Skip to content
Pharmacy Notes

Arrhythmia - Pathophysiology, Clinical features, Treatment

Document25 pagesB.Pharm, Pharm.D

Download PDF
Loading…

About this document

Notes on Arrhythmia - Pathophysiology, Clinical features, Treatment

  • cardiac arrhythmias
  • pathophysiology
  • antiarrhythmic drugs
  • clinical features
  • treatment

By Dr. Ayesha Fatima

Download PDF
Text of these pages
  1. Page 1. GENESIS OF CARDIAC ARRHYTHMIAS 1. NORMAL HEART RHYTHM (STARTING POINT) SA node generates impulse ↓ Impulse spreads through atria ↓ AV node delays impulse ↓ His–Purkinje system conducts rapidly ↓ Coordinated atrial & ventricular contraction ↓ NORMAL SINUS RHYTHM Arrhythmias occur when impulse generation , impulse conduction , or both become abnormal. DISTURBANCE IN ELECTRICAL ACTIVITY ↓ Three Fundamental Mechanisms ↓ 1. Abnormal Impulse Generation 2. Triggered Activity (After depolarisation) 3. Abnormal Impulse Conduction 1. ABNORMAL IMPULSE GENERATION : (Problem at the pacemaker level) Normally, SA node controls heart rate. Arrhythmias occur when:  SA node fires too slowly  SA node fires too fast  Other cells start acting as pacemakers A. DECREASED AUTOMATICITY → SLOW RHYTHMS =  Sinus bradycardia, AV Block, Asystole  These patients often need pacemakers , not drugs. ↓ SA node fails to generate impulses properly OR Impulse fails to pass through AV node ↓ Heart rate slows ↓ BRADYARRHYTHMIAS B. INCREASED AUTOMATICITY → FAST RHYTHMS ↓ Steeper phase-4 depolarisation ↓ Cells reach threshold faster ↓ SA node or ectopic focus fires rapidly
  2. Page 2. ↓ TACHYARRHYTHMIAS + Ectopic beats  Where ectopic pacemakers arise from Atria, AV node, Purkinje fibres, Ventricular myocardium  Common triggers : Ischaemia, Hypokalaemia, Catecholamines, Digitalis toxicity 2. TRIGGERED ACTIVITY (Impulse triggered after a normal beat) Occurs when normal AP triggers extra abnormal depolarisations. The problem is not automaticity , but abnormal depolarisations occurring after an action potential . Normal action potential ↓ Abnormal calcium influx into cardiac myocyte during or immediately after phase 3 repolarisation ↓ After-depolarisations ↓ Extra (triggered) beat ↓ Arrhythmia (Seld sustained and depends on proceeding AP) Not self-initiated or spontaneous A. DELAYED AFTER-DEPOLARISATIONS (DAD) Occurs AFTER repolarisation (Phase 4) ↓ Intracellular Ca²⁺ overload ↓ Extra depolarisation reaches threshold ↓ Triggered tachycardia  Exacerbated in Digitalis toxicity, High sympathetic activity, Myocardial ischemia  DADs are rate-dependent → worse at fast heart rates. B. EARLY AFTER-DEPOLARISATIONS (EAD) => Prolong cardiac repolarisation phase Occurs DURING repolarisation (Phase 2 or 3) ↓ Action potential becomes prolonged ↓ Reactivation of Na⁺ / Ca²⁺ channels ↓ Triggered beat ↓ Polymorphic VT (Torsades de Pointes) associated with Prolonged QT → dangerous ventricular arrhythmias. 5. ABNORMAL IMPULSE CONDUCTION: (Impulse formed normally but travels abnormally) Normal impulse generation ↓ Abnormal impulse propagation ↓ Three mechanisms
  3. Page 3. 1. Conduction Block 2. Re-entry Phenomenon 3. Accessory tract pathways A. CONDUCTION BLOCK  result in AV nodal block, Bundle branch block ↓ Impulse partially or completely blocked ↓ Delayed or absent ventricular activation ↓ BRADYARRHYTHMIAS B. RE-ENTRY PHENOMENON (Most common mechanism – ~80–90%)  Observed in Atrial flutter, VT, AVNRT An impulse keeps circulating in a loop instead of dying out. Two conduction pathways present ↓ Unidirectional block in one pathway ↓ Slow conduction in the other pathway ↓ Previously blocked tissue recovers ↓ Impulse re-enters ↓ RE-ENTRY PHENOMENON (Mechanism of Tachyarrhythmias) WHAT IS