HYPOXIA AND OXYGEN THERAPY Dr. Sami Abu-Halaweh Associate prof The University of Jordan Jordan University Hospital

HYPOXIA (1) Definition HYPOXIA:- is reduced Oxygen for tissue respiration Anoxia:- complete absence of oxygen in tissues Hypoxia Vs Hypoxemia

PHYSIOLOGICAL PRINCIPLES (1) Oxygen Delivery to the Tissues This depends on three important factors: 1- The SUPPLY of oxygen during inspiration 2- The TRANSFER of oxygen from the alveoli to the pulmonary capillaries 3- The TRANSPORTATION of oxygen by the blood to the tissues

PHYSIOLOGICAL PRINCIPLES (CONT.) (2) Oxygen Cascade This represents the series of partial pressure of oxygen (PO2) decline from Atmosphere (at sea level) to the Mitochondria in the cell. It is formed by the following pressures: 1- Atmospheric Air = 160 mmHg (21 KPa) 2- Humidified Tracheal Gas = 150 mmHg (19.8 KPa) 3- The Alveolar Gas = 106 mmHg (14 KPa) 4- The Arterial Blood = 100 mmHg (13.3 KPa) 5- The Capillary Blood = mmHg (6.7 KPa) 6- The Mitochondria = mmHg (1-5 KPa) Reduction of PO2 at any stage in the cascade causes reduction in subsequent steps. This risks inadequate mitochondrial PO2 for AEROBIC METABOLISM.

PHYSILOGICAL PRINCIPLES (CONT.) (3) Oxygen Flux Is the same as Available Oxygen or Oxygen Delivery, which is the amount of oxygen delivered to the tissues per unit time (usually per minute). This equals: COxO2 bound to Haemoglobin + O2 dissolved in plasma = CO/100(HbxSaO2x1.34)+(PaO2x0.003) Where: CO = Cardiac Output in ml/min Hb = Haemoglobin Concentration in g/dL SaO2 = Arterial Oxygen Saturation of Haemoglobin 1.34 = Huefner`s Constant (amount of oxygen in ml bound to each gram of haemoglobin) PaO2 = Partial Pressure of Oxygen in Arterial Blood in mmHg = Amount of Oxygen in ml dissolved in plasma per mmHg PaO2 THE AMOUNT OF OXYGEN FLUX IS NORMALLY ML/MIN OR ML/MIN/M 2

PHYSIOLOGICAL PRINCIPLES (CONT.) (4) Oxygen Consumption Is the amount of Oxygen consumed by the body per unit time (usually per minute). It is calculated as fallows: O2 consumption = CO x (Arterial Oxygen Content – Mixed Venous Oxygen Content) O2 Consumption = ml/min AT REST ( ml/min/m 2 ). It is increased in : Fever, Sepsis, Shivering, Restlessness, Hypercatabolism It is decreased in : Cooling, Paralysis, Mechanical Ventilation

HYPOXIA (CONT.) (2) Types of Hypoxia 1- Hypoxic Hypoxia in inadequate arterial oxygenation 2- Anemic Hypoxia in inadequate hemoglobin content 3- Circulatory Hypoxia in inadequate perfusion 4- Histotoxic Hypoxia in inability of the cell to utilize oxygen

HYPOXIA (CONT.) (3) Acute Hypoxia It can be due to : 1- Respiratory depression 2- Airway obstruction 3- Atetectasis 4- Ventilation/Perfusion mismatch 5- Reduced Functional Residual Capacity (FRC)

HYPOXIA (CONT.) (4) Direct Effects of Acute Hypoxia 1- Cyanosis 2- Confusion, Drowsiness 3- Excitement 4- Headache 5- Nausea 6- Myocardial Depression 7- Arrhythmias 8- Bradycardia 9- Renal Impairment

HYPOXIA (CONT.) (5) Indirect Effects of Acute Hypoxia These are mediated through stimulation of Carotid and Aortic Bodies : 1- Tachycardia 2- Hypertension 3- Hyperventilation

HYPOXIA (CONT.) (6) Degrees of Acute Hypoxia Acute Hypoxia can cause the following according to the degree of oxygen saturation in arterial blood: % Saturation = Mental Impairment % Saturation = Severe Mental Impairment % Saturation = Unconsciousness

HYPOXIA (CONT.) (7) Chronic Hypoxia This develops after adaptation for high altitude and chronically developing lung diseases affecting oxygen transfer in the lung.

