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  1. Pain: that which hurts or is unpleasant
    • Fear: short-lived phenomenon, disappears when the threat passes
    • Anxiety: a learned response, arises from anticipation
    • Analgesia: Diminution or elimination of pain
  2. Local anesthesia:
    Elimination of sensation, especially of pain, in one part of the body by topical or regional injection of a drug.
  3. Conscious sedation:
    (CA) A minimally depressed level of consciousness that retains the patient’s ability to independently and continuously maintain an airway and respond appropriately to physical stimulation OR verbal command caused by a pharmacologic, non-pharamcologic agent or combination thereof. Respiration and CV not affected. (Similar to ADA moderate sedation)
  4. Deep sedation:
    (CA) A controlled state of depressed consciousness, accompanied by a partial loss of protective reflexes including, inability to respond purposefully to verbal command. Ability to maintain ventilator function may be impaired.
  5. General anesthesia:
    (CA) Controlled state of unconcsiouness accompanied by partial or complete loss of protective reflexes, including inability to independently maintain an airway and respond appropriately to stimuli. CV may be impaired.
  6. discuss the relationship between the patient, a noxious stimulus, and the environment in terms of how they can influence pain.
    Anesthesia is a continuum; there are not distinct stages. As the provider, you must be able to rescue the patient from one level deeper than you intend the patient to remain at. The less sedated a patient is, the more likely the analgesia will not work. Contrarily, the more sedated a patient is, the more likely the analgesia will work (i.e. N2O vs GA). Patients that are extremely anxious will have a much tougher time becoming numb with just LA alone; they may require additional sedation for the LA to begin working.
  7. Compare and contrast conscious sedation and general anesthesia
    • Conscious Sedation (Moderate Sedation)
    • Patient is conscious, cooperative
    • Protective reflexes intact
    • Vital signs stable
    • Pre-Op fasting sometimes required
    • General Anesthesia
    • Patient is unconscious
    • Protective reflexes absent
    • Vital signs unstable
    • Pre-Op fasting REQUIRED
  8. Indications for Sedation:
    Anxiety or fear in adults, young children, mental or physical disability, medically compromised patient, extensive invasive procedure, extended care during a single appointment, significant gag reflex, LA problems.
  9. discuss the parameters involved with cardiac output and blood pressure in the healthy patient and will also have an understanding of the physiologic changes that occur with common cardiovascular pathology (hypertension, MI, cardiac failure, etc.)
    • Cardiac Output: Stroke Volume X Heart Rate
    • Controlled by auto-regulation of the tissues
    • Stroke volume is controlled by preload, afterload, contractility and left ventricular dyssnergy
    • Afterload is most similar to BP, usually only a problem if patient has uncontrolled HTN
    • MAP is increased with HTN also, will cause higher necessary CO
    • Contractility can decrease with MI or cardiomyopathy due to weak heart or from B-blockers or Ca channel blockers, will decrease CO
    • Heart Rate is affected by SANS and PANS (dominant), as well as baroreceptors on carotid body and atoric arch. Tachycardias can cause hypotension by decreasing the pre-load
  10. ↑CO
    • ↑HR
    • ↑Venous Return
    • ↑Endogenous or exogenous catecholatmines (NE/EPI)
    • ↑Sympathetic Autonomic Nervous System
  11. ↓CO
    • Intrinsic Myocardial Disease
    • ↓Venous Return
    • Peripheral vasoconstriction
    • ↑Parasympathetic Stimulation
  12. describe the effect of sedative drugs on the normal and diseased cardiovascular system.
    Sedative drugs decrease the sympathetic nervous system firing by calming the patient. Will cause the dominant parasympathetic nervous system to control the heart rate and arterial pressure. HR will decrease slightly or will be normal, BP should be WNL with some vasodilation.
  13. discuss ventilation, gaseous exchange, and the mechanisms of regulation of respiration.
