Cardiac Action Potential Overview

What is primarily responsible for making the interior of a resting cardiac cell electrically negative?

During which phase of the action potential does rapid influx of Na+ occur?

What occurs during Phase 2 of the cardiac action potential?

What characterizes WPW syndrome?

Which of the following describes first-degree AV conduction block?

What mechanism restores Na+ and K+ ion concentrations in the heart cell after an action potential?

What is the primary outcome during Phase 3 of the cardiac action potential?

What effect do Class IA antiarrhythmic drugs have on action potential duration (APD)?

Which event characterizes Phase 1 of the cardiac action potential?

What is a primary effect of Class IB antiarrhythmic drugs on conduction properties?

Which of the following statements about antiarrhythmic drugs is accurate?

What happens during Phase 4 of the cardiac action potential?

Which of the following ions are mainly extracellular in the resting state of the cardiac action potential?

Which of the following best represents a characteristic of Class II antiarrhythmic drugs?

In the Vaughan Williams classification system, which class would Quinidine fall under?

What mechanism characterizes the action of most antiarrhythmic drugs?

What is primarily indicated by an increase in the slope of phase 4 in cardiac action potentials?

Which structure serves as the dominant pacemaker under normal physiological conditions?

What term is used to describe the spontaneous repetitive firing of myocardial cells under certain pathological conditions?

Which of the following components conducts electrical impulses from the SA node to the ventricles?

In an ECG, what does the P wave represent?

Normal myocardial cells are characterized by which of the following?

What type of cells compete with the SA node for control of the heart under pathological conditions?

What physiological change occurs during tachycardia?

What does the QRS complex represent?

Which of the following is NOT a cause of cardiac arrhythmia?

Ectopic beats can be caused by which of the following abnormalities?

What characterizes re-entry in cardiac impulses?

Atrial flutter and fibrillation are commonly caused by which phenomenon?

Which of the following is specifically an example of re-entry?

Ventricular repolarization is represented by which part of the ECG?

Which arrhythmia is characterized by a slow heart rate?

Which class of drugs primarily blocks Na+ channels and does not affect ERP?

What effect do beta-blockers have on AV conduction?

Which drug is classified as a potassium channel blocker?

What is the primary action of Class IV drugs in cardiac treatment?

Which of the following drugs is NOT classified under beta-blockers?

What effect do Class III K+ channel blockers primarily have on ERP?

Which of the following is an unclassified cardiac drug?

Which class of drugs has a significant effect on AV conduction via direct inhibition?

AV conduction can be completely blocked in third-degree heart block.

Class IB antiarrhythmic drugs, such as lidocaine, primarily increase the effective refractory period (ERP).

Automaticity is one of the factors that antiarrhythmic drugs affect.

The Vaughan Williams classification system assumes that each antiarrhythmic drug has multiple main mechanisms of action.

First-degree AV block is characterized by a delayed conduction without complete block.

Class IA antiarrhythmic drugs are known for their ability to strongly reduce sodium channel activity.

Class II antiarrhythmic drugs specifically act as Na+ channel blockers.

Ventricular tachycardia can be associated with an accessory AV pathway.

The QRS complex represents the spread of depolarization wave through the atria.

Abnormal impulse generation can lead to arrhythmias, such as sinus tachycardia.

Re-entry is a phenomenon that causes impulses to circulate around an area in a bidirectional manner.

Wolff–Parkinson–White syndrome is a type of defined re-entry condition.

Atrial flutter and fibrillation are primarily caused by abnormal impulse conduction.

Sinus bradycardia is an example of extranodal abnormal impulse generation.

The ST segment in an ECG represents atrial contraction.

The slope of phase 4 indicates when the first action potential begins.

Ectopic beats can result from both abnormal impulse generation and conduction.

Cardiac automaticity allows normal myocardial cells to generate electrical impulses.

Ectopic pacemakers gain control over the heart by having lower automaticity than the SA node.

The P wave in an ECG represents ventricular contraction.

The bundle of His is responsible for the rapid propagation of electrical impulses to the SA node.

Under normal conditions, the SA node exhibits the lowest automaticity in the heart.

The electrical activity in the heart transitions from the AV node to the atria.

Increased slope of phase 4 in the cardiac action potential is associated with bradycardia.

In the resting state of a cardiac cell, K+ ions are primarily extracellular.

Phase 2 of the action potential is characterized by a rapid outflow of K+ ions.

The Na+/K+ pump restores Na+ ions inside the cell during Phase 4 of the cardiac action potential.

