Cardiac Arrhythmia Drugs Flashcards
What are arrhythmias?
Heart condition where disturbances in:
- Pacemaker impulse formation
- Contraction impulse conduction
- Combination of the two
Results in rate and/or timing of contraction of heart muscle that may be insufficient to maintain normal cardiac output.
What creates the resting potential?
Unequal distribution of ions (interior of the cell is negative with respect to the outside).
Na+ higher outside than inside the cell
Ca2+ much higher outside than inside
K+ higher inside than outside.
It is maintained by ion selective channels, active pumps ad exchangers
Explain the ventricular cardiac action potential
Phase 0 - Opening of voltage gated Na channels
Phase 1 - Transient outward K+ current
Phase 2 - Opening of voltage gated Ca2+ channels (some K+ channels also open).
Phase 3 - Ca2+ channels inactivate, voltage gated K+ channels open.
Phase 4 - resting.
What effect do class 1 drugs have?
Block Na channels which slow the conduction in tissue (phase 0). It has a minor effect on action potential duration.
What effects do class 2 drugs have?
Beta blockers which bloke sympathetic action (act on B1 adrenoreceptors in the heart) so, decrease the slope of the pacemaker potential in the SA node and slow conduction at AV node.
What effects do class 3 drugs have?
Block K+ channels so prolong plateau phase and increase AP duration.
This prolongs the refractory period.
What effects do class 4 drugs have?
Ca2+ channel blockers which decrease inward Ca2+ currents resulting in a decrease of phase 4 spontaneous depolarisation.
They decrease slope of AP at SA node, decrease AV nodal conduction, decrease force of contraction (negative isotropy)
Where is slow cardiac action potential?
SA and AV node
Explain the slow cardiac action potential
Pacemaker potential / Funny current (If)- Na+ in via HCN channels.
Opening of voltage gated Ca2+ channels.
Then opening of voltage gated K+ channels so K+out
How do Ca2+ channel blockers affect slow Cardiac AP?
Reduce conduction velocity
Decrease AV nodal conduction
Decrease slope of AP at SA node.
Decrease force of contraction
What drugs affect automaticity?
Catecholamines (B agonist)- increase phase 4
Muscarinic agonist and adenosine - slow down phase 4
What are some mechanisms of arrhythmias?
Abnormal impulse generation - Automatic rhythms (enhanced normal automaticity and exotic focus), triggered rhythms (delayed and early afterdepolarisations)
Abnormal conduction - conduction block (1st, 2nd, 3rd), reentry loops (circus movements, reflection)
Where can reentry occur?
WPW - ventricles to atrium and visa versa (AV node, bundles, pathway and renter atrium)
AV node - split into slow and fast pathway
If abnormal rhythm generation how could drugs work?
Decrease of phase 4 slope in pacemaker cells
Raise the threshold
In the case of abnormal conduction, how could drugs work?
Decrease conduction velocity
Increase (ERP) effective refractory period (so the cell won’t be reexcited again)
What are antiarrhythmic drugs used for?
They aim to restore normal sinus rhythm and conduction to prevent more serious and possibly lethal arrhythmias from occurring.
They are used to:
Decrease conduction velocity
Change duration of ERP
Suppress abnormal automaticity
Give examples of class 1A agents
Procainamide, quinidine, disopyramide.
What effects do class 1A agents have on cardiac activity?
Decrease conduction
Increase refractory period
Decrease automaticity
Increase threshold
What are class 1A drugs used for?
Wide spectrum
Quinidine: Maintain sinus rhythm in Atrial fibrillation and atrial flutter and to precent recurrence, brugada syndrome.
Procainamide: acute IV treatment of SV and Ventricular arrhythmias.
ADRs of 1A?
Hypotension, reduced CO, Proarrythmias, DIzziness, confusion, insomnia, seizures, GI effects, Lupus-like syndrome.
Give examples of class IB agents?
Lidocaine( IV), mexiletine (oral)
How do 1B agents affect cardiac activity?
Increase threshold
Decrease phase 0 conduction in fast beating or ischaemic tissue.
APD slightly decreased
When do you use 1B agents?
Ventricular tachycardia
Side effects of iB?
Less side effects than 1A
GI upset
Dizziness, drowsiness
IC example?
Flecainide and propafenone
1C effect on cardiac activity?
Very slow binding offset kinetics
Substantially decrease phase 0 in normal
Decrease automaticity (increase threshold)
Increase APD and refractory period especially in rapidly depolarising tissue.
What are 1C used for?
SV arrhythmias (fibrilation and flutter)
Premature ventricular contractions
WPW syndrome
What are the side effects of iC?
Proarrhythmias and sudden death (especially chronic use)
Increase ventricular reasons to SV arrhythmias.
CNS and GI effects
What is a CAST?