    • Ventilation is the movement of gases between the atmosphere and the alveoli. It is measured via vital capacity and minute volume. If you are breathing really slowly, can get more minute volume, if you are hyperventilating, will not get enough O2 to the alveoli due to the small volume. Gas exchange occurs via simple diffusion. O2 is transported primarily by hemoglobin where as CO2 is transported primarily as bicarbonate ion.
    • Ventilation is controlled by the respiratory center in the medulla with some protective measures: central hypercapnic drive and peripheral hypoxemic drive. Chemoreceptors sense the H+ from carbonic acid (bicarbonate ion dissociated). The CO2 can cross the BBB and then dissociates to form the H+, which triggers the hypercapnic drive to stimulate ventilation. The peripheral hypoxemic drive senses the PaO2 at the carotid bodies and the aortic arch. If PaO2<60mmHg, triggers CN IX and CN X activation to stimulate respiratory center.
  14. Vital Capacity:
    Tidal Volume + In Rate + Ex Rate (how much space you have in your lungs for gas exchange)
  15. Tidal Volume:
    The amount of air you breath in with each breath
  16. Minute Volume:
    Tidal Volume X RR (how much air you are breathing per minute)
  17. effect of various sedative drugs on the respiratory system of normal and compromised patients.
    All sedative opioids and general anesthetics DEPRESS ventilation; opioids work on the hypercapnic drive, benzodiazapines and inhalation anesthetics work on the hypoxemic drive. Opioids and N2O (volatile anesthetics) require the PaCO2 to be higher than normal in order for the hypercapnic drive to kick in (these shift the curve to the right). Benzodiazepines and propofol decrease minute volume per increase in PaCO2 compared to normal. So, if you were that hypercapnic without the drugs, would be breathing faster than with the drugs, these decrease the slope on the response curve). Central etiologies and metabolic acidosis cause a left shift in the curve meaning that you are breathing faster at lower PaCO2 than normal.
  18. discuss the peripheral transmission of orofacial pain.
    • This is in the form of first pain (sharp, prickling, fast, localized, myelinated fibers—A-delta, reflex withdrawal) and second pain (dull, aching, slow, diffuse, unmyelinated fibersC)
    • Inflammatory Pain: synthesis and release of prostaglandins, bradykinin, histamine
    • Dentinal Pain: hydrodynamic
    • Pulpal pain: free nerve endings in pulp and blood vessels
    • Periodontal pain: CN V
  19. discuss the central mechanisms of orofacial pain.
    A-delta and C fibers transmit nociception to trigeminal nucleus caudalis, which functions like the dorsal horn of the spinal column. These are transmitted to projection neurons, the thalamus and eventually the cortex (periaqueductal gray matter).
  20. discuss the major pain theories.
    • 1) Intensity theory: when receptor overstimulated, pain is perceived
    • 2) Specificity theory: pain is a specific sensation, like sight and has direct lines of communication. When a receptor feel a noxious stim, pain will ALWAYS be felt according to this theory
    • 3) Gate Control Theory: Noxious stim sets up impulses in a small diameter to excite transmission cells to the spinal cord. Non-painful input will close the gate
  21. Know the basic neuroanatomy of the trigeminal system.
    • Sensory Nucleus of Trigemina system has 2 components
    • i) Main sensory nucleus
    • ii) Spinal Nucleus
    • (1) Nucleus oralis
    • (2) Nucleus interpolaris
    • (3) Nucleus Caudalis: pain information from the face (like dorsal horn of spinal column)
    • (a) Nociceptive fibers->painprojection neuronsthalamuscortex
    • (b) LA blocks pain by preventing stimulation of nociceptive fibers
    • This transmits pain via projection neurons to the thalamus, then to the PAG
  22. discuss the endogenous pain suppression system.