Phase 1 of the action potential involves a short period of rapid depolarization due to Na+ influx.

The interior of a resting cardiac cell is electrically positive due to the presence of Na+ and Ca2+ ions.

During Phase 3 of the action potential, there is a rapid influx of Ca2+ ions.

Rapid redistribution of ions across the cell membrane occurs during four phases of action potential.

Phase 4 is the phase where the cell is prepared for the next action potential.

Class I antiarrhythmic drugs primarily block K+ channels and have no effect on ERP.

Class III antiarrhythmic drugs primarily increase the effective refractory period (ERP).

Calcium channel blockers mainly inhibit Na+ channels and decrease ERP.

Beta-blockers exert their effects by decreasing AV conduction and inhibiting phase 4 depolarization.

The unclassified drug digoxin predominantly blocks Na+ channels in cardiac cells.

Dronedarone is an example of a Class II antiarrhythmic drug.

Amiodarone is a drug that inhibits mainly K+ channels and increases ERP.

Phase 4 depolarization is significantly inhibited by Class I antiarrhythmic drugs.

What does the ST segment and T wave in an ECG represent?

What is re-entry in the context of cardiac arrhythmias?

Identify one example of abnormal impulse generation related to arrhythmias.

Describe the primary distinction between normal impulse generation and extranodal abnormality.

What common arrhythmia results from a re-entry circuit?

What can be classified as a disturbance in the normal heart rhythm?

Give one example of an abnormal impulse conduction issue.

What does the QRS complex represent in an ECG?

What is the relationship between the slope of phase 4 and heart rate variability?

Which cells in the heart primarily exhibit automaticity under normal conditions?

What occurs when myocardial cells gain abnormal automaticity?

How does electrical activity propagate from the SA node to the ventricles?

What does the P wave represent in an ECG?

What characteristic distinguishes normal myocardial cells from those that exhibit automaticity?

What impact does a pathological condition have on myocardial cells regarding automaticity?

In the context of cardiac cycles, what does tachycardia indicate about the slope of phase 4?

What is the primary effect of Class IC antiarrhythmic drugs on ion channels?

How do beta-blockers, as classified in Class II, alter AV conduction?

What is the primary action of Class III antiarrhythmic drugs like amiodarone?

What ion channels are predominantly affected by Class IV antiarrhythmic drugs?

What distinguishes unclassified drugs like digoxin from the traditional antiarrhythmic classes?

Explain how Class III K+ channel blockers affect the effective refractory period (ERP).

What is a notable physiological outcome of using sodium channel blockers in Class I antiarrhythmic drugs?

Identify one major effect of potassium channel blockers on cardiac action potential duration.

What role do accessory AV pathways play in WPW syndrome?

Describe the primary impact of Class IA antiarrhythmic drugs on cardiac action potentials.

What defines the mechanism of action for Class IB antiarrhythmic drugs?

What does third-degree AV block indicate about conduction in the heart?

How do antiarrhythmic drugs affect membrane responsiveness in cardiac cells?

What is the significance of refractory periods in the action of antiarrhythmic agents?

What characterizes Class II antiarrhythmic drugs and their action on the heart?

Explain the importance of understanding action potential duration (APD) in cardiology.

During which phase of the cardiac action potential does a plateau occur and why?

What role do K+ ions play during Phase 1 of the cardiac action potential?

How do Na+/K+ pumps contribute to Phase 4 of the cardiac action potential?

Which ion movements characterize the transition from the resting state to Phase 0 in cardiac action potential?

What is the significance of Ca++ ion influx during the cardiac action potential?

Explain the basic electrical situation of a resting cardiac cell.

What characterizes Phase 3 of the cardiac action potential?

Describe the phases of action potential and their role in cardiac function.

In the resting state, K+ ions are found mainly ______, while Na+ and Ca2+ are mainly extracellular.

During Phase 0 of the cardiac action potential, there is a rapid influx of ______.

Phase 2 of the action potential is characterized by a 'plateau' due to slow influx of ______.

Phase 3 of the cardiac action potential involves rapid outflow of ______.

Phase 4 of the action potential refers to the ______ state being restored.

The Na+/K+ pump is responsible for extruding Na+ ions out of the cell and returning ______ ions back.

A characteristic of antiarrhythmic drugs is that they can affect ______ in cardiac action potentials.

Class IA antiarrhythmic drugs are known for their ability to strongly reduce ______ channel activity.

The QRS complex represents the spread of depolarization wave through the ______.

The ST segment and T wave represent ventricular ______.

