoea, cough or sputum production) and a necessity to change their usual medications.2 ‘Exacerbations’ with accompanying ventilatory failure in patients with severe COPD are a frequent cause of admission to hospital. We report an individual admitted in ventilatory failure who was initially diagnosed as having an exacerbation of COPD, but examination and investigations in clinic revealed that a tonsillar cyst was causing obstructive sleep apnoea, which upon removal led to substantial improvements.

Poor sleep quality is associated with late noninvasive ventilation failure in patients with acute hypercapnic respiratory failure*

To determine whether sleep quality helps to predict noninvasive ventilation outcome in patients with acute hypercapnic respiratory failure. Despite an initial clinical improvement, nearly one fourth of patients may fail noninvasive ventilation after several days. Because late intubation is associated with a poor prognosis, it may be useful to identify factors that may predict or explain late noninvasive ventilation failure. We prospectively studied 27 hypercapnic patients in a medical intensive care unit who required noninvasive ventilation for >48 hrs. A 17-hr sleep polysomnography (3 PM-8 AM) was recorded 2 days to 4 days after noninvasive ventilation initiation. Late noninvasive ventilation failure was defined as death, endotracheal intubation, or persistent need for noninvasive ventilation on day 6. An abnormal electroencephalographic pattern that eluded analysis by standard sleep-scoring criteria was noted in seven (50%) of the 14 patients with late noninvasive ventilation failure compared with one (8%) of the 13 patients successfully treated with noninvasive ventilation (p = .03). No clinical or laboratory variables explained the electroencephalographic differences. Patients failing noninvasive ventilation had poorer sleep quality with greater circadian sleep-cycle disruption and less nocturnal rapid eye movement sleep (6 mins [range, 0-12] vs. 26 mins [range, 6-49], p = .03), compared with patients successfully treated with noninvasive ventilation. Noninvasive ventilation failure was associated with delirium during the intensive care unit stay (64% vs. 0%). Late noninvasive ventilation failure in elderly patients with acute hypercapnic respiratory failure was associated with early sleep disturbances including an abnormal electroencephalographic pattern, disruption of the circadian sleep cycle, and decreased rapid eye movement sleep.

Predictors of noninvasive ventilation failure in patients with hematologic malignancy and acute respiratory failure*

The current trend to manage critically ill hematologic patients admitted with acute respiratory failure is to perform noninvasive ventilation to avoid endotracheal intubation. However, failure of noninvasive ventilation may lead to an increased mortality. Retrospective study to determine the frequency of noninvasive ventilation failure and identify its determinants. Medical intensive care unit in a University hospital. All consecutive patients with hematologic malignancies admitted to the intensive care unit over a 10-yr period who received noninvasive ventilation. A total of 99 patients were studied. Simplified Acute Physiology Score II at admission was 49 (median, interquartile range, 39-57). Fifty-three patients (54%) failed noninvasive ventilation and required endotracheal intubation. Their PaO2/FiO2 ratio was significantly lower (175 [101-236] vs. 248 [134-337]) and their respiratory rate under noninvasive ventilation was significantly higher (32 breaths/min [30-36] vs. 28 [27-30]). Forty-seven patients (89%) who failed noninvasive ventilation required vasopressors. Hospital mortality was 79% in those who failed noninvasive ventilation, and 41% in those who succeeded. Patients who failed noninvasive ventilation had a significantly longer intensive care unit stay (13 days [8-23] vs. 5 [2-8]) and a significantly higher rate of intensive care unit-acquired infections (32% compared with 7%). Factors independently associated with noninvasive ventilation failure by multivariate analysis were respiratory rate under noninvasive ventilation, longer delay between admission and noninvasive ventilation first use, need for vasopressors or renal replacement therapy, and acute respiratory distress syndrome. Failure of noninvasive ventilation occurs in half the critically ill hematologic patients and is associated with an increased mortality. Predictors of noninvasive ventilation failure might be used to guide decisions regarding intubation.

