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Anesthesia Pharm > Week 4 - ANS Physiology/Pharmacology > Flashcards

Week 4 - ANS Physiology/Pharmacology Flashcards

1
Q

What is the function of the ANS?

A

Controls visceral body functions and modulates BP, GI motility & secretion, bladder emptying, sweating & temperature maintenance

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2
Q

Where does activation of the ANS occur?

A

Hypothalamus: response to stress, BP control, Temp regulation

Brain stem (Medulla/Pons): hemodynamic and ventilatory control

Spinal cord

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3
Q

What are the divisions of the Autonomic Nervous System?

A

Sympathetic Nervous System
Parasympathetic Nervous System
Enteric Nervous System

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4
Q

What is the location of the SNS and its response?

A

Thoracolumbar – Fight, Flight, or Fright

-Increases responses

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5
Q

What is the location of the PNS and its response?

A

Craniosacral – Rest and Digest

  • Relaxes and targets responses
  • Salivation, Lacrimation, Urination, Digestion/Defecation, Sexual arousal
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6
Q

What is the Enteric Nervous System?

A

Third branch of ANS

A system of neurons and supporting cells within the walls of the GI tract including cells of the pancreas and gall bladder

Locally autonomous in contrast to sympathetic and parasympathetic but influenced by the SNS and PNS activity

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7
Q

What organs only have sympathetic innervation?

A

Spleen
Certain blood vessels
Piloerector muscles

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8
Q

What is response to SNS stimulation on the heart?

A
  • Increased HR (SA node)
  • Increased conduction velocity of AV node
  • Increased automaticity, conduction velocity of His-Purkinje system
  • Increased contractility, conduction velocity of the ventricles
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9
Q

What is response to PNS stimulation on the heart?

A
  • Decreased HR (SA node)
  • Decreased conduction velocity of AV node
  • Minimal effect on His-Purkinje system
  • Minimal effects with possible slight decrease in contractility of the ventricles
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10
Q

What is response to SNS and PNS stimulation on bronchial smooth muscle?

A

SNS = bronchial relaxation

PNS = bronchial contraction

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11
Q

What is response to SNS stimulation on the GI tract?

A
  • Decrease motility
  • Decrease secretion
  • Sphincter contraction
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12
Q

What is response to PNS stimulation on the GI tract?

A
  • Increase motility
  • Increase secretion
  • Sphincter relaxation
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13
Q

What is response to SNS stimulation on the urinary bladder?

A
  • Smooth muscle relaxation

- Sphincter contraction

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14
Q

What is response to PNS stimulation on the urinary bladder?

A
  • Smooth muscle contraction

- Sphincter relaxation

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15
Q

What is response to SNS stimulation on the eye?

A
  • Mydriasis (pupil dilation)

- Relaxation of ciliary muscle for far vision

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16
Q

What is response to PNS stimulation on the eye?

A
  • Miosis (pupil constriction)

- Contraction of ciliary muscle for near vision

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17
Q

What is response to SNS stimulation on the liver?

A

Glycogenolysis and Gluconeogenesis

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18
Q

What is response to PNS stimulation on the liver?

A

Glycogen synthesis

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19
Q

What is response to SNS and PNS stimulation on salivary gland secretion?

A

SNS = increase

PNS = marked increase

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20
Q

What receptors are SNS?

A

Adrenergic:

  • Alpha-1/Alpha-2
  • Beta-1/Beta-2
  • Dopa-1/Dopa-2
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21
Q

What receptors are PNS?

A

Cholinergic:

  • Muscarinic - M1,2,3,4
  • Nicotinic - N1,2
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22
Q

What nerve conducts 75% of PNS signals?

A

Vagus nerve (CN X)

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23
Q

A local anesthetic blockade of the Stellate Ganglion causes what syndrome?

A

Horner’s Syndrome

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24
Q

What is Cushing’s Triad?

A

Increased ICP, Bradycardia, and Hypertension

  • Intracranial HTN –> SNS mediated systemic HTN
  • Activation of the PNS medullary centers via the baroreceptor slows the heart rate (baroreceptor response not enough to reduce HTN)
  • Results in increased blood flow to the brain and further increased ICP
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25
Q

What is Autonomic Hyperreflexia?

