module 6 Flashcards
Heart Failure Drugs
The heart is unable to pump blood in sufficient amounts from the ventricles to meet the body’s metabolic needs Symptoms depend on the cardiac area affected Systolic dysfunction Diastolic dysfunction • Less common
Heart Failure: Causes
Cardiac defect Myocardial infarction Valve deficiency Defect outside the heart Coronary artery disease Pulmonary hypertension Diabetes Supraventricular dysrhythmias Atrial fibrillation Atrial flutter
Drug Therapy for Heart Failure
Positive inotropic drugs Increase the force of myocardial contraction Positive chronotropic drugs Increase heart rate Positive dromotropic drugs Accelerate cardiac conduction Used to treat heart muscle failure
Drug Therapy for Heart Failure
ACE inhibitors Angiotensin II receptor blockers B-type natriuretic peptides Phosphodiesterase inhibitors Cardiac glycosides
ACE inhibitors
end in pril
Prevent sodium and water resorption by
inhibiting aldosterone secretion
Diuresis results, which decreases preload, or
the left ventricular end-volume, and the work
of the heart
Examples: lisinopril, enalapril, captopril
lisinopril(Prinivil, Zestril) (C in women in 1st trimester; D in 2nd & 3rd can cause fetal death in these trimesters)
Ace inhibitor; used for HTN, HF & acute MI;
Hyperkalemia ma occur with any ACE inhibitor & K+ supplmentaion or K+ sparing diuretics need to be used with caution. SE-dry cough & possible decreased renal function
enalapril,
Hyperkalemia ma occur with any ACE inhibitor & K+ supplmentaion or K+ sparing diuretics need to be used with caution. SE-dry cough & possible decreased renal function
captopril
Hyperkalemia ma occur with any ACE inhibitor & K+ supplmentaion or K+ sparing diuretics need to be used with caution. SE-dry cough & possible decreased renal function
Angiotensin II Receptor Blockers(ARB)
end in artan
Potent vasodilators; decrease systemic
vascular resistance (afterload)
Examples: valsartan, candesartan, losartan
valsartan(Diovan) (D)
ARBS are potent vasodilators; used alone or in combo with other drugs such as diuretics in tx of HTN & HF.Most commonly used; Less likely to cause cough or hyperkalemia
candesartan(Atacand)(D)
ARBS are potent vasodilators; used alone or in combo with other drugs such as diuretics in tx of HTN & HFMost commonly used; Less likely to cause cough or hyperkalemia
losartan(Cozaar) (D)
ARBS are potent vasodilators; used alone or in combo with other drugs such as diuretics in tx of HTN & HFMost commonly used; Less likely to cause cough or hyperkalemia
B-type Natiuretic Peptides
nesiritide (Natrecor)
Used in se ere life threatening heart fail re
severe, life-failure
B-type Natiuretic Peptides:
Mechanism of Action
Vasodilating effects on arteries and veins
Indirectly increases cardiac output
Suppresses renin-angiotensin system
Diuresis
Phosphodiesterase Inhibitors
Work by inhibiting the enzyme phosphodiesterase Results in: Positive inotropic response Vasodilation Two drugs (inodilators) Inamrinone and milrinone
Inamrinone
Phosphodiesterase Inhibitors,Work by inhibiting the enzyme phosphodiesterase
Results in:
Positive inotropic response
Vasodilation(inodilators)
milrinone
Phosphodiesterase Inhibitors,Work by inhibiting the enzyme phosphodiesterase
Results in:
Positive inotropic response
Vasodilation(inodilators)
Phosphodiesterase Inhibitors:
Indications
Short-term management of heart failure
Given when patient does not respond to treatment with digoxin, diuretics, and/or vasodilators
AHA and ACC advise against weekly infusions
No improvement of clinical status
Phosphodiesterase Inhibitors:
Adverse Effects
