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Pharm II > Anticholinergics and Vasoconstrictors > Flashcards

Anticholinergics and Vasoconstrictors Flashcards

1
Q

What do anticholinergics do at the muscarinic and nicotinic receptors?

A

Antagonize the effects of ACh at the muscarinic receptors

Exert little or no effect at the nicotinic receptors

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2
Q

What are the types of anticholinergic drugs?

A 
Naturally occurring tertiary amines
Semisynthetic congeners (quaternary amines)
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3
Q

What are the naturally occurring tertiary amines for anticholinergics?

A

Atropine and Scopalamine

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4
Q

What are the quaternary amines for anticholinergics?

A

Glycopyrrolate

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5
Q

Are anticholinergics agonists or antagonists?

A

Primarily competitive antagonists

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6
Q

How do anticholinergics work?

A

Reversibly bind with muscarinic receptor preventing ACh from binding
Increasing ACh overcomes the effect of the drug

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7
Q

Do anticholinergics drug/receptor combo alter the membrane?

A

No

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8
Q

T/F: Anticholinergics prevent the release of ACh and react with it

A

False, does not prevent the release of ACh or react with it

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9
Q

What are the 5 subtypes of anticholinergics?

A 
M1: CNS and stomach
M2: Lungs and heart
M3: CNS, airway, smooth muscle, glandular tissue
M4: CNS
M5: CNS
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10
Q

Which muscarinic receptors are the most sensitive?

A

M3>M2>M1
Smallest doses decrease salivation
Dose to decrease H secretion will also affect M2 and M3 receptors

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11
Q

What are the doses of anticholinergics to work as an antisialagogue?

A

Atropine 10-20 mcg/kg
Scopalamine 5 mcg/kg
Glycopyrrolate 5-8 mcg/kg

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12
Q

T/F: At small doses all 3 drugs can produce heart rate slowing due to direct agonist effects

A

True

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13
Q

What are the other effects of anticholinergics?

A

Agonist at low doses
Indirect (interfere with the normal inhibition of release of endogenous NE)
Block the ACh inhibited release of NE
Presynaptic effects
Drugs have an effect like a sympathomimetic

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14
Q

What is the onset time for IV Atropine and Glycopyrrolate?

A

Atropine: 1 min
Glyco: 2-3 mins

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15
Q

What is the duration for Atropine and glycol?

A

30-60 mins

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16
Q

What are the uses of Anticholinergics>

A 
Preop medication: sedation, antisaialagogue, and prevent vagal reflexes
Treat reflex-mediated bradycardia
Combined with anticholinesterase drugs
Bronchodilation
Prevent motion-induced nausea
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17
Q

Does atropine or glycol have increased incidence of memory deficits?

A

Atropine

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18
Q

What are some of the unwanted effects of anticholinergics when used as preop sedation?

A

Can be associated with restlessness to somnolence
Delay awakening particularly in elderly patients
Inhaled anesthetics can potentiate the CNS effects
Reverse with physostigimine

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19
Q

Use anticholinergics with caution in which type of patients?

A

Glaucoma and parturients
Mydriatic effect could increase IOP
Atropine and scope cross the placenta

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20
Q

Which aticholinergic is the most potent antisialagogue?

A

Scopalamine 3x more potent than atropine

Glyco 2x more potent than atropine with a longer DOA

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21
Q

Which drug is used frequently to blunt the vagal reflex associated with laryngoscopy for peds patients?

A

Atropine

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22
Q

What is the drug of choice for treatment of intraop bradycardia (laryngoscopy, carotid sinus, insufflation)

A

Atropine 15-70 mcg/kg IV

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23
Q

How do anticholinergics work when treating reflex-mediated bradycardia?

A

Act by blocking the effects of ACh on the SA node. Effect most evident on young adulats

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24
Q

What do anticholinergics do when combined with anticholinesterases?

A

Prevent the parasympathomimetic effects of anticholinesterases

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25
Q

How do anticholingerics work for bronchodilitation?

A

Due to antagonism of ACh effects of airway smooth muscle
Predominantly effect large and medium sized airways
Decrease airway resistance and increase dead space in bronchial asthma and chronic bronchitis

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26
Q

What are some less common uses that anticholinergics are used for?

A

Biliary and ureteral smooth muscle relaxant
Mydriasis and cycloplegia
Antagonize gastric H secretion
Non-prescription cold remedy

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27
Q

What is central anticholinergic syndrome?

A

Scope and atropine enter the CNS

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28
Q

What are the symptoms of anticholinergic syndrome?

A

Restlessness and hallucinations to somnolence and unconsciousness

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29
Q

How do you treat central anticholinergic syndrome?

