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anesthesia pharm midterm 2 > ANS Physiology & Pharmacology > Flashcards

ANS Physiology & Pharmacology Flashcards

1
Q

Sympathetic Nervous System arises from what spinal cord level?

A

T1-L3 (per the textbook)

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2
Q

Parasympathetic Nervous System arises from what spinal cord level?

A

Cranial Nerves II, VII, IX and X

S2-S4 (per the textbook)

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3
Q

Blocking what ganglion can lead to Horner’s syndrome?

A

Local anesthetic blockade of stellate ganglion (inferior cervical ganglion) causes Horner’s syndrome
Horner’s syndrome: ptosis, miosis, enophthalmos, and anhydrosis on affected side

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4
Q

Synthesis of Norepi and Epi

A

From tyrosine in the adrenal medulla: “That Damn Dog’s Not Eating”
T: tyrosine
D: Dopa
D:Dopamine
N: Norepi
E: Epi
-Release of norepi int synaptic clef is Ca2+ dependent
-Diffusion away from synaptic clef, metabolism by MAO & COMT terminates the action of norepi at synapse
-A2 receptors are pre synaptic and provide a negative feedback look that modulates the release of norepi by inhibiting Ca2+ release mechanism

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5
Q

Ach: preganglionic and post ganglionic location

A

Ach is the pre ganglionic SNS and PSNS NTM

AND postganglionic PSNS NTM and sweat glands

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6
Q

Norepi: ganglionic location

A

-SNS post-ganglionic

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7
Q

Cushings Triad

A

ANS Reflex

  • Increase in ICP, Bradycardia and Hypertension
  • Intracranial HTN leads to SNS meditated systemic HTN
  • activation of the PSNS medullary centers via the baroreceptor slows the heart rate (baroreceptor not enough to slow HR though)
  • results in increased blood flow to the brain and further increase in ICP
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8
Q

Autonomic Hyperreflexia

A
  • Disruption of efferent impulses down the spinal cord from T5 or higher
  • exaggerated SNS response to bowel, bladder, or surgical stimulation d/t receptor sensitivity due to denervation
  • loss of inhibitory impulses results in pure SNS response significant HTN***
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9
Q

Thermogenesis reflex

A
  • sweating controlled by cholingeric fibers (blocked by atropine or nerve blocks)
  • shivering decreased in elderly, absent in newborn/infants, blocked by NDMR’s
  • general anesthetics impair thermogenesis
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10
Q

Baroreceptor reflex

A
  • stretch receptors in aorta and carotid arteries sense increased pressure
  • send signals via n. hering & vagus to medulla
  • decreased HR, decreased BP, decreased contractility, decreased PVR
  • phenylephrine (a1 agonist) increases BP and reflex decreases HR
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11
Q

Chemoreceptor reflex

A

-central sense increased arterial CO2 and/or decrease arterial pH (hypercapnia increases minute vent)

  • peripheral in carotid body responds to decreased PO2
    (n. hering and vagus increase respiratory rate and tidal volumes which leads to increased minute vent)
  • -may also see increased HR and CO
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12
Q

Bainbridge reflex

A
  • increased CVP activates stretch receptors in the atria
  • afferent impulses though vagus inhibit PSNS output
  • tachycardia
  • seen during labor when contractions auto transfuse and increase CVP
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13
Q

Bezold-Jarisch reflex

A
  • Hypotension, bradycardia, coronary dilation
  • noxious stimuli sensed in cardiac ventricles
  • unmyelinated C fibers of Vagus send signal to:
    1. enhance baroreceptor response
    2. inhibit sympathetic output
    3. decrease PVR to make it easier for heart to pump

-increased blood flow to the myocardium to decrease work of heart (cardioprotective)

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14
Q

Valsalva reflex

A
  • increasd intrathoracic pressure, decreased venous return, decrease cardiac filling, decreased BP
  • baroreceptor increases HR, increases inotropy which leads to increased BP
  • baroreceptors cause PSNS induced decrease in HR
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15
Q

Oculocardiac (Five and Dime reflex)

A
  • afferent impulses to pressur eont eh eye or pulling on eye muscle
  • efferent slowing of HR via the Vagus nerve
  • muscarinic response blocked by atropine or glycopyrrolate (side note: glyco does not cross BBB so it takes longer to work)
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16
Q

A2 agonist affects on anesthetic needs?

