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Basic Pharmacology > Pharmacology of Cardiovascular Drugs > Flashcards

Pharmacology of Cardiovascular Drugs Flashcards

1
Q

what is heart failure or congestive heart failure?

A

heart is unable to adequately circulate blood to meet the needs of the body

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2
Q

what direct effects on the heart do cardiovascular drugs have?

A

chronotropy: rate, rhythm
intropy: contractility

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3
Q

how do cardiovascular drugs change vascular tone?

A

vasodilation/constriction
ateriodilation/constriction: decrease/increase peripheral resistance
venodilation: increase venous capacity

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4
Q

how do cardiovascular drugs change vascular volume?

A

change volume of blood: increase or decrease
change venous capacity: venodilation

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5
Q

many drugs effects both the heart and the vascular system directly, and there are ____________________________ between the two “systems”

A

homeostatic control mechanisms

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6
Q

what is increased survival from cardiovascular drugs linked to?

A

decreased sympathetic input to the heart, which decreases likelihood of fatal cardiac arrhythmias and decreases overall stress on the heart
decreased hormonal input that reduces secondary inflammation and remodeling (helps to decrease disease progression)

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7
Q

what drugs are chronotropes?

A

adrenergic drugs
cholinergic drugs

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8
Q

what drugs are inotropes?

A

adrenergic drugs
inodilators
cardiac glycosides

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9
Q

what are the class I antiarrhythmics?

A

sodium channel blockers

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10
Q

what are the effects of beta1 agonists?

A

increase rate and force of contraction
no direct effects on arteries

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11
Q

what is dopamine?

A

positive chronotrope/inotrope

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12
Q

what receptors is dopamine an agonist for?

A

dopamine
beta1
alpha-receptors
depends on concentration

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13
Q

what is dopamine IV used for?

A

immediate inotropic support

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14
Q

what does dobutamine do?

A

inotrope with little chronotropic effect
beta1

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15
Q

what are the main cardiac chronotropic effects of beta blockers?

A

decrease heart rate
slow AV conduction
prolong refractory period in conducting tissues
decrease spontaneous depolarization
suppress catecholamine-induced arrhythmias

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16
Q

what are beta blockers used for?

A

supraventricular tachycardias

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17
Q

what are some supraventricular tachycardias?

A

elevated heart rate
atrial fibrillation

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18
Q

what receptors do beta blockers affect?

A

block beta1 and/or beta2 receptors

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19
Q

when is dobutamine used?

A

acute, in hospital situations, for immediate inotropic support

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20
Q

what is the mechanism of anticholinergic agents (positive chronotropes)?

A

muscarinic receptor antagonists

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21
Q

what is atenolol?

A

selective beta-1 blocker

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22
Q

what is atenolol used for in cats?

A

hypertrophic cardiomyopathy

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23
Q

what are the adverse effects of positive chronotropes (anticholinergics)?

A

increased peripheral resistance
ileus
decrease salivary and bronchiolar secretions
urinary retention
mydriasis and associated photophobia

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24
Q

inotropes that also decrease neurohormonal (sympathetic) input to the heart have ______________________ or ____________________, depending on magnitude of decreases in neurohormonal input

A

neutral effects on survivability (digoxin)
beneficial effects (pimobendan)

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25
Q

how does pimobendan increase contractility?

A

increases affinity of troponin C complex for calcium, leading to increased contractility without increasing calcium concentrations

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26
Q

what is the key property of pimobendan?

A

increases cardiac contractility without increasing myocardial oxygen consumption

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27
Q

how does pimobendan cause vasodilation?

A

phosphodiesterase III inhibition

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28
Q

what does pimobendan do with the heart?

A

modulates neurohormonal input to the heart

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29
Q

what drug is the only positive inotrope that has been evaluated in clinical trials in the dog?

A

pimobendan

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30
Q

what is pimobendan approved for in dogs?