A
  • Disruption of efferent impulses down the spinal cord from T5 or higher
  • Exaggerated SNS response to bowel, bladder, or surgical stimulation due to receptor sensitivity secondary to denervation
  • Loss of inhibitory impulses results in pure SNS response (HTN)
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26
Q

What is the Thermogenesis Reflex?

A
  • Sweating controlled by cholinergic fibers (blocked by atropine or nerve blocks)
  • Shivering decreased in elderly, absent in newborns/infants, blocked by NDMR’s
  • General anesthetics impair thermogenesis
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27
Q

What is the Baroreceptor Reflex?

A
  • Stretch receptors in aorta and carotid arteries sense increased pressure which sends signals via Hering nerve and Vagus nerve to the medulla
  • Causes decreased HR, BP, Contractility and PVR
  • Phenylephrine (alpha1 agonist) increases BP and reflex decreases HR
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28
Q

What is the Chemoreceptor reflex?

A
  • Central sense increased arterial CO2 and/or decreased arterial pH (hypercarbia increases minute ventilation
  • Peripheral in carotid body respond to decreased pO2 (Hering/Vegus nerve increases RR and tidal volume –> increased minute ventilation) (may also see increased HR/CO)
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29
Q

What is the Bainbridge reflex?

A
  • Increased CVP activates stretch receptors in the atria
  • Afferent impulses through vagus inhibit PNS output resulting in tachycardia
  • Seen during labor when contractions autotransfuse and increase CVP
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30
Q

What is the Bezold-Jarisch reflex?

A

Hypotension, Bradycardia, Coronary Dilation

  • Noxious stimuli sensed in the cardiac ventricles
  • Unmyelinated C-fibers of vagus send signal to enhance baroreceptor response, inhibit sympathetic output, and decrease PVR to make it easier for the heart to pump
  • Increased blood flow to the myocardium to decreased work of the heart (cardioprotective)
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31
Q

What is the Valsalva reflex?

A

Increased intrathoracic pressure, Decreased venous return, Decreased cardiac filling, Decreased BP

  • Baroreceptor increases HR, increases inotropy –> increased BP
  • Baroreceptors cause PNS induced decrease HR
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32
Q

What is the Oculocardiac (Five & Dime) Reflex?

A
  • Afferent impulses to pressure on the eye or pulling on eye muscle
  • Efferent slowing of HR via the Vagus nerve
  • Muscarinic response blocked by Atropine or Glycopyrrolate
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33
Q

What are some anesthetic interactions with the ANS?

A
  • Alpha2 agonists (inhibitory) reduce anesthetic needs
  • Fentanyl depresses SNS tone and promotes vagal activation
  • Desflurane depresses the ANS, stimulates the SNS
  • Depression of the SNS by anesthetics appears to dominate
  • Regional anesthesia and SNS blockade
  • Postoperative complications secondary to ANS dysfunction
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34
Q

How does aging affect the ANS?

A
  • HTN and orthostasis
  • Temperature regulation (increased or decreased)
  • Increased circulating norepinephrine (receptor down-regulation/decreased responses to exogenous catecholamines)
  • Beta agonists are going to have decreased effects on HR, CO, and vasodilation secondary to reduced receptor response
  • Decreased renin, decreased aldosterone, increased atrial natriuretic factor leads to salt wasting and hypovolemia
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35
Q

What affect does DM have on the ANS?

A

20-40% insulin dependent DM have neuropathies (ANS)

Labile BP, gastroparesis, thermoregulation, vagal dysfunction

Increased aspiration risk, aggressive temp maintenance, increased c/o

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36
Q

How does dysautonomia affect the ANS?

A

Shy-Drager syndrome
Guillain-Barre
Lamber-Eaton
Familial

Orthostatic Hypotension, HR variability, BP lability

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37
Q

Where is norepinephrine and epinephrine synthesized?

A

From tyrosine in the adrenal medulla

80% epinephrine 20% norepinephrine

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38
Q

What is the release of Norepinephrine into the synaptic cleft dependent on?

A

Calcium

*Alpha2 receptors are pre-synaptic and provides a negative feedback loop that modulates the release of Norepi by inhibiting the Ca++ release mechanism

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39
Q

What terminates the action of Norepinephrine at the synapse?

A

Diffusion away from the synaptic cleft and metabolism by MAO & COMT

Reuptake = 80% Metabolism = 20%

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40
Q

How does reuptake of Norepinephrine occur and what is it dependent on?

A

Via two active transport mechanisms:
-One into varicosities & Second into cytoplasm synaptic vesicle for storage

Dependent on magnesium and ATP, cytoplasm may be blocked by drugs (cocaine & tricyclics)

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41
Q

How is Norepinephrine metabolized?

A

By MAO - although it is minimal (mostly reuptake)
Residual vulnerable to metabolism by COMT

COMT not affected by drugs – MAO inhibitors can increase levels of NE
Metabolized NE is excreted in urine as metabolite VMA (high levels of VMA indicate pheochromocytoma)

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42
Q

How is ACh synthesized, stored, and metabolized?

A

Synthesized in pre and post ganglionic parasympathetic nerves
-Choline acetyltransferase catalyzes acetyl coA in mitochondria to form ACh

Stored in synaptic vesicles, released via PNS

Metabolism: rapidly hydrolyzed by AChE, plasma cholinesterase is too slow to metabolize ACh unless succinylcholine or mivacuriumn is given

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43
Q

What is the neurotransmitter for the SNS?

A

Norepi = SNS post-ganglionic

ACh = SNS pre-ganglionic

44
Q

What is the neurotransmitter for the PNS?

A

ACh = PNS pre-ganglionic and post-ganglionic

45
Q

What receptors does epinephrine act on?

A

+ Alpha
++ Beta1
++ Beta2

  • Direct action
  • Has CNS stimulation
46
Q

What are the physiologic effects of epinephrine?

A
  • Moderate increase in CO and HR
  • Marked increase in dysrhythmias
  • Arteriolar vasoconstriction/Pulmonary artery vasoconstriction
  • Moderate decrease in renal blood flow
  • Minimal increase in MAP
  • Moderate decrease in airway resistance
47
Q

What are the Adrenal standard secretion rates of Epi and Norepi?

A

Epi = 0.2 mcg/kg/min

Norepi = 0.05 mcg/kg/min

48
Q

What are the exogenous infusion rates for Epinephrine?

A

Continuous Infusion: 1-20 mcg/min
2-10 mcg/min (beta1, beta2)
>10 mcg/min (alpha1)

  1. 2-0.5mg SubQ for anaphylaxis
    * Beta2 receptors are more sensitive to lower epi doses while effects on alpha1 receptors predominate at higher doses
49
Q

What receptors does Norepinephrine act on?

A

+++ Alpha
++ Beta1
+ Beta2
Greater alpha and less beta effects than Epi

  • Direct action
  • No CNS stimulation
50
Q

What are the physiologic effects of Norepinephrine?

A
  • Minimal decrease in CO and HR
  • Minimal increase in dysrhythmias
  • Marked Increase in Peripheral Vascular Resistance
  • Marked decrease in renal blood flow
  • Marked increase in MAP
51
Q

What is the dose for Norepinephrine?

A

4-12 mcg/min (4-16 mcg/min according to the table on slide 27)

  • Low dose - beta1 dominates and BP increases secondary to increased CO
  • High dose - alpha1 dominates and BP increases and HR/CO may decrease secondary to baroreceptor reflex
52
Q

What are the endogenous catecholamines?

A

Epinephrine
Norepinephrine
Dopamine

53
Q

What receptors does Dopamine act on?

A 
Dopamine1
Dopamine2
\++ Alpha
\++ Beta1
\+ Beta2
  • Direct action
  • No CNS stimulation
54
Q

What are the physiologic effects of Dopamine?

A
  • Marked increase in CO
  • Minimal increase in HR/dysrhythmias
  • Minimal increase in peripheral vascular resistance
  • Marked increase in renal blood flow
  • Minimal increase in MAP
55
Q

What is dopamine?

A

Precursor to Norepi and Epi

Central and peripheral neural transmission

Exogenous does not cross BBB (endogenous does)

56
Q

What are the doses for Dopamine? What receptors are activated at each dose?

A

2-20 mcg/kg/min

Low Dose: 1-3 mcg/kg/min (D1 activation: coronary, renal, mesenteric, and cerebral vasodilation and inhibit Na/K pump)
Moderate Dose: 3-10 mcg/kg/min (Beta-1)
High Dose: >10 mcg/kg/min (Alpha-1)

*Dose dependent model false – no renal dose

57
Q

How are catecholamines metabolized?

A

COMT is intracellular
MAO in nerve terminal mitochondria (analyze metanephrines and VMA for pheochromocytoma)

*Exogenous catecholamines may resist COMT and MAO metabolism

58
Q

What is Fenoldopam? Dose?

A

Partial D1 receptor agonist – Exogenous Catecholamine

  • Minimal D2, alpha, or beta effects
  • 10x potency of dopamine

Dose: 0.1-0.8 mcg/kg/min
-0.1-0.2 mcg/kg/min produce renal vasodilation, increases renal blood flow and GFR, and increases Na excretion

*Improved outcome in CABG pts with less renal failure

59
Q

What are the effects of alpha1 agonists on BP, CO, HR, and MVO2?

A

Increase BP
No effect on CO
Decrease HR (baroreceptor response)
Increase MVO2 supply

60
Q

What is Phenylephrine?

A

Synthetic Noncatecholamine – Direct Acting
Almost purely alpha agonist

Greater veno-constricion than arterial constriction (increases venous return, maintains CO, HR decreases secondary to baroreceptors)

NOT contraindicated in OB

61
Q

What is Methoxamine?

A

Synthetic Noncatecholamine – Alpha1 Agonist – Direct acting

Greater arterial constriction than veno-constriction
Longer acting

*NO longer in clinical use

62
Q

What is the class, use, and duration of Midodrine?

A

Synthetic Noncatecholamine – Alpha1 agonist – Direct acting

PO - used for dialysis induced hypotension

T1/2 = 3 hrs Duration = 4-6 hrs

63
Q

What is the dose for Phenylephrine?

A

Single dose = 50-100 mcg

Infusion dose = 20-50 mcg/min

64
Q

How do indirect acting sympathomimetics work?

A

Cause the release of “stored” norepinephrine in the synaptic vesicles

*Beware in pts taking TCAs (NE reuptake inhibition) and MAOIs (NE breakdown inhibition)

65
Q

What is Ephedrine?

A

Synthetic Noncatecholamine

Indirect and Direct actions on alpha and beta receptors (++ alpha, + beta)
-Competes with NE for reuptake in vesicles so NE stays at receptor sites longer

Increases HR, CO, and BP
Tachyphylaxis (becomes less effective due to depletion of NE stores)
May increase MAC secondary to stimulatory effects on CNS

66
Q

What is the dose of Ephedrine?

A

10-25 mcg (single dose) — Infusions not used

Given IV or IM

67
Q

What class is amphetamine, methamphetamine, and methylphenidate?

A

Exogenous Catecholamines – Indirect acting sympathomimetics

Amphetamine and Methamphetamine:

  • CNS stimulants, alpha/beta stimulants
  • Cause release of and inhibit reuptake of stimulating neurotransmitters
  • Effects related to alpha/beta stimulation
  • Treatment of OD may include Dantrolene to decrease temp

Methylphenidate: similar effects but milder, used to treat ADHD

68
Q

What are the effects of alpha2 agonists?

A
  • Decreased CNS sympathetic output
  • Decreased presynaptic Norepi release
  • Sedation, hypnosis, sympatholysis (blocks SNS), neuroprotection, diuresis, inhibition of insulin and HGH secretion
  • Rapid delivery may increase BP secondary to postsynaptic alpha2b receptor mediated arterial and venoconstriction
69
Q

What are the beneficial anesthetic effects of alpha2 agonists?

A

Anxiolysis
Sedation
Decreased MAC
Decreased opioid induced chest wall rigidity
Decreased BP response to ETT, extubation, and incision
Decreased post-anesthesia shivering

70
Q

What is Dexmedetomidine, its benefits, and its dose?

A

Selective alpha2 agonist

  • PACU pts on Dex require less morphine
  • Decreased postop analgesics, beta blockers, antiemetics, diuretics, and Epi for CABG pts

Load Dose: 1 mcg/kg/hr over 10-20 min
Infusion Dose: 0.2-0.7 mcg/kg/hr

*Beware hypotension and bradycardia (overtime due to blockage of NE release)

71
Q

What is Clonidine and its dose?

A

Alpha2 Agonist (220:1 alpha2:alpha1)

Oral dosing Q8 hours (do not hold preop due to rebound HTN)
Intrathecal: 10-50 mcg, epidural 75-150 mcg
-Black box for pregnant women

72
Q

What receptors does Isoproterenol act on?

A

+++ Beta1
+++ Beta2
No Alpha

  • Direct action
  • Has CNS stimulation
73
Q

What are the physiologic effects of Isoproterenol?

A
  • Marked increase in CO, HR, and dysrhythmias
  • Moderate decrease in peripheral vascular resistance
  • Minimal decrease in renal blood flow
  • Marked decrease in airway resistance

*Nonselective beta agonist

74
Q

What is the dose for Isoproterenol?

A

Single Dose: 1-4 mcg (metabolized very quickly)

Infusion: 1-5 mcg/min

-High dose causes tachycardia and hypotension

May be used as a chemical pacemaker (mostly used in heart blocks)

75
Q

What receptors does Dobutamine act on?

A

+++ Beta1
+ Beta2

*Direct acting

76
Q

What are the physiologic effects of Dobutamine?

A
  • Marked increase in CO
  • Minimal increase in HR
  • Moderate increase in renal blood flow
  • Minimal increase in MAP
  • Decreases LV filling
77
Q

What is the dose for Dobutamine?

A

2-10 mcg/kg/min

-Prolonged infusion can cause myocarditis

78
Q

Rank the following in their potency on alpha1 arterial/venous vasoconstriction:
-Epinephrine, Norepinephrine, Dopamine, Phenylephrine, Ephedrine, Methoxamine, Isoproterenol, Dobutamine

Table on slide 38

A 
Norepinephrine +++++/+++++
Phenylephrine ++++/+++++
Epinephrine ++++/++++ (at high doses)
Dopamine ++++/+++ (at high doses)
Methoxamine +++++/++++
Ephedrine ++/+++
Dobutamine 0
Isoproterenol 0
79
Q

What are the physiologic effects of alpha1 receptor activation?

A

Vasoconstriction of blood vessels of skin, GI tract, Kidney, Brain

Contraction of smooth muscles of ureter, vas deferens, urethral sphincter, uterus, ciliary body (mydiarisis)

Glucose metabolism: gluconeogenesis, glycolysis

80
Q

What are the physiologic effects of alpha2 receptor activation?

A

Glucose metabolism: inhibits insulin release, stimulates glucagon release

Contraction of anal sphincter

Inhibits release of Norepi

81
Q

What are the physiologic effects of beta1 receptor activation?

A

Increase HR (+ chronotropic)
Increase impulse conduction (+ dromotropic)
Increase contraction (+ inotropic)
Increase ejection fraction
Increase renin release by Juxtaglomerular cells
Increase hunger (increase ghrelin release by stomach)

82
Q

What are the physiologic effects of beta2 receptor activation?

A

Smooth muscle relaxation of bronchus, bronchioles, detrusor muscle, uterine muscle
Contraction of urethral sphincter
Increase renin release by Juxtaglomerular cells
Glucose metabolism: inhibits insulin release, stimulates gluconeogenesis, glycolysis
Lipolysis
Thickened salivary secretion

83
Q

What are Metaproterenol, Albuterol, Salmeterol, and Isoetharine inhalers?

A

Beta2 agonists
Used for Asthma and COPD treatment

Bronchodilation without systemic effects – overdosing causes beta1 effects

84
Q

What are Terbutaline and Ritodrine?

A

Beta2 agonists
Used for tocolysis in pregnancy (stops contractions)

Beta2 mediated relaxation of uterine smooth muscle

85
Q

What is Vasopressin and its dose?

A

Endogenous hormone that regulates urine volume and plasma osmolality

Higher concentrations act on the V1 receptors in vascular smooth muscle to vasoconstrict (via the phosphoinositol pathway)

Dose: used intraoperatively in 1-8 unit doses (1-2 units at a time dose is real nice)

  • 40 unit bolus instead of Epi 1mg in a code
  • Used to treat refractory hypotension — ACE or ARB induced refractory hypotension
86
Q

What is the mechanism of action of adrenergic blockers?

A

Act post-synaptically competitively blocking the alpha and beta receptors

Beta blockers target cardiac and vascular smooth muscle

87
Q

What do Phenoxybenzamine and Phentolamine do?

A

Block alpha receptors and cause vascular dilation

Phenoxybenzamine = 1st choice to produce alpha blockade in pheochromocytoma pts (irreversible, non-competitive blocker T1/2 = 18-24 hrs) — 10-20 mg PO BID
-also used to treat neurogenic bladder and BPH

Phentolamine used for infiltration when Norepi infusion inflitrates

88
Q

Which of the following drugs are beta1 selective and which are non-selective?

Propanolol, Labetalol, Atenolol, Metoprolol, Esmolol

A

Propanolol and Labetalol = beta1 and beta2 blockade (non=selective)

Atenolol, Metoprolol, and Esmolol = beta1 selective (cardioselective)

89
Q

What do Reserpine and alpha-methyldopa do?

A

block synthesis and storage of Norepi

90
Q

What does Guanethidine do?

A

blocks release of Norepi

91
Q

What is Prazosin

A

Alpha adrenergic blocker
-has high affinity for alpha receptors

Used to treat HTN
PO at bedtime

92
Q

What are Doxazosin and Tamsulosin?

A

Alpha adrenergic blockers

Typically used for BPH

93
Q

What are some adverse effects of beta adrenergic blockers?

A
  • Can cause problems with bronchospasm and peripheral vascular disease
  • Can lead to bradycardia, asystole, HF, inhibit gluconeogenesis (bad for DM), Raynaud’s phenomenon
  • Can cause severe HTN in certain pts (pheo) if they are given prior to instituting alpha blockade
94
Q

Beta blockers ____ surgical M&M in patients with CAD.

A

Reduce

-be careful about initiating beta blockade but if the pt is on them give them

95
Q

What can happen by holding beta blockers for surgery?

A

may lead to rebound HTN that could last up to 6 days post-op

96
Q

What is Esmolol and its onset, T1/2, and dose?

A

Selective beta1 blocker
Onset: 90 seconds T1/2: 9-10 minutes
Dose: 10-20-40 mg boluses to reduce HTN
Non-specific red cell esterase metabolism (not metabolized by pseudocholinesterase)

*Fast BP control desired but short duration needed

97
Q

What is Labetalol and its onset, duration, and dose?

A

alpha1, beta1, and beta2 blockade (alpha:beta ratio 1:7)

Peak: 5-10 min Duration: 4-6 hr
Dose: 5-10 mg boluses every 5-10 min (wait for effect)

  • Continued BP control desired and tired of giving repeated boluses of Esmolol
  • Peripheral vasodilation with reflex tachycardia
98
Q

What is Metoprolol and its dose?

A

Primarily beta1 (B1:B2 - 30:1)

Dose: 2-5mg every 2-5 min up to total dose of 15mg
(Max beta1 blockade seen at 0.2 mg/kg)

*Typically given to control HR when BP reduction is not needed or desired

99
Q

What is the effect of activation of postjunctional muscarinic receptors of ACh in the heart and smooth muscle?

A

In the heart – leads to bradycardia

In smooth muscle – leads to bronchoconstriction, miosis, and increased GI motility and secretion

100
Q

What is the effect of activation of muscarinic receptors by ACh at the presynaptic SNS terminals in the CV and coronaries?

A

Leads to decreased Norepi release

101
Q

Nicotinic receptors activate postganglionic junctions in ______.

A

Both the SNS and PNS

NMJ nicotinic receptors are blocked by Succinylcholine which is an agonist at these sites

102
Q

What is the mechanism of action of muscarinic blockers?

A

competitively inhibit ACh by reversibly binding to muscarinic receptors

103
Q

What are Atropine and Scopolamine?

A

Muscarinic blockers

Tertiary amine (can cross BBB and have CNS effects)

These effects may include augmenting vagal outflow and result in bradycardia at low doses (<0.5mg)

104
Q

What is Glycopyrrolate?

A

Muscarinic blocker

Quaternary amine (does NOT cross BBB and had no CNS effects)

More potent and longer acting at peripheral muscarinic receptors than Atropine

105
Q

Where do Acetylcholinesterase (AChE) inhibitors act?

A

they act indirectly resulting in an increase in ACh at ALL ACh receptor sites – acts postsynaptically

Directly inhibits the action of both TRUE or acetyl-cholinesterase and plasma or pseudo-cholinesterase

106
Q

What are Neostigmine, Pyridostigmine, Physostigmine, Edrophonium, and Echothiophate?

A

Cholinesterase Inhibitors

Neostigmine, Pyridostigmine, Physostigmine, Edrophonium = NDMR reversal agents

Echothiophate = eye drop

107
Q

What receptors cause the desired effects and undesired effects of cholinesterase inhibitors (NDMR reversal agents)?

A

Desired = Nicotinic receptors

Undesired = Muscarinic receptors (administer a muscarinic blocking agent at the same time)

Anesthesia Pharm (18 decks)

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