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Heart drugs Flashcards

1
Q

quinidine

A

Class 1a antiarrhythmic
blocks Na+ channels (use-dependent) slowed upstorke
blocks K+ channels –> delay repolarization

vagal inhibitor (anti-cholinergic) 
a-receptor antagonist 
use treat:
re-entrant arrhythmias 
atrial flutter
Atrial fibrillation
Atrial tachycardia(30% success rate)
Ventricular tachycardias/fibrillation (frequent)
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2
Q

procainamide

A

Class 1a antiarrhythmic
blocks Na+ channels (use-dependent) slowed upstorke
blocks K+ channels –> delay repolarization

use treat:
re-entrant arrhythmias 
atrial flutter
Atrial fibrillation
Atrial tachycardia(30% success rate)
AV reentrant Tachycardia
Ventricular tachycardias/fibrillation (frequent)
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3
Q

lidocaine

A 
Class 1b antiarrhythmic
blocks Na+ channels (use-dependent) slowed upstorke (milder effect than 1a and 1c) 
Purest form of class 1 drugs
use treat:
re-entrant arrhythmias 
atrial flutter
Atrial fibrillation
Atrial tachycardia(30% success rate)
Ventricular tachycardias/fibrillation (frequent)
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4
Q

phenytoin.

A

Class 1b antiarrhythmic
blocks Na+ channels (use-dependent) slowed upstorke (milder effect than 1a and 1c)

use treat:
re-entrant arrhythmias
atrial flutter
Atrial fibrillation
Atrial tachycardia(30% success rate)
Ventricular tachycardias/fibrillation (frequent)
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5
Q

propafenone

A

Class 1c antiarrhythmic
blocks Na+ channels (use-dependent) and prolongs phase 2
powerful prolongation of tissue refractory period

use treat:
re-entrant arrhythmias 
atrial flutter
Atrial fibrillation
Atrial tachycardia(30% success rate)
Ventricular tachycardias/fibrillation(frequent)
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6
Q

flecainide

A

Class 1c antiarrhythmic
blocks Na+ channels (use-dependent) and prolongs phase 2
powerful prolongation of tissue refractory period

use treat:
re-entrant arrhythmias 
atrial flutter
Atrial fibrillation
Atrial tachycardia(30% success rate)
Ventricular tachycardias/fibrillation (frequent)
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7
Q

propranolol

A

class II antiarrhythmic drug B-blocker

reduce If, L-type Ca2+, Ks current –>reduces the upstroke rate and slows repolarization particuarly in AV nodal myocytes. —-> pacing and refractory period is prolonged in SA and AV nodal cells.

Used to treat
atrial flutter (slow conduction in 1:1 situation)
atrial fibrillation (controlling ventricular rate)
Atrial tachycardia(30% success rate)
AV nodal reentrant tachycardia (acute and chronic)
Ventricular tachycardias/fibrillation (frequent)
long QT syndrome(prevent Torsades)
hypertrophic obstructive cardiomyopathy(decrease contractility)

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8
Q

metoprolol

A

class II antiarrhythmic drug B-blocker

reduce If, L-type Ca2+, Ks current –>reduces the upstroke rate and slows repolarization particuarly in AV nodal myocytes. —-> pacing and refractory period is prolonged in SA and AV nodal cells.

Used to treat
atrial flutter (slow conduction in 1:1 situation)
atrial fibrillation (controlling ventricular rate)
Atrial tachycardia(30% success rate)
AV nodal reentrant tachycardia (acute and chronic)
Ventricular tachycardias/fibrillation (frequent)
long QT syndrome(prevent Torsades)
hypertrophic obstructive cardiomyopathy(decrease contractility)

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9
Q

esmolol

A

class II antiarrhythmic drug B-blocker

reduce If, L-type Ca2+, Ks current –>reduces the upstroke rate and slows repolarization particuarly in AV nodal myocytes. —-> pacing and refractory period is prolonged in SA and AV nodal cells.

