Complications of Positive Pressure Ventilation
PPV can affect circulation because of the transmission of increased mean airway pressure
to the thoracic cavity.
With increased intrathoracic pressure, thoracic vessels are compressed resulting in
decreased venous return to the heart, decreased left ventricular end-diastolic volume
(preload), decreased CO, and hypotension. Mean airway pressure is further increased if
titrating PEEP (>5 cm H 2) to improve oxygenation.
As lung inflation pressures increase, risk of barotrauma increases.
o Patients with compliant lungs (e.g., COPD) are at greater risk for barotraumas.
o Air can escape into the pleural space from alveoli or interstitium, accumulate, and
become trapped causing a pneumothorax.
o For some patients, chest tubes may be placed prophylactically.
Pneumomediastinum usually begins with rupture of alveoli into the lung interstitium;
progressive air movement then occurs into the mediastinum and subcutaneous neck
tissue. This is commonly followed by pneumothorax.
Volutrauma in PPV relates to the lung injury that occurs when large tidal volumes are
used to ventilate noncompliant lungs (e.g., ARDS).
o Volutrauma results in alveolar fractures and movement of fluids and proteins into
the alveolar spaces.
Hypoventilation can be caused by inappropriate ventilator settings, leakage of air from
the ventilator tubing or around the ET tube or tracheostomy cuff, lung secretions or
obstruction, and low ventilation/perfusion ratio.
o Interventions include turning the patient every 1 to 2 hours, providing chest
physical therapy to lung areas with increased secretions, encouraging deep
breathing and coughing, and suctioning as needed.
Respiratory alkalosis can occur if the respiratory rate orTV is set too high (mechanical
overventilation) or if the patient receiving assisted ventilation is hyperventilating.
o If hyperventilation is spontaneous, it is important to determine the cause (e.g.,
hypoxemia, pain, fear, anxiety, or compensation for metabolic acidosis) and treat
Ventilator-associated pneumonia (VAP) is defined as a pneumonia that occurs 48 hours
or more after endotracheal intubation and occurs in 9% to 27% of all intubated patients
with 50% of the occurrences developing within the first 4 days of mechanical ventilation.
o Clinical evidence suggesting VAP includes fever, elevated white blood cell count,
purulent sputum, odorous sputum, crackles or rhonchi on auscultation, and
pulmonary infiltrates noted on chest x-ray. o Evidenced - based guidelines on VAP prevention include (1) HOB elevation at a
minimum of 30 degrees to 45 degrees unless medically contraindicated, (2) no
routine changes of the patient’s ventilator circuit tubing, and (3) the use of an ET
with a dorsal lumen above the cuff to allow continuous suctioning of secretions in
the subglottic area. Condensation that collects in the ventilator tubing should be
drained away from the patient as it collects.
Progressive fluid retention often occurs after 48 to 72 hours of PPV especially PPV with
PEEP. It is associated with decreased urinary output and increased sodium retention.
o Fluid balance changes may be due to decreased CO.
o Results include diminished renal perfusion, the release of renin with subsequent
production of angiotensin and aldosterone resulting in sodium and water
o Pressure changes within the thorax are associated with decreased release of atrial
natriuretic peptide, also causing sodium retention.
o As a part of the stress response, release of antidiuretic hormone (ADH) and
cortisol may be increased, contributing to sodium and water retention.
In patients with head injury, PPV, especially with PEEP, can impair cerebral blood flow.
Elevating the head of th