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anesthesia pharm II > inhalational agents: MOA; effects on ventilation and circulation > Flashcards

inhalational agents: MOA; effects on ventilation and circulation Flashcards

1
Q

what defines anesthesia?

A
  • muscle relaxation
  • unconsciousness
  • analgesia
  • suppression of autonomic reflexes
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2
Q

according to Eger, what is absolutely essential for anesthesia?

A
  • immobility (r/t spinal cord)
  • amnesia (r/t higher CNS, brain)
  • analgesia cant be assessed under anesthesia
  • unconsciousness and muscle relaxation not important as long as pt. is still and has amnesia
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3
Q

what is the MOA for immobility caused by inhalation agents?

A
  • site of action: spinal cord
  • not sure exactly where in spinal cord
  • one suggestion is the motor neuron
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4
Q

describe the theory of effect on receptors as MOA for immobility

A
  • indirect effect
  • depression of excitatory receptors N-methyl-D-asparate (NMDA) and AMPA; both mediate fast excitatory transmission at most synapses in the CNS
  • responds to changes in extracellular ligands like glutamate, the main excitatory neurotransmitter CNS
  • Na ion channels- hyperpolarized; inhibit presynaptic release of NTs, esp. glutamate (how lidocaine decreases MAC)
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5
Q

which receptors do not affect MAC

A
  • GABA
  • ACh
  • 5-HT
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6
Q

describe the Meyer Overton hypothesis for immobility MOA of inhalation agents

A

states that there is a direct correlation b/w the anesthetic potency and the lipophilicity (oil:gas partition coefficient)

  • suggests the site of action is likely lipid portion of the membrane, on the neuronal lipid bilayers
  • and indirect relationship b/w MAC and oil:gas partition coefficient (greater the coefficient, more lipophilic and higher the potency or lower MAC)
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7
Q

describe the membrane expansion theory of MOA for immobility r/t inhalation agents

A
  • agent moves into the lipid portion of the lipid bilayer causing a disruption of synaptic transmission or receptor function
  • 1950s study showed that anesthetized animals could be awakened by hyper pressurizing them to 100 atm. which “restored the cell membranes to the pre-anesthetic density”
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8
Q

what were the facts contradicting Meyer Overton (M-O) theory?

A
  • some transitional agents take much higher concentrations than M-O would suggest to cause immobility
  • other non-immobilizers, never cause immobility although M-O would suggest that it could (lipophilic but don’t cause immobility)
  • alcohols have a greater potency than M-O would suggest (hydrophilic but good immobilizers)
  • all three of these have water solubility or hydrophilicity component
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9
Q

what is the 3rd theory for MOA of inhalation agents to cause immobility?

A
  • anesthetic agents must be lipophilic and hydrophilic to work on both lipid and water portion of the lipid bilayer membrane
  • in doing so, agents change the amount or order of the motion of the lipid constituents; this changes the surface tension and the cellular and membrane function
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10
Q

describe the 5-angstrom theory of immobility from inhalation agents

A
  • site of action may actually be two sites of action (5 angstrom apart)
  • maximum potency is achieved w/ a molecule of 5 carbons long w/ two active sites at each end (less than or over 5, not as potent)
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11
Q

describe the MOA of inhalational agents to cause amnesia

A
  • site not at the spinal cord
  • possible site: reticular activating system- enhance inhibitory synaptic transmission, esp. involving GABA, the major inhibitory NT in the brain
  • Glycine: inhibitory NT in the cord and brainstem, is enhanced
  • other possible sites: hippocampus, amygdala, caudate putamen, parts of the cerebral cortex
  • may be d/t inhibition of release of excitatory NTs: may be d/t action on presynaptic Na channels or calcium ion channels
  • occurs at a site deeper than the membrane than site causing immobility
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12
Q

what is the theory for the MOA causing narcosis?

A
  • inhaled agents bind to specific sites on the membranes of proteins as opposed to disrupting lipid bilayers
  • sites may be GABA-a and glycine receptors
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13
Q

describe Geudel’s Stage 1

A
  • analgesia

- ends w/ loss of eyelash reflex and unconsciousness

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14
Q

describe Geudel’s Stage 2

A
  • excitement
  • irregular breathing, struggling
  • dilated pupils
  • susceptible to vomiting, coughing, laryngospasm
  • ends w/ onset of automatic breathing and loss of eyelid reflex
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15
Q

describe Geudel’s Stage 3, plane I

A
  • until eyes central w/ loss of conjunctival reflex
  • pupils normal or small
  • lacrimation increased (can tell if pt. getting light)
  • pharyngeal reflex abolished
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16
Q

describe Geudel’s Stage 3, plane II

A
  • until onset of intercostal paralysis
  • deep regular breathing
  • laryngeal reflexes abolished
  • loss of corneal reflex
  • pupils larger
  • when diaphragm pulls down, may see chest sink in
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17
Q

describe Geudel’s Stage 3, plane III

A
  • until complete intercostal paralysis
  • shallow breathing
  • lacrimation depressed
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18
Q

describe Geudel’s Stage 3, plane IV

A
  • until diaphragmatic paralysis

- carinal reflexes abolished

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19
Q

describe Geudel’s Stage 4

A
  • overdose
  • apnea
  • dilated pupils
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20
Q

what are signs of light anesthesia?

A
  • lacrimation, tearing
  • tachycardia
  • HTN
  • sweating
  • reactive, dilated pupils (can be d/t anticholinergics, opioids, etc.)
  • movement and laryngospasm (if no NMB utilized)
  • SNS stimulation seen since MAC BAR much higher than MAC
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21
Q

what are the effects of inhalation agents on ventilation in regards to depression?

A

dose related respiratory depression

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22
Q

what are the effects of response to CO2 and O2?

A
  • dose dependent depressed response to increase in CO2

- non dose dependent depressed response to decrease in O2 (oxyhemoglobin saturation)

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23
Q

describe breathing w/ light anesthesia compared to deeper planes

A
  • light: breath holding, irregular pattern of breathing; irregular depths of breaths
  • as anesthesia deepens, breathing changes to regular, faster rate w/ smaller tidal volumes (Vm changes little, but alveolar ventilation decreases w/ smaller Vt causing more dead space ventilation)
  • even deep plane, intercostal muscle function fails (may need help w/ positive pressure)
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24
Q

how is ventilation affected by inhalation agents?

A
  • minute ventilation may not change
  • alveolar ventilation decreases w/ increased dead space ventilation
  • resp. rate may be increased, tidal volume decreased
  • PaCO2 increases during spontaneous ventilation in proportion w/ the increase in the concentration of inhaled agent (response curve shifts right)
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25
Q

how does nitrous oxide affect the respiratory depression caused by potent volatile agents?

A
  • does not increase the CO2
  • if used, and concentration of volatile agent is decreased, there is less ventilatory depression compared to equivalent MAC of volatile alone
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26
Q

how do volatile agents shift the CO2 response curve?

A
  • response curve shifted right
  • takes a higher CO2 to produce the increase in Vm
  • opioids also shift curve right (additive effect), so don’t give opioids on induction
  • response improves overtime, but not to normal (5 hrs better than at 1 hr)
27
Q

at 1 MAC of either halothane, isoflurane, or desflurane, how much CO2 is required to stimulate breathing?

A
  • halothane: 42 mmHg CO2
  • isoflurane: 45 mmHg CO2
  • desflurane: 50 mmHg CO2
28
Q

at what levels do desflurane and sevoflurane lead to apnea?

A

b/w 1.5 and 2 MAC

29
Q

how can surgical stimulation affect CO2 response shift?

A
  • stimulation of surgery increase Vm by 40% and can decrease PaCO2 by 10%
  • increased production of CO2 offsets Vm
  • so w/ LMA, if deep for incision, may get apneic, but will start to breathe again on incision d/t stimulation
30
Q

what effect do inhalation agents have on hypoxic drive?

A
  • depress the response to hypoxemia, when PaO2 falls below 55 torr
  • response is blunted (50-70% depression) by as little as 0.1 MAC of halothane, isoflurane, and sevoflurane (not dose dependent)
  • 0.1 MAC of desflurane decreased the response by 30% w/ hypercapnia (w/ normocarbia, des doesn’t affect hypoxic drive much if at all)
  • 1.1 MAC causes 100% depression of hypoxic response
31
Q

what is doxepram good for?

A
  • respiratory stimulation
  • makes carotid bodies think PaO2 is as low as 38 mmHg
  • good for COPD pts., esp. if need to put deep but still want to breathe
32
Q

what are the effects of volatile agents on bronchi?

A
  • all agents cause bronchodilation if constricted (good for asthmatics)
  • greatest to least: sevoflurane-isoflurane-desflurane
  • w/o preexisting bronchoconstriction, airway resistance is essentially unchanged (may see 5% increase in resistance d/t low bronchomotor tone)
  • desflurane causes increased resistance in smokers
33
Q

what blunts the irritability of airways caused by desflurane?

A
  • prior administration of fentanyl 1 mcg/kg or morphine 0.1 mg/kg
  • addition of nitrous also blunts irritability
  • both desflurane and sevoflurane have been given to asthma pts. w/o causing vasoconstriction
34
Q

how much desflurane is ok to use, not causing bronchoconstriction?

A
  • up to 1 MAC, should be bronchodilation
  • over 1 MAC causes bronchoconstriction
  • can use desflurane w/ RAD, but if any slight signs of constriction (increases PiPs) just be safe and switch agents
35
Q

why is airway diameter reduced w/ volatile agents?

A
  • reduced lung volumes
  • reduced elastic forces keeping small, non-cartilaginous airways open
  • smaller airways (children) will see significant retractions so give positive pressure to help keep airways open
36
Q

describe airway irritation caused by some agents

A
  • pungent desflurane is an bronchial irritant above 6% (1 MAC), but does not cause irritation below 6%
  • increases w/ concentrations greater than MAC of isoflurane also
  • higher incidence in smokers
  • increases in mucociliary activity may reflect the effect of the airway irritant (desflurane-isoflurane/halothane)
  • only sevoflurane good for inhalation inductions
37
Q

what are ways to minimize airway irritation?

A
  • premedicate w/ an opioid (fentanyl 1.5 mcg/kg)
  • slower increase in desflurane concentration
  • induction w/ propofol (v. inhalation induction)
  • humidification of inspired gases
38
Q

what is the effect of inhalation agents on hypoxic pulmonary vasoconstriction (HPV)?

A
  • all can alter HPV, but at clinical doses of inhaled anesthetics, do not prevent HPV
  • typically causes vasodilation, but little effect on pulmonary vasculature
39
Q

describe the effects of inhalation agents on mean arterial pressure

A
  • dose-dependent decrease in MAP w/ all agents
  • at 2 MAC, BP decreases by 50% w/o stimulation
  • surgical stimulation minimizes decrease
  • lower MAP d/t changes in cardiac output, venous capacitance, and SVR
  • more drastic in elderly
  • different agents alter BP by different mechanisms
  • substituting a portion of the MAC w/ N2O decreases extent of drop on MAP
40
Q

by what mechanism does each agent decrease MAP?

A
  • halothane: decrease in inotropic effect (CO and SV)
  • all others decrease by drop in SVR
  • iso and des to a greater extent than sevo
41
Q

how do inhalation agents affect cardiac output?

A
  • all cause myocardial depression to some degree in a dose-dependent manner
  • LV stroke volume decreased 15-30%
  • decreased LV stroke volume may not translate into decreased CO d/t vasodilation and decreased SVR caused by des, iso, and sevo
  • *halothane cause dose dependent decrease in CO in healthy volunteers (greatest effect of depression)
42
Q

what does decreased myocardial contractility result in?

A

dose-dependent reduction in O2 demand

  • protectant
  • however, excessive concentrations can cause CV collapse
43
Q

what is unique about N2O effect on CO?

A
  • directly a myocardial depressant

- d/t mild sympathomimetic effects w/ increased catecholamine, usu. see an increase in CO

44
Q

describe inhalation agents effect on right atrial pressure

A
  • all agents BUT SEVO cause increased RAP (decreased function of LV cause fluid back up)
  • decreased forward pump causes higher pressure in the venous side or right atrium
  • N2O increases RAP d/t increased pulmonary vascular resistance (PVR)(avoid w/ pulm. HTN, congenital hearts, r to l shunts)
45
Q

describe inhalation agents effect on systemic vascular resistance

A
  • inhaled agents decrease the resistance to the skin, muscle, and the brain; but increase resistance to the splanchnic system
  • venodilators (decrease in venous return)
  • attenuate vasoconstriction r/t sympathetic stimulation
  • more exaggerated hypotension seen w/ HTN pts. when normotensive pt. (even if well controlled)
  • *can use to your advantage to dilate peripheral veins for IV
46
Q

w/ decreased SVR causing increase peripheral blood flow to skin, muscle, and brain, what are the results?

A

increased perfusion to these areas, resulting in :

  • skin: temp decreases and heat loss; high risk for hypothermia and shivering
  • muscle: delivery of NMB improved
  • brain: increased CBF; increased ICP
  • wasted perfusion compared to needs
47
Q

which agent has the better beta 2 agonist effect (vasodilation)?

A

isoflurane

48
Q

what is N2O effect on SVR?

A
  • does not decrease SVR
  • may actually cause vasoconstriction of cutaneous vessels
  • may offset drop in SVR
49
Q

how do agents compare in order from greatest change to least change in SVR?

A

isoflurane-desflurane-sevoflurane

50
Q

how do agents affect pulmonary vascular resistance (PVR)?

A
  • little effect of volatile agents on PVR
  • N2O causes increased pulmonary vascular resistance
  • neonates are vulnerable (closure not complete; increased PVR can open back up)
  • congenital heart defects/ shunts may be increased
51
Q

how do agents affect heart rate?

A
  • agent specific effect and concentration specific effect
  • sevo increases HR only at concentrations more than 1.5 MAC
  • iso and des increased HR at lower concentration
  • des worst offender (control by increasing slowly)
  • halothane does not increase HR d/t conduction effects (bradycardia)
  • response not impeded by meds (beta blockers)
  • effects ANS activity, SA node firing, and myocardial conduction
52
Q

who are increases in HR more frequently seen w/?

A
  • younger patients

- accentuated by vagolytic agents like atropine and pancuronium

53
Q

how do agents affect the baroreceptor reflex response?

A
  • dose dependent depression of the reflex responses
  • some agents eliminate baroreceptor reflex at low concentration
  • des attenuates response, but does not abolish
  • iso abolishes at 1.25 MAC v. 1.5
  • sevo, increasing to 4% (about 2 MAC) decreases response
54
Q

what happens when the baroreceptor reflex is abolished?

A
  • when BP decreases, there is no reflex response of an increase in HR
  • impacts us clinically r/t volume loss or position changes during anesthesia
55
Q

describe the volatile agents effect on coronary blood flow

A
  • coronary vasodilators acting on SMALL coronary arteries, can cause shift of blood from ischemic areas to non ischemic areas
  • coronary steal syndrome w/ iso (not clinically significant)
56
Q

describe cardioprotectant effects of inhalation agents

A
  • preconditioning
  • brief exposure of myocardium to volatile agents before myocardial ischemia results in faster recovery after reperfusion of ischemic myocardium and reduction in infarct size
  • similar effect on vascular endothelium may provide protection to other tissues also
  • isoflurane as low as 0.25 MAC may be effective
  • sevo has ben shown to be protective for CPB pts.
57
Q

define reperfusion injury

A

cellular injury caused by the reinstitution of the blood flow, not d/t the ischemia itself

58
Q

what are signs of a reversible reperfusion injury?

A
  • cardiac dysrhythmias
  • contractile dysfunction
  • microvascular injury
59
Q

what may be the MOA of cardioprotectant?

A

-protection probably results from an action on ATP-dependent potassium channels

60
Q

with 1-1.5 MAC in healthy individuals, in what order from greatest to least do agents decrease MAP?

A

halothane/isoflurane/desflurane-sevoflurane

61
Q

with 1-1.5 MAC in healthy individuals, in what order from greatest to least do agents decrease SVR?

A

isoflurane/desflurane-sevoflurane

  • none w/ halothane
  • w/ HTN, SVR effect is much more dramatic
62
Q

with 1-1.5 MAC in healthy individuals, in what order from greatest to least do agents decrease CO?

A

halothane-sevoflurane-(maybe a little w/ desflurane)

*none w/ isoflurane

63
Q

with 1-1.5 MAC in healthy individuals, in what order from greatest to least do agents increase HR?

A

isoflurane-desflurane (unless concentration increased slow)

  • none w/ sevoflurane
  • decreased HR w/ halothane
64
Q

with 1-1.5 MAC, which agent increases sensitivity to catecholamines?

A

halothane

anesthesia pharm II (5 decks)

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