Ch. 17: Effects of PPV on the Pulmonary System

Pulmonary Complications

High pressures and large tidal volumes can cause lung injury.
Barotrauma – trauma caused by pressure.
Volutrauma – trauma caused by high distending volumes. High volume results in overdistension.
Pressure alone may not cause lung injury.
Biotrauma – alveolar overdistension leads to release of inflammatory mediators that can cause damage to other organs.
Shear stress – generated by repeated opening and closing of lung-units, causing tissue damage and loss of surfactant.
Atelectrauma – another term for shear stress injury and loss of surfactant.
VALI and VILI are often synonymous terms used to describe lung injury caused by or associated with mechanical ventilation.
- VALI – Ventilator associated lung injury.
- VILI – ventilator-induced lung injury.

When lung injury is identified as a consequence of mechanical ventilation.
Forms include – Ventilator Acquired Pneumonia, Air-trapping, Patient-Ventilator Dyssynchrony, Pneumothorax, and Pneumomediastinum.
Barotrauma, (extra alveolar air) – may be caused by pressures as low as 30-35 cm H2O.
Subcutaneous Emphysema – visible puffing of the skin over chest, neck, or face. Skin feels crepitant to touch. Clears without treatment. May be sign of pneumothorax.
Pneumomediastinum – may compress great vessels, esophagus. If severe, air must be removed as it may cause cardiac tamponade.
Pneumothorax – most common form of extra-alveolar air in “70s.” Less common now with intro of lower VT.
- A Pneumothorax may become a tension-pneumothorax in which air accumulates in pleural space but cannot escape. A tension pneumothorax is “Life-Threatening.”
- Treatment involves placement of a 14 -gauge needle into the anterior 2nd or 3rd intercostal space. RCP can decrease mean airway pressure and may need to manually ventilate the patient with 100% O2.
- Treatment for most pneumothoraces typically involves placement of a chest tube. However, pneumothoraces < 15-20% may only require close monitoring.
- A less than 15-20% pneumothorax will reabsorb at a rate of 2% per day in a patient breathing RA. Using supplemental O2 increases reabsorption 4 X.

Increasing volume now accepted as cause of overdistension caused by high transpulmonary pressure.
Overdistension causes excess stretching of alveolar cells.
Edema formation.
Release of chemical or inflammatory mediators = biotrauma.

Occurs at the level of the acinus.
Includes biotrauma, and atelectrauma.
VILI – resembles ARDS.
Practitioners must remember that PPV is not always benign.
Atelectrauma – injury that occurs because of repeated opening and closing of lung units at lower volumes. Can occur when low VT’s are used with inadequate levels of PEEP. Alveoli open on inspiration and close on expiration.
Shear Stress – occurs when an alveolus with normal compliance is adjacent to one that is atelectatic.
Surfactant Alteration – a secondary consequence of atelectrauma.
Biotrauma – Pulmonary cells distort with PPV when overstretched releasing cytokines and other chemical mediators.
Multiple-Organ Dysfunction Syndrome – Chemical mediators released in lung leak into blood vessels causing an inflammatory reaction.
Vascular Endothelial Injury – During PPV alveolar capillaries flatten, but the corner microvessels open wider.

Recent studies have shown that imposing too little stress on the diaphragm during MV by lowering the demands on a pt’s resp. muscles can induce resp. muscle weakness
Prolonged controlled MV can lead to significant decrease in cross- sectional area of diaphragmatic fibers.

In Spontaneous breathing patient lying supine – “the greatest displacement of the diaphragm occurs in the dependant region of the lung, near the back.”
When anesthesia is administered, the opposite occurs – the diaphragm moves cephalad.
Increase in Dead Space – the conductive airways increase in diameter with PPV, and so increase dead space.

Normal pulmonary blood flow favors gravity-dependent central areas.
PPV may shift pulmonary perfusion to periphery of lung rather than central areas.
PPV especially with high PEEP compresses capillaries and increases pulmonary vascular resistance.

Hypoventilation – inadequate ventilation leads to acidosis and subsequent effects.
Hyperventilation – leads to alkalosis and subsequent effects.
Metabolic Acidosis – requires greater ventilation to compensate. May require bicarbonate administration.

Increased RAW – in the spontaneously breathing patient, causes an impedance to both inspiratory and expiratory flow.
Increased RAW – with PPV, the “increased alveolar pressure is transmitted to the intrapleural space like an artificial PEEP effect.”

In the mechanically ventilated patient, defined as unintentional PEEP. Occurs when a new breath has begun before expiration has ended.
Can lead to barotrauma
“TE must be at least 3-4 time-constants for the lungs to empty 98% of the inspired volume.”
Dynamic hyperinflation – failure of lung volume to return to passive FRC.
Easiest way to detect auto-PEEP is to examine the flow-time curve.
CS = VT/(plateau – PEEP) However to be accurate PEEP should not be just set PEEP, but all or total PEEP.

O2 Toxicity – exact safe level not known. > 60% for more than 48 hours generally agreed to increase risk of toxicity.
Absorption Atelectasis - 100% O2 quickly absorbed out of hypoventilated lung units causing alveolar collapse.
Depression of Ventilation – may occur with COPD patients with CO2 retention.

Work of Breathing – can be high depending on mode.
As the support is decreased the patient’s WOB increases.
WOB is increased by spontaneous breathing through OETT and ventilator circuit
WOB imposed by artificial airway: Using the larges airway possible is always recommended.
Machine Sensitivity – sensitivity must be set appropriately for each patient in order to reduce WOB.

Note

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