Used to treat:
atrial flutter (slow conduction in 1:1 situation)
atrial fibrillation (controlling ventricular rate)
Atrial tachycardia(30% success rate)
AV nodal reentrant tachycardia (acute and chronic)
Ventricular tachycardias/fibrillation (frequent)
long QT syndrome(prevent Torsades)
hypertrophic obstructive cardiomyopathy(decrease contractility)

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10
Q

amiodarone

A

class III antiarrhythmic drug (long half-life)

blocks cardiac K+ channels —> prolongation of fast response phase 2 –> prominent prolongation of refractory period
blocks Na+ channels reduces conduction velocity and increases refractory period
decreases the rate of diastolic depolarizaton in autonomic cells —> reduces firing rate

used to treat:
re-entrant arrhythmias  
atrial flutter
Atrial fibrillation
Atrial tachycardia(30% success rate)
Ventricular tachycardias/fibrillation (acute and chronic)
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11
Q

sotalol

A

class III antiarrhythmic drug

blocks cardiac K+ channels —> prolongation of fast response phase 2 –> prominent prolongation of refractory period
B-blocker

used to treat:
re-entrant arrhythmias  
atrial flutter
Atrial fibrillation
Atrial tachycardia(30% success rate)
Ventricular tachycardias/fibrillation (frequent)
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12
Q

ibutilide

A

class III antiarrhythmic drug

blocks cardiac K+ channels —> prolongation of fast response phase 2 –> prominent prolongation of refractory period
Specifically blocks Kr

used to treat:
re-entrant arrhythmias  
atrial flutter
Atrial fibrillation
Atrial tachycardia(30% success rate)
Ventricular tachycardias/fibrillation (frequent)
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13
Q

dofetilide

A

class III antiarrhythmic drug

blocks cardiac K+ channels —> prolongation of fast response phase 2 –> prominent prolongation of refractory period
Specifically blocks Kr

used to treat:
re-entrant arrhythmias
atrial flutter
Atrial fibrillation
Atrial tachycardia(30% success rate)
Ventricular tachycardias/fibrillation (frequent)
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14
Q

bretylium

A

class III antiarrhythmic drug

blocks cardiac K+ channels —> prolongation of fast response phase 2 –> prominent prolongation of refractory period

used to treat:
re-entrant arrhythmias
atrial flutter
Atrial fibrillation
Atrial tachycardia(30% success rate)
Ventricular tachycardias/fibrillation (frequent)
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15
Q

verapamil

A

class IV antiarrhythmic drug

slow down Ca2+ dependent upstoke in slow response tissue –> slows condcution velocity (principal effect)
prolong refractory period —> suppress re-entrant arrhythmias, particularly in the AV node.

Used to treat:
atrial flutter (slow conduction in 1:1 situation)
Atrial tachycardia(30% success rate)
AV nodal reentrant tachycardia (acute and chronic)
Ventricular tachycardias/fibrillation(frequent)
hypertrophic obstructive cardiomyopathy(decrease contractility)

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16
Q

diltiazem

A

class IV antiarrhythmic drug

slow down Ca2+ dependent upstoke in slow response tissue –> slows condcution velocity (principal effect)
prolong refractory period —> suppress re-entrant arrhythmias, particularly in the AV node.

Used to treat:
atrial flutter (slow conduction in 1:1 situation)
Atrial tachycardia(30% success rate)
AV nodal reentrant tachycardia (acute and chronic)
Ventricular tachycardias/fibrillation(frequent)
hypertrophic obstructive cardiomyopathy(decrease contractility)

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17
Q

Adenosine

A

Antiarrhythmic drug
acts on A1 adenosine receptor –> Gi coupled antagonizes sympathetic action in nodal cells

Activates K+ channel activates by Ach (parasympathetic)

reduction in SA and AV node firing rate + reduced conduction rate in AV node.

Used to treat:
AV nodal reentrant tachycardia (acute)

18
Q

digoxin

A

Inotrope
Half life 38 hours
Na/K ATPase inhibitor:
Increases Ca2+ load via NCX

p-glycoprotein substrate (narrow therapeutic window)

Increases Baroreceptor sensitivity
Slows the sinus rate (SA node effect) 
slowed conduction (AV node effect)
decreased norepeniphrine serum concentration 
decresed RAAS activation

Recommended for:
Patients with HFrEF in sinus rhythm or atrial fibrillation
All patients with sever symptoms EF <25%, big heart on X-ray
Paroxysmal supraventricular tachycardia

19
Q

Hydralazine

A

direct arterial vasodilation
decrease in afterload

combination Hydralazine and Isosorbite dinitrate:
reduce mortality and morbidity in African-Americans with HFrEF
also to patients who can’t be give ACE inhibitor or ARBS

