anatomy physiology for nitrous oxide n.
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ANATOMY & PHYSIOLOGY for NITROUS OXIDE

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ANATOMY & PHYSIOLOGY for NITROUS OXIDE

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ANATOMY & PHYSIOLOGY for NITROUS OXIDE

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  1. ANATOMY & PHYSIOLOGYfor NITROUS OXIDE

  2. Respiratory System Two functional parts Conducting zone Respiratory zone

  3. Conducting Zone Transports gases from outside to respiratory zone Includes anatomic deadspace (150 ml)

  4. Conducting Zone Nasal passages Pharynx Nasopharynx Oropharynx Hypopharynx

  5. Conducting Zone (cont.) Larynx Trachea Bronchi (left and right mainstem) Bronchioles

  6. Respiratory Zone Portion of lung where exchange of gases occurs between blood and air

  7. Respiratory Zone Respiratory bronchioles Alveolar ducts Alveolar sacs Alveoli

  8. Alveolus Unit in which actual gas exchange occurs Around 300 million total A pocket of air surrounded by thin membrane (1-2 micrometers in thickness) containing capillaries

  9. Alveolus Wall consists of 4 thin layers Mucinous covering Alveolar epithelium (incomplete) Interstitial layer Endothelial cells (pulmonary capillaries)

  10. Physiology of Respiration Inhaled gases travel through conducting zone to respiratory zone Gases diffuse across alveolar membranes according to pressure gradients Pulmonary capillaries are a pool of blood vessels (70 sq meters)

  11. Respiratory Mechanics Pre inspiration - resting - -5cm H2O pleural Peak inspiration - more negative pressures End inspiration - negative pleural, 0 alveolar Peak expiration -positive alveolar End expiration - -5cm pleural, 0 alveolar

  12. Respiratory Mechanics Muscles Involved Primary - Diaphragm Intercostals Accessory - Abdominals, Scalenes, Sternocleidomastoid Some back muscles

  13. Respiratory Mechanics Resting pleural cavity pressure = - 5 cm H20 Thorax expands, increasing negative pressure Air flows into lungs/alveoli until positive pressure develops and gas exchange occurs Air flows out of lungs to return to resting pleural pressure of negative 5 cm H20

  14. Nitrous Oxide Inhalational Sedation May Represent the Most Ideal Sedation Technique

  15. PHARMACOLOGY OFNITROUS OXIDE

  16. Preparation of Nitrous Oxide Ammonium nitrate crystals heated to 240 degrees celsius Decomposition to nitrous oxide and water

  17. Preparation of Nitrous Oxide heat NH4NO3 =======> N2O + 2 H2O 240 deg.C

  18. Preparation of Nitrous Oxide N20 is chemically scrubbed 99.5% pure Stored in compressed form in metal cylinders 30% in liquid form in full cylinder Nitric oxide (NO) is the most dangerous impurity (use only medical grade N2O)

  19. Physical Properties N2O is a nonirritating, sweet-smelling, colorless gas Only inorganic substance other than CO2 to have CNS depressant properties Only inorganic gas used to produce anesthesia in humans

  20. Physical Properties N2O liquid requires heat for vaporization into gaseous state Relatively insoluble in the blood; Blood-gas solubility coefficient is 0.47 at 37 deg. C

  21. Potency of Nitrous Oxide Least potent of anesthetic gases 35 more times soluble than N2 in plasma 100 times more soluble than O2 in plasma N2O + O2 can produce CNS depression

  22. Potency of Nitrous Oxide N2O in subanesthetic doses can produce analgesia N2O +O2 at 20%/80% is equal-analgesic to 10 to 15 mg of morphine Optimal concentration is 35%

  23. Pharmacology of Nitrous Oxide N2O is rapidly absorbed into the CV system, due to large concentration gradient of N2O between alveolar sacs and blood N2O rapidly fills air-filled body cavities

  24. Pharmacology of Nitrous Oxide Due to rapid uptake, two phenomena are seen Concentration effect - higher concentrations cause more rapid uptake of N2O Second gas effect - a second anesthetic gas will also be taken up more rapidly than usual when added to N2O

  25. Concentration Effect Seen only when using high concentrations of a gas The higher the concentration inhaled, the more rapidly the arterial tension of the gas increases The diffusion gradient from the lungs into blood results in a greater uptake of gas into lungs

  26. Second Gas Effect Occurs when another inhalation anesthetic is used with N2O Rapid uptake of N2O produces a vacuum in alveoli Second gas also undergoes rapid uptake along with N2O

  27. Absorption CNS saturation occurs by displacement of N2 by N2O, usually in 3-5 minutes Tissues with greater blood flow (brain, heart, liver, kidney) receive greater amounts of N2O

  28. Absorption Tissues with poor blood supply (fat, muscle, connective tissue) absorb small amounts Slow absorption occurs once primary saturation is completed Therefore no body reservoir present to slow recovery once N2O terminated

  29. Biotransformation N2O undergoes no biotransformation in the body Majority of N2O is exhaled unchanged 3 to 5 mins. following termination of delivery 1% eliminated via skin and lungs in 24 hours

  30. Diffusion Hypoxia Can occur following termination of N2O if patient is allowed to breathe only room air “Hangover” effect (headache,nausea,lethargy) is produced Prevented by having the patient breathe 100% O2 for minimum of 3 to 5 minutes

  31. Diffusion Hypoxia Rapid diffusion of N2O from blood to lungs results in decreased CO2 arterial tension with decreased stimulus for respiration Rapid diffusion of N2O back into lungs dilutes alveolar O2 with resultant hypoxia

  32. Pharmacology of Nitrous Oxide N2O is non-allergenic Least toxic of inhalational agents

  33. Effects of Nitrous Oxideon Organ Systems

  34. Central Nervous System Actual mechanism unknown Mild depression of CNS (cerebral cortex) in conjunction with physiological levels of O2 (greater than 20%) Sensations depressed (sight, hearing, touch, pain)

  35. Cardiovascular System No changes in heart rate or cardiac output Blood pressure remains stable with only slight decrease Cutaneous vasodilation

  36. Respiratory System N2O is non-irritating to pulmonary epithelium Changes (drop) in rate and depth more likely due to anxiolytic effects Slight elevation of resting respiratory minute volume at 50%/50%

  37. GI System No clinically significant effects, unless there is a closed space (obstruction) N/V rarely seen unless hypoxia present Can be used in hepatic dysfunction

  38. Hematopoietic System Long-term exposure (greater than 24 hours) can produce transient bone marrow depression

  39. Musculoskeletal System No direct relaxation of skeletal muscle Anxiolytic effects help relaxation