Antidysrhymic Drugs Flashcards
Dysrhythmia
abnormaility in rhythm of heartbeat
- if severe can disable heart so NO BLOOD PUMPs
2 types of dysrhythmia
Tachydysrhythmias- increased HR
Brady dysthrhythmias-
decreased HR
what is important to know before prescribing antidysthmias drugs
- can cause dysrhythmias
- increased risk of death
what is replacing antidysrhythic drugs
Implantable defibrillators
Arrhythmia radio frequency ablation- destroys cells that cause dysrhythmias
What do dysrhythmias result from?
alternation of cardiac electrical impulses
SA node
heart PACEMAKER
- spont. depolariztion
- atria contracts in unison
AV node
impulse delayed
- allows complete atrial contraction
His-Purkinjie System
spreads impulse rapidly to all parts of ventricles
- ventricles contract in unison
2 kinds of cardiac action potentials
1) fast potentials
- contractile cardiac tissue
2) Slow potentials
- self-excitable cardiac tissue
Fast Potentials- what happens
0: depolarization
- influx of Na+
- drugs that block Na+ channels slow ventricle depolarization
- Rapid, partial repolariztation
- no effects of drugs - Prolonged plateau
- drugs that reduce calcium influx reduce myocardial contractility - Rapid depolarization due to efflux K+
- K+ channel blockers delay polarization
= prolonged time between 2 heartbeats - Under pathological conditions depolarization may occur in all cardiac cells
- dysrhythmia
Slow potential Pathway
Draw it too :)
- depolarization by slow influx of Ca2+
- drugs that suppress Ca2+ influx slow/stop AV node contraction
2 and 3. repolarization
- NO effect of drugs here
- SA node and AV node cells begin next depolarization
- beta blockers and calcium channel blockers suppress here = decrease SA node activity
ECG measures
electrical activity of Fast Potentials
-CONTRACTILE CELLS
DRAW ecg normal
P wave
Q, R, S
T wave
PR interval
lengthening
- conduction delayed through AV node
- several drugs increase PR interva
QRS will widen if
conduction through ventricles is slowed
QT interval is prolonged by
prolonged by drugs that delay ventricular repolarization
ST segment
what drug depresses it
end of QRS to beginning of T
Digoxin depresses ST segment
2 causes of Dysrhythmias
1) Disturbances of impulse formation (automaticity)
2) Disturbances of impulse conduction
Causes of Dysrhythmias
(6)
hypoxia
electrolyte imbalance
cardiac surgery
reduced coronary blood flow,
myocardial infarction (MI)
antidysrhythmic drugs
disturbance of impulse formation
occur in cells capable of automaticity, but can occur in others that don’t express automaticity (contractile cells)
increased Purkinje fiber automaticity
- Common cause of dysrhythmias
Disturbances of impulse conduction
first degree block: impulse is delayed but NOT blocked
second degree block: some impulses go through but not others
Third degree block: all traffic through AV node stops
Re-entry (recirculating Activation)
mechanism that produces dysrhythmias
started by a self-sustaining circuit of repetitive cardiac stimulation
Re-entrant Activation
one-way conduction block
impulses can’t travel downward in Branch 1
BUT can travel upward in branch 1 (because muscle impulses are very strong)
Results: impulse travels up Branch 1, and then back down Branch 2
Process continues to repeat itself
= repetitive ectopic beats
Drug Effect I and II
I: eliminates block in branch 1
2: drug converts one-way block to a two-way block
4 groups of Antidysrhythmic Drugs
Class I: sodium channel blockers
class II: beta blockers
class III: potassium channel blockers
class iv: calcium channel blockers
class I drug function
sodium channel blockers
slows impulse conduction in atria, ventricles and His-Purkinje system
Class II function
Beta blockers
reduce calcium entry
= SA (reduce automaticity), AV (slow conduction), atria/ ventricle, reduces contractility
Class III function
Potassium Channel Blockers
