Combining O2 High Flow Nasal or Non-Invasive Ventilation with Cooperative Sedation to Avoid Intubation in Early Diffuse Severe Respiratory Distress Syndrome, Especially in Immunocompromised or COVID Patients?
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31. Okt. 2024
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Artikel-Kategorie: Review
Online veröffentlicht: 31. Okt. 2024
Seitenbereich: 291 - 315
Eingereicht: 22. März 2024
Akzeptiert: 01. Aug. 2024
DOI: https://doi.org/10.2478/jccm-2024-0035
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© 2024 Fabrice Petitjeans et al., published by Sciendo
This work is licensed under the Creative Commons Attribution 4.0 International License.
Fig. 1.
![From non-invasive to invasive ventilatory assistance in the setting of severe ARDS.
The clinical signs of ventilatory failure are: discomfort, intolerance to device, mental deterioration, diaphoresis, dyspnea (hyperpnea> tachypnea), inspiratory effort [use of accessory muscles, phasic activation of the sternomastoid muscle (palpation of the sterno-mastoid muscle as an index of drive in ARDS [69]), tracheal tug [69], thoraco-abdominal swing, suprasternal notch retraction (index of large negative esophageal pressure change), intercostal recession [69], nasal flaring, gasping [70]], copious respiratory secretions [71], airway bleeding, circulatory instability, electrocardiographic changes, P/F trend. An index of drive, airway occlusion pressure (P0.1), is set to 0.5 ms in the spontaneous breathing setting (P0.5) [125] and used as such.
Isolated “silent hypoxemia” without signs of labored breathing as the principal symptom: HFN/VHFN is the logical therapy. A multimodal approach complements HFN/VHFN to allow for an extended period of optimization and observation.
Labored breathing as the principal symptom: continued or intensified labored breathing should be interrupted to avoid transitioning from impending to overt failure and arrest. HFN/VHFN allows one to simultaneously buy time, observe, carry on the ancillary work (insertion of lines, chest X Ray, ECG, CT scan, bronchoscopy, pleural-pulmonary-cardiac ultrasounds, etc.) and addressing hypoxemia. Repeated assessments of the tidal volume (under mask NIV) and other signs of ventilatory failure or nasal/esophageal pressure [70] changes will allow one to assess improvement or deterioration within 2 h (NIV failure vs success respectively: Vt: 9.6–12 vs. 7.6–10.2 mL.kg−1 with NIV set to Vt=6–8 mL.kg−1 [72]; NIV success: reduction in esophageal pressure change≥10 cm H2O [2]; nasal pressure change mirrors esophageal pressure change [70]). Criteria for escalation from HFN to NIV are P/F<100, and/or RR>25 bpm, and/or respiratory distress and dyspnea despite HFN>60 L.min−1 [70]. Absence of improvement or deterioration within 2 h suggests switching to helmet NIV to achieve higher PEEP, restore a fluid-like lung behavior and reduced work of breathing. Absence of improvement or deterioration implies running through a multimodal approach again, looking for sepsis, coronary artery, delirium tremens, etc., then escalating up to intubation+CMV and avoiding overt failure.
NIV is set to avoid dyssynchrony: low inspiratory trigger, high pressurization time, lowest expiratory trigger. Helmet NIV requires faster pressurization time≤50 ms, cycling off=30% of peak inspiratory flow, higher PS level (+33–50%) and PEEP. High inspiratory assistance should not sum up with negative esophageal pressure change to avoid high transpulmonary pressure and further inflammation. HFN or NIV allows one to buy time and combine physiological tools (circulatory, respiratory, ventilatory, autonomic) within a multimodal approach. The check list is (Vt, RR)=f(temperature, agitation, cardiac output, microcirculation-arterial lactate, inflammation, lung water-diuresis, systemic pH, PaCO2, PaO2):
1)fever control [156, 157]: 36<θ<35°C, i.e. first [paracetamol, wet sheet+fan or BairHugger®] then alpha-2 agonist (“no bolus, start slow-go slow, fill them up-then open them up”; dexmedetomidine or clonidine up to 1.5 or 2 µg.kg−1.h−1, respectively). Alpha-2 agonists develop favorable effects slowly (≥3 h) if a slow administration is used to avoid bradycardia or hypotension, after iterative echocardiographic assessment and passive leg raising.
