Effect of Atypical Sleep EEG Patterns on Weaning From Prolonged Mechanical Ventilation.

BACKGROUND: Approximately one-third of acute ICU patients display atypical sleep patterns that cannot be interpreted by using standard EEG criteria for sleep. Atypical sleep patterns have been associated with poor weaning outcomes in acute ICUs. RESEARCH QUESTION: Do patients being weaned from prolonged mechanical ventilation experience atypical sleep EEG patterns, and are these patterns linked with weaning outcomes? STUDY DESIGN AND METHODS: EEG power spectral analysis during wakefulness and overnight polysomnogram were performed on alert, nondelirious patients at a long-term acute care facility. RESULTS: Forty-four patients had been ventilated for a median duration of 38 days at the time of the polysomnogram study. Eleven patients (25%) exhibited atypical sleep EEG. During wakefulness, relative EEG power spectral analysis revealed higher relative delta power in patients with atypical sleep than in patients with usual sleep (53% vs 41%; P < .001) and a higher slow-to-fast power ratio during wakefulness: 4.39 vs 2.17 (P < .001). Patients with atypical sleep displayed more subsyndromal delirium (36% vs 6%; P = .027) and less rapid eye movement sleep (4% vs 11% total sleep time; P < .02). Weaning failure was more common in the atypical sleep group than in the usual sleep group: 91% vs 45% (P = .013). INTERPRETATION: This study provides the first evidence that patients in a long-term acute care facility being weaned from prolonged ventilation exhibit atypical sleep EEG patterns that are associated with weaning failure. Patients with atypical sleep EEG patterns had higher rates of subsyndromal delirium and slowing of the wakeful EEG, suggesting that these two findings represent a biological signal for brain dysfunction.

Setting positive end-expiratory pressure in the severely obstructive patient.

PURPOSE OF REVIEW: The response to positive end-expiratory pressure (PEEP) in patients with chronic obstructive pulmonary disease (COPD) requiring mechanical ventilation depends on the underlying pathophysiology. This review focuses on the pathophysiology of COPD, especially intrinsic PEEP (PEEPi) and its consequences, and the benefits of applying external PEEP during assisted ventilation when PEEPi is present. RECENT FINDINGS: The presence of expiratory airflow limitation and increased airway resistance promotes the development of dynamic hyperinflation in patients with COPD during acute respiratory failure. Dynamic hyperinflation and the associated development of PEEPi increases work of breathing and contributes to ineffective triggering of the ventilator. In the presence of airflow limitation, application of external PEEP during patient-triggered ventilation has been shown to reduce inspiratory effort, facilitate ventilatory triggering and enhance patient-ventilator interaction. To minimize the risk of hyperinflation, it is advisable to limit the level of external PEEP during assisted ventilation after optimization of ventilator settings to about 70% of the level of PEEPi (measured during passive ventilation). SUMMARY: In patients with COPD and dynamic hyperinflation receiving assisted mechanical ventilation, the application of low levels of external PEEP can minimize work of breathing, facilitate ventilator triggering and improve patient-ventilator interaction.

The central nervous system during lung injury and mechanical ventilation: a narrative review.

Mechanical ventilation induces a number of systemic responses for which the brain plays an essential role. During the last decade, substantial evidence has emerged showing that the brain modifies pulmonary responses to physical and biological stimuli by various mechanisms, including the modulation of neuroinflammatory reflexes and the onset of abnormal breathing patterns. Afferent signals and circulating factors from injured peripheral tissues, including the lung, can induce neuronal reprogramming, potentially contributing to neurocognitive dysfunction and psychological alterations seen in critically ill patients. These impairments are ubiquitous in the presence of positive pressure ventilation. This narrative review summarises current evidence of lung-brain crosstalk in patients receiving mechanical ventilation and describes the clinical implications of this crosstalk. Further, it proposes directions for future research ranging from identifying mechanisms of multiorgan failure to mitigating long-term sequelae after critical illness.

How to ventilate obstructive and asthmatic patients.

Exacerbations are part of the natural history of chronic obstructive pulmonary disease and asthma. Severe exacerbations can cause acute respiratory failure, which may ultimately require mechanical ventilation. This review summarizes practical ventilator strategies for the management of patients with obstructive airway disease. Such strategies include non-invasive mechanical ventilation to prevent intubation, invasive mechanical ventilation, from the time of intubation to weaning, and strategies intended to prevent post-extubation acute respiratory failure. The role of tracheostomy, the long-term prognosis, and potential future adjunctive strategies are also discussed. Finally, the physiological background that underlies these strategies is detailed.

Misconceptions of pathophysiology of happy hypoxemia and implications for management of COVID-19.

In the article "The pathophysiology of 'happy' hypoxemia in COVID-19," Dhont et al. (Respir Res 21:198, 2020) discuss pathophysiological mechanisms that may be responsible for the absence of dyspnea in patients with COVID-19 who exhibit severe hypoxemia. The authors review well-known mechanisms that contribute to development of hypoxemia in patients with pneumonia, but are less clear as to why patients should be free of respiratory discomfort despite arterial oxygen levels commonly regarded as life threatening. The authors propose a number of therapeutic measures for patients with COVID-19 and happy hypoxemia; we believe readers should be alerted to problems with the authors' interpretations and recommendations.

Inhibition of central activation of the diaphragm: a mechanism of weaning failure.

