B.26 Ventricular Arrhythmia Flashcards

1
Q

B.26 Ventricular Arrhythmia

define

A

A group of tachyarrhythmias that originate below the atrioventricular node.

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2
Q

B.26 Ventricular Arrhythmia

Types:

A
  • ventricular ectopics (premature ventricular contractions)
  • ventricular tachycardia (monomorphic or polymorphic)
  • ventricular flutter
  • ventricular fibrillation
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3
Q

B.26 Ventricular Arrhythmia

Premature ventricular beats

A

Premature ventricular beats are ectopic beats that originate from a ventricular source. They may occur due to conditions such as hypoxia, hyperthyroidism, or electrolyte imbalances.

Ectopic beat that originates from a ventricular focus

Due to hypoxia, hyperthyroidism, electrolyte abnormalitie

Premature, wide QRS complex that is not preceded by a P wave

Compensatory pause after the premature beat

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4
Q

B.26 Ventricular Arrhythmia

Premature ventricular beats ECG

A

These beats are characterized by a wide QRS complex that is not preceded by a P wave and are often followed by a compensatory pause after the ectopic beat.

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5
Q

B.26 Ventricular Arrhythmia

Premature ventricular beats

Etiology

A

Etiology

  • Idiopathic causes
  • Cardiovascular diseases (e.g., coronary artery disease, myocarditis)
  • Electrolyte imbalances (e.g., hypokalemia, hypomagnesemia)
  • Side effects of certain medications (e.g., digoxin, psychiatric drugs)
  • Caffeine and alcohol consumption
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6
Q

B.26 Ventricular Arrhythmia

Premature ventricular beats Classification

A

Classification

  • Monomorphic PVCs: Each PVC has the same configuration, indicating an identical origin.
  • Polymorphic PVCs: PVCs exhibit different configurations, signifying multiple foci.
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7
Q

B.26 Ventricular Arrhythmia

Premature ventricular beats Clinical

A

Clinical Features

  • Most patients are asymptomatic.
  • May experience a skipped beat.
  • If PVCs are frequent, they can lead to lightheadedness, dizziness, palpitations, or an irregular heartbeat.
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8
Q

B.26 Ventricular Arrhythmia

Premature ventricular beats DX

A

ECG Characteristics
- QRS duration ≥ 120 ms with a block-like morphology.
- PVCs often followed by a compensatory pause.
- Patterns of Arrhythmia
- Single PVC / Couplets: Two PVCs in a row.
- Bigeminy: One normal beat followed by one PVC.
- Trigeminy: One normal beat, one PVC, and then another normal beat.

PVCs are frequently identified during routine ECGs. Further evaluation is not typically necessary for asymptomatic patients.

Additional Procedures
- Only recommended for frequent, symptomatic PVCs.
- 24-hour Holter monitor.
- Exercise stress test.
- Echocardiography.

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9
Q

B.26 Ventricular Arrhythmia

Premature ventricular beats TX

A

Treatment

  • Most patients do not need treatment.
  • Address any underlying conditions (e.g., CAD, myocarditis).
  • Only intervene for frequent and significantly symptomatic PVCs:
  • Antiarrhythmic therapy (e.g., IV amiodarone).
  • Catheter ablation if antiarrhythmic therapy is ineffective.
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10
Q

B.26 Ventricular Arrhythmia

Ventricular tachycardia

A

Causes:
Coronary artery disease
Myocardial infarction
Structural heart diseas
ECG findings:
- Regular, rapid rhythm
- Wide QRS complexes (≥ 3 consecutive premature ventricular beats)
Monomorphic VT (most common): single QRS morphology
Polymorphic VT: multiple QRS morphologies
- AV dissociation (P waves may or may not be discernible

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11
Q

B.26 Ventricular Arrhythmia

Ventricular tachycardia Etiology

A
  • Cardiac Scars (often due to infarction; can also be iatrogenic or postoperative)
  • Conduction Disorders
  • Medications (e.g., digitalis, antiarrhythmics)
  • Drugs Associated with Long-QT Syndrome
  • Congenital Long-QT Syndrome
  • Acquired Long-QT Syndrome

Antiarrhythmics
- Class Ia (e.g., quinidine, disopyramide)
- Class III (e.g., sotalol, amiodarone)

