Arrhythmias

Question 1

What is a first-degree atrioventricular block (AV) block?

Answer 1

First-degree atrioventricular (AV) block is a bradyarrhythmia characterized by abnormally slow conduction through the AV node that is defined by ECG changes that include a PR interval of greater than 200 ms without disruption of atrial to ventricular conduction, i.e. each P wave is followed by a QRS complex. First-degree atrioventricular block is benign.

Question 2

What is second-degree atrioventricular block Mobitz Type 1 (Wenckebach)?

Answer 2

In second-degree atrioventricular block Mobitz Type 1 (Wenckebach) there is a progressive prolongation of the PR interval until eventually an atrial impulse is completely blocked. When an atrial impulse is completely blocked there will be a P wave without a QRS complex.

This type of atrioventricular block is physiologically mediated by the vagus nerve, and it occurs within the AV node.

Question 3

What is second-degree atrioventricular block Mobitz Type 2?

Answer 3

Second-degree atrioventricular block Mobitz Type 2 is a bradyarrhythmia characterized by a constant PR interval across the rhythm strip both before and after the non-conducted atrial beat. Each P wave is associated with a QRS complex until there is one atrial conduction of a P wave that is not followed by a QRS complex.

This type of atrioventricular block is pathologic and indicates that the site of conduction delay is at or below the level of the His bundle.

Second-degree atrioventricular block Mobitz Type 2 requires a pacemaker!

Question 4

What is third-degree atrioventricular block?

Answer 4

Third-degree atrioventricular block is a bradyarrhythmia characterized by a complete loss of communication between the atria and the ventricles. The rate of ventricular contraction does not exceed the rate of atrial contraction.

Third-degree atrioventricular block is almost always pathologic. Depending on the location of the block, the QRS complex might be a narrow morphology (junctional escape QRS complex) or a wide morphology (ventricular escape QRS complex).

Third-degree atrioventricular block almost always requires a pacemaker!

Question 5

What are the electrocardiographic characteristics of a left bundle branch block?

Answer 5

The criteria for a left bundle branch block to be diagnosed with an electrocardiogram are the following:

1) QRS duration > 120 ms (3 small boxes)
2) In V1 there is an absent R wave and a prominent S wave
3) In V6 there is a broad notched R wave

Question 6

What are the common causes of a left bundle branch block?

Answer 6

The common causes of a left bundle branch block include the following: degenerative fibrosis of the conduction system (Lenore or Lev disease), ischemic heart disease (e.g. anteroseptal MI) and dilated cardiomyopathy.

Question 7

What are the common causes of a right bundle branch block?

Answer 7

The common causes of a right bundle branch block include the following: degenerative fibrosis of the conduction system (Lenore or Lev disease), pulmonary embolus, right ventricle (RV) hypertrophy or cor pulmonale.

Question 8

What are the electrocardiographic characteristics of a right bundle branch block?

Answer 8

The criteria for a right bundle branch to be diagnosed with an electrocardiogram are the following:

1) QRS duration > 120 ms (3 small boxes)
2) In V1 and V2 there is an RSR’ wave
3) In V6 there is a wide, slurred S wave

Question 9

What is Torsade de Pointes?

Answer 9

Torsade de Pointes is pointes a rapid, unstable polymorphic ventricular tachycardia in which the QRS complexes appear to twist or shift electrical orientation around the isoelectric line of the electrocardiogram. It often occurs as a lifethreatening effect of electrolyte disturbances (such as hypomagnesemia or hypokalemia) or of a medication (such as quinidine, amiodarone, or a tricyclic antidepressant) that prolongs the Q-T interval but may also complicate congenital long QT syndromes. Intravenous magnesium sulfate may be used to treat this arrhythmia.

Question 10

What are the criteria to diagnose left ventricular hypertrophy (LVH) on electrocardiogram?

Answer 10

Diagnostic criteria for left ventricular hypertrophy (LVH) include one or more of the following:

Voltage Criteria:
R in aVL > 11 mm
R in I > 15 mm
S in V1 and R in V5 or V6 > 35 mm

Cornell Criteria:
S in V3 and R in aVL > 28 mm (men) or > 20 (women)

Question 11

What are the prototype drugs for Class 1A anti-arrhythmics, and what are the characteristics of these drugs?

Answer 11

The prototype drugs for Class 1A anti-arrhythmics are procainamide, quinidine and dysopyramide.

Mechanism: Moderate Na+ channel blockade, moderate K+ channel blockade

Therapeutic uses:
1) Atrial arrhythmias
2) Ventricular arrhythmias, especially reentrant and ectopic supraventricular tachycardia (SVT) and
ventricular tachycardia (VT)

Adverse effects:

All: Tosades de Pointes due to prolongation of the QT interval, thrombocytopenia

Quinidine: Cinchonism (eg, headache, tinnitus)

Procainamide: Systemic lupus erythematous (SLE)-like syndrome

Disopyramide: Heart failure

Question 12

What are the prototype drugs for Class 1B anti-arrhythmics, and what are the characteristics of these drugs?

Answer 12

The prototype drugs for Class 1B anti-arrhythmics are lidocaine, phenytoin, and mexiletine.

Mechanism: : Weak Na+ channel blockade

Therapeutic uses:
1) Acute ventricular arrhythmias (especially post myocardial infarction (MI))

Adverse Effects:

All: CNS stimulation/depression, cardiovascular depression

Question 13

What is the prototype drug for Class 1C anti-arrhythmics, and what are the characteristics of this drug?

