2.3 Cardiac Arrhythmias, Conduction Blocks & BLS/ACLS Algorithms

Classification & Evaluation of Tachyarrhythmias

Tachyarrhythmias (heart rate > 100 bpm) are systematically evaluated based on two foundational clinical questions: Is the patient hemodynamically stable? and What is the QRS morphology on the 12-lead ECG?

Clinical Stability Assessment

Hemodynamic instability is defined by the presence of any of the following five adverse features caused by the rapid heart rate:

1. Hypotension (systolic blood pressure < 90 mmHg or mean arterial pressure < 65 mmHg)
2. Acutely altered mental status (confusion, lethargy, syncope)
3. Ischemic chest pain or discomfort
4. Acute pulmonary edema or heart failure signs (rales, elevated JVP)
5. Signs of shock (cold clammy extremities, delayed capillary refill, oliguria)

Electrical Treatment: Unstable organized tachyarrhythmia with a pulse requires immediate synchronized cardioversion. Sustained polymorphic VT requires unsynchronized defibrillation because synchronization is unreliable. For sinus tachycardia, treat the underlying cause.

Electrocardiographic Morphological Triage

For the stable patient, the 12-lead ECG is categorized by QRS duration and ventricular rhythm regularity:

+-----------------------------------------------------------------------------------------+
|                                Tachyarrhythmia (> 100 bpm)                              |
+-----------------------------------------------------------------------------------------+
                                             |
                   +-------------------------+-------------------------+
                   |                                                   |
                   v                                                   v
         [ Narrow QRS (< 120 ms) ]                           [ Broad QRS (>= 120 ms) ]
                   |                                                   |
         +---------+---------+                               +---------+---------+
         |                   |                               |                   |
         v                   v                               v                   v
     [ Regular ]       [ Irregular ]                     [ Regular ]       [ Irregular ]
         |                   |                               |                   |
     - AVNRT             - Atrial Fib                    - Ventricular       - AF with Aberrancy
     - AVRT              - Atrial Flutter                  Tachycardia (80%) - Pre-excited AF
     - Atrial Flutter      with variable block           - SVT with            (WPW)
     - Sinus Tachycardia - Multifocal Atrial               aberrancy (20%)   - Polymorphic VT
                           Tachycardia (MAT)                                   / Torsades

Acute Management of Supraventricular Tachycardia (SVT)

Paroxysmal supraventricular tachycardias (pSVT)—predominantly Atrioventricular Nodal Re-entrant Tachycardia (AVNRT) (~60%) and Atrioventricular Re-entrant Tachycardia (AVRT) involving an accessory pathway (~30%)—present with abrupt-onset regular palpitations, neck pounding (due to cannon A waves), and lightheadedness.

Sequential Management in Stable SVT

1. Vagal Maneuvers:
   • Modified Valsalva Maneuver: The patient undertakes standard forced expiration (blowing into a 10 mL syringe to achieve 40 mmHg pressure) for 15 seconds in a semi-recumbent position, followed immediately by supine repositioning with passive leg elevation to 45 degrees for 15 seconds. This technique achieves cardioversion in over 40% of patients compared to 17% with standard Valsalva.
   • Carotid Sinus Massage: Steady pressure applied over the right carotid bifurcation below the angle of the jaw for 5 to 10 seconds. Contraindicated in patients with carotid bruits or history of stroke/TIA in the past 3 months.
2. Intravenous Adenosine:
   • If vagal maneuvers fail, Adenosine is the first-line pharmacologic agent. It stimulates A1 adenosine receptors in the AV node, activating inward rectifier potassium currents and suppressing calcium influx, producing profound, transient AV nodal conduction block (half-life < 10 seconds).
   • Administration Technique: Must be administered as an extremely rapid IV push over 1 to 2 seconds via a large-bore cannula in an antecubital vein, followed immediately by a 20 mL normal saline flush with arm elevation.
   • Dosing Regimen: Initial dose of 6 mg rapid IV push. If no conversion occurs within 1 to 2 minutes, administer a second dose of 12 mg rapid IV push. A third dose of 12 mg may be administered if required.
   • Dose Adjustments: Reduce initial dose to 3 mg if given through a central venous line, in cardiac transplant recipients, or in patients taking dipyridamole. Higher doses are required in patients consuming high levels of caffeine or theophylline.
   • Patient Education: Warn the patient in advance of profound transient symptoms: facial flushing, chest tightness, dyspnea, and impending doom. A transient period of asystole or sinus arrest (up to 3-6 seconds) commonly precedes sinus rhythm resumption on the cardiac monitor.
   • Contraindications: Severe active bronchospastic asthma (may trigger severe bronchospasm; use verapamil instead) and pre-excited atrial fibrillation.
3. Second-Line Pharmacotherapy:
   • If adenosine fails to terminate the arrhythmia, non-dihydropyridine calcium channel blockers (IV Verapamil 2.5-5 mg IV over 2 minutes, repeated at 5-10 mg after 15-30 minutes) or IV Diltiazem (0.25 mg/kg IV bolus over 2 minutes) are highly effective alternatives in patients with preserved ejection fraction.

The Broad-Complex Regular Tachycardia Dilemma

Any broad-complex tachycardia (QRS >= 120 ms) must be managed as Ventricular Tachycardia (VT) until conclusively proven otherwise. Over 80% of broad regular tachycardias are VT. Administration of intravenous verapamil or diltiazem to a patient in VT is a catastrophic error that precipitates rapid vasodilation, negative inotropy, and fatal cardiogenic shock or ventricular fibrillation.

For stable monomorphic VT:

• Intravenous Amiodarone: 150 mg IV infused over 10 minutes, followed by 1 mg/min infusion for 6 hours, then 0.5 mg/min for 18 hours.
• Intravenous Procainamide: 20 to 50 mg/min IV until arrhythmia stops, hypotension occurs, QRS widens > 50%, or 17 mg/kg is reached. Avoid in prolonged QT or congestive heart failure.
• Synchronized Electrical Cardioversion: Should be performed promptly if pharmacotherapy is ineffective or at any point if stability deteriorates.

Atrial Fibrillation: Rate, Rhythm & Anticoagulation

Atrial fibrillation (AF) is characterized by disorganized atrial electrical activity at 350-600 bpm with an irregularly irregular ventricular response and absence of discernible P waves.

Rate Control vs. Rhythm Control

• Rate Control (AF Without Preexcitation): First-line for most elderly, asymptomatic, or minimally symptomatic patients. Target resting heart rate is < 110 bpm (lenient rate control, RACE II study). Pharmacological agents include:
  • Beta-Blockers: Metoprolol tartrate/succinate, bisoprolol, or atenolol. Preferred in coronary disease or adrenergic drive.
  • Non-dihydropyridine CCBs: Diltiazem or verapamil. Highly effective for rapid symptom relief, but strictly contraindicated in HFrEF (LVEF <= 40%).
  • Digoxin: Inhibits Na+/K+-ATPase, enhancing vagal tone. Slower onset; effective at rest but ineffective during physical exertion. Valuable adjunct in sedentary elderly patients or co-existing HFrEF.
• Rhythm Control: Consider for symptomatic or recently diagnosed AF, tachycardiomyopathy, or inadequate rate control. Options include electrical cardioversion, amiodarone, or flecainide/propafenone when significant structural or ischemic heart disease is absent. Pre-excited AF (WPW) requires a different approach: cardiovert immediately if unstable; if stable, use electrical cardioversion or expert-guided IV procainamide/ibutilide. Avoid adenosine, beta-blockers, verapamil/diltiazem, digoxin and IV amiodarone because they can precipitate VF.
• Cardioversion and Anticoagulation (AHA Approach): For elective cardioversion when AF has lasted >= 48 hours or its duration is unknown, provide at least 3 weeks of uninterrupted therapeutic anticoagulation, or perform TEE to exclude intracardiac thrombus with therapeutic anticoagulation established before cardioversion. Continue anticoagulation for at least 4 weeks afterwards with either approach, then according to long-term stroke risk. A shorter reported duration does not eliminate embolic risk; assess duration and stroke risk before cardioversion. If AF causes life-threatening hemodynamic instability, perform immediate synchronized cardioversion without waiting for TEE or 3 weeks of anticoagulation; establish anticoagulation as soon as feasible.

Thromboembolic Risk Stratification: CHA2DS2-VASc

All patients with non-valvular atrial fibrillation must be stratified for long-term systemic thromboembolism risk using the CHA2DS2-VASc scoring system:

• Anticoagulation Thresholds:
  • Score >= 2 in men or >= 3 in women: Oral anticoagulation is strongly recommended.
  • Score 1 in men or 2 in women: Oral anticoagulation should be considered based on individual bleeding risk and shared decision-making.
  • Score 0 in men or 1 in women: No antithrombotic therapy indicated.
• Direct Oral Anticoagulants (DOACs) (Apixaban, Rivaroxaban, Dabigatran, Edoxaban) are preferred over Warfarin due to superior safety profiles (significantly lower intracranial hemorrhage risk), fixed dosing, and lack of routine INR monitoring. Warfarin remains mandatory in patients with mechanical prosthetic heart valves or moderate-to-severe mitral stenosis (target INR 2.5-3.5 or 2.0-3.0 depending on valve type/position).
• Bleeding Risk: Quantified using the HAS-BLED score (Hypertension, Abnormal renal/liver function, Stroke, Bleeding history, Labile INR, Elderly > 65, Drugs/alcohol). A high score (>= 3) does not exclude anticoagulation but mandates aggressive mitigation of reversible bleeding risk factors.

Bradyarrhythmias & Conduction Blocks

Bradyarrhythmias (heart rate < 50-60 bpm) stem from sinus node dysfunction or atrioventricular (AV) conduction failure.

Atrioventricular Conduction Blocks

1. First-Degree AV Block: Consistent prolongation of the PR interval > 200 ms (0.20 seconds) with a 1:1 P to QRS ratio. Benign conduction delay within the AV node. Generally asymptomatic; no treatment needed.
2. Second-Degree AV Block, Mobitz Type I (Wenckebach):
   • Electrocardiography: Progressive, cyclical prolongation of the PR interval until a P wave fails to conduct (dropped QRS). The PR interval following the pause is the shortest.
   • Location: Nodal level. Often physiological (high vagal tone in athletes) or due to inferior myocardial ischemia.
   • Prognosis & Treatment: Low risk of progression to complete heart block. Rarely requires treatment unless symptomatic; responds readily to atropine.
3. Second-Degree AV Block, Mobitz Type II:
   • Electrocardiography: Intermittent non-conducted P waves with constant, fixed PR intervals in conducted beats.
   • Location: Infranodal defect (His bundle or bundle branches). Pathological; commonly associated with anterior myocardial infarction or extensive conduction system sclerosis (Lenègre-Lev disease).
   • Prognosis & Treatment: High risk of progression to complete block. Arrange urgent monitored specialist care and pacing capability; atropine is unreliable. Use temporary pacing for hemodynamic compromise. Permanent pacing is indicated when acquired Mobitz II is not due to a reversible or physiological cause.
4. Third-Degree (Complete) AV Block:
   • Electrocardiography: Complete atrioventricular dissociation. P waves march out at a regular intrinsic atrial rate (60-90 bpm), and QRS complexes march out at an independent, slower escape rate (20-40 bpm). No relationship between P waves and QRS complexes.
   • Symptoms: Severe fatigue, syncope (Stokes-Adams attacks), cardiogenic shock, sudden death.
   • Treatment: Stabilize hemodynamic compromise with temporary pacing, identify reversible causes, and obtain urgent specialist assessment. Permanent pacing is indicated for acquired complete block without a reversible or physiological cause.

