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Oxygen Therapy Dr.Dhaher JS Al-habbo FRCP London UK Assistant Professor in Medicine DEPARTMENT OF MEDICINE 1 Oxygen Therapy • Oxygen was discovered independently by the Swedish apothecary Karl W.Scheele, in 1772, and by the English amateur chemist Joseph Priestly,in August 1774. • Priestley first liberated oxygen by intensely heating 'mercurius calcinatus' (mercuric oxide) placed over liquid mercury in a closed vessel. He called this new gas "dephlogisticated air, "oxygenated." 2 Karl W.Scheele in 1772 Joseph Priestly in1774 3 Oxygen Therapy • Joseph Priestley and Carl Wilhelm Scheele both independently discovered oxygen, but Priestly is usually given credit for the discovery. • Priestley called the gas produced in his experiments 'dephlogisticated air' and Scheele called his 'fire air'. • The name oxygen was created by Antoine Lavoisier who incorrectly believed that oxygen was necessary to form all acids. The Element Oxygen • • • • • • • • • Atomic Number: 8 Atomic Weight: 15.9994 Melting Point: 54.36 K (-218.79°C or -361.82°F) Boiling Point: 90.20 K (-182.95°C or -297.31°F) Density: 0.001429 grams per cubic centimeter Phase at Room Temperature: Gas Element Classification: Non-metal Period Number: 2 Group Number: 16 Group Name: Chalcoge Oxygen is a drug • • • • Colorless, odorless, tasteless gas, makes up 21% of room air .It is NOT flammable but does support combustion. should be regarded as a drug . Has a Drug Identification Number (DIN) Oxygen must be prescribed in all situations (except for the immediate management of critical illness). Oxygen should be prescribed to achieve a target saturation (Sp02), which should be written on the drug chart . 6 Basic Concepts of Oxygen • Composition of Room Air Nitrogen 78.08% ~78% Oxygen 20.946% ~21% Trace gases ~1% • Normal PO2 in arterial blood (PaO2) ≥ 95mmHg: • • • • decrease with age. PO2 in mitochondria ≥ 18 mmHg required to generate high energy phosphate bonds e.x ATP At rest the average adult male consumes about 225250 ml of O2/min. This can increase up to 10 folds during exercise. There’s very small O2 reserve that can be consumed within 4-6 minutes of cessation of spontaneous ventilation. 7 Oxygen content of blood • The theoretical maximum oxygen carrying capacity is 1.39 ml O2/g Hb, but direct measurement gives a capacity of 1.34 ml O2/g Hb.1.34 is also known as Hüfner’s constant. • The oxygen content of blood is the volume of oxygen carried in each 100 ml blood. It is calculated by: (O2 carried by Hb) + (O2 in solution) = (1.34 x Hb x SpO2 x 0.01) + (0.023 x PaO2) 10 Mechanisms of Hypoxia O2 Utilization O2 Utilization O2 Delivery O2 Delivery Shift from aerobic to anaerobic metabolism Increase Lactic acid Progressive Acidosis Cell Death 9 Basic Concepts of Oxygen Oxygen Cascade: Inspired = 150 mmHg at Sea Level ↓ Alveolar PO2= 103 ↓ Arterial=100 ↓ Capillary= 51 ↓ Mitochondrial= 1-10 (FiO2 expressed as 0.21-1.0 or 21- 100%) 10 Clinical Conditions With Increased Risk of Hypoxia • Myocardial infarction • Acute pulmonary disorders • Sepsis • Drug overdose • Liver failure • Head trauma • CHF • Hypovolemic shock • Blunt chest trauma • Acute neuromuscular disease • Acute abdomen (splinting) • Acute pancreatitis • Spinal cord injury Indications for Oxygen Therapy • • • • • • • • Tachypnea Cyanosis Restlessness Disorientation Cardiac arrhythmias Slow bounding pulse Tachycardia Hypertension • Dyspnea • Coma • Labored breathing (use of accessory muscles, nasal flaring) • Lethargy • Tremors/seizure activity Oxygen Therapy • “Generally speaking”, a patient who is breathing less than 12 and more than 24 times a minute needs oxygen of some kind 13 Oxygen therapy To ensure safe and effective treatment • Oxygen is required for the functioning and survival of all body tissues and deprivation for more than a few minutes is fatal. • In immediately life threatening situations oxygen should be administered. • Hypoxaemia. Acute hypotension. Breathing