Oxygen Therapy - CVTS Reference: Cardiopulmonary & CASH (10 Marks)

1. DEFINITION AND PHYSIOLOGICAL BASIS

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

DO2 = Cardiac Output × [(Hb × 1.360 × % Arterial Saturation) + (PaO2 × 0.0030)]

2. INDICATIONS FOR OXYGEN THERAPY

A. Definite Indications

• Arterial hypoxemia: PaO2 < 60 mmHg or SaO2 < 90% - the most certain indication
• Cardiac or respiratory arrest: 100% O2 is mandatory
• Carbon monoxide (CO) poisoning: 100% O2 by non-rebreather mask; reduces carboxyhemoglobin half-life from 4-5 hours (room air) to ~1 hour
• Shock states: hemorrhagic, vasodilatory, low cardiac output, obstructive - all lead to tissue hypoxia and benefit from supplemental O2
• Severe trauma: until tissue hypoxia is excluded

B. Cardiopulmonary Specific Indications

• Acute Myocardial Infarction (AMI): Only in patients with hypoxemia (SpO2 < 90%), signs of heart failure, shock, or respiratory distress. The AHA does NOT recommend routine O2 in normoxic AMI patients. A randomized trial of STEMI patients showed O2 increased infarct size (assessed by peak enzymes and cardiac MRI at 6 months) compared to room air
• Heart failure / cardiogenic shock: O2 relieves tissue hypoxia by improving delivery
• Pulmonary hypertension / Cor pulmonale: O2 relieves hypoxic pulmonary vasoconstriction, decreases pulmonary vascular resistance, improves CO, lessens renal vasoconstriction, and improves urinary sodium excretion. SpO2 < 90% at rest, exercise, or sleep is the threshold for supplemental O2
• Post-cardiac arrest: Titrate to SpO2 94-99% to prevent oxygen toxicity during reperfusion

C. Acute Stroke

3. CONTRAINDICATIONS

• Relative: COPD patients with CO2 retention (PaCO2 > 40 mmHg) - administer cautiously, recognizing risk of respiratory acidosis. Do NOT withhold oxygen, but titrate carefully.
• Never withhold oxygen from a hypoxemic patient for fear of complications.

4. METHODS OF OXYGEN DELIVERY (Devices)

A. Low-Flow Systems

B. High-Flow Systems

• Uses the Bernoulli effect and jet mixing to deliver precise, controlled FiO2
• Available in 24%, 28%, 31%, 35%, 40%, 60% FiO2 settings
• Preferred in COPD patients where precise O2 titration is needed
• "Titratable" - used more in inpatient/ICU settings than ED

• Uses high-pressure O2, air blender, humidifier, and large-bore tubing
• Delivers flow rates often exceeding 60 L/min
• Benefits: washes out nasopharyngeal dead space, provides PEEP effect, improves mucociliary clearance, reduces work of breathing
• Post-cardiothoracic surgery: A landmark trial of 830 cardiothoracic surgical patients showed HFNC was equivalent to BiPAP for post-extubation respiratory failure. Prophylactic HFNC immediately after extubation following cardiothoracic surgery reduced reintubation and escalation of respiratory support compared with conventional O2 therapy.

5. MONITORING

• Pulse oximetry (SpO2): Non-invasive; target SpO2 ≥ 94% in most patients (94-98% in general; 88-92% in COPD)
• Arterial Blood Gas (ABG): PaO2, PaCO2, pH - essential in COPD/CO2 retainers
• Measurements in pulmonary hypertension patients: at rest, with exertion, and during sleep
• Normal arterial PaO2 = 75-100 mmHg; Hypoxemic respiratory failure = PaO2 < 60 mmHg

6. HAZARDS AND COMPLICATIONS (CASH Perspective)

A. Oxygen Toxicity (Pulmonary)

• Occurs with prolonged high FiO2 (>60%)
• Free radicals overwhelm cellular detoxification machinery
• Histopathology: tissue inflammation, capillary leak, cellular necrosis and apoptosis, septal fibrosis
• Clinically: tracheobronchitis, ARDS-like picture

B. Resorption Atelectasis

• High FiO2 washes out alveolar nitrogen (the "splint" gas)
• Alveolar O2 is absorbed faster than ventilation replaces it
• Result: alveolar collapse - worsens V/Q mismatch and hypoxemia paradoxically
• Compounded by positive-pressure ventilation

C. Hyperoxia - Systemic Effects

• Generalized vasoconstriction due to regulatory mechanisms reducing O2 delivery
• Coronary vasoconstriction leading to increased myocardial injury and decreased cardiac function
• Cerebral vasoconstriction - decreased cerebral blood flow; poor outcomes in stroke and traumatic brain injury
• Hyperoxia is associated with increased mortality in neurologic injury and post-cardiac arrest patients

D. CO2 Retention (Hypercapnic Respiratory Failure)

• Classically in COPD: excess O2 blunts hypoxic drive to breathe, leads to hypercapnia and respiratory acidosis
• Mechanism debated but clinically significant
• Management: titrate to SpO2 88-92%; use Venturi mask for precise delivery

E. Fire Hazard

• O2 is highly combustible; must not be used near flames or by patients who smoke (facial burns have been reported from nasal cannula use while smoking)

7. OXYGEN THERAPY IN CARDIOPULMONARY RESUSCITATION (CPR/CASH)

• Goals of CPR: restore energy to the heart; ensure adequate O2 supply to the brain during resuscitation
• During arrest, blood flow (not O2 content) is the primary limiting factor
• 100% FiO2 (1.0) should be administered during active cardiac arrest in adults, children, and neonates to maximize O2 delivery to vital organs

• Titrate FiO2 to the lowest level required to achieve SpO2 ≥ 94%
• Avoid hyperoxemia during reperfusion: excess O2 generates free radicals during reperfusion phase causing reperfusion injury
• Target: SpO2 94-99%; avoid PaO2 > 300 mmHg
• Optimal FiO2 in the immediate post-arrest period remains debated but current consensus favors titrated, not 100%, O2

8. SPECIAL CLINICAL SCENARIOS IN CVTS

9. NURSING CONSIDERATIONS (CASH Context)

1. Assessment: Record baseline SpO2, respiratory rate, ABG values, level of consciousness before initiating O2
2. Device selection: Choose based on required FiO2 and patient tolerance; ensure proper fit to prevent pressure sores
3. Humidification: Oxygen should be humidified at flow rates >4 L/min to prevent drying of nasal/oral mucosa and inspissation of secretions
4. Documentation: Record device, flow rate, SpO2 response, time of initiation
5. Safety: No smoking, no flammable materials near O2 source; fire extinguisher accessible
6. Monitoring: Continuous pulse oximetry; ABG in CO2 retainers; check for signs of O2 toxicity with prolonged high FiO2
7. Weaning: Reduce O2 gradually when SpO2 stable; sudden withdrawal can cause rebound hypoxia
8. Patient education: Explain purpose, safety precautions, importance of keeping device in place

• Roberts and Hedges' Clinical Procedures in Emergency Medicine, Oxygen Therapy Chapter
• Fishman's Pulmonary Diseases and Disorders, 2-Volume Set - Pulmonary Hypertension / Postoperative Oxygen sections
• Murray & Nadel's Textbook of Respiratory Medicine - Devices and Interfaces
• Rosen's Emergency Medicine - Oxygen Therapy section
• AHA Guidelines for CPR and Emergency Cardiovascular Care (summarized in Roberts & Hedges' Box 3.1)