RE-ENTRY? (Core Concept) Re-entry is a mechanism of arrhythmia in which a single electrical impulse repeatedly circulates in a closed loop, re-exciting the myocardium instead of extinguishing normally. The impulse goes around in circles and keeps the heart beating fast. NORMAL IMPULSE CONDUCTION (FOR CONTRAST) : Normal conduction is one-way and self- terminating . Impulse generated in SA node ↓ Travels through atria ↓ Passes AV node ↓ Conducted via His–Purkinje system ↓ Activates ventricles once ↓ Impulse dies out (tissue becomes refractory) CONDITIONS REQUIRED FOR RE-ENTRY : (All three must be present) 1. Two conduction pathways 2. Unidirectional block in one pathway
  4. Page 4. 3. Slow conduction in the other pathway Without all three , re-entry cannot occur. HOW RE-ENTRY DEVELOPS (STEP-BY-STEP) Step 1: Two Parallel Pathways Exist  These may be: o Two AV nodal pathways (fast and slow) o Normal pathway + accessory pathway (Bundle of Kent) o Normal myocardium + damaged (ischemic) tissue Pathway A – fast conduction, long refractory period Pathway B – slow conduction, short refractory period Step 2: Premature Impulse Occurs  A premature atrial or ventricular beat arrives early. Premature impulse reaches pathways ↓ Pathway A still refractory → impulse blocked Pathway B excitable → impulse conducts slowly ➡ This creates a unidirectional block Step 3: Impulse Travels Slowly Through Alternate Pathway Impulse moves down slow pathway ↓ Time delay allows Pathway A to recover excitability Step 4: Retrograde Conduction (Re-entry) Impulse reaches distal end ↓ Travels backward (retrograde) through recovered Pathway A ↓ Re-excites the original tissue Step 5: Self-Sustaining Loop Impulse keeps circulating ↓ Repeated myocardial activation ↓ SUSTAINED TACHYCARDIA The impulse is now trapped in a loop , producing rapid heart rate. C. ACCESSORY PATHWAYS (WPW SYNDROME) ↓ Extra pathway (Bundle of Kent) ↓ Impulse bypasses AV node ↓ Very rapid ventricular activation ↓ Re-entry circuit ↓ Paroxysmal SVT
  5. Page 5. Arrhythmia Clinical Presentation ECG Features Supraventricular Tachycardias (SVT – General) Asymptomatic to palpitations, irregular pulse, dizziness, syncope, chest discomfort, choking/pressure sensation; may precipitate HF Narrow QRS tachycardia (usually), rapid ventricular rate Atrial Fibrillation (AF) Palpitations, dyspnea, fatigue, chest pain; syncope uncommon; risk of embolic stroke due to atrial stasis Irregularly irregular rhythm, no P waves, variable RR intervals Atrial Flutter (AFl) Similar to AF; severe symptoms in 1:1 conduction (≈300 bpm); worse in mitral stenosis, cardiomyopathy Saw-tooth flutter waves, atrial rate ≈300 bpm, ventricular rate 150/100/75 Paroxysmal SVT (Re- entry) Sudden onset & termination of palpitations; chest pressure or neck pounding; syncope if very fast Regular narrow-QRS tachycardia; P waves hidden in QRS or T wave Premature Ventricular Contractions (PVCs) Often asymptomatic; palpitations or “missed beats” sensation Early wide QRS complex followed by compensatory pause Ventricular Tachycardia (VT) Asymptomatic to dizziness, syncope, hypotension, collapse; severity ↑ with poor LV function Wide-QRS tachycardia; monomorphic or polymorphic Torsades de Pointes (TdP) Dizziness, syncope, sudden death risk Polymorphic VT with twisting QRS, prolonged QT Ventricular Fibrillation (VF) Immediate hemodynamic collapse, syncope, cardiac arrest Chaotic, disorganized ECG with no identifiable QRS Bradyarrhythmias Dizziness, syncope, fatigue, confusion; worse
