Cardiac Rhythm Disturbances

1. THE PHYSIOLOGICAL FOUNDATION

• The Electrophysiological Engine: Cardiac dysrhythmias are broadly classified by their electrophysiologic origin (supraventricular vs. ventricular), their ECG appearance (narrow vs. wide QRS), and their ventricular rate. They arise either from abnormal impulse generation (automaticity/triggered activity) or abnormal conduction (reentry circuits) (External Knowledge).
• The Hemodynamic Crisis: The clinical significance of any dysrhythmia is determined by its impact on systemic perfusion. At extremes of rate (e.g., typically \(>150\) beats/min or \(<50\) beats/min), the heart fails to maintain adequate stroke volume and cardiac output. This demand-supply mismatch results in coronary hypoperfusion (ischemic chest pain), pulmonary edema (dyspnea), and cerebral hypoperfusion (altered sensorium or syncope).

2. THE MATHEMATICAL / DIAGNOSTIC ENGINE

• QRS Duration Cutoffs:
• Narrow-Complex: \(\le 0.09\) seconds in pediatrics, or \(< 0.12\) seconds in adults. Primarily represents sinus tachycardia or supraventricular tachycardia (SVT).
• Wide-Complex: \(\ge 0.12\) seconds. Must be presumed to be Ventricular Tachycardia (VT) or SVT with aberrant conduction.
• The Instability Criteria: A patient is defined as "unstable" if the dysrhythmia directly causes any of the following:
• Hypotension (e.g., SBP \(< 90\) mm Hg).
• Acutely altered mental status.
• Signs of shock or systemic hypoperfusion.
• Ischemic chest discomfort.
• Acute heart failure / pulmonary edema.
• Torsades de Pointes (TdP) Equation: TdP strictly requires the presence of polymorphic ventricular tachycardia (PVT) and a prolonged QTc interval. PVT without a prolonged QT is most commonly caused by myocardial ischemia, not TdP.

3. THE CRASHING PATIENT PROTOCOL

Management is strictly bifurcated based on the presence of a pulse and the presence of hemodynamic instability.

• The Pulseless Patient (Cardiac Arrest):
• Shockable (VF / pVT): Immediate defibrillation (200 J biphasic or 360 J monophasic), followed by 2 minutes of CPR. Epinephrine 1 mg IV every 3–5 mins. Amiodarone (300 mg, then 150 mg) or Lidocaine (1-1.5 mg/kg, then 0.5-0.75 mg/kg) for refractory rhythms.
• Non-Shockable (Asystole / PEA): Epinephrine ASAP and continuous CPR. Aggressively hunt for the Reversible Causes (The 5 H's and 5 T's).
• The Unstable Patient WITH a Pulse:
• Tachycardia: Immediate synchronized cardioversion. Consider sedation if feasible, but do not delay therapy.
• Bradycardia: Atropine 1 mg IV bolus. If ineffective, rapidly transition to Transcutaneous Pacing OR Dopamine infusion OR Epinephrine infusion.
• The Stable Patient:
• Narrow/Regular Tachycardia: Vagal maneuvers, then Adenosine. If refractory, use Beta-blockers or Calcium Channel Blockers.
• Wide Tachycardia: Assume VT. Consider Amiodarone or Procainamide infusions. Seek expert consultation.

4. THE PHARMACOLOGY MATRIX

• Adenosine
• Target: Purinergic receptors (transiently blocks AV node conduction) (External Knowledge).
• Dose: 6 mg rapid IV push with a saline flush. If unsuccessful, give a second dose of 12 mg. Indicated for regular, monomorphic tachycardias.
• Amiodarone
• Target: Class III antiarrhythmic (potassium-channel blocker with Class I, II, and IV properties) (External Knowledge).
• Dose (Stable Wide-QRS): 150 mg IV over 10 minutes. Follow with a maintenance infusion of 1 mg/min for the first 6 hours.
• Procainamide
• Target: Class Ia antiarrhythmic (sodium-channel blocker) (External Knowledge).
• Dose: 20–50 mg/min until arrhythmia is suppressed, hypotension ensues, QRS duration increases \(>50%\), or a maximum dose of 17 mg/kg is reached. Maintenance: 1-4 mg/min.
• Atropine
• Target: Muscarinic antagonist (vagolytic) (External Knowledge).
• Dose: 1 mg IV bolus, repeated every 3-5 minutes up to a maximum of 3 mg.
• Diltiazem
• Target: Calcium channel blocker (slows ventricular rate in atrial fibrillation/flutter).
• Dose: 15–20 mg IV bolus over 2 mins. If rate response is satisfactory, begin infusion at 5–10 mg/hr.

