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CPR Week 4 > 3.4.2. Vasodilator Drugs > Flashcards

3.4.2. Vasodilator Drugs Flashcards

1
Q

Purpose of vasodilators acting on arteries

A

arteries → reduce peripheral resistance (greater blood flow)

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2
Q

Purpose of vasodilators acting on veins

A

veins → increase capacitance (larger volume stored in venous system)

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3
Q

Purpose of vasodilators acting on coronary arteries

A

CORONARY arteries → improve cardiac blood flow

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4
Q

Propranolol, Sotalol

A

β1 & β2-adrenoceptor antagonists = Propranolol, Sotalol

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5
Q

metoprolol, Atenolol

A

β1-adrenoceptor selective antagonists = metoprolol, Atenolol,

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6
Q

Labetalol, Carvedilol

A

α1- & β-adrenoceptor antagonists = Labetalol, Carvedilol

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7
Q

Norepinephrine depletion drugs

A

Guanadrel, Reserpine

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8
Q

α2A-adrenoceptor agonists

A

Clonidine, Guanabenz, Guanfacine

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9
Q

fenoldopam

A

Dopamine D1 receptor agonists

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10
Q

Drug types acting through autonomic nervous system

A

ACE inhibitors
ARBs (Angiotensin Receptor Blockers)
Aldosterone receptor antagonists
Renin inhibitors

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11
Q

Captopril

A

ACE inhibitor

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12
Q

Losartan

A

ARB

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13
Q

Spironolactone and Eplerenone

A

Aldosterone receptor antagonists

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14
Q

Aliskiren

A

Renin inhibitor

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15
Q

MOA for Guanadrel

A

This is an exogenous false neurotransmitter that is accumulated, stored, and released like NE but is inactive at adrenergic receptors. Basically kicks out NE and takes its place.

  • NET actively transports guanadrel into adrenergic neuronal storage vesicles.
  • NE is displaced, resulting in specific inhibition of peripheral post-ganglionic adrenergic neurons
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16
Q

Adverse effects for Guanadrel

A
  • effector cells become supersensitive to NE during adrenergic neuron blockade. This response is similar to that produced by postganglionic sympathetic denervation.
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17
Q

MOA for Reserpine

A
  • binds tightly to adrenergic storage vesicles in central
    and peripheral adrenergic neurons and remains bound for prolonged period of time
  • the vesicular catecholamine transporter that facilitates vesicular storage is inhibited
  • thus, nerve endings
    lose their capacity to concentrate and store NE and dopamine
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18
Q

Adverse effects for reserpine

A
  • sympathetic dysfunction and antihypertensive effects observed in reserpine-induced depletion of biogenic amines, so central and peripheral effects likely contribute to these effects
  • Recovery of sympathetic function requires synthesis of new
    storage vesicles, which takes days to weeks after discontinuation of the drug
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19
Q

What are our Centrally-acting sympatholytic agents

A

Clonidine
Guanabenz
Guanfacine

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20
Q

MOA for Centrally acting sympatholytic agents

A
  • α2A adrenergic receptors in the brainstem are stimulated
  • sympathetic outflow from the CNS is reduced
  • plasma NE concentrations decrease (direct relationship w/sympathetic activity)
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21
Q

Side effects for centrally acting sympatholytic agents

A
  • at HIGHER doses, α2B receptors on vascular smooth muscle can be activated, inducing vasoconstriction
  • loss of therapeutic effect observed at high doses
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22
Q

What are the following drugs examples of?

Clonidine
Guanabenz
Guanfacine

A

Centrally-acting sympatholytic agents

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23
Q

When do we use Hydralazine?

A

Clin Use: Severe HTN, CHF, HTN in pregnancy w/ methyldopa; frequently coadministered with B-blockers

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24
Q

MOA for Hydralazine

A

Increase cGMP → smooth muscle relaxation; vasodilates arterioles more than veins; afterload reduction

It seems to prevent the development of nitrate tolerance, perhaps by inhibiting vascular superoxide production

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25
Q

Side Effects for Hydralazine

A
  • reflex-related increases in HR
  • cardiac contractility
  • Lupus-like syndrome
  • fluid retention
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26
Q

Hydralazine is contraindicated in who?

A

contraindicated in patients with both hypertension and coronary artery disease

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27
Q

MOA for Minoxidil

A

K+ channel OPENER

  • metabolized to the active metabolite minoxidil sulfate that activates the ATP-modulated K+ channel
  • channel opening causes hyperpolarization and relaxation (mainly in arteriolar smooth muscle, little effect on veins)
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28
Q

Side effects for Minoxidil

A

similar adverse effects to that of hydralazine

  • also: plasma renin activity and fluid retention
  • increases contractility and oxygen demand in the heart (can lead to cardiac ischemia)
29
Q

Minoxadril is contraindicated in who?

A

contraindicated in hypertensive patients with coronary artery disease and patients with ventricular hypertrophy

30
Q

MOA for Sodium nitroprusside

A

NO donor

  • the “nitroso” functional group spontaneously and nonenzymatically releases a single NO molec
  • vessel relaxation by NO is non-specific, so arteries and veins are BOTH affected
31
Q

Side effects for sodium nitroprusside

A
  • Excessive cyanide accumulation can lead to acid-base disturbances, cardiac arrhythmias, and even death
  • Thiocyanate toxicity can also occur in patients with impaired renal function, causing disorientation, psychosis, muscle spasms, and convulsions
32
Q

What are the following drugs an example of?

Sodium nitroprusside
Hydralazine
Minoxadril

A

Direct vasodilator drugs acting on vascular smooth muscle

and/or the adjacent vascular endothelium

33
Q

All Ca Channel blockers cause what

A

ALL Ca-C blockers:

Reduction in contractility in vascular smooth muscle and the heart

34
Q

Order of strength of vascular smooth muscle contraction by Ca Channel blockers

A

Vasc Smooth Muscle: amlodipine = nifedipine > diltiazem > verapamil

35
Q

Order of strength of heart contraction by Ca Channel blockers

A

Heart: verapamil > diltiazem > amlodipine = nifedipine (verapamil = ventricle)

36
Q

Which Ca Channel blockers are dihydropyridine?

A

nifedipine, amlodipine,
nimodipine,
clevidipine

37
Q

Which Ca Channel blockers are non dihydropyridine?

A

diltiazem, verapamil

38
Q

General MOA for all Ca Channel blockers

A
  • inhibition/blockage of L-type Ca channels (specifically binds to the alpha-1 subunit)
39
Q

Effect of Ca Channel blockers in smooth muscle

A
  • in SMOOTH MUSCLE: decreased Ca influx keeps intracellular [Ca] low
  • Ca/CaM-mediated activation of myosin light chain kinase, actin-myosin
    interaction, and smooth muscle contractility are all reduced
40
Q

Effect of Ca Channel blockers in cardiac muscle

A
  • in CARDIAC MUSCLE:

decreased Ca influx decreases myocardial contractility, SA node pacemaker rate, and AV node conduction velocity

41
Q

Effect of Ca Channel blockers in skeletal muscle?

A
  • in SKELETAL MUSCLE:

not significantly affected by Ca channel blockers b/c these cells depend on Ca release from the SR

42
Q

Side Effects of dihydropyridine Ca Channel blockers

A
  • Excessive vasodilation

- depression of cardiac output

43
Q

What do we use non dihydropyridine Ca Channel blockers for that we don’t use dihydropyridine Ca Channel blockers for?

A

Atrial fibrillation/flutter

44
Q

Side effects of nondihydropyridine Ca Channel blockers

A
  • Excessive vasodilation
  • depression of cardiac output
  • AV nodal block
  • potential precipitation of congestive heart failure
45
Q

Verapamil is similar to ___ in effect

A

B blockers

46
Q

____ is similar to nitrates in effect

A

nifedipine

47
Q

This drug is contraindicated in patients with pheochromocytoma

A

Guanadrel is contraindicated in Pts with pheochromocytoma.

48
Q

What is Theophylline?

A

Non-specific PDE inhibitor

49
Q

MOA for PDE inhibitors

A
  • prevent the hydrolysis of cyclic nucleotides (cAMP or cGMP) to their inactive monophosphate forms (AMP or GMP)
  • increased cAMP causes positive inotropism in the heart, and dilation of both resistance and capacitance vessels in the peripheral vasculature
50
Q

Which drugs are PDE 3 specific?

A

amrinone, milrinone, vesnarinone,

dipyridamole

51
Q

Which drugs are PDE 5 specific?

A

sildenafil, vardenafil, tadalefil

52
Q

Where do we find PDE 3 specific PDE inhibitors

A

Cardiac and smooth muscle

53
Q

Where do we find PDE 5 specific PDE inhibitors

A

Erectile smooth muscle.

Some amounts in retina and systemic vasculature

54
Q

Side effects of all PDE inhibitors

A
  • thrombocytopenia in about 10% of patients

- severe side effects related to excessive vasodilation such as hypotension, MI, and sudden death can occur

55
Q

Distinguish between oral and IV dose of Guandrel

A

When administered IV, an initial increase in arterial BP is seen because the sudden bolus causes a “surge” of NE displacement.. This response isn’t seen with oral administration because of a more gradual NE release; MAO has time to degrade NE as it is slowly displaced.

56
Q

What is special about K+ channel openers?

A

Because K+ channel openers act by a mechanism that is entirely different from that of other vasodilators, these agents represent a potent family of drugs that can be used to treat hypertension refractory to other antihypertensive therapeutics

57
Q

Use of Nitroprusside in the clinic

A

Used intravenously for potent hemodynamic control in hypertensive emergencies and severe cardiac failure. Because of its rapid onset of action, short duration of action, and high efficacy, sodium nitroprusside must be infused with continuous blood pressure monitoring and careful titration of drug dose to drug effect.

58
Q

Which type of Ca Channel blocker is better at causing vasodilation?

A

Dihydropyridines.

Both do it, but DH are better than NonDH

59
Q

Effect of Ca Channel blockers on AV conduction

A

Dihydro does not affect this

Nondihydros decrease the conduction

60
Q

Effect of Ca Channel blockers on rate of recovery of the Ca channels

A

Dihydro does not affect this

Nondihydros decrease the rate of recovery

61
Q

Effect of Ca Channel blockers on cardiac contractility

A

Dihydro increases HR by reflex

Nondihydros decrease contractility

62
Q

Effect of Ca Channel blockers on HR

A

Dihydro increases HR by reflex

Nondihydros decrease HR dramatically

63
Q

Drugs that we use for HTN EMERGENCIES

A

Nick can never find self HELP

Nicardipine
Clevidipine
Nitroglycerin
Fenoldopam
Sodium nitroprusside
Hydralazine
Esmolol
Labetalol
Phentolamine
64
Q

Nicardipine vs. Clevidipine

A

Nicardipine has a long terminal half life

65
Q

What emergency hypertensive is best for those with kidney issues

A

Fenoldopam

66
Q

We use this emergency Hypertensive s/p CABG

A

Nitroglycerine

67
Q

Our go to drug for aortic dissection

A

Esmolol

68
Q

When we have HTN emergency in a pregnancy related eclampsia, we use this

A

Hydralazine

CPR Week 4 (19 decks)

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