    • a) Endogenous Opioid Peptides (EOP)
    • i) Enkephalin, Dynorphin, B-endorphin
    • ii) Similar properties to exogenous opioids
    • b) Works top-down
    • c) EOP: stimulates PAG, then down to the nucleus caudalis
    • d) Level 1 (Highest): Periaqueductal Gray Matter (PAG)
    • i) Integrate info from cortex and brainstem with incoming pain signals
    • ii) Has enkephalin and dynorphin interneurons
    • iii) Opiate injection here: long-lasting analgesia
    • iv) Remember opioid antagonist: naloxone (reduces effects of PAG stimulation)
    • e) Level 2: Nucleus Raphe Magnus, Medullary Reticular Nuclei, Locus Ceruleus
    • i) Descending fibers serotinergic and noradrenergic
    • ii) Analgesia of morphine inhibited by 5HT and norepi antagonists
    • f) Level 3 (lowest): Medullary and Spinal Dorsal Horns
    • i) Pain signals suppression: Direct/indirect/both action of descending fibers
    • g) Activated by pain or stress
  23. discuss the difference between pain threshold and pain tolerance
    • Pain threshold: level of stimulus at which pain is first PERCEIVED
    • Pain tolerance: level of stimulus when there is a PAIN RESPONSE
  24. list psychological factors that may alter pain tolerance, such as past experience, personality variables, age, fatigue ...
    • Factors that Decrease pain tolerance
    • Increasing age (possibly reversed in dentistry), fatigue, females, cultural variable (Japanes show less response), depression, chronic anxiety
  25. discuss theories as to how nitrous oxide works
    • 1. Conformational changes in membrane proteins
    • 2. NMDA Antagonist
    • 3. Increased GABA-A effect
  26. discuss the pharmacologic effects of nitrous oxide on the body’s systems
    • **Note: sedation is about 30% and anesthesia is 70%
    • CNS
    • Sedation: mild depression, analgesia equivalent to one dose morphine
    • Anesthesia: unconsciousness, total amnesia, nausea, high analgesia
    • CVS
    • Sedation: Minor changes in BP/HR, cutaneous vasodilation, very stable
    • Anesthesia: myocardial depression, increased sympathetic tone
    • Respiratory
    • Sedation: regular, mild increase in RR, reflexes intact (except gag), no hypoxia, increased PO2
    • Anesthesia: irregular, altered reflexes, hypoxia if > 70%, lower hypoxemic and hypercapnic drives (hypoxemic more so)
    • Musculature
    • Sedation: mild relaxation
    • Anesthesia: possible rigidity
  27. recognize the signs and symptoms of nitrous oxide inhalation
    • a) 10-30% N2O
    • i) Body warmth, tingling of hands/feet
    • ii) Analgesia
    • iii) Circumoral numbess
    • b) 20-40%
    • i) Numbness of hands/feet
    • ii) Body heavy/light
    • iii) Vision, hearing distinct but distant
    • iv) Sedation and sleepiness
    • v) Increased analgesia
    • vi) Most pts sedated 30-40%
    • vii) Possible euphoria, profound ideation, droning sounds
    • c) 30-50%
    • i) Detachment or disorientation
    • ii) Amnesia
    • iii) Nausea unlikely
    • iv) Sweating or nervous
    • v) Slow response
    • vi) Somnolence (drowsiness)
    • d) 40-60%
    • i) Dreaming.hallucinations
    • ii) Profound analgesia
    • iii) Unable to follow commands
    • iv) Lethargy, uncoordinated
    • v) Increased nausea
    • e) >50%
    • i) Unconsciousness and light general anesthesia
  28. discuss the movement of nitrous oxide from the alveolus to the blood and ultimately to the central nervous system, and vice versa.
    N2O is insoluble, therefore, there is fast uptake into the alveolus when inspired. Percentage of inspired N2O X 760mmHg is the partial pressure according to Dalton’s Law. This is the same partial pressure (tension) as in the blood (Henry’s Law). Use Blood/gas coefficient to calculate actual concentration of N2O in the blood (0.47 x Partial Pressure). The vessel rich groups pick up the N2O first, then the muscle group and finally the fat group. Since the brain is highly perfused, it’s concentration is almost the same as the arterial concentration. As we breathe a constant PP of the gas, over time the concentration in the brain increases. This is because as we breathe, there is a leak of N2O into surrounding tissues. Our body picks up more N2O everytime we breathe, so the concentration gradually rises as some leaks out to the VRG, MG and FG. N2O crosses the BBB, so gets into the brain quite readily and quickly.
  29. discuss how the distribution of nitrous oxide to body tissues is influenced by regional blood flow.
    Anything that increases delivery of the drug to the alveoli will hasten the onset of anesthetic and vice versa, anything that decreases the PP will slow the onset of anesthesia. For example, talking will decrease the PP of N2O, because blowing off drug prior to uptake in the alveoli. Moving muscles around will pull blood away from the brain and slow the onset of the drug. Hypocarbia causes vasoconstriction and therefore bad blood flow to the brain, which will slow onset. Increasing the amount of blood to the lungs via high CO, will delay equilibrium with the gas and therefore onset. Hyperventilation decreases cerebral blood flow because hypocarbia causes vasoconstriction. Therefore, want slow, deep breaths to allow for the drug to be taken up at the highest concentration possible.
  30. Metabolism of nitrous oxide
    Enteric bacteria metabolize N2O into nitrosamines, however most of it is eliminated by breathing it out. The metabolism of N2O causes the oxidation of B12-dependent enzymes, which will decrease DNA replication if exposed continuously over long periods of time.
  31. Elimination of nitrous oxide
    Reverse uptake with residuum in fat. Fat and muscle groups taper off the longer the patient is not breathing N2O. Lungs, blood and high flow viscera such as the brain have the highest concentration during inhalation, when the N2O is turned off, these taper drastically. Muscle and fat groups rise gradually throughout administration and taper slowly after termination. Very obese patients may have residual effects of N2O due to the high concentration of N2O in the fat if administered for a long period of time.
  32. list the components of a nitrous oxide machine and understand the function of each.
    O2 (green) and N2O (blue) cylinders, Regulators (reduce high cylinder pressure to low line pressure), N2O head (has the flow meters, flow valves, O2 flush, fail safe and flow safe), Breathing circuit (reservoir bag, elephant tube, breathing tubes and slide), Nasal mask or hood
  33. explain the importance of “fail-safe” and “flow-safe” mechanisms built into the machine.
    • Fail-safe: if the O2 runs out before the N2O, the N2O will automatically shut off until the pressure of O2 is returned above the fail-safe threshold.
    • Flow-safe: you cannot administer anything under 2-3L of O2 at any given time. Therefore, will never be only administering N2O without O2.
  34. describe the main implication of the different storage states of nitrous oxide and oxygen.
    • O2 stored as gas with 2000psi, will gradually taper as you use it
    • N2O stored as a liquid with a 750psi, will not taper until almost empty
    • Need to know if the N2O tank has been used or not in order to know if it is full, half, or close to empty because the meter will not tell you.
  35. List the aspects of preparation of the patient for sedation.
    Take all normal meds, eat normally. Use bathroom ahead of time. Review medical history. Take and record vital signs and place chair in semisupine position. No escort needed
  36. List the steps of the sedation technique.
    • 1) Prepare the equipment
    • 2) Prepare the patient
    • 3) Adjust flow with O2 only so it is good (7-8 L/min)
    • 4) Titrate slowly
    • a. ½ L increments or by 10%
    • b. Record proper amount and keep constant
    • 5) Evaluate patient for proper effects
    • 6) Procedure
    • 7) Turn off N2O when done and turn on 100% O2 for 5 minutes
    • 8) Check and record vital signs again
    • 9) Discharge patient and write a discharge note
  37. Able to recognize the objective signs of the proper level of sedation.
    Awake, alert and responds to commands. Marked analgesia. Relaxed but not euphoric
  38. List the complications that may occur during nitrous oxide-oxygen sedation.
    Spontaneous mouth-breathing, uncomfortable “too intense” feeling, behavior problems, excessive perspiration, nausea, vasodilation, responding slowly, unconscious
  39. describe prevention and treatment of nausea and vomiting.
