Nitrous oxide, Oxygen and Hyperbaric Oxygen Dr Ashton Resident Anaesthesia

Nitrous oxide, 0xygen and hyperbaric oxygen

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  • 1.Nitrous oxide, Oxygen and Hyperbaric Oxygen Dr Ashton Resident Anaesthesia

2. Nitrous Oxide 1771-1772: Oxygen and nitrous oxide were discovered by Joseph Priestley. 1799: Sir Humprey Davy discovered the euphoric effects and called it laughing gas. 1884: Gardener Quincy Colton a travelling showman conducted a demonstration exhibiting the intoxicating effects of nitrous oxide 3. Horace wells a young dentist saw this and used nitrous oxide to extract one of his own teeth and felt no pain. January 20,1845: Horace Wells public demonstration was a failure. 1863: Introduced into dental practice on a large scale by Gardener Quincy Colton. 4. Preparation In laboratory: by allowing iron to react with nitric acid, Nitric oxide is produced first which is then reduced to nitrous oxide by an excess of iron. Commercially: By Heating ammonium nitrate to between 245 to 270C. This produces ammonia, nitrous oxide, nitrogen and nitrogen dioxide. Gases are passed through water scrubbers to remove ammonia and nitric acid. 5. Then acid scrubbers remove nitrogen dioxide. The gases then dried in an aluminium drier. The compressed and dried gases are then expanded in a liquifier with resultant liquefaction of nitrous oxide and escape of gaseous nitrogen. Purified nitrous oxide is now evaporated compressed into a liquid and passed to a second aluminium drier to the cylinder filling line 6. Physical Properties: Only inorganic gas in clinical use. Colorless and odorless. Non explosive and non combustible yet supports combustion. It exists as a gas at room temperature and ambient pressure Its critical temperature lies above room temperature. 7. Physical properties( contd. ) -molecular weight - 44 -MAC -105 -Blood gas partition coefficient - 0.47 -critical temperature - +36.5C 8. N2O Cylinder N2O cylinder, color-blue, Pin index - 3,5 Stored as a liquified gas. Pressure depends on vapor pressure of the liquid and is not an indication of the amount of gas in the cylinder as contents are in the liquid phase. The pressure remains nearly constant until all the liquid is evaporated after which it decreases till the cylinder is exhausted. 9. Concentration effect N2O is about 20 times more soluble than O2 and N2. During induction the volume of N2O entering the pulmonary capillaries is greater than the N2 leaving the blood and entering the alveolus. As a result the volume of the alveolus decreases, thereby increasing the fractional concentration of the remaining gases. This process augments ventilation as bronchial and tracheal gas is drawn into the alveolus to make good the diminished alveolar volume. 10. Second gas effect Rapid absorption from alveoli causes an rise in the alveolar concentration of the other inhalational anaesthetic agent administered at the same time. 11. Diffusion hypoxia First described by Fink in 1955 The elimination of nitrous oxide may proceed at a greater rate as its uptake The volume of N2O entering the alveolus from blood is greater than the volume of N2 entering the pulmonary capillary blood. Effectively dilutes alveolar air, and available oxygen, so that when room air is inspired hypoxia may result 12. SYSTEMIC EFFECTS CENTRAL NERVOUS SYSTEM -EEG: Frequency is decreased and voltage is increased -SEIZURE ACTIVITY: It may increase motor activity with clonus and opisthotonus, even tonic clonic seizure has been described -AWARENESS: Requires greater than 0.5 to 0.6MAC to prevent it. -CEREBRAL BLOOD FLOW: Increased -INTRACRANIAL PRESSURE: Increased 13. CIRCULATORY EFFECTS -SYSTEMIC BLOOD PRESSURE:, HEART RATE, CARDIAC OUTPUT: No change or modest increase -RIGHT ATRIAL PRESSURE: Increased -SYSTEMIC VASCULAR RESISTANCE: No change -PULMONARY VASCULAR RESISTANCE: -Increased -This mild sympathomimetic activity may be due to central effect regulating beta adrenergic outflow. 