Tachyarrhythmias: Fast rhythms from atria or ventricles.

Bradyarrhythmias (not detailed here but implied as opposite): Slow heart rhythms.

Cardiac arrest context: Most arrhythmias are ventricular in origin (~80%).

TOO  FAST				TOO  SLOW
NARROW COMPLEX		BROAD COMPLEX		NARROW COMPLEX		BROAD COMPLEX
REGUALR	IRREGULAR	REGULAR	IRREGULAR
SVT Flutter Sinus Tachy	AF A-flutter with variable block	VT Conduction abN	VF AF with LBBB	Sinus (medications) AF (medications) SSS(sick sinus Syndrome) 2nd degree heart block		BBB 3rd degree HB Poisoned Heart (hypoxia, acidosis, overdose, hypothermia)
TOO  FAST				TOO  SLOW
Compromised		Stable		Compromised	Stable
Electricity		Medical Management		= treat rhythm Atropine Adrenaline Pacemaker	= treat cause Ischaemia Medications SSS ABG, K+
Check K+, Mg, Digoxin toxicity, B-Blocker, Systemic illness

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Management

from https://www.anzcor.org/home/adult-advanced-life-support/guideline-11-9-managing-acute-dysrhythmias/

Broad-Complex Tachycardia (QRS ≥ 0.12s)

Regular

• Assume VT unless proven otherwise.
• GCS 15
  • First-line: Amiodarone 300 mg IV (with 250 mL 5% glucose) over 20–60 min → Infuse 900 mg/24 hr
  • Consider electrical cardioversion if unstable or persistent.
  • Transvenous pacing if refractory to cardioversion.
  • IV lignocaine: useful if post-MI VT.
  • Avoid: Verapamil/Diltiazem in wide-QRS tachycardia unless proven SVT
• GCS not 15/Cardiac Arrest
  • Shockable VT/VF: Adrenaline: 1 mg every 3-5 minutes
  • Non-Shockable Asystole/PEA: Adrenaline: 1 mg every 3-5 minutes (every 2nd loop)

Irregular

• Most likely: AF with bundle branch block.
• Other causes:
  • Pre-excited AF (e.g., WPW)
  • Polymorphic VT (torsades de pointes)
• Pre-excited AF: Avoid AV blockers (adenosine, digoxin, verapamil, diltiazem).
  • Electrical cardioversion preferred.
• Torsades:
  • MgSO₄ 5 mmol IV over 10 min ± repeat → then 20 mmol over 4 hrs.
  • Stop QT-prolonging drugs; correct electrolytes.
  • Acute pacing or isoprenaline if bradycardia or pause-dependent.
  • Calcium Gluconate: 1 g to replenish calcium (often administered together with magnesium)

2. Narrow-Complex Tachycardia (QRS < 0.12s)

Regular

• Types:
  • Sinus tachycardia
  • AVNRT
  • AVRT (e.g. WPW)
  • Atrial flutter with fixed block
• If unstable: Immediate synchronised cardioversion.
• If stable:
  • Vagal manoeuvres → adenosine (6 mg → 12 mg × 2)
  • If fails: Verapamil 2.5–5 mg IV or Diltiazem 15–20 mg IV

Irregular

• Most common: Atrial fibrillation
• Consider atrial flutter with variable block
• If unstable: Immediate cardioversion.
• If stable:
  • Rate control:
    • Beta-blockers (e.g., metoprolol 5 mg IV)
    • Digoxin (250–500 mcg IV or PO)
    • Verapamil/Diltiazem (IV)
  • Avoid if pre-excitation present.
  • Consider anticoagulation if AF > 48 hrs (unless TOE rules out clot).

Supraventricular Tachycardia (SVT):

• Adenosine:
  • 3 mg → 6 mg → 12 mg (adult)
  • 0.04 to 0.25 mg/kg (children)
  • Note: May cause pain, anxiety, sense of doom
  • Contraindications: Sick sinus syndrome, symptomatic bradycardia, second and third degree AV block, allergy, caution with asthma and COPD

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Atrial Fibrillation (AF) – Acute Management

If unstable

• Synchronised cardioversion (after sedation)

If stable

• Rate control:
  • First-line: β-blockers or CCBs (unless HF)
  • HF or LV dysfunction: Digoxin or amiodarone
• Pharmacological Evidence:
  • Class A: Use β-blockers or ND-CCBs unless contraindicated (LOE II)
  • Class B: Combination therapy reasonable (LOE II)
  • Class C: Avoid digoxin as monotherapy in paroxysmal AF

