Basing intubation of acutely hypoxemic patients on physiologic principles.

The decision to intubate a patient with acute hypoxemic respiratory failure who is not in apparent respiratory distress is one of the most difficult clinical decisions faced by intensivists. A conservative approach exposes patients to the dangers of hypoxemia, while a liberal approach exposes them to the dangers of inserting an endotracheal tube and invasive mechanical ventilation. To assist intensivists in this decision, investigators have used various thresholds of peripheral or arterial oxygen saturation, partial pressure of oxygen, partial pressure of oxygen-to-fraction of inspired oxygen ratio, and arterial oxygen content. In this review we will discuss how each of these oxygenation indices provides inaccurate information about the volume of oxygen transported in the arterial blood (convective oxygen delivery) or the pressure gradient driving oxygen from the capillaries to the cells (diffusive oxygen delivery). The decision to intubate hypoxemic patients is further complicated by our nescience of the critical point below which global and cerebral oxygen supply become delivery-dependent in the individual patient. Accordingly, intubation requires a nuanced understanding of oxygenation indexes. In this review, we will also discuss our approach to intubation based on clinical observations and physiologic principles. Specifically, we consider intubation when hypoxemic patients, who are neither in apparent respiratory distress nor in shock, become cognitively impaired suggesting emergent cerebral hypoxia. When deciding to intubate, we also consider additional factors including estimates of cardiac function, peripheral perfusion, arterial oxygen content and its determinants. It is not possible, however, to pick an oxygenation breakpoint below which the benefits of mechanical ventilation decidedly outweigh its hazards. It is futile to imagine that decision making about instituting mechanical ventilation in an individual patient can be condensed into an algorithm with absolute numbers at each nodal point. In sum, an algorithm cannot replace the presence of a physician well skilled in the art of clinical evaluation who has a deep understanding of pathophysiologic principles.

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.

Long-Term Acute Care Hospital Outcomes of Mechanically Ventilated Patients With Coronavirus Disease 2019.

OBJECTIVES: To describe the clinical characteristics and outcomes of adult patients with coronavirus disease 2019 requiring weaning from prolonged mechanical ventilation. DESIGN: Observational cohort study of patients admitted to two long-term acute care hospitals from April 1, 2020, to March 31, 2021. SETTING: Two long-term acute care hospitals specialized in weaning from prolonged mechanical ventilation in the Chicagoland area, Illinois, United States. PATIENTS: Adult (≥ 18 yr old) ICU survivors of respiratory failure caused by severe acute respiratory syndrome coronavirus 2 pneumonia receiving prolonged mechanical ventilation. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: During the study period, 158 consecutive patients were transferred to the long-term acute care hospitals for weaning from prolonged ventilation. Demographic, clinical, and laboratory data were collected and analyzed. Final date of follow-up was June 1, 2021. Prior to long-term acute care hospital transfer, median length of stay at the acute care hospital was 41.0 days and median number of ventilator days was 35. Median age was 60.0 years, 34.8% of patients were women, 91.8% had a least one comorbidity, most commonly hypertension (65.8%) and diabetes (53.2%). The percentage of weaning success was 70.9%. The median duration of successful weaning was 8 days. Mortality was 9.6%. As of June 1, 2021, 19.0% of patients had been discharged home, 70.3% had been discharged to other facilities, and 1.3% were still in the long-term acute care hospitals. CONCLUSIONS: Most patients with coronavirus disease 2019 transferred to two Chicago-area long-term acute care hospitals successfully weaned from prolonged mechanical ventilation.

Ultrasound and non-ultrasound imaging techniques in the assessment of diaphragmatic dysfunction.

Diaphragm muscle dysfunction is increasingly recognized as an important element of several diseases including neuromuscular disease, chronic obstructive pulmonary disease and diaphragm dysfunction in critically ill patients. Functional evaluation of the diaphragm is challenging. Use of volitional maneuvers to test the diaphragm can be limited by patient effort. Non-volitional tests such as those using neuromuscular stimulation are technically complex, since the muscle itself is relatively inaccessible. As such, there is a growing interest in using imaging techniques to characterize diaphragm muscle dysfunction. Selecting the appropriate imaging technique for a given clinical scenario is a critical step in the evaluation of patients suspected of having diaphragm dysfunction. In this review, we aim to present a detailed analysis of evidence for the use of ultrasound and non-ultrasound imaging techniques in the assessment of diaphragm dysfunction. We highlight the utility of the qualitative information gathered by ultrasound imaging as a means to assess integrity, excursion, thickness, and thickening of the diaphragm. In contrast, quantitative ultrasound analysis of the diaphragm is marred by inherent limitations of this technique, and we provide a detailed examination of these limitations. We evaluate non-ultrasound imaging modalities that apply static techniques (chest radiograph, computerized tomography and magnetic resonance imaging), used to assess muscle position, shape and dimension. We also evaluate non-ultrasound imaging modalities that apply dynamic imaging (fluoroscopy and dynamic magnetic resonance imaging) to assess diaphragm motion. Finally, we critically review the application of each of these techniques in the clinical setting when diaphragm dysfunction is suspected.