inadequacy. Trauma. Acute illness. CO poisoning. Severe anaemia. During the peri14 operative period. Oxygen therapy • Oxygen therapy Humidification Is recommended if more than 4 litres/min is delivered. • Helps prevent drying of mucous membranes. • Helps prevent the formation of tenacious sputum. • Oxygen concentrations will be affected with all delivery systems if not fitted correctly or tubing becomes kinked and ports 15 obstructed. The oxyhaemoglobin dissociation curve showing the relation between partial pressure of oxygen and haemoglobin saturation 16 Methods of Oxygen Delivery • Most common methods of oxygen delivery include – – – – Nasal Cannula Venturi Mask 100% Non-Rebreather Mask Mechanical Ventilation Oxygen Delivery Methods • Nasal Cannula • Comfortable, convenient, mouth breathing will not effect % of O2 delivered • Liters/min = % – – – – – 2 l/m = 24-28% 3 l/m = 28-30% 4 l/m = 32-36% 5 l/m = 36-40% 6 l/m = 40-44% • Cannot administer > 6 liters/minute (44%) Nasal Cannula • • • • • • Provides limited oxygen concentration Used when patients cannot tolerate mask Prongs and other uses Concentration of 24 to 44% Flow rate set between 1 to 6 liters For every liter per minute of flow delivered, the oxygen concentration the patient inhales increases by 4% 19 Venturi Mask Provides precise FiO2 Delivery concentrations of Blue 24% Yellow 28% White 31% Green 35% oxygen Pink 40% Entrainment valve to Concerns adjust oxygen delivery Tight seal is a must Interferes with Mostly used in the hospital eating/drinking setting for COPD Condensation collection patients 20 Venturi Mask Red 40% 10/L/M Blue 24% 2/L/M Yellow 35% 8/L/M White28% 4/L/M Green 60% 15/L/M Orange 31% 6/L/M 21 Oxygen Delivery Methods 100% Non-Rebreather • Delivery percentages – 6 l/min = 55 – 60 % – 8 l/min = 60 – 80 % – 10 l/min = 80 – 90 % – >12 l/min = 90 + % • Benefit: Has a one way expiratory valve that prevents rebreathing expired gases • Concern – May lead to O2 toxicity 100% Non-Rebreather Mask partial rebreather Mask 23 Oxygen Delivery Methods Mechanical Ventilation • Allows administration of 100% oxygen • Controls breathing pattern for patients who are unable to maintain adequate ventilation • Is a temporary support that “buys time” for correcting the primary pathologic process Indications for Mechanical Ventilation • Mechanical Failure • Ventilatory Failure • Oxygenation Failure • General Anesthesia • Post-Cardiac Arrest Mechanical Ventilation Two categories of ventilators – Negative pressure ventilators • Iron lung • Cuirass ventilator – Positive pressure ventilators • Two categories – Volume-cycled (volumepreset) – Pressure-cycled (pressurepreset) Iron Lung Mechanical Ventilation PEEP • Description – Maintains a preset positive airway pressure at the end of expiration – Increases PaO2 so that FiO2 can be decreased – Increases DO2 (amt of delivered O2 to tissue) – Maximizes pulmonary compliance – Minimized pulmonary shunting • Indications – PaO2 < 60 on FiO2 > 60% by recruiting dysfunctional alveoli – Increases intrapulmonary pressure after cardiac surgery to decrease intrathoracic bleeding (research does not support this idea) Mechanical Ventilation PEEP • Advantages – Improves PaO2 and SaO2 while allowing FiO2 to be decreased – Decreases the work of breathing – Keeps airways from closing at end expiration (esp. in pts with surfactant deficiency) • Disadvantages – Increased functional residual capacity (increases risk for barotrauma) – Can cause increased dead space and increased ICP – In pts with increased ICP, must assure CO2 elimination – Contraindicated: hypovolemia, drug induced low cardiac output, unilateral lung disease, COPD 29 Mechanical Ventilation CPAP • Description – Constant positive pressure is applied throughout the respiratory cycle to keep alveoli open • Indications – To wean without having to remove the ventilator and having to connect to additional equipment 31 Mechanical Ventilation CPAP • Advantages – Takes advantage of