3.3 Dysrhythmias, ECG & ACLS

Systematic Rhythm Interpretation

Interpret every strip the same way: (1) determine the rate (300 divided by the number of large boxes between R waves for a regular rhythm), (2) assess regularity, (3) evaluate the P waves and their relationship to each QRS, (4) measure the PR interval (normal 0.12-0.20 seconds), and (5) measure the QRS width (normal under 0.12 seconds; a wide QRS suggests a ventricular or bundle-branch origin). This disciplined five-step read separates narrow- from wide-complex and organized from disorganized rhythms — the same axis that drives every ACLS decision at the bedside.

Lethal Arrest Rhythms

In cardiac arrest, the CCRN expects you to sort four rhythms into shockable and non-shockable because that decision drives the entire ACLS pathway.

• Ventricular fibrillation (VF) — chaotic, disorganized ventricular activity with no effective contraction. Shockable.
• Pulseless ventricular tachycardia (pVT) — organized wide-complex tachycardia with no pulse. Shockable.
• Asystole — flatline, no electrical activity. Non-shockable.
• Pulseless electrical activity (PEA) — organized electrical rhythm on the monitor but no palpable pulse. Non-shockable.

For shockable rhythms: deliver an immediate defibrillation (biphasic 120-200 J per manufacturer), resume high-quality CPR for 2 minutes, give epinephrine 1 mg IV every 3-5 minutes, and after the second shock give amiodarone 300 mg IV push (then 150 mg), or lidocaine as an alternative. For non-shockable rhythms: CPR, epinephrine as soon as possible, and aggressively search for and treat the reversible H's and T's (hypovolemia, hypoxia, hydrogen ion/acidosis, hypo-/hyperkalemia, hypothermia; tension pneumothorax, tamponade, toxins, thrombosis-pulmonary, thrombosis-coronary).

Defibrillation versus Synchronized Cardioversion

This distinction is heavily tested.

• Defibrillation is UNsynchronized — it delivers a shock at any point in the cycle. Used for pulseless VF and pVT (and polymorphic/torsades where syncing is impossible).
• Synchronized cardioversion times the shock to the R wave to avoid the vulnerable T wave (which could induce VF). Used for unstable rhythms that still have a pulse: unstable SVT, unstable atrial fibrillation or flutter, and stable-but-unstable monomorphic VT with a pulse. Signs of instability include hypotension, altered mentation, ischemic chest pain, and acute heart failure.

A monitored patient in wide-complex tachycardia who becomes pulseless needs immediate defibrillation, not cardioversion — once there is no pulse, the rhythm is treated as VF/pVT.

Tachydysrhythmias with a Pulse

• Supraventricular tachycardia (SVT) — regular narrow-complex tachycardia (150-250/min). If stable: vagal maneuvers, then adenosine 6 mg rapid IV push followed by a saline flush; repeat 12 mg if needed. If unstable: synchronized cardioversion.
• Atrial fibrillation — irregularly irregular, no discrete P waves. Atrial flutter — sawtooth flutter waves, often 2:1 or 4:1 conduction. Management: rate control with a beta-blocker or a non-dihydropyridine calcium channel blocker (diltiazem); rhythm control when indicated; and anticoagulation. Because atrial thrombus can form, any AF or flutter present more than 48 hours requires anticoagulation or a transesophageal echocardiogram to exclude clot before elective cardioversion. If the patient is unstable, perform immediate synchronized cardioversion.
• Torsades de pointes — polymorphic VT with a twisting axis, associated with a prolonged QT. Treat with IV magnesium sulfate; defibrillate if pulseless.

Other Common Rhythms

Premature ventricular contractions (PVCs) are early, wide beats; frequent multifocal PVCs, couplets, or the R-on-T phenomenon can herald ventricular tachycardia. Junctional rhythms arise from the AV node when the SA node fails, producing a narrow-complex rhythm at 40-60/min with absent, inverted, or retrograde P waves. Accelerated idioventricular rhythm (AIVR) is a benign, wide, slow rhythm (40-100/min) frequently seen as a reperfusion marker after successful PCI or fibrinolysis and usually needs no treatment. Recognizing these largely stable rhythms — and not reflexively shocking them — prevents unnecessary and harmful interventions.

Bradydysrhythmias and Heart Blocks

Symptomatic bradycardia (rate under 50 with hypotension, altered mentation, ischemic chest pain, or shock): first-line drug is atropine 1 mg