Drugs used in Cardiac Arrythmias Flashcards
(53 cards)
<p>What are the Class 1A Sodium Channel Blocking drugs?</p>
<p>– Quinidine – Procainamide – Disopyramide</p>
<p>What are the class 1B Sodium blocking drugs</p>
<p>Lidocaine
Mexiletine</p>
<p>What are the class 1C drugs</p>
<p>Flecainide
Propafenone</p>
<p>What are the class 2 Beta blockers?</p>
<p>Esmolol
Propranolol</p>
<p>what are the class 3 Potassium channel blocking drugs</p>
<p>Amiodarone – Sotalol – Dofetilide – Ibutilide</p>
<p>What are the class 4 cardioactive calcium channel blockers</p>
<p>–
Verapamil
–
Diltiazem</p>
<p>what are the Miscellaneous agents for antiarrhythmic drugs</p>
<p>Adenosine</p>
<p>what are the phases is the fast action potential in cardiac muscle</p>
<p>Phase 0: voltage dependent fast Na + channels open
as a result of depolarization; Na enters the cells
down its electrochemical gradient
Phase 1: K + exits cells down its gradient, while fast
Na + channels close, resulting in some repolarization
Phase 2: plateau phase results from K + exiting cells
offset by and Ca 2+ entering through slow voltage
dependent Ca 2+ channels
Phase 3: Ca 2+ channels close and K + begins to exit
more rapidly resulting in repolarization
Phase 4: Resting membrane potential is gradually
restored by Na ++/K + ATPase and the Na ++/Ca 2+
exchanger</p>
<p>what are the phases of the Pacemaker Action potential</p>
<p>Phase 4: Slow spontaneous depolarization
-Poorly selective ionic influx (Na ++, K ++) known as pacemaker
current (Funny current, I f ) activated by hyperpolarization
-Slow Ca 2+ influx [via T type transient )
Phase 0: Upstroke of Action Potential
–Ca 2+ influx through the relatively slow L type ( long acting )
Ca 2+ channels
Phase 3 : Repolarization
–Inactivation of calcium channels with increased K efflux</p>
<p>Mechanism of action for Class 1A drugs</p>
<p>Block sodium channels
- reduce slope of phase 0
- prolong QRS of the ECG
BLock Potassium channels
- prolong the action potential duration
- prolong the QT interval</p>
<p>Procainamide characteristics: clinical use and adverse effects</p>
<p>Class 1A sodium channel blocker
Is effective in sustained ventricular tachycardias and
arrhythmias associated with myocardial infarction (not a
first choice drug for these indications)
Adverse effects:
•QT interval prolongation and induction of torsade de
pointes arrhythmias and syncope
•Lupus erythematosus syndrome with arthritis, pleuritis,
pulmonary disease, hepatitis and fever
•Hypotension</p>
<p>Quinidine Characteristics: Clinical and adverse effects</p>
<p>Class 1A drug sodium channel blocker
Natural alkaloid from Cinchona bark
•Affords antimuscarinic effect on the heart may enhance AV
conductance
•May cause hypotension tachycardia
•Rarely used because of cardiac and extracardiac adverse
effects and the availability of better tolerated antiarrhythmic
drugs
Adverse effects
•
Cardiac:
–QT interval prolongation and induction of torsade de
pointes arrhythmia and syncope
–GI side effects (diarrhea, nausea, vomiting)
–Tinnitus, hearing loss, confusion, delirium, disturbances
in vision, and psychosis (known as cinchonism
–Thrombocytopenia, hepatitis, fever</p>
<p>Disopyramide: Characteristics and clinical and adverse effects</p>
<p>Class 1A drug Sodium channel blocker
Affords strong antimuscarinic effect on the heart
Clinical use
•Recurrent ventricular arrhythmias
Adverse effects
•QT interval prolongation and induction of torsade de
pointes arrhythmia and syncope
•Negative inotropic effect may precipitate heart failure
•Atropine like symptoms tachycardia, urinary
retention, dry mouth, blurred vision, constipation,
exacerbation of glaucoma</p>
<p>Mechanism of action of Class 1B drugs</p>
<p>BLock sodium channels specifically sodium channels
