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90 Cards in this Set
- Front
- Back
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Anesthesia vs. general anesthesia vs. local anesthesia
- loss of sensation |
anesthesia
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Anesthesia vs. general anesthesia vs. local anesthesia
- loss of sensation associated with loss of consciousness |
general anesthesia
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Anesthesia vs. general anesthesia vs. local anesthesia
- localized loss of sensation without loss of consciousness |
local anesthesia
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T/F: All anesthetics produce reversible actions manifest by depression of excitable tissues such as nerves, smooth muscles, and myocardium.
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T.
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Four objectives of anesthesia.
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- hypnosis (amnesia): loss of consciousness. Level should be as mild as possible.
- analgesia: loss of pain, also obtunded CNS so that body would not cause reflex protective mechanisms to noxious stimulus. - hyporeflexia: decreased spinal reflex such as BP elevation, release of catecholamines, withdrawal of limbs. - neuromuscular blockade: adequate muscle relaxation. |
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What is balanced anesthesia?
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More than one agents may be needed to achieve the desired objectives required for a particular operation.
- pre-anesthetics: sedatives, analegesics, anticholinergic muscarinic blockers to dry secretions and reduce reflexes. - anesthetics - adjunctive: neuromuscular blocking drugs |
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What are some preanesthetic medications?
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- sedatives
- analegesics - anticholinergic muscarinic blockers to dry secretions and reduce reflexes. |
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What are some adjunctive agents for anesthesia?
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neuromuscular blocking agents
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What are the 4 stages of anesthesia?
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Stage I: analgesia
Stage II: excitement Stage III: surgical anesthesia Stage IV: medullary depression |
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Which stage of anesthesia is this?
- interruption of sensory transmission in spinothalemic tract, including nociceptive stimuli due to sensitive ells in the substantia gelatinosa in the dorsal horn of spinal cord. - minimal CNS depression - some amnesia - normal respiration and pupils - no eye movements - intact reflexes |
Stage I: analgesia
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Which stage of anesthesia is this?
- seen only with diethyl ether - blockade of small inhibitory neurons such as Glogi type II cells. Release and facilitation of catecholamines due to irritation of respiratory mucosa. - dilated pupils - marked eye movements - no blink reflex - irregular respiration, coughing |
Stage II: Excitement
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Which stage of anesthesia is this?
- progressive depression of ascending pathways in the reticular activating system (ARAS) - normal respiration - normal pupil - diminished eye movement to fixed stare - loss of swallowing, conjunctival and pharyngeal reflexes |
plane 1 of Stage III (surgical)
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Which stage of anesthesia is this?
- progressive depression of ascending pathways in the reticular activating system (ARAS) - slight depression of respiratory movements - loss of laryngeal and corneal reflexes - adequate for tonsillectomy |
plane 2 of Stage III (surgical)
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Which stage of anesthesia is this?
- progressive depression of ascending pathways in the reticular activating system (ARAS) - marked decrease in depth of inspiration - suppression of spinal reflex -> muscle relaxation - need mechanical respirator - preferred level for most surgeries |
plane 3 of Stage III (surgical)
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Which stage of anesthesia is this?
- progressive depression of ascending pathways in the reticular activating system (ARAS) - decreased depth of expiration - dilated pupil, won't respond to light - loose carinal reflex |
plane 4 of Stage III (surgical)
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Which stage of anesthesia is this?
- cardio-respiratry collapse due to depression of respiratory and vasomotor center of medulla - observed only at toxic doses - fixed dilated pupils |
stage IV (medullary depression)
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Induction phase correspond to to which Guedel stages?
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I and II
- the shorter the better |
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How to shorten the induction phase for a ventilation-limited GA?
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- hyperventilate
- decrease cardiac output |
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Ventilation-limited GA woulf have shorter or longer induction phase in these people?
- children - patients in shock or with thyrotoxicosis |
shorter
- high respiratory rate -> increased GA partial pressure |
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What can lengthen induction phase of perfusion-limited GA?
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- hyperventilation
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What can lengthen induction phase of ventilation-limited GA?
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- hypoventilation
- increased cardiac output/right-left shunt - COPD |
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T/F: the more soluble an anesthetic is in the blood, the higher will be the blood:gas(Oswald) coefficient, and the longer the induction phase and recovery periods.
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T.
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During the maintenance phase, what would produce deeper anesthesia and what would produce lighter anesthesia?
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- deeper: increase partial pressure or increase minute ventilation
- lighter: decrease partial pressure or decrease minute ventilation |
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Which is more soluble in blood, N2O or halothane?
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halothane: longer induction phase
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What are the three phases of distribution of GA?
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1. pulmonary
- related to partial pressure and solubility of GA in the blood 2. circulatory - vessel rich group (VRG) of highly perfused organs has low capacity and high flow. 75% cardiac output - muscle skin (MG) has high capacity and moderate flow - fat group (FG) has high capacity and low flow - 25% cardiac output goes to MG and FG (90% body mass) 3. tissue - brain must be perfused with a stable GA concentration - "lean" tissue have tissue/blood coefficient of 1 - perfusion limited transfer of GA at the lungs and tissues - potency of GA is directly related to lipid solubility |
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Ventilation or perfusion limited GA?
- slow, rate limiting equilibration of alveolar with inspire partial pressures - slow induction, slow recovery - can speed up by increase partial pressure in alveolar |
ventilation limited GA
- diethyl ether - enflurane - isoflurane - halothane |
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Ventilation or perfusion limited GA?
- quick induction and recovery - agents that are less soluble in blood induce anesthesia faster |
perfusion limited GA
- N2O - desflurane - sevoflurane |
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Ventilation or perfusion limited GA?
- diethyl ether - enflurane - isoflurane - halothane |
ventilation limited GA
- slow, rate limiting equilibration of alveolar with inspire partial pressures - slow induction, slow recovery - can speed up by increase partial pressure in alveolar |
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Ventilation or perfusion limited GA?
- N2O - desflurane - sevoflurane |
perfusion limited GA
- quick induction and recovery - agents that are less soluble in blood induce anesthesia faster |
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What are the cardiac output distribution and volume capacacity of the following organs?
- brain - liver - kidney |
VRG
- 75% cardiac output, 10% body mass - low volume capacity - high flow |
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What are the cardiac output distribution and volume capacacity of the following organs?
- muscle - skin - fat |
MG and FG (25% cardiac output, 90% body mass)
- MG (muscle and skin): high volume capacity and moderate flow) - FG (fat): high volume capacity and low flow |
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What are the cardiac output distribution and volume capacacity of the following organs?
- bone - cartilage - ligaments |
VPG
- negligible flow and capacity - ignored in calculations |
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What is the tissue/blood coefficient of "lean" tissue?
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1
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Ventilation or perfusion limited?
- transfer of GA in lungs and tissue during tissue phase |
perfusion limited
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Where do GAs with high lipid solubility concentrate?
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body fat
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Potency of GAs is directly related to ____.
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lipid solubility
- as oil/gas partition coefficient increase, potency increases (Meyer-Overton rule) |
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What is MAC?
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minimal alveolar concentration
- median effective anesthetic dose (ED50) - inversely proportional to potency |
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How to get TI (therapeutic indices)?
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TI = LD50/MAC
- LD50: lethal dose - MAC: ED50 |
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T/F: Anesthetics have steep dose-response curve and high therapeutic indices.
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F.
Anesthetics have steep dose-response curve and LOW therapeutic indices. |
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What is analgesic index?
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AI = MAC/AP50
- AP50: partial pressure causing analgesia in 50% of patients |
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What does high AI (analgeic index) mean?
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Analgesia is induced at partial pressure lower than that required for surgical anesthesia.
AI = MAC/AP50 - AP50: partial pressure causing analgesia in 50% of patients |
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Are there antagonists to correct GA overdose?
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NO!
But can closely regulate partial pressure in CNS by regulating partial pressure of inspired gas. |
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What is the major route of GA elimination?
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expiration
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Why are patients ventilated with O2 for a period of time after terminating anesthetics?
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To prevent diffusion hypoxia.
- exhalation of gases with low blood/gas coefficient is too rapid -> back diffusion displaces O2 in alveoli |
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How is halogenated GAs eliminated?
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- undergo microsomal liver metabolism
- may produce toxicity to liver and kidney due to free halogen radials produced |
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Since halogenated GAs may cause liver and kidney damage, why use it?
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halogenated GAs are noninflammable and nonexplosive -> safety factor
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What are the three major GA mechanism of action?
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1. activate K+ channels -> membrane hyperpolarization
2. directly activate GABA Cl channels (inhaled or IV anesthetics) 3. inhibit NMDA receptor (N2O, ketamine, xenon) |
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What are the physiological effect of GAs on CNS?
