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Vasospastic (Prinzmetal) Angina

Arrhythmia

Background 

Arrhythmia, also known as dysrhythmia, refers to any abnormality in the heart’s rhythm—be it irregular, too fast, or too slow. It can originate from the atria, AV node, or ventricles, and may result in a wide spectrum of clinical manifestations ranging from asymptomatic to life-threatening. While some arrhythmias are benign and transient, others can result in hemodynamic compromise, embolic events, or sudden cardiac death. 

Arrhythmia is caused by disruptions in the generation or conduction of electrical impulses in the heart. It may involve: 

  • Rate disturbances: bradyarrhythmias (<60 bpm) or tachyarrhythmias (>100 bpm). 
  • Rhythm disturbances: irregular (e.g., atrial fibrillation) or ectopic rhythms (e.g., PVCs). 
  • Conduction abnormalities: heart blocks, reentry circuits, or accessory pathways. 

 

Classification/Types

I) By Rate: 

  • Bradyarrhythmias: Sinus bradycardia, AV blocks, junctional  rhythms. 
  • Tachyarrhythmias: Atrial fibrillation, atrial flutter, SVT, VT, VF. 

II) By Origin: 

  • Supraventricular: Atrial fibrillation/flutter, SVT, WPW syndrome. 
  • Ventricular: PVCs, VT, VF. 
  • Junctional: Junctional escape or tachycardia. 

III) By Clinical Impact: 

  • Benign/Physiologic: Sinus arrhythmia, isolated PVCs. 
  • Pathologic: Sustained VT, AF with RVR, complete heart block. 

 

Pathophysiology 

Arrhythmias arise from abnormalities in: 

  • Impulse formation: Enhanced automaticity, triggered activity (e.g., afterdepolarizations). 
  • Impulse conduction: Reentry circuits, conduction delays or blocks. 
  • The effect of arrhythmias on cardiac output depends on rate, rhythm regularity, and underlying cardiac function. They may cause hypotension, ischemia, thromboembolism, or syncope. 

 

Epidemiology 

  • Atrial fibrillation is the most common arrhythmia worldwide, affecting over 3 million people in the U.S. 
  • Bradyarrhythmias are more common in the elderly due to conduction system degeneration. 
  • Supraventricular tachycardias are more frequent in younger individuals. 
  • Ventricular arrhythmias are often associated with structural heart disease and post-MI patients. 

 

Etiology 

I. Causes 

  • Electrolyte abnormalities (e.g., hypokalemia, hyperkalemia, hypomagnesemia). 
  • Ischemic heart disease (especially post-MI). 
  • Heart failure, cardiomyopathy, valvular disease. 
  • Medications: Digoxin, antiarrhythmics, beta-blockers, QT-prolonging drugs. 
  • Structural heart defects: Congenital or acquired. 
  • Infiltrative diseases: Amyloidosis, sarcoidosis. 
  • Infections: Myocarditis, endocarditis. 
  • Endocrine/metabolic: Hyperthyroidism (AF), hypothyroidism (bradycardia), hypoxia. 
  • Substance use: Alcohol (“holiday heart”), cocaine, caffeine. 

II. Risk Factors 

  • Age >60 
  • Hypertension, diabetes, CAD 
  • Heart failure or LV dysfunction 
  • Obstructive sleep apnea 
  • Valvular heart disease 
  • Family history of arrhythmias or sudden death 

 

Clinical Presentation 

I. History (Symptoms) 

  • Palpitations (fluttering, pounding, skipped beats) 
  • Dizziness, lightheadedness 
  • Syncope or near-syncope 
  • Chest discomfort or pressure 
  • Dyspnea, fatigue 
  • Sudden cardiac arrest (in malignant ventricular arrhythmias) 
  • May be asymptomatic and discovered incidentally 

II. Physical Exam (Signs) 

Vital Signs: 

  • Bradycardia or tachycardia 
  • Irregularly irregular pulse (e.g., AF) 
  • Hypotension (in low-output states) 
  • Narrow or wide pulse pressure depending on hemodynamic compromise 

General Appearance: 

  • May appear normal at rest 
  • In distress if rapid arrhythmia or poor perfusion 
  • Diaphoretic or pale during symptomatic episodes 

Cardiovascular: 

  • Irregular rhythm or rate on auscultation 
  • Canon “a” waves (in AV dissociation) 
  • Variable S1 intensity (e.g., AF) 
  • Possible gallop (S3/S4) in heart failure 

Neurologic: 

  • Syncope or altered mental status in profound arrhythmias 
  • Transient weakness or confusion 
  • Stroke symptoms (from AF-related embolism) 

Respiratory: 

  • Tachypnea or dyspnea 
  • Bibasilar crackles if heart failure develops 

Skin/Extremities: 