Relationships between Dyspnea, Respiratory Muscle Strength, and Ventilatory Failure in Patients with Amyotrophic Lateral Sclerosis

The purpose of this study was to investigate the relationships between dyspnea, respiratory muscle strength, and ventilatory failure in patients with amyotrophic lateral sclerosis (ALS). A cross-sectional study, based on patients' medical records, was performed at a primary care hospital in Japan. Twenty-five patients diagnosed with ALS who received care as outpatients or inpatients were included in this study, and patients' characteristics, dyspnea on the subscale of the revised ALS Functional Rating Scale, sniff nasal inspiratory pressure (SNIP), an indicator of respiratory muscle strength, and arterial carbon dioxide pressure (PaCO2) were selected as main outcome measures. All data were collected from patients' medical records. For patients with dyspnea, SNIP was significantly lower and PaCO2 tended to be higher than in patients without dyspnea. There were no significant differences in both bulbar symptoms and types of disease onset between the patients with and without dyspnea. In patients with ALS, it is suggested that dyspnea reflects respiratory muscle weakness and ventilatory failure. For the assessment of respiratory function in patients with ALS, it may be important to evaluate dyspnea in addition to SNIP and PaCO2.

Effects of Inhaled Fenoterol and Positive End-Expiratory Pressure on the Respiratory Mechanics of Patients with Chronic Obstructive Pulmonary Disease

During acute ventilatory failure in patients with chronic obstructive pulmonary disease (COPD), applying external positive end-expiratory pressure (PEEPe) will reopen small airways and, thus, may enhance peripheral deposition as well as the physiological effects of inhaled beta-2 agonists. To investigate the efficacy of inhaled fenoterol applied by zero end-expiratory pressure (ZEEPe) or PEEPe. Ten patients with COPD who were intubated and mechanically ventilated received fenoterol (10 mg/4 mL) via the ventilator using a jet nebulizer for 30 min on ZEEPe and PEEPe set at 80% of the total PEEP in a random order. The total resistance of the respiratory system (rapid airway occlusion technique), change in end-expiratory lung volume and expiratory flow limitation were assessed before and 5 min, 15 min, 30 min, 60 min and 240 min after fenoterol inhalation. Before inhalation and 60 min after inhalation, the total PEEP, the change in end-expiratory lung volume and the total resistance of the respiratory system were 8+/-3 cmH2O and 6+/-3 cmH2O, 0.61+/-0.34 L and 0.43+/-0.32 L, and 26+/-7 cmH2O/L/s and 23+/-6 cmH2O/L/s, respectively, with ZEEPe, and 9+/-3 cmH2O and 8+/-3 cmH2O (P<0.05 versus ZEEPe), 0.62+/-0.34 L and 0.62+/-0.37 L (P<0.05 versus ZEEPe), and 26+/-9 H2O/L/s and 25+/-9 H2O/L/s, respectively, with PEEPe. Three patients became not flow-limited under the combination of PEEPe and fenoterol. In patients with COPD, fenoterol combined with PEEPe has opposing effects on respiratory mechanics. First, it does not significantly reduce lung hyperinflation or inspiratory resistances. Second, it allows expiratory flow limitation reversal in some patients. These findings result from the net effect on end-expiratory lung volume of each intervention. This implies that if fenoterol is used in combination with PEEPe, the level of PEEPe should be reassessed during the time course of the drug to prevent any further lung hyperinflation.

Clinical practice guideline for the use of noninvasive positive pressure ventilation in COPD patients with acute respiratory failure

Noninvasive positive pressure ventilation has been demonstrated to be of benefit in preventing endotracheal intubation and reducing mortality in specific patients in the setting of acute exacerbations of chronic obstructive pulmonary disease. The successful application of noninvasive positive pressure ventilation depends on a multitude of factors, including patient selection, choice of interface, physician experience, and patient-ventilator synchrony. The use of clinical practice guidelines has been shown to improve the process and outcomes of care. This paper presents a guideline for the use of noninvasive positive pressure ventilation in the setting of acute ventilatory failure in patients with acute exacerbations of chronic obstructive pulmonary disease.

Effects of muscle relaxation therapy using specially designed plates in patients with pulmonary emphysema.

It has been suggested that respiratory muscle dysfunction plays a major role in the development of acute ventilatory failure in patients with chronic obstructive pulmonary disease (COPD). In this study, we devised a respiratory muscle relaxation maneuver using wedge-shaped wooden plates, with which pressure was exerted on the intercostal and accessory respiratory muscles by hand, or by tapping with a wooden hammer, for 15-20 minutes twice a day. The muscle relaxation maneuver was performed in 5 moderate to severe pulmonary emphysema patients for 4 weeks and in 7 emphysema patients for 6 weeks, and the effects on pulmonary function were examined. After the therapy, inspiratory capacity (IC) and vital capacity (VC) in both the 4 weeks-and 6 weeks-treated groups, and the forced expiratory volume in 1 second (FEV 1.0) in the 6 weeks-treated group were significantly increased, and CO2 retention had also improved. Daily peak expiratory flow (PEF) showed significant increases from 2 weeks after the initiation of the therapy. These results suggest that the respiratory muscle relaxation maneuver is effective for improving the pulmonary function of pulmonary emphysema patients.