delay repolarization
- prolong action potential and refractory period
Class IV function
calcium channel blockers
Verapamil/diltiazem/ same effects as Class II
–> reduce calcium entry
2 groups of dysrhythmias
1) Supraventricular (above ventricle)
2) Ventricular (more dangerous)
2 phases of treatment for dysrhythmias
1) dysrhythmia termination
- electrical countershock, drugs, or both)
followed by
2) long-term suppression with drugs
can also be treated with
-ICD: fxns as pacemaker and defibrillator
- destroying small areas of cardiac cells
Treatment for Supraventricular Dysrhythmias (SA)
arise in SA and AV node
only dangerous if results in increased rate of ventricular contraction
= ventricle filling imcomplete and CO reduced
Treatment: block impulse through AV node
- not by eliminating dysthymia itself
Drug Class II, Class IV, adenosine and digoxin
Treatment for Atrial Fibrillation
most common sustained dysrhythmia
- rapid random firing of atrial ectopic foci
- high risk of stroke (potential clot formation)
Treatment: beta blocker = restore normal rhythm or slow ventricular rate
Warfarin to prevent stroke
Sustained Supraventricular Tachycardia
due to AV node Re-entrant activation
= HR 200 bpm
Treatment: IV beta blocker or calcium channel blocker
Ventricular Dysrhythmias
LIFE threating emergency
Cause:
multiple ventricular ectopic foci firing
localized twitching takes place all over the ventricle
= coordinated contraction IMPOSSIBLE
Result:
loss of consciousness and tissue become CYANOTIC/ DEATH soon follows
Treatment:
Immediate defibrillation
Amiodarone
Ventricular Tachycardia
Arise from SINGLE rapid firing ectopic focus
- generally location of an old infarction
Long-term Treatment:
ICD
Amiodarone
Torsades de Pointes
potentially fatal dysrhythmia due to PROLONGATION OF QT INTERVAL
Treatment
Class I or III drugs
Class I : Sodium Channel Blockers drug name
Quinidine
source: natural source from bark of Cichona Tree
Mechanism of Class 1: Sodium Channel Blockers
Blocking Na+ channels
= widening of QRS by slowing ventricle depolarization and increase QT (delays repolarization
Class I Adverse Effects
Diarrhea: immediate and intense
- can result in treatment being discontinued
Cardiotoxicity:
high conc. of quinidine = disrupt ventricle contractions
Class I Drug Interactions
Quinidine can double Digoxin levels
Class II Drug Interactions
Propranolol
Class II mech of action
beta blockers act on calcium channels
blocks beta1 (heart) and beta2 receptors (lungs)
decreases SA node automaticity
Decreased AV node conduction
Decreases myocardial contractility
Prolongs PR interval
Class II Therapeutic Use
treating dysrhythmias caused by excessive Sympathetic NS stimulation
Adverse Effects
Heart: cause heart failure, AV block
Lungs: asthma pts can cause bronchospasm
Class III drug name
Amiodarone
Class III mechanism
delay repolarization in fast potentials (SA, AV)
Prolonged action potential duration and QT interval
Class III therapeutic Use
effective against atrial and ventricle dysrhytmias
-serious toxicities
PO and IV
Class III Adverse Effects
Lung damage main concern in high-dose, long-term patients, visual impairment
still frequently used
Class IV drug name
Verapamil and Diltiazem
Class IV mechanism of action
Slow ventricular rate in atrial fibrillation patients
IV: effects in minutes
Class IV adverse effects
bradycardia
av block
heart failure
Class IV drug interactions
Elevate Digoxin levels
- digoxin toxicity
Other antidysrhythmic drugs
Adenosine
Digoxin
Adenosine
drug choice for Supraventricular Dysrhythmias (SRV)
Mechanism
inhibition of cAMP-induced calcium influx
= decreased automaticity in SA node and slows conduction through AV node
IV
Digoxin
Primary indication is heart failure
suppresses dysrhythmias by decreasing automaticity of AV node and conduction through AV node
adverse effects: dysrhythmias