  6. Page 6. PATIENT WITH RHYTHM DISTURBANCE ↓ Assess Symptoms ↓ 1. Palpitations 2. Dizziness / Syncope 3. Chest pain 4. Dyspnea / HF 5. Collapse ↓ Perform ECG ↓ Is QRS Narrow or Wide? Narrow-QRS Arrhythmias ↓ Regular rhythm? ↓ YES → PSVT NO → AF or AFl ↓ ECG Analysis • AF → Irregular, no P waves • AFl → Saw-tooth flutter waves Wide-QRS Arrhythmias ↓ Is rhythm organized? ↓ YES → Ventricular Tachycardia NO → Ventricular Fibrillation ↓ Check QT Interval ↓ Prolonged QT → Torsades de Pointes Slow Heart Rate ↓ Bradycardia with symptoms ↓ ECG Evaluation ↓ • Sinus bradycardia • AV block (1st / 2nd / 3rd degree)
  7. Page 7. A. Supraventricular Tachyarrhythmias Supraventricular tachycardias produce a wide spectrum of symptoms, ranging from no symptoms to palpitations and irregular pulse, and in severe cases, dizziness, syncope, chest pain, or worsening heart failure. Many patients describe a choking or pressure sensation in the neck or chest, especially during re-entrant tachycardias due to simultaneous atrial and ventricular contraction. B. Atrial Fibrillation & Atrial Flutter AF and AFl usually do not cause syncope or hemodynamic collapse, except in cases of 1:1 atrial flutter or in patients with underlying heart disease. The most important complication of AF is arterial embolization, leading to ischemic stroke due to atrial stasis and thrombus formation. On ECG:  AF shows an irregularly irregular rhythm with absent P waves .  AFl shows organized atrial activity with flutter (saw-tooth) waves . C. Paroxysmal Supraventricular Tachycardia (PSVT) PSVT typically presents as sudden episodes of rapid heart rate that start and stop abruptly. Symptoms include palpitations, dizziness, and chest pressure. In AV nodal re-entry, patients often complain of neck pounding, due to atrial contraction against a closed tricuspid valve. ECG usually shows a regular narrow-QRS tachycardia with hidden P waves. D. Ventricular Arrhythmias PVCs PVCs are usually benign and asymptomatic. Patients feel palpitations due to the post- PVC compensatory pause, not the PVC itself. Ventricular Tachycardia VT symptoms depend on
  8. Page 8. Treatment Goals: 1. Relieve symptoms 2. Prevent hemodynamic compromise 3. Prevent progression to more dangerous arrhythmias 4. Reduce morbidity and mortality 5. Avoid treatment-related harm (proarrhythmia) Pharmacological Treatment I. CLINICAL (DESCRIPTIVE) CLASSIFICATION (Based on the type of arrhythmia treated) Category Drugs Clinical Use Drugs used for supraventricular arrhythmias Adenosine, Verapamil, Diltiazem PSVT, AV nodal–dependent tachycardias, rate control in AF/AFl Drugs used for ventricular arrhythmias Lignocaine (Lidocaine), Mexiletine, Bretylium Ventricular tachycardia, ventricular ectopy Drugs used for both supraventricular and ventricular arrhythmias Amiodarone, β-blockers, Disopyramide, Procainamide AF, AFl, VT, mixed arrhythmias
  9. Page 9. Type of Arrhythmia Goals of Treatment Supraventricular Tachyarrhythmias (PSVT, AF, AFl, atrial tachycardia) 1. Relieve symptoms (palpitations, dizziness, chest discomfort) 2. Control ventricular rate 3. Restore sinus rhythm when appropriate 4. Prevent recurrence of tachyarrhythmia 5. Prevent hemodynamic compromise and ischemia 6. Improve functional status and quality of life Atrial Fibrillation (AF) 1. Control ventricular rate 2. Prevent thromboembolism (stroke prevention) 3. Restore and maintain sinus rhythm in selected patients 4. Prevent recurrence of AF 5. Improve symptoms and exercise tolerance 6. Reduce risk of heart failure and mortality Atrial Flutter (AFl) 1. Control ventricular rate 2. Restore sinus rhythm (cardioversion or ablation when appropriate) 3. Prevent recurrence 4. Prevent thromboembolic complications 5. Improve hemodynamics and symptoms Paroxysmal Supraventricular Tachycardia (PSVT) 1. Terminate acute tachycardia episodes 2. Prevent recurrence of episodes 3. Reduce symptom burden (palpitations, dizziness, neck pressure) 4. Avoid hemodynamic compromise 5. Minimize need for invasive therapy Ventricular Tachycardia (VT) 1. Terminate acute VT, especially if unstable 2. Prevent degeneration into ventricular fibrillation 3. Prevent sudden cardiac death 4. Reduce recurrence of VT 5. Improve survival and hemodynamic stability 6. Treat underlying causes (ischemia, structural heart disease) Torsades de Pointes (TdP) 1. Terminate the arrhythmia promptly 2. Correct p
