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Vocabulary-style practice flashcards covering cardiac conduction, action potentials, ECG intervals, arrhythmia types, and the Vaughan-Williams classification of anti-dysrhythmic drugs.
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Sinoatrial (SA) node
The key structure in the right atrium responsible for generating a regular heartbeat, often called the pacemaker of the heart because its self-excitation generates the action potential that initiates contraction.
Effective refractory period (ERP)
The duration of time during which a cardiac cell is unable to respond to a new excitation or initiate a new action potential.
Phase 4 (Non-pacemaker cells)
The resting phase where the resting potential is maintained at −90mV by a constant outward leak of K+ through rectifier channels while Na+ and Ca2+ channels remain closed.
Phase 0 (Depolarization in cardiomyocytes)
Phase where fast Na+ channels open, allowing Na+ to leak into the cell and rapidly depolarize the Transmembrane Potential (TMP) to 0mV or slightly above.
Phase 2 (Plateau phase)
A period where L-type Ca2+ channels are open, creating a constant inward current of Ca2+ that balances K+ leak to maintain a potential just below 0mV.
Funny current (If)
A spontaneous phase 4 depolarization found in pacemaker cells (SA and AV nodes) involving Na+ entry through slow HCN channels and Ca2+ through T-type channels.
P wave
The portion of the electrocardiogram (ECG) that represents atrial depolarization.
QRS complex
The portion of the ECG representing ventricular depolarization, occurring simultaneously with atrial repolarization.
PR interval
The time between the onset of the P wave and the onset of the QRS complex; an increase in this interval indicates a delay in AV conduction.
QT interval
The time measured from the onset of the QRS complex to the completion of the T wave; drugs that delay ventricular repolarization will increase this interval.
Reentry
The most common cause of arrhythmias, occurring when a unidirectional block leads to an abnormal conduction pathway that causes re-excitation of cardiac muscle.
Atrial fibrillation
An arrhythmia with an atrial rate of approximately 350beats/min, characterized by multiple atrial ectopic foci and an irregular pulse.
Ventricular tachycardia (VT)
Arrhythmias originating from the ventricular myocardium or His-Purkinje system with a heart rate faster than 100 (or 120) beats/min.
Ventricular fibrillation (VF)
A life-threatening medical emergency where the ventricular rate is usually greater than 300beats/min, preventing the heart from pumping blood and leading to cardiac arrest.
Class IA antiarrhythmic drugs
Sodium channel blockers like Quinidine, Procainamide, and Disopyramide that slow Phase 0 depolarization and Phase 3 repolarization, leading to an increased ERP and QT prolongation.
Cinchonism
A set of adverse effects associated with large doses of quinidine, including blurred vision, tinnitus, headache, disorientation, and psychosis.
Class IB antiarrhythmic drugs
Weak sodium channel blockers such as Lidocaine and Mexiletine that rapidly associate and dissociate from channels and shorten phase 3 repolarization.
Class IC antiarrhythmic drugs
Strong sodium channel blockers like Flecainide and Propafenone that slowly dissociate from channels, markedly slow conduction, and have minimal effect on the QT interval.
Class II antiarrhythmic drugs
Beta-blockers (e.g., Metoprolol, Esmolol) that treat arrhythmias by decreasing SA node automaticity, AV conduction, and myocardial contractility.
Class III antiarrhythmic drugs
Potassium channel blockers (e.g., Amiodarone, Sotalol, Dofetilide) that prolong the duration of the action potential and the effective refractory period by diminishing outward K+ current during repolarization.
Amiodarone
A Class III drug with a long half-life (25−110days) that blocks K+, Na+, and Ca2+ channels; it is structurally similar to thyroxine and can cause pulmonary fibrosis or thyroid dysfunction.
Class IV antiarrhythmic drugs
Non-dihydropyridine calcium channel blockers (Verapamil, Diltiazem) that decrease the inward Ca2+ current, slowing spontaneous phase 4 depolarization and conduction in the AV and SA nodes.
Adenosine
An endogenous metabolite with an extremely short duration of action (10−15seconds) used intravenously to convert acute supraventricular tachycardias by depressing SA and AV node activity.