Common lifesaving intervention for critically ill patients in respiratory failure due to a wide variety of etiologies.
The overall goal of mechanical ventilation is to maintain acceptable gas exchange to meet the body’s metabolic demands and to minimize adverse effects in its application.
Combination of diaphragmatic inactivity and mechanical ventilation for prolonged periods, more than 18 hours, is associated with atrophy of muscle fibers in the human diaphragm (Levine).
Almost 800,000 patients require mechanical ventilation per year.
ARDS represents only a portion of more than the 13 million people worldwide to require mechanical ventilation for respiratory failure each year.
Estimated approximately 310 persons per hundred thousand adult population undergo invasive ventilation for non-surgical indications.
Purpose of mechanical ventilation is to rest the respiratory muscles and to provide adequate gas exchange.
Invasive mechanical ventilation in critically ill adults involves adjusting the fraction of inspired oxygen to maintain arterial oxygen saturation: the oxygen saturation target to optimize clinical outcomes in this patient population is unknown.
Among critically ill adults receiving mechanical ventilation, the number of ventilator free days did not differ among groups in which goal of 90%, 94%, or 98% were reached (Semler M).
Prolonged diaphragmatic inactivity of 18-69 hours, and mechanical ventilation associated with atrophy of slow-twitch and fast-twitch fibers of the diaphragm.
A lifesaving strategy in patients with acute respiratory failure.
Indications: airway protection for a patient with a decreased level of consciousness, hypercapnic respiratory failure due to to airway, chest wall, or respiratory muscle diseases, hypoxemic respiratory failure or, for circulatory failure in which sedation and mechanical valve ventilation could decrease the oxygen cost of breathing.
Associated with significant morbidity including: pneumonia, weakness, and delirium, all which increases with duration of mechanical ventilation.
Patient-ventilator dyssynchronies arefrequent and associated with worse outcomes.
Its benefits in respiratory failure must be balanced with known risks.
Unequivocal evidence suggests that MV has the potential to aggravate and precipitate lung injury.
In acute respiratory distress syndrome and in acute lung injury mechanical ventilation can cause ventilator associated lung injury.
Complications of ventilation include barotrauma, that is, gross air leaks, oxygen toxicity, and hemodynamic compromise.
Mechanical ventilation with injurious tidal volumes, excessive airway pressures, inadequate end-expiratory pressure, and unmatched patient respiratory demand can lead to volume trauma which is alveoli overdistension leading to inflammation and iatrogenic lung injury, barotrauma with pneumothorax and or pneumomediastinum, atelecttrauma with damage from repetitive opening and closing of alveoli, and patient-ventilator asynchrony, respectively.
Trigger phase of mechanical ventilation initiates a breath, when the ventilator is fully controlled the trigger variable is the time, indicating a breath is initiated at fixed intervals.
When mechanical ventilation synchronizes the breath delivery with the signal that is related to the patients effort, inspiration is initiated when a given flow or pressure decrease is detected by the ventilator.
Respirator lung describes diffuse alveolar infiltrates and hyaline membranes found on postmortem examination of patients who had previously had mechanical ventilation.
MV can cause worsening lung injury in patients with previously damaged lungs and it can damage previously normal lungs.
Ventilator associated lung injury is a frequent complication in critically ill patients and its development increases morbidity and mortality.
Lung damage from mechanical ventilation includes inflammatory cell infiltrates, hyaline membranes, increased vascular permeability, and pulmonary edema: the constellation of pulmonary consequences are termed ventilator induced lung injury.
High tidal volumes are associated with repetitive opening and closing of aveolo, albeolar rupture, and excessive alveolar dissension resulting in ventilated induced lung injury, leading to increased mortality compared with the strategy of lung protective mechanical ventilation that uses lower tidal volumes.
Low tidal volume ventilation avoids alveolar collapse through the use of positive end-expiratory pressure (PEEP).
Using low tidal volume improves survival in ventilation use with acute respiratory distress syndrome.
Low tidal volume use may be associated with a lower number of pulmonary complications in patients without adult respiratory distress syndrome, and it may shorten the time spent on the ventilator and duration of time spent in the ICU and hospital.
In patients in the ICU without adult respiratory distress syndrome, low total volume strategy did not result in a greater number of ventilator free days than an intermediate tidal volume strategy ( Effect of the Low versus Intermediate Tidal Volume Strategy on Ventilator-free days in Intensive care unit Patients without ARDS).