    • Prevention: avoid deep, long sedation. Do not change patient position drastically or frequently. Do not alter the concentration often or drastically (roller-coaster)
    • Treatment: Position appropriately, suction, remove equipment and give 100% O2
  40. Able to recognize oversedation.
    Closing of mouth, mouth breathing, sluggish response, unconscious, “too intense”, nausea
  41. List the evaluation procedures completed before the patient is discharged.
    Make sure patient is aware, alert, responsive and ambulatory. Check vital signs.
  42. describe signs and symptoms of nitrous oxide abuse.
    • Signs: Romberg Sign (drunk driver test), Muscle weakness in distal legs and arms, impaired sense of touch
    • Symptoms: Lhermitte Sign (electrical sensation runs down the back and into the limbs), numbness, impairment of gait, inability to walk unassisted, impotence, impairment of sphincter control, altered mood, inability to work.
  43. discuss the potential effects of long-term, low dose exposure to nitrous oxide- oxygen.
    • 1) Inhibits vitamin B12-dependent enzymes
    • a. Methionine Synthase
    • i. Forms methionine from homocystine
    • ii. If inhibited, build up of homocystine leads to hypercoaguable state
    • iii. Decreased DNA synthesis due to decreased amounts of dTMP and Folate
    • iv. Altered B12 metabolism shown by toxicity in bone marrow
    • b. Methylmalonyl-CoA mutase
    • c. Leucine 2,3-aminomutase
    • 2) Can cause pernicious anemia due to impaired conversion of dUMP to thymidien monophastate
    • 3) Spontaneous abortion, reduced fertility
  44. discuss techniques to limit nitrous oxide exposure
    • 1) Use scavenging equipment (REQUIRED)
    • a. Use max vacuum
    • b. Check all fittings for leaks
    • c. Ensure that operatory ventilation and air circulation is adequate
    • d. Use appropriate gas flow and well fitting mask
    • e. Administer 100% O2 for 3-5 minutes
    • 2) Adhere to the government recommended exposure limits (25-50ppm over 8hr time period)
    • 3) CalOSHA Requirements: permissible amount 50ppm with ceiling of 75ppm
    • 4) Use monitoring equipment to measure employee exposure
  45. Able to evaluate the patient’s medical history and assign to an anesthetic risk category.
    • ASA I (no risk): healthy pt
    • ASA II (low risk): mild systemic disease
    • Phobic, autism, CONTROLLED HTN/seizure/asthma/DM
    • ASA III (moderate risk): severe systemic disease limiting activity but not incapacitating
    • UNCONTROLLED HTN/asthma/seizure/DM, stable angina
    • ASA IV: Incapacitating disease that is threat to life
    • Unstable angina, transplants, liver failure, etc
    • ASA V: will not live 24 hrs
    • ASA VI: dead, organ donor
    • TREAT ASA I-III in office
  46. Able to decide if sedation is safe and indicated for the patient, taking into consideration concomitant drug therapy and possible disease states which may indicate or contraindicate the use of sedation.
    • For Nitrous:
    • Absolute contraindications: acute nasopharyngeal/respiratory disease, cannot breathe thru nose
    • Relative contraindications: pregnancy, chronic pulmonary disease, CNS medications, MTHFR deficiency, psychosis, claustrophobic, retinal surgery, otitis media
    • Multiple drug therapy: more control of side effects, get additive effects of sedation
  47. Able to list the advantages for the different routes of administration of sedative drugs.
    • Oral
    • Advantages: highly acceptable, cheap, easy admin, low amount of adverse effects, no special equipment/training required (other than children)
    • Disadvantages: rely upon compliance, unpredictable latent period, erratic absorption, cannot titrate effect, need escort
    • IM Sedation
    • Advantages: Onset in 15-30 minutes, more predictable absorption, no patient coop
    • Disadvantages: cannot tirate, cannot always reverse, pain on injection, need escort
    • IV Sedation
    • Advantages: safe, rapid onset, lesser recovery period, can titrate effect
    • Disadvantages: Must start an IV, special training required, need coop, injury to vein, cannot always reverse, need escort
  48. discuss the advantages and disadvantages of IV sedation as compared to other routes of sedation.
    • Advantages
    • Rapid Onset
    • Titrate to effect
    • Shorter recovery period
    • Continous IV access
    • Nausea nad vomiting uncommon
    • Gag reflex diminished
    • Disadvantages
    • Venipuncture necessary
    • More intensive monitoring required
    • Escort necessary
    • Cannot reverse all agents
    • NPO required
  49. Diazepam (Valium)
    • Family: Benzodiazepine
    • Duration: ~45mins
    • Long duration of action for sedation 20-80hrs
    • Metabolism: Multiple ACTIVE METABOLITES
    • Pharm: Amnesia:10-15mins
    • CNS depression, respiratory depression
    • Adverse: Throbophlebitis
  50. Midazolam (Versed)
    • Benzodiazepine, not available in tablet form, only oral for KIDS
    • ~45mins
    • SHORT DURATION of action 1.2-12.3hrs
    • Inactive metabolites, short duration
    • Amnesia: Up to 45 mins
    • CNS depression, respiratory depression
    • Adverse: Interactions with CYP3A4 inhibitors, will have longer effect if on one of these
  51. Lorazepam (Ativan)
    • Benzodiazapine
    • Short duration of action
    • Inactive metabolites
    • CNS depression, respiratory depression
    • Supraadditive effect with other CNS depressants
  52. Triazolam (Halcion)
    • Benzodiazapine
    • Short duration, MOST popular for adults Inactive metabolites
    • CNS depression, respiratory depression
    • Supraadditive effect with other CNS depressants
  53. Pentobarbital (Nembutal)
    • Barbiturate, not used that much in dentistry
    • 2-3hrs
    • CNS depression, respiratory depression
    • Contraindicated with certain porphyrias, CNS depression while increasing responses to noxious stimuli
  54. Meperidine, (Demerol)
    • Opioid
    • 60-90mins
    • CNS depression, respiratory depression
    • Contraindicated with MAO inhibitors (must be off for 2-3 weeks prior to use), can cause severe HTN
  55. Fentanyl (Sublimaze)
    • Opioid
    • 30-45mins
    • CNS depression, respiratory depression
    • Rapid bolus may lead to stiff-chest syndrome (give naloxone for reversal)
  56. Zolpidem (Ambien)
    • Non-Benzodiazepine
    • Fast onset, good for night before
    • Minimal sedation
    • CNS depression, respiratory depression, paradoxical effects, good for pregnant women
  57. Promethazine (Phenergan)
    • Antihistamine
    • Mild sedation
    • Antiemetic, antimuscarinic
    • Respiratory depression, Hypotensive potential
  58. Hydroxyzine (Atarax)
    • Antihistamine
    • Mild sdedation
    • Anticholinergic and antiemetic effects
    • Respiratory depression, Hypotensive potential
  59. list the types of drugs used in I.V. sedation.
    • Diazepam (Valium): Benzodiazepine ~45mins 10-15mins Throbophlebitis
    • Midazolam (Versed): Benzodiazepine, not available in tablet form, only oral for KIDS ~45mins Up to 45 mins Interactions with CYP3A4 inhibitors, will have longer effect if on one of these
    • Pentobarbital (Nembutal): Barbiturate, not used that much in dentistry 2-3hrs NONE Contraindicated with certain porphyrias, CNS depression while increasing responses to noxious stimuli
    • Meperidine, (Demerol): Opioid 60-90mins NONE Contraindicated with MAO inhibitors (must be off for 2-3 weeks prior to use), can cause severe HTN
    • Fentanyl (Sublimaze): Opioid 30-45mins NONE Rapid bolus may lead to stiff-chest syndrome (give naloxone for reversal)
  60. list necessary monitors for I.V. sedation
    • 1) Pretracheal stethoscope
    • 2) Sphygmomanometer (automatic)
    • 3) Pulse oximeter
  61. California regulations concerning I.V. sedation.
    • Requires completion of a course for moderate sedation
    • Must be at least 60hrs didactic, 20 patient cases
    • Pediatric ORAL moderate sedation requires permit if kid under 13yrs old
    • OMFS, Pedo, Perio, GPR, AEGD, Dental Anethesia residency
    • 25hrs course
  62. discuss the different needs of these special groups as compared to the “normal” patient.