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.

New device for nonvolitional evaluation of quadriceps force in ventilated patients.

INTRODUCTION: In mechanically ventilated patients, nonvolitional assessment of quadriceps weakness using femoral-nerve stimulation (twitch force) while the leg rests on a right-angle trapezoid or dangles from the bed edge is impractical. Accordingly, we developed a knee-support apparatus for use in ventilated patients. METHODS: Ninety subjects (12 ventilated patients, 28 ambulatory patients, and 50 healthy subjects) were enrolled. Twitches with leg-dangling, trapezoid, and knee-support setups were compared. RESULTS: Knee-support twitches were similar to trapezoid twitches but smaller than leg-dangling twitches (P < 0.0001). Inter- and intraoperator agreement was high for knee-support twitches at 1 week and 1 month. In ventilated patients, knee-support twitches were smaller than in healthy subjects and ambulatory patients (P < 0.004). DISCUSSION: The new knee-support apparatus allows accurate recording of quadriceps twitches. The ease of use in ventilated patients and excellent inter- and intraoperator agreement suggest that this technique is suitable for cross-sectional and longitudinal studies in critically ill patients. Muscle Nerve 57: 784-791, 2018.

Respiratory muscle testing in amyotrophic lateral sclerosis: a practical approach.

In amyotrophic lateral sclerosis (ALS), respiratory muscle weakness leads to respiratory failure and death. Non-invasive positive pressure ventilation (NIPPV) appears to reduce lung function decline, thus improving survival and quality-of-life of patients affected by the disease. Unfortunately, clinical features and timing to start NIPPV are not well defined. Starting from recent findings, we examine established and novel tests of respiratory muscle function that could help clinicians decide whether and when to start NIPPV in ALS. Non-invasive tests estimate the function of inspiratory, expiratory, and bulbar muscles, whereas clinical examination allows to assess the overall neurologic and respiratory symptoms and general conditions. Most of the studies recommend that together with a thorough clinical evaluation of the patient according to current guidelines, vital capacity, maximal static and sniff nasal inspiratory pressures, maximal static expiratory pressures and peak cough expiratory flow, and nocturnal pulse oximetry be measured. A sound understanding of physiology can guide the physician also through the current armamentarium for additional supportive treatments for ALS, such as symptomatic drugs and new treatments to manage sialorrhea and thickened saliva, cough assistance, air stacking, and physiotherapy. In conclusion, careful clinical and functional evaluation of respiratory function and patient's preference are key determinants to decide "when" and "to whom" respiratory treatments can be provided.

Weaning from mechanical ventilation.

For many critically ill patients admitted to an intensive care unit, the insertion of an endotracheal tube and the initiation of mechanical ventilation (MV) can be lifesaving procedures. Subsequent patient care often requires intensivists to manage the complex interaction of multiple failing organ systems. The shift in the intensivists' focus toward the discontinuation of MV can thus occur late in the course of critical illness. The dangers of MV, however, make it imperative to wean patients at the earliest possible time. Premature weaning trials, however, trigger significant respiratory distress, which can cause setbacks in the patient's clinical course. Premature extubation is also risky. To reduce delayed weaning and premature extubation, a three-step diagnostic strategy is suggested: measurement of weaning predictors, a trial of unassisted breathing (T-tube trial), and a trial of extubation. Since each step constitutes a diagnostic test, clinicians must not only command a thorough understanding of each test but must also be aware of the principles of clinical decision making when interpreting the information generated by each step. Many difficult aspects of pulmonary pathophysiology encroach on weaning management. Accordingly, weaning commands sophisticated, individualized care. Few other responsibilities of an intensivist require a more analytical effort and carry more promise for improving patient outcome than the application of physiologic principles in the weaning of patients.

Diaphragmatic neuromechanical coupling and mechanisms of hypercapnia during inspiratory loading.

We hypothesized that improved diaphragmatic neuromechanical coupling during inspiratory loading is not sufficient to prevent alveolar hypoventilation and task failure, and that the latter results primarily from central-output inhibition of the diaphragm and air hunger rather than contractile fatigue. Eighteen subjects underwent progressive inspiratory loading. By task failure all developed hypercapnia. Tidal transdiaphragmatic pressure (ΔPdi) and diaphragmatic electrical activity (ΔEAdi) increased during loading - the former more than the latter; thus, neuromechanical coupling (ΔPdi/ΔEAdi) increased during loading. Progressive increase in extra-diaphragmatic muscle contribution to tidal breathing, expiratory muscle recruitment, and decreased end-expiratory lung volume contributed to improved neuromechanical coupling. At task failure, subjects experienced intolerable breathing discomfort, at which point mean ΔEAdi was 74.9±4.9% of maximum, indicating that the primary mechanism of hypercapnia was submaximal diaphragmatic recruitment. Contractile fatigue was an inconsistent finding. In conclusion, hypercapnia during acute loading primarily resulted from central-output inhibition of the diaphragm suggesting that acute loading responses are controlled by the cortex rather than bulbopontine centers.