  10. Page 10. Ventricular Fibrillation (VF) 1. Immediate restoration of effective cardiac output 2. Prevent sudden cardiac death 3. Correct reversible causes (ischemia, electrolyte imbalance) 4. Prevent recurrence of VF 5. Maintain long-term survival Bradyarrhythmias (General)(Sinus bradycardia, AV block) 1. Restore adequate heart rate 2. Improve cardiac output and organ perfusion 3. Relieve symptoms of hypotension (dizziness, syncope, fatigue) 4. Prevent syncope and sudden cardiac arrest 5. Prevent worsening of heart failure Atrioventricular (AV) Block 1. Maintain adequate ventricular rate 2. Prevent syncope and hypotension 3. Improve quality of life 4. Prevent progression to complete heart block 5. Reduce mortality (often via pacing)
  11. Page 12. Class I A Drug Common Side Effects Serious / Important Effects Disopyramide Dry mouth, constipation, urinary retention, blurred vision TdP, heart failure (HF), ventricular arrhythmias Procainamide Hypotension TdP, worsening HF, ventricular arrhythmias Quinidine GI upset (diarrhea, nausea, vomiting), cinchonism (tinnitus, headache) TdP, hypotension, thrombocytopenia, hemolytic anemia Class I B Lidocaine Dizziness, sedation, confusion, paresthesia Seizures, sinus arrest, conduction disturbances Mexiletine Dizziness, tremor, nausea, vomiting Ventricular arrhythmias, conduction disturbances Class I C Flecainide Dizziness, blurred vision, headache Worsening HF, ventricular arrhythmias Propafenone Dizziness, fatigue, metallic taste, nausea Bradycardia, AV block, worsening HF Class III Amiodarone Tremor, insomnia, nausea, photosensitivity Pulmonary fibrosis, thyroid dysfunction, liver toxicity, bradycardia Dofetilide Headache, dizziness TdP Dronedarone Nausea, diarrhea, ↑ serum creatinine Worsening HF, liver toxicity, TdP (rare) Ibutilide Headache TdP, hypotension Sotalol Fatigue, dizziness, bradycardia TdP, bronchospasm, worsening HF
  12. Page 13. A. Emergency / Acute (IV) Use Ventricular Arrhythmias & AF Termination Drug Used For Easy-to-Remember IV Dose Amiodarone Pulseless VT/VF 300 mg IV push, then 150 mg if needed → infusion 1 mg/min (6 h) → 0.5 mg/min Stable VT (pulse) 150 mg IV over 10 min → infusion AF termination 5 mg/kg IV over 30 min → infusion Lidocaine VT/VF 1–1.5 mg/kg IV bolus, repeat → max 3 mg/kg, then infusion Procainamide AF / Stable VT 15–18 mg/kg IV over 60 min → infusion Ibutilide AF termination 1 mg IV over 10 min, repeat once Sotalol VT / AF 75–150 mg IV over 5 h Rate Control (SVT / AF) Drug Used For Easy IV Dose Diltiazem PSVT, AF 0.25 mg/kg IV bolus → infusion 5–15 mg/h Verapamil PSVT, AF 2.5–5 mg IV, repeat → infusion 2.5–10 mg/h B. Long-Term (Oral Maintenance Therapy) Chronic Rhythm / Rate Control Drug Simple Oral Dose Disopyramide 100–150 mg q6h OR 200–300 mg q12h (SR) Quinidine 200–300 mg q6h Mexiletine 200–300 mg q8h Flecainide 50–200 mg q12h Propafenone 150–300 mg q8h OR 225–425 mg q12h (SR) Amiodarone Loading: 400 mg 2–3×/day → Maintenance: 200–400 mg/day Dofetilide 500 mcg q12h Dronedarone 400 mg q12h with meals Sotalol 80–160 mg q12h