2)agitation [167] addressed to stringent quietness (−2<RASS<0; cooperative sedation: alpha-2 agonist as first-line sedative [15]; “breakthrough”: haloperidol 2.5–10 mg bolus or 5 mg bolus up to 4 administrations; supplementation: infusion up to 50 mg/day).
3)normalized cardiac output [4, 46]: iterative echocardiography coupled with volume, vasopressors, inotropes, pulmonary vasodilators.
4)normalized microcirculation and pH (systemic and regional): the alpha-2 agonist normalizes the sympathetic vascular activity, revascularizes the microcirculation, normalizes the local pH and arterial lactate and inflammation linked to acidosis.
5)anti-inflammation (source control; alveolar antiinflammation: adequate PEEP to suppress atelectrauma; systemic indirect antiinflammation i.e., alpha-2 agonist, steroids).
6)reduced lung water: volume loading before PEEP and administration of alpha-2 agonists then according to clinical signs, lowered PCWP [241] or iterative echocardiography. Increased CO or BP upon passive leg raising does not necessarily imply further volume loading. Only peripheral perfusion dictates volume load: mottling, capillary refill time, diuresis, lactate, pH, CO2 gap, mixed venous saturation. The alpha-2 agonist produces anti-ADH effect, diuresis and kaliuresis.
7)normalized CO2: lowered activity of the respiratory generator and inspiratory muscles through fever control (36<θ<35°C), microcirculation and pH with an alpha-2 agonist. PS level is as necessary to suppress the additional work of breathing caused by the valves and tubings (3–7 cm H2O) [116].
8)normalized hypoxic drive [78]: Oxygen therapy is the first line upon admission. a) FiO2=1 as briefly as possible (absorption atelectasis, toxicity) lowered step by step to 0.4, without lowering the flow, i.e. keeping PEEP on. Normalization of systemic CO2 and pH are key before normalizing the hypoxic drive. b) PEEP according to the disease : focal ARDS : 5 cm H2O; COVID-ARDS: 8–10 cm H2O; diffuse ARDS: 16 cm H2O. An esophageal balloon individualizes PEEP as early as possible. Leaks in the setting of NIV limit the ability to use very high PEEP.
9)upright position [7]: reverse Trendelenburg, 60° head up, 45° leg down. Upright position makes compression stockings or military antishock trouser sometimes useful.
10)lowered intra-abdominal pressure: gastric and bladder decompression, increased colonic motility (mild laxative).
Abbreviations: HFN: O2 high flow nasal; VHFN: very high flow nasal; NIV: non-invasive ventilation; CMV: controlled mandatory ventilation; PEEP: positive end-expiratory pressure; PS: pressure support, inspiratory assistance.](https://sciendo-parsed.s3.eu-central-1.amazonaws.com/678a6069082aa65dea3d1793/j_jccm-2024-0035_fig_001.jpg?X-Amz-Algorithm=AWS4-HMAC-SHA256&X-Amz-Content-Sha256=UNSIGNED-PAYLOAD&X-Amz-Credential=AKIA6AP2G7AKOUXAVR44%2F20250911%2Feu-central-1%2Fs3%2Faws4_request&X-Amz-Date=20250911T081910Z&X-Amz-Expires=3600&X-Amz-Signature=afc7d795f349c501fb6219b8c5adb6a5db0d20548cb31dc1bc5281789a06486d&X-Amz-SignedHeaders=host&x-amz-checksum-mode=ENABLED&x-id=GetObject)
Criteria for non-invasive ventilatory failure [76]
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Absence of improvement or worsening of clinical signs observed on admission, including oxygenation data and increased respiratory rate Appearance of signs of ventilatory muscle fatigue or use of accessory muscles Presence of acidosis, both respiratory and metabolic Inability to properly clear respiratory secretions Signs of circulatory instability, including hyperlactatemia Deterioration of consciousness or presence of seizures Intolerance to device, especially mask wearers |