14. VENTILATION EFFECTS -FREQUENCY: Increased, - TIDAL VOLUME: Decreased -VENTILATORY RESPONSE TO HYPOXIA: Depressed 15. BONE MARROW FUNCTION - Megaloblastic changes and agranulocytosis. PERIPHERAL NEUROPATHY -Ataxia and spinal cord and peripheral nerve degeneration causing sensorimotor polyneuropathy. 16. METABOLISM - About 0.004% of absorbed dose of nitrous oxide undergoes reductive metabolism to nitrogen in the gastrointestinal tract. - Anerobic bacteria are responsible for this - Oxygen concentration of >10% in GIT and antibiotics inhibit its metabolism by anerobic bacteria 17. SIDE EFFECTS HEMATOLOGIC: Mild Megaloblastic changes.(due to irreversible oxidation of cobalt atom in Vit B12 affects methionine synthetase) NEUROTOXICITY: Sub acute combined degeneration of spinal cord. REPRODUCTION AND DEVELOPMENT: - Reduced fertility and increased spontaneous abortion rate in operation theatre personal. 18. OXYGEN 19. INTRODUCTION - Independently discovered by CARL WILHELM SCHEELE in 1773 and JOSEPH PRIESTLY in 1774. - Name OXYGEN was coined by ANTOINE LOVOISIER in 1777. - Atomic number-8, atomic weight- 15.9994g/mol - Critical temperature- -119C - Colourless, odourless, tasteless diatomic gas with the formula O2. - Oxygen cylinder, color - Black with white shoulder pin index-2,5 20. Production: By Fractional Distillation of liquid air 1.Liquefaction of air: Air is compressed heat thus produced is got rid of and air is allowed to expand. As it expands it cools.(Joule Thompson Effect) By repetition of this there is a progressive fall in temp till it cools enough to liquefy. 21. Distillation of liquid air: In liquid air, nitrogen and oxygen can be separated as the more volatile nitrogen (boiling pt at 760mmHg= -1960C) is siphoned at the top Oxygen is separated at the bottom 22. Oxygen Cascade The O2 content in air (at sea level) is about 159.6mm Hg. (760 mm Hg x 0.21), falling to 10-15 mm Hg. (0.5 KPa) in the mitochondria where it is utilized. The transport of O 2 down this concentration gradient is described as "Oxygen cascade". 23. 1.Starting point At sea level, the atmospheric pressure is 760mmHg, and oxygen makes up 21% (20.094% to be exact) of inspired air: so oxygen exerts a partial pressure of 760 x 0.21 160mmHg. 2.First drop Water vapor, humidifies inspired air, and dilutes the amount of oxygen, by reducing the partial pressure by the saturated vapor pressure (47mmHg). PIO2 (the partial pressure of inspired oxygen), (760 - 47) x 0.2094 24. 3.ALVEOLI Alveolar oxygen tension(PAO2) is less than PiO2 because some oxygen is absorbed in exchange for CO2. By the Alveolar Gas Equation. PAO2 =PiO2-(PACO2/RQ)=103.5mmHg R is the respiratory quotient, which represents the amount of carbon dioxide excreted for the amount of oxygen utilized, and this in turn depends on the carbon content of food (carbohydrates high, fat low). RQ8 25. 4.ALVEOLI TO BLOOD FICKS LAW OF DIFFUSION Rate of gas transfer= (k * A) P/D K is a constant called the diffusion coefficient A is the cross sectional area across which diffusion is taking place P/D is the concentration gradient (any factor that increases the thickness of membrane such as pulmonary edema interferes with diffusion of oxygen more than with that of CO2) 26. In alveolar air, the O 2 tension is 106 mm Hg and in venous blood entering the pulmonary capillary is 40mm Hg. (pressure gradient difference of 66 mm Hg) O 2 diffuses rapidly across the AC- membrane, on reaching the blood, the O 2 first dissolves in plasma and finally combines with Hb for its carriage to the tissues. 27. Arterial Pao2 is now roughly100mmof Hg The difference between alveolar and arterial PO2 (A-a gradient) is 5-10mmHg Increase in the difference between alveolar and arterial PO2 is due to 1. Increased PIO2 2. V/Q mismatch 3. Rt to Left shunting 28. 