  13. Page 14. Treatment of Atrial Fibrillation (AF) and Atrial Flutter Management of AF is done in sequential steps, with three main goals: 1. Goals of Treatment in Atrial Fibrillation o AF management follows three sequential goals:  Acute stabilization – control ventricular rate and relieve symptoms  Restoration of sinus rhythm – if clinically indicated  Prevention of complications – stroke, thromboembolism, recurrence o Rate control and anticoagulation are essential even if rhythm control is planned. o Choice of therapy depends on hemodynamic stability, AF duration, LV function, and stroke risk. 2. Immediate Assessment: Hemodynamic Status a. Management of Hemodynamically Unstable AF  Hemodynamic instability includes: o Severe hypotension o Angina o Pulmonary edema o Shock  Immediate synchronized direct-current cardioversion (DCC) is indicated.  Anticoagulation status should not delay cardioversion.  DCC rapidly restores sinus rhythm and improves cardiac output. b. Hemodynamically Stable AF ✔ Primary focus: Ventricular Rate Control 3. Ventricular Rate Control (First-Line Strategy) : Slow ventricular response and improve symptoms. Why Rate Control?  AF causes rapid ventricular response  Leads to ↓ cardiac output, ischemia, HF  Slowing AV nodal conduction improves symptoms  Rate control is the initial strategy in stable patients.  Drugs act by slowing AV nodal conduction.  Target heart rate:  <80 bpm (strict control)  <110 bpm (lenient control) AV Nodal Blocking Agents Patien
  14. Page 15. High adrenergic state IV β-blockers (first choice) LVEF ≤40% Avoid diltiazem & verapamil; use β-blockers cautiously Heart failure exacerbation IV digoxin or IV amiodarone Refractory or contraindicated to others IV amiodarone 4. Reassessment After Rate Control After adequate AV nodal blockade: ✔ Reassess symptoms ✔ Evaluate AF duration ✔ Decide on rhythm control vs rate control strategy ✔ Once ventricular rate is controlled: → Assess whether sinus rhythm restoration is needed Rhythm control is preferred in:  Younger patients  First episode AF  Highly symptomatic patients AF causing HF or ischemia A. Stroke Risk Assessment in AF (CHADS₂ Score)  AF increases risk of thromboembolic stroke .  CHADS₂ score assesses stroke risk. Risk Factor Score CHF 1 Hypertension 1 Age >75 yrs 1 Diabetes 1 Prior stroke/TIA 2 CHADS₂ Score Stroke Risk Recommendation 0 Low No therapy preferred; aspirin optional 1 Intermediate Oral anticoagulation preferred ≥2 High Oral anticoagulation mandatory
  15. Page 16. B. Long-Term Antithrombotic Therapy Options  Indicated to prevent stroke and systemic embolism .  Options include: o Warfarin (INR 2–3) o Dabigatran o Rivaroxaban o Apixaban Drug Dose Key Points Warfarin INR 2–3 Requires monitoring Dabigatran 150 mg twice daily CrCl >30 mL/min Rivaroxaban 20 mg once daily Moderate–high stroke risk Apixaban 5 mg twice daily Alternative to warfarin or aspirin ✔ Nonvalvular AF: All above are acceptable ✔ Low-risk patients: No therapy preferred over aspirin  In nonvalvular AF , all above agents are effective.  Aspirin is inferior to anticoagulants and reserved for low-risk patients.  Dual antiplatelet therapy (aspirin + clopidogrel) is used only if anticoagulation is not feasible. 6. Anticoagulation Before Cardioversion Based on Duration of AF Duration of AF Anticoagulation Strategy <48 hours No prior anticoagulation required; give IV heparin or LMWH at presentation >48 hours or unknown Anticoagulation for ≥3 weeks before cardioversion Post-Cardioversion: ✔ Continue anticoagulation for at least 4 weeks (warfarin or dabigatran) To Restoration of atrial contraction ↑ risk of thromboembolism 7. Methods to Restore Sinus Rhythm  Rhythm control is considered after rate control.  Indicated in: o Young patients o First-episode AF o Severe symptoms o AF causing HF or ischemia
  16. Page 17. A. Electrical Cardioversion (DCC) Advantage Disadvantage Rapid, highly effective Requires anesthesia Higher success rate Risk of sinus arrest, ventricular arrhythmias B. Pharmacologic Cardioversion Drug Class Examples Class III (IK blockers) Ibutilide, dofetilide Class Ic Flecainide, propafenone Class III Amiodarone (oral or IV) C. “Pill in the Pocket” Approach  Single oral dose of flecainide or propafenone taken by patient during AF episode.  Suitable only for selected patients: o No structural heart disease o No AV or sinus node dysfunction o No QT prolongation or Brugada syndrome  Must be tested successfully in hospital before outpatient use. Reduces hospital visits and improves patient autonomy D. Long-Term Maintenance of Sinus Rhythm  AF commonly recurs due to structural heart disease and atrial remodeling.  Antiarrhythmic drugs used: o Class Ic: Flecainide, propafenone (avoid in structural heart disease) o Class III: Amiodarone (most effective)  Quinidine maintains rhythm but increases mortality.  Amiodarone requires monitoring for thyroid, lung, and liver toxicity. Drug Key Points Quinidine Maintains rhythm but ↑ mortality Class Ic agents Avoid in structural heart disease Amiodarone Most effective; risk of organ toxicity
  17. Page 18. PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA (PSVT) – TREATMENT 1. Principles of PSVT Management  Treatment depends on: o Severity of symptoms o Hemodynamic stability o Frequency of episodes  Management has two phases:  Termination of acute episode  Prevention of recurrence 2. Acute Management of PSVT (Stepwise Approach) Step 1: Assess Symptom Severity Clinical Status Examples Severe symptoms Syncope, near syncope, angina, severe heart failure Mild–moderate symptoms Palpitations, dizziness, mild dyspnea Step 2: Immediate Treatment Based on Severity A. Hemodynamically Unstable / Severe Symptoms ✔ Synchronized Direct-Current Cardioversion (DCC)  First-line therapy  Rapid and highly effective  Restores sinus rhythm immediately o Used when drug therapy may be too slow or unsafe B. Hemodynamically Stable / Mild–Moderate Symptoms  Non-Pharmacologic (First Attempt)  Vagal Maneuver Mechanism Valsalva maneuver ↑ vagal tone → slows AV nodal conduction Unilateral carotid sinus massage Reflex AV nodal inhibition Step 3: Pharmacologic Therapy (If Vagal Maneuvers Fail) Drug Therapy for Acute PSVT (Based on QRS Width) Drug Group Mechanism Examples ↑ Vagal tone Indirect AV nodal inhibition Digoxin Slow Ca²⁺-dependent conduction AV nodal blockade Adenosine, β-blockers, verapamil, diltiazem Fast Na⁺-dependent conduction Suppress atrial/ventricular conduction Quinidine, procainamide, disopyramide, flecainide 4. Adenosine – Drug of First Choice Reasons:
  18. Page 19.  Very short half-life (seconds)  Rapid onset and offset  Safer if diagnosis is uncertain (wide QRS tachycardia may be VT) 5. Long-Term Prophylaxis of PSVT When Is Long-Term Therapy Indicated?  Frequent PSVT episodes requiring treatment  Infrequent but severely symptomatic episodes Methods for Long-Term Management Strategy Explanation Antiarrhythmic drug therapy Prevents recurrence Monitoring Holter monitor or event recorder Electrophysiologic testing Identifies arrhythmia mechanism PREMATURE VENTRICULAR COMPLEXES (PVCs) – TREATMENT 1. Overview of PVC Management  Treatment depends on: o Presence of structural heart disease o Risk of arrhythmic death  PVCs are common and often benign. 2. Management in Apparently Healthy Individuals  ✔ No drug therapy required  Reason:  PVCs without heart disease carry little or no risk  Antiarrhythmic drugs may cause more harm than benefit 3. Management in High-Risk Patients High-Risk Features  Recent myocardial infarction  Left ventricular dysfunction  Frequent or complex PVCs Preferred Therapy ✔ β-Blockers only Reason Explanation Mortality benefit Only drugs proven to reduce death Antiarrhythmic effect Reduce PVC frequency Cardioprotective Reduce sympathetic activity
  19. Page 20. VENTRICULAR TACHYCARDIA – TREATMENT 1. Ventricular Tachycardia (VT)  VT is a rapid rhythm originating from the ventricles.  It can be life-threatening due to reduced cardiac output and risk of degeneration into VF.  Management depends on: o Hemodynamic stability o Presence of symptoms o Underlying cause 2. Acute Ventricular Tachycardia Step 1: Assess Symptom Severity Clinical Status Examples Severe symptoms Hypotension, syncope, angina, acute HF Mild or no symptoms Palpitations, dizziness, stable BP A. Acute VT with Severe Symptoms ✔ Immediate synchronized direct-current cardioversion (DCC) Key points:  Rapidly restores sinus rhythm  Prevents progression to VF  Correct precipitating factors (ischemia, electrolyte imbalance, drug toxicity)  If VT is due to a transient cause (e.g., acute MI, digitalis toxicity), long-term antiarrhythmic therapy is not required once the cause is corrected. B. Acute VT with Mild or No Symptoms ✔ Initial pharmacologic therapy Drug Comments IV Procainamide Effective for monomorphic VT IV Amiodarone Useful in structural heart disease IV Sotalol Class III effect IV Lidocaine Alternative agent ✔ Proceed to synchronized DCC if:  Patient deteriorates  VT degenerates into VF  Drug therapy fails
  20. Page 21. 3. Sustained Ventricular Tachycardia (Chronic / Recurrent) Definition  VT lasting >30 seconds or requiring intervention for termination. Key Features  Patients are at very high risk of sudden cardiac death .  Trial-and-error drug testing is unsafe and ineffective . Preferred Management Strategy ✔ Nondrug approaches are favored Approach Explanation Implantable Cardioverter-Defibrillator (ICD) Detects and terminates VT/VF automatically Drug therapy alone Not reliable for mortality reduction ICD is the most effective method for preventing sudden death in sustained VT. 4. Ventricular Proarrhythmia Definition  Worsening or induction of arrhythmia caused by antiarrhythmic drugs. Common Cause  Class Ic drugs (flecainide, propafenone) Typical Features  Rapid, sustained monomorphic VT  Sinusoidal QRS pattern  Often resistant to cardioversion Management Treatment Rationale IV Lidocaine Competes at sodium channel Sodium bicarbonate Reverses sodium channel blockade These agents counteract excessive sodium channel inhibition. 5. Torsade de Pointes (TdP) Definition  Polymorphic VT associated with QT interval prolongation . Acute Management of TdP ✔ Direct-current cardioversion (DCC)  Required in most acute episodes  TdP often recurs after DCC Prevention of Recurrence ✔ IV Magnesium sulfate – Drug of choice ✔ If magnesium is ineffective:
  21. Page 22.  Increase heart rate to shorten QT interval Method Details Temporary pacing 105–120 beats/min Pharmacologic pacing Isoproterenol or epinephrine infusion Additional Measures ✔ Discontinue QT-prolonging drugs ✔ Correct electrolyte abnormalities:  Hypokalemia  Hypomagnesemia Contraindicated drugs:  Procainamide  Other QT-prolonging agents Lidocaine is usually ineffective in TdP. 6. Ventricular Fibrillation (VF) Definition  Chaotic ventricular activity with no effective cardiac output . Management of VF / Pulseless VT ✔ Treat according to American Heart Association (AHA) CPR guidelines Key steps include:  Immediate defibrillation  High-quality CPR  Advanced cardiac life support (ACLS) VF is a medical emergency requiring immediate intervention.
  22. Page 23. Treatment of Bradyarrhythmias Bradyarrhythmias are rhythms with abnormally slow heart rate. 1) Common causes: a) Sinus node dysfunction b) Carotid sinus hypersensitivity c) Vasovagal syncope d) AV conduction blocks 2) Treatment depends on: a) Presence of symptoms b) Hemodynamic impact c) Reversibility of cause Treat symptoms, not just heart rate. a) Sinus Node Dysfunction (Sick Sinus Syndrome): Sinus node dysfunction refers to inappropriate sinus bradycardia, sinus pauses, or sinoatrial block , often associated with bradycardia–tachycardia syndrome . Goals 2) Eliminate symptomatic bradycardia 3) Prevent syncope and hypotension 4) Manage associated tachyarrhythmias (e.g., AF) a) Clinical Features  Symptomatic sinus bradycardia  Sinus pauses  Alternating bradycardia and tachycardia (e.g., AF) Treatment Approach Situation Management Asymptomatic bradycardia No treatment required Symptomatic bradycardia Permanent pacemaker Bradycardia–tachycardia syndrome Pacemaker + manage tachyarrhythmia  Drugs used for supraventricular tachycardias (β-blockers, CCBs, digoxin): o Can worsen bradycardia o Should be used only if a pacemaker is in place Role of Permanent Pacemaker in Bradyarrhythmias  Permanent ventricular pacemaker is the long-term treatment of choice for: o Symptomatic sinus node dysfunction o Symptomatic carotid sinus hypersensitivity o Chronic symptomatic AV block Pacemaker prevents:  Syncope  Hypotension  Sudden cardiac arrest due to extreme bradycardia
  23. Page 24. b) Carotid Sinus Hypersensitivity  Exaggerated vagal response to carotid sinus stimulation  Causes bradycardia, hypotension, or syncope Treatment Condition Therapy Symptomatic patients Permanent pacemaker Persistent symptoms Add α-adrenergic agonist (midodrine) Midodrine increases peripheral vascular tone and blood pressure. C) Vasovagal Syncope Mechanism  Trigger → sympathetic surge → forceful ventricular contraction  Followed by reflex bradycardia and hypotension Drug Therapy for Vasovagal Syncope Drug Class Examples Mechanism β-blockers Metoprolol Blunts sympathetic surge Mineralocorticoids Fludrocortisone Expands plasma volume Anticholinergics Scopolamine, disopyramide Reduce vagal tone α-agonists Midodrine ↑ Peripheral resistance Adenosine antagonists Theophylline, dipyridamole Increase heart rate SSRIs Sertraline, paroxetine Modulate autonomic reflexes ATRIOVENTRICULAR (AV) BLOCK – TREATMENT  AV block is a delay or interruption of impulse conduction from atria to ventricles.  Types of AV Block (Clinical Relevance) Type Severity First degree Usually benign Mobitz I Often transient Mobitz II Dangerous Third degree (complete block) Life-threatening Acute Management of Symptomatic AV Block Indications for Emergency Treatment  Altered mental status  Chest pain  Hypotension  Shock Stepwise Acute Treatment
  24. Page 25. Step Therapy Dose / Notes 1 Atropine 0.5 mg IV every 3–5 min (max 3 mg) 2 Transcutaneous pacing If atropine fails 3 Epinephrine infusion 2–10 mcg/min 4 Dopamine infusion 2–10 mcg/kg/min Atropine, dopamine, and epinephrine are often ineffective in:  Mobitz II block  Infranodal or trifascicular block Chronic Management of AV Block Long-Term Therapy Patient Type Management Symptomatic AV block Permanent pacemaker Asymptomatic AV block Close monitoring

More on Pharmacotherapeutics