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Inhaled Anesthetics Review > Inhaled Anesthetics- General > Flashcards

Inhaled Anesthetics- General Flashcards

1
Q

Meyer-Overton Correlation

A

Dependent upon affinity for water or affinity for fat (fat/water partition coefficient). States anesthetics are soluble in fat

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2
Q

Unitary Theory

A

Cell membranes mostly lipid therefore majority of anesthetic effects come from effects on cell membranes

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3
Q

Concept of MAC

A

Analogous to plasma EC50 - 50% of nonparalyzed do not move with surgical stimulus. Universal measurement for inhaled anesthetic potency

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4
Q

Protein Centered Theory

A

Signaling proteins (ion channels/receptors) are the molecular site of action

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5
Q

Effects of Inhaled anesthetics on ligand gated ion channels

A

Potentiate GABA & Glycine, Inhibit Acetylcholine & glutamate

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6
Q

Effects of inhaled anesthetics on voltage gated ion channels

A

Nervous system - reduction in amplitude through sodium channels, CV system - reduction in amplitude and duration through calcium & potassium channels

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7
Q

Intracellular signaling mechanisms that inhaled anesthetics work on

A

G-protein coupled receptors, protein phosphorylation, gene expression

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8
Q

Cellular mechanisms of inhaled anesthetics

A

Hyperpolarize neurons - decrease neuronal excitability (determined by resting membrane potential, threshold potential & input resistance. Alter transmitter release presynaptic & neurotransmitter responses postsynaptic

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9
Q

How do volatile anesthetics enhance inhibitory synaptic transmission postsynaptically?

A

Potentiating ligand-gated ion channels activated by GABA & glycine, extrasynaptically by enhancing GABA receptors & leak currents, & presynaptically by enhancing basal GABA release

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10
Q

How do volatile anesthetics suppress excitatory synaptic transmission?

A

Presynaptically by reducing glutamate release (volatile agents) and postsynaptically by inhibiting excitatory ionotropic receptors activated by glutamate (gaseous agents)

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11
Q

Desired effects of inhalation agents

A

Immobility, unconsciousness, no learning/memory, sedation, neuroprotection, CV & respiratory protectants

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12
Q

How immobility is mediated

A

Probably by spinal cord NMDA receptors, requires 2.5-4X MAC needed for amnesia & unconsciousness

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13
Q

How unconsciousness is mediated

A

Hyperpolarization of thalamic sites, dimmer, not on/off, depends on interrupting synchronicity between multiple neural networks

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14
Q

How learning & memory is mediated

A

Possibly hippocampal & amygdala dependent (usually 0.3-0.4 MAC is enough)

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15
Q

How sedation is mediated in potent agents vs gases?

A

Potent agents probably stimulate GABA, gases (N2O & Xenon) possibly antagonize NMDA

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16
Q

How neuroprotection is mediated

A

All potent agents prevent apoptosis, decrease CMRO2 (by increasing inhibitory and decreasing excitatory transmission).

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17
Q

What is a neurological risk of inhaled anesthetics

A

Neurotoxicity- irreversible cell damage by N2O & less by potent agents

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18
Q

CV Effects of gases - general

A

Dose dependent myocardial depression, hypotension, SVR, direct negative chronotropic effects, sensitized to arrhythmogenicity, direct coronary artery vasodilation in vitron, coronary vasoconstriction in vivo

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19
Q

Pulmonary Effects of gases - general

A

Significant respiratory depression via central depression

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20
Q

Why are volatile anesthetics fluorinated?

A

Reduce or eliminate toxicity via metabolism, reduce/eliminate flammability, allow increased speed of induction and recovery from anesthesia

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21
Q

Basic hydrocarbon structures useful as fluorinated anesthetics include what?

A

ethane, methyl ethyl ether & propyl methyl ether

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22
Q

Most to least pungent anesthetic

A

Desflurane, isoflurane, halothane, sevoflurane

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23
Q

Potent inhaled anesthetics pulmonary effects- specifics

A

Decrease tidal volume in dose dependent manner (get less than adequate increase in RR & increased resting end tidal CO2). Decrease FRC, bronchodilation, increase activity of laryngeal irritant receptors and decrease activity of pulmonary irritant receptors, can adversely effect hypoxic pulmonary vasoconstriction. Effects on PVR are relatively small

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24
Q

Why does FRC decrease

A

Loss of intercostals, altered respiratory pattern, cephalad movement of diaphragm, altered thoracic blood volume

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25
Q

How are potent inhaled anesthetics bronchodilators

A

Decreases intracellular calcium concentration & reduces calcium sensitivity- Relaxes airway smooth muscle by directly depressing smooth muscle contractility- it directly effects bronchial epithelium and airway smooth muscle cells through phosphorylated myosin light chain, and indirectly inhibits reflex neural pathways.

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26
Q

What does an increase in pulmonary vascular resistance cause

A

Corresponding increase in pulmonary arterial pressure which promotes interstitial fluid transudation

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27
Q

When is pulmonary vascular resistance lowest

A

At lung volume equivalent to FRC

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28
Q

How do inhaled anesthetics effects hypoxic pulmonary vasoconstriction

A

Through vasodilation of pulmonary vascular bed and dose dependent myocardial depression, blood flow will get to the area that was restricted (such as in the case of a tumor)

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29
Q

Inhaled anesthetics protein binding site, effect & target

A

Amphiphilic site, effect: conformational flexibility/ligand binding, target: ion channels/receptors and signaling proteins

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30
Q

Inhaled anesthetics action potential site, effect & target

A

Site: Nervous system Effect: small reduction in amplitude, target: sodium channels. Site: CV system Effect: reduced amplitude & duration Target: Calcium & Potassium channels

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31
Q

Inhaled anesthetic inhibitory site, effect & target

A

Site: Presynaptic terminal Effect: enhanced transmitter release Target: unknown Site: Postsynaptic terminal Effect: enhanced transmitter effect Target: Glycine & GABAa receptors

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32
Q

Inhaled anesthetic excitatory site, effect & target

A

Site: Presynaptic terminal Effect: reduced transmitter release Target: sodium & K2P (2 pore potassium) channels Site: Postsynaptic receptors Effect: reduced transmitter effects Target: NMDA, nicotinic and acetycholine receptors

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33
Q

Inhaled anesthetic site, effect & target in neuronal networks

A

Site: neuronal circuit & integration Effect: Altered long term potential/depression, rhythmicity & coherence Target: synaptic plasticity HCN (non-selective ligand gated) channels, K2P (2 pore potassium) channels, extrasynaptic GABAa receptors

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34
Q

Inhaled anesthetic site of action, effect & target in CNS

A

Site: Neocortex/hippocampus/amygdala Effect: sedation & amnesia Target: delta & gamma rhythms, synchrony
Site: Diencephalon (thalamus) & brainstem (reticular formation) Effect: unconsciousness Target: ?gamma band
Site: Spinal cord Effect: immobility Target: nocifensive reflex, ?thalamic deafferentation

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35
Q

Inhaled anesthetic site of action, effect & target in CV system

A

Site: Myocardium Effect: negative inotropy Target: excitation-contraction coupling
Site: Conduction system Effect: dysrhythmias Target: action potential
Site: Vasodilation Effect: vasodilation Target: direct/indirect vasoregulation

36
Q

CO2 response curves with inhaled anesthetics

A

Expected to shift right, will get higher end tidal CO2 (secondary to medullary depression) and suppressed ventilatory response to hypercapnia in dose-dependent fashion (<0.2 MAC depress peripheral chemoreflex loop)

37
Q

Central & peripheral chemoreceptors & pulmonary effect with inhaled anesthetics

A

Respiratory controller in pontine (pneumotaxic center & apneustic center) & medullary (dorsal & ventral respiratory group) signal with GABAergic to inhibit drive of inspiratory and expiratory premotor neurons- sends inhibitory message to spinal cord/phrenic nerve to go to muscles of inspiration & expiration

38
Q

Central chemical control of respiration

A

Located near ventrolateral medulla, respond to changes in hydrogen ion concentration in CSF– NOT altered by arterial CO2 or pH. More profoundly affected by respiratory than by metabolic alterations in arterial carbon dioxide tension

39
Q

Peripheral chemical control of respiration

A

located in carotid bodies, sensitive to changes in arterial CO2 tension, pH & arterial oxygen tension

40
Q

Hypoxemia response to volatile anesthetics

A

All volatile anesthetics & N2O decrease ventilatory response to hypoxia in dose-dependent manner as low as 0.1 MAC

41
Q

What does the cephalad shifting of the diaphragm cause?

A

Decrease lung volumes FRC, increases V/Q mismatching in bases of lungs. As FRC decreases, closing volume increases & eventually overtakes the FRC so some alveoli never open = atelactesis

42
Q

About how much is the apneic threshold during spontaneous return of respiration for CO2

A

2-5 mmHg less than PaCO2 (if you give a big breath, CO2 will drop and patient will become apneic quickly)

43
Q

How inhaled anesthetics cause dose dependent depression of myocardial contractility

A

Alterations in intracellular Calcium homeostasis, inhibition of NaCa exchange, LV afterload reduction, LA myocardial depression & possibly LV diastolic dysfunction

44
Q

How inhaled anesthetics cause dose dependent hypotension

A

Decrease myocardial contractility & cardiac output. LV afterload reduction by iso, des & sevo

45
Q

How inhaled anesthetics cause direct negative chronotropic effects

A

Depression of SA node via direct & indirect effects on SA node automaticity (may produce bradycardia & AV conduction abnormalities) & baroreceptor reflex activity

46
Q

How inhaled anesthetics cause arrhythmogenicity

A

Sensitize myocardium to effects of epinephrine. *Halothane & iso have been shown to be cardioprotective against VFib from occlusion/reperfusion.. des/iso/sevo do not sensitize heart to PVCs

47
Q

How inhaled anesthetics cause coronary vasodilation

A

Reduced MVO2 and simultaneous decreased O2 extraction are indicative of coronary vasodilation

48
Q

Inhaled anesthetic neurologic effects

A

All increase CBF by decreasing cerebrovascular resistance = increased ICP (Halothane > Iso = Des = Sevo).
All decrease CMROs (iso slight cerebral protection)
Halothane blunts autoregulatory response of cerebral vasculature, sevo uncouples this by dilating cerebral vessels
Burst suppression effects
All depress SSEP & MEP - use TIVA

49
Q

Inhaled anesthetic neuromuscular effects

A

All have centrally mediated muscle relaxant properties. Iso=Des=Sevo>Halothane

50
Q

Inhaled anesthetic MH triggering properties

A

Halothane> Iso=Des=Sevo (N2O does not trigger!)

51
Q

Inhaled anesthetic hepatic effects

A

Decreased hepatic blood flow (as liver receives its blood supply from hepatic artery & portal vein): halothane>iso>des=sevo
Affected by age/gender/disease/genetics

52
Q

Hepatic metabolism of inhalation agents

A

Halothane>Iso>Des=Sevo .. iso/des/hal all metabolize to a trifluoroacetylated protein that may produce liver injury in susceptible patients (usually if they are hypoxic at same time). Iso & Des preserve hepatic artery blood flow better – probably maintain hepatic oxygen supply better than halothane. N2O not metabolized

53
Q

How inhalation agents are metabolized?

A

Catalyzed by phase 1 (CYP450) or phase 2 (uridine 5’ diphosphate transferase) enzymes

54
Q

Inhalation agents renal effects

A

Similar decreases in renal blood flow, glomerular filtration rate & urine output.

55
Q

Inhalation agents obstetrical effects

A

Decrease in uterine blood flow & contractility (don’t give postpartum = bleeding). Halothane>Iso=Des=Sevo

56
Q

Time Constant defined

A

A way of describing the amount of change that is occurring in a dynamic system

57
Q

Time Constant equation

A

capacity of the system (about 7 L) divided by flow into the system (in L/Min)

58
Q

How much is 1 TC, 2 TC, 3 TC & 4 TC

A

1- 63%
2- 85%
3- 95%
4- 98%

59
Q

How to calculate oxygen percentage of flow into the system

A

Say you have 3 L of oxygen (that is 100% oxygen), and 2 L air (21% oxygen, 79% nitrogen)… you will take 3 multiplied by 100 percent = 3, and 2 multiplied by 21% = 0.42..
3+ 0.42 = 3.42 then divide that by 7 (3.42/7)= 0.488 = 49% oxygen flowing into the system

60
Q

MAC awake

A

1/3-1/4 MAC

61
Q

MAC intubation

A

higher than classic MAC, this is more stimulating than incision

62
Q

MAC Incision

A

regular MAC

63
Q

MAC BAR

A

“blunt autonomic responses” 30-40% greater than MAC

64
Q

Factors that decrease MAC

A

advanced age, opioids, ketamine, IV local anesthetics, alpha2 agonists

65
Q

Factors that increase MAC

A

young age (up to 9 months, then drops over time)

66
Q

Awareness defined

A

postoperative recall of events occurring during general anesthesia

67
Q

Amnesic wakefulness defined

A

responsiveness during general anesthesia without postoperative recall

68
Q

Dreaming defined

A

any experience (excluding awareness) that patients are able to recall postoperatively that they think occurred during general anesthesia and that they believe is dreaming

69
Q

Explicit memory defined

A

Conscious recollection of previous experiences (“awareness” is evidence of explicit memory)

70
Q

Implicit memory defined

A

changes in performance or behavior that are produced by previous experiences but without any conscious recollection of those experiences (“unconscious memory formation” during general anesthesia)

71
Q

Uptake is related to (equation)

A

Q * lamda * [(Pa-Pv)/barometric pressure]
Q = cardiac output
lamda = blood/gas solubility
(pa-Pv) = alveolar to venous partial pressure gradient in mm Hg (%gas)
– low numbers decrease uptake, high increase uptake. No cardiac output = no uptake, no tissue gradient = no uptake

72
Q

Henry’s law

A

Amount of gas that dissolves in a liquid is directly proportional to the partial pressure of the gas over the liquid

73
Q

How to figure out partial pressure of gas

A

Barometric pressure multiplied by vol% of gas (6% des = 0.06 x 760 = 46 mmHg des)

74
Q

High Pa agent

A

High Fi = higher delivered concentration = greater uptake

75
Q

High Pv agent

A

High Fe = high tissue concentration = less uptake

76
Q

VRG (body weight & CO)

A

10% body weight, 75% cardiac output

77
Q

Muscle Group (body weight & CO)

A

50% body weight, 19% cardiac output

78
Q

Fat Group (body weight & CO)

A

20% body weight, 6% cardiac output

79
Q

FA/Fi ratio and difference between soluble & insoluble agents

A

insoluble agents reach higher FA/Fi, soluble are lower. A higher concentration of agent will cause ratio to be higher.

80
Q

Cardiac output and rate of rise of FA/Fi

A

Lower cardiac output increases rapidity of rise because less is taken up by blood and by tissues - leaves more in the alveoli

81
Q

Minute ventilation and rate of rise of FA/Fi

A

Greater minute ventilation increases rise more rapidly because more agent going to the lungs and tissues (no different in insoluble agents)

82
Q

What if CO & minute ventilation rise together - what happens to FA/Fi ratio

A

Rises faster

83
Q

Children Fa/Fi ratio

A

Have a larger VRG so proportion of CO to VRG is higher- faster induction in kids

84
Q

Deadspace and uptake of agents

A

Minimal effects

85
Q

R to L intrapulmonary shunts such as with R mainstem ETT what happens with uptake?

A

Over ventilated = more uptake, under ventilated = less uptake, evens out - less effect with soluble agents

86
Q

If 2/3 of inhaled anesthetic is taken up, how soluble is it and what is the Fa/Fi ratio?

A

Highly soluble, 33%

87
Q

If 1/4 of inhaled anesthetic is taken up, how soluble is it and what is the Fa/Fi ratio?

A

low solubility, 75%

Inhaled Anesthetics Review (6 decks)

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