Cardiology Pharmacology Quiz

The ability of a cell to spontaneously generate an electrical impulse.

The ability of a cell to transmit an electrical impulse to neighboring cells.

The regular pattern of electrical impulses generated by heart cells.

The ability of a cell to respond to an electrical stimulus.

A phase of repolarization where the cell can be re-excited if the stimulus is strong enough.

A phase of repolarization where the cell is completely unresponsive to any stimulus.

The process of the heart muscle relaxing after contraction.

The ability of a cell to contract with increased force.

A synthetic, noncardioselective beta-blocker with antianginal, antiarrhythmic, and antihypertensive properties. It is a racemic mixture of 2 enantiomers with the S(-)-enantiomer having a significantly higher affinity for beta-adrenergic receptors (β1: β2 affinity is equal).

Propranolol is effective in treating hypertrophic obstructive cardiomyopathies (HOCM), a condition where the heart muscle thickens.

The effects of propranolol are most pronounced during exercise or stress. This is because beta-receptors are activated during increased physical demands.

Propranolol is metabolized in the liver, producing various metabolites, some of which remain active. The half-life of certain drugs, like amide local anesthetics, can be prolonged by propranolol.

Propranolol is used in divided doses to achieve a resting heart rate of 55-60 beats per minute. It is administered intravenously in higher doses until this targeted heart rate is reached.

The ability of cardiac cells to spontaneously generate electrical impulses.

When a cardiac cell generates an electrical impulse due to a previous stimulus, even if it should be in its resting state.

A reentrant circuit where an electrical impulse keeps looping around, causing a continuous rhythm disturbance.

A type of antiarrhythmic drug that blocks the fast sodium channels, slowing down electrical impulses.

A subgroup of Class I antiarrhythmics that moderately slows down the heart muscle and extends the repolarization phase.

A type of Class IA antiarrhythmic, known by its old name 'Cardioquin'.

A type of antiarrhythmic drug that blocks the beta-adrenergic receptors, slowing down the heart rate.

A type of antiarrhythmic drug that blocks the potassium channels, prolonging the repolarization phase.

A type of antiarrhythmic drug that blocks the slow calcium channels, decreasing the heart's contractility.

A class IA antiarrhythmic that is an analog of procainamide and has similar properties but has different pharmacokinetic properties.

A class IA antiarrhythmic that has potent sodium-channel blocking and potassium-channel blocking properties.

A subgroup of Class I antiarrhythmics that have a weaker effect on sodium channels and a shorter action on repolarization.

A class IB antiarrhythmic known for its effectiveness against ventricular arrhythmias.

A subgroup of Class I antiarrhythmics that have a strong blocking effect on sodium channels with minimal effect on repolarization.

A class IC antiarrhythmic that has a fast onset of action and a long duration of action.

A non-iodinated antiarrhythmic agent structurally similar to amiodarone. It exhibits properties of all four antiarrhythmic classes and is available only as an oral medication.

Prolongs action potential duration by inhibiting sodium and potassium channels, leading to a longer refractory period, which helps stabilize heart rhythms.

A type of ventricular tachycardia that occurs when the heart beat is unstable due to prolonged QT intervals.

A long-acting, non-cardioselective beta blocker that prolongs the action potential of the ventricles, atria, and accessory bypass tracts. It also has class III antiarrhythmic properties at higher doses.

A 'pure' class III antiarrhythmic drug used to convert recent onset atrial fibrillation or flutter to normal sinus rhythm.

A life-threatening condition characterized by inflammation of the lungs and accumulation of fluids.

A common side effect of dronedarone, sotalol, and amiodarone that can result in irregular heart rhythms and potential life-threatening conditions.

The ability of the heart muscle to relax after contraction, an essential aspect of the cardiac cycle.

The ability of the heart muscle to contract with increased force. It is essential for efficient pumping of blood throughout the body.

The tendency of some drugs to cause the heart muscle to relax and become less efficient at pumping blood.

A 'pure' potent potassium channel blocker indicated for chemical cardioversion and maintenance of normal sinus rhythm (NSR) from atrial fibrillation and flutter. It prolongs the action potential duration and effective refractory period of accessory pathways.

A long-acting, potent antiarrhythmic drug with multiple effects. It acts on potassium and sodium channels, prolonging the action potential duration and effective refractory period. It also blocks beta-adrenergic receptors, reducing heart rate and contractility.

A drug used for chemical cardioversion and increasing ventricular fibrillation (VF) threshold. It acts by prolonging the action potential duration and effective refractory period in Purkinje fibers and ventricular tissue.

A racemic mixture of calcium channel blockers that is used to terminate paroxysmal SVT and control ventricular rate in atrial fibrillation/flutter. It inhibits the flux of calcium ions, decreasing the rate of spontaneous phase 4 depolarization.

IV: 1-2 mg/kg over 10 minutes. Used to suppress ventricular tachycardia (VT) and premature ventricular contractions (PVCs), as well as atrial tachyarrhythmias.

A potent local anesthetic with a strong affinity for the sodium channels. It's used to prevent paroxysmal ventricular tachycardia, PVCs, and atrial tachyarrhythmias.

A short and rapid-acting beta-blocker specifically targeting the beta-1 receptors in the heart.

A potent local anesthetic analog of procainamide that possesses local anesthetic and negative inotropic activity. Used in suppressing ventricular tachycardia, PVCs, atrial tachyarrhythmias, and Wolf-Parkinson-White syndrome.

Used in suppressing ventricular arrhythmias associated with digitalis toxicity, but less effective in VT from other causes.

IV dose is 100 mg (1.5 mg/kg) every 5 minutes until arrhythmia is controlled to a maximum of 10-15 mg/kg (or 1000 mg).

An amine analog of lidocaine used orally for suppression of chronic VT. Similar electrophysiologic function to lidocaine.

An oral antiarrhythmic drug used to suppress chronic ventricular tachycardia. It blocks sodium channels and has similar electrophysiologic effects as lidocaine.

A phenothiazine derivative with potent local anesthetic properties. It blocks fast sodium channel conductance during Phase 0, decreasing inward sodium current, and also has properties of Class IB and IC.

Effective in preventing paroxysmal ventricular tachycardia and PVCs, as well as atrial tachyarrhythmias. It also exhibits some beta-blocker effects.

A drug that is effective in suppressing ventricular arrhythmias associated with digitalis toxicity. It's less effective in VT from other causes.

May be effective in prolonged QTc interval induced torsades de pointes. It shortens the QTc interval more than any other antiarrhythmic drug.

Has beta-blocker effects, such as bradycardia and bronchospasm.

Used in conjunction with other antiarrhythmics, it can diminish the dosage of all components.