module 12- cardiac drugs

Question 1

Class IB antiarrythmic drugs

drugs, ECG changes, modes of action, complications

Answer 1

drugs: lidocaine, phenytoin, mexiletine, tocainide
ECG: no significant changes
MOA: act selectively on diseased or ischemic tissue by shortening the action potential and inhibiting fast sodium current- minimal slowing
complications: NA

Question 2

Class IC antiarrhythmics

drugs, ECG changes, modes of action, complications

Answer 2

Drugs: flocainide, propafenone (treats paroxymal SV & V tachycardias-only when other treatment unsuccessful)
ECG: Prolonged PR, prolonged QRS(inhibitory affect on HIS-Purkinje)
MOA: Strong inhibitors of sodium channel causing marked depressing of action potential (phase O), variably prolong action potential duration, marked inhibitory affects on HIS-Purkinje
Complications: proarrhythmic, worsen existing arrhythmias or produce new ones.

Question 3

Class II antiarrhythmic - Beta-adrenergic antagonists
Drugs, indications, contradictions

opie- “the best drug of choice for general administration”

Answer 3

drugs: atenolol, metoprolol, timolol, propanolol
indications: inappropriate sinus tachycardia, hereditary prolonged QT syndrome, heart failure, arrhythmias associated with mitral valve prolapse, reduction in cardiac death in patients with controlled heart failure, non-ischemic recurrent VT, ventricular fibrillation, symptomatic VT.
contradictions: pulmonary problems, conduction defects, overt untreated heart failure.

Question 4

Class III antiarrhythmic drugs

drugs, ECG changes, modes of action, complications

Answer 4

drugs: amiodarone, sotalol(both more beneficial than Class I drugs), pure: ibutilide, dofetilide.
MOA: prolong action potential and refractory period- ultimately prolongs QT interval. in addition amiodarone acts as a sodium channel blocker and sotalol as a beta-blocker. conduction can be slowed
complications: a prolonged ST in conjunction with other disorders that cause QT prolongation results in torsades de pointes VT.

Question 5

Class IV antiarrhythmic drugs

drugs, electrophysical change, modes of action, contradictions

Answer 5

drugs: verapamil, dilitiazem - calcium channel blockers
MOA: calcium channel blockade slows conduction through AV node, increased refractory period in nodal tissue.
electrophysically: slow ventricular response in atrial arrhythmias, prevent AV nodal re-entry tachycardias
contradictions: ventricular tachyarrhythmias bc of hemodynamic nature

Question 6

Class IV- like antiarrhythmic drugs

Drugs, side affects, contradictions

Answer 6

drugs: adenosine- first line drug used for terminating narrow complex SV tachyarrhythmias and for diagnosis of wide complex tachycardias of unknown origin.
Side effects: headache, chest pain, flushing, excess sinus or AV node inhibition.
Contradictions: asthma, history of asthma, second or third degree heart block, sick sinus syndrome, atrial flutter

Question 7

Class IA antiarrythmic drugs

drugs, ECG changes, modes of action, complications

Answer 7

drugs: quinidine, procainamide, & disopyramide.
ECG- prolonged PR and QRS duration
MOA- inhibit fast sodium channels, depression of phase O of action potential, prolongation of action potential(mild class III affects)
Complications: proarrythmic complications (prolonging QT interval or by depression conduction promoting re-entry tachycardias)

Question 8

Roles and indications to ACE(angiotensin-converting enzyme) inhibitors

Answer 8

Roles: reduce hypertension (indirect), decrease LV hypertension(indirect), anti-hypertension effect, inhibit carotid atherogenesis, inhibit carotid thrombogenesis, antiarrhythmic effects, lessen wall stress -> reduce remodeling(post infarct), decrease incidence of L heart failure (post infarct)
indications: cardiovascular protection, heart failure, acute myocardial infarction, hypertension, post infarct, renal protection, diabetic nephropathy

Question 9

ACE inhibitors

drugs, side effects, moa

Answer 9

drugs: captopril (class I), ramipril (class II), lisinopril (class III)
side effects: cough - as a result of pulmonary congestion associated with left heart failure & hypertension.
MOA: used to treat heart failure, hypertension, and for cardiovascular protection. work primarily by lessening the effects of angiotensin II

Question 10

ARB’s (angiotensin receptor blockers)

Answer 10

can be combined with ACE inhibitors to treat heart failure- direct antagonist to angiotensin II. Fewer related side affects due to specificity.
common drugs: losartan(cozaar), candesartan(atacand), telmisartan(micardis).

Question 11

Nitrates

Answer 11

potent coronary vasodilators (nitro), antianginals-manage stable and unstable angina pectoris. Administered sublingually(spray, tablet)(short acting nitrate), intravenously, or transdermal (patch)(long acting nitrate)

Question 12

Nitrates

indications, side effects, contraindications

Answer 12

indication: angina attacks, acute myocardial infarction, congestive heart failure, acute pulmonary edema.
side effects: headache, syncope, tachycardia
contraindications: hypertrophic obstructive cardiomyopathy, acute inferior wall infarction with RV involvement, cor pulmonale
a big drawback of nitrates is the bodies ability to develop a tolerance

Question 13

HMG CoA reductase inhibitors (statins) benefits

Answer 13

lipid lowering agent that reduces total cholesterol, reduces low density lipid C, Increase high density lipid C. also helps reduce atherosclerotic plaque- improve endothelial function, stabilizing platelets, reducing fibrinogen, inhibiting inflammatory response w atherogenesis.

Question 14

HMG CoA reductase inhibitors (statins)

drugs and side effects

Answer 14

atrovastatin(lipitor), lovastatin(mevacor), mevastatin, pravastatin(lipostat), simvastatin(zocor)
complications: liver damage and myopathy