A
  • A2 agonists- inhibitory- reduce anesthetic needs

example: dex and clonodine

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17
Q

How does fentanyl affect SNS tone?

A
  • depresses SNS tone and promotes vagal activation

- lowers BP and slows HR

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18
Q

Des affect on ANS and SNS?

A
  • depresses ANS

- stimulates SNS (HTN and tachycardia w/ des)

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19
Q

Aging

A
  • HTN and orthostasis (low venous return to heart)
  • temperature regulation decreases
  • increased circulating norepi: receptor down regulated and created responses to exogenous catecholamines. B agonist are going to have decreased effects on HR, CO, and vasodilation due to reduced receptor response
  • decreased renin, decreased aldosterone, increase in atrial natriuretic factor leads to salt wasting and hypovolemia
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20
Q

Diabetes Mellitus

A
  • 20-40% insulin dependent DM have neuropathies (ANS)
  • labil BP, gastroparesis, thermoregulation, ?vagal dysfunction
  • increased aspiration risk, aggressive temp maintenance, increased CO
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21
Q

Dysautonomia

A
  • shy-drager syndrome, GB, Lambert-Eaton, familial

- orthostatic hypotension, HR variability, BP lability

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22
Q

Endogenous catecholamines: Epi

A
  • Produced in adrenal medulla (80% epi, 20% norepi)
  • Adrenal standard secretion rates: 0.2 mcg/kg/min epi and 0.05 mcg/kg/min norepi

Exogenous infusions:
2-10 mcg/min (B1,B2)
>10 mcg/min (A1)

Anaphylyaxis: 0.20.5 mg SQ

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23
Q

Endogenous catecholamines: Norepi

A
  • Norepi has more alpha 1 than epi (textbook: greater arterial and venous vascular constriction than epi)
  • NO beta2 effects like Epi does

Dosing:
4-12 mcg/min (alpha 1, beta 1)
Low dose: B1 predominates. Increase in BP d/t increased CO
High dose: A1 dominates and BP increases, but HR and CO may decrease d/t baroreceptor reflex
-beware effect on pulmonary alpha1 and possible pulmonary HTN or right heart failure.

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24
Q

Dopamine

A
  • precursor to Norepi and Epi
  • central and peripheral neural transmission
  • exogenous does NOT cross BBB (only L dopa for parkinson’s patients)
  • low dose: 1-3 mcg/kg/min leads to D1 activation-coronary, renal and mesenteric vasodilation
  • moderate dose: 3-10 mcg/kg/min B1 effects
  • high dose: > 10 mcg/kgmin A1 effects
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25
Q

Metabolism of catecholamines

A

-COMT: intracellular
-MAO in nerve terminal mitochondria
Note: exogenous catecholamines may resist COMT and MAO metabolism

26
Q

Dopamine D1 receptor agonist: Fenoldopam

A
  • Minimal D2, alpha or B effects
  • 10X potency of dopamine
  • Dose: 0.1-0.8 mcg/kg/min
  • 0.1-0.2 mcg/kg/min produce renal vasodilation, increased renal blood flow and GFR, and Na+ excretion
  • improved outcome in CABG patients with less renal failure
27
Q

Exogenous catecholamines: alpha 1 agonists

A
  • Increase BP, CO same, Decrease HR

- Increase MVO2 supply

28
Q

Exogenous catecholamines: phenylephrine

A

-almost purely alpha agonist
>venoconstriction than arterial (increases venous return, maintains CO, HR decreases d/t baroreceptors
-NOT contraindicated in OB (but not better then ephedrine)
-Neosyphrine nasal spray

29
Q

Exogenous catecholamines: methoxamine

A

> arterial constriction than venoconstriction

  • longer acting
  • no longer clinically used
30
Q

Exogenous catecholamines: midodrine

A
  • oral alpha 1 agonist used for dialysis induced hypotension
  • t1/2 3 hours
  • duration: 4-6 hours
31
Q

Predominant effects: artery

A

a1>a2
contraction in splanchnic, renal, pulmonary, and especially skin, muscle, and cerebral vasculature
D: vasodilation, especially in renal & mesenteric vasculature