Incidence of respiratory complications following Spinal Cord Injury

From 1985 to 1990 five Model Regional Spinal Cord Injury (SCI) Care Systems participated in a collaborative effort to prospectively document the occurrence of adult respiratory distress syndrome (ARDS), aspiration, atelectasis, bronchitis, bronchospasm, lung abscess, pleural effusion, pneumonia, pneumo/hemothorax, pulmonary edema, pulmonary thromboembolism, tracheitis, upper respiratory infection, and ventilatory failure in patients admitted within 48 hours of SCI with a level of C1-T12 and Frankel Grade A, B, or C. The mean, standard deviation and range was calculated for the time of onset and duration of each complication. Of the 261 patients who entered the study, 175 (67%) experience 544 respiratory complications with atelectasis being the most common (36.4%) followed by pneumonia (31.4%) and ventilatory failure (22.6%). These complications occurred on the average of 17.7 days, 24.5 days and 4.5 days postinjury and lasted 12.8 days, 15.5 days, and 35.9 days, respectively. Twenty-two percent, 47%, and 31% had injury levels at C1-4, C5-8, T1-12, respectively with the majority being Frankel Grade A (78%). Eighty-four percent of C1-4, 60% of the C5-8, and 65% of the T1-12 had respiratory complications. Statistical analysis revealed complications to be significantly greater (p < .05) and of longer duration (p < .05) for the C1-4 group. Ventilatory failure and aspiration were the earliest to occur (at 4.5 days) for all SCI patients. Surprisingly, however, complications overall occurred significantly sooner (p < .05) in the T1-12 group. In conclusion, patients who sustain SCI have a high incidence of respiratory complications; however, some occur earlier and more frequently depending on the level of injury.

Ventilatory drive and carbon dioxide response in ventilatory failure due to myasthenia gravis and Guillain-Barré syndrome.

To test the hypothesis that either decreased ventilatory drive or decreased CO2 responsiveness accounts for the hypoventilation observed in patients during acute ventilatory failure from myasthenia gravis or Guillain-Barré syndrome. Prospective, consecutive case series evaluating trials of ventilatory muscle performance, ventilatory drive, and CO2 response in patients during recovery from ventilatory failure until they were weaned from mechanical ventilation. Neurosciences critical care unit in a university hospital. Seven intubated, mechanically ventilated patients with myasthenia gravis or Guillain-Barré syndrome. Patients repeatedly performed mechanically unsupported, spontaneous breathing trials to the limits of endurance. After spontaneous breathing trials, patients underwent CO2 rebreathing studies. Seventy-three breathing trials were performed in three patients with Guillain-Barré syndrome and four patients with myasthenia gravis. Patients were unable to sustain spontaneous ventilation in 55 trials averaging 27 +/- 5 mins. In these trials, significant increases occurred in mean end-tidal CO2 (41 +/- 1 to 44 +/- 1 torr [5.6 +/- 0.1 to 6.0 +/- 0.1 kPa]) and respiratory rate (31 +/- 1 to 35 +/- 1 breaths/min, p < .01). Ventilatory drive (as measured by airway occlusion pressure for 100 msecs) increased significantly p < .01 from 3.7 +/- 0.3 to 4.9 +/- 0.3 cm H2O. The response of airway occlusion pressure to CO2 rebreathing after these trials was 0.33 +/- 0.07 cm H2O/sec/mm Hg, while the minute ventilation response to CO2 rebreathing was only 0.30 +/- 0.06 L/min/mm Hg. These results suggest that ventilatory drive increases during acute hypoventilation, and the ventilatory drive response to CO2 remains intact, even when the minute ventilation response to CO2 is poor. Therefore, a decrease in ventilatory drive or CO2 response is unlikely to account for hypoventilation during ventilatory failure in patients with myasthenia gravis or Guillain-Barré syndrome.