A

Physostigmine 15-60 mcg/kg IV

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30
Q

What are the symptoms is you overdose on anticholinergics?

A

Dry mouth, blurred vision, photophobia, tachycardia
Dry and flushed skin
Increased tempt due to inhibition of sweating
Skeletal muscle weakness
Orthostatic hypotension
Can lead to fatal events (seizure, coma, medullary ventilator center paralysis)

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31
Q

What is the treatment for overdose of anticholinergics?

A

Physostigmine 15-60 mcg/kg IV

May need to repeat dose since it is metabolized rapidly

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32
Q

What are the direct and indirect effects of vasoactive drugs?

A

Direct effects on the heart and vasculature

Indirect effects mediated by the nervous system

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33
Q

What is the site of action for vasoconstrictors?

A

Arterial and venous smooth muscle

Systemic and pulmonary circulation

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34
Q

What are the 2 mechanisms of action for vasoconstrictors?

A

Receptor activation: Alpha1 agonists initiate a cascade of reactions through an intermediary G protein. The terminal products, protein kinase C and inositol triphosphate trigger the release of intracellular calcium resulting in smooth muscle contraction
Direct action: on smooth muscle (angiotensin)

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35
Q

What are the hemodynamic effects of vasoconstrictors?

A

Increase arterial resistance and afterload: Increase SVR and usually MAP
Increase venous return: increase preload and CO
In a failing heart, decreased SV may occur

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36
Q

What are the reflex changes for vasoconstrictors?

A

Decreased HR
Decreased conduction
Occasionally, decreased contractility

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37
Q

What are the indication for vasoconstrictors?

A

Decreased arterial resistance (hypotension)
-Could be iatrogenic (SAB, general anesthesia, vasodilator overdose) or physiologic (endotoxic or septic shock, hemorrhage)
Myocardial ischemia
CPR
Anaphylactic shock
Intracardiac right to left shunts
Hypovolemia

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38
Q

How do vasoconstrictors work for myocardial ischemia?

A

Maintain coronary perfusion
Used with coronary venodilators
Could worsen ischemia by increasing preload and wall tension

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39
Q

How do vasoconstrictors work for CPR?

A

Restore perfusion pressure to vital organs

Used in conjunction with other appropriate cardiac drugs

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40
Q

What are the contraindications/complications to vasoconstrictors?

A

Can worsen LV failure
Can exacerbate RV failure
Can decrease renal blood flow
Can mask hypovolemia

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41
Q

What are the types of vasoconstrictors?

A

Pure Alpha1 agonists

Mixed alpha1 and beta adrenergic compounds

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42
Q

What are the pure alpha1 agonists?

A

Phenylephrine and methoxamine

43
Q

What are the mixed alpha1 and beta adrenergic compounds?

A 
Norepi (D)
Metaraminol (I & D)
Epi (D)
Dopamine (I & D)
Ephedrine (I & D)
Mephentermine (I)
44
Q

What are the natural catecholamines?

A

Epi
Norepi
Dopamine

45
Q

What are sympathomimetics?

A

Sympathetics that act on the nervous system
Compounds that resemble catecholamines except that hydroxyl groups are not present in both the 3 and 4 positions of the benzene ring
Classified according to their selectivity for stimulating alpha and/or beta receptors
Naturally occurring catecholamines (endogenous)

46
Q

What are Indirect sympathomimetics?

A

Synthetic non-catecholamines

Release endogenous neurotransmitter NE from postganglionic sympathetic nerve endings

47
Q

What are direct-acting sympathomimetics?

A

Catecholamines and synthetic non-catecholamines

48
Q

What are the pharmacologic effects of sympathomimetics?

A
  • Vasoconstriction (cutaneous and renal circulations)
  • Vasodilation of skeletal muscle
  • Cardiac stimulation (increased HR and myocardial contractility and vulnerability to dysrhythmias
  • Hepatic: glycogenolysis
  • Liberation of free fatty acids from adipose tissues
  • Modulation of hormone secretion: insulin, renin, and pituitary
  • CNS stimulation
49
Q

What are the clinical uses of sympathomimetics?

A

Most often used as positive inotropes to improved cardiac contractility. Vasopressor to elevate blood pressure from unacceptable lows

50
Q

What are the less often used clinical uses of sympathomimetics?

A

Treatment of bronchospasm in the asthmatic patient
Management of anaphylaxis
Addition to local anesthetic to slow systemic absorption of local anesthetic from site of infiltration or injection

51
Q

What is the mechanism of action of sympathomimetics?

A
  • The pharmacologic response caused by a sympathomimetic is related to the density of the alpha and beta adrenergic receptors in the tissues
  • There is an inverse relationship between the concentration of available sympathomimetic and the number of receptors
52
Q

Why does norepi have minimal effects on airway resistance?

A

Because adrenergic receptors in bronchial smooth muscle are mostly beta2 and thus not stimulated by this catecholamine

53
Q

T/F: oral administration of catecholamines is effective

A

False, not effective

54
Q

What is the metabolism for synthetic non-catecholamines?

A

Lack a 3-hydroxyl group: not metabolized by COMT
Dependent on MAO for metabolism
Metabolism is often slower than that of catechols

55
Q

What drug interacts with synthetic non-catecholamines?

A

Patients on MAO inhibitors may manifest exaggerated responses when treated with synthetic non-catecholamines because inhibition of MAO may prolong their duration

56
Q

The effect of ephedrine is primarily mediated thru what?

A

Direct and indirect action thru the release of NE

57
Q

What is the principle mechanism of ephedrine?

A

Increased myocardial contractility

58
Q

What are some of the actions of Ephedrine?

A

Venoconstriction greater than arteriolar constriction increases preload and with increased HR and myocardial contractility, results in increased CO (beta1 receptor action)
Increases BP as a result
Tachyphylaxis can occur
Preserves or increases uterine blood flow
Bronchial smooth muscle relaxant

59
Q

What is the onset and duration of ephedrine?

A

Onset 1 min

Duration 5-10 mins

60
Q

What type of catecholamine is phenylephrine?

A

Synthetic non-catecholamine

61
Q

What are some adverse effects of phenylephrine?

A

Causes reflex bradycardia
Decreases renal and splanchnic blood flow
Increases pulmonary artery resistance and pressure
No dysrhythmias as a direct effect
Reverses right to left shunt in tetralogy of fallot

62
Q

What is the onset and duration of phenylephrine?

A

Onset: 1-2 mins
Duration: 5-10 mins

63
Q

Which drug is phenylephrine like?

A

Norepi but less potent and lasts longer

64
Q

What are some other uses of norepi?

A

Drug induced priapism
Mydriatic agent
Nasal decongestant

65
Q

What is norepinephrine?

A

Endogenous neurotransmitter responsible for maintaining BP by adjusting SVR (alpha1 effects)
Increases systolic, diastolic and mean arterial pressure

66
Q

Levo is a potent vasoconstrictor of renal, mesenteric and cutaneous vascular beds so what does this mean for the renal system?

A

May decrease renal blood flow and cause oliguria
May lead to mesenteric infarct
Peripheral hypoperfusion can lead to gangrene of digit

67
Q

What type of agonist is Levo?

A

Primarily alpha1 agonist
Beta1 effects are overshadowed by alpha1 effects
Beta2 effects minimal

68
Q

What happens to CO with Levo?

A

At low doses, CO may increase because of increased venous return and beta effects
At higher doses CO may decrease because of increased afterload and baroreceptor-mediated reflex bradycardia

69
Q

What is the most potent activator of Alpha1 receptors?

A

Epi

70
Q

What is epinephrine?

A

Prototypical catecholamine

Stimulates Alpha1, beta1, and beta2 receptors

71
Q

What type of effect does low dose epi have?

A

Beta2
Stimulate alpha1 receptors in the skin, mucosa, and hepatorenal system while beta2 receptors are stimulated in skeletal muscle

72
Q

What is the net effect of beta2 in low dose epi?

A

Decreased SVR and distribution of blood to skeletal muscle, MAP remains essentially the same

73
Q

What type of effect does intermediate doses of epi have?

A

Beta1
Increased HR and contractility and increased CO
Increased automaticity which may lead to dysrhythmias (PVCs) in sensitized myocardium

74
Q

What type of effect does high dose epi have?

A

Alpha1
Potent vasoconstrictor including cutaneous, splanchnic and renal vascular beds
Used to maintain myocardial and cerebral perfusion but reflex bradycardia can occur

75
Q

What is epi used to treat?

A

Asthma
Anaphylaxis
Cardiac arrest
Bleeding and to prolong regional anesthesia as well as decrease systemic absorption of local anesthetics
Increases lipolysis, glycogenolysis, and inhibits secretion of insulin (increases blood sugar due to the stress of surgery)

76
Q

T/F: Epinephrine increases renal blood flow even in the absence of changes in systemic BP

A

False, decreases renal blood flow

77
Q

Does tachyphylaxis occur with epi?

A

No

78
Q

How do you give epi down an ETT?