32
Q

Predominant effects: vein

A

a2>a1: contraction

33
Q

Predominant effects: kidney

A

D: vasodilation
a2: diuresis (opposes arginine)

34
Q

Predominant effects: GI tract

A

a2: relaxation (slow transit time)

35
Q

Predominant effects: bladder

A

a1: contraction (trigone and sphincter)

36
Q

Predominant effects: eye radial muscle

A

a1: contraction (mydriasis)

* remember D in myDriasis= dilation even though muscle contracts

37
Q

Predominant effects: pancreas

A

a2: glucagon release, inhibit insulin secretion

38
Q

Predominant effects: adipose cells

A

a2: inhibit lipolysis

39
Q

Predominant effects: uterus

A

a1: contraction

40
Q

Exogenous catecholamines: alpha2 agonist

A
  • decrease CNS sympathetic output
  • decrease presynaptic norepi release
  • sedation, hyponosis, sympatholysis, neuroprotection, diuresis, inhibition of insulin and HGH secretion
  • rapid delivery may increase BP secondary to post synaptic alpha2 (beta) receptor mediated arterial and venoconstriction
  • beneficial anesthetic effects include:
    1. anxiolysis/sedation
    2. decreasd MAC, decreased opioid induced chest wall rigidity
    3. decreased BP response to ETT, extubation and incision
    4. Decreased post-anesthesia shivering
41
Q

Exogenous catecholamines: Dexmedetomidine

A

selective alpha 2 agonist (1620:1 a2:a1)

  • PACU pt on dex infusion require less morphine
  • decreased post op analgesics, beta blockers, antiemetics, diuretics and epi for CABG patients

Dosing:
Load 1 mcg/kg/hr over 10-20 min
0.2-0.7 mcg/kg/hr infusion
beware hypotension and bradycardia

42
Q

Exogenous catecholamines: Clonidine

A

220: 1 a2: a1 activity
- oral dosing q8 hours- DO NOT hold= rebound HTN
- can be used epidural but inconsistent results

43
Q

Exogenous catecholamines: B1 receptor agonist: Isoproterenol

A

-isopropyl derivitive of epi
nonselective activity at B1 and B2
high dose cause tachycardia and hypotension-BAD
-may be used as a chemical pacemaker

44
Q

Exogenous catecholamines: Dobutamine

A
  • derivative of dopamine
  • B1 agonist and alpha 1 antagonist, minimal B2 effects
  • increased CO, decreased LV filling pressure, same HR, same SVR until dose > 10-20 m/k/min
  • dobutamine stress tests
45
Q

Exogenous Catecholamines: B2 agonists (lungs)

A
  • asthma and COPD
  • metaproterenol, albuterol, salmeterol, isoetharine inhalers
  • bronchodilation without system effects
  • overdosing causes B1 effects
46
Q

Exogenous Catecholamines: Terbutaline and Ritodrine

A
  • used for tocolysis in pregnancy

- b2 mediated relaxation of uterine smooth muscle

47
Q

Exogenous Catecholamines: INDIRECT acting sympathomimetics

A
  • causes the release of “Stored” norepi in the synaptic vesicles
  • BEWARE in patients taking TCAs (NE reuptake inhibition) and MAOIs (NE breakdown inhibition)
48
Q

Ephederine

A
  • chemically an alkaloid with phenethylamine skeleton
  • INDIRECT and direct actions on alph and beta receptors
  • competes with NE for repute in vesicles so NE stays at receptor sites longer
  • increased HR, increased CO, increased BP
  • tachyphylaxis– less of a response over time because you’re using up stores
  • May increase MAC due to stimulatory effects on CNS
49
Q

Amphetamine and METHamphetamine

A
  • CNS stimulants, alpha and beta stimulants
  • cause release of and inhibit repute of stimulating NTM
  • effects related to alpha and beta stimulation like other SNS stimulants
  • treatment of OD may include dantrolene to decrease temp

Methylphenidate (Ritaline)
-effects similar but milder
-used to treat ADHD
(Ephederine will not work for these patients-already using norepi stores)

