Pulmonary Alterations and Mechanical Ventilation (Video Notes)

A set of Q&A flashcards covering pulmonary anatomy, diffusion, ABG interpretation, oxygen therapy, ventilation, ARDS, thoracic trauma, VAP prevention, and PE management.

Endotracheal tube placement relative to the carina

2–3 cm above the carina to ensure both lungs inflate and to prevent single-lung ventilation.

Pleural membranes and their function

Parietal pleura lines the chest wall; visceral pleura covers the lung; pleural fluid allows sliding for normal lung movement.

Pleural pressure and lung inflation

Negative intrapleural pressure (about -5 cm H2O) between the pleura helps keep the lungs inflated.

Type II alveolar cells function

Produce surfactant, which lowers surface tension, increases compliance, and prevents alveolar collapse.

Ventilation, perfusion, diffusion definitions

Ventilation: air movement in/out; Perfusion: blood flow through pulmonary capillaries; Diffusion: gas movement across the alveolar-capillary membrane.

Factors affecting alveolar diffusion

Surface area, membrane thickness, partial pressures of gases, and gas solubility (CO2 diffuses ~20x faster than O2).

Oxygen transport and saturation measurement

Oxygen is ~97% bound to hemoglobin (SaO2) and ~3% dissolved (PaO2); saturation measured by SaO2; PaO2 from ABG.

Normal ABG values

pH 7.35–7.45; PaO2 80–100 mmHg; SaO2 93–99%; PaCO2 35–45 mmHg; HCO3- 22–26 mEq/L.

ABG parameter that indicates ventilation status

PaCO2; high PaCO2 indicates hypoventilation, low PaCO2 indicates hyperventilation.

Signs of hypoxemia

Tachypnea, dyspnea, use of accessory muscles, restlessness, agitation, confusion; tachycardia, hypertension; chest pain, dysrhythmias; cyanosis is a late sign.

ABG interpretation steps (ROME approach)

1) Evaluate pH; 2) Evaluate PaCO2; 3) Evaluate HCO3-; 4) Determine primary disorder; 5) Determine compensation; 6) Evaluate oxygenation; 7) Compare with prior ABGs.

Correction vs. compensation in ABG interpretation

Correction is when the same system changes to normalize pH; compensation is when the other system adjusts to help normalize pH.

Shunt vs. dead space vs. normal ventilation units

Shunt: perfusion exceeds ventilation with no gas exchange; Deadspace: ventilation without perfusion; Normal unit: balanced ventilation and perfusion.

Primary respiratory vs metabolic acid-base disorders

Respiratory disorders involve PaCO2; metabolic disorders involve HCO3-; pH shows the overall balance and guides diagnosis.

Oxygen therapy devices and approximate FiO2 ranges

Nasal cannula 1–6 L/min (21–44%); HFNC up to 60 L/min (21–100%); Face mask ~40–60% (5–10 L/min); Venturi 25–60% (4–15 L/min); Nonrebreather 85–95% (10–15 L/min).

Non-invasive ventilation modes

CPAP provides continuous positive airway pressure; BiPAP provides different inspiratory (IPAP) and expiratory (EPAP) pressures.

Endotracheal tube placement indicators

Cuff inflation on ETT, correct placement shown by ETCO2 color change (purple to yellow), breath sounds equal bilaterally, chest X-ray confirmation.

Key ventilator modes: AC vs SIMV vs PSV

AC delivers preset tidal volume at a preset rate with possible patient-triggered breaths; SIMV delivers preset breaths with spontaneous breaths in between; PSV assists inspiratory effort to reduce work of breathing.

Purpose and typical value of PEEP

Maintains alveolar recruitment at end expiration to improve oxygenation; typical starting at 5 cm H2O, adjustable as needed.

Common complications of mechanical ventilation

Aspiration, barotrauma/volutrauma, VAP, decreased cardiac output with high PEEP, immobility‑related issues, GI problems, muscle weakness, self-extubation, ventilator dependence.

Weaning and spontaneous breathing trials (SBT)

SBT/CPAP trials assess readiness to wean: monitor RR, SpO2, tidal volume, work of breathing; stop criteria include RR >35, SpO2

Neuromuscular blockade and monitoring

NMBA reduces oxygen demand in severe disease; require sedation; BIS monitoring and Train-of-Four (TOF) to prevent over-paralysis; baseline TOF 4/4.

ARDS/ALI definitions

ALI: acute non-cardiogenic pulmonary edema; ARDS: more severe form with bilateral edema and refractory hypoxemia due to alveolar-capillary disruption.

Pathophysiology of ARDS

Surfactant dysfunction and alveolar flooding cause decreased lung compliance and severe hypoxemia despite ventilation; bilateral infiltrates on imaging.

Pneumothorax: open vs closed and management

Open: chest wound; cover with a three-sided occlusive dressing to allow air escape; Closed: no visible wound; can become tension pneumothorax requiring immediate decompression.

Hemothorax features and management

Blood in pleural space causing hypotension and hypovolemic shock; dullness to percussion; managed with chest tube drainage.

Flail chest

Multiple rib fractures causing paradoxical chest movement; reduces negative intrathoracic pressure and tidal volume; treat with oxygenation/ventilation and pain control; may need ventilation.

Chest tubes and thoracostomy care

Chest tubes drain air or fluid from pleural space to re-expand lung; monitor drainage quantity/type, assess for air leaks, ensure patency, and manage suction or water-seal as ordered.

Pulmonary embolism: diagnosis and treatment

Massive or nonmassive PE from DVT; CTA is gold standard; D-dimer supportive; treatments include heparin, thrombolysis, embolectomy; IVC filter if anticoagulation is contraindicated.

Key characteristics of Asthma exacerbation

Bronchoconstriction, airway inflammation, and increased mucus production leading to wheezing, dyspnea, and cough; often triggered by allergens, exercise, or infections.

Management of Asthma exacerbation

Short-acting beta-agonists (SABAs) for bronchodilation, systemic corticosteroids for inflammation, and oxygen therapy if hypoxic. May require heliox or magnesium sulfate in severe cases.

Key characteristics of COPD exacerbation

Acute worsening of respiratory symptoms (dyspnea, cough, sputum production) beyond daily variation; often triggered by bacterial or viral infections, or environmental pollutants.

Management of COPD exacerbation

Bronchodilators (SABAs, anticholinergics), systemic corticosteroids, antibiotics if bacterial infection suspected, and oxygen therapy aiming for SpO2 88-92%. Non-invasive ventilation (NIV) may be used for respiratory acidosis.

Peak Inspiratory Pressure (PIP) and Plateau Pressure (Pplat)

PIP is the maximum pressure during inspiration, reflecting airway resistance and lung compliance. Pplat is the pressure measured during an end-inspiratory pause, reflecting alveolar pressure and lung compliance, excluding airway resistance. Pplat is a better indicator of alveolar distention and risk of barotrauma.