Untitled Quiz

Effects of Positive Pressure Ventilation on the Pulmonary System

• Positive pressure ventilation carries inherent risks and complications including ventilator-associated and ventilator-induced lung injury, gas distribution/blood flow effects, hypo/hyperventilation, air trapping, oxygen toxicity, increased work of breathing (WOB), patient-ventilator asynchrony, mechanical problems, and artificial airway complications.

• Lung Injury: High pressures (greater than 45cm H₂O) and volumes (10-12 mL/kg) during ventilation can cause lung injury (barotrauma, volutrauma). Volutrauma stems from overdistention due to high volumes, while barotrauma is caused by high pressures.

• Barotrauma (Extraalveolar Air): Positive pressure ventilation can cause alveolar rupture, leading to extraalveolar air leaks like subcutaneous emphysema, pneumothorax, pneumomediastinum, pneumoperitoneum, and pneumopericardium. This is a significant risk, particularly in patients with lung bullae or chest injury. Factors that increase risk are high peak airway pressures with low end-expiratory pressure, bullous lung disease (emphysema, tuberculosis), high levels of positive end-expiratory pressure (PEEP) with high tidal volumes (VT), aspiration of gastric acid, and necrotizing pneumonias.

• Pneumothorax: Extraalveolar air may accumulate in the pleural space, causing lung collapse and mediastinal shift. Diagnosis involves percussion (hyperresonance), absence of breath sounds, and imaging (radiographs). Treatment involves chest tube insertion.

• Tension Pneumothorax: A life-threatening complication where air is trapped in the pleural space, causing pressure buildup that shifts mediastinal structures. Immediate intervention is required.

• Pneumomediastinum: A more diffuse air-filled space surrounding the lung.

• Subcutaneous Emphysema: Air in the subcutaneous tissues, characterized by crepitus.

• Pneumoperitoneum: Air in the peritoneal cavity, potentially causing diaphragm dysfunction.

• Biotrauma: Repeated opening/closing of lung units during ventilation creates shear stress and surfactant loss. Excessive opening and closing of lung units may also affect inflammatory mediators potentially leading to multisystem organ failure (biotrauma).

• Ventilator-Associated Lung Injury (VALI): Lung injury resulting from mechanical ventilation.

• Ventilator-Induced Lung Injury (VILI): Microscopic lung injury occurring at the level of the acinus, it resembles ARDS. Difficult to diagnose in humans.

Chest Wall and Transpulmonary Pressures

• Transpulmonary Pressure (PL): Difference between alveolar (airway) pressure and intrapleural pressure.
• High PL values increase risk of lung injury.

Chest Wall Compliance and Protection from Overdistention

• Forces from ribs, muscles, diaphragm and abdomen create chest wall pressure.
• Forces on the diaphragm and vena cava increase with abdominal pressure (>20cmH2O).

Difficulty Triggering in Patients With Chronic Obstructive Pulmonary Disease (COPD)

• Reduced inspiratory capacity with increased WOB, decreased VE.
• Indicators of difficulty are: progressive peak pressure increase, decreased tidal volume.

Acid-Base Imbalances

• Hypoventilation: Increased PaCO₂ (hypercapnia) and acidosis (leading to right shift in oxyhemoglobin dissociation curve, reduced capacity to carry O₂), possible coma.
• Hyperventilation: Reduced PaCO₂ and alkalosis (leading to left shift of oxyhemoglobin dissociation curve, reduced O₂ delivery). Possible tetany, cerebral hypoxia.

Clinical and Electrocardiographic (ECG) Changes Associated With Respiratory Acidosis and Alkalosis

• Clinical signs: Cool skin (decreased PaCO₂), twitching, tetany.
• ECG changes: Elevated and peaked T waves, ST-segment depression, widened QRS complexes, prolonged P-R interval (with hypokalemia).
• ECG changes: Prolonged Q-T interval, low, rounded T waves, depressed ST segment, inverted T waves, inverted P waves, atrioventricular block, premature ventricular contractions, paroxysmal tachycardia, and atrial flutter (with hypokalemia).

Air Trapping (Auto-PEEP)

• Auto-PEEP is increased airway resistance during exhalation, caused by the time taken to exhale.
• Factors that increase risk are airway obstruction (COPD, asthma), short expiratory times, and mechanical devices that impede exhalation.
• This leads to an increase in functional residual capacity (FRC), reduced venous return, and increased cardiac workload.

Work of Breathing (WOB)

• Normal WOB is about 0.5 J/L. High WOB (>1.5J/L) leads to fatigue and difficulty weaning.
• Methods to reduce WOB include use of proper ET size, minimizing auto-PEEP and using appropriate ventilator settings (e.g., higher flow rate, shorter inspiratory time).

Patient-Ventilator Synchrony

• Trigger, flow, cycle, and mode synchrony can be difficult due to the delay in sensor response.
• Auto-PEEP can hinder patient-ventilator synchrony.

Ventilator Mechanical and Operational Hazards

• Malfunctions like disconnection, power issues, alarm failures, or humidification/heating issues can occur.
• Inadequate alarm systems and staffing issues can make detection and intervention of failures more difficult.
• Mechanical/operational issues can increase complications.