25%–50%.
The influx of extracellular sodium (Na) and the efflux of intracellular potassium (K).
The membrane potential at which the cell membrane depolarizes and generates an action potential.
The minimal interval between action potentials, including absolute and relative refractory periods.
Sustained depolarization (plateau) due to transient outward flow of K and opening of voltage-gated Ca channels.
The characteristic of spontaneously depolarizing cardiac cells, such as pacemaker cells.
A deviation of the heart from its normal rhythm.
Sinus bradycardia and hypotension.
Disturbance in impulse formation and/or disturbance in impulse conduction.
Used for most atrial and ventricular arrhythmias and as a second choice for sustained ventricular arrhythmias associated with acute myocardial infarction.
Rapid repolarization occurs as Ca channels inactivate and K continues to leave the cell.
They block activated and inactivated L-type calcium channels.
4-7 hours.
Ibutilide is used for the acute conversion of atrial flutter and atrial fibrillation to normal sinus rhythm.
Dose-related blurred vision.
They block sodium channels and reduce the sodium current (INa).
Hypotension and reversible lupus-related symptoms with long-term therapy.
60-100 beats per minute.
Vernakalant proved more effective than placebo or amiodarone in terminating atrial fibrillation in a 90-minute period.
Dronedarone is a structural analog of Amiodarone with iodine atoms removed and a methanesulfonyl group added.
Above 150 bpm.
Lupus-like syndrome.
Rapid depolarization due to the opening of voltage-gated Na channels and Na influx.
It prolongs the action potential duration and QT interval on the ECG by blockade of IKr.
They can prevent recurrent infarction and sudden death in patients recovering from acute myocardial infarction.
To relax the ventricles and allow them to fill with blood.
Sotalol has both beta-adrenergic receptor blocking and action potential prolonging action.
Class 1: Sodium channel blockade, Class 2: Sympatholytic, Class 3: Prolongation of action potential duration, Class 4: Calcium current blockade.
500 bpm.
Borja, De Sagun, Lim, Morin, Talampas, Vanguardía.
Contraction of the atria.
From the SA Node, the pacemaker of the heart.
Digoxin.
Restore pacemaker activity, modify impaired conduction, and minimize risk.
GIT problems such as nausea and vomiting.
Flecainide.
The voltage-dependent recovery of Na-channel inactivation.
During the repolarization phase of the heart.
They prolong the effective refractory period by blocking potassium channels.
It is used to treat serious ventricular arrhythmias and is highly effective for supraventricular arrhythmias like atrial fibrillation.
To eliminate the cause, firm diagnosis, and determine baseline condition.
They prolong the action potential duration by blocking the rapid component of the delayed rectifier potassium current.
It serves as the primary pacemaker, initiating electrical stimulation at a rate of 60-100 beats per minute.
The half-life of Amiodarone is 3-10 days.
An increase in the slope of phase 4 depolarization and a decrease in resting membrane potential.
Supraventricular tachycardia.
Dofetilide prolongs action potential duration by blocking the rapid component of the delayed rectifier potassium current.
Dose-related pulmonary toxicity.
Slows conduction velocity and pacemaker rate, prolongs action potential duration, and has direct depressant effects on SA and AV nodes.
They are forms of triggered activity that require a prior normal action potential to trigger an abnormal one.
40-60 beats per minute.
It is effective in maintaining sinus rhythm in patients with atrial fibrillation and preventing recurrent ventricular tachycardia.
Atrial flutter.
It controls the ventricular rate and slows conduction through the AV node.
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Systole (depolarization) and Diastole (repolarization).
It causes frequency- and voltage-dependent block of early and late components of the sodium current.
After repolarization is complete.
They can contribute to the risk of Torsades De Pointes, especially at slow rates.
60-100 bpm.
It increases heart rate in bradycardia and heart blocks.
It blocks the muscarinic potassium current IKACh, which is activated in atrial fibrillation.
It produces only mild QT-interval prolongation.
It can produce bradycardia and heart block in patients with preexisting sinus or AV node disease.
Beta adrenoceptor activation, hypokalemia, and stretching of cardiac muscles.
Sotalol is eliminated by the kidneys in unchanged form.
They prolong the action potential duration and dissociate from the sodium channel with intermediate kinetics.
They competitively block catecholamine-induced stimulation of cardiac beta-receptors.
Sodium (Na), Potassium (K), and Calcium (Ca).
The cell's ability to raise the resting membrane potential above the threshold value to initiate an action potential spontaneously.
Adenosine.
Excessive QT interval prolongation and Torsades De Pointes, requiring continuous ECG monitoring.
A process where an excitatory wavefront circulates around an inexcitable region, causing one impulse to re-enter and excite areas of the heart multiple times.
Magnesium.
It is useful for treating hypomagnesemic digitalis-induced arrhythmias.
