CVS - ARRYTHMIA
84 important questions on CVS - ARRYTHMIA
What is the mode of action for Class I antiarrhythmic drugs?
Class I antiarrhythmic drugs are Na+ Channels Blockers. They are divided into:
- IA: Prolong action potential
- IB: Shorten repolarization (AP duration)
- IC: Less effect on repolarization
What are the first choice drugs for Atrial fibrillation/flutter?
- Verapamil
- Diltiazem
- β-blocker
Name the drugs classified under Class IA antiarrhythmics.
Class IA antiarrhythmics include:
- Quinidine
- Procainamide
- Disopyramide
- Ajmaline I.V.
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What are the alternative choices for Atrial fibrillation/flutter?
- Digoxin
- Class IA, IC drugs
- Low dose amiodarone
What is the function of cardiac glycosides like Digoxin and Digitalis?
Cardiac glycosides activate vagus nerves, slowing sinus rate and prolonging AV conduction time. They are used in treatment of atrial fibrillation, in combination with β-blockers and verapamil.
What is the mode of action for Class II antiarrhythmic drugs?
Class II antiarrhythmic drugs are Beta-Adrenergic Blockers. Examples include:
- Propanolol
- Metopropol
- Esmolol
- Acebutolol, etc.
What are the first choice drugs for Supraventricular tachycardia?
- Adenosine
- Verapamil
- Diltiazem
What channels do Class IV drugs block on myocardial cells?
Class IV drugs block the L-type Ca2+ channels on myocardial cells. These drugs are calcium channel blockers (CCBs) with higher affinity to myocardium, such as Verapamil and Diltiazem.
How does adenosine function as an antiarrhythmic drug?
Adenosine is a K+-channel opener that activates atrial A1-adenosine receptor IK channel opening, causing hyperpolarization. It slows spontaneous depolarization and reduces sinus rate and AV conduction.
Which drugs are included in Class III antiarrhythmics?
Class III antiarrhythmics include:
- Amiodarone
- Sotalol
- Ibutilide
- Bretylium
- Dofetilide
What are the alternative choices for Supraventricular tachycardia?
- Class II drugs
- Digoxin
- Class IA, IC, II, or IV drugs
What is the function of Class III drugs (K+ channel blockers)?
Class III drugs block the repolarizing K+ channel, thereby prolonging AP duration and lengthening the RP. Amiodarone blocks several ionic channels and possesses both α- and β-adrenoceptor antagonist effect.
Which CCBs are used due to their higher affinity to myocardium?
Only CCBs with higher affinity to myocardium, i.e. phenylalkylamines e.g. Verapamil, Gallopamil and/or benzothiazepine derivatives e.g. Diltiazem, are used.
What is the mode of action for Class IV antiarrhythmic drugs?
Class IV antiarrhythmic drugs are Calcium Channel (L-type) Blockers. Examples include:
- Verapamil
- Diltiazem
What is the first choice treatment for Sustained Ventricular Tachycardia?
- Cardioversion (safest & effective option)
- Lidocaine
What are examples of Class II drugs (β adrenoceptor antagonists)?
Examples include Propranolol, Atenolol, Metoprolol, and Esmolol. These drugs are β adrenoceptor antagonists used to manage various cardiac conditions.
What effects do Class IV drugs have on sinus rate and AV conduction?
They reduce sinus rate, slow AV conduction, prolong RP of AV node, and exert a strong (-ve) inotropic and vasodilator effect.
List the drugs classified under miscellaneous antiarrhythmics.
Miscellaneous antiarrhythmics include:
- Adenosine
- Magnesium
- Alnidine
- Atropine
- Digoxin
What effect does the clinical use have on the QT interval?
It can prolong the QT interval. Overall slower depolarization leads to slower conduction of the AP throughout the heart, hence a slow heart rate.
What effects do Class II drugs have on sinus rate and AV conduction?
They reduce sinus rate, exert (-ve) inotropic effects, and slow AV conduction. These actions help manage heart rhythm and function effectively.
Where do Class IV drugs exert their strongest electrophysiological effects?
Exert strongest electrophysiological effects on SA N and AV N (where AP are mediated by Ca2+).
What are the alternative choices for Sustained Ventricular Tachycardia?
- Procainamide
- Bretylium or Amiodarone
- Sotalol
- Class IA, IB, II, III
What is the first choice treatment for Ventricular Fibrillation?
- Defibrillation is treatment of choice
- Lidocaine to prevent recurrence
What do Quinidine and Procainamide inhibit in Class 1A?
- Inhibit the Na+ channels and K+ channels on atrial and ventricular myocytes and cells of the purkinje fibers.
What are the clinical uses for treating arrhythmias?
Clinical uses include treating both supraventricular and ventricular arrhythmias. It is contraindicated in heart failure due to a negative inotropic effect on the heart and could lead to hypotension.
How do Class II drugs affect automaticity and membrane responsiveness?
They reduce automaticity, membrane responsiveness, and the effective refractory period of Purkinje fibres, aiding in controlling heart rhythm.
