Cardiac Arrhythmia Drugs Flashcards
The P wave of an ECG corresponds to what event in the cardiac cycle?
Contraction of the atria
The R wave of an ECG corresponds to what event in the cardiac cycle?
Contraction of the ventricles
The T wave of an ECG corresponds to what event in the cardiac cycle?
Repolarization of the ventricles
Arrhythmias can be defined as disturbances in what?
Pacemaker impulse formation (SA/AV node)
Contraction impulse conduction (Bundle of His)
Both of these
Arrthymias can result in “blackouts” as a result of what?
Rate and/or timing of contraction of heart musle that is insufficient to maintain normal cardiac output (CO)
Draw a graph (action potential vs. time) showing the fast action potential of cardiac myocytes over time
Explain what is happening at each stage
Using the graph you have drawn showing cardiac action potential to show where drugs blocking Na+ channels act
Phase 0
Using the graph you have drawn showing cardiac action potential to show where drugs beta blockers act
Phase 4
Using the graph you have drawn showing cardiac action potential to show where drugs blocking K+ channels act
Late phase 3 (refractory period)
Using the graph you have drawn showing cardiac action potential to show where drugs blocking calcium channels act
Phase 2
Draw a graph showing the slow action potential of the SA/AV node
Where in the heart does this type of AP originate?
In the pacemakers (SA or AV node) of the heart
Where would a fast actional potential occur within the heart?
In ventricular cardiac myocytes
Where would a slow actional potential occur within the heart?
Atrium (specifically SA/AV nodes)
Give two general types of abnormal impulse generation
Abnormal automaticity- spontaneous firing
Triggered rhythms- myocytes contract twice when stimulated once
Give two examples of abnormal automaticity
- Enhanced normal automaticity
Increased number of action potentials from the SA node
- Ectopic foci
Action potentials arise from sites other than the SA node
Give two types of triggered rhythm and explain the difference between the two
- Delayed afterdepolarization
AP arises from the resting potential
- Early afterdepolarization
AP arises from the plateau phase
e.g. Torsade de Pointes
What are the two general types of abnormal conduction?
Conduction block
Reentry
Describe the four types of conduction block
1st degree- slowed impulses through the conducting system (usually asymptomatic and does not require treatment)
2nd degree, Mobitz Type I- electrical impulses are delayed further and further with each subsequent heartbeat until a beat fails to reach to the ventricles entirely
2nd degree, Mobitz Type II- some electrical impulses are unable to reach the ventricles
3rd degree- none of the electrical impulses from the atria reach the ventricles
Bundle branch block- electrical impulses are slowed or blocked as they travel through His in one of the two ventricles.
Descibe how first degree heart block might look on an ECG
Why might you see these changes?
Prolonged P-R interval (>200ms)
Everything else is normal
Why: Problem at the AV node-conducton from here to ventricles is slowed, everything else is functioning ok
Describe how second degree type I heart block might look on an ECG
Why might you see these changes?
Progressive prolongation of the P-R interval until a QRS complex is completely dropped
Why? Problem most likely functional deficit at the AV node structurally intact
Describe how second degree type II heart block might look on an ECG
Why might you see these changes?
Intermittent non-conducted P waves without progressive prolongation of the PR interval
PR interval remains the same
Wide QRS
Dropped QRS, P waves remain
Why: Block is below the AV node (in the His or Purkinje system), more likely due to structural damage
Describe how thrid degree heart block might look on an ECG
Why might you see these changes?
P waves and R waves are independent
(Atrial and ventriclar activities are not synchronous)
No PR to QRS relationship
Why: Complete AV dissociation from the ventricles
Perfusing rhythm is maintained by a junctional or ventricular escape rhythm
Explain what is meant by “re-entry” in relation to abnormal conduction leading to arrhytmias
Re-entry is a defect which occurs when the action potential fails to extinguish itself and reactivates a region that has recovered from the previous AP
Image B
What is reflection type reentry in relation to abnormal AP conducton?
Reflection is when an AP front travels in a forward direction through tissue that is then re-excited by a wave front that propagates backward.
A on the image
What is Wolff-Parkinson-White syndrome?
The commonest form of ventricular preexcitation
Presence of an acessory pathway (Bundle of Kent) which provides an alternative route for ventricular depolarisation
(avoids AV node, exciting the ventricles)
Intermitted tachycardia results
At which points could we use drugs for the treatment of:
1) Abnormal AP generation
2) Abnormal AP conduction
1) Decrease the slope of phase 4 in the pacemakers cells - making it harder for the rhythm to be generated
Raise the threshold
2) Decrese conduction velocity
Increase effective refractory period (harder for the cell to be re-excited)
What are the two main goals of pharmacological treatment of arrhytmias?
Restore normal sinus rhythm and conduction
Prevent more serious and possibly lethal arrhythmias from occuring
What are the three main ways in which drugs can act to improve arrhytmias?
1) Decrease conduction velocity
2) Change ERP duration
3) Supress abnormal automaticity
Where do class I A antiarrhytmic drugs have their action?
Give some examples of such drugs
Moderate reduction in conduction of phase 0 (Na+)
e.g. Quinidine, procainmide
Where do class I B antiarrhytmic drugs have their action?
Give some examples of such drugs
No change in phase 0
Increased threshold of (Na+)
e.g. Lidocaine
Where do class I C antiarrhytmic drugs have their action?
Give an example of such
Marked reduction in phase 0 through strong blockade of Na+ channels
Increased AP duration through blockade of K+ channels
e.g. Flecainide
Where do class II antiarrhytmic drugs have their action?
Give some examples of such drugs
Beta-adrenergic receptor blockers
Increase the action potential duration and refractory period in AV node to SLOW AV conduction velocity
Decrease phase 4 repol.
e.g. Propanolol, bisoprolol, esmolol
Where do class III antiarrhytmic drugs have their action?
Give some examples of such drugs
Increase the refractory period and the action potential duration (K+ channel block)
Decrease phase 0 and coduction (Na+ channel block)
Decrease pahase 4 (beta block and Ca2+ block)
e.g. Amiodarone, Sotalol, Dofetalide, Ibutilide
Where do class IV antiarrhytmic drugs have their action?
Give some examples of such drugs
Calcium channel blockers
Slow conduction through the AV node
Increase refractory period in AV node Increase phase 4 slope
e.g. Verapamil, Diltiazem
Why is it important to check if a patient is asthmatic before starting them on a Class II antiarrhythmic drug?
These drugs block b-adrenergic receptors and cause bonchospasm which may worsen their asthma symptoms
Which drugs could be used to treat AF?
Rate control (reduce ventricular response):
Bisoprolol
Verapamil
Diltiazem
+/- Digoxin
Rhythm control (stop AF):
Sotalol
Flecainide + bisoprolol
Amiodarone (central line)
Which IV drugs might you use to treat ventricular tachycardia?
Depending on what is already prescribed:
(All IV):
Metoprolol
Lignocaine
Amiodarone
Should Flecainide be used alone to treat atrial flutter?
No
If you slow the flutter rate to that the AV node takes the beat “flecainide flutter” which is a one to one conduction- patient will go into asystole
NEED Bisoprolol with this
Which is the best drug to use to treat WPW syndrome?
Flecainide - oral, long-term
Amiodarone- NOT long-term
Which drugs could be used to treat re-entrant SVT both
1) Acutely
2) Chronically
1) Acutely: (IV)
Adenosine
Verapamil
Flecainide
2) Chronic: (Oral)
Bisoprolol
Verapamil
Sotalol
Flecainide
Procainamide
Which drugs would you use to treat ectopic beats?
First line: Bisoprolol
Flecanide, Sotalol, Amiodarone (ONLY IF NO structural/IHD)
Which drugs would you use to treat sinus tachycardia?
Ivabradine
Bisoprolol
Verapamil
