Alveolar rupture appears to require sustained hyperexpansion of fragile alveoli. Despite the presumed importance of peak tidal alveolar pressure, there are many contributing predisposing variables: necrotizing and heterogeneous lung pathology, youth, copious retained airway secretions, and extended duration of positive-pressure ventilation (Tib]®!). As major determinants of peak and mean transalveolar pressures, minute ventilation requirements and high levels of PEEP (positive end-expiratory pressure) contribute to the hazard. Peak dynamic and static airway pressures ( PD and PS) appear to contribute most to the multivariate risk equation; when considered separately from its influence on inspiratory pressure, PEEP contributes little to the risk of barotrauma.
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As a general rule, high peak pressures applied to a stiff lung cause less alveolar stretch than the same pressures applied to a compliant lung. Pneumothorax becomes much more likely at peak ventilator cycling pressures above 40 cmH2O. However, the inherent susceptibility of lung tissue to rupture, chest wall compliance, and the degree of regional inhomogeneity also play crucial roles. Largely for these reasons, there is no sharp threshold value of peak ventilator cycling pressure below which lung rupture does not occur. A peak static (plateau) pressure above 35 cmH 2O usually achieves or exceeds the alveolar volume corresponding to total lung capacity in a patient with a normal chest wall. However, when the chest wall stiffens, higher plateau pressures may be well tolerated. Secretions, blood clots, or foreign objects in the airway can give rise to heterogeneity or ball-valve mechanisms that encourage barotrauma. The crucial roles of parenchymal inhomogeneity and inflammation in producing barotrauma may explain why pneumothorax tends to develop 1 to 3 weeks after the onset of diffuse lung injury, when some regions are healing while others remain actively inflamed.
Diagnosis of barotrauma
Pneumothorax frequently presents with tachypnea, respiratory distress, tachycardia, diaphoresis, cyanosis, or agitation. In patients receiving volume-cycled ventilation, peak inspiratory (and peak static) airway pressures typically increase, and compliance falls as pneumothorax develops, particularly if tension is present. Volume-cycled ventilators may 'pressure limit' or 'pop off', resulting in ineffective ventilation. During pressure-controlled ventilation, tidal volume and/or minute ventilation decrease, while airway pressures remain unaffected.
Massive gas trapping and auto-PEEP effectively mimic tension pneumothorax, particularly if hyperinflation or infiltration is asymmetrically distributed. Tension is reflected in elevations of central venous, right atrial, and pulmonary arterial pressures.
Two useful markers of occult pneumothorax visible on supine films are the deep sulcus sign and hyperlucency centered over the ipsilateral abdominal upper quadrant. In bedridden patients, a lateral decubitus view facilitates visualization by allowing air to collect along the upper margin of the hemithorax. An expiratory chest film thickens the stripe of pleural gas. Pneumothorax under tension can be strongly suspected on a single film when diaphragmatic inversion or extreme mediastinal shift occurs. Obtaining a sequence of films to demonstrate progressive migration of mediastinal contents into the contralateral hemithorax delays diagnosis but confirms validity. Life-threatening tension can exist without complete lung collapse or mediastinal displacement if the lung adheres to the pleura or is densely infiltrated. Tension without mediastinal shift may also develop if the airway becomes obstructed, or the mediastinum is immobilized by infection, fibrosis, neoplasm, or previous surgery.
Thoracic CT scanning is an invaluable aid in determining whether a lucency represents parenchymal or pleural air. Indeed, accurate chest tube placement into a loculated pocket of gas or fluid may require CT-guided insertion.
Management of pneumothorax
The key interventions aimed at avoiding barotrauma (Ta.b.!§...2.) are as follows.
1. Treat the underlying disease, particularly suppurative processes.
2. Relieve bronchospasm and maintain effective bronchial hygiene, but minimize unnecessary coughing.
3. Reduce minute ventilation requirement by treating agitation, fever, metabolic acidosis, and bronchospasm. Consider sedation (or paralysis) to enforce hypoventilation and permissive hypercapnia.
4. Reduce peak and mean alveolar pressures by limiting PEEP and auto-PEEP, using small tidal volumes, and increasing the percentage of spontaneous versus machine-aided breaths.
5. Drain the pleural space of air using the least effective suction.
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Table 2 Preventing ventilator-related lung rupture
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