*inamrinone Thrombocytopenia Dysrhythmia, nausea, hypotension Elevated liver enzymes with long-term use * milrinone Dysrhythmia, mainly ventricular Hypotension, angina, hypokalemia, tremor, thrombocytopenia
Cardiac Glycosides
No longer used as first-line treatment
Originally obtained from Digitalis plant,
foxglove
Digoxin
Used in heart failure and to control ventricular
response to atrial fibrillation or flutter
Cardiac Glycosides:
Mechanism of Action
Increase myocardial contractility Change electrical conduction properties of the heart Decrease rate of electrical conduction Prolong the refractory period • Area between SA node and AV node
Cardiac Glycosides:
Drug Effects
Positive inotropic effect
Increased force and velocity of myocardial contraction
Negative chronotropic effect
Reduced heart rate
Negative dromotropic effect
Decreased automaticity at SA node, decreased AV nodal
conduction
Cardiac Glycosides:
Drug Effects
Increased stroke volume
Reduction in heart size during diastole
Decrease in venous BP and vein engorgement
Increase in coronary circulation
Promotion of diuresis due to improved blood circulation
decreased exertional and paroxysmal nocturnal dyspnea, cough, and cyanosis
Cardiac Glycosides:
Indications
Heart failure
Supraventricular dysrhythmias
Atrial fibrillation and atrial flutter
Cardiac Glycosides:
Adverse Effects
digoxin (Lanoxin) Very narrow therapeutic range and low TI Drug levels must be monitored • 0.5 to 2 ng/mL Hypokalemia increases its toxicity Electrolyte levels must be monitored
Digoxin:
Adverse Effects
digoxin (Lanoxin) (cont’d)
Cardiovascular
• Dysrhythmias, including bradycardia or tachycardia
CNS
• Headaches, fatigue, malaise, confusion, convulsions
Digoxin Toxicity
digoxin immune Fab (Digibind) therapy
Life-threatening digoxin overdose
Life-threatening cardiac dysrhythmias
Digibind
Used in digoxin overdose
Life-threatening cardiac dysrhythmias
Antidysrhythmic Drugs
Dysrhythmia
Any deviation from the normal rhythm of the heart
Antidysrhythmics
Used for the treatment and prevention of
disturbances in cardiac rhythm
Cardiac Cell
Inside the resting cardiac cell there exists a
net negative charge relative to the outside of
the cell
This difference in the electronegative charge
results from an uneven distribution of ions
(sodium, potassium, calcium) across the cell
membrane
Resting membrane potential (RMP)
Resting Membrane Potential
An energy-requiring pump is needed to
maintain this uneven distribution of ions
Sodium-potassium ATPase pump
Action Potential
A change in the distribution of ions causes cardiac cells to become excited
The movement of ions across the cardiac cell’s membrane results in an electrical impulse spreading
across the cardiac cells
This electrical impulse leads to contraction
of the myocardial muscle
Action Potential Duration
Absolute or effective refractory period
Relative refractory period
Threshold potential
Automaticity or pacemaker activity
Electrocardiogram
ECG or EKG P wave PR interval QRS complex ST segment T wave
Common Dysrhythmias
Supraventricular dysrhythmias
Ventricular dysrhythmias
Ectopic foci
Conduction blocks
Vaughan Williams Classification
System commonly used to classify
antidysrhythmic drugs
Based on the electrophysiologic effect of
particular drugs on the action potential
Vaughan Williams
Classification
Class I
Class Ia
Class Ib
Class Ic
Class II
Class III
Class IV
OtherVaughan Williams Classification:
Mechanism of Action
Class I Membrane-stabilizing drugs Fast sodium channel blockers Divided into Ia, Ib, and Ic drugs, according to effects
Vaughan Williams Classification:
Mechanism of Action and Indications
Class I: moricizine
General class I drug
Has characteristics of all three subclasses
Used for symptomatic ventricular and life-threatening dysrhythmias
Vaughan Williams Classification:
Mechanism of Action and Indications
Class Ia: quinidine, procainamide,
disopyramide
Block sodium (fast) channels
Delay repolarization
Increase the APD
Used for atrial fibrillation, premature atrial
contractions, premature ventricular contractions, ventricular tachycardia
quinidine(C)
Antiarrhythmic;Class Ia:Sodium channel blocker;decrease myocardial excitability & slow conduction velocity. tx restoration & maintenance of sinus rhythm in pt with a.fib.or flutter & prevention of recurrent ventricular arrhythmias
procainamide,(C)
Antiarrhythmic;Class Ia:Sodium channel blocker;decrease myocardial excitability & slow conduction velocity;tx wide variety of ventricular & atrial arrhythmias & maintance of normal sinus rhythm
disopyramide(C)(Norpace, Norpace CR)
Antiarrhythmic;Class Ia:Sodium channel blocker;decrease myocardial excitability & slow conduction velocity. Has anticholinergic properties.Little effect on HR but has a direct neg. inotropic effect.tx ventricular tachycardia
Vaughan Williams Classification:
Mechanism of Action and Indications
Class Ib: phenytoin, lidocaine Block sodium channels Accelerate repolarization Increase or decrease the APD Used for ventricular dysrhythmias only Premature ventricular contractions, ventricular tachycardia,ventricular fibrillation
phenytoin(D) (Dilantin,Phenytek)
lidocaine(also used as anticonvulsant) Class 1b:Limits seizure progagation by altering ion transport, may also decrease synaptic transmission, antiarrhythmic porerties as a result of shortening the action potentenial & decreasein automaticity. tx termination of ventricular arrhythmias
lidocaine(B)(Lido Pen, Xylocaine, Lindoderm,etc)
lidocaine(also used anesthetic topical local) Class 1b: given IV suppresses automaticity & spontaneous depolarization of the ventricles during diastole by altering the flux of sodium ions across cell membranes with little or no effect on HR. tx control of ventricular arrhythmias
Vaughan Williams Classification:
Mechanism of Action and Indications
Class Ic: flecainide, propafenone
Block sodium channels
Little effect on APD or repolarization
Used for severe ventricular dysrhythmias
May be used in atrial fibrillation/flutter,
supraventricular tachycardia dysrhythmias
flecainide(C)(Tambocor)
Antiarrhythmic Class 1c; Slows conduction in cardiac tissue by altering transport of ions across cell membrane. tx ventricular arrhythmias & ventricular tachycardia
propafenone(C)(Rythmol, Rythmol SR)
Antiarrhythmic Class 1c;Slows conduction in cardiac tissue by altering transport of ions across cell membrane. tx ventricular arrhythmias & ventricular tachycardia(immediate release only)
Vaughan Williams Classification:
Mechanism of Action and Indications
Class II: Beta-blockers: atenolol, esmolol,
metoprolol, propranolol
Reduce or block sympathetic nervous system
stimulation, thus reducing transmission of impulses in the heart’s conduction system
General myocardial depressants for both
supraventricular and ventricular dysrhythmias
Also used as antianginal & drugs
atenolol(D)(Tenormin)
antihypertensive,antianginal,Atihypertensive ClassII Reduce or block sympathetic nervous system
stimulation, thus reducing transmission of impulses in the heart’s conduction system
General myocardial depressants for both
supraventricular and ventricular dysrhythmias
esmolol(C)(Brevibloc)
antihypertensive,antianginal,Atihypertensive ClassII. Reduce or block sympathetic nervous system
stimulation, thus reducing transmission of impulses in the heart’s conduction system
General myocardial depressants for both
supraventricular and ventricular dysrhythmias
metoprolol(C)(Lopressor, Toprol-XL)
antihypertensive,antianginal,Atihypertensive Class II Reduce or block sympathetic nervous system
stimulation, thus reducing transmission of impulses in the heart’s conduction system
General myocardial depressants for both
supraventricular and ventricular dysrhythmias
propranolol(C)(Inderal, InnoPran)
Antiarrhythmic, antianginals, antihypertensives vascular HA suppressant ClassII; Beta Blocker-decrease HR & BP, suppression of arrhythmias, prevention of MI.tx mgnt HTN,angina, arrhythmias hypertrophic cardiomyopathy, thyrotoxicossis, pheochromocytoma(a tumor on andrenal gland),preventn & mgnt of MI and vascular HA
Vaughan Williams Classification:
Mechanism of Action and Indications
Class III: amiodarone, sotalol*, ibutilide
Increase APD
Prolong repolarization
Used for dysrhythmias that are difficult to
treat
Life-threatening ventricular tachycardia or
fibrillation, atrial fibrillation or flutter—resistant to other drugs
Sustained ventricular tachycardia
*Sotalol also exhibits Class II properties
Sotalol(B)(Betapace, Sorine)
Antiarrhythmia Class III;Blocks stimulation of beta1 & beta 2 ; tx mgnt of ventricular arrhythmia; Betaspace AF-maintence of normal sinus rhythm in pt with highly symptomatic A.Fib. who are currently in sinus rhythm.
Vaughan Williams Classification:
Mechanism of Action and Indications
Class IV: verapamil, diltiazem
Calcium channel blockers
Inhibit slow-channel (calcium-dependent) pathways
Depress depolarization
Reduce AV node conduction
Used for paroxysmal supraventricular tachycardia;rate control for atrial fibrillation and flutter
verapamil(C)(Calan, Covera-HS, IsoptinSR, Verelan)
Antihypertensive, antiarrhythmic, antianginals, vascular HA suppressant; Calcium Channel Blocker- inhibits the transport of Ca+ into myocardial & vascular smooth muscle cells, resulting inhibition of exitation and contraction coupling & subsequent contraction; decreases SA& AV conduction & prolongs AV refactory period in conduction tissue. tx mgnt HTN, angina. mgnt suprventricular arrhythmia, rapid ventricular rates in a. fib.
diltiazem(C)(Cardizem, Cartia, Dilacor, Taxtia etc.)
Antihypertensive, antiarrhythmic, antianginals, vascular HA suppressant; Calcium Channel Blocker- inhibits the transport of Ca+ into myocardial & vascular smooth muscle cells, resulting inhibition of exitation and contraction coupling & subsequent contraction; decreases SA& AV conduction & prolongs AV refactory period in conduction tissue.tx HTN, angina, suprventricular tachyarrhymias, rapid ventricular rates in a. fib.
Vaughan Williams Classification:
Other Antidysrhythmics
digoxin, adenosine
Have properties of several classes and are not placed into one particular class
digoxin(C)(Lanoxin)
Antidysrhythmics; increaeses the force of myocardial contraction, prolongs refractory period of the AV node, decreases conduction through the SA & AV node. tx HF, A. Fib & flutter, parosysmal atrial tachycardia
adenosine(C)(Adenocard, Adenoscan)
Antidysrhythmics;restores normal sinus rhythm by interrupting re-entrant pathways in the AV node, slows conduction time through AV node, produces coronary artery vasodialation.tx paroxysmal supraventicular tachycardia(PSVT), used as diagnostic agent for myocardial perfusion defects as result of coronary artery disease
Unclassified Antidysrhythmic
adenosine (Adenocard)
Slows conduction through the AV node
Used to convert paroxysmal supraventricular
tachycardia to sinus rhythm
Very short half-life—less than 10 seconds
Only administered as fast IV push
May cause asystole for a few seconds
Antidysrhythmics: Adverse
Effects
ALL antidysrhythmics can cause dysrhythmias! Hypersensitivity reactions Nausea Vomiting Diarrhea Dizziness Blurred vision Headache
