see also:

• assisted ventilation

• the application of positive pressure ventilation creates changes to the body which may not be beneficial.
• these adverse effects need to be recognised and mitigated where possible
• some of these are inevitable if ventilation is prolonged, and for this reason, invasive ventilation is generally NOT recommended for those with severe chronic obstructive pulmonary disease (COPD) who do not have an immediately reversible problem, as they are not likely to be weaned off the ventilator as a result of their risk of further impaired pulmonary function from sputum retention, atelectasis, pneumonia, and lung injury combined with atrophy of diaphragm and respiratory muscles.

• barotrauma:
  • may result in pneumothorax (30% of which will develop into tension pneumothorax), subcutaneous emphysema (usually self-limiting), pneumomediastinum (most are self-limiting although rarely may develop tension), and, rarely, pneumoperitoneum
  • risk factors include:
    • asthma
    • chronic interstitial lung disease
    • Acute Respiratory Distress Syndrome (ARDS)
    • plateau airway pressure (a good indicator of alveolar pressures) > 35 cm H2O
    • NB. peak airway pressure does not predict pulmonary barotrauma
• auto-PEEP:
  • is caused by incomplete exhalation due to either:
    • high minute volumes
    • prolonged inspiratory time (reduces expiratory time)
    • expiratory flow resistance such as obstructive airway disease, airway/ETT secretions, narrow ETT, or ventilator tubing
    • non-uniform emptying of lung units such as in obstructive airway disease
  • may result in:
    • barotrauma
    • impaired ability of patient to trigger a ventilator-assisted breath
    • incorrect estimation of the mean alveolar pressure and static lung compliance
    • decreased venous return and hypotension
  • suspect if:
    • continued expiratory airflow from the preceding breath when the next breath is triggered
    • measure airway pressure at the end of the 0.5-1.0 sec breath hold
  • reduce auto-PEEP by:
    • changing ventilator settings to increase expiratory time
    • reduce airway obstruction - suction secretions, beta 2 adrenergic agonists, wide ETT
    • reduce demand for high minute volume - reduce pain or fever
• ventilator-associated lung injury (VALI)
  • alveolar over-distension “alveolar strain”
    • due to relative high tidal volume for the amount of ventilated lung
  • cyclic atelectasis
    • most commonly occurs in injured lung and is exacerbated by repeated closure of alveoli
    • reduce with PEEP
  • see Acute Respiratory Distress Syndrome (ARDS)
• non-uniform ventilation
  • compliant non-dependent regions of the lung with low airway resistance will be ventilated best
• increased physiologic dead space
  • this is due to ventilation of lung which is not necessarily perfused as well as less well ventilated areas
• increased physiologic shunt
  • dependent lung is no long pulled open by diaphragmatic contraction resulting in perfused focal atelectasis and V/Q shunting
• disuse atrophy of diaphragm
  • may develop within 1st 24hrs
• respiratory muscle atrophy
  • combination of disuse and general muscle catabolism during critical illness
• impaired mucociliary motility
  • results in sputum retention and risk of pneumonia

• decreased venous return
  • increased intrathoracic pressure from positive pressure ventilation reduces the pressure gradient of extrathoracic veins to right atrium driving blood back to the heart
  • this is made worse by intravascular hypovolaemia, auto-PEEP, applied PEEP, and compression on the IVC as when intrabdominal pressures are sufficiently high to prevent venous return from the legs
  • this may be beneficial in patients with cardiac failure as it reduces preload
• increased pulmonary vascular resistance and reduced right ventricular output
  • due to positive pressure in alveoli
  • this can also shift the interventricular septum to the left, impair diastolic filling of the LV, and reduce LV output

• gastric stress ulcers
  • prolonged ventilation > 48hrs exacerbated by PEEP, decreases splanchnic perfusion as shown by increased lactate dehydrogenase levels, and risk of gastric stress ulcers
• other GIT complications during prolonged ventilation:
  • erosive esophagitis
  • diarrhea
  • acalculous cholecystitis
  • GIT hypomotility
• acute kidney injury (AKI) / acute renal failure (ARF)
  • mech. ventilation appears to independently double risk of ARF
• raised intracranial pressure
  • presumably via impairing cerebral venous outflow due to raised intrathoracic pressures
• systemic muscle weakness
  • presumably associated with disuse, perhaps neuro-muscular blockers, and catabolic effects of critical illness
• increased inflammatory response
  • particularly with high tidal volume ventilation
• disordered sleep