During a T-tube trial following disconnection of mechanical ventilation, patients failing the trial do not develop contractile diaphragmatic fatigue despite increases in inspiratory pressure output. Studies in volunteers, patients, and animals raise the possibility of spinal and supraspinal reflex mechanisms that inhibit central-neural output under loaded conditions. We hypothesized that diaphragmatic recruitment is submaximal at the end of a failed weaning trial despite concurrent respiratory distress. Tidal transdiaphragmatic pressure (ΔPdi) and electrical activity (ΔEAdi) were recorded with esophago-gastric catheters during a T-tube trial in 20 critically ill patients. During the T-tube trial, ∆EAdi was greater in weaning failure patients than in weaning success patients (P = 0.049). Despite increases in ΔPdi, from 18.1 ± 2.5 to 25.9 ± 3.7 cm H2O (P < 0.001), rate of transdiaphragmatic pressure development (from 22.6 ± 3.1 to 37.8 ± 6.7 cm H2O/s; P < 0.0004), and concurrent respiratory distress, ∆EAdi at the end of a failed T-tube trial was half of maximum, signifying inhibition of central neural output to the diaphragm. The increase in ΔPdi in the weaning failure group, while ∆EAdi remained constant, indicates unexpected improvement in diaphragmatic neuromuscular coupling (from 46.7 ± 6.5 to 57.8 ± 8.4 cm H2O/%; P = 0.006). Redistribution of neural output to the respiratory muscles characterized by a progressive increase in rib cage and accessory muscle contribution to tidal breathing and expiratory muscle recruitment contributed to enhanced coupling. In conclusion, diaphragmatic recruitment is submaximal at the end of a failed weaning trial despite concurrent respiratory distress. This finding signifies that reflex inhibition of central neural output to the diaphragm contributes to weaning failure.NEW & NOTEWORTHY Research into pathophysiology of failure to wean from mechanical ventilation has excluded several factors, including contractile fatigue, but the precise mechanism remains unknown. We recorded transdiaphragmatic pressure and diaphragmatic electrical activity in patients undergoing a T-tube trial. Diaphragmatic recruitment was submaximal at the end of a failed trial despite concurrent respiratory distress, signifying that inhibition of central neural output to the diaphragm is an important mechanism of weaning failure.

Why COVID-19 Silent Hypoxemia Is Baffling to Physicians.

Patients with coronavirus disease (COVID-19) are described as exhibiting oxygen levels incompatible with life without dyspnea. The pairing-dubbed happy hypoxia but more precisely termed silent hypoxemia-is especially bewildering to physicians and is considered as defying basic biology. This combination has attracted extensive coverage in media but has not been discussed in medical journals. It is possible that coronavirus has an idiosyncratic action on receptors involved in chemosensitivity to oxygen, but well-established pathophysiological mechanisms can account for most, if not all, cases of silent hypoxemia. These mechanisms include the way dyspnea and the respiratory centers respond to low levels of oxygen, the way the prevailing carbon dioxide tension (PaCO2) blunts the brain's response to hypoxia, effects of disease and age on control of breathing, inaccuracy of pulse oximetry at low oxygen saturations, and temperature-induced shifts in the oxygen dissociation curve. Without knowledge of these mechanisms, physicians caring for patients with hypoxemia free of dyspnea are operating in the dark, placing vulnerable patients with COVID-19 at considerable risk. In conclusion, features of COVID-19 that physicians find baffling become less strange when viewed in light of long-established principles of respiratory physiology; an understanding of these mechanisms will enhance patient care if the much-anticipated second wave emerges.

Long-Term Outcome after Prolonged Mechanical Ventilation. A Long-Term Acute-Care Hospital Study.

Rationale: Patients managed at a long-term acute-care hospital (LTACH) for weaning from prolonged mechanical ventilation are at risk for profound muscle weakness and disability. Objectives: To investigate effects of prolonged ventilation on survival, muscle function, and its impact on quality of life at 6 and 12 months after LTACH discharge. Methods: This was a prospective, longitudinal study conducted in 315 patients being weaned from prolonged ventilation at an LTACH. Measurements and Main Results: At discharge, 53.7% of patients were detached from the ventilator and 1-year survival was 66.9%. On enrollment, maximum inspiratory pressure (Pimax) was 41.3 (95% confidence interval, 39.4-43.2) cm H2O (53.1% predicted), whereas handgrip strength was 16.4 (95% confidence interval, 14.4-18.7) kPa (21.5% predicted). At discharge, Pimax did not change, whereas handgrip strength increased by 34.8% (P < 0.001). Between discharge and 6 months, handgrip strength increased 6.2 times more than did Pimax. Between discharge and 6 months, Katz activities-of-daily-living summary score improved by 64.4%; improvement in Katz summary score was related to improvement in handgrip strength (r = -0.51; P < 0.001). By 12 months, physical summary score and mental summary score of 36-item Short-Form Survey returned to preillness values. When asked, 84.7% of survivors indicated willingness to undergo mechanical ventilation again. Conclusions: Among patients receiving prolonged mechanical ventilation at an LTACH, 53.7% were detached from the ventilator at discharge and 1-year survival was 66.9%. Respiratory strength was well maintained, whereas peripheral strength was severely impaired throughout hospitalization. Six months after discharge, improvement in muscle function enabled patients to perform daily activities, and 84.7% indicated willingness to undergo mechanical ventilation again.