20
Q

Isosorbite dinitrate

A

venous dilation
decrease in preload

combination Hydralazine and Isosorbite dinitrate:
reduce mortality and morbidity in African-Americans with HFrEF
also to patients who can’t be give ACE inhibitor or ARBS

21
Q

Captopril

A

ACE inhibitor:(short half-life)
prevents formation of Angiotensin II
prevents breakdown of Bradykinin

Blocks action of Angiotenisn II:
arterial constriction
increased sympathetic output (cardiac output)
Aldosterone secretion (Na+ resorption)
ADH secretion(increase water absorption)
Direct kidney effects (Na+ resorption + water retention)

Side effects:
cough (bradykinin) 
hyperkalemia 
angioedema
hypotension
renal dysfunction(NSAID make it worse)

Recommended in patients with HFrER and currret or priop symptoms.

22
Q

Enatopril

A

ACE inhibitor: (6h half life)
prevents formation of Angiotensin II
prevents breakdown of Bradykinin

Blocks action of Angiotenis II:
arterial constriction
increased sympathetic output (cardiac output)
Aldosterone secretion (Na+ resorption)
ADH secretion(increase water absorption)
Direct kidney effects (Na+ resorption + water retention)

Side effects:
cough (bradykinin) 
hyperkalemia 
angioedema
hypotension
renal dysfunction(NSAID make it worse)

Recommended in patients with HFrER and currret or priop symptoms.

23
Q

Lisonopril

A

ACE inhibitor:(12 h half life)
prevents formation of Angiotensin II
prevents breakdown of Bradykinin

Blocks action of Angiotenis II:
arterial constriction
increased sympathetic output (cardiac output)
Aldosterone secretion (Na+ resorption, fibrosis, hypertrophy)
ADH secretion(increase water absorption)
Direct kidney effects (Na+ resorption + water retention)

Side effects:
cough (bradykinin) 
hyperkalemia 
angioedema
hypotension
renal dysfunction(NSAID make it worse)

Recommended in patients with HFrER and currret or priop symptoms.

24
Q

Losartan

A

Angiotensin II receptor blocker: ARB

block angiotensin receptor 1

prevent: 
aldosterone secretion(Na+ retention, fibrosis, hypertrophy) 
vascular constriction 
dyspogenic response (drinking) 
renal/inotropic response
angiotensiongen gene expression

Recommended
Patients with HFrEF, intolerant to ACE inhibitors (reduce mortality)
Maybe addition to ACE inhibitors, intolerant to aldosterone antagonist

25
Q

Candesartan

A

Angiotensin II receptor blocker: ARB

block angiotensin receptor 1

prevent: 
aldosterone secretion(Na+ retention, fibrosis, hypertrophy) 
vascular constriction 
dyspogenic response (drinking) 
renal/inotropic response
angiotensiongen gene expression

Recommended
Patients with HFrEF, intolerant to ACE inhibitors (reduce mortality)
Maybe addition to ACE inhibitors, intolerant to aldosterone antagonist

26
Q

Valsartan

A

block angiotensin receptor 1

prevent: 
aldosterone secretion(Na+ retention, fibrosis, hypertrophy) 
vascular constriction 
dyspogenic response (drinking) 
renal/inotropic response
angiotensiongen gene expression

Recommended
Patients with HFrEF, intolerant to ACE inhibitors (reduce mortality)
Maybe addition to ACE inhibitors, intolerant to aldosterone antagonist

27
Q

Carvedilol

A

Beta-blocker:

prevents down regulation of B-1 receptor 
prevents apoptosis/oxidative stress
prevents hypertrophy/fibrosis
prevents increased arrhythmia potential 
vasodilation

recommended for patients with current or prior symptoms of HFrEF to reduce mobritdiy and mortality

28
Q

Bisoprolol

A

Beta-blocker:

prevents down regulation of B-1 receptor 
prevents apoptosis/oxidative stress
prevents hypertrophy/fibrosis
prevents increased arrhythmia potential 
vasodilation

recommended for patients with current or prior symptoms of HFrEF to reduce mobritdiy and mortality