Acute Emergency Management of Bradycardia

For symptomatic bradycardia (hypotension, altered mental status, chest pain, shock):

• Atropine: First-line pharmacological agent. Administer 0.5 to 1.0 mg IV bolus, repeated every 3 to 5 minutes to a maximum cumulative dose of 3.0 mg (full vagolytic dose). Ineffective in infranodal blocks (Mobitz II and wide-QRS 3rd-degree block) or denervated hearts (heart transplants).
• Transcutaneous Pacing (TCP): Initiate for persistent hemodynamic compromise when atropine is ineffective; do not delay pacing in unstable high-grade infranodal block. Sedate if conscious. Set demand rate at 60-80 bpm; increase current (milliamperes) until consistent electrical capture (wide QRS and broad T wave following every pacer spike) and mechanical capture (palpable femoral or radial pulse matching the pacer rate) are confirmed.
• Chronotropic Infusions: While awaiting or bridging pacing: Adrenaline (Epinephrine) infusion at 2 to 10 mcg/min, or Dopamine infusion at 5 to 20 mcg/kg/min titrated to heart rate and blood pressure.

BLS & ACLS Algorithms for Cardiac Arrest

High-quality cardiopulmonary resuscitation (CPR) and rapid defibrillation remain the cardinal determinants of cardiac arrest survival.

High-Quality CPR Quality Metrics

• Chest Compression Rate: 100 to 120 compressions per minute.
• Compression Depth: 5 to 6 cm (2 to 2.4 inches) in adults.
• Chest Recoil: Allow complete recoil between compressions; do not lean on the chest.
• Minimize Interruptions: Chest compression fraction (CCF) should exceed 80%; pauses for pulse/rhythm checks limited to < 10 seconds.
• Ventilation: 30 compressions to 2 ventilations without advanced airway. Once an advanced airway (endotracheal tube or supraglottic airway) is secured, provide continuous compressions with 1 breath every 6 seconds (10 breaths/min) without pausing. Avoid hyperventilation (which increases intrathoracic pressure, impeding venous return and cardiac output).

Shockable vs. Non-Shockable Pathways

+-----------------------------------------------------------------------------------------+
|                                 ADULT CARDIAC ARREST                                    |
|                           Start CPR - Attach Monitor/Defibrillator                       |
+-----------------------------------------------------------------------------------------+
                                             |
                   +-------------------------+-------------------------+
                   |                                                   |
                   v                                                   v
         [ SHOCKABLE RHYTHM ]                                [ NON-SHOCKABLE RHYTHM ]
        (VF / Pulseless VT)                                       (PEA / Asystole)
                   |                                                   |
                   v                                                   v
         DELIVER 1 SHOCK                                     Immediate CPR (2 min)
      (Biphasic 120-200 J)                                   Give Adrenaline 1 mg IV/IO
                   |                                         as early as possible
                   v                                                   |
         Immediate CPR (2 min)                                         v
                   |                                         Repeat Adrenaline
                   v                                         every 3-5 min
         Rhythm Check -> Shockable?                                    |
                   |                                                   v
                   v                                         Search & Treat Reversible
         DELIVER 2nd SHOCK                                   Causes: 4 Hs & 4 Ts
         Resume CPR immediately                                        |
         Give Adrenaline 1 mg IV/IO                                    v
         (repeat every 3-5 min)                              Rhythm Check every 2 min
                   |
                   v
         Rhythm Check -> Shockable?
                   |
                   v
         DELIVER 3rd SHOCK
         Resume CPR immediately
         Give Amiodarone 300 mg IV/IO
         (or Lidocaine 1-1.5 mg/kg)
                   |
                   v
         Subsequent Shocks:
         Amiodarone 150 mg after 5th shock

The Reversible Causes: 4 Hs and 4 Ts

Throughout CPR, especially in PEA and asystole, clinicians must systematically evaluate and reverse the underlying drivers: