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Cardio Week 1 > CV Stimulants > Flashcards

CV Stimulants Flashcards

1
Q

What are some CV stimulants?

A
  • Epi
  • Nor
  • Dopamine
  • Dobutamine
  • Isoproterenol
  • Phenylephine
  • Ephedrine
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2
Q

What does stimulation of beta receptors in the heart (B1) lead to?

A
  • accelerated SA/AV node (HR up)
  • accelerated ectopic pacemakers
  • increased contractility
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3
Q

What does stimulation of beta receptors in skeletal muscle vasculature lead to?

A

relaxation via preventing the entry of calcium that is critical to the contraction of vascular smooth muscle.

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4
Q

What does binding of epinephrine or NE to β adrenoceptors result in?

A

Stimulates adenylyl cyclase by activating the stimulatory G
protein, Gs, which leads to the dissociation of its alpha subunit charged with GTP. This activated αs subunit directly activates adenylyl cyclase, resulting in an increased rate of synthesis of cAMP.

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5
Q

What does binding of epinephrine or NE to a2 adrenoceptors result in?

A

Binding of presynaptic alpha2-adrenoceptor ligands inhibits adenylyl cyclase by causing dissociation of the inhibitory G protein, Gi, into its subunits; ie, an activated αi subunit charged with GTP and a β-γ unit.

The mechanism by which these subunits inhibit adenylyl cyclase is uncertain.

cAMP binds to the regulatory subunit (R) of cAMP-dependent protein kinase, leading to the liberation of
active catalytic subunits (C) that phosphorylate specific protein substrates and modify their activity.

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6
Q

Which receptors are linked to the Gq protein?

A

a1
M1
M3

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7
Q

Which receptors are linked to the Gi protein?

A

a2
D2
M2

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8
Q

Which receptors are linked to the Gs protein?

A

B1/B2

D1

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9
Q

Which sympathomimetic agents act on a-receptors?

A
  • Epi (locally vasoconstrict)
  • NE
  • DA (at higher dose)
  • Dobutamine
  • Phenylephrine
  • Ephedrine
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10
Q

Which sympathomimetic agents act on B-receptors?

A
  • Epi
  • DA (at higher dose)
  • Dobutamine
  • Isoproterenol
  • Ephedrine
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11
Q

Sympathomimetic drugs are classified based upon their mechanism of action either in the pre-synaptic terminal or on the post-synaptic membrane. What do direct acting drugs do?

A

stimulate postsynaptic receptors

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12
Q

What do indirect acting drugs do?

A

Indirectly-acting drugs cause an increase of E or NE via:

  • causing release from pre-synaptic terminals
  • blocking transport into sympathetic neurons (cocaine)
  • blocking metabolizing enzymes
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13
Q

What are some stimulant metabolizing enzymes?

A
  • monoamine oxidase (MAO)

- catechol-O-methyltransferase (COMT)

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14
Q

Drugs that cause a release of neurotransmitter, but they also themselves stimulate the receptors are called what?

A

mixed-acting drugs

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15
Q

What are some direct acting selective adrenergic agonists?

A

a1-phenylephrine
a2-clonidine
B1-dobutamine
B2-terbutaline

please call dad tomorrow

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16
Q

What are some direct acting non-selective adrenergic agonists?

A

a1/2 oxymetazoline
B1/2 isoproterenol
a1/2, B1/2 Epi
a1/2, B1- Nor

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17
Q

T or F. Both selective and non-selective direct acting adrenergic agnostic are not reduced by reserpine pretreatment

A

T. May actually increase because NE induces changes that up-regulate receptors or enhance signaling pathway

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18
Q

What are some mixed acting adrenergic agnostic?

A

Ephredrine

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19
Q

Is Ephredrine reduced by prior treatment with reserpine?

A

Effects are blunted, but not abolished

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20
Q

What are some indirect acting adrenergic agonists?

A
  • Cocaine
  • MOAI/COMTI
  • Tyramine
  • Amphetamine
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21
Q

How do MAOIs or COMTIs cause indirect effects?

A

By preventing the breakdown of released

neurotransmitter

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22
Q

How doe Tyramine and Amphetamine cause indirect effects?

A

cause the release of preformed transmitter that is normally stored successfully in the presynaptic vesicles

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23
Q

What does reserpine do?

A

depletes NE from sympathetic neurons

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24
Q

Does pretreatment with reserpine affect the effects of indirect adrenergic agonists?

A

Yes, abolishes them

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25
Q

What is the receptor specificity for Dobutamine?

A

B1 more than B2, alpha

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26
Q

What are the uses of Dobutamine?