A

Triple the dose and dilute in 10 ml NS

79
Q

How do you treat bronchospasm with epi?

A

.3 mg subq q 20 mins to max of 3 doses

80
Q

What are the drug interactions that occur with epi?

A

Alpha blockers: “epi reversal” beta2 response (hypotension)

Beta blockers: unopposed alpha response

81
Q

what is racemic epi?

A

Mixture of levo and dextrorotatory isomers that constrict edematous mucosa

82
Q

What does racemic epi treat?

A

Sever croup and post extubation or traumatic airway edema
Lasts 30-60 mins
Observe for 2 hours after treatment to watch for rebound

83
Q

What are the side effects of epi?

A 
No CNS effects
Hyperglycemia
Mydriasis
Platelet aggregation
Sweating
Headache
Tremor
Nausea
Arrhythmia
84
Q

What type of effects does Dopamine have?

A

Endogenous catecholamine
Beta and alpha effects at 10-20 mcg/kg/min
Over 5 mcg/kg/min causes NE to be released contributing to cardiac stimulation
Over 10 mcg/kg/min alpha effects start to predominate

85
Q

What is Metaraminol (aramine)?

A 
Direct alpha agonist
Beta agonist at low doses
Indirect effects (endogenous release of NE)
86
Q

What does Metaraminol do?

A

Increases BP and CO

Reflex bradycardia occurs

87
Q

What are some adverse effects that occur with Metaraminol?

A

Cardiac dysrhythmias (beta stimulation)

88
Q

What drug interactions occur with Metaraminol?

A

Pure alpha agonists can activate baroreceptor reflex-mediated bradycardia and possibly decrease CO
Antihypertensives may decrease the pressor response to indirect acting drugs or enhance the response to direct acting drugs (denervation hypersensitivity)

89
Q

What drugs can interact with vasoconstrictors?

A

Tricyclic antidepressants and MAO inhibitors
Cocaine
Natural weight loss products that contain ma huang (ephedra)

90
Q

Is it okay to continue with tricyclic antidepressants and MAOIs in the perioperative period?

A

Yes, use a decreased dose of direct acting drugs

91
Q

How does cocaine interact with vasoconstrictors?

A

Interferes with reuptake of catecholamines, both exogenous and endogenous catecholamines exhibit enhanced effects

92
Q

What happens if cocaine interacts with vasoconstrictors?

A

Produces central and peripheral sympathetic stimulation, resulting in vasoconstriction, tachycardia and potentially arrhythmias

93
Q

Acute toxicity of cocaine and vasoconstrictors can best be managed how?

A

With adrenergic blockade (labetalol with alpha and beta effects)

94
Q

How does ephedra interact with vasoconstrictors?

A

It contains ephedrine, pseudoephedrine
Long-term use results in tachyphylaxis from depletion of endogenous catecholamine stores and may contribute to perioperative hemodynamic instability and cardiovascular collapse.
Stop product at least 24 hours prior to surgery

95
Q

How do you treat extravasation?

A

Phentolamine

96
Q

How does Phentolamine work?

A

Alpha1 and 2 antagonist
Peripheral vasodilator
Treats skin necrosis secondary to norepi, dopamine and epi

97
Q

What are the vasoconstrictors that are posterior pituitary hormones?

A

Arginine vasopressin (AVP, formerly known as ADH)
Oxytocin (Pitocin)
DDAVP (desmopressin)

98
Q

What is arginine vasopressin used for?

A

To preserve cardiocirculatory homeostasis in patients with advanced vasodilitory shock
(Patients who have failed or resistant to conventional vasopressor therapy, Patients who experience the adverse effects of conventional vasopressor therapy)

99
Q

How is arginine vasopressin different than other catecholamines?

A

Effects of arginine vasopressin are preserved during hypoxia and severe acidosis

100
Q

How does arginine vasopressin work?

A

Causes vasoconstriction in most vascular beds (strongest in splanchnic, muscular, and cutaneous vasculature. Paradoxical vasodilatation in pulomonary, coronary, and vertebrobasilar circulation

101
Q

What are the ACLS guidelines for vasopressin?

A

40 units IV
Treat vfib and vtach for patients who haven’t responded to 3 attempts at defib
Also an alternative to ep

102
Q

What is the goal in CPR?

A

To increase cerebral perfusion pressure to improve blood flow to the heart and brain and subsequently restore function

103
Q

What are the advantages of vasopressin over epi?

A

Epi increases myocardial oxygen consumption which contributes to the risk of developing post-resuscitation MI and arrhythmias
Catecholamines may not work well in acidic environment associated with CPR

Pharm II (8 decks)

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