Answer 13

The prototype drugs for Class 1C anti-arrhythmics are flecainide and propane one.

Mechanism: Strong Na+ channel blockade.

Therapeutic uses:
1) Supraventricular arrhythmias (SVT) including atrial fibrillation.

Adverse effects: Proarrhythmic, especially post-myocardial infarction (MI). Class 1C anti-arrhythmias are contraindicated in structural and ischemic heart disease.

Question 14

What is the prototype drugs for Class 2 anti-arrhythmics, and what are the characteristics of this drug?

Answer 14

The prototype drugs for Class 2 anti-arrhythmics are the beta-blockers metropolol, propranolol, esmolol, atenolol, timolol, and carvedilol.

Mechanism: Decrease sinoatrial (SA) and atrioventricular (AV) nodal activity by decreasing cAMP and decreasing Ca2+ currents

Therapeutic uses:
1) Slows atrioventricular (AV) nodal conduction and ventricular rate in atrial fibrillation and atrial flutter
2) May prevent atrioventricular nodal reentrant tachycardia (AVNRT) of atrioventricular reentrant tachycardia (AVRT) by slowing AV node conduction
3) May suppress ventricular tachycardia (VT)
4) Prolongs life in patients with systolic heart failure

Side Effects: Fatigue, depression, sexual dysfunction, bradycardia, hypotension

Question 15

What are the prototype drugs for Class 3 anti-arrhythmics, and what are the characteristics of these drug?

Answer 15

The prototype drugs for Class 3 anti-arrhythmics are amiodarone, ibutilide, dofetilide, and sotalol.

Mechanism: K+ channel blockade

Therapeutic uses:
1) Atrial fibrillation
2) Atrial flutter
3) Ventricular tachycardia

Adverse effects:

Amiodarone: Pulmonary fibrosis, hepatotoxity, hypothyroidism or hyperthyroidism, corneal deposit, blue/gray skin deposits resulting in photodermatitis), neurological effects, constipation, cardiovascular effects (bradycardia, heart block, heart failure).

Remember to check PFTs, LFTs, and TFTs when using amiodarone

Note that although amiodarone prolongs the QT interval, it is has very little risk of inducing torsades de pointes

Question 16

What is the prototype drug for Class 2, 3, 4 anti-arrhythmics, and what are the characteristics of this drug?

Answer 16

The prototype drug for Class 2, 3, 4 anti-arrhythmics is amiodarone.

Mechanisms of action (MOAs):
1) K+ channel blocker, prolongs QT interval
2) Beta-1 adrenergic receptor blocker
3) Calcium channel blocker

Therapeutic uses:

Amiodarone is the most effective drug to maintain sinus rhythm.

 1) Prevent atrial fibrillation and atrial flutter 
 2) Prevent or treat ventricular tachycardia 
 3) Treatment for cardiac arrest

Side Effects: QT prolongation, Torsades de Pointes, liver injury, Hypothyroidism, Hyperthyroidism, Interstitial lung disease, Corneal deposits, Blue skin discoloration

Question 17

What are the prototype drugs for Class 4 anti-arrhythmics, and what are the characteristics of these drugs?

Answer 17

The prototype drugs for Class 4 anti-arrhythmics are verapimil (nondihydropyridine) and diltiazem.

Mechanisms: Blocks calcium channels in pacemaker tissue (in the sinoatrial (SA) node and the atrioventricular (AV) node.

Therapeutic uses:
1) Control ventricular rate in atrial fibrillation and atrial flutter
2) May prevent atrioventricular nodal reentrant tachycardia (AVNRT) or atrioventricular reentrant tachycardia (AVRT)

Adverse effects: Constipation, flushing, edema, cardiovascular effects (heart failure, atrioventricular (AC) block, sinus node depression).

Question 18

What is the mechanism of action, the therapeutic uses, and the adverse effects of adenosine?

Answer 18

Mechanism: Interacts with A1 receptors on cardiac cells and activates K+ channels, increasing K+ conductance. Causes a transient conduction delay through the atrioventricular (AV) node

Therapeutic Use: Acute termination of paroxysmal supraventricular tachycardia (PSVT)

Adverse Effects: Heart block, transient asystole, bronchoconstriction, flushing (mast cell degranulation)

Note that adenosine is rapidly metabolized in the blood and tissues and has a very brief duration of action

Question 19

What is the mechanism of action, the therapeutic uses, and the side effects of digoxin?

Answer 19

Mechanism:

(1) Direct inhibition the Na+/K+-ATPase and indirect inhibition of the Na+/Ca2+ exchanger which leads to an increase in the. Intracellular concentration of Ca2+ and positive ionotropy

(2) Stimulation of the vagus nerves which decreased heart rate

Therapeutic uses:

(1) Heart failure (increases contractility)
(2) Atrial fibrillation (decreases conduction at the atrioventricular (AV) node and depresses the sinoatrial (SA) node

Adverse Effects: Cholinergic effects (nausea, vomiting, diarrhea), blurry yellow vision, atrial and ventricular arrhythmia, AV nodal block, hyperkalemia

Question 20

What is sick sinus syndrome?

Answer 20

Sick sinus syndrome is any of several diseases of the sinoatrial node of the heart in which the node fails to generate impulses appropriately, resulting in long pauses, bradycardia, or brady cardia alternating with tachycardia. It is an occasional cause of palpitations, breathlessness, or loss of consciousness.

Treatment: A pacemaker should be inserted. Anticoagulant therapy may be required to prevent thromboembolism.