Cardiac Arrhythmias 1 Flashcards

1
Q

What is a Cardiac Arrhythmia

A

Cardiac arrhythmias (dysrhythmias) are disturbances in cardiac rhythm, including abnormalities in the site of origin, rate, or conduction of the cardiac impulse, disrupting normal activation in the atria or ventricles.

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2
Q

What are the 2 mechanisms behind arrhythmias?

A

Arrhythmias result from either abnormal impulse generation/initiation, abnormal impulse conduction, or both.

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3
Q

How are arrhythmias classified based on the origin of the abnormal impulse?

A

Arrhythmias are classified as:

Supraventricular: Originating in the SA node, atria, or AV node.
Ventricular: Originating in the His-Purkinje system or ventricles.

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4
Q

What are tachyarrhythmias and bradyarrhythmias?

A

Tachyarrhythmias: Arrhythmias with an increased heart rate.

Bradyarrhythmias: Arrhythmias with a decreased heart rate.

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5
Q

What are the 3 subtypes of tachyarrhythmias?

A

Tachyarrhythmias include:
Tachycardia: Sustained run of regular premature beats.
Flutter: Very rapid, regular premature beats.
Fibrillation: Rapid, irregular, and chaotic depolarizations.

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6
Q

List specific types of arrhythmias

A

Common arrhythmias include:

Ventricular Premature Contractions (PVCs)
Ventricular Tachycardia (VT)
Ventricular Fibrillation (VF)
Atrial Flutter
Atrial Fibrillation (AF)

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7
Q

What are the primary causes of cardiac arrhythmias?

A

Causes include:
Ischemia, hypoxia, and acidosis
Electrolyte abnormalities: Mainly K+, Mg++, and Ca++ imbalances.
Heart tissue changes: Infarction, fibrosis, structural abnormalities.
Genetic mutations: e.g., Long QT Syndrome.
Drug toxicity: e.g., digoxin toxicity.
Enhanced autonomic influences: Sympathetic or parasympathetic.

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8
Q

3 Things commonly associated with Arrhythmias

A
  • Drug Therapy - 25% of patients on digitalis
  • Anaesthetic Use - 50% of patients
  • Heart Disease - 80% of patents
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9
Q

What are possible clinical consequences of arrhythmias?

A

Consequences depend on arrhythmia frequency, duration, impact on cardiac/vital organ function, and underlying heart disease. They may range from being asymptomatic, symptomatic (dizziness, palpitations, syncope), to lethal (cardiac arrest, sudden death).

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10
Q

Describe abnormal impulse generation mechanisms in arrhythmias

A

Mechanisms include:
- Altered normal automaticity: Changes in the rate of firing of normal pacemaker cells.
Enhanced automaticity: Leads to tachyarrhythmias.
Depressed automaticity: Leads to bradyarrhythmias.

  • Abnormal automaticity: Spontaneous firing of partially depolarized cells, often in atrial or ventricular muscle or Purkinje fibers. (MDP -50mV) Also involve generation of slow type cardiac action potentials
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11
Q

What is triggered activity in cardiac arrhythmias?

A

Triggered activity refers to abnormal impulses resulting from a previous normal impulse, occurring as either:

Early Afterdepolarizations (EADs): Depolarisations occur before full repolarization of the initiating impulse
Delayed Afterdepolarizations (DADs): Depolarisations occur after full repolarization of the initiating impulse

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12
Q

Describe the 2 types of abnormal impulse conduction in arrhythmias

A

Conduction block: Occurs between the sinus node and atria, or within the AV node/His-Purkinje system.

Reentrant mechanisms: A cardiac impulse repeatedly excites the same region due to:
-slow conduction
-unidirectional conduction block
(often causing continuous arrhythmic loops)

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13
Q

Diagram of reenterant mechanisms

A
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14
Q

What are the general principles of arrhythmia management and the 3 criteria for treatment?

A

Consideration of risks and benefits: Treatments may have adverse effects.

3 Criteria for treatment: Treatment is needed if the arrhythmia causes severe hemodynamic failure, predicts/instigates serious or lethal arrhythmias, or causes significant distress.

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15
Q

What are the 5 C’s for arrhythmia management?

A

Causes: Treat/remove underlying causes.
Coagulation: Anticoagulation to prevent stroke.
Cardioversion: Convert heart to a normal sinus rhythm.
Control: Managing ventricular rate to maintain adequate CO.
Cure: Permanently terminate the arrhythmia.

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16
Q

Describe the pharmacological and the 3 non-pharmacological treatment options for arrhythmias.

A

Pharmacological: Antiarrhythmic drugs (Classes I-IV), digoxin, adenosine, magnesium, etc.

Non-Pharmacological:
1) Non-Surgical Procedures - RF catheter ablation, DC cardioversion/defibrillation
2) Medical Devices - pacemakers, ICDs
3) Surgical Procedures - Maze procedure

17
Q

What are the 3 mechanisms to supress Arrhythmias?

A

1) Inhibition of inward/depolarizing currents:
- Blocking voltage-gated Na+ and Ca+ channels to prevent rapid influx.
2) Prolonging the effective refractory period (ERP):
- Blockade of K+ channels to delay outward/repolarising currents
3) Inhibiting sympathetic effects autonomic effects on heart:
- Beta Adrenoceptor blockade

18
Q

Summarize the Vaughan Williams Classification of antiarrhythmic agents.

A

Class I: Na+ Channel Blockers
-Inhibit/block fast voltage-gated Na+ channels (e.g., lidocaine, encainide).
Class II: Beta-blockers
-Inhibit/block adrenergic activity in the heart (e.g., atenolol, metoprolol).
Class III: K+ channel blockers
-delay action potential repolarisation and inc ERP (e.g., amiodarone, d-sotalol).
Class IV: Ca++ channel blockers
-Inhibit/block slow voltage-gated Ca channels (e.g., verapamil, diltiazem).

19
Q

Explain the Harrison-Campbell sub-classification of Class I agents.

A

Class IA:
- moderate inhibition of fast voltage-gated Na channel
- prolong repolarisation (prolong APD)
- moderately slow binding-unbinding kinetics
Class IB:
- mild inhibition of fast voltage-gated Na channel
- (marked inhibition in depolarised myocardial cells)
- accelerate repolarisation (shorten APD)
- rapid binding-unbinding kinetics
Class IC:
-marked inhibition of fast voltage-gated Na channel
- little or no effect on repolarisation / APD
- slow binding-unbinding kinetics

20
Q

Diagram of Class 1a vs 1b vs 1c of Antiarrhythmic Agents

A
21
Q

What are the different drugs for each of the sub-classifications of Class 1 antiarrhythmic drugs

A

Class IA:
- Disopyramide
- Quinidine
- Procainamide
Class IB:
-Lidocaine
- Mexiletine
- Tocainide
- Phenytoin
Class IC:
- Flecainide
- Encainide
- Propafenone