Cardiac Arrhythmia Suppression Trial
Class II examples?
Propranolol, Bisoprolol, Metoprolol, esmolol
B blockers
How does Class II work on cardiac tissue?
Increase APD and refractory period in AV node and to slow AV conduction velocity.
Decrease phase 4 depolarisation (catecholamine dependant)
Effect of class II on ECG?
Increase PR and decrease HR
CLass II uses?
All arrhythmias (almost)
Treating sinus and catecholamine dependant tachycardia
Converting reentrant arrhythmias at AV node
Protecting the ventricles from high atrial rates (slow AV conduction)
ADRS of class II?
Bronchospasm
Hypotension
Don’t use in partial AV block or acute heart failure (used in stable HF)
Class III agent examples?
Amiodarone
Sotalol
CLass III cardiac effects?
Increase refractory period and increase APD
Decrease phase 0 and conduction
Increase threshold
Decrease phase 4
Decrease speed of AV conduction.
Effect of lLass III on ECG?
Increase PR, QRS, QT
Decrease HR
What is amiodarone used for
Very wide spectrum.
Effective for most arrhythmias.
Side effects of class III (amiodarone)?
Many serious side effects that may increase with time
Pulmonary fibrosis Hepatic injury Increase LDL cholesterol Thyroid disease Photosensitivity Optic neuritis (transient blindness)
Cardiac effects of sotalol?
Increase APD and refractory period in both atrial and ventricular tissue.
Slow phase 4 (B bloker)
Slow AV conduction
ECG effects of sotalol?
Increase QT and decrease HR
Uses of sotalol?
Wide spectrum: Supraventricular and ventricular tachycardia
Side effects of sotalol?
Proarrythmia, fatigue, insomnia
Class IV examples?
Verapamil and diltiazem
Cardiac effects of Class IV?
Slow conduction through AV node (Ca2+)
Increase refractory period in AV node
Increase slow of phase 4 in SA to slow HR.
CLass IV Effects on ECG?
Increase PR, alters heart rate (depending on BP response and baroreflex).
Uses of class IV?
Control ventricles during SVT
Concert SVT (re-entry around AV)
Side effects of class IV agents?
Caution when partial AV block is present. Can get systole if B blocker is on board.
Caution when hypotension, decrease CO or sick sinus
Some GI problems (constipation).
Adenosine mechanism?
Natural nucleoside that binds A1 receptors and activates K+ currents in AV and S.A. nodes.
Decrease APD, hyperpolarosation - decrease HR.
What are the cardiac effects of adenosine?
Slow AV coditction
Use of adenosine?
Convert re-entrant SV arrhythmias diagnosis of coronary artery disease (scans).
Mechanism of vernakalant?
Blocks atrial specific K+ channels (outwards channel class 3)
Cardiac effects of vernakalant?
Slows atrial conduction
Increase 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
Ivabraine mechanism and cardiac effects?
Blocks If ion current highly expressed in sinus node.
Slows the sinus node but does not affect BP.
Side effects of Ivabradine?
Flashing lights
Teratogenicity not known (avoid in pregnancy)
Uses of ivabradine?
Reduce inappropriate sinus tachycardia
Reduce heart rate in heart failure and angina (avoiding blood pressure drops)
Digoxin mehanism?
Enhances vagal activity
Slows AV conduction and slows HR
Digoxin uses?
Treatment to reduce ventricular rates in atrial fibrillation and atrial flutter.
Atropine mechanism and cardiac effects and uses?
Selective muscarininc antagonist.
Blocks vagal activity to speed AV conduction and increase HR.
Used to treat vagal bradycardia
Which drugs could be used in AF?
Rate control: Bisoprolol, verapamil, diltiazem +/- digoxin.
Rhythm control: Sotalol, flecainide with bisoprolol, amiodarone
Which IV drug first for VT?
Depends on what drugs are already prescribed.
Metoprolol / bisoprolol (1st line if no meds)
Lignocaine/ mexoletine
Amiodarone
Should flecainide be used alone for atrial flutter?
No
Give AV nodal blocking drugs to reduce ventricular rates in atrial flutter.
Best drugs for WPW?
Flecainide
Amiodarone
List drugs used in re-entrant SVT?
Acutely (IV):
Adenosine, Verapamil, Flecainide
Chronic (repeated episodes, orally):
Bisoprolol, verapamil, Sotalol, Flecainide, Procainamide, Amiodarone
Which drug for ectopic beats
Bisoprolol first line
Flecainide, sotalol or amiodarone
Which drugs for sinus tachycardia?
Ivabradine, Bosoprolol, verapamil
What is catheter ablation?
Catheter ablation is a minimally invasive procedure in which the doctor threads a flexible thin tube (catheter) through the blood vessels to your heart to terminate (ablate) abnormal electrical pathways in the heart tissue.
