Oxygen Therapy: Definition, Types, Delivery Devices, and O2 Toxicity

Definition

1. Inspired partial pressure of O2
2. Alveolar ventilation
3. Pulmonary gas exchange
4. Oxygen-carrying capacity of blood (hemoglobin)
5. Cardiac output

• Roberts & Hedges' Clinical Procedures in Emergency Medicine

Indications

• Definite: Arterial hypoxemia - PaO2 < 60 mmHg or SaO2 < 90%
• Shock states: Hemorrhagic, septic, cardiogenic, obstructive - administer until hypoxia is excluded
• Carbon monoxide poisoning: 100% O2 via non-rebreather mask (reduces carboxyhemoglobin half-life from ~5 h to ~1 h)
• Cardiac arrest / resuscitation: 100% O2
• High-altitude illness: Low flow (1-2 L/min) for AMS; higher flows for HACE/HAPE

Note: O2 is NOT routinely indicated in acute MI without hypoxemia (may worsen infarct size), and routine use in stroke without documented hypoxia is not recommended by current guidelines.

Types of Oxygen Therapy Systems

1. Low-Flow Systems

• Flow: 1-6 L/min
• FiO2: ~24-45% (increases ~3-4% per L/min)
• Well tolerated, allows eating/speaking
• Limitation: FiO2 fluctuates with respiratory rate and tidal volume; requires nasal patency; high flows dry mucosa (humidification advised above 4 L/min)

• Flow: up to 15 L/min
• FiO2: ~50-70%
• Three-channel design; should not be confused with heated high-flow nasal cannula (HFNC)

• Flow: 5-10 L/min
• FiO2: ~35-60%
• Minimum flow of 5 L/min needed to flush exhaled CO2 from the mask
• Well tolerated; FiO2 still variable with breathing effort

2. Reservoir Systems

• Flow: 10-15 L/min
• FiO2: ~50-75%
• No one-way valves; patient rebreathes a small amount of exhaled gas (first portion from dead space, which is O2-rich)

• Flow: 10-15 L/min
• FiO2: ~60-95% (up to ~95% at 15 L/min when tightly sealed)
• One-way valves prevent rebreathing exhaled CO2
• First-line for critically ill patients requiring high FiO2
• Limitation: FiO2 varies with respiratory distress; cannot be titrated below 10 L/min

3. High-Flow Systems

• Flow: varies by valve color-coded for FiO2
• FiO2: precisely controlled at 24%, 28%, 31%, 35%, 40%, or 60%
• Based on the Bernoulli/Venturi principle - O2 jet creates a fixed entrainment of room air
• Best choice when precise FiO2 is needed (COPD, titrated therapy)

• Flow: up to 60 L/min of heated, humidified O2
• FiO2: 21-100%, titrated independently
• Provides positive nasopharyngeal pressure (~1 cmH2O per 10 L/min)
• Reduces work of breathing, flushes CO2 from anatomical dead space
• Evidence-based for acute hypoxemic respiratory failure; reduces need for intubation

• CPAP delivers continuous positive airway pressure
• BiPAP delivers two levels: IPAP (inspiratory) and EPAP (expiratory)
• FiO2: 21-100%
• Used for COPD exacerbations, cardiogenic pulmonary edema, OSA, hypoxemic failure

• FiO2: 21-100%
• Fully controlled delivery via endotracheal tube

4. Specialized Systems

• 100% O2 at >1 ATA (typically 2.0-3.0 ATA)
• Dramatically increases dissolved plasma O2
• Indications: CO poisoning, decompression sickness, gas gangrene, non-healing wounds, radiation necrosis

• Domiciliary O2 for COPD patients with resting PaO2 ≤ 55 mmHg (or ≤ 60 mmHg with cor pulmonale/polycythemia)
• Via concentrators (stationary) or portable liquid O2/cylinders
• Oxygen-conserving devices (pulse-dose systems, transtracheal catheters) reduce usage by 50-75%

Oxygen Delivery Devices at a Glance

Oxygen Toxicity

Biochemical Mechanism

• Lipid peroxidation - membrane dysfunction
• Protein oxidation - enzymatic failure
• DNA/nucleic acid damage - cell death or mutagenesis
• Fishman's Pulmonary Diseases and Disorders

Two Main Clinical Forms

1. Pulmonary Oxygen Toxicity (Low-Pressure / Normobaric)

• Occurs with FiO2 > 0.5 for prolonged periods (typically >12-24 h at high FiO2)
• Clinical toxicity generally absent when FiO2 < 0.5

• Exudative phase (days 3-4): Death of type I pneumocytes and endothelial cells, interstitial edema, neutrophil infiltration, alveolar exudate
• Proliferative phase: Type II pneumocyte and endothelial proliferation, fibroblast expansion, interstitial scarring

• Substernal chest pain and cough (tracheobronchitis)
• Decreased vital capacity and DLCO
• Reduced lung compliance
• Progressive ARDS-like picture at high exposures

1. Absorption atelectasis - Breathing high FiO2 washes out nitrogen (the "stent" that keeps alveoli open); alveolar collapse follows, worsened with 100% O2 pre-oxygenation
2. Hypercapnic respiratory failure (CO2 retention in COPD) - Mechanisms include: abolition of hypoxic pulmonary vasoconstriction (worsening V/Q mismatch), Haldane effect (O2 displaces CO2 from hemoglobin), and possible blunting of hypoxic drive
3. ARDS - High FiO2 in mechanically ventilated patients contributes to lung injury
4. Bronchopulmonary dysplasia (BPD) in premature neonates

2. CNS (Cerebral) Oxygen Toxicity (High-Pressure / Hyperbaric)

• Occurs at pO2 > 1.4-1.6 ATA (short duration exposure)
• Classic in diving and HBOT

• Visual disturbances (tunnel vision)
• Ear symptoms (tinnitus)
• Nausea
• Twitching (facial/lip muscles)
• Irritability
• Dizziness

Other Toxic Effects

• Retinopathy of prematurity (ROP): High O2 in premature infants causes abnormal retinal vascularization
• Oxygen-induced hypercapnia in COPD: Use Venturi mask to titrate to SpO2 88-92% in COPD
• Coronary effects: Hyperoxia causes coronary vasoconstriction and may worsen myocardial infarction - avoid in normoxic MI patients

Safe Thresholds (Clinical Guidance)

Key principle: Never withhold oxygen from a hypoxemic patient out of fear of complications - the risks of hypoxemia always outweigh those of judicious O2 use. However, titrate to the lowest effective FiO2 once the patient is stabilized.