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In contrast to skeletal muscle, which contracts
only when it receives a stimulus, the heart
contains specialized cells that exhibit
automaticity. ““pacemaker” cells “
Ventricular VS.
SA node (pace-maker) action potential
Cardiac muscle action potential
Class I (sodium channel blockers)
IA : Quinidine IB : lidocaine
• Adverse effects:
• Quinidine:
-arrhythmia (k + channel block)
-cinchonism
• Lidocaine:
- wide therapeutic index
- CNS effects
Mechanism of action:
-Several studies have cast serious doubts on the safety of
the class IC drugs, particularly in patients with structural
heart disease.
- Flecainide:
-generally well tolerated
- blurred vision, dizziness, and nausea
- Propafenone:
-similar side effect profile
-may cause bronchospasm due to its β-blocking effects
Adverse effects
Class II : B- blockers (ex: metoprolol)
Mechanism of action:
CLASS III ANTIARRHYTHMIC DRUGS:
Amiodarone
Mechanism of action:
Digoxin
inhibits the Na+/K+-ATPase pump, ultimately shortening the refractory
period in atrial and ventricular myocardial cells while prolonging the
effective refractory period and diminishing conduction velocity in the
AV node.
Bradycardia:
A slow ventricular rate, usually defined as <60bpm, but may be
absolute (<40bpm) or relative
-If asymptomatic and rate >40bpm, no treatment is required.
-If rate <40bpm or patient is symptomatic:
Follow the next algorithm
Tachyarrhythmias
Narrow complex
ECG shows rate of
>100bpm and QRS
complex duration of
<120ms
Wide complex
ECG shows rate of >100
and QRS complexes
>120ms (>3 small
squares).
• Vagal maneuvres
• Adenosine (DOC)
• Verapamil - B- blocker
Carotid sinus massage and IV adenosine transiently block the AV node
and may unmask flutter waves.
Cardioversion may be indicated (anticoagulate before). Anti-AF drugs
may not work—but consider amiodarone to restore sinus rhythm, and
amiodarone or sotalol to maintain it. Aim to control rate as above; if
the IV route is needed, a b-blocker is preferred.
Ventricular extrasystoles (ectopics)
- the commonest post-MI arrhythmia.
- Post-MI they suggest electrical instability, and the risk is VF
if the ‘R on T’ pattern (ie no gap before the T wave) is seen.
- If frequent (>10/min), consider amiodarone IV as above.
Otherwise, just observe patient.
Antiarrhythmic drugs

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Antiarrhythmic drugs

  • 1.
  • 2. In contrast to skeletal muscle, which contracts only when it receives a stimulus, the heart contains specialized cells that exhibit automaticity. ““pacemaker” cells “
  • 3. Ventricular VS. SA node (pace-maker) action potential
  • 5.
  • 6.
  • 7. Class I (sodium channel blockers) IA : Quinidine IB : lidocaine • Adverse effects: • Quinidine: -arrhythmia (k + channel block) -cinchonism • Lidocaine: - wide therapeutic index - CNS effects Mechanism of action:
  • 8.
  • 9. -Several studies have cast serious doubts on the safety of the class IC drugs, particularly in patients with structural heart disease. - Flecainide: -generally well tolerated - blurred vision, dizziness, and nausea - Propafenone: -similar side effect profile -may cause bronchospasm due to its β-blocking effects Adverse effects
  • 10. Class II : B- blockers (ex: metoprolol) Mechanism of action:
  • 11. CLASS III ANTIARRHYTHMIC DRUGS: Amiodarone Mechanism of action:
  • 12.
  • 13.
  • 14.
  • 15. Digoxin inhibits the Na+/K+-ATPase pump, ultimately shortening the refractory period in atrial and ventricular myocardial cells while prolonging the effective refractory period and diminishing conduction velocity in the AV node.
  • 16.
  • 17. Bradycardia: A slow ventricular rate, usually defined as <60bpm, but may be absolute (<40bpm) or relative -If asymptomatic and rate >40bpm, no treatment is required. -If rate <40bpm or patient is symptomatic: Follow the next algorithm
  • 18.
  • 19. Tachyarrhythmias Narrow complex ECG shows rate of >100bpm and QRS complex duration of <120ms Wide complex ECG shows rate of >100 and QRS complexes >120ms (>3 small squares).
  • 20.
  • 21. • Vagal maneuvres • Adenosine (DOC) • Verapamil - B- blocker
  • 22.
  • 23. Carotid sinus massage and IV adenosine transiently block the AV node and may unmask flutter waves. Cardioversion may be indicated (anticoagulate before). Anti-AF drugs may not work—but consider amiodarone to restore sinus rhythm, and amiodarone or sotalol to maintain it. Aim to control rate as above; if the IV route is needed, a b-blocker is preferred.
  • 24.
  • 25.
  • 26.
  • 27.
  • 28. Ventricular extrasystoles (ectopics) - the commonest post-MI arrhythmia. - Post-MI they suggest electrical instability, and the risk is VF if the ‘R on T’ pattern (ie no gap before the T wave) is seen. - If frequent (>10/min), consider amiodarone IV as above. Otherwise, just observe patient.