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52 Cards in this Set
- Front
- Back
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Three anesthetics that dominated the first 100 years of anesthesia
M & M Ch 7: Inhalation Anesthetics |
Nitrous oxide
chloroform Ether |
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inhalational agents currently used
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Nitrous oxide
Isoflurane Desflurane Sevoflurane |
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Mechanism of action of inhalational agents
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unknown but thought to depend on attainment of a therapeutic tissue concentration in the CNS
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what does the actual composition of the inspired gas mixture depend on
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*Fresh gas flow rate
*Volume of the breathing system *Any absorption by the machine or breathing or breating circuit |
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How does uptake effect rate of induction
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The greater the uptake of anesthetic agent, the greater the difference between inspired and alveolar concentrations, and slower the rate of induction
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What are the three factors that affect anesthetic uptake
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1. solubility in the blood
2. alveolar blood flow 3. difference in partial pressure between alveolar gas and venous blood |
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how does the solubility of an anesthetic affect onset of action
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insoluble agents are taken up by the blood less avidly than soluble agents leading to the alveolar concetration of the insoluble agent rising quickly leading to a faster induction
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how are the relative solubilities of an anesthetic in the air, blood, and tissues expressed
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partition coefficients
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what is a partition coefficient
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the ratio of the concentrations of the anesthetic gas of the anesthetic gas in each of two phases of equilibrium
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what is equilibrium
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equal partial pressures in two phases
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what does a higher blood/gas coefficient translate into for an anesthetic
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the higher the blood/gas coefficient, the greater the anesthetic's solubility and the greater its uptake by the pulmonary circulation; the alveolar partial pressure rises more slowly and induction is prolonged
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in the absence of pulmonary shunting, what is alveolar blood flow essentially equal to
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cardiac output
(if cardiac output drops to zero, so will anesthetic uptake) |
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what does low output states predispose the patient to
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overdosage with soluble agents, as the rate of rise in alveolar concentrations will be markely increased
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what is the gradient of partial pressures between alveolar gas and venous blood dependent on
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tissue uptake
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what 3 factors determine the anesthetic transfer from blood to tissues
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1. tissue solubility of the agent
2. tissue blood flow 3.the difference in partial pressure between arterial blood and the tissue |
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what are the four groups that tissues can be divided into based on solubility and blood flow
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1.vessel-rich group
2.muscle group 3.fat group 4.vessel poor group |
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which is the first group to take up appreciable amounts of anesthetic and what organs are inlcuded
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the highly perfused vessel group which includes the brain, heart, liver, kidney, and endocrine organs
it is the first to fill |
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what is included in the muscle group and how long will uptake will be sustained
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skin and muscle
uptake is slower has larger volume so uptake will be sustained for hours |
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what does perfusion of the fat group nearly equal to
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muscle group
tremendous volume would take days to fill with anesthetic |
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what organs are included in the vessel poor group and how much uptake does it account for
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bones, ligaments, teeth, hair, and cartilage which have minimal perfusion leading to insignificant uptake
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what can lowering of the alveolar parital pressure be countered by
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increasing alveolar ventilation
(i.e. constantly replacing anesthetic taken up by the pulmonary bloodstream results in better maintenance of alveolar concentration) |
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what is the concentration effect
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increasing the inspired concentration which increases Fa/Fi and alveolar concentration
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what is the concentration effect a result of
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1. concentration effect
2. augmented inflow effect |
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what is the concentration effect more significant with
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more with nitrous oxide than with volatile anesthetics because volatile anesthetics can be used in much higher concentrations
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what are the routes of elimination for anesthetics
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biotransformation
transcutaneous loss exhalation |
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what factors speed recovery from an anesthetic
(most of which also speed induction) |
*elimination of rebreathing
*high fresh gas flows *low anesthetic-circuit volume *low absorption by the anesthetic circuit *decreased solubility *high cerebral blood flow (CBF) *increased ventilation *length of time the anesthetic has been administered |
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what is diffusion hypoxia