29
Q

LC2696

A

combinatin of neprilysin inhibitor + ARB

neptrilysin degrades BNP

30
Q

Dobutamine

A

Inotrope
B1 agonist

Increases cardiac output

Used in patients:
Cold and wet/dry

31
Q

Milrinone

A

Inotrope
phosphodiaesterase inhibitors

prevents breakdown of cAMP
Increases cardiac output

Used in patients:
Cold and wet/dry
advanced heart failure and low out syndrome

32
Q

Dopamine

A

endogenous precursor of norepinephrine

directly simulates adrenergic receptors
release norepinephrine from nerves

renal, inotrope, pressor

33
Q

furosemide

A

Loop Diuretic
inhibit Na-K-2Cl- transporter (NKCC2) —> decrease water reabsorption
effected augmented with Na restricted diet

adverse reactions:
decrease Mg+ and Ca2+ reabsroption
hypokalemic metabolic alkalosis(ectopic pacemaker and arrhythmias) 
hypouricemia (same transport)
Ototoxicity
34
Q

bumetanide

A 
Loop Diuretic (more reliable bioavailability) 
inhibit Na-K-2Cl- transporter (NKCC2) ---> decrease water reabsorption 
effected augmented with Na restricted diet 
adverse reactions:
decrease Mg+ and Ca2+ reabsroption
hypokalemic metabolic alkalosis(ectopic pacemaker and arrhythmias) 
hypouricemia (same transport)
Ototoxicity
35
Q

torsemide

A 
Loop Diuretic (more reliable bioavailability) 
inhibit Na-K-2Cl- transporter (NKCC2) ---> decrease water reabsorption 
effected augmented with Na restricted diet 
adverse reactions:
decrease Mg+ and Ca2+ reabsroption
hypokalemic metabolic alkalosis(ectopic pacemaker and arrhythmias) 
hypouricemia (same transport)
Ototoxicity
allergic sulfa reaction.
36
Q

Hydrochlorothiazide

A

Na/Cl contransporter inhibitor –> increasing urinary excretion of NaCl
prototype thiazide, 2x daily dose

increase Ca2+ reabsorption

clinical uses:
congestive heart failure in combination with loop diuretics.
hypertension
hypocalcuria.

Adverse reactions/toxicities:

hypokalemia ---> ectopic pacemkaers 
impaired carbohydrate tolerance (hyperglycemia)
hyperuricemia 
hyperlipidemia (long term)
allergic sulfa reaction.
37
Q

Metolazone

A

Na/Cl contransporter inhibitor –> increasing urinary excretion of NaCl
1x daily dose (longer duration, acts well with loop diuretics)

increase Ca2+ reabsorption

clinical uses:
congestive heart failure in combination with loop diuretics.
hypertension
hypocalcuria.

Adverse reactions/toxicities:

hypokalemia ---> ectopic pacemkaers 
impaired carbohydrate tolerance (hyperglycemia)
hyperuricemia 
hyperlipidemia (long term)
allergic sulfa reaction
38
Q

Spironolactone

A

Potassium-Sparing Diurectic
aldosterone receptor antagonist
poor oral absorption

prevent increased activity and number of Na+ (ENaC leak) channels, K+ leak channels and Na-K ATPase —> less Na+ absorobed more K+ and H+ excreted.

Clinical uses:
congestive heart failure —> anti remodeling action + raising serum potassium to counter the action of K+ wasting diuretics.

Hypertension in combination with thiazides

Adeverse reactions:

hyperkalemia —> EKG changes, conduction abnormalitis, arrhythmias.

gynecomastia

39
Q

Eplerenone

A

Potassium-Sparing Diurectic
aldosterone receptor antagonist
good oral absorption metabolized by CYP3A4

prevent increased activity and number of Na+ (ENaC leak) channels, K+ leak channels and Na-K ATPase —> less Na+ absorobed more K+ and H+ excreted.

Clinical uses:
congestive heart failure —> anti remodeling action + raising serum potassium to counter the action of K+ wasting diuretics.

Hypertension in combination with thiazides

Adeverse reactions:
hyperkalemia —> EKG changes, conduction abnormalitis, arrhythmias.

40
Q

Triamterene

A

Potassium-Sparing Diurectic

direct effect to block the Na+ channels on the collecting duct —> decrease Na+ reabsorption —> decrease coupled K+ excretion.

41
Q

Amiloride

A

Potassium-Sparing Diurectic
direct effect to block the Na+ channels on the collecting duct —> decrease Na+ reabsorption —> decrease coupled K+ excretion

heart drugs (2 decks)

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