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1
Q

ALPHA 1 -
Signal Transduction
Effector
Second Messenger

A

Gq
Increase Phospholipase C
Increase IP3, DAG, Ca+2

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2
Q

ALPHA 2 -
Signal Transduction
Effector
Second Messenger

A

Gi
Decrease Adenylate cyclase
Decrease cAMP

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3
Q

BETA 1 -
Signal Transduction
Effector
Second Messenger

A

Gs
Increase Adenylate cyclase
Increase cAMP

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4
Q

BETA 2 -
Signal Transduction
Effector
Second Messenger

A

Gs
Increase Adenylate cyclase
Incrase cAMP

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5
Q

MUSCARINIC 1/3/5 -
Signal Transduction
Effector
Second Messenger

A

Gq
Increase Phospholipase C
Increase IP3, DAG, Ca+2

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6
Q

MUSCARINIC 2/4-
Signal Transduction
Effector
Second Messenger

A

Gi
Decrease Adenylate cyclase
Decrease cAMP

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7
Q

NICOTINIC (ANS ganglia, NMJ, & CNS)
Signal Transduction
Effector
Second Messenger

A

Ion channels
N/A
N/A

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8
Q

DOPAMINE 1 (post-synaptic)
Signal Transduction
Effector
Second Messenger

A

Gs
Increase Adenylate cyclase
Increase cAMP

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9
Q

DOPAMINE 2 (pre-synaptic)
Signal Transduction
Effector
Second Messenger

A

Gi
Decrease Adenylate cyclase
Decrease cAMP

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10
Q

VASOPRESSIN 1 (vasculature) -
Signal Transduction
Effector
Second Messenger

A

Gq
Increase Phospholipase C
Increase IP3, DAG, Ca+2

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11
Q

VASOPRESSIN 2 (renal tubules) -
Signal Transduction
Effector
Second Messenger

A

Gs
Increase Adenylate cyclase
Increase cAMP

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12
Q

HISTAMINE 1 -
Signal Transduction
Effector
Second Messenger

A

Gq
Increase Phospholipase C
Increase IP3, DAG, Ca+2

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13
Q

HISTAMINE 2-
Signal Transduction
Effector
Second Messenger

A

Gs
Increase Adenylate cyclase
Increase cAMP

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14
Q

MYOCARDIUM
SNS Receptor
Action

A

B1

Increased contractility

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15
Q

MYOCARDIUM
PNS Receptor
Action

A

M2

Decreased contractility

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16
Q

CONDUCTION SYSTEN
SNS Receptor
Action

A

B1

Increased HR, Increased conduction speed

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17
Q

CONDUCTION SYSTEN
PNS Receptor
Action

A

M2

Decreased HR, Decreased conduction speed

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18
Q

ARTERIES
SNS Receptor
Action

A

A1 > A2
Vasoconstriction

*No PNS receptors

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19
Q

VEINS
SNS Receptor
Action

A

A2 > A1
Vasoconstriction

*No PNS receptors

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20
Q

MYOCARDIUM VASCULATURE
SNS Receptor
Action

A

B2
Vasodilation

*No PNS receptors

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21
Q

SKELETAL MUSCLE VASCULATURE
SNS Receptor
Action

A

B2
Vasodilation

*No PNS receptors

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22
Q

RENAL VASCULATURE
SNS Receptor
Action

A

DA
Vasodilation

*No PNS receptors

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23
Q

MESENTERIC VASCULATURE
SNS Receptor
Action

A

DA
Vasodilation

*No PNS receptors

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24
Q

BRONCHIAL TREE
SNS Receptor
Action

A

B2

Bronchodilation

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25
BRONCHIAL TREE PNS Receptor Action
M3 | Bronchoconstriction
26
RENAL TUBULES SNS Receptor Action
A2 Diuresis *No PNS receptors
27
RENIN RELEASE SNS Receptor Action
B1 Increased renin release *No PNS receptors
28
SPHINCTER MUSCLE (IRIS) SNS Receptor Action
No SNS receptor
29
SPHINCTER MUSCLE (IRIS) PNS Receptor Action
M3, M2 | Contraction (miosis)
30
RADIAL MUSCLE (IRIS) SNS Receptor Action
A1 Contraction (mydriasis) *No PNS receptor
31
CILIARY MUSCLE SNS Receptor Action
B2 | Relaxation (far vision)
32
CILIARY MUSCLE PNS Receptor Action
M3, M2 | Contraction (near vision)
33
SPHINCTERS SNS Receptor Action
A1 | Contraction
34
SPHINCTERS PNS Receptor Action
M | Relaxation
35
GI MOTILITY & TONE SNS Receptor Action
A1/A2/B1/B2 | Decrease
36
GI MOTILITY & TONE PNS Receptor Action
M | Increase
37
SALIVARY GLANDS SNS Receptor Action
A2 | Decrease
38
SALIVARY GLANDS PNS Receptor Action
M | Increase
39
GALLBLADDER & DUCTS SNS Receptor Action
B2 | Relaxation
40
GALLBLADDER & DUCTS PNS Receptor Action
M | Contraction
41
BETA CELLS - Alpha and Beta SNS Receptor Action
A2 - Decrease insulin release B2 - Increase insulin release *No PNS receptor
42
LIVER SNS Receptor Action
A1/B2 | Increase serum glucose
43
UTERUS - Alpha and Beta SNS Receptor Action
A1 - Contraction B2 - Relaxation *No PNS receptor
44
BLADDER TRIGONE & SPHINCTER SNS Receptor Action
A1 | Contraction
45
BLADDER DETRUSOR SNS Receptor Action
B2 | Relaxation
46
BLADDER TRIGONE & SPHINCTER PNS Receptor Action
M | Relaxation
47
BLADDER DETRUSOR PNS Receptor Action
M | Contraction
48
SWEAT GLANDS SNS Receptor Action
A1 | Increase secretion
49
SWEAT GLANDS PNS Receptor Action
M | Increase secretion
50
ANS innervation of eye | A1 stimulation
radial muscle contraction | mydriasis = pupil DILATION
51
ANS innervation of eye | Muscarinic stimulation
sphincter muscle contraction | miosis = pupil CONSTRICTION
52
BRR | If the heart rate increases in setting of hypotension OR decrease in setting of hypertension, BRR is said to be
preserved
53
Volatile gas | Decrease or Increase effectiveness of BRR
Decrease in dose-dependent
54
Volatile gas | which gas impairs BRR lease
Iso | mild B1 agonist properties
55
IV Induction agents and BRR | Thiopental
Preserves
56
IV Induction agents and BRR | Propofol
Depresses - decrease in HR with decrease in SVR
57
IV Induction agents and BRR | Ketamine
activates SNS - increase HR but no change in SVR | In critically ill pts, with exhausted catecholamine reserve, myocardial depressant effects may be noticed
58
IV Induction agents and BRR | Etomidate
No change in HR, small decrease in SVR. Hypovolemic pts my experience hypotension
59
Vasodilators and BRR | Hydralazine
Preserves BRR | Decrease in SVR with Increase in HR
60
Vasodilators and BRR | Nitroprusside
Preserves BRR
61
Vasodilators and BRR | Nitroglycerine
Preserves BRR
62
Beta blockers and BRR
May prevent a compensatory rise in HR in setting of hypotension
63
BB and BRR | Labetalol
BB Also antagonizes A-1 receptor May increase the risk of orthostatic hypotension
64
Catecholamines and BRR | NE
Effect on HR is dose-dependent Lower doses - B1 chronotropic effects prevail Higher doses - A1 vasoconstrictive effects overshadow B1 = BRR fall in HR
65
Catecholamines and BRR | epi, dobutamine, isoproterenol, dopamine
BRR NOT preserved | HR increases
66
Phenylephrine and BRR
BRR is preserved Bradycardia is side effect Not a catecholamine
67
Adrenergic Agonists | NE
``` Low dose - B1 selective (increase HR, increase inotropy) High dose ( - stimulates A1, A2, B1 - increase SVR to increase BP and decrease HR via BRR ``` 0.02-0.4 mcg/kg
68
Adrenergic Agonists NE When is ideal to use?
Ideal drug for low SVR states like sepsis or post-CPB hypotension due to low afterload
69
Adrenergic Agonists NE When to avoid use?
In the setting of cardiogenic shock bc it increase afterload and MVO2
70
Treatment of NE extravasation
Injection with phentolamine (2.5-10 mg in 10 mL of dilute) | Stellate ganglion block
71
Adrenergic Agonists | Epi
``` Low dose (0.01-0.03 mcg/kg) - b1 and B2 (increase HR, increase CO, increase inotropy, decrease SVR) Intermediate dose(0.03-0.15 mcg/kg) - Mixed alpha and beta High dose (>0.15)- Alpha effects predominate and SVT common ```
72
Adrenergic Agonists Epi Key points
Bronchodilation - think bronchospasm! Mast cell stabilization - think anaphylaxis! Prolongs duration of LA Increases serum glucose Causes hypokalemia due to transcellular K+ shift
73
Adrenergic Agonists | Dopamine
``` Low dose (1-2 mcg/kg) - Renal vasodilation and incrase RBF Intermediate (2-10 mcg/kg) - Increase HR, increase inotropy, increase CO High dose (10-20 mcg/kg) - Vasopressor effect - Alpha effects overshadow ```
74
Adrenergic Agonists | Isoproterenol
Synthetic catecholamine derived from dopamine Stimulates B1, B2 0.02-0.5 mcg/kg increase HR, incrase inotropy, incrase CO Vasodilation decrease SVR Can cause dysrthymias and tachycardia
75
Adrenergic Agonists Isoproterenol What to be aware/cautious of?
reduction in SVR can be so severe as to drop DBP, and this can impair CPP Also makes it a poor choice for septic shock
76
Adrenergic Agonists Isoproterenol Key points
chemical PM for bradycardia unresponsive to atropine or for the pt w a denervated heart Treatment of bronchoconstriction Treatment of cor pulmonale
77
Adrenergic Agonists | Dobutamine
Sympathomimetic amine Potent B1 and mild B2 agonist Increase HR, Increase inotropy, increase CO 0.5-15 mcg/kg
78
Adrenergic agent | Phenylephrine
Alpha1 receptor Direct acting Increases SVR Increases CPP Reflex bradycardia Good for conditions where increase afterload is required, such as hypertrophic cardiomyopathy or tetralogy of Fallot Infusion 10-200 mcg/min
79
Adrenergic agent | Ephedrine
Non-catecholamine Direct and Indirect A1, A2, B1, B2 Increase HR, Increase inotropy, increase CO, increase SVR Multiple doses can cause tachyphylaxis - progressively smaller response to a given dose after multiple administrations
80
Adrenergic agent Ephedrine When doesn't ephedrine work?
When neuronal catecholamine stores are: 1. depleted - SEPSIS 2. absent - denervated heart (HEART TRANSPLANT)
81
Adrenergic agent Ephedrine Pts on MAOI are at risk for what?
Hypertensive crisis
82
Adrenergic agent Vasopressin Where does it come from?
Produced by the hypothalamus and released by the Posterior Pituitary Gland
83
Adrenergic agent Vasopressin How does it restore BP?
1. V1 receptor simulation causes intense vasoconstriction 2. V2 receptor simulation stimulates the synthesis and insertion of aquaporins into the walls of the collecting ducts. This increase water (but not solute) reabsorption and lowers serum osmolarity
84
Adrenergic agent Vasopressin Key points
IV bolus - 0.5-1 unit IV infusion - 0.01-0.04 units/min First line therapy for ACEI or ARB induced vasoplegia that's refractory to catecholamines *NOTE: methylene blue is next best drug
85
Adrenergic agent Vasopressin Overdose can cause what?
Hyponatremia and seizures
86
What causes K+ to shift into cells?
Alkalosis - Activating Na+/K+ pump B2 agonists (albuterol, ritodrine, epi) Theophylline Insulin
87
What causes K+ to shift out of cells?
Acidosis - Activating H+/K+ pump Cell lysis Hyperosmolarity Succ

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