50
Q

Arginine Vasopressin

A
  • NOT a catecholamine
  • endogenous hormone that regulates urine volume and plasma osmolality
  • higher concentrations act on V1alpha receptors in vascular smooth muscle to vasoconstrictor

dose:
40 unit bolus instead of EPI 1 mg in code
used intraoperatively in 1-8 unit doses
-used to treat refractory hypotension
-ACE or ARB induced refractory hypotension: works VERY well for this*
-1-2 units a dose is good

51
Q

Adrenergic Blockers

A
  • act post-synpatically competitively blocking the alph and beta receptors
  • phenoxybenzamine and phentolamine block alpha receptors and vascular dilation occurs
52
Q

Generalized B1 and B2 blockade

A

B1 and B2 blockade: propranolol and labetalol
B1 specific: atenolol, metoprolol, esmolol

  • resperine and a-methyldopa block synthesis and storage of NE
  • guanethidine blocks release of NE
53
Q

Adrenergic Blocker-a: Phenoxybenzamine

A

1st choice to produce alpha blocked in pheochromocytoma patients

  • irreversible, non competitive blocker (T 1/2 18-24 hours)
  • 10-20 mg BIG for pheo
  • also used to treat neurogenic bladder with BPH

phentolamine used for interrelation when NE infusion infiltrates*

  • prazosin has high affinity for alpha receptors and is used to treat HTN. Oral at bedtime
  • Doxazosin and tamulosin typically used in BPH
54
Q

Adrenergic Blockers: B2

A

B2 blockade can cause problems with bronchospasm and peripheral vascular disease

  • B blockade can lead to bradycardia, asystole, HF, inhibit gluconeogenesis, Raynaud’s phenomenon
  • can cause severe HTN in certain patients (pheo) if they are given prior to instituting alpha blockade
  • reduce surgical M&M in patients with CAD (if pt on beta blocker make sure they take them day of surgery)
  • holding beta blockers for surgery may lead to rebound HTN that could last up to 6 days post op
55
Q

Esmolol

A

-selective B1 blocker
-90 second onset, T 1/2: 9-0 minutes
-non specific red cell esterase metabolism (NOT pseudocholinesterase)
10-20-40 mg boluses to reduce HTN
Fast BP control desired but short duration needed

56
Q

Labetolol

A

alpha 1, beta 1 and beta 2 blockade (a:b ratio= 1:7)
peripheral vasodilation with reflex tachycardia
peaks 5-15 min, duration 4-6 hours
50-10 mg boluses every 5-10minutes; wait for effect
-continued BP control desired and tired of giving repeated esmolol doses

57
Q

Metoprolol

A

primarily Beta 1 (b1:b2 ratio= 30:1)
2-5 mg every 2-5 minutes up to total dose of 15 mg
maximum beta 1 blockade see at 0.2 mg/kg
typically given to control HR when BP reduction is not needed or desired

58
Q

Activation of cholingeric receptors

A
  • activation of post junctional muscarinic receptors by acetylcholine leaders to:
  • in the heart= bradycardia
  • in smooth muscle= bronchoconstriction, miosis, and increase GI motility and secretion

activation of muscarinic receptors by Acetylcholine
-at presynaptic SNS terminals in CV and coronaries= decreased NE release

nicotinic receptors activate post ganglionic junction sin both the SNS and PSNS
-NMJ nicotinic receptors are blocked by Succ, which is an AGONIST at these sites

59
Q

Muscarinic Blockers

A
  • anticholingeric drugs (atropine, stop, glyco) competitively inhibit ACH by reversibly binding to muscarinic receptors
  • Atropine and scop are tertiary mines so they can cross BBB and have CNS effects (may include augmenting vagal outflow an result in bradycardia at low doses
60
Q

Cholinesterase Inhibitors

A
  • AchE inhibitors act indirectly resulting in an increase in Ach at ALL Ach receptors sites****
  • directly inhibits the action of both TRUE or acetylcholinesterase and plasma or pseudo-cholinesterase
  • AchE is found post-synaptically so AchE inhibitors are post-synpatically
  • Neostigmine, pyridostigmine, physostigmine, edrophonium (all NDMR reversal agents) and echiothiophate (eye drops)
  • the desired effects at the NMJ are primarily at nicotinic receptors on NMJ
  • most of the undesired effects of NMDR reversal agents occur at muscarinic receptors (so we administer a muscarinic blocking agent at the same time)

anesthesia pharm midterm 2 (8 decks)

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