• Respiratory rate RR >38 bpm for 5 minutes or <6bpm • SpO2 < 92% • Tidal volume < 325 mL • Heart rate: HR > 140 OR 25% above baseline OR HR<60 • Blood pressure: SBP 40 mm Hg above baseline • Worsening agitation, anxiety or discomfort despite reassurance • Rapid shallow breathing index (RSBI) = RR/ TV Most consistent and powerful predictor RSBI > 105 min/L predicted failure well, but if used rigidly may slow the weaning process

• Anticipated need for the patient to return to the OR • ICP numbers out of normal range >20 (N: 7-15mmhg) • NMBA still being administered. • Nitric Oxide, ECMO, Flo-Lan • Glasgow Coma score <8

• Lung disease stable or resolving • FiO2 (lower than 50%) (he says 30%) • PEEP Less than 8 (he says 5) • Hemodynamically stable • Spontaneous breaths/Neuromuscular function (little to no pressors) • ABG within normal ranges

Ventilator: • PSV/CPAP • Peep of 5 or lower • PS of 10 or lower • FIO2--Lower then 50% (he says 30%) • Minimum of 30 minutes to Maximum of 120 minutes T-Piece (old School) • T-shaped tubing at ET tube • What about Peep? Going to have internal peep (normal peep)

Overdistention causes the release of chemical mediators

damage to the delicate tissue lining the alveoli (air sacs) in the lungs and the surrounding pulmonary capillaries, caused by the application of positive pressure ventilation (PPV), often during mechanical ventilation, leading to potential complications like fluid leakage into the lung tissue and impaired gas exchange; this injury is primarily caused by excessive stretching of the lung tissue due to high tidal volumes, a phenomenon known as "volutrauma" or "barotrauma.".

PPV is a hemodynamic monitoring index that's based on changes in TPP and pleural pressure. A high PPV can be used to monitor the mechanical ventilation cycle and guide circulation-protective ventilation.

PPV stands for prone position ventilation, which is a recommended treatment for patients with acute respiratory distress syndrome (ARDS) to improve oxygenation. PPV is considered an essential therapeutic approach for ARDS, and multiple randomized controlled clinical trials have shown its effectiveness. However, some concerns remain, such as whether prolonged prone ventilation can worsen hyperoxia and whether abdominal compression can worsen permissive hypercapnia acidosis.

Cytokines Mechanical ventilation can cause a cytokine response, including increased expression of tumor necrosis factor alpha (TNFalpha) and interleukin-6 (IL-6) mRNA. Prostacyclin Hyperventilation with PPV can cause an almost immediate increase in prostacyclin release. Alveolar-capillary permeability Mechanical stress from PPV can increase alveolar-capillary permeability, which allows inflammatory mediators to be released and translocated. Other effects of PPV include: Hemodynamic effects PPV can compress the pulmonary vasculature and mediastinal structures, which can increase right ventricular afterload. Neurohormonal effects PPV can alter neurohormonal systems, including the renin-angiotensin axis, sympathetic outflow, and nonosmotic vasopressin release. Pulmonary edema Increased intra-vascular pressure from PPV can contribute to pulmonary edema, which can affect oxygenation and lung compliance.