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Basic Pharmacology > Pharmacology of Cardiovascular Drugs > Flashcards

Pharmacology of Cardiovascular Drugs Flashcards

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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
how does pimobendan increase contractility?
increases affinity of troponin C complex for calcium, leading to increased contractility without increasing calcium concentrations
26
what is the key property of pimobendan?
increases cardiac contractility without increasing myocardial oxygen consumption
27
how does pimobendan cause vasodilation?
phosphodiesterase III inhibition
28
what does pimobendan do with the heart?
modulates neurohormonal input to the heart
29
what drug is the only positive inotrope that has been evaluated in clinical trials in the dog?
pimobendan
30
what is pimobendan approved for in dogs?
management of signs of congestive heart failure due to dilated cardiomyopathy (DCM) and myxomatous mitral valve disease (MMVD)
31
what has pimobendan shown in dogs with changes in function or cardiomegaly that do not have CHF?
significant delayed onset of congestive heart failure and/or death for both dilated cardiomyopathy and myxomatous mitral valve disease
32
what does digoxin (cardiac glycoside, positive inotrope) do?
inhibits Na/K ATPase pump on cardiac myocytes increases vagal tone
33
how is digoxin cleared?
primarily by kidney
34
what is the therapeutic range of digoxin like?
narrow: therapeutic drug monitoring useful
35
what are some adverse effects of digoxin?
gastrointestinal distress arrhythmias
36
what are the clinical indications of digoxin?
primarily to slow ventricular response rate in dogs with atrial fibrillation horses: protect against increased ventricular response rate
37
what is supraventricular arrhythmia?
abnormal rate/rhythm that originates above the ventricle
38
what is ventricular arrhythmia?
abnormal rate/rhythm that originates in the ventricle
39
what do antiarrhythmic drugs do generally?
alter automaticity alter conduction velocity change excitability of cardiac cells during effective refractory period alter membrane ion conductance to affect the action potential
40
what are class 1 antiarrhythmic drugs?
Na-channel blockers
41
what are class 2 antiarrhythmic drugs?
beta-blockers
42
what are class 3 antiarrhythmic drugs?
K-channel blockers
43
what are class 4 antiarrhythmic drugs?
Ca-channel blockers
44
what class of antiarrhythmic drugs includes atropine and digoxin?
miscellaneous
45
what does lidocaine do?
blocks inactive Na-channels no increase in effective refractory period
46
where does lidocaine have its greatest effect?
abnormal ventricular cardiac tissue
47
what is lidocaine a drug of choice for?
acute ventricular arrhythmias
48
what does procainamide do?
blocks open Na channels, slower off rate increases effective refractory period
49
what does quinidine do?
blocks open Na channels, slow off rate increases effective refractory period significant vagolytic effect and is an alpha1-blocker
50
what is the primary treatment for atrial fibrillation in horses?
quinidine
51
what do class 3 antiarrhythmics do?
prolong action potential and extend effective refractory period likely through effect on K-channels
52
what is the most clinically relevant class 3 antiarrhythmic/potassium channel blocker?
sotalol
53
how do class 4 antiarrhythmics work?
block slow calcium channels in cardiac cells and vascular smooth muscle
54
what do calcium channel blockers do?
slow heart rate (SA node) and AV conductance decrease myocardial contraction cause peripheral vasodilation
55
what is diltiazem?
calcium channel blocker
56
what is diltiazem used for?
atrial fibrillation in dogs
57
what drugs do we use in the adrenergic system to modify vasodilation and vasoconstriction?
alpha1 adrenergic receptor antagonists alpha1 agonists alpha2 agonists beta-blockers and beta-agonists
58
what is amlodipine preferred for?
calcium channel blocker for peripheral vasodilation
59
what does amlodipine target?
systemic arteriolar smooth muscle
60
what is amlodipine used for?
severe mitral valve regurgitation in dogs systemic hypertension
61
what do nitric oxide producers do?
cause arterial and venodilation by conversion to nitric oxide
62
what are nitric oxide producers used for?
acute management of cardiac failure
63
angiotensin converting enzyme is located primarily in the endothelial cells of the __________________. __________ quantitively most important
lungs and kidneys lungs
64
what do angiotensin converting enzyme inhibitors lead to?
significant vasodilation decrease in aldosterone, leading to diuresis decrease sympathetic input to heart
65
what are the primary ACE inhibitors used?
benzapril enalaprilremain
66
what are the approved veterinary ACE inhibitors?
enalapril benazepril
67
are ACE inhibitors for acute therapy or management?
management
68
how do diuretics reduce blood volume?
by increasing urine production
69
what are the diuretics of choice?
furosemide torsemide
70
what is spironolactone?
diuretic aldosterone antagonist
71
how are ACE inhibitors diuretics?
decrease aldosterone production
72
what is key to prolonged survivability?
decreasing sympathetic and neurohormonal input to the heart
73
who is more sensitive to the CNS adverse effects of dobutamine?
cats
74
what do beta blockers do with atrial fibrillation?
decrease ventricular response rate
75
where are beta-2 receptors found other than the heart?
lungs bladder some vasculature
76
when should you avoid using beta-blockers?
animal in overt heart failure pulmonary pathology present
77
what is propanolol?
non-selective beta blocker largely supplanted by atenolol: beta-1 selective blocker
78
why is it important that carvedilol also blocks alpha-1 adrenergic receptors and mat possess antioxidant properties?
protects against increased resistance from unopposed beta-2 block antioxidant properties may protect heart
79
what is generally the drug of choice for beta-blockade?
atenolol: selectivity, data, cost
80
what are the effects of cholinergic drugs?
SA node: slow heart rate AV node: slow heart rate atrium: decrease contractility ventricle: decrease contractility
81
what are some positive chronotropes?
atropine glycopyrrolate
82
does atropine and/or glycopyrrolate cross the blood-brain barrier?
atropine does
83
how do positive chronotropes increase heart rate?
inhibit M2 actions
84
what are some negative inotropes?
adrenergic antagonists calcium channel blockers
85
what has been shown with life expectancy and pure positive inotropes?
negative impact
86
what is the half life of pimobendan's active metabolite?
2 hours
87
what are the adverse effects of pimobendan?
relatively safe diarrhea tachycardia or ventricular arrhythmia hyperexcitability worsening dynamic outflow obstruction
88
what positive inotrope has been evaluated in clinical trials for dogs?
pimobendan only
89
what is the half-life of digoxin?
24 hours
90
what do arrhythmias with digoxin result from?
high vagal tone and direct effects on heart
91
how do anti-arrhythmics affect the action potential?
alter membrane ion conductance
92
do sodium channel blockers affect the SA/AV nodes?
not really directly
93
what are the adverse effects of lidocaine?
skeletal muscle fasciculation, vomiting seizures
94
can you use lidocaine containing epinephrine?
no
95
how do potassium channel blockade drugs/class III affect the heart?
prolong action potential and extend effective refractory period
96
what does diltiazem do?
decreases SA/AV node with limited effect on inotropy mild peripheral vasodilatory effect
97
what is phenylephrine?
alpha1 agonist: selective for alpha1 receptors, IV only
98
what is ephedrine?
alpha1 agonist: non-selective alpha/beta agonist and may stimulate release of norepinephrine
99
what is norepinephrine?
alpha1 agonist: alpha 1, 2, and beta-1 receptor agonist
100
what is the primary alpha1 adrenergic receptor antagonist?
prazosin

Basic Pharmacology (37 decks)

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