Arrhythmia means disturbance in the normal heart ______.

Abnormal impulse generation can lead to arrhythmias, such as sinus ______.

Re-entry is a circus movement of an impulse that circulates around a certain area in a ______ direction.

Wolff–Parkinson–White syndrome is an example of a defined ______.

Ectopic beats can be caused by either abnormal impulse generation or ______.

Atrial flutter and fibrillation are commonly caused by ______ re-entry.

The slope of phase 4 determines when the 2nd action potential starts. When the slope is increased, the distance between 2 cardiac cycles shortens (i.e. ______).

Cardiac automaticity refers to the ability of certain cells to self-generate electrical impulses that spread throughout the ______.

Under normal conditions, the SA node is the dominant ______ (i.e. has the highest automaticity).

In the ECG, the P wave represents the spread of depolarization wave through the ______ (atrial contraction).

Normal myocardial cells don’t have automaticity i.e. cannot generate ______.

Ectopic pacemakers compete with the SA node for control of the ______.

Impulse conduction spreads from the SA node to the ventricles via the AV node and the bundle of ______.

Under certain pathological conditions, some myocardial cells may acquire spontaneous repetitive firing, this is called abnormal automaticity or ______.

Class IC drugs, such as ______, strongly block Na+ channels.

Beta-blockers, like ______, inhibit phase 4 depolarization.

Class III K+ channel blockers include drugs like ______ and dronedarone.

Class IV drugs primarily inhibit ______ channels and increase ERP.

An example of an unclassified drug is ______.

Class III drugs primarily affect ______ channel activity and ERP.

The drug ______ is known to block both sodium and potassium channels.

Calcium channel blockers like ______ are used to affect AV conduction.

WPW syndrome is a type of atrioventricular re-entry tachycardia caused by an accessory AV ______ pathway.

Antiarrhythmic drugs can alter factors such as automaticity, conduction velocity, refractory period, and membrane ______.

Class IA antiarrhythmic drugs, such as quinidine and procainamide, moderately block Na+ channels and increase ______.

Class IB antiarrhythmic drugs, like lidocaine, weakly block Na+ channels and decrease ______.

Heart block can be classified as first-degree, second-degree, or third-degree, with third-degree being ______ blocked.

The Vaughan Williams classification assumes that each antiarrhythmic drug has one main mechanism of ______.

Most antiarrhythmic drugs have more than one ______ of action.

Class II antiarrhythmic drugs primarily act on ______ channels.

Match the following classes of antiarrhythmic drugs with their primary action:

Match the following antiarrhythmic drugs with their class:

Match the following drugs with their unique characteristic:

Match the following terms with their corresponding definitions:

Match the following actions with the drug class responsible:

Match the following drug effects with their corresponding classes:

Match the following antiarrhythmic drugs with their specific function:

Match the following cardiac conditions with the appropriate drug class treatment:

Match the following cardiac terms with their definitions:

Match the following ECG waveforms with their meanings:

Match the following cardiac arrhythmia mechanisms with their descriptions:

Match the following terms with their definitions:

Match the following cardiac phases with their characteristics:

Match the following types of arrhythmias with their descriptions:

Match the following arrhythmias with their causes:

Match the following cardiac conduction components with their functions:

Match the following ECG waveforms with their representative actions:

Match the following concepts in cardiac physiology with their relevant examples:

Match the following conditions with their effects on the heart:

Match the following terms to their related cardiac events:

Match the following types of myocardial cells with their characteristics:

Match the following types of arrhythmias with their characteristics:

Match the following definitions with the correct terms:

Match the following types of cardiac cells or rhythms with their definitions:

Match the antiarrhythmic drug subclass to its primary mechanism of action:

Match the antiarrhythmic drug to its corresponding example:

Match the classification of heart block to its description:

Match the effect of Class IA antiarrhythmic drugs to their function:

Match the antiarrhythmic drug class to its specific clinical effect:

Match the cardiac condition to its associated treatment:

Match the mechanism of action to its effect on cardiac action potentials:

Match the drug to the class it belongs to based on clinical usage:

Match the phases of cardiac action potential with their descriptions:

Match the antiarrhythmic drug classes with their primary mechanisms:

Match the ion with its location during the resting state of the cardiac cell:

Match the concept with its definition in cardiac physiology:

Match the effect with the respective class of antiarrhythmic drugs:

Match the physiological effects to their respective phases of the cardiac action potential:

Match the terminology with its relevant clinical significance:

Match the type of cardiac arrhythmias with their characteristics: