Anti-Arrhythmic (General) Flashcards
Arrhythmia
Electrical impulses that coordinate the heart no longer function properly
–> Fast, Slow, Irregular patterns
Heart Rate
Number of times the heart beats per minute
- BPM
Heart Rhythm
Pattern of heart beat
- Fast, Slow, Irregular
Rate Control
Drugs that reduce rapid ventricular rate
- Negatively chronotropic drugs
- electrophysical interventions
Rhythm Control
Restore normal sinus rhythm by:
- Antiarrhythmic Medication
- Cardioversion
- Surgery
Electrical Activity of Pacemaker Cell
- Pacemaker Potential (Initial)
Initial spontaneous (Slow) depolarization
- Funny Channels open
–> Na+ Moves in
Electrical Activity of Pacemaker Cell
- Pacemaker Potential (Latter)
Latter spontaneous depolarization
- T-Type Ca2+ Channels open
–> Ca2+ Moves in
Electrical Activity of Pacemaker Cell
- Rapid Depolarization
L-Type Fast Ca2+ Channels Open
- Ca2+ Moves in
Electrical Activity of Pacemaker Cell
- Rapid Repolarization
K+ Channels open
- K+ moves out of cell
Sympathetic Activity effect on Heart
NE/EP act on Beta1 receptors on SA node
–> Increased open state of funny calcium channels
–> Increased rate of spontaneous depolarization
–> Increased Heart Rate
Parasympathetic Activity effect on Heart
Vagus Nerve acts on Muscarinic Cholinergic Receptors on SA node
- Increased open state of K+ Channels
- Increased closed state of Ca2+ Channels
–> Decrease rate of spontaneous depolarization and Hyperpolarizes cell
–> Decrease Heart Rate
Electrical Activity of Contractile Cell
- 0 Stage
Rapid Depolarization
- Na+ Channels Open
–> Na+ moves in
Electrical Activity of Contractile Cell
- 1 Stage
Small Repolarization
- Na+ Channels Inactivated
–> Na+ decreases in cell
Electrical Activity of Contractile Cell
- 2 Stage
Plateau
- K+ Channels Close
–> Small K+ out of cell
- Ca2+ L-Type Channels Open
–> Ca2+ into cell
Electrical Activity of Contractile Cell
- 3 Stage
Repolarization
- Delayed K+ Channels Open
–> K+ out of cell
- Ca2+ L-Type Channels Close
–> Less Ca2+ into cell
Electrical Activity of Contractile Cell
- 4 Stage
Resting Potential
- Both types of K+ open
–> K+ out of cell
Na+ and Ca2+ stay close
Refractory Period
Time when cell is incapable of repeating an action
Define ERP
Effective Refractory Period:
- Longest interval when a cell can not respond to stimuli
What is worse Atricular or Ventricular Fibrillation
Ventricular Fibrillation is worse as blood is not being pumped across the body
- Articular Fibrillation just increases chances of a stroke
P Wave
Atrial Depolarization
QRS Complex
Ventricular Depolarization
(Atrial Repolarization is mixed in)
T Wave
Ventricular Repolarization
PQ Segment
AV Nodal Delay
(Atrial Depolarization)
- Time for ventricle to fill
QT Segment
Ventricular Systole
TQ Interval
Ventricular Diastole
RR Interval
Heart Rate
Atrial Fibrilation
Blood in atrium is pumping irregularly to the ventricles
Ventricular Fibrillation
Cardiac Arrest
- Signal is occurring but ventricle is not contracting and pushing blood to body
Heart Block
Signal from atrial fails to transfer to ventricle
Long QT Syndrome
Disorders that delay repolarization of ventricle
- Causes prolonged ventricular AP
–> Long pauses on ECG
Causes of Arrhythmias
- Impulse Formations
- Impulse Conduction/Propagation
Arrhythmia Causes
(Impulse Formations)
Altered Automaticity
- Increased (Sympathetic)
- Decreased (Parasympathetic)
- Escape Rhythm
–> (AV node is firing quicker than SA node)
- Enhanced latent pacemakers
–> (SA node is firing quicker than AV node)
Abnormal Automaticity
Triggered Activity
- Early afterdepolarization
–> Prolonged AP, enough to trigger another depolarization
- Delayed afterdepolarization
–> Excess intracellular Ca2+
Arrhythmia Causes
(Altered Impulse Conduction)
Conduction Block
- Impulse is blocked
Unidirectional Block (Reentry)
- Electrical signal repeatedly circles around
–> Occurs in cells with heterogenous refractory periods
Altered Impulse Conduction
(Re-entry)
One side is fast pathway
- Fast conduction, long refractory period
One side is slow pathway
- Slow conduction, short refractory period
Signal goes down the slow path and up the fast path.
- By the time the fast signal reaches the start the slow path is ready for another AP
- Signal goes through cycle again
–> Constant recycle leading to tachycardia
Class I Anti-Arryhthmics
Sodium Channel Blockers
MOA:
- Bind to alpha subunit of Na+ Channels and blocks Na+ Channel
–> Blocks phase 0 depolarization
–> Slows conduction velocity
Works better at High HR - Terminates Afib
Class IA
Moderate Effect Phase 0 (Prolong AP)
- Associate/Dissociate Midway
- Treat large variety of Arrhythmia
Class IB
Weak Effect Phase 0
- Associate/Dissociate Rapidly
- Treat Ventricular Arrhythmia
Class IC
Strong Effect Phase 0
- Associate/Dissociate Slowly
- Treat Ventricular Arrhythmia
Class 1(Three States of Sodium Channels)
Open: Ions flow
Close: Ions do not flow
- Channel can be depolarized
Inactivated: Ions do not flow
- Channel is repolarizing and can not be activated
To ensure that Class I drugs do not influence normal heart activity
–> Only target open/inactivated states
–> Only prolongs repolarization, does not cause random depolarization
Class II Anti-Arryhthmics
Beta-Adrenoceptors Antagonists
- Decrease Heart Rate and Contractility
- Indirectly impacts calcium channels
Class II - Anti-Arryhthmics
(Pacemaker Cells)
Targets Na+ and Ca2+ currents
- Slows pacemaker potential
- Decrease repolarization
- Slows conduction of AV node
Class II - Anti-Arryhthmics
(Contractile Cells)
Lowers Calcium:
- Regulates intracellular Ca2+
- Decrease contraction force, rate
- Inhibits afterdepolarization
–> Decrease Heart Rate
Class III - Anti-Arryhthmics
Potassium Channel Blockers
- Delays repolarization, increases refractory period
Works better at Low HR - Prevents Afib
Class IV - Anti-Arrhythmic
Calcium Channel Blockers
- Blocks L-Type Calcium Channels
- Decreases Contractility
- Decreases Heart Rate
- Decreases Conduction Velocity
L-Type Calcium Channels
Long Type
- Pacemaker Cells, Myocytes, Vasculature
T-Type Calcium Channels
Transient (Short) Type
- Pacemaker Cells
Non-Dihydropines
Calcium Channel Blockers
- Focuses on Contractile Cells (Heart)
–> Binds to high frequency L-Type Channels that undergo constant depolarization
(Pacemaker, Myocyte)
MOA:
- Decreases Cardiac Contractility
- Decreases Heart Rate
Dihydropine
Calcium Channel Blockers
- Focuses on Arterial Blood Vessels (Vasculature)
- Favours the inactivated state
MOA:
- Vasodilation
- Reduce Peripheral Vascular Resistance
Contraindications of Class IV
Do not combine calcium channel blockers with beta blockers