HYPOXIA (CONT.) (8) Effects of Chronic Hypoxia 1- Hyperventilation 2- Polycythaemia 3- Increased 2-3-DPG 4- Proliferation of peripheral capillaries 5- Alteration in Intracellular Oxidative Enzymes

Hypoxic Hypoxia → Normal O2 carrying capacity and blood flow → Low PaO2 Causes: → Low PO2 in inspired air- high altitude → Decreased pulmonary ventilation- airway obstruction, paralysis of respiratory muscle, narcotics → Defect in exchange of gases through the membrane → A-V shunts- cyanotic congenital heart disease

Characteristic features: → PaO2- 40 mm Hg; PvO2- 2 mm Hg → %O2 saturation- arterial 75%; venous 45% → O2 content- arterial 14 ml/dL; venous 9 ml/dL → O2 utilization- 5 ml/dL → A-V PO2 difference- 15 mm Hg

Hypoxic hypoxia Via peripheral chemoreceptors Respiratory center Increased pulmonary ventilation Reduced PaCO2 Shift to left of O2-Hb curve Reduced O2 release from Hb Tissue hypoxia

Anemic Hypoxia Arterial PO2 is normal Reduced Hb content Causes: (iv) Anemia (v) Carbon monoxide poisoning

Characteristic features: → PaO2- 95 mm Hg; PvO2- 40 mm Hg → Reduced % saturation of Hb → O2 content of blood is reduced Hypoxia is not severe at rest because of increase in 2,3 DPG Severe hypoxia during exercise

Carbon monoxide poisoning CO combines with Hb at the same point where O2 combines CO has 250 times more affinity than O2 Shifts O2-Hb dissociation curve to left Treated with 100% O2

Stagnant Hypoxia Normal Hb% and PaO 2 Reduced blood flow to tissues Causes: (iv) Circulatory failure (v) Hemorrhage

Histotoxic Hypoxia Tissue utilization of O2 is hampered Normal O2 supply to tissues Cause: cyanide poisoning

Characteristic features: → PO2- arterial 95 mm Hg; venous 90 mm Hg → %O2 saturation- arterial 97%; venous 96% → O2 content- arterial 19 ml/dL; venous 18.5 ml/dL

Treatment of hypoxia Oxygen administration is of importance in hypoxic hypoxia. A. Inhalation of 100% O2 at normal atmospheric pressure B. Hyperbaric oxygen therapy

OXYGEN THERAPY (CONT.) (2) Oxygen Therapy Apparatus Requirements 1- Control of Fractional Inspired Oxygen Concentration (FiO2) 2- Prevention of CO2-Accumulation 3- Minimal Resistance to Breathing 4- Acceptable to the Patient

OXYGEN THERAPY (1) Indications 1- Cardio Pulmonary Resuscitation (CPR) 2- Respiratory Failure 3- Cardiac Failure 4- Shock of any Cause 5- Increased Metabolic Demands 6- Carbon Monoxide (CO)-Poisoning 7- Postoperative States

Normobaric 100% O 2 therapy It is useful in hypoxic hypoxia. Dangers of inhaling 100% oxygen: - → Produce nasal congestion, throat pain, cough, substernal discomfort, etc by stimulating irritant receptors. → Cause bronchopneumonia if given for more than 24 hrs by inhibiting alveolar macrophages → Newborns should not be given more than 40% oxygen

Hyperbaric O 2 Therapy Useful in anemic, stagnant and histotoxic hypoxia Inhalation of 100% O2 at 1 atm can increase arterial PO2 to 673 mm Hg as it includes PCO2 of 40 mm Hg and PH2O of 47 mm Hg At 1 atmospheric pressure, oxygen dissolved in plasma is 2ml/dL (i.e 673 x 0.003) 3 atm of pure O2 will deliver resting O2 needs

Oxygen toxicity will occur early Inhibits tissue enzyme activity Cerebral vasoconstriction Muscular twitches,tinnitus,convulsions and coma

OXYGEN THERAPY (CONT.) (3) Types of Oxygen Therapy Apparatus 1- Fixed Performance Systems : FiO2 is independent of patients factors : A- High Flow Venturi -Type Mask B- Low Flow Anesthesia Breathing System (with CO2-absorber) 2- Variable Performance Systems : FiO2 depends upon O2-flow and patient`s factors : A- No Capacity Systems - Nasal Catheter with Low Flow B- Small Capacity Systems – a- Nasal Catheter with High Flow b- Simple Face Mask c- Tracheostomy Mask or T-Piece d- Face Tent C- Large Capacity Systems – a- Soft Plastic Mask b- Oxygen Head Box c- Oxygen Tent d- Incubator

OXYGEN THERAPY (CONT.) (4) Oxygen Toxicity 1- Retrolental Fibroplasia : In Neonates (especially prematures) if breathing Oxygen Concentration more than 40 % (FiO2 more than o.4) 2- Lung Toxicity : In Adults if breathing Oxygen Concentration more than 60 % (FiO2 more than 0.6) for a long time

OXYGEN THERAPY (CONT.) (5) Hazards of Oxygen Therapy 1- CO2 Narcosis 2- Barotrauma 3- Fires