Oxygen

• Oxygen is a drug, not just a "vital sign fixer." It has a dose-response curve and real toxicity at high doses or prolonged exposure. The goal is to treat hypoxemia, not to make every SpO₂ read 100%.
• Most critically ill adults: Target SpO₂ ≈ 92–96% (PaO₂ roughly 60–90 mmHg). Above this, outcome data show harm from hyperoxia in sepsis, post-cardiac arrest, stroke, and STEMI. Avoid sustained SpO₂ >96% in most patients once stabilized.
• Chronic hypercapnic respiratory disease (e.g., COPD with CO₂ retention, obesity hypoventilation, severe neuromuscular disease): Target SpO₂ ≈ 88–92% and avoid over-oxygenation, which can worsen hypercapnia and acidosis.
• Immediate high-FiO₂ use is appropriate when patients are unstable or peri-arrest (e.g., bag-mask or NRB at 15 L/min, 100% FiO₂ on the ventilator). Once ROSC or stabilization is achieved, FiO₂ should be titrated down quickly to avoid hyperoxia.
• Common delivery devices: Nasal cannula 1–6 L/min (FiO₂ ≈ 0.24–0.44), simple mask 5–10 L/min (FiO₂ ≈ 0.35–0.60), nonrebreather mask 10–15 L/min (FiO₂ up to ~0.80–0.90), Venturi mask (fixed FiO₂ 0.24–0.60), high-flow nasal cannula (up to 60 L/min, FiO₂ 0.21–1.0), and invasive/noninvasive ventilators (FiO₂ 0.21–1.0).
• Special high-flow indications: 100% FiO₂ via NRB or ETT for carbon monoxide poisoning or cyanide/CO co-toxicity; 12–15 L/min 100% O₂ NRB for cluster headache therapy.
• Key complications: Hyperoxia-related vasoconstriction (coronary, cerebral), increased oxidative stress, absorption atelectasis, expansion of gas-filled spaces (pneumothorax), and CO₂ retention in susceptible patients. Oxygen also poses a significant fire risk, especially with open flames, cautery, or smoking nearby.

• Generic Name: Oxygen (medical gas)
• Brand Names: Medical-grade oxygen supplied via bulk tanks, cylinders, or concentrators; various manufacturers – institution-specific

Medical gas; inhaled oxidant; essential metabolic substrate; vasoactive and neuroactive agent

Mechanism of Action:

• Oxygen therapy increases the fraction of inspired oxygen (FiO₂), raising alveolar partial pressure of oxygen (P_AO₂) according to the alveolar gas equation, increasing the gradient driving diffusion into pulmonary capillary blood
• In hypoxemic respiratory failure, oxygen improves arterial oxygen content (CaO₂) primarily by increasing hemoglobin saturation (SaO₂)
• Once hemoglobin is nearly fully saturated, further increases in PaO₂ contribute very little to CaO₂ but do increase dissolved oxygen and oxidative stress
• Hyperoxia can cause vasoconstriction in coronary and cerebral vessels, reduce cardiac output, and increase systemic vascular resistance
• High FiO₂ can lead to absorption atelectasis: nitrogen washout from alveoli leads to collapse in poorly ventilated units, worsening shunt
• In chronic hypercapnic patients, high FiO₂ can worsen CO₂ retention via reduced hypoxic respiratory drive, increased V/Q mismatch, and the Haldane effect (reduced CO₂ carrying capacity of oxyhemoglobin)

Pharmacokinetics:

• Absorption: Taken up across the alveolar–capillary membrane by passive diffusion, driven by partial pressure gradients
• Distribution: Transported largely bound to hemoglobin with a small fraction dissolved in plasma; tissue delivery depends on CaO₂ and cardiac output (DO₂ = CaO₂ × CO × 10)
• Metabolism: Consumed in mitochondrial oxidative phosphorylation to generate ATP and water; excess oxygen contributes to reactive oxygen species generation
• Elimination: Exhaled via the lungs as unused oxygen and as CO₂ produced by metabolism; no hepatic or renal clearance in the traditional sense
• Time Course: Arterial oxygenation responds within seconds to minutes to changes in FiO₂, but the clinical impact on tissue hypoxia and lactate may lag depending on perfusion and underlying pathology

• Documented hypoxemia: PaO₂ <60 mmHg or SpO₂ <90–92% on room air (or below individualized target in chronic lung disease)
• Acute respiratory distress with clinical suspicion for hypoxemia while definitive assessment (SpO₂/ABG) is obtained
• Acute hypoxemic respiratory failure (e.g., pneumonia, ARDS, pulmonary edema, PE) as part of supportive care while the underlying cause is addressed
• Peri-arrest and cardiac arrest: 100% FiO₂ during resuscitation; FiO₂ titrated down after ROSC to avoid hyperoxia
• Shock states (sepsis, cardiogenic, obstructive, hypovolemic) with impaired tissue oxygen delivery; oxygen improves CaO₂ while hemodynamics are corrected
• Carbon monoxide poisoning and smoke inhalation: high-flow 100% oxygen to accelerate CO elimination; hyperbaric oxygen in selected cases
• Cluster headache: high-flow 100% O₂ delivered via NRB at 12–15 L/min for abortive therapy
• Periprocedural oxygenation for sedation, RSI preoxygenation, and transport of critically ill patients

Available Forms:

• Medical-grade oxygen gas: bulk liquid oxygen systems, compressed gas cylinders (various sizes), and oxygen concentrators
• Delivery systems: nasal cannula, simple face mask, nonrebreather mask, Venturi mask, high-flow nasal cannula (HFNC), noninvasive ventilation (BiPAP/CPAP), invasive mechanical ventilation, and hyperbaric oxygen chambers

Delivery Devices & Typical FiO₂ / Flows (Adult):

Dosing – Practical Titration Targets (Adults):

Additional Dosing & Administration Notes:

• Titrate oxygen to the lowest FiO₂ that achieves the target saturation appropriate for the clinical context; reassess targets regularly as the patient improves or decompensates
• Pulse oximetry has limitations in shock, severe anemia, vasoconstriction, dark skin pigmentation, or dyshemoglobinemias; use ABG/venous gas and co-oximetry when accuracy is in doubt
• In ARDS, lung-protective ventilation, appropriate PEEP, prone positioning, and hemodynamic optimization often have greater impact than simply turning up FiO₂
• Preoxygenation for RSI focuses on maximizing oxygen reservoir and denitrogenation (e.g., 3–5 minutes of high-flow NC/NRB and/or NIV/HFNC) to prolong safe apnea time; high FiO₂ is appropriate in this setting, then reduced once the airway is secured and the patient is stable
• Home oxygen and long-term oxygen therapy require separate assessment (e.g., resting PaO₂ ≤55 mmHg or SpO₂ ≤88%); this reference focuses on acute ED/ICU use

Absolute Contraindications:

• No absolute contraindications in hypoxemic or critically ill patients when oxygen is indicated and titrated appropriately

Major Precautions:

• Chronic hypercapnic respiratory failure (COPD, obesity hypoventilation, some neuromuscular diseases): Avoid over-oxygenation; monitor PaCO₂ and pH when increasing FiO₂
• Acute coronary syndromes and ischemic stroke: Avoid routine oxygen if SpO₂ is normal; hyperoxia may worsen outcomes via vasoconstriction and oxidative stress
• Post-cardiac arrest, sepsis, and other critical illness: Emerging data associate hyperoxia with worse outcomes; titrate oxygen down once hypoxemia is corrected
• Premature neonates: High FiO₂ is associated with retinopathy of prematurity and oxidative lung injury; neonatal protocols use carefully titrated oxygen

Common / Important:

• Dryness of nasal passages and upper airway; epistaxis at higher nasal cannula flows without humidification
• Mild absorption atelectasis at moderate FiO₂, especially in patients with low lung volumes
• CO₂ retention and narcosis in susceptible hypercapnic patients when FiO₂ is increased excessively
• Mask intolerance, claustrophobia, and difficulty eating or speaking with face masks or NIV interfaces

Serious:

• Hyperoxic vasoconstriction: Reduced coronary or cerebral blood flow, potentially worsening outcomes in MI, stroke, and post-arrest states
• Severe absorption atelectasis: High FiO₂ (particularly >0.8) with low PEEP, exacerbating shunt and hypoxemia
• Oxygen toxicity: Prolonged high FiO₂ exposure (e.g., >0.6 for many hours to days), contributing to diffuse lung injury and ARDS-like pathology
• Fire and explosion: Severe burns in oxygen-enriched environments with ignition sources
• Retinopathy of prematurity: In premature neonates exposed to high FiO₂

COPD & Chronic Hypercapnic Disease:

• Use controlled oxygen delivery (Venturi mask or low-flow nasal cannula) with target SpO₂ 88–92%
• Monitor ABG for CO₂ retention and acidosis when titrating oxygen upward
• Consider early escalation to noninvasive ventilation if work of breathing increases or CO₂ rises

Cardiac & Stroke Patients:

• Avoid routine oxygen therapy in normoxemic patients with acute coronary syndrome or stroke
• Only administer oxygen if SpO₂ <90–92%; target SpO₂ 92–96%
• Hyperoxia may cause coronary and cerebral vasoconstriction, potentially worsening outcomes

Post-Cardiac Arrest:

• Use 100% FiO₂ during active resuscitation
• After ROSC, rapidly titrate FiO₂ down to avoid hyperoxia (target SpO₂ 94–98%)
• Monitor with frequent ABGs and adjust based on PaO₂ and clinical status

Pregnancy & Lactation:

• Oxygen is safe and indicated for maternal hypoxemia
• Fetal oxygenation depends on maternal oxygen delivery; treat maternal hypoxemia appropriately

Pediatric & Neonatal:

• Neonates, especially premature infants, are at risk for retinopathy of prematurity and bronchopulmonary dysplasia with prolonged high FiO₂
• Use targeted oxygen saturation ranges per neonatal/pediatric protocols

Clinical Monitoring:

• Continuous pulse oximetry for any patient on supplemental oxygen, with regular documentation of SpO₂ trends and FiO₂/flow settings
• Respiratory rate, work of breathing, accessory muscle use, mental status, and ability to speak in sentences
• Hemodynamics: blood pressure, heart rate, and perfusion, particularly when high FiO₂ is used in shock or post-arrest patients

Laboratory Monitoring:

• ABGs or venous blood gases with co-oximetry when needed to assess PaO₂, PaCO₂, pH, lactate, and dyshemoglobins in unstable or complex patients
• For CO poisoning: Carboxyhemoglobin levels via co-oximetry (pulse oximetry is unreliable)

For High-Flow and Ventilated Patients:

• Ventilator parameters (FiO₂, PEEP, tidal volume, plateau pressure)
• Imaging (CXR, POCUS) to assess lung recruitment and complications

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• 4. Kilgannon, J. H., Jones, A. E., Shapiro, N. I., Angelos, M. G., Milcarek, B., Hunter, K., Parrillo, J. E., & Trzeciak, S. (2010). Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality. JAMA, 303(21), 2165–2171. https://doi.org/10.1001/jama.2010.707
• 5. Chu, D. K., Kim, L. H.-Y., Young, P. J., Zamiri, N., Almenawer, S. A., Jaeschke, R., Szczeklik, W., Schünemann, H. J., Neary, J. D., & Alhazzani, W. (2018). Mortality and morbidity in acutely ill adults treated with liberal versus conservative oxygen therapy (IOTA): A systematic review and meta-analysis. Lancet, 391(10131), 1693–1705. https://doi.org/10.1016/S0140-6736(18)30479-3