Drugs Affecting Cardiac Rhythm

Normal duration of PR interval

120-200 ms

Normal duration of QRS interval

60-100 ms

abnormal if above 120 ms

Normal duration of QT interval

~400 ms

abnormal if below 390 or above 450

a prolonged PR interval is a red flag for

AV conduction issues

A prolonged QT interval is a red flag for

arrhythmia risk (Torsades de pointes)

These classes of antiarrhythmias are mainly for rhythm control// restoring normal sinus rhythm and often lead to what change in the ECG?

• Class I (Na+ blockers)

• Class III (K+ blockers)

widen QT interval

These classes of antiarrhythmias are mainly for rate control// restoring normal sinus rhythm and often lead to what change in the ECG?

• Class II (Beta-blockers)

• Class IV (Ca2+ blockers)

• Digoxin

affect the PR interval

Common side effects of Class I antiarrhythmics

proarrhythmic risk

• quinidine —> cinchonism

• Torsades de pointes

• procainamide —> Lupus-like symptoms

Common side effects of Class II antiarrhythmics

• Bradycardia

• bronchospasm

• fatigue

Common side effects of Class III antiarrhythmics

• Amiodarone → pulmonary toxicity

• thyroid dysfunction

• hepatotoxicity

• blue skin

Common side effects of Class IV antiarrhythmics

• heart block

• hypotension

Common side effects of Adenosine as an antiarrhythmic

• transient asystole

• flushing

• chest discomfort

Common contraindications of Class I antiarrhythmics

Avoid class IC (flecainide) in structural heart disease (e.g. heart failure)

Common contraindications of Class II antiarrhythmics

avoid in:

• asthma

• severe bradycardia

Common contraindications of Class III antiarrhythmics

Should be avoided in severe lung disease like COPD (e.g. avoid Amiodarone)

Common contraindications of Class IV antiarrhythmics

avoid in:

• heart failure

• high-degree AV block

(Ca+ channel blockers selectively affect SA nodal tissue)

Amiodarone has a ______ T1/2 (half-life) such that the patient should _________

LONG (20-100 days); be continuously monitored

Adenosine has a _______ T1/2 (half-life) such that the patient should ________

SHORT (<10 sec); rapidly metabolize the drug

Quinidine (IA):

Oral Bioavailability:

T1/2:

Metabolism/Clearance:

Oral Bioavailability: ~80%

T1/2: 6-8 hrs

Metabolism/Clearance: Hepatic metabolism (CYP3A4)

Lidocaine (IB):

Oral Bioavailability:

T1/2:

Metabolism/Clearance:

Oral Bioavailability: IV → 100% bioavailable

T1/2: 1-2 hrs

Metabolism/Clearance: Hepatic clearance

Flecainide (IC):

Oral Bioavailability:

T1/2:

Metabolism/Clearance:

Oral Bioavailability: ~90%

T1/2: 12-20 hrs

Metabolism/Clearance: Hepatic/Renal Clearance

Metoprolol (II)

Oral Bioavailability:

T1/2:

Metabolism/Clearance:

Oral Bioavailability: ~50%

T1/2: 3-7 hrs

Metabolism/Clearance: Hepatic Metabolism

Verapamil (IV):

Oral Bioavailability:

T1/2:

Metabolism/Clearance:

Oral Bioavailability: ~20-35% (LOW)

T1/2: 3-7 hrs

Metabolism/Clearance: Hepatic Metabolism

Digoxin:

Oral Bioavailability:

T1/2:

Metabolism/Clearance:

Oral Bioavailability: ~70-80%

T1/2: 30-48 hrs

Metabolism/Clearance: N/A

Class IA drugs are for rhythm control in _____________ arrhythmias. An example is _________ for A-fib

Atrial/Ventricular; quinidine

Class IB drugs are for rhythm control in _____________ arrhythmias. Some examples are _________ and _________, usually post-MI

Ventricular; Lidocaine, Mexilitine

Class IC drugs are for rhythm control in _____________ arrhythmias and sustained ventricular tachycardia. An example is _________ for paroxysmal A-fib

Supraventricular arrhythmias; flecainide

Class ID drugs are for rhythm control to suppress ____________, an example is the drug ________

V-Tach; Ranolazine

Class II/IV drugs are for rate control in _______ (arrhythmia type). Examples are _________ and __________

A-Fib; metoprolol and diltiazem

Class III drugs are for rhythm control in _____________ arrhythmias. An example is _________

A-fib/VT; amiodarone

drug that can treat acute SVT

adenosine

drug that slows AV nodal conduction for Afib

Digoxin/Magnesium

Ivabradine (class 0) targets _______________ (arrhythmia/dysfunction) by selectively blocking the If “funny” currents in the SA node

Sinus Tachycardia

Ranolazine (class Id) targets _____________ (arrhythmia/dysfunction) by inhibiting the late inward sodium current (INa,L) - prevents Ca+ overload —> QT prolongation and risk of torsades

Chronic Angina

Adenosine (class IIe) targets _____________ (arrhythmia/dysfunction) by acting as an A1 receptor agonist hyperpolarizing the AV node and causing a transient therapeutic asystole

Acute SVT

Digoxin (class IId) targets _____________ (arrhythmia/dysfunction) by inhibiting Na+/K+ ATPase and enhancing central vagal tone

A-Fib for rate control thereof

Magnesium sulfate (unclassified) targets _____________ (arrhythmia/dysfunction) by blocking Ca+ (naturally) and therefore suppressing early afterdepolarizations

Torsades de Pointes and digitalis-induced arhythmias

Class I antiarrhythmics serve as

sodium channel blockers

target Atrial and Ventricular Muscle (His-Purkinje Fibers)

Class II antiarrhythmics serve as

Beta Receptor Blockers

target SA and AV nodal cells

Class III antiarrhythmics serve as

Potassium Channel Blockers

target AP repolarization - blocking it to extend the QT interval

Class IV antiarrhythmics serve as

Calcium Channel Blockers (Non-Dihydropyridines)

target: SA and AV nodal cells (should not be used in combo w/ Class II (Beta Blockers))

Class Ia

(intermediate)

Class Ib

(rapid)

Class Ic

(slow)

Types of SVT arrhythmias

• A-Fib/Flutter

  • commonly associated with heart block, 50-250 bpm

  • atria quiver

  • can lead to formation of blood clots in the atria

• AVNRT (AV nodal reentrant tachycardia) —> e.g. WPW syndrome

• AVRT (AV reentrant tachycardia) —> often mimics V-tach

• Junctional Tachycardia —> often seen in digitais toxicity or heart block

indicates a 1st degree heart block

prolongation of PR interval

indicates a 2nd degree heart block

intermittent failure of atrial impulses, dropping of QRS complexes

indicates a 3rd degree heart block

total electrical dissociation between the atria and ventricles

hypokalemia results in ________________ of the heart whereas hyperkalemia results in ___________ of the heart

uncontrolled acceleration of activity; stopping (inactivated Na+ channels due to sustained depolarization)