Do not block potassium channels
-shorten action potential</p>
<p>Lidocaine characteristics, clinical use and adverse effects</p>
<p>Class 1B drug (sodium channel blocker)
Extensive first pass metabolism used only by the
intravenous route
Clinical use
•Termination of ventricular tachycardia in the setting
of acute myocardial ischemia
Adverse effects
•The least toxic of all Class 1 drugs, proarrhythmic
effects are uncommon
•May cause hypotension in patients with heart
failure by inhibiting cardiac contractility
•Neurological side effects: paresthesias, tremor,
slurred speech, convulsions</p>
<p>Mexiletine characteristics clinical use and adverse effect</p>
<p>Class 1B sodium blocker – Orally active congener of lidocaine – Electrophysiological and antiarrhythmic effects are similar to lidocaine
Clinical use
•Ventricular arrhythmias
•To relieve chronic pain, especially pain due to
diabetic neuropathy and nerve injury
– Adverse effects •Tremor •Blurred vision •Nausea •Lethargy</p>
<p>Mechanism of action of Class 1C drugs</p>
<p>BLock sodium channels and certain potassium channels
does not prolong action potential duration and QT interval
does prolong the QRS interval</p>
<p>Flecaninide characteristics and adverse effects</p>
<p>Class 1C drug sodium channel blocker
•In patients with otherwise normal hearts who have
supraventricular arrhythmias
•Refractory ventricular arrhythmias that are life
threatening
–Adverse effects
•May cause severe exacerbation of ventricular
arrhythmias when administered to
–Patients with preexisting ventricular
tachyarrhythmias
–Patients with a previous myocardial infarction
–Patients with ventricular ectopic rhythms</p>
<p>Propafenone characteristics, adverse effects, clinical use</p>
<p>–Sodium channel blocking kinetics is similar to
flecainide
–Possesses weak beta blocking activity
Clinical use: Supraventricular arrhythmias in patients without
structural disease
Adverse effects: Exacerbation of ventricular arrhythmias (similar
to flecainide)</p>
<p>Mechanism of action of class 2 Beta blockers</p>
<p>Decrease HR via the Sinoatrial Node
- increased RR interval
- decreased slope due to effects on If and T type Ca channels
Decrease AV conductance on the AV node
-increased PR interval (increased threshold of L-type Ca channels)</p>
<p>Propranolol characteristics and clinical use</p>
<p>–Clinical use of propranolol in cardiac arrhythmias
•Arrhythmias associated with stress and thyroid
storm
•Atrial fibrillation and flutter
•Paroxysmal supraventricular arrhythmias
•Arrhythmias associated with MI (decrease mortality
in patients with MI)</p>
<p>Esmolol characteristics and clinical use</p>
<p>– Short acting selective beta 1 blocker – Half life is 10 min, due to hydrolysis by blood esterases – Used as a continuous i.v. infusion, with rapid onset and termination of its action
–
Clinical use
•Supraventricular arrhythmias
•Arrhythmias associated with thyrotoxicosis
•Myocardial ischemia or acute myocardial infarction
with arrhythmias
•As an adjunct drug in general anesthesia to control
arrhythmias in perioperative period</p>
<p>what are the adverse effects of Beta blockers</p>
<p>– Reduced cardiac output – Bronchoconstriction – Impaired liver glucose mobilization – Produce an unfavorable blood lipoprotein profile (increase VLDL and decrease HDL) – Sedation, depression – Withdrawal syndrome associated with sympathetic hyperresponsiveness</p>
<p>what are the contraindications to the use of Beta blockers</p>
<p>– Asthma – Peripheral vascular disease – Raynaud’s syndrome – Type 1 diabetics on insulin – Bradyarrhythmias and AV conduction abnormalities – Severe depression of cardiac function</p>
what is the MOA of Class 3 drugs for arrhythmias?