5.Artery to tissue. The PO2 falls progressively form the arterial to the venous end of the capillaries and from capillaries to the cell and is lowest in the mitochondria. O2 tension in tissue is 40mm of Hg. (O2 transfers via plasma from RBC to tissue via diffusion) About 30% of O2 is liberated from blood to supply the tissue O2 consumption cannot take place below a mitochondrial PO2 of 1 -2 mmHg is known as 29. Oxygen Transport 30. Oxygen carriage by the blood The amount of oxygen in the bloodstream is determined by the oxygen binding capacity of hemoglobin the serum hemoglobin level, the percentage of this hemoglobin saturated with oxygen the amount of oxygen dissolved 31. Dissolved O2 in plasma Small quantity of O2 about (3%) 0.3ml/100ml of blood at a PaO2 of 100 mm Hg is physically dissolved in the plasma. i) It reflects the tension of oxygen (PO2) in the blood ii) Acts as a pathway for supply of O2 to Hb. PO2 in the blood is first transferred to the cells, while its place is rapidly being taken up by more O2 liberated from the Hb. 32. b) O2 combined with Hb: Most of the O2 (97%) in the blood is transported in combination with Hb. Hemoglobin: Consists of the protein globin joined with the pigment haem, which is a Fe- containing porphyrin. Normal adult Hb consists of: Hb (A 1 ): 98% and Hb (A 2 ): 2%. Hb has 4 binding sites for oxygen. Each gram of Hb can carry 1.34ml of oxygen. With a Hb concentration of 15g/dl, the O2 33. Oxygen flux: The amount of O2 leaving the Lt. Ventricle per minute in the arterial blood has been termed the "oxygen flux". It represents O2 delivers to the tissues. O 2 flux = CO x Arterial O2 saturation x Hb conc x 1.31.= 5000 ml/min x 98/100 x 15.6/ 100g / ml x 1.31 ml/gm. = l000ml/min. Normally about 250ml of this O2 is used up in cellular metabolism and the rest returned to the lungs in the mixed venous blood 34. The 3 variables in the equation: Cardiac output, arterial O2 saturation and Hb concentration are multiplied together Trivial reduction of any may result in a catastrophic reduction in O2 flux. Lowest tolerable value of O2 flux is 400 ml/min. Oxygen flux decreased in anaemia, CCF, metabolic acidosis, respiratory acidosis Oxygen flux is increased in exercise, thyrotoxicosis, halothane shakes, pain and shivering. 35. OXYHAEMOGLOBIN DISSOCIATION CURVE(ODC) The percent of Hb saturation with oxygen (PO2) at different partial pressures of O2 in blood is described by the ODC. It expresses the relation between oxygen tension taken on the X axis and % of Hb saturation taken on the Y axis at 37 C, pH: 7.4, PCO2 40 mmHg. It is a sigmoid curve. 36. Bohr Effect: EFFECT-shift in position of ODC caused by CO2 entering or leaving blood. CO2+H2OH+ +HCO3. A fall in pH shift the ODC to the "right" and a rise a shift of the ODC to the left Double Bohr Effect: The transfer of H+ ions from the fetal blood into the maternal intervillous spaces causes the fetal pH to rise and increase the affinity of fetal blood to O 2 (shift to left). H + ions acids passing to the maternal circulation causes the maternal pH to fall, reducing the affinity of maternal blood for O 2 (shift to right) so further O 2 is released to the fetus. 37. Oxygen content of blood =(SO2*1.34*Hb*0.01)+(0.023*PO2) Arterial blood(CaO2)=20.4ml/100ml Venous blood(CvO2)=15.2ml/100ml O2 Delivery(DO2) and O2 Uptake(VO2) DO2=CaO2 * CO(cardiac output) =1005ml/min VO2=DO2-oxygen return =DO2-(CvO2*CO) =245ml/min O2 Extraction Ratio=VO2/DO2=25% Increased tissue demand increase in CO Extreme conditionsCvO2 falls, extraction ratio increases 38. HYPOXIA Hypoxia, is a pathological condition in which the body as a whole (generalized hypoxia) or a region of the body (tissue hypoxia) is deprived of adequate oxygen supply. CLASSIFICATION -hypoxemic hypoxia -hypemic hypoxia -histotoxic hypoxia -ischemic or stagnant hypoxia 39. HYPOXEMIC HYPOXIA: Reduction in PO2 -high altitude -switching from inhaled anesthesia atmospheric air-FINK EFFECT -sleep apnea -COPD or pulmonary arrest -shunts HYPEMIC HYPOXIA: O2 content of arterial blood is reduced -carbon monoxide poisoning -methhemoglobinemia 40. HISTOTOXIC HYPOXIA:Poisoning of the electron transfer chain -cyanide poisoning ISCHEMIC OR STAGNANT HYPOXIA -cerebral ischemia, IHD. SYMPTOMS OF HYPOXIA -headaches,fatigue -shortness of breath -feeling of euphoria and nausea -changes in level of conciousness -seizures -coma -death 41. OXYGEN THERAPY INDICATIONS In adults and infants > 1 months SPO2