OXYGEN TOXICITY Prepared and presented by: Dr Debora, Dr.Gibonce-DEPARTMENT OF ANAESTHESIOLOGY AND ICU BMC19 th of May,2016.

OXYGEN TOXICITY OUTLINE a)Introduction b)Functions/Indications c)Measurements of O2 d)Mechanisms of O2 toxicity e)Protective mechanisms against Reactive Oxygen Species(ROS). g)Complications of Oxygen toxicity h)Take home message

INTRODUCTION Oxygen is a chemical element with symbol O and atomic number 8. By mass, oxygen is the third-most abundant element in the universe, after hydrogen and helium,comprising about 21% of atmospheric air. OXYGEN IS A DRUG AND IS PRESCRIBED!! Oxygen therapy is the administration of O2 at a concentration greater than a room air(21%) with a goal of treating/preventing symptoms and manifestations of hypoxia.

MEDICAL OXYGEN SOURCE The sources of medical O2 are: 1)Oxygen Cylinders. 2)Oxygen concentrators. 3) oxygen plant.

USES OF MEDICAL OXYGEN The aerobic metabolic system functions using the Krebs Cycle, a complex series of chemical reactions that use oxygen to convert nutrients (carbohydrates, fats, and protein) to carbon dioxide and adenosine triphosphate (ATP), an energy-rich compound.

INDICATIONS  The main indication of O2 thearpy is treatment/prevention of Hypoxia(i.e state of low O2 concentration reaching the tissues).

CAUSES OF HYPOXIA  Reduced partial pressure of oxygen in air.  Inadequate alveolar ventilation.  Impaired pulmonary uptake. 14-Jun-16 7  PO 2 in air Inadequate alveolar ventilation Inadequate blood flow to tissues Impaired O 2 uptake Poisoning or inadequate cellular enzymes

 Venous – arterial shunt.  Inadequate flow of blood to tissues.  Poisoning or inadequate cellular enzymes. 14-Jun-16 8  PO 2 in air Inadequate alveolar ventilation Inadequate blood flow to tissues Impaired O 2 uptake Poisoning or inadequate cellular enzymes

SIGNS OF HYPOXIA Generally the pt will present with signs of respiratory distress which include:  Dyspnea.  Tachypnea.  Severe hypoxaemia (decreased oxygen concentration in the blood)  Pulmonary hypertension.  Cyanosis,etc.

MEASUREMENTS OF O2 LEVELS IN THE BODY The most common methods used are: a) Pulse oxymeter. b) Arterial blood gases analysis(ABG).  ABG is more accurate than Pulse oxymeter because it measures the actual concentration of O2 in the blood in relation to other blood gases.  Factors hindering P/oxymeter accuracy are:-poor peripheral blood flow(i.e hypotension),coldness,nail polish,etc.

Need of O2 is determined by: Clinical evaluation plus measured O2 level- By- Pulse oxymeter or ABG Generally agreed indication for O2 therapy-Persistent SPO2<90%.

OXYGEN TOXICITY  Not only is too little oxygen a problem, too much is as well. Defn:  Oxygen toxicity is a condition resulting from the harmful effects of breathing molecular oxygen (O2) at increased partial pressures.

Exposure time matters alot… Oxygen toxicity – can occur with Fio2 > 60% longer than 36 hrs Fio2>80%longer than 24 hrs Fio2>100%longer than 12hrs

MECHANISM OF OXYGEN TOXICITY  Usually Reactive Oxygen Species (ROS ) are produced during normal physiological processes like Electron Transport Chain(ETC),etc.  The most commonly produced ROS are: - Superoxide anion (O 2 - ) -Hydroxyl radical (OH) -Hydrogen peroxide (H 2 O 2 ) -Hypochlorous acid (HOCl )

ELECTRON TRANSPORT CHAIN

 Under normal circumstances the body is able to handle the ROS produced using anti oxidants but can be overwhelmed incase of excessive production of ROS,hence toxic effects of O2.  Glutathione is the mother of all anti oxidants.  Others Anti-oxidants are catalase,superoxide dismutase,vitaminC,E.

SOURCES OF ROS Reactive Oxygen Species (ROS) are a natural occurrence:  Accidental products of nonenzymatic and enzymatic processes.  Deliberate production by immune cells killing pathogens.  UV irradiation, radioactive chemicals, Xrays

HYDROXYL RADICAL Is the most reactive oxygen species OH  Two nonenzymatic reactions can form OH by transfer of single e-.  Metals Fe 2+ or Cu + are kept sequestered.

Harmful effects of these radicals… Oxygen radicals react with cell components: Lipid peroxidation of membranes. Increased permeability → influx Ca 2+ → mitochondrial damage. Proteins oxidized and degraded. DNA oxidized → breakage.

PROTECTIVE MECHANISMS OF THE BODY  Antioxidant scavenging enzymes (red).  Nonenzymatic antioxidants (free radical scavengers).  Compartmentalization.  Repair of damaged components.  Metal sequestration. SOD = superoxide dismutase converts O2- to H2O2 GSH = glutathione Catalase=reduces H2O2 to H2O

COMPLICATIONS OF OXYGEN TOXICITY  The common affected sytems/organs are:- a) CNS - Convulsions(tonic–clonic seizure). b) Pulmonary - Atelectasis. c) Eyes - Retinal damage.

TAKE HOME MESSAGE  We need to emphasize on good use of O2 due to the following reasons: a) Detrimental effects of unnecessary O2 therapy. b) Cost effective utilization of O2. - Very expensive. c) Risk of fire hazards. -Highly inflammable gas. -Needs good and safe storage conditions.

SUGGESTIONS  O2 therapy should be used only if there are confirmed indications.  Causative problem of Hypoxia should be identified and intervened appropriately-giving O2 alone is not a solution.  Use of appropriate P/oxymeter size to age.  Close monitoring of the pts on O2 therapy(i.e O2 saturation level).  Avoid combustive materials close to cylinders,eg- oil,kerosene,etc.

Refferences: Clinical Anesthesia-Barash.,7 th ed. Clinical Anesthesia-Morgan and Mikhail.,5 th ed. Harper's Biochemistry.,30 th ed. The ICU Book..,4 th ed.