block potassium channels -prolongs the action potential Prolongs the QT interval -due to prolonging the refractory period
Amiodarone Characteristics and clinical use
– Pharmacodynamics •Blocks potassium channels •Prolongs QT interval and APD uniformly over a wide range of heart rates •Blocks inactivated sodium channels •Possesses adrenolytic activity •Has calcium channel blocking activities •Causes bradycardia and slows AV conduction ``` Clinical use: - Recurrent ventricular tachycardia - Atrial fibrillation
Adverse effects of Amiodarone
•AV block and bradycardia •Incidence of torsade de pointes is low as compared to other Class 3 drugs •Fatal pulmonary fibrosis •Hepatitis •Photodermatitis, deposits in the skin, gives blue grey skin discoloration in sun exposed areas •Deposits of drug in cornea and other eye tissues, optical neuritis •Blocks the peripheral conversion of thyroxine to triiodothyronine, also a source of inorganic iodine in the body may cause hypo or hyperthyroidism
Sotalol: characteristcs, clinical use, and adverse effets
– Class 2 (non selective beta blocker) and class 3 agent (prolongs APD) ``` Clinical use •Treatment of life threatening ventricular arrhythmias •Maintenance of sinus rhythm in patients with atrial fibrillation Adverse effects •Depression of cardiac function •Provokes torsade de pointes
Dofetilide, Ibutilide: charaacteristics, clinical use, and adverse effects
Class 3 drug that blocks potassium channel –Specifically block rapid component of the delayed rectifier potassium current Clinical use •Restore sinus rhythm in patients with atrial fibrillation •Maintain the sinus rhythm after cardioversion in patients with atrial fibrillation ( dofetilide Adverse effects •QT interval prolongation and increased risk of ventricular arrhythmias
what is the Mechanism of action of Class 4 drugs for arrythmias?
– Block L type calcium channels Active in cells exhibiting pacemaker potential •Decrease the slope of phase 0 depolarization •Increase L type Ca 2+ channel threshold potential –Slow sinoatrial node depolarization to reduce heart rate –Prolong conduction time and refractory period in AV node
Verapamil, Diltiazem clinical use and adverse effects
CLass type 4 : L type calcium channel blocker– Clinical use •Termination and prevention of paroxysmal supraventricular tachycardia •Ventricular rate control in atrial fibrillation and flutter ``` Adverse effects •Cardiac –Negative inotropy –AV block –Sinoatrial node arrest –Bradyarrhythmias –Hypotension •Extracardiac –Constipation (Verapamil)
```MOA of Adenosine
Activates A1 adenosine receptor via Gi coupled GPCR enhances potassium current and inhibits Ca channel and funny channels to hyperpolarize and suppress the AP of pacemaker cells inhibit AV conduction and increase AV nodal refractory period
Clinical use and adverse effects of Adenosine
Clinical use •Conversion to sinus rhythm in paroxysmal supraventricular tachycardia (given intravenously to provide rapid relief) ``` Adverse effects •Shortness of breath •Bronchoconstriction (both A 1 and A 2B adenosine receptors cause bronchoconstriction) •Chest burning •AV block •Hypotension
```what does Proarrythmia mean?
is a drug that induces a significant new arrhythmia or worsens and already existing arrhythmia
what are 4 non pharmacological approaches to treatment of cardiac arrhythmias
–Catheter ablation –Implantable cardioverter defibrillator –Artificial cardiac pacemaker –Direct current cardioversion
Class 1A and Class 3 drugs can trigger what fatal arrhythmias?
Excessive slowing of repolarization leading to torsades de pointes
Class 1A and 1C drugs can cause what fatal arrhythmias?
excessive slowing of conduction leading to persistent ventricular tachycardias
What can Atrial fibrillation cause?
organized atrial contraction is lost leading to reduced ventricular filling leading to - Fatigue weakness, and decreased excerise tolerance - hypotension - Pulmonary congestion - Exacerbation of heart failure
what is the MOA of atrial fibrillation?
Reentry circuit that means an impulse reenters and excites the area of the heart more than once -due to: - There must be an obstacle to homogeneous conduction that will contribute to the formation of a circuit – There must be a unidirectional block at some point of the circuit – Conduction time around the circuit must exceed the effective refractory period
what is the rhythm control of Afib
Direct current cardioversion Chemical cardioversion using specific antiarrhythmic drugs ``` Class 1C agents will effectively block fast Na channel to selectively reduce retrograde conduction through damaged tissue to terminate reentry ``` ``` Class 3 agents will block K channels to keep cells in their refractory period to terminate reentry
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