A

HF (ino over chrontropic), stress tests

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27
Q

What is the receptor specificity for DA?

A

D1=D2 more than B more than alpha

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28
Q

What are the uses of DA?

A
  • unstable bradycardia
  • HF
  • shock
  • inotropic and chronotropic effects predominate at high doses
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29
Q

What is the receptor specificity for Epi?

A

a1=a2; B1=B2

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30
Q

What are the uses of Epi?

A
  • anaphylaxis
  • cardiac arrest
  • hypotension
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31
Q

What is the receptor specificity for Isoproterenol?

A

B1=B2

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32
Q

What are the uses of Isoproterenol? Side-effect?

A

-electrophysiologic evaluation of tachyarryhthmia

can worsen ischemia

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33
Q

What is the receptor specificity for Nor?

A

a1 over a2 over B1

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34
Q

What are the uses of Nor? But?

A

hypotension, but decreases renal perfusion

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35
Q

What is the receptor specificity for Phenylephrine?

A

a1 over a2

36
Q

What are the uses of Phenylephrine?

A

hypotension (vasoconstrictor)

37
Q

What is the receptor specificity for Ephedrine?

A

a1 over a2 over B1

38
Q

What are the uses of Ephedrine?

A
  • hypotension of anesthesia
  • narcolepsy
  • nasal congestion
  • asthma
  • bronchospasm

NoBody asks henry nelson

39
Q

At low doses, which receptors dominate for DA?

A

D1/D2 receptors

40
Q

At intermediate doses, which receptors dominate for DA?

A

b-receptors

41
Q

At high doses, which receptors dominate for DA?

A

a-receptors

42
Q

What does Epi cause at low dose?

A

produces a widening of pulse pressure (difference between systolic and diastolic) though effects upon beta-2 receptors

43
Q

What does Epi cause at high dose?

A

produce overall vasoconstriction via a strong alpha-1

mediated action.

44
Q

What does NE do to BP?

A

NE produces a strong vasoconstrictive action via alpha-1 receptors, leading to a rise in SBP and DBP and in MAP

45
Q

What does NE do to pulse?

A

Pulse rate is reduced via a baroreceptor mediated

reflexive action.

46
Q

What does Epi do to BP?

A

By contrast, E, with its beta-2 mediated relaxation of

skeletal muscle vasculature, produces a widening of pulse pressure, but no significant change in MAP

47
Q

What does Epi do to pulse?

A

increase in pulse rate mediated by beta-1 stimulation that is
unopposed by the baroreceptor reflexive mechanism.

48
Q

What does Iso do to BP?

A

This drug also stimulates beta-2 receptors leading to a fall in DBP, but the small rise in SBP is attributable to the beta-1 mediated increase in cardiac output, rather than to nonexistent alpha-1 effects.

49
Q

What does Iso do to pulse?

A

In comparison with Epi, isoproterenol tends to increase pulse rate more and reduce peripheral resistance more for the same reason, a lack of alpha-1 mediated effect.

50
Q

An important “take home” message is that the net effect of any drug depends not only on its relative receptor selectivity, but also by compensatory baroreflex mechanisms aimed at restoring BP homeostasis

A

An important “take home” message is that the net effect of any drug depends not only on its relative receptor selectivity, but also by compensatory baroreflex mechanisms aimed at restoring BP homeostasis

51
Q

How is Epi given?

A

IV, inhaled, IM, or SC (which has the most potent vasoconstrictive effects)

52
Q

Adverse effects of Epi?

A
  • cerebral hemorrhage
  • angina
  • ventricular arrhythmias
53
Q

Uses of Epi?

A
  • hypersensitivity rxns
  • vasoconstrictor with local anesthetics
  • restoring cardiac rhythm in patients with cardiac arrest
54
Q

How does Epi affect the heart?

A
  • powerful direct cardiac stimulant
  • increases HR, CO, and O2 consumption and shortens systole
  • increases relaxation rate of ventricular muscle
  • accelerates SA node action
  • shortens AV refractory period
  • activates latent pacemaker cells in the SA node
55
Q

T or F. Premature ventricular contractions can occur via Epi

A

T.

56
Q

Epi primarily acts on what kinds of vessels?

A
  • smaller arterioles

- precapillary sphincters

57
Q

What are the main effects on blood distribution of Epi?

A
  • decreased cutaneous BF and renal BF

- increased B2 mediated skeletal muscle BF, coronary BF, and pulmonary BF

58
Q

How does Epi affect the kidneys?

A

increases renal vascular resistance; decreases renal BF

does not affect GFR, but causes decreased excretion of Na+, K+, and Cl- and increased renin secretion (B1 receptors in JGA)

59
Q

What lung conditions would be contraindicated with Epi?