  • Cool extremities if poor perfusion 
  • Cyanosis or mottling in cardiogenic shock 
  • Delayed capillary refill 

 

Differential Diagnosis (DDx) 

  • Sinus arrhythmia (normal variant) 
  • Ectopic atrial rhythm or PACs 
  • AV block (first to third degree) 
  • Atrial fibrillation/flutter 
  • SVT (e.g., AVNRT, AVRT) 
  • Ventricular tachycardia or fibrillation 
  • Sick sinus syndrome 
  • Electrolyte imbalance 
  • Hyperthyroidism 
  • Drug toxicity (e.g., digoxin, antiarrhythmics) 

 

Diagnostic Tests 

  • ECG: Essential for rhythm diagnosis. 
  • AF: Irregularly irregular, no P waves. 
  • VT: Wide QRS tachycardia. 
  • SVT: Narrow QRS tachycardia. 
  • AV block: Prolonged PR or dropped beats. 
  • Electrolytes, Mg²⁺, Ca²⁺, TSH 
  • Cardiac enzymes if ischemia suspected 
  • TTE: Evaluate structural heart disease 
  • Holter monitor or event monitor for intermittent symptoms 
  • Telemetry in hospitalized patients 
  • Electrophysiology study for complex or refractory arrhythmias 

 

Treatment 

I. Acute Management 

A) Unstable Patient (e.g., hypotension, syncope): 

  • Immediate synchronized cardioversion (e.g., AF with RVR, VT with pulse) 
  • Defibrillation for pulseless VT/VF 
  • IV medications
  • AF: Diltiazem, beta-blockers, amiodarone 
  • VT: Amiodarone, lidocaine 
  • SVT: Adenosine 

B) Stable Patient: 

  • Rate or rhythm control depending on type 
  • Correct underlying cause (e.g., electrolytes, ischemia, drug toxicity) 

II. Chronic Management 

  • AF: Rate control (BB, CCB), anticoagulation (CHA₂DS₂-VASc), rhythm control (AADs or ablation) 
  • SVT: AV nodal blockers, catheter ablation 
  • VT: Beta-blockers, amiodarone, ICD if high-risk 
  • Bradyarrhythmias: Pacemaker if symptomatic or advanced AV block 

 

Medications 

Drug Class 

Examples 

Notes 

Beta-blockers 

Metoprolol, Esmolol 

Rate control; avoid in decompensated HF 

Calcium blockers 

Diltiazem, Verapamil 

Rate control in AF 

Antiarrhythmics 

Amiodarone, Sotalol, Flecainide 

Rhythm control or VT suppression 

Adenosine 

— 

Termination of SVT (transient AV block) 

Anticoagulants 

Warfarin, DOACs 

Stroke prevention in AF 

Electrolyte repletion 

Mg²⁺, K⁺ 

Essential in correcting trigger factors 

 

Device Therapy 

  • Pacemaker: For symptomatic bradycardia or heart block 
  • Implantable Cardioverter-Defibrillator (ICD): For secondary prevention (e.g., survived VT/VF) or primary prevention (EF <35% with cardiomyopathy) 
  • Ablation: For AF, SVT, and some forms of VT 

 

Consults

  • Cardiology: For all sustained or symptomatic arrhythmias 
  • Electrophysiology: For ablation consideration or complex rhythm issues 
  • Neurology: If stroke suspected 
  • Endocrinology: For thyroid-related arrhythmias 

 

Patient Education 

Education 

  • Recognize symptoms (palpitations, syncope) 
  • Adherence to medications and follow-up 
  • Avoid stimulants (caffeine, alcohol, illicit drugs) 
  • Importance of anticoagulation in AF 

Screening

  • Routine ECG in high-risk individuals 
  • Ambulatory monitoring for unexplained syncope 
  • Genetic screening in family history of sudden death (e.g., Long QT syndrome) 

Vaccinations 

  • Influenza and pneumococcal vaccines reduce cardiovascular complications 

 

Follow-Up 

Short-Term: 

  • Monitor for recurrence after intervention 
  • Assess for medication side effects 

Long-Term: 

  • Repeat ECG or Holter if indicated 
  • Monitor anticoagulation (if on warfarin) 
  • Device checks for pacemakers or ICDs 
  • Monitor for progression to structural heart disease 

 

Prognosis 

  • Benign arrhythmias (e.g., PACs, sinus arrhythmia): Excellent. 
  • AF: Increased risk of stroke and heart failure if untreated. 
  • VT/VF: Potentially fatal without intervention. 
  • ICD recipients: Improved survival in high-risk populations. 
  • Prognosis depends on type, underlying cardiac function, and timely management. 
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