Heart drugs Flashcards
quinidine
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)
procainamide
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)
lidocaine
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)
phenytoin.
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)
propafenone
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)
flecainide
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)
propranolol
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)
metoprolol
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)
esmolol
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)
amiodarone
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)
sotalol
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)
ibutilide
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)
dofetilide
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)
bretylium
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)
verapamil
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)
diltiazem
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)
Adenosine
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)
digoxin
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
Hydralazine
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
Isosorbite dinitrate
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
Captopril
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.
Enatopril
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.
Lisonopril
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.
Losartan
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