ANS Physiology & Pharmacology Flashcards
(60 cards)
1
Q
Sympathetic Nervous System arises from what spinal cord level?
A
T1-L3 (per the textbook)
2
Q
Parasympathetic Nervous System arises from what spinal cord level?
A
Cranial Nerves II, VII, IX and X
S2-S4 (per the textbook)
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
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
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
6
Q
Norepi: ganglionic location
A
-SNS post-ganglionic
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
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***
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
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
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
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
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)
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
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)
16
Q
A2 agonist affects on anesthetic needs?
A
- A2 agonists- inhibitory- reduce anesthetic needs
example: dex and clonodine
17
Q
How does fentanyl affect SNS tone?
A
- depresses SNS tone and promotes vagal activation
- lowers BP and slows HR
18
Q
Des affect on ANS and SNS?
A
- depresses ANS
- stimulates SNS (HTN and tachycardia w/ des)
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
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
21
Q
Dysautonomia
A
- shy-drager syndrome, GB, Lambert-Eaton, familial
- orthostatic hypotension, HR variability, BP lability
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
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.
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
25
Metabolism of catecholamines
-COMT: intracellular
-MAO in nerve terminal mitochondria
Note: exogenous catecholamines may resist COMT and MAO metabolism
26
Dopamine D1 receptor agonist: Fenoldopam
- 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
Exogenous catecholamines: alpha 1 agonists
- Increase BP, CO same, Decrease HR
| - Increase MVO2 supply
28
Exogenous catecholamines: phenylephrine
-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
Exogenous catecholamines: methoxamine
> arterial constriction than venoconstriction
- longer acting
- no longer clinically used
30
Exogenous catecholamines: midodrine
- oral alpha 1 agonist used for dialysis induced hypotension
- t1/2 3 hours
- duration: 4-6 hours
31
Predominant effects: artery
a1>a2
contraction in splanchnic, renal, pulmonary, and especially skin, muscle, and cerebral vasculature
D: vasodilation, especially in renal & mesenteric vasculature
32
Predominant effects: vein
a2>a1: contraction
33
Predominant effects: kidney
D: vasodilation
a2: diuresis (opposes arginine)
34
Predominant effects: GI tract
a2: relaxation (slow transit time)
35
Predominant effects: bladder
a1: contraction (trigone and sphincter)
36
Predominant effects: eye radial muscle
a1: contraction (mydriasis)
| * remember D in myDriasis= dilation even though muscle contracts
37
Predominant effects: pancreas
a2: glucagon release, inhibit insulin secretion
38
Predominant effects: adipose cells
a2: inhibit lipolysis
39
Predominant effects: uterus
a1: contraction
40
Exogenous catecholamines: alpha2 agonist
- 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
Exogenous catecholamines: Dexmedetomidine
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
Exogenous catecholamines: Clonidine
220: 1 a2: a1 activity
- oral dosing q8 hours- DO NOT hold= rebound HTN
- can be used epidural but inconsistent results
43
Exogenous catecholamines: B1 receptor agonist: Isoproterenol
-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
Exogenous catecholamines: Dobutamine
- 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
Exogenous Catecholamines: B2 agonists (lungs)
- asthma and COPD
- metaproterenol, albuterol, salmeterol, isoetharine inhalers
- bronchodilation without system effects
- overdosing causes B1 effects
46
Exogenous Catecholamines: Terbutaline and Ritodrine
- used for tocolysis in pregnancy
| - b2 mediated relaxation of uterine smooth muscle
47
Exogenous Catecholamines: INDIRECT acting sympathomimetics
- causes the release of "Stored" norepi in the synaptic vesicles
- BEWARE in patients taking TCAs (NE reuptake inhibition) and MAOIs (NE breakdown inhibition)
48
Ephederine
- 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
Amphetamine and METHamphetamine
- 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
Arginine Vasopressin
- 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
Adrenergic Blockers
- act post-synpatically competitively blocking the alph and beta receptors
- phenoxybenzamine and phentolamine block alpha receptors and vascular dilation occurs
52
Generalized B1 and B2 blockade
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
Adrenergic Blocker-a: Phenoxybenzamine
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
Adrenergic Blockers: B2
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
Esmolol
-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
Labetolol
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
Metoprolol
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
Activation of cholingeric receptors
- 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
Muscarinic Blockers
- 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
Cholinesterase Inhibitors
- 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)