Pharmacological Options in AF (Rate Control)

Drug	Indication	Avoid In	Notes
β-blockers	Most AF cases, especially active patients	Bronchospasm, acute HF	IV/Oral; monitor hypotension
Verapamil/Diltiazem	Alternative to β-blockers	LV dysfunction, hypotension	Good for rate + BP control
Digoxin	Sedentary, LV dysfunction, HF	Pre-excitation, monotherapy in paroxysmal AF	Good for rest HR
Amiodarone	Refractory cases, HF	Long-term use without monitoring	QT prolongation, many side effects

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Bradycardia

• Bradyarrhythmia = HR < 60/min
• Not always pathological — may be physiological (e.g., athletes, during sleep)
• Emergency treatment required only if symptomatic or associated with adverse signs

Symptoms Suggestive of Clinically Significant Bradycardia

• Syncope (fainting)
• Shortness of breath
• Dizziness
• Chest pain

Adverse Features Suggesting Need for Urgent Intervention

• Systolic BP < 90 mmHg
• HR < 40 bpm
• Ventricular arrhythmias
• Signs of heart failure

If pulseless, manage as cardiac arrest (ANZCOR 11.2)

Pharmacological Management

🥇 First-line

• Atropine IV:
  • Dose: 500–600 mcg IV every 3–5 min
  • Max total dose: 3 mg
  • Level of Evidence: III-2

Second-line (if atropine ineffective)

• Adrenaline IV infusion:
  • Dose: 2–10 mcg/min
  • Goal: Maintain MAP ≥ 70 mmHg
• Isoprenaline: 2–5 mcg/min
• Dopamine: 2–5 mcg/kg/min
• Theophylline (evidence: III-2)
• Glycopyrrolate

Caution

• Beta-blocker or CCB toxicity:
  • Consider IV glucagon
  • Insulin-glucose-potassium therapy (Level IV evidence)
• Cardiac transplant:
  • Do not give atropine — may induce paradoxical AV block

Pacing (if pharmacological therapy fails or high-risk features)

Indications for Electrical Pacing

• Recent asystole
• Mobitz II AV block
• Complete heart block (especially with:
  • Broad QRS
  • Initial HR < 40 bpm)
• Ventricular standstill > 3 sec

Technical Setup

• Use external or internal pacing
• Demand mode: Set to 70–80 bpm
  • Start current at ~30 mA
  • Increase until electrical capture
• In pre-hospital/transport: Use fixed (asynchronous) mode to avoid artefact interference

Patient Comfort

• External pacing stimulates skeletal muscle → can cause discomfort/pain

Class A Recommendation Summary (https://www.anzcor.org)-

Management Step	Recommendation	Evidence Level
Atropine first-line	Yes	III-2
Adrenaline, Isoprenaline, Dopamine	Yes (2nd-line)	III-2
Glucagon/Insulin-Glucose-K	If BB/CCB-induced	IV
External pacing for high-risk	Yes	A
Avoid atropine post-transplant	Yes	1

🔍 Special Considerations for AV Block in Acute Myocardial Infarction (AMI)

🟢 Inferior MI

• Location of Block: Typically at the AV node (supra-Hisian).
• Mechanism: Often due to increased vagal tone or ischemia to the AV node (supplied by RCA).
• Prognosis:
  • Usually transient and self-limiting
  • Rarely progresses to complete heart block
• Management:
  • Atropine often effective
  • Temporary pacing rarely required
  • Monitor closely; resolution often occurs within 72 hours

🔴 Anterior MI

• Location of Block: Typically at the His-Purkinje system (infra-Hisian or intraventricular conduction system)
• Mechanism: Structural damage to the conduction system from large infarct area (usually LAD territory)
• Prognosis:
  • Often permanent
  • Associated with poor outcomes and high mortality
• Management:
  • Atropine often ineffective
  • Emergency transvenous pacing usually indicated
  • Consider early permanent pacing if conduction fails to recover

🚑 Key Clinical Distinctions

Feature	Inferior MI	Anterior MI
Site of Block	AV node	Bundle of His or below
Likely Type	Mobitz I or complete HB	Mobitz II or complete HB
Responsiveness to Atropine	Usually effective	Often ineffective
Need for Pacing	Rarely	Frequently (emergency pacing)
Prognosis	Usually benign	High risk; may be fatal