Complications associated with mechanical ventilation are primarily related to the use of positive pressure applied to the lungs and the artificial airways required to provide invasive ventilation. Positive pressure not only damages sensitive lung tissue but also may inhibit blood flow returning to the heart. Each of these effects can then go on to affect other organ systems such as the kidneys and brain.
Ventilator induced lung injury (VILI) occurs when the alveoli capillary membrane is damaged during mechanical ventilation. VILI can be the result of barotrauma, volutrauma, atelectrauma, and biotrauma.
Barotrauma occurs when high ventilatory pressures rupture the small airways and alveoli. Barotrauma may become life threatening if it leads to tension pneumothorax. A tension pneumothorax is a condition in which air enters the pleural space with each breath but cannot exit.
Volutrauma occurs when alveoli are over distended due to high tidal volume use. This damages the epithelial cells lining the alveoli. Volutrauma can also occur even when the tidal volume is set appropriately. This is because air will follow the path of least resistance. So, when a tidal volume is delivered to a diseased lung the healthy regions of the lung may receive the bulk of the tidal volume breath as compared to diseased non-compliant regions of the lung.
Atelectrauma occurs when collapsed alveoli are repeatedly snapped open with each breath only to then re-collapse again after exhalation. This creates shearing forces which damage the epithelial cells of the alveoli. As a result, cellular proteins leak into the extracellular fluid leading to pulmonary edema.
Biotrauma occurs when aforementioned traumas fill the alveoli with cytokines, proteins, white blood cells, and neutrophils. These bio-elements cause further damage to the alveolar-capillary membrane by allowing bacteria into the bloodstream. This leads to an even more severe systemic inflammatory response as a result.
Alveolar damage may is associated with prolonged use of high FiO2’s for greater than 48 hours.
Absorption atelectasis also may occur due to high fio2 use.
Neonatal retinopathy is also associated with exposure of the neonate to high FiO2.
Hypotension and decreased cardiac output may occur when increased intra-thoracic pressure from positive pressure ventilation and PEEP use decreases venous blood returning to the right atrium. The same affect can occur with patients who are using CPAP for sleep apnea.
Increased pulmonary vascular resistance also may result from the reduced cardiac output caused by PPV and the use of PEEP. The use of PEEP increases pressure applied to the alveoli and may compress pulmonary vasculature.
Neurological & Neuromuscular Hazards
Increased intracranial pressure is common in patients with traumatic brain injury or stroke. The use of PEEP during mechanical ventilation may increase ICP by reducing central venous blood return leaving the brain. Increased carbon dioxide levels may decrease cerebral blood flow and increase ICP as a result.
Cerebral hypo perfusion can occur when high mean airway pressures are used during mechanical ventilation. This may occur when high MAP decreases overall blood pressure.
Delirium is a common problem for patient’s on prolonged mechanical ventilation. The use of Benzodiazepines are associated with delirium in the ICU.
Poly neruopathy and myopathy is a common occurrence in patient’s receiving mechanical ventilation. This may make weaning difficult due to diaphragmatic dysfunction.
Ventilator Associated Pneumonia (VAP) occurs when oropharyngeal secretions slip past the endotracheal tube cuff and are aspirated into the lungs. Though, VAP is really more the result of artificial airway use rather than mechanical ventilation.
The definition and diagnosis of VAP has evolved over the years. Currently, VAP is defined as a pneumonia occurring greater than 48 hours after initiation of invasive mechanical ventilation.
Some general guidelines for VAP prevention include:
- Maintain good oral hygiene by brushing the teeth, suctioning excess oral secretions and providing an antiseptic mouth rinse such as chlorhexidine for example.
- Avoid breaking (opening) and routinely changing the ventilator circuit.
- Minimize unnecessary transports. Transports have been associated with contamination of the airway and an increased risk of VAP.
- Maintain the head of the bead greater than a 30 degree angle.
- Using endotracheal tubes with subglottic suction ports can help remove secretions pooling on top of the cuff before they can be aspirated.
- Use PEEP
Impaired mucocilliary clearance during mechanical ventilation due to the use of an artificial airway may lead to increased secretion retention and buildup in the lungs.
Trauma and edema may also result from the use of artificial airways.
Tracheo-esophageal fistula, a rare complication of long term mechanical ventilation creates a connection between the trachea and esophagus. Gastric distention may then result as air passes into the esophagus rather than solely the trachea.
Hypervolemia (fluid overload) can occur as a result of decreased cardiac output associated with positive pressure ventilation. Decreased cardiac output decreases perfusion of the kidneys which also decreases the production of urine as a result.
Stress ulcers may occur in the GI system of patients receiving mechanical ventilation for greater than 48 hours.
Gastric distention may occur during non-invasive ventilation when using high inspiratory pressures.
Respiratory muscle catabolism may result due to underfeeding of the patient.
Increased metabolic rate
Patient-ventilator asynchrony can lead to all sorts of problems. Delay of ventilator liberation…
Inappropriate flow, I-time, tidal volume, rate
Loss of power or gas source
Vent circuit leaks