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elimination of nitrous oxide is so rapid that alveolar oxygen and CO2 are diluted resulting in diffusion hypoxia
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how can diffusion hypoxia be prevented
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administration of 100% O2 for 5-10 minutes after discontinuing nitrous oxide
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what is the definition of general anesthesia
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altered physiological state characterized by reversible loss of consciousness, analgesia of the entire body, amnesia, and some degree of muscle relaxation
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what is the unitary hypothesis
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all inhalation agents share a common mechanism of action at the molecular level
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what is the myer-overton rule
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anesthetic potency of inhalation agents correlates directly with their lipid solubility
(supports the unitary hypothesis) |
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what is the minimum alveolar concentration (MAC) of an inhaled anesthetic
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the alveolar concentration that prevents movement in 50% of patients in response to a standardiazed stimulus
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why is MAC useful
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*it mirrors brain partial pressure
*allows comparisons of potency between agents *provides a standard for experimental evaluations |
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what should the anesthetist keep in mind about the MAC
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*it is a statistical average
*limited value in managing individual patients, particularly during times of rapidly changing alveolar concentrations (i.e.induction) |
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what is MAC equivalent to
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median effective dose (ED50)
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what does 1.3 MAC of any volatile anesthetic roughly equal
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the level that will prevent movement in 95% of patients (an approximation of ED95)
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what is 0.3 - 0.4 MAC associated with
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awakening from anesthesia (MAC awake)
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what happens to MAC with increase in age of the pt
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6% decrease in MAC per decade of age, regardless of the volatile anesthetic
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factors that decrease MAC
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*hypothermia
*hyerthermia *elderly *acute intoxication *anemia (hct <10%) *PaO2 <40mmhg *PaCO2 >95 mmhg *BP with MAP <40mmhg *hypercalcemia *hyponatremia *pregnancy (decreased by 1/3 at 8 weeks; normal by 72 h postpartum |
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what drugs decrease MAC
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*local anesthetics
*opioids *ketamine *barbituates *benzos *verapamil *lithium *methlydopa *clonidine *precedex *chronic amphetamine use |
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factors that increase MAC
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*young age
*chronic alcohol abuse *hypernatremia *acute amphetamine use *cocaine *ephedrine |
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physical properties of nitrous oxide
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*only inorganic anesthetic
*colorless/odorless *supports combustion *gas at room temp and ambient pressure *inexpensive |
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cardiovascular effects of nitrous
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*stimulates SNS
*depresses myocardial contractility *no change in arterial BP, CO and HR *increases pulmonary vscualr resistance leading to elevation of RV end diastolic pressure *may be associated with a higher incidence of epinephrine induced arrythmias |
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respiratory effects of nitrous
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*increases resp rate
*decreases tidal volume *depressed hypoxic drive *minimal change in minute ventilation |
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effects of nitrous on cerebral
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*by increasing CBF and cerebral blood volume, nitrous produces mild elevation of ICP
*increases cerebral oxygen consumption *levels below MAC provide analgesia in dental surgery and oter minor procedures |
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effects of nitrous on neuromuscular system
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*no significant muscle relaxation
*NOT triggering agent of malignant hyperthermia *skeletal rigidity in high concentrations |
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renal effects from nitrous
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*decrease renal blood flow by increasing renal vascular resistance
*decrease GFR and UO |
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nitrous effects on GI
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*PONV
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what can prolonged exposure to anesthetic concentration of nitrous lead to
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bone marrow depression (megaloblastic anemia) and neurological deficiencies (peripheral neuropthies and pernicious anemia)
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contraindications of nitrous use
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*air embolism
*pneumothorax *acute intestinal obstruction *intracranial air (tension pneumocephalus or pneumoencephalography) *pulmonary air cysts *intraocular air bubbles *tympanic membrane grafting *pt with trach |
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physiucal properties of halothane
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*halogenated alkane
*nonflammable *thymol preservative (retards spontaneous oxidatvie decomposition) *least expensive volatile |
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effects of halothane on cardiovascular
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*dose dependent reduction of arterial BP due to direct myocardial depression (2.0 MAC of halothane results in a 50% decrease in BP and CO)
*coronary artery vasodilator *decreses coronary blood flow due to decrease in arterial BP *compensatory rise in HR and decrease in vagal stimulation becuse of hypotensio *junctional rhythm or bradycardia ***sensitizes heart to arrythomogenic effects of epinephrine so that doses above 1.5 mcg/kg should be avoided *SVR unchanged |