    • Pediatric: may ne unable to communicate, cooperate, or uncontrollable. More easily depressed and may not always maintain an airway
    • Geriatric: understand that the have decreased functional reserve and are not able to cope with stress as well as “normal” pops, which is an indication for mild sedation. May also take longer to clear the drug and are much more likely to have drug-drug interactions
    • Disabled: OK to sedate if high functioning. Otherwise, gotta do general anesthesia
    • Renal disease: treat day after dialysis
    • Seizure disorder: use benzos
    • Hyperthyroidism: decreased response
    • Hypothyroidism: increased response
  63. List appropriate sedative goals for these patients and techniques of sedation which are most likely to safely meet these goals.
    • Want conscious sedation: maintain protective reflexes. Maintain a continuous airway. Must be arousable, responsive to commands, conscious, not notable CVS depression
    • Remember: watch for over-sedation and if it isn’t working, it’s okay to give up and try again another day. Also: don’t use fucking chloral hydrate.
    • Also, must have a special certificate to sedate patients under age 13
  64. Extra-venous injection
    • Prevention: make sure you are in the vein by lowering the bag and seeing blood run into the line
    • Diagnosis: acute pain and swelling in immediate area
    • Treatment: will have delayed or no drug effect
  65. Intra-arterial injection
    • P: look to see if pulsatile blood running into line
    • D: pain radiating toward fingers caused by arteriospasm
    • T: Give 1% procaine (LA and vasodilator)
  66. Thrombosis
    • P: avoid unstable IV, small veins
    • D: redness, inflammation, pain
    • T: immobilize, heat, aspirin, elevation
  67. Nausea and vomiting
    • P: avoid opioids, predisposed pts
    • D: obvious
    • T: position, suction, anti-emetics (dexamethasone, diphenhydramine), avoid aspiration
  68. Emergence delirium
    • P: often with scopolamine, diazepam, midazolam
    • D: transient delirium, anxiety, rage
    • T: give physostigmine
  69. Respiratory Depression
    • P: avoid oversedation
    • D: not breathing properly, cyanosis
    • T: BLS, reversal agents (flumazenil for nbenzo, naloxone for opioids)
  70. Respiratory Obstruction
    • P: avoid oversedation, foreign bodies
    • D: difficulty breathing, cyanosis
    • T: head-tilt chin-lift. Good airflow: encourage cough. Bad airflow: Heimlich or abdominal thrusts
  71. Hypotension
    • P: know about meds, avoid getting up quickly
    • D: dizziness, nausea
    • T: trendelenberg
  72. define general anesthesia
    General anesthesia: (CA) Controlled state of unconcsiouness accompanied by partial or complete loss of protective reflexes, including inability to independently maintain an airway and respond appropriately to stimuli. CV may be impaired
  73. list the four stages and four planes of classic general anesthesia.
    • Stage 1: Analgesia (where we want patients with N2O)
    • Stage 2: Excitement stage (BAD for patients, may vomit, or salivate)
    • Stage 3: General Anesthesia, surgical plane
    • Stage 4: Respiratory paralysis (ALMOST DEAD)
  74. List recent hypotheses of the mechanism of action of general anesthesia.
    • 1) Lipid Theory: general anethestics act on the plasma membrane, causes fluidity
    • 2) Ion Channels: general anethestics inihibit excitatory functions of some CNS receptors such as neuronal ACh, glutamate or 5-HT3 receptors. Some others excite inhibitory receptors such as GABA-A (propofol and thiopental). In general they may decrease transmitter release presynaptically or decrease excitability of postsynaptic neurons
  75. list three common potent volatile anesthetics and discuss their advantages and disadvantages.