Prolonged mechanical ventilation is defined as more than 21 days, accounts for more than 13% of ventilated patients and 37% of intensive care unit cost.
Muscle inactivity effects oxidative stress and increases cytosolic calcium concentration increasing the activity of proteases that cause dissociation of the myofibrillar lattice, the initial step in proteolysis.
Patients found to have decreased diaphragmatic glutathione concentration and increase in active capase-3 suggesting increased protein release from the myofibrillar lattice.
Following protein release from the lattice, proteolysis occurs via the ubiquitin-protease pathway.
Higher tidal volumes during ventilation causes the alveoli to overstretch in a process called volutrauma.
Volutrauma is the main cause of ventilator associated lung injury.
The use of lower tidal volume ventilation reduces morbidity and mortality in patients with ARDS or ALI ( acute lung injury).
Low tidal volumes, may be associated with patient ventilator asynchrony and hypercapnia.
Low tidal volume ventilation results in relative hypoxemia and hypercarbia which can increase patient ventilator drive and often make it difficult to maintain low tidal volumes in synchronous ventilated interactions.
In a meta-analysis protective ventilation with lower tidal volumes is associated with better clinical outcomes (Neto AS et al).
A lung protective ventilation strategy targets a tidal volume of 6 mL per kilogram body weight is the current consensus recommendation for a patient with ARDS.
Because patients cannot eat normally, artificial nutrition is often provided in patients with acute lung injury and with long duration of mechanical ventilation.
The two most common weaning methods from ventilators are pressure support and spontaneous breathing trials.
Enteral nutrition targeting full caloric needs is advocated over parenteral nutrition during mechanical ventilation.
Advantage of Tracheostomy over prolonged translaryngeal endotracheal intubation include: increased patient comfort, decreased sedative use, faster weaning, decreased nosocomial pneumonia and shorter hospital stay.
Metaanalysis suggests early tracheostomy reduces duration of mechanical ventilation, hospital stay, and mortality (Griffiths J et al, Rumbak MJ et al).
In the UK. mechanically ventilated patients treated with tracheostomy within 4 days of critical care admission was not associated with improvement in 30 day mortality or other secondary outcomes: clinicians ability to predict which patients will require extended ventilatory therapy is limited (Young D et al).
Most critically ill patients on mechanical ventilation will develop endoscopic evidence of stress ulceration in the upper G.I. tract, and 10 to 25% of these patients will manifest overt signs and symptoms of G.I. bleeding, and another 5% will progress clinically significant hemorrhage.
Approximately 1 million hospitalizations in United States annually require mechanical ventilation and are risk for stress-related G.I. hemorrhage.
((Proton pump inhibitors)) are associated with greater risk of G.I. bleeding, pneumonia, and C. difficile infections then H2RAs in mechanically ventilated patients (MacLaren R et al.).
Ventilator bundles to prevent ventilator-associated pneumonia include: head of bed elevation, daily interruption of sedative infusions, daily spontaneous breathing trial su, thromboembolism prophylaxis, stress ulcer prophylaxis, and oral care with chlorhexidine gluconate.
Ventilator bundles reduce ventilator-associated pneumonia.
Among patients with agitated delirium receiving mechanical ventilation the addition of dexmedetomidine results in more ventilator free hours at seven days.
Among mechanically ventilated ICU patients, mortality at 90 days did not differ significantly between those on no sedation in those on light sedation with daily interruption (Olsen HT).
In patients receiving mechanical ventilation treated with chlorhexidine, decontamination of the digestive tract and selective oropharyngeal decontamination did not reduced multi drug resistant gram-negative bacteremia compared with standard care.
Prolonged mechanical ventilation is associated with significant morbidity among critically ill children, including secondary infections, exposure to potentially neurotoxic sedatives, and muscle wasting: adversely affecting childhood development.
Prone positioning with invasive mechanical ventilation for acute respiratory distress syndrome may result in increased lung volume, homogenized pleural pressure, and reduced shunting, and may be associated with a lower risk of death for moderate to severe acute respiratory distress syndrome.
Among adults undergoing mechanical ventilation in the ICU early mobilization did not result in a greater number of days patients were alive and out of the hospital than usual mobilization efforts.