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Pharmacology Exam 3 > Cardiovascular Drugs > Flashcards

Cardiovascular Drugs Flashcards

1
Q

what is the normal heart rhymthm?

A

SA node (pacemaker)-> atrial muscle-> av node-> ventricles

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2
Q

what is arrhythmia?

A

alteration in the normal impulse pathway
alteration in the pacemaker
ectopic focus is source of rhythm start
alteration in the transmission pathway
ventricular fibrillation is lifethreatening
ventricular arrhythmias are the major cause of cardiac death

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3
Q

what is the electrophysiology of cardiac cell

A

Na2+ influx, Ca2+ influx, K+ efflux

recovery

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4
Q

what are some non-drug treatments of arrhythmia?

A

no treatment
non drug treatment is preferable
pacemaker implantation
cardioversion- global depolarization of heart
automatic defibrillator implanted
surgical removal of ectopic focus- ablation

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5
Q

what are the class 1 drugs?

A

sodium channel blockers
local anesthetics
decrease rate of depolarization

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6
Q

which drugs are in 1a?

A

quinidine, procainamide, disopyramide

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7
Q

tell me about quinidine

A 
sodium channel blocker class 1a
for all arrythmias 
depresses all muscle function
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8
Q

what are the side effects of quinidine?

A 
anticholinergic effects (antivagal effects)
GI- nausea, vomiting
naus
anorexia
CNS- tinnitus, altered color vision
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9
Q

tell me about procainamide

A 
sodium channel blocker class 1a
like quinidine
does not enter the cns
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10
Q

what are the side effects of procainamide?

A

lupus like syndrome in slow acetylators

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11
Q

tell me about disopyramide

A

sodium channel blocker class 1a

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12
Q

what are the side effects of disopyramide?

A

antimuscarinic effect

strong antivagal effects

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13
Q

what drugs are in 1b?

A

lidocaine

mexiletine

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14
Q

tell me about lidocaine

A

sodium channel blocker class 1b
given IV- first pass effect
less likely to cause arrhythmias
useful for treating ventricular tachycardia

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15
Q

side effects of lidocaine

A

can enter cns- tumors, seizures

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16
Q

tell me about mexiletine

A 
sodium channel blocker class 1b
like lidocaine but can be given orally
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17
Q

what are the class 2 drugs?

A

beta blockers
block b1 receptors in the heart
effectively slows heart rate
propranolol, metoprolol, esmolol

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18
Q

propranolol

A

decrease pacemaker firing rate

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19
Q

metoprolol

A

more selective- less B2 effects

selective B1

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20
Q

esmolol

A

more rapid onset of action

selective B1

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21
Q

side effects of class 2

A

brady cardia
hypotension
b2 effects (propranolol)-asthma

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22
Q

what are the class 3 drugs?

A

potassium channel blockers
sotalol
amiodarone
dronedarone

23
Q

tell me about sotalol

A

potassium channel blocker

beta blocker that also blocks potassium channels

24
Q

tell me about amiodarone

A

potassium channel blocker
acts like all 4 classes of antiarrhythmia
most effective antiarrhythmic
DOC in cases of cardiac arrest

25
side effects of amiodarone
``` potentially fatal pulmonary fibrosis liver damage corneal deposits- optic neuritis deposition in skin-- causes blue grey skin coloration gi upset ```
26
tell me about dronedarone
potassium channel blocker analog of amiodarone fewer side effects, less efficacy
27
what are the class 4 drugs
calcium channel blockers verapamil diltiazem nifedipine
28
verapamil diltiazem nifedipine
calcium channel blocker block calcium transport in cardiac cells increase refractory period useful for all but ventricular arrhythmia
29
tell me about adenosine
``` given iv binds to an adenosine receptor and decreases firing rate of av node very short half life for atrial tachycardia coronary vasodilator ```
30
definition of angina
not enough blood flow to heart muscle chest pain usually after exercise- if at rest, then it's unstable angina treatment by increase blood flow to the heart or decrease oxygen demand
31
behavioral treatment of angina
exercise- develop collateral circulation
32
what are the nitrates?
``` glyceryl trinitrate (nitroglycerin) isosorbide dinitrate ```
33
tell me about glyceryl trinitrate (nitroglycerin)
generally given sublingual treatment of angina rapidly dilates all blood vessels (including coronary artery) GTN->nitric oxide->activates guanylate cyclase->cGMP-> vascular dilation can develop rapid tolerance to nitric oxide
34
side effects of nitroglycerin
hypotension skin flushing headache
35
tell me about isosorbide dinitrate
treatment of angina | slow release nitrate formulation- can be given orally
36
what are the other agents used in treament about angina?
use agents that decrease heart work beta blockers- olols calcium channel blocker- ipine
37
congestive heart failure definition
heart muscle doesn't contract strongly enough blood doesn't leave heart fast enough tissue doesn't get enough oxygenated blood heart begins to enlarge-> pulmonary congestion decrease ability to breathe kidney is not well perfused kidney causes retention of sodium ions and fluid- peripheral edema
38
what are the causes of congestive heart failure?
cardiac damage
39
how does the heart adapts to congestive heart failure?
Apparent loss of blood because tissues are underperfused thus release of epinephrine, NE, Angiotensin II Increase BP, increase HR, vasoconstriction Increase blood volume→ Angiotensin II→ increase sodium retention→increase aldosterone secretion→ increase Na+ --- K+exchange (increase Na+) Enlargement of heart- increase force of contraction due to stretching of cardiac muscle Heart works harder These compensation actually damage the heart
40
treatment of cardiac insufficiency
increase cardiac muscle contractility (inotropic agents- increase amount of calcium in the heart muscle)
41
digoxin
cardiac glycoside
42
digoxin mechanism of action
All about Ca2+ In order for muscle to relax after contraction, calcium must be removed Digoxin inhibit the Na+/K+ ATPase Na+ remains in cell, this prevents the loss of calcium (Na+/Ca2+ exchanger)- net result- Ca2+ remains high in system Greater Ca2+→greater contractility
43
SE of digoxin
Cardiac arrhythmia CNS effects: yellow green tinting of vision Hallucinations: activation of chemoreceptor trigger zone→severe nausea
44
effects of digoxin is greatly enhanced in what individuals?
hypokalemic (low k+)
45
what is digoxin poisoning treated with?
anti-digoxin antibody
46
what other inotropic agents are used to treat congestive heart failure
dobutamine
47
what is dobutamine
beta 1 agonist | strong inotropic effect- increase force of contraction
48
current best treatment of congestive heart failure
``` ace inhibitors beta blockers vasodilators diuretics want to decrease BP, decrease fluid retention, decrease heart rate ```
49
what are the agents that increase blood flow to selected organs?
Sildenafil Vardenafil Tadalafil Avanafil
50
how do the afils work?
Inhibitors of types of cGMP phosphodiesterase Nitrates→ NO→ increase cGMP→smooth muscle relaxation cGMP is broken down into 5’GMP by type 5 phosphodiesterase
51
side effects of afils
Metabolized by p450→ drug interactions Stroke, myocardial infraction Visual disturbances- impaired blue/green color discrimination NAION- some potential for damage to the retina induced by cGMP phosphodiesterase inhibitors
52
cautions of using afils
Slight dec BP | Do not use with alpha 1 blockers or nitrates→ dramatic decrease in BP
53
what else is afils useful for?
Useful for treatment of pulmonary hypertension
54
what is alprostadil?
another agent for increase blood flow to selective organs | ingestable pge1- vasodilation- when injected directly into penis- lead to erection

Pharmacology Exam 3 (4 decks)

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