  • Antibiotics (e.g., macrolides, fluroquinolones)
  • Antidepressants (most tricyclics and tetracyclics, lithium)
  • Antipsychotics (e.g., haloperidol)
  • Electrolyte Imbalances (hypokalemia, hypomagnesemia, hypocalcemia)
  • Ischemic Stroke or Intracranial Hemorrhage
  • Endocrine Disorders (e.g., hypothyroidism)
  • Eating Disorders (e.g., anorexia nervosa)
  • In rare cases, VT may occur in individuals with healthy hearts.
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12
Q

B.26 Ventricular Arrhythmia

Ventricular tachycardia Pathophys

A

Monomorphic VT (all QRS complexes appear similar)

  • Increased automaticity
  • Re-entry circuit

Polymorphic VT (varied QRS complexes)
- Caused by abnormal ventricular repolarization (e.g., long QT syndrome, drug toxicity, electrolyte abnormalities)

  • Decreased Cardiac Output
  • Asynchronous atrial and ventricular beats combined with rapid ventricular rhythm
  • Leads to reduced blood flow into the ventricle during diastole, resulting in hemodynamic compromise and symptoms such as syncope, myocardial infarction, and angina.
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13
Q

B.26 Ventricular Arrhythmia

Ventricular tachycardia Clinical

A

Clinical Features

  • Often asymptomatic, particularly in nonsustained cases.
  • Common symptoms of sustained VT may include:
  • Palpitations
  • Hypotension
  • Syncope

In more severe instances:
- Chest pain/pressure (often in conjunction with myocardial infarction)

  • Cardiogenic shock
  • Loss of consciousness
  • Progression to ventricular fibrillation
  • Sudden cardiac death
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14
Q

B.26 Ventricular Arrhythmia

Ventricular tachycardia : Torsade de pointes tachycardia

A

Torsades de Pointes

  • Polymorphic VT characterized by QRS complexes that seem to twist around the isoelectric line.
  • The most severe complication is the progression to life-threatening ventricular arrhythmia.
  • Cause: Prolonged QT interval due to congenital conditions, electrolyte imbalances, or medications.
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15
Q

B.26 Ventricular Arrhythmia

Ventricular tachycardia : Torsade de pointes tachycardia Acute TX

A
  • If hemodynamically unstable: Administer defibrillation.
  • If hemodynamically stable: Administer IV magnesium sulfate, beta-blockers, and consider a pacemaker.
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16
Q

B.26 Ventricular Arrhythmia
Ventricular tachycardia : Torsade de pointes tachycardia ECG

A

ECG Criteria
- Three or more consecutive premature ventricular beats (i.e., widened QRS).

  • Heart rate: > 120 bpm.
  • Duration:
  • Nonsustained: < 30 seconds
  • Sustained: > 30 seconds.

Morphology
- Monomorphic: All QRS complexes appear similar (identical origin).

  • Polymorphic: QRS complexes differ (multiple origins).
17
Q

B.26 Ventricular Arrhythmia

Ventricular tachycardia Torsade de pointes tachycardia DX

A
  • Holter Monitor: Useful for identifying intermittent VT that may not appear on a single ECG.
  • Patient-Activated Event Recorder: A wearable monitor that requires activation by the patient at the onset of symptoms.
  • Echocardiography: Provides insights into potential causes of VT (e.g., structural heart disease, prior MI) and serves as a valuable tool for evaluating VT.
18
Q

B.26 Ventricular Arrhythmia

Ventricular tachycardia Torsade de pointes tachycardia DDX

A

Supraventricular Tachycardia with Aberrancy (RBBB, LBBB, Wolf-Parkinson-White)
- It’s crucial to differentiate between SVT with aberrancy and VT, as treatment for both conditions differs and may influence the choice of hemodynamic agents (e.g., using AV-node blocking drugs in patients with SVT).

Signs Indicating SVT Rather Than VT:
- Age > 35 (high prevalence of prior heart disease)
- A history of prior heart disease or myocardial infarction
- AV dissociation, fusion beats, and capture beats

Signs Suggesting Bundle Branch Block in Prior ECG:
- Documentation of aberrant conduction

If there is any uncertainty regarding the diagnosis, assess the VT rhythm accordingly.

19
Q

B.26 Ventricular Arrhythmia

Ventricular tachycardia Torsade de pointes tachycardia intial TX

A

If the patient is hemodynamically unstable (hypotension, loss of consciousness):

VT → cardioversion

If VT is nonsustained → defibrillation

If the patient is hemodynamically stable:

Antiarhythmics: typically lidocaine, procainamide, or amiodarone

Cardioversion: if medical therapy fails

In all patients, investigate and address potential causes of VT, such as:

Electrolyte imbalances (e.g., hypokalemia) → correct any identified abnormalities

Consideration of QT prolongation and any offending medications, along with digoxin in cases of digoxin toxicity

20
Q

B.26 Ventricular Arrhythmia

Ventricular tachycardia Torsade de pointes tachycardia long Term TX

A

Implantable Cardioverter Defibrillator (ICD): the most effective therapy to reduce mortality; indicated in cases of VT that does not respond to other treatments.

Catheter Ablation

Antiarhythmics: typically Class I or III medications.

21
Q

B.26 Ventricular Arrhythmia

Ventricular fibrillation define

A

Ventricular Fibrillation (Ventricular Fibrillation and Ventricular Flutter)

Ventricular Fibrillation (VF or “V-fit”) is a life-threatening cardiac arrhythmia marked by chaotic, high-frequency contractions of the ventricles, leading to reduced cardiac output and hemodynamic collapse.

22
Q

B.26 Ventricular Arrhythmia

Ventricular fibrillation etiology

A
  • Underlying Cardiovascular Diseases
  • Most common: Coronary Artery Disease (CAD)
  • Other factors: Previous Myocardial Infarction (MI), myocarditis, cardiomyopathy, severe congestive heart failure (CHF), heart valve disease
  • Congenital Heart Defects
  • Example: Pulmonary Atresia
  • Electrophysiologic Disorders
  • Wolff-Parkinson-White Syndrome
  • Long-QT Syndrome, leading to Torsades de Pointes
23
Q

B.26 Ventricular Arrhythmia

Ventricular fibrillation pathophys

A

Normal electrical conduction can be disrupted by:

  • Re-entry: Chaotic, circulating excitation of the myocardium (ventricular fibrillation) resulting in multiple foci of activation, leading to insufficient cardiac output, hemodynamic collapse, loss of consciousness, and potentially sudden death.

Causes of Re-entry:

  • Changes in the conduction pathway (e.g., unexcitable scar tissue from a previous myocardial infarction (MI))
  • Abnormal patterns of activation:
  • If the activation and recovery period of myocardial tissue exceeds the duration of an action potential (e.g., in long-QT syndrome)
  • If activation occurs outside the normal sequence of myocardial activation (e.g., premature ventricular complex, PVC)
24
Q

B.26 Ventricular Arrhythmia

Ventricular fibrillation clinical

A

Possible Early Signs:

  • Chest pain
  • Palpitations
  • Fatigue
  • Shortness of breath
  • Dizziness

Ultimately: Loss of consciousness, death

25
Q

B.26 Ventricular Arrhythmia

Ventricular fibrillation ECG

A
  • Often preceded by ventricular tachycardia
  • General Appearance:
  • Arrhythmic, fibrillatory baseline, typically exceeding 300 bpm
  • Irregular undulations with indistinguishable QRS complexes
  • Absence of atrial P waves
26
Q

B.26 Ventricular Arrhythmia

Ventricular fibrillation DX

A

Laboratory Tests:
- Cardiac enzymes
- Electrolytes
- Thyroid-stimulating hormone (TSH)
- Drug levels and toxicology screening
- Arterial blood gases

Imaging:
- Coronary angiography
- Echocardiography
- Nuclear imaging

27
Q

B.26 Ventricular Arrhythmia

Ventricular fibrillation TX

A

Resuscitation for V-Fib:
- Advanced Cardiac Life Support (ACLS)
- If V-Fib is refractory to standard ACLS protocol, consider administering lidocaine, procainamide, or magnesium.

Post-Resuscitation Care:
- Intensive Cardiac Monitoring:
- Monitor vital signs closely and address acute metabolic imbalances (e.g., electrolyte disturbances).

  • Be vigilant for therapeutic hypothermia.
  • Continue antiarrhythmics as indicated, typically amiodarone or IV lidocaine.
  • Assess the need for beta blockers based on patient condition.
  • Consider implantation of an ICD in patients with recurrent or high-risk hemodynamically significant V-Fib.