Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
46 Cards in this Set
- Front
- Back
Meyer-Overton Theory |
Agent affects neuronal membrane by distortion of Na channels, leading to fewer action potentials |
|
Hepatic metabolism percentages of each anesthetic agent |
Des- .02% Iso- 0.2% Sevo- 2-5% Halo- 20% |
|
Gas uptake formula |
solubility x CO x (PA-PV)/PB
(PB- barometric pressure) |
|
Factors that affect uptake of gas from circuit to alveoli |
1. Inspired partial pressure 2. Alveolar ventilation 3. Circuit length, gas absorption in circuit |
|
Factors that affect transfer of gas from alveoli to arterial blood |
1. Blood:gas coefficient 2. cardiac output 3. Aa gradient |
|
Factors that affect transfer of gas from arterial blood to brain |
1. Brain:blood coefficient 2. CBF 3. Art-ven partial pressure gradient |
|
Solubility definition |
-the affinity of the anesthetic gas for blood and for gas at equilibrium (equal partial pressures)
|
|
Are insoluble agents taken up in the blood quickly or slowly? |
Quickly (slow uptake causes a faster increase in alveolar concentration) |
|
How does CO affect speed of induction |
The higher the CO, the lower the alveolar partial pressure, so induction is slower. Inversely, lower CO causes faster rise in alveolar concentration, so induction is quicker
R -> L shunt = slower induction L -> R shunt = faster induction |
|
Children have relatively high CO. Why is induction fast in children compared to adults? |
Low FRC, greater blood flow to vessel-rich group (75% of CO) |
|
Name the tissue compartments and their correlating percentage of blood flow (in adults) |
Vessel-rich (brain, heart, liver, kidneys) = 75% Muscle- 19% Fat- 6% Vessel-poor (tendons, bones) - negligible |
|
What is overpressuring? |
Increased inspired concentration of agent speeds uptake and alveolar concentration (makes soluble agent act like insoluble) |
|
What is second-gas effect? |
N20 leaves alveolus quickly, which leaves behind a relatively higher concentration of second gas, increasing its alveolar concentration |
|
Factors that increase speed of induction |
Low B:G coefficient Low CO Over-pressuring Low FRC High flows, MV L to R shunt |
|
Factors that slow speed of induction |
High B:G coefficient High CO Low alveolar ventilation R to L shunt |
|
How do anesthetic agents affect neuronal membrane function |
Alteration of gated ion channels in CNS (mainly GABAa) causing Cl- channels to open (inhibition of AP) and closure of calcium channels
Inhibition of excitatory NT's (mainly NMDA and AMPA/Kainate) |
|
Name the main excitatory neurotransmitters of the CNS |
Glutamate (principle excitatory NT) NMDA AMPA Kainate |
|
What does halogenation do to inhaled agents? |
supports their nonflammable status |
|
Describe the metabolism of halothane |
20% oxidative metabolism Can undergo reductive metabolism during hypoxia, causing nephrotoxicity |
|
What causes Compound A production? |
Interaction of soda lime and sevo Low flows increase risk Nephrotoxic |
|
Inhaled agents' effects on CBF and CMRO2? |
Increases CBF, decreases CMRO2 (uncoupling), except for N20 |
|
Inhaled agent effects on CV |
Decrease SVR (esp forane and desflurane) Decrease CO (esp halothane d/t direct myocardial depression) SA node depression, altered barorecptor reflex - esp halothane, except sevo, forane Forane dilates coronary vessels (inverse steal) |
|
How does halothane predispose to ventricular arrythmias? |
increases myocardial sensitization to epi Slows conduction through bundle of his and purkinje fibers, causing re-entry impulse |