the ventilator alarm systems providing psychological security of the ventilator being there • Disadvantages – Patient may sense resistance as he breathes through the ventilator tubing Mechanical Ventilation Complications • Respiratory arrest from disconnection • Respiratory infection (VAP) • Acid-base imbalances • Oxygen toxicity • • • • Pneumothorax GI bleeding Barotrauma Decreased cardiac output Ventilator Weaning • • • • • • • Vital Capacity at least 10 – 15 ml/kg Tidal Volume > 5 ml/kg Resting minute volume > 10 L per minute ABG’s adequate on < 40% FiO2 Stable vital signs Intact airway protective reflexes (strong cough) Absence of dyspnea, neuromuscular fatigue, pain, diaphoresis, restlessness, use of accessory muscles Primary Acid-base Disorders: Respiratory Alkalosis Respiratory alkalosis - A primary disorder where the first change is a lowering of PaCO2, resulting in an elevated pH. Compensation (bringing the pH back down toward normal) is a secondary lowering of bicarbonate (HCO3) by the kidneys; this reduction in HCO3- is not metabolic acidosis, since it is not a primary process. Primary Event HCO3↑ pH ~ ------↓ PaCO2 Compensatory Event ↓HCO3- ↑ pH ~ -------↓ PaCO2 Primary Acid-base Disorders: Respiratory Acidosis Respiratory acidosis - A primary disorder where the first change is an elevation of PaCO2, resulting in decreased pH. Compensation (bringing pH back up toward normal) is a secondary retention of bicarbonate by the kidneys; this elevation of HCO3- is not metabolic alkalosis since it is not a primary process. Primary Event HCO3↓ pH ~ --------↑PaCO2 Compensatory Event ↑ HCO3- ↓ pH ~ --------↑ PaCO2 Primary Acid-base Disorders: Metabolic Acidosis Metabolic acidosis - A primary acid-base disorder where the first change is a lowering of HCO3-, resulting in decreased pH. Compensation (bringing pH back up toward normal) is a secondary hyperventilation; this lowering of PaCO2 is not respiratory alkalosis since it is not a primary process. Primary Event ↓ HCO3↓ pH ~ -----------PaCO2 Compensatory Event ↓HCO3↓ pH ~ -----------↓ PaCO2 Primary Acid-base Disorders: Metabolic Alkalosis Metabolic alkalosis - A primary acid-base disorder where the first change is an elevation of HCO3-, resulting in increased pH. Compensation is a secondary hypoventilation (increased PaCO2), which is not respiratory acidosis since it is not a primary process. Compensation for metabolic alkalosis (attempting to bring pH back down toward normal) is less predictable than for the other three acid-base disorders. ↑ pH ~ Primary Event Compensatory Event ↑ HCO3------------ ↑HCO3↑ pH ~ --------- PaCO2 PaCO2 ↑ Metabolic Acid-base Disorders: Some Clinical Causes METABOLIC ACIDOSIS ↓HCO3- & ↓ pH - Increased anion gap • lactic acidosis; ketoacidosis; drug poisonings (e.g., aspirin, ethylene glycol, methanol) - Normal anion gap • diarrhea; some kidney problems (e.g., renal tubular acidosis, interstitial nephritis) METABOLIC ALKALOSIS ↑ HCO3- & ↑ pH Chloride responsive (responds to NaCl or KCl therapy): contraction alkalosis, diuretics, corticosteroids, gastric suctioning, vomiting Chloride resistant: any hyperaldosterone state (e.g., Cushing’s syndrome, Bartter’s syndrome, severe K+ depletion) Respiratory Acid-base Disorders: Some Clinical Causes RESPIRATORY ACIDOSIS ↑PaCO2 & ↓ pH Central nervous system depression (e.g., drug overdose) Chest bellows dysfunction (e.g., Guillain-Barré syndrome, myasthenia gravis) Disease of lungs and/or upper airway (e.g., chronic obstructive lung disease, severe asthma attack, severe pulmonary edema) RESPIRATORY ALKALOSIS ↓PaCO2 & ↑ pH Hypoxemia (includes altitude) Anxiety Sepsis Any acute pulmonary insult (e.g., pneumonia, mild asthma attack, early pulmonary edema, pulmonary embolism) Production of the hemoglobin-hyerpolymers from pig blood Haemoglobin Haemoglobin Multimeres Polymerisation PEGylated Multimeres Monomeres Oligomeres Surface Modification Separation One-vessel- reaction 41 Hyperpolymeres Tamaulipas 10-2007