A

pulmonary edema can be precipitated by high concentrations of Epi

60
Q

What does the increase in coronary BF caused by Epi cause?

A
  • increased aortic pressure

- increased O2 myocardium consumption

61
Q

What are the main effects of Nor?

A
  • decrease CO
  • increase total peripheral resistance and stroke volume
  • predisposes to arryhthmias

-does not play a major role in stimulating HR

62
Q

How does Nor affect blood distribution?

A

-increase coronary BF

63
Q

How is Nor given?

A

IV

64
Q

What are the side effects of Nor?

A

same as Epi but increase in BP are more prominent- careful monitoring needed

-necrosis at infusion site

65
Q

Where are dopamine receptors found?

A

most notably in the renal vasculature where activation of D1 receptors leads to vasodilation

66
Q

Indications for dopamine?

A
  • CHD
  • RF

Having a short
duration of action the drug is only suitable for inpatient treatment.

67
Q

How is dopamine given?

A

IV infusion (monitor urine output as a 2ndary marker of drug effect)

68
Q

What does low dose DA cause?

A
  • mainly D1 action
  • vasodilation of renal, mesenteric, coronary, and intracerebral vasculature
  • improves GFR
69
Q

What does moderate dose DA cause?

A
  • mainly D1 + B1
  • increase CO (contractility over HR) and vasodilation
  • release of NE
70
Q

What does high dose DA cause?

A
  • a-agonism dominate

- increased peripheral vascular resistance and renal vasoconstriction

71
Q

What are the effects of dobutamine?

A
  • increased CO, stroke volume
  • does not affect HR
  • increased myocardial contractility with decreased left ventricular filing pressure
  • increased urinary output 2ndary to increased CO
72
Q

What is dobutamine indicated for?

A

short term treatment of cardiac decompensation after cardiac surgery, CHF, or acute MI

73
Q

How is dobutamine given?

A

infusion: T1/2= 2min (very short)

74
Q

What are the effects of isoproterenol?

A
  • mainly B receptors
  • increased CO (into and chronotropic)
  • decreased diastolic BP
75
Q

Side effects of isoproterenol?

A
  • palpitations common
  • sinus tachycardia
  • arrhythmias
  • headache
  • flushing
76
Q

How is iso given?

A

parenterol or aerosol

77
Q

What is iso used for?

A

not commonly used today but used in emergency to stimulate HR in patients with bradycardia or heart block, particularly in anticipation of inserting an artificial cardiac pacemaker or in patients with the ventricular arrhythmia tornadoes de pointes

78
Q

What does phenylephrine cause?

A
  • a1 agonist with systemic vasoconstrictor

- increased SBP and DBP

79
Q

How is phenylephrine given?

A

SC, IM, IV

80
Q

What is phenylephrine used for?

A

control of hypotension, including hypotension associated with regional or spinal anesthesia

Phenylephrine is also mixed with some local anesthetics as a vasoconstrictive agent and is employed to produce mydriasis prior to ophthalmologic examination

81
Q

Adverse effects of phenylephrine?

A
  • angina
  • anxiety
  • hallucinations
  • HTN
  • dizziness
  • insomnia/ restlessness/excitability
  • pallor
82
Q

What does ephedrine cause?

A

direct agonist at both a- and b-receptors that enhances release of NE from neurons that causes:

  • increased HR, CO, and BP
  • increased cardiac workload=possible angina
83
Q

Side effects of ephedrine?

A
  • angina
  • stimulates myocardium and may cause ventricular dysfunction, palpitations, and s-TACH
  • fatal arrhtyhmias
84
Q

Uses of ephedrine.

A
  • hypotensions
  • treatment of asthma and bronchospam (stimulates beta-receptors directly, particularly in bronchiolar smooth muscle.)
  • cooking that crystal
85
Q

Ephedra or Ma Huang (a family of botanicals) contains primarily ephedrine, with some pseudoephedrine and lesser levels of ephedra alkaloids. Ma Huang was once promoted as a dietary supplement for several conditions, including weight loss. In the early 2000s the FDA took action under the 1994 Dietary Supplement Health and Education Act (DSHEA) provisions for banning a dietary supplement that presents a significant and unreasonable human health risk.

A

The FDA reviewed an extensive amount of data, which confirmed CV risks, including HTN, heart problems and stroke from the use of the herb; conversely, there was little evidence of effectiveness except for use for short-term weight loss. Given its bronchodilatory effects, ephedrine continues to be available in many OTC cold and sinus
products.

Cardio Week 1 (22 decks)

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