|
Inhaled agents effect on respiratory system |
-Decreased TV, increased rate (directly affects -medulla and intercostal function) -Decreased response to hypoxia -Reduces airway resistance (bronchodilation) -Reduces HPV
|
|
Properties of an ideal inhaled agent |
-fast onset (low B:G solubility) -Cheap -not airway irritating -predictable -no PONV -bronchodilator -no metabolism -no adverse CV, hepatic, renal effects -CBF/CMRO2 uncoupling
|
|
Definition of MAC |
agent concentration which prevents movement in response to surgical stimulation in 50% of the population |
|
What MAC corresponds to ED95? |
1.3-1.5 MAC (MAC-BAR) |
|
What is MAC Awake? |
MAC when patients respond to verbal stimulus (~MAC 0.2) |
|
Factors that increase MAC requirements |
-young age -chronic ETOH -cocaine -MAOI, Tricyclic antidepressants -laudanosine -increased sympathetic activity -hypernatremia |
|
Factors that decrease MAC requirements |
-advanced age -hypoxia less than 38 torr -hypotension -hypothermia -acute ETOH -lidocaine -clonidine -hyponatremia -pregnancy -adjunct sedatives/narcotics |
|
Nitrous oxide values for Blood:gas, oil:gas, vapor pressure |
B:G- 0.47 O:G- 1.4 VP- 38,770 |
|
How does N20 affect CV function? |
Myocardial depression, counteracted by catecholamine release |
|
How is N20 teratogenic? |
oxidizes cobalt in vitamin B12, inhibits methionine synthetase (needed for myelin formation) and thymidylate synthetase (needed for DNA synthesis) |
|
Contraindications for N20 use |
-VAE -middle ear surgery -pneumo -bowel obstruction -COPD/emphysema -early pregnancy (teratogenic) -use of cement |
|
How does N20 cause gas expansion within a closed cavity? |
N20 is more soluble than nitrogen, so diffuses into cavities 34x faster than nitrogen leaves, causing gas expansion |
|
What is diffusion hypoxia? |
-as N20 is turned off during emergence, N20 diffuses from blood to alveoli, diluting O2 concentration (greatest in first 5 minutes) -Tx: high O2 flows |
|
Unique characteristics of halothane |
-undergoes 2 types of metabolism (oxidative, reductive in obesity or low PO2) -20% hepatic metabolism (hepatotoxicity) -can cause ventricular arrythmias - sensitizes heart to catecholamines -most effective bronchodilator -most potent cerebral vasodilator
|
|
Unique characteristics of ethrane |
- can cause seizure activity at 2 MAC, PaCO2 at 30 torr -increased CSF production, decreased absorption -2-5% hepatic metabolism, can cause release of fluoride molecules causing nephrotoxicity
|
|
Unique characteristics of isoflurane |
-potent peripheral vasodilator, decreases MAP by SVR reduction, CO is unaffected -reflexive increase in HR -can cause coronary steal -increases hepatic artery flow, decreases portal vein flow (increased hepatic oxygenation) -pungent (airway irritant) |
|
Unique characteristics of desflurane |
-high vapor pressure, boils at room temp -pungent (airway irritant) -causes transient increase in HR, BP and catecholamine levels during rapid increase |
|
Unique characteristics of sevoflurane |
-non pungent -3-5% degraded to fluoride in liver -compound A -possible proximal tubule injury (increased urinary secretion of N-acetyl-b-glucosaminidase) |
|
Desflurane Blood:gas, oil:gas, vapor pressure |
B:G- 0.42 O:G- 18.7 VP- 664 |
|
Sevoflurane Blood:gas, oil:gas, vapor pressure |
B:G- 0.65 O:G- 55 VP- 158 |
|
Isoflurane Blood:gas, oil:gas, vapor pressure |
B:G- 1.4 O:G- 91 VP- 238 |
|
Enflurane Blood:gas, oil:gas, vapor pressure |
B:G- 1.9 O:G- 96 VP- 172 |
|
Halothane Blood:gas, oil:gas, vapor pressure |
B:G- 2.3 O:G- 224 VP- 243 |