    • 1) Isoflurane
    • 2) Sevoflurane
    • 3) Desflurane-as soluble as N2O, very fast uptake
    • 4) N2O (not in hospital setting)
  76. list I.V. drugs commonly used for the induction of anesthesia.
    • 1) Propofol: almost everyone uses it
    • 2) Midazolam (benzodiazepines)
    • 3) Opiates (fentanyl or remifentanil)
    • 4) Ketamine (good for kids)
    • 5) Methohexital (Barbiturate): not used much anymore
  77. Cardiac Workload
    • (rate pressure product)
    • Systolic blood pressure x heart rate
    • Correlates myocardial oxygen consumption in pt with IHD
    • Relates to the onset of angina
    • Safe up to 20,000 in healthy pt.
    • 12,000 - compromised pt
  78. _________is released from the pituitary gland under conditions of stress and pain
    • B-endorphin
    • OS pts pretreated with dexamethasone had lower levels of circulating B-endorphin and significantly greater levels of postoperative pain
  79. A delta and C fibers from the orofacial region transmit nociceptive signals to the ________
    trigeminal nucleus caudalis
  80. Pain tolerance is ______ in the elderly, depressed, anxious and fatigued
  81. MAC for N2O
    • 104%
    • alveolar concentration at which 50% of the population will not react to surgical stimulus
  82. B/G coeff of N2O
  83. How can onset of anesthesia be delayed?
    • Increased blood flow to the lungs, delays equilibrium
    • Lots of patient movement will increase the muscle uptake and brain concentration will rise more slowly.
    • Hyperventilation decreases cerebral blood flow
  84. Notable medical conditions with N2O administration:
    • Bowel obstruction
    • Otitis media
    • Recent eye surgery using perfluoropropane (C3F8)
    • pneumothorax
    • nitrous oxide enters the gas-filled space faster than N2 can leave it.
    • Gas volume and pressure may become very high
  85. E cylinder has ______
    • 659 L of oxygen in the tank;
    • Also has 1590 L of nitrogen.
    • note: you will run through your nitrogen supply faster than your oxygen supply
    • -KNOW the size of G and H,K (the big cylinders)  about 10x the size of the E cylinder
  86. N2O abuse sequelae:
    • Nitrous oxide induced cobalamin deficiency
    • subacute combined degeneration of the spinal cord
  87. enzymes that need B12
    • Methionine synthase
    • Catalyzes the synthesis of methionine and tetrahydrofolate from homocysteine and 5-methyltetrahydrofolate
    • Methylmalonyl-CoA mutase
    • Leucine 2,3-aminomutase
  88. Verrill’s sign
    point when the pt’s eyes are halfway open), this is the end point for IV sedation
  89. minor patient
  90. old ages of note
    • >65: Geriatric
    • >80: ASA II
  91. Intra-arterial drug administration
    • Pain radiating towards fingers
    • Arteriospasm
    • Leave cannula in place, may administer 1% procaineER
  92. you will see thrombophlebitis occurring with _____
    • diazepam
    • (Inflammation precedes clot formation)
  93. Anaphylaxis vs. anaphylactoid
    • Consider diphenhydramine for skin reactions (50 mg IM/IV)
    • Use epinephrine for airway compromise (0.3 mg SQ/IM)
    • anaphylactoid: happens with meperidine
  94. emergence delirium Treatment
    • Give physostigmine
    • Reversible anticholinesterase
  95. respiratory depression tx:
    • Benzo’s - flumazenil
    • Opioids - naloxone
  96. IV placement and anesthesia maintenance
    • IV propofol and remifentanil for all cases
    • Ultrashort acting
    • Antinauseant (propofol)
  97. oversedation
    • falling asleep
    • uncooperative
    • laughs or cries uncontrollably
    • uncoordinated movements
Card Set:
2013-08-26 19:39:18

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