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- depress excitable tissue
- depress frequency of EEG (beta, alpha, delta waves) - decrease metabolic rate of brain - decrease cerebral resistance -> increase crerebral blood flow -> increase intracranial pressure (need to ventilate patient and keep PCO2 low) - poly-synaptic relexes are depressed more than mono-synaptic reflexes |
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What are the physiological effect of GAs on respiratory system?
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- suppressed RAS -> loose drive to increase ventilation during hypozia
- depressed respiratory center -> reduced sensitivity to CO2 - increase Pa(CO2) - depressed amplitude of respiration -> depressed Vt - increased rate of respiration, but insufficient to compensate for depressed Vt - depressed mucociliary function -> atelectasis, infections |
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Inhaled GAs can be used to treat status asthmaticus. How?
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bronchodilator
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What are GA effects on CV system?
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- altered vagal stimulation
- altered sympathoadrenal discharge - depressed baroreceptor reflexes result in - decreased CO - bradycardia |
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What are the effects of halogenated GA on CV system?
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- sensitize the myocardium to cardiac arrhythmias, in the presence of elevated levels of catecholamines (catecholamine sensitization)
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Which GA protects the myocardium from catecholamine sensitization by halogenated GAs?
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diethyl ether
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Mechaninis of catecholamine sensitization by halogenated GAs.
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local re-entry (Wolff-Parkinson-White syndrome)
- inhibition of myocardial gap junction communication. |
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What can you do to minimize the effect of catecholamine sensitization by halogenated GAs?
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- adequate O2 supply to keep minimum CO2 build up (prevent catecholamine release)
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Effects of GA on renal system.
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decrease urine output:
- decreased BP - vasoconstriction of kidney - central ADH stimulation |
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Effects of halogenated GA on renal system.
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direct nephrotoxicity
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Effects of GA on liver.
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decrease hepatic blood flow
- related to increase CO2, low O2, or catecholamine release |
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Effects of halogenated GA on liver.
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severe liver damage in people with defective hepatic cell membrane
- autoimmune response -> necrosis - most common with repeated short term exposure in women and obese patients |
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Effects of halogenated GA on uterus.
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uterine smooth muscle relaxation
- beneficial for intrauterine fetal manipulation during delivery |
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Name a GA that is excellent in both analgesia and muscle relaxation.
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diethyl ether
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Name a GA that is excellent in analgesia, but not really in muscle relaxation.
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N2O
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Name a GA that is excellent in muscle relaxation but not quiet in analgesia.
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- enflurane
- isoflurane |
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What is this GA?
- excellent analgesic and muscle relaxant - stimulate respiration down to plane 3 of stage 3 - bronchodilation - large safety margin - explosive, flammable - cause post-operative nausea and vomiting |
diethyl ether
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What is this GA?
- most commonly used in children and ischemic heart disease - smooth induction and recovery - bronchodilation - uterine relaxation, but may lead to increased blood loss after C-section - poor analgesia - profound myocardial depression - respiratory depression - may produce malignant hyperthermia |
halothane
- standard against which other GA are compared |
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What type of people are more susceptible to malignant hyperthermia?
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- AD characteristics linked to chromosome 19 which affects ryanodine receptor in sarcoplasmic reticulum Ca channel.
- males > 3 y.o., peak at age 20 |
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What should you worry about when you see these after giving GA?
- myopathy/neuropathy - muscle spasm/pain - elevated serum creatine phosphokinase - difficulty to intubate patient |
these are warning signs of malignant hyperthermia
- difficulty to intubate patient: prodromal sign. Muscle hypertonus in masseter muscle in response to succinylcholine (muscle relaxant) |
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What does this person have?
- body temperature rises 1 degree every 5-10 min - sinus tachycardia, myoglobinemia, hyperkalemia, metabolic acidosis - increased liver enzymes - increase in myoplasmic Ca2+ |
malignant hyperthermia
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Treatment for malignant hyperthermia.
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- stop the GA
- total body cooling - correct acidosis using sodium bicarbonate - continued high O2 supply - antedote: procaine or procainamide, or Dantrolene (block Ca release from SR) - correct hyperkalemia with insulin and glucose - IV manitol to clear myoglobin and prevent renal failure |
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What is this GA?
- non-flammable - excellent muscle relaxant - little or no sensitization toward arrhythmias - less risk of acidosis - may cause coronary steal - no EKG changes - less hepatic or renal toxicity - relaxes uterine smooth muscle - may cause cough, breath holding during induction - direct bronchiolar smooth muscle, good for status asthmaticus |
isoflurane
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What is this GA?
- good for outpatient surgery due to rapid induction and recovery - no liver or renal toxicity - cause respiratory irritation, coughing, breath holding, laryngeal spasm - cause increased BP and HR due to central sympathetic stimulation |
desflurane
- not recommended for patients with hypertension and heart disease |
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What is this GA?
- excellent analgesic and amnesic - no respiratory depression or CV depression if given 20% O2 - rapid induction and recovery - not capable of producing surgical anesthesia in un-premedicated patient - danger of diffusion hypoxia at the end of anesthesia. |
N2O
- MAC = 105, danger of hypoxia if given high dose -> dilutes O2 in alveoli, displaces N2 (increased pressure in bowel, middle ear, pneumothorax, pneumocephalus) - used at >50% but less than 70% in combination with volatile liquid GAs. |
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What is this GA?
- popular for outpatient anesthesia - does not produce tachycardia - most effective bronchodilation - forms toxic products if soda lime is used to absorb CO2 in anesthetic circuit |
sevoflurane
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What type of anesthetic is this?
- patient is awake and responsive but has catatonia, amnesia, and selective analgesia - acts on limbic system and cortex rather than RAS |
dissociative anesthetics
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What is this drug?
- produce good analgesia and amnesia - airway reflexes maintained - increases CO, HR, BP - may cause energence delirium - poor visceral analgesia thus not used in thoracic or abdominal surgery - contraindicated in neurosurgical procedures due to increased cerebral blood flow, O2 consumption, amd intracranial presusre |
ketamine (dissociative anesthetics)
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How to controll the emergence delirium caused by ketamine (dissociative anesthetic)?
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- barbituates (thiopenthal)
- benzodiazepine (diazepam) - psycho-sedatives (droperidol) |
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What type of anesthetic drug is this?
- patient is indifferent to surrounding along with recuced motor activity - patient remains responsive to voice instructions |
Neuroleptanalgesia (Innovar)
- fentanyl or sufentanil - droperidol analgesia produced by adding N2O |
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Adverse effect of Innovar.
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- fentanyl: cardiac slowing, hypotension, severe respiratory depression
- droperidol: QT prolongation -> torsade de pointes - combined: increase CSF pressure, nausea, vomit, extrapyramidal muscle movements |
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Name some induction agents.
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- ultra-short acting IV babituates (thiopenthal): highly fat soluble
- etomidate - propofol: IV emulsion |
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Disadvantage of IV analgesics.
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- loss of moment to moment control
- must wait for circulatory, renal and metabolic system to lower blood levels |
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Advantage of IV analgesics.
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- rapid induction: bypass pulmonary phase
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Which induction agent is this?
- short duration of action (5-10min): first dose only - redistribution from CNS to tissue: VRG, then MG, then FG - marked CNS depression -> respiratory depression - poor analgesia and muscle relaxation - useful in patients with cerebral edema |
ultra-short acting barbituates (eg thiopenthal)
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When is ultra-short acting barbituates contraindicated?
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patients with acute intermittent porphyria
- induces liver enzyme ALA synthase - affect liver microsomes - aggravate porphyria |
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Which induction agent is this?
- mild reflex tachycardia and transient apnea - cause nausea, vomit, injection pain, myoclonus - may cause phlebitis, thrombosis - may cause adrenal suppresion after single injection |
etomidate
- contraindicated for children <10yrs, pregnancy, and in delivery |
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Which induction agent is this?
- used for prolonged sedation in critical care unit because of rapid metabolism - most - inotrope - may lower coronary blood flow and CSF pressure - used for sedation during regional anesthesia and in patients requiring controlled ventilation |
propofol
- contraindicated for children in ICU |
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When is etomidate contraindicated?
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- children <10yrs
- pregnancy - in delivery |
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When is propofol contraindicated?
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children in ICU
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Which adjunctive drug to use?
- smooth induction |
- sedatives
- antihistamines |
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Which adjunctive drug to use?
- preoperative and postoperative pain |
- narcotics
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Which adjunctive drug to use?
- to dry respiratory and GI secretions - block vagal reflexes |
anticholinergics
- atropine - scopolamine |
