الفهرس 
PULMONARY VENTILATIONOnly 14 pages are availabe for public view
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Abstract
Mechanical ventilation is a life-saving intervention its indication rather than acute respiratory failure are, coma , acute exacerbation of chronic obstructive pulmonary disease , neuromuscular disorders, and other disorders including; acute respiratory distress syndrome, heart failure, pneumonia, sepsis, complications of surgery, and trauma.
Complications of mechanical ventilation are common for ventilator-dependent patients to experience injuries related to mechanical ventilation.
Pulmonary complications of long-term mechanical ventilation (LTMV) are probably less common compared with the incidence of complications that occur in the acute setting. Ventilator-induced lung injury (VILI) has become a well-recognized side effect of mechanical ventilation. Alveolar damage and capillary leak caused by over-stretching of the alveolar spaces have been suggested to be major contributors to VILI.
The primary factors that induce VALI are barotrauma, volutrauma, hyperoxia and the underlying disease process. More specifically these include, air leak, alveolar shearing, edematous lungs, fluid and protein leakage, reduced compliance, absorption atelectasis, and physiological shunting.
Pulmonary barotrauma refers to alveolar rupture due to elevated transalveolar pressure (the alveolar pressure minus the pressure in the adjacent interstitial space). Common consequences include PTX, pneumomediastinum, pneumoperitoneum, and subcutaneous emphysema.
Volutrauma describes the parenchymal injury that occurs secondary to the change in volume from end inspiration to end expiration. This parenchymal injury is commonly referred to as alveolar shearing and has been attributed to the force from cyclic opening and closing of adjacent alveoli which is exacerbated by high transpulmonary pressures at end inspiration and the retention of insufficient functional residual capacity at end expiration. This shearing effect results in alveolar injury and fibrotic changes which further reduces compliance.
Biotrauma is a relatively new term that is used to describe the release of cytokines secondary to epithelial injury in the lung which then contributes to a systemic inflammatory cascade.
Hyperoxia difined as a consequence of ventilating with a high FiO2, compliance is reduced secondary to fibrotic changes, vascular permeability alters which exacerbates pulmonary edema and extrinsic and mitochondrial cell death pathways are activated. Exposure of humans to elevated levels of inspired oxygen results in lung injury. This injury, which may occur as a result of increased generation in the lung of reactive oxygen species, may be mitigated by the presence of antioxidants.
Airway complications is complications of mechanical ventilation are related to compromising the airway because of tracheal injury by the endotracheal tube (ETT), retained secretions, and the adverse effects of tracheostomy. Upper airway injury from prolonged ETT exposure can occur anywhere along path of the tube and may contribute to weaning failure even after tracheostomy.
VAP is estimated to be responsible for 27-47% of intensive care unit (ICU)-acquired infections, and it is the second most common nosocomial infection. VAP occurs in 10–20% of patients receiving mechanical ventilation for more than 48 hours, and it is associated with increased ICU length of stay and mortality.
Patients receiving LTMV often have significant cardiac dysfunction that may be unrecognized and may interfere with the ability to wean. In weaning trials, occult myocardial ischemia and acute left ventricular dilatation have an incidence range of 6% to 47%. Other potential cardiovascular, direct complications of mechanical ventilation are related to volutrauma. Pneumomediastinum rarely causes hemodynamic demise comparable with that seen with a large PTX .
Neurological complications include increased intracranial pressure during suctioning and possibly with PEEP application; induced cerebrovascular vasoconstriction caused by hyperventilation, which results in reduction in cerebral blood flow and the worsening of ischemia; and, rarely, pulmonary venous air embolism. Most VAIs already have underlying central neurologic or neuromuscular dysfunctions, which are caused by their chronic morbidities or after acute severe illness and care in ICU.
Mechanically ventilated patients who develop pulmonary barotrauma, we suggest that the plateau airway pressure be immediately lowered . An appropriate goal is a plateau airway pressure ≤35 cm H2O.
Also this may require lowering the tidal volume, positive end-expiratory pressure, or inspiratory flow, as well as increasing sedation, administering neuromuscular blockade, or advancing treatment of the underlying medical condition (e.g. bronchodilators for asthma).
For mechanically ventilated patients who develop pneumothorax, management is virtually the same as the management of secondary spontaneous pneumothorax as will as must be monitored closely.
Pneumomediastinum, pneumoperitoneum, and subcutaneous emphysema generally require supportive care only. In rare instances that tension physiology develops, decompression may be necessary.
For patients have VAP preventive strategies aimed at reducing either incidence or the severity of pneumonia that occar by choosing appropriate therapy for VAP include knowledge of organisms likely to be present, local resistance patterns within the ICU, a rational antibiotic regimen, and a rationale for antibiotic de-escalation or stoppage. Although the clinician could know the organisms and sensitivities prior to the development of VAP, this is often not the case
The role of NIV, instead of conventional mechanical ventilation in patients with acute respiratory failure due to COPD or acute cardiogenic pulmonary edema, lead to a significantly lower risk of nosocomial pneumonia, less antibiotic use, shorter ICU stay, and lower mortality.