What are the alternative choices for Ventricular Fibrillation?
- Amiodarone
- Procainamide
- Bretylium to prevent recurrence
What effects do Class I Drugs (Na+ channel blockers) have on Action Potential (AP) amplitude and depolarization velocity?
They suppress Action Potential (AP) amplitude, reduce fast depolarization velocity and propagation velocity.
What happens when Na+ channels are blocked in Class 1A?
- There is a decrease in the amount of Na entering the cell causing a slower depolarization which means a decrease in the slope during phase zero.
How do Class I Drugs affect the total Refractory Period (RP) and automaticity?
They prolong total Refractory Period (RP) and reduce automaticity.
What is the first choice drug for Torsades de pointes?
- Magnesium sulfate
What are the targets of Class I antiarrhythmic drugs?
Class I antiarrhythmic drugs, such as flecainide, target the I(Na) channels. These channels are responsible for the movement of Na+ ions.
What is the effect of blocking K+ channels in Class 1A?
- There is less K+ leaving the cell and it leads to a slower rate of repolarization and a longer phase of phase 1, 2, and 3 (prolonged AP) which means there is a longer effective refractory period.
How does Class 1A affect the ECG?
- This shows up as a longer QRS complex and a longer T-Q segment.
What is the mechanism of action for antiarrhythmic drugs?
Antiarrhythmic drugs act by altering ion fluxes within excitable tissues in the myocardium. Three ions of primary importance are Na+, Ca2+, and K+.
Which ions are involved in Class IV antiarrhythmic drug action?
Class IV antiarrhythmic drugs, like verapamil, target the I(Ca.L) channels, which involve the movement of Ca++ ions.
What are the alternative choices for Torsades de pointes?
- Potassium (if hypokalemic)
- Isoprenaline
What influence do Class I Drugs have on slow Ca2+ mediated APs in SA or AV node cells?
They have little or no influence on slow Ca2+ mediated APs (e.g. in SA or AV node cells).
What are the first choice drugs for Bradyarrhythmia?
- Atropine
- Ipratropium
What is the role of Class II antiarrhythmic drugs?
Class II antiarrhythmic drugs, such as propranolol, affect Na+ channels and are influenced by sympathomimetics and vagal nerve stimulation.
What are the types of disturbances in impulse generation in cardiac arrhythmias?
- Disturbance in impulse generation, e.g., increased/decreased automaticity due to ectopic focus.
- Disturbance in impulse conduction, e.g., AV block.
- Re-entry arrhythmias, e.g., decreased retrograde conduction (backward conduction from AV node to the atria).
What is the aim of therapy for arrhythmias?
The aim of therapy of the arrhythmias is to reduce ectopic pacemaker activity and modify conduction or refractoriness in re-entry circuits to disable circus movement.
What is the alternative choice for Bradyarrhythmia?
- Cardiac pacing
How do Class III antiarrhythmic drugs function?
Class III antiarrhythmic drugs, like d-sotalol, target I(K.r) channels, affecting K+ ion movement. They have indirect effects via T3-antagonism by amiodarone or dronedarone.
What is atrial flutter?
Rapid contraction of the atria (up to 300 bpm) at a rate too rapid for the ventricles to pump efficiently.
What are the major mechanisms available for achieving the goals of arrhythmia therapy?
- Sodium channel blockade
- Blockade of sympathetic autonomic effects in the heart
- Prolongation of the effective refractory period
- Calcium channel blockade
What substances can influence action potential propagation?
Action potential propagation can be influenced by Na+, Ca++, K+, H+, loss of ATP, ischemic metabolites, Halothane, Isoflurane, etc.
What is the normal heart rate range for determining arrhythmia?
A heart rate outside the normal range of 60 – 100 bpm is a criterion for determining arrhythmia. It indicates an abnormal heart condition.
Describe atrial fibrillation.
Irregular and rapid atrial contraction, resulting in a quivering of the atria and causing an irregular and inefficient ventricular contraction.
What is the normal resting heart rate range for adults?
The normal resting heart rate for adults ranges from 60 to 100bpm. A lower heart rate at rest implies more efficient heart function.
What indicates an arrhythmia if the rhythm is not originating from a specific node?
Rhythm not originating from the SA node, the natural pacemaker that generates electrical impulses, indicates arrhythmia. This is one of the criteria for determining arrhythmia.
What characterizes premature ventricular contractions?
Beats originating in the ventricles instead of the sinoatrial node in the atria, causing the ventricles to contract before the atria and resulting in a decrease in the amount of blood pumped to the body.
What is ventricular tachycardia?
A rapid heartbeat with a rate of more than 100 bpm, usually originating in the ventricles.
What ions are involved in the action potential of cardiac tissue during Phase 0?
During Phase 0, fast Na+ entry occurs. This phase is characterized by the rapid influx of sodium ions into the cardiac cells.
How is arrhythmia defined in terms of heart rhythm disturbance?
Arrhythmia is a disturbance of normal heart rhythm either resulting in:
- A faster rhythm (Tachycardia, >100bpm)
- Faster arrhythmia (Tachyarrhythmia, >150 - 250bpm)
- A flutter >250 – 350bpm
- Fibrillation, >350bpm
- Slowed rhythm (Bradyarrhythmia,
What are the two types of abnormal conduction that can determine arrhythmia?
- Abnormal conduction pathway
- Abnormal conduction velocity
What contributes to each phase of the cardiac action potential?
Specific ionic currents contribute to each phase of the cardiac action potential, hence difference in drug activity.
Describe the ion movement during Phases 1 and 2 of cardiac action potential.
In Phases 1 and 2, slow Ca2+ entry occurs along with some Na+ entry. Calcium ions play a crucial role in these phases.
What are the characteristics of a faster heart rhythm in arrhythmia?
A faster rhythm in arrhythmia is characterized by:
- Tachycardia, >100bpm
- Tachyarrhythmia, >150 - 250bpm
- A flutter >250 – 350bpm
- Fibrillation, >350bpm
Describe ventricular fibrillation.
Rapid disorganized contractions of the ventricles resulting in the inability of the heart to pump any blood to the body, which will result in death unless treated.
What is the refractory period after an action potential (AP)?
The rest period after an AP initiates the cardiac cell is unable to initiate another AP for some time (time shorter than the period for the true AP; 250 milliseconds (ms) or 0.25 seconds (sec)).
How many phases does the cardiac transmembrane action potential consist of?
The cardiac transmembrane action potential consists of five phases.
What is the definition of a slowed heart rhythm in arrhythmia?
A slowed rhythm in arrhythmia is defined as Bradyarrhythmia, with a heart rate of
What happens during Phase 3 of the cardiac action potential?
Phase 3 involves K+ exit. Potassium ions leave the cardiac cells, contributing to the repolarization of the membrane potential.
What happens during depolarization in terms of membrane potential?
During depolarization, the movement of the cell's membrane potential shifts to a more positive value. This involves the rapid rise in membrane potential and opening of Na+ channels.
What occurs during Phase 0 of the cardiac action potential?
Phase 0 involves Rapid depolarization.
How does the refractory period protect the heart?
This period helps to protect the heart as it is the recovery period, the resting period after excitation.
Explain the refractory period in the context of cardiac action potential.
The refractory period is a phase where the cardiac cells are unable to respond to new stimuli, ensuring proper timing of heart contractions.
Where does the cardiac action potential (AP) originate?
The cardiac action potential (AP) originates from the sinus node spontaneously at regular rate.
What is the effective refractory period?
Effective Refractory period is defined as no response to stimulus/no production of an AP.
What causes the large influx of Na+ ions during depolarization?
The large influx of Na+ ions during depolarization is caused by the opening of Na+ channels in the cellular membrane, resulting in positively charged Na+ ions rushing into the cell.
What happens in Phase 1 of the cardiac action potential?
Phase 1 is characterized by Early rapid repolarization.
What is the significance of the rate of depolarization in cardiac action potential?
The rate of depolarization affects how quickly the membrane potential changes, influencing the overall timing and strength of cardiac contractions.
What are the two types of cardiac tissue?
- Conducting tissue: Includes SA node, AV node, and Purkinje fibers. They are automatic and can initiate impulses. The SA node acts as the pacemaker.
- Contractile tissue: Includes Atria and Ventricular muscles. They are not automatic, cannot initiate impulses, but are excitable and respond to impulses.
What is an AP in cardiac tissue?
An AP is a rapid sequence of changes in the voltage across a cell membrane.
Describe the absolute refractory period.
Absolute Refractory period is absolutely impossible to stimulate an action potential, corresponds to depolarization and repolarization.
How does repolarization affect membrane potential?
Repolarization involves the change in membrane potential from a positive to a negative value. This process includes rapid sodium channel inactivation and a large efflux of k ions.
Describe what occurs during Phase 2 of the cardiac action potential.
Phase 2 is the Plateau phase, involving a sharp increase in membrane potential with Ca+2 influx and K efflux, and closure of Na+.
How is the cardiac AP measured?
The cardiac AP is the measurement of the membrane of the myocytes in terms of the electrical activity of the cell during the contraction and relaxation of the heart.
What role do ion channels play in repolarization?
During repolarization, rapid sodium channel inactivation and the large efflux of k ions are caused by the closing of Na ion channels and opening of k+ ion channels.
What does the relative refractory period correspond to?
Relative refractory period corresponds to hyperpolarization.
What is the main event in Phase 3 of the cardiac action potential?
Phase 3 involves Final rapid repolarization.
How is the membrane voltage or potential determined?
The membrane voltage or potential is determined at any time by the relative ratio of ions in terms of concentration between the intracellular and extracellular as well as the permeability of each ion.
What characterizes Phase 4 of the cardiac action potential?
Phase 4 is characterized by Resting membrane potential and diastolic depolarization.
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