A

management of signs of congestive heart failure due to dilated cardiomyopathy (DCM) and myxomatous mitral valve disease (MMVD)

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31
Q

what has pimobendan shown in dogs with changes in function or cardiomegaly that do not have CHF?

A

significant delayed onset of congestive heart failure and/or death for both dilated cardiomyopathy and myxomatous mitral valve disease

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32
Q

what does digoxin (cardiac glycoside, positive inotrope) do?

A

inhibits Na/K ATPase pump on cardiac myocytes
increases vagal tone

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33
Q

how is digoxin cleared?

A

primarily by kidney

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34
Q

what is the therapeutic range of digoxin like?

A

narrow: therapeutic drug monitoring useful

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35
Q

what are some adverse effects of digoxin?

A

gastrointestinal distress
arrhythmias

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36
Q

what are the clinical indications of digoxin?

A

primarily to slow ventricular response rate in dogs with atrial fibrillation
horses: protect against increased ventricular response rate

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37
Q

what is supraventricular arrhythmia?

A

abnormal rate/rhythm that originates above the ventricle

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38
Q

what is ventricular arrhythmia?

A

abnormal rate/rhythm that originates in the ventricle

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39
Q

what do antiarrhythmic drugs do generally?

A

alter automaticity
alter conduction velocity
change excitability of cardiac cells during effective refractory period
alter membrane ion conductance to affect the action potential

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40
Q

what are class 1 antiarrhythmic drugs?

A

Na-channel blockers

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41
Q

what are class 2 antiarrhythmic drugs?

A

beta-blockers

42
Q

what are class 3 antiarrhythmic drugs?

A

K-channel blockers

43
Q

what are class 4 antiarrhythmic drugs?

A

Ca-channel blockers

44
Q

what class of antiarrhythmic drugs includes atropine and digoxin?

A

miscellaneous

45
Q

what does lidocaine do?

A

blocks inactive Na-channels
no increase in effective refractory period

46
Q

where does lidocaine have its greatest effect?

A

abnormal ventricular cardiac tissue

47
Q

what is lidocaine a drug of choice for?

A

acute ventricular arrhythmias

48
Q

what does procainamide do?

A

blocks open Na channels, slower off rate
increases effective refractory period

49
Q

what does quinidine do?

A

blocks open Na channels, slow off rate
increases effective refractory period
significant vagolytic effect and is an alpha1-blocker

50
Q

what is the primary treatment for atrial fibrillation in horses?

A

quinidine

51
Q

what do class 3 antiarrhythmics do?

A

prolong action potential and extend effective refractory period
likely through effect on K-channels

52
Q

what is the most clinically relevant class 3 antiarrhythmic/potassium channel blocker?

A

sotalol

53
Q

how do class 4 antiarrhythmics work?

A

block slow calcium channels in cardiac cells and vascular smooth muscle

54
Q

what do calcium channel blockers do?

A

slow heart rate (SA node) and AV conductance
decrease myocardial contraction
cause peripheral vasodilation

55
Q

what is diltiazem?

A

calcium channel blocker

56
Q

what is diltiazem used for?

A

atrial fibrillation in dogs

57
Q

what drugs do we use in the adrenergic system to modify vasodilation and vasoconstriction?

A

alpha1 adrenergic receptor antagonists
alpha1 agonists
alpha2 agonists
beta-blockers and beta-agonists

58
Q

what is amlodipine preferred for?

A

calcium channel blocker for peripheral vasodilation

59
Q

what does amlodipine target?

A

systemic arteriolar smooth muscle

60
Q

what is amlodipine used for?

A

severe mitral valve regurgitation in dogs
systemic hypertension

61
Q

what do nitric oxide producers do?

A

cause arterial and venodilation by conversion to nitric oxide

62
Q

what are nitric oxide producers used for?

A

acute management of cardiac failure

63
Q

angiotensin converting enzyme is located primarily in the endothelial cells of the __________________. __________ quantitively most important

A

lungs and kidneys
lungs

64
Q

what do angiotensin converting enzyme inhibitors lead to?

A

significant vasodilation
decrease in aldosterone, leading to diuresis
decrease sympathetic input to heart

65
Q

what are the primary ACE inhibitors used?

A

benzapril
enalaprilremain

66
Q

what are the approved veterinary ACE inhibitors?

A

enalapril
benazepril

67
Q

are ACE inhibitors for acute therapy or management?

A

management

68
Q

how do diuretics reduce blood volume?

A

by increasing urine production

69
Q

what are the diuretics of choice?

A

furosemide
torsemide

70
Q

what is spironolactone?

A

diuretic
aldosterone antagonist

71
Q

how are ACE inhibitors diuretics?

A

decrease aldosterone production

72
Q

what is key to prolonged survivability?

A

decreasing sympathetic and neurohormonal input to the heart

73
Q

who is more sensitive to the CNS adverse effects of dobutamine?

A

cats

74
Q

what do beta blockers do with atrial fibrillation?

A

decrease ventricular response rate

75
Q

where are beta-2 receptors found other than the heart?

A

lungs
bladder
some vasculature

76
Q

when should you avoid using beta-blockers?

A

animal in overt heart failure
pulmonary pathology present

77
Q

what is propanolol?

A

non-selective beta blocker
largely supplanted by atenolol: beta-1 selective blocker

78
Q

why is it important that carvedilol also blocks alpha-1 adrenergic receptors and mat possess antioxidant properties?

A

protects against increased resistance from unopposed beta-2 block
antioxidant properties may protect heart

79
Q

what is generally the drug of choice for beta-blockade?

A

atenolol: selectivity, data, cost

80
Q

what are the effects of cholinergic drugs?

A

SA node: slow heart rate
AV node: slow heart rate
atrium: decrease contractility
ventricle: decrease contractility

81
Q

what are some positive chronotropes?

A

atropine
glycopyrrolate

82
Q

does atropine and/or glycopyrrolate cross the blood-brain barrier?

A

atropine does

83
Q

how do positive chronotropes increase heart rate?

A

inhibit M2 actions

84
Q

what are some negative inotropes?

A

adrenergic antagonists
calcium channel blockers

85
Q

what has been shown with life expectancy and pure positive inotropes?

A

negative impact

86
Q

what is the half life of pimobendan’s active metabolite?

A

2 hours

87
Q

what are the adverse effects of pimobendan?

A

relatively safe
diarrhea
tachycardia or ventricular arrhythmia
hyperexcitability
worsening dynamic outflow obstruction

88
Q

what positive inotrope has been evaluated in clinical trials for dogs?

A

pimobendan only

89
Q

what is the half-life of digoxin?

A

24 hours

90
Q

what do arrhythmias with digoxin result from?

A

high vagal tone and direct effects on heart

91
Q

how do anti-arrhythmics affect the action potential?

A

alter membrane ion conductance

92
Q

do sodium channel blockers affect the SA/AV nodes?

A

not really directly

93
Q

what are the adverse effects of lidocaine?

A

skeletal muscle fasciculation, vomiting
seizures

94
Q

can you use lidocaine containing epinephrine?

A

no

95
Q

how do potassium channel blockade drugs/class III affect the heart?

A

prolong action potential and extend effective refractory period

96
Q

what does diltiazem do?

A

decreases SA/AV node with limited effect on inotropy
mild peripheral vasodilatory effect

97
Q

what is phenylephrine?

A

alpha1 agonist: selective for alpha1 receptors, IV only

98
Q

what is ephedrine?

A

alpha1 agonist: non-selective alpha/beta agonist and may stimulate release of norepinephrine

99
Q

what is norepinephrine?

A

alpha1 agonist: alpha 1, 2, and beta-1 receptor agonist

100
Q

what is the primary alpha1 adrenergic receptor antagonist?

A

prazosin

Basic Pharmacology (37 decks)

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