5. THE TITRATION & MONITORING GRID

• Hunting the Reversible Causes (Hs and Ts): For any refractory dysrhythmia or cardiac arrest, actively correct: Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypo-/hyperkalemia, Hypothermia, Tension pneumothorax, Tamponade (cardiac), Toxins, Thrombosis (pulmonary/coronary).
• Vasopressor Titration for Bradycardia: If utilizing infusions for unstable bradycardia, titrate Dopamine at 5–20 mcg/kg/min or Epinephrine at 2–10 mcg/min specifically to the patient's hemodynamic response and taper slowly once stable.
• Sodium Bicarbonate Titration: In wide-complex tachycardia suspected to be caused by Sodium-channel blocker toxicity (e.g., Tricyclic Antidepressant overdose), administer 1 mEq/kg Sodium Bicarbonate IV slowly.

6. THE DANGER ZONE

• The "Polypharmacy" Trap: Do not sequentially administer Amiodarone and Procainamide for a stable wide-complex tachycardia. Both medications prolong the QRS and QTc intervals; combining them drastically increases the risk of precipitating Torsades de Pointes or fatal cardiovascular collapse.
• The "Undifferentiated Wide QRS" Trap: Administering an AV-nodal blocker (Verapamil or Diltiazem) to a patient with an undifferentiated wide-complex tachycardia. If the rhythm is VT or WPW with antidromic conduction, blocking the AV node can accelerate ventricular rates and induce ventricular fibrillation (External Knowledge).
• The Hyperkalemia Mimic: A patient presenting with profound weakness, peaked T waves, absent P waves, and a dangerously wide QRS (e.g., 240 ms) must not be treated with standard antiarrhythmics. This is severe hyperkalemia; the immediate, lifesaving treatment is IV Calcium to stabilize the myocyte membrane and narrow the QRS.

7. MCQ MASTERCLASS

• The "Twisting" Rhythm Buzzword: A board question describing a "polymorphic VT twisting around the isoelectric line" with a history of a prolonged QTc or malnutrition is testing Torsades de Pointes. The first-line therapy is IV Magnesium.
• The "Fusion/Capture Beat" Distractor: An ECG describing a wide-complex tachycardia at 160 bpm that exhibits occasional "fusion beats," "capture beats," or AV dissociation is definitively Ventricular Tachycardia, completely ruling out SVT with aberrancy.
• The "Ischemic Pain" Pairing: If a patient with a heart rate of 170 bpm is complaining of crushing chest pain and their blood pressure is 85/50, they are unstable. Written boards will often offer Adenosine or Amiodarone as distractors. The correct action is always Synchronized Cardioversion.

8. THE ER RESIDENCY SCRIPT

"Cardiology/ICU team, I am calling to hand off a 65-year-old male who presented in extremis with an unstable, monomorphic wide-complex tachycardia. Initial vitals demonstrated a heart rate of 185 bpm with a systolic blood pressure of 78 mm Hg and acutely altered mentation, meeting AHA criteria for cardiovascular instability. An immediate 12-lead ECG confirmed a wide QRS of 160 ms with AV dissociation, highly suggestive of ventricular tachycardia. Given the profound instability, he underwent immediate synchronized cardioversion at 100 Joules, which successfully converted him to normal sinus rhythm with a MAP now > 65 on room air. Post-cardioversion ECG shows no acute ST-elevation. His labs are pending, including potassium and magnesium, but he remains hemodynamically stable on a prophylactic Amiodarone infusion at 1 mg/min. He requires admission to the CCU for continuous rhythm monitoring, evaluation for ischemic drivers, and potential EP studies."