3.1 Cardiac Arrhythmia Drugs Flashcards
Arrhythmias can be due to disturbances in..
Pacemaker impulse formation
Contraction impulse conduction
Combination
What is the consequence of arrhythmia?
Rate or timing of contraction of heart muscle that is insufficient to maintain normal cardiac output
What is the effect of drugs that block Na channels? Fast
Slowing of conduction in tissue (phase 0)
Upslope of AP offset to the right
Minor effects on duration of AP
What effect do beta blockers have in the AP? Fast
Diminish phase 4 depolarisation and automaticity
Affects the plateau
Increases duration slightly
What is the effect of potassium blocking drugs on AP? Fast
Increase duration
Because increases refractory period
What effect can calcium blockers have on AP? Fast
Decrease calcium inward currents
Results in decrease of phase 4 spontaneous depolarisation
Effects plateau phase
What effect can calcium channel blockers have on slow cardiac AP?
Decreased slope of phase 0
Prolonged refractory period
Name some drugs that effect automaticity
Beta agonists increase slope
Muscarinic agonists and adenosine decrease slope
Where can fast action potentials be found?
Cardiac tissue
Where can slow action potentials be found?
SAN or AVN
What two types of rhythms can be generated by abnormal impulse generation?
Automatic and triggered
What can automatic rhythms lead to?
Enhanced normal automaticity and ectopic focus
What can triggered rhythms lead to?
Delayed after depolarisation and early after depolarisation
Name two types of abnormal conduction
Conduction clock
Reentry
What is conduction block and how is it treated?
When impulse isn’t conducted from atria to ventricles
Treated by pacemakers
Name a location in the heart where there could be an accessory pathway in WPW
Bundle of Kent
What is a condition caused by abnormal anatomical conduction?
Wolf Parkinson white syndrome
What is the affect of scarred heart tissue on depolarisation?
Causes a functional block of depolarisation
What do you want to do to the slop of the AP in abnormal generation of rhythms ? Which class of drugs?
Decrease of phase 4 slope
Raises the threshold
Give calcium channel blocker
Harder to generate rhythm
What three things can antiarrhythmic Drugs be used to do?
Decrease conduction velocity
Change the duration of ERP
Suppress abnormal automaticity
Name some class 1a agents?
Procainamide, quinidine, disopyramide
How can class 1a agents be given?
Oral or IV
What effects do class 1a agents have in cardiac activity?
Decreased conduction (decrease phase 0)
Increase refractory period
Decreased automaticity
Increase Na threshold
What effects may class 1a agents produce on ECG?
Increased QRS,
increased QT
What channel do class 1a agents block?
Sodium
Two uses of quinidine
Maintain sinus rhythm in AF and flutter and prevent reoccurrence
Brugada syndrome
Use of procainamide
Acute IV treatment of supraventricular and ventricular arrhythmias
Side effects of class 1a agents
Hypotension - duento recpduced CO Proarrhythmia Dizzy, confused, insomnia, seizure GI effects Lupus like syndrome especially procainamide
Name some class 1b agents and the route of administration
Lidocaine - IV
Mexiletine - oral
Effects of class 1b agents on cardiac activity
Fast binding offset kinetics No change in phase 0 in normal tissue APD slightly decreases in normal tissue Increased Na threshold Decreased phase 0 conduction in fast beating or ischaemic Tissue
Effects on ecg of class 1b agents
None in normal tissue
Increased QRS in fast beating or ischaemic
Uses of 1b agents
Ventricular tachycardia
Not used in atrial arrhythmias or av junctions arrhythmias
Advantage of class 1b agents over class 1a
Less pro arrhythmic as less QT effect
Side effects of class 1b agents
Dizzy, drowsy
Abdominal upset
Name some class 1c agents and their route of administration
Flecainide and propafenone
Oral or IV
Effect of class 1c agents on cardiac activity
Very slow binding offset kinetics
Substantial decrease in phase 0 Na
Decrease automaticity so increased threshold
Increased apd (k) and increased refractory period
Effect of class 1c agents on ecg
Increased PR, QRS and QT
What are some uses for class 1C agents?
Supraventricular arrhythmias (fibrillation and flutter)
Premature ventricular contractions
Wolff-Parkinson-White Syndrome
What are some side effects of class 1c agents?
Proarrhythmia and sudden death
Increases the ventricular response to supreventricular rhythms (flutter)
CNS and GI effects
Why should you avoid using a class 1C agent in flutter?
They increase the ventricular response to the flutter so need to block the AVN with another drug if using these drugs
Name some class II agents?
Propranolol, bisoprolol, metoprolol, esmolol
How can propanolol be administered?
IV and oral
Which class II agent can be given IV only?
Esmolol
What are the cardiac effects of Class II agents?
Increased APD and refractory period in AV node to slow AV conduction velocity
Decrease phase 4 depolarisation - catecholamine dependent
What effects can be seen on the ECG due to class II agents?
Increase PR
Decrease HR
Uses of Class II agents
Treat sinus and catecholamine dependent tachycardia
Converting re-entrant arrhythmias at AVN
Protect ventricles from high atrial rates due to slowing of conduction at AVN
Side effects of class II agents
Bronchospasm
Hypotension
When should Class II agents not be used? Why?
In partial AV block or ventricular heart failure
As it will further increase the AV block
Name some class III agents
Amiodarone, sotalol
Why is amiodarone very effective?
Because it effects all phases of action potential
What are the cardiac effects of amiodarone?
Increase refractory period and ADP (K+) Decrease phase 0 and conduction (Na+) Increase threshold Decrease phase 4 (B block and Ca block) Decrease speed of AV conduction
Effects on ECG of amiodarone
Increase PR, QRS, QT
Decrease HR
Why is amiodarone useful for very wide spectrum?
Very fat soluble
Which drug has side effects which increase with time?
Amiodarone
Name some side effects of amiodarone
Pulmonary fibrosis- breathess Hepatic injury Increase LDL cholesterol Thyroid disease (hypo or hyper) Photosensitivity Optic neuritis - transient blindness
Which drugs may need to be reduced or monitored more if taking amiodarone?
digoxin and warfarin
How is sotalol administered?
Oral
Cardiac effects of sotalol
Increased APD and refractory period in atrial and ventricular tissue
Slow pahse 4 (B blocker)
Slow AV conduction
ECG effects of sotalol
Increase QT - effects K channels
Decrease HR
Uses of sotalol
Wide spectrum
Supracentricular and ventricular tachycardia
Side effects of sotalol
Pro-arrhythmia, fatigue, insomnia
Why is sotalol pro-arrhythmic?
It effects QT interval
Name some class IV agents
Verapamil, dilltiazem
Cardiac effects of class IV agents
Slow conduction through AV (Ca++)
Increase refractory period in AVN
Increase slope of phase 4 in SA to slow HR
Effects of class IV agents on ECG
Increase PR (dec conduction through AVN) Increase or decrease HR depending on bloop pressure response and baroreflex
Uses of Class IV
Control ventricles during supra ventricular tachycardia
Convert supraventricular tachycardia (reentry around AVN)
When should caution be used in prescribing class IV agents?
Partial AV block
Hypotension, decreased CO or sick sinus
What is the relevance of the type of administration of adenosine?
Rapid IV bolus
Very short half life - seconds
Stops conduction at AVN for 20 seconds whilst drugs gets metabolised
What is the mechanism of action of adenosine?
Binds A1 receptors and activates K currents in AVN and SAN
Decreases APD, hyperpolarisation causing decreased HR
Decrease Ca current = Increased refractory period at AVN
What are the effects of adenosine on the heart?
Slows AVN conduction
Uses of adenosine
Convert re-entrant supravenricular arrhythmias
Hypotension during surgery
Diagnosis of coronary artery disease by looking for perfusion defects
How is vernakalant administered?
IV bolus over 10mins
Mechanism of action of vernakalant
Blocks ATRIAL specific K channels
What are the cardiac effects of vernakalant?
Slows atrial conduction
Increased potency with higher heart rates
Side effects of vernakalant
Hypotension, AV block
Sneezing and taste disturbances
Uses of vernakalant
Convert RECENT onset AF to normal sinus rhythm
What is the mechanism of action of Ivabradine?
Blocks If ion current which is highly expressed in sinus node
What are the cardiac effects of ivabradine?
Slows the sinus node
Doesn’t effect BP
Uses of ivabradine
Reduce inappropriate sinus tachycardia
Reduce HR in angina and HF
What group of drugs does digoxin belong to?
Cardiac glycosides
What is the mechanism of action of digoxin?
Enhances vagal activity
Slows AV conduction and slows HR
How does digoxin enhance vagal activity?
Increase K current
Decrease Ca current
Increases refractory period
Uses of digoxin
Reduce ventricular rate in AF and flutter
How should digoxin be added to a treatment programme?
As an adjunct
What is the mechanism of action of atropine?
Selective muscarinic antagonist
What are the cardiac effects of atropine?
Block vagal activity to speed AV conduction and increase HR
Uses of atropine
Treat vagal bradycardia
Which drugs can be used in AF?
Rate control
- Bisoprolol, verapamil, diltiazem +/- digoxin
Rhythm control
- Sotalol, flecainide with isoprolol, amiodarone
Should flecainide be used alone in AF?
No
Give AV nodal blocking drugs to reduce ventricular rates in flutter
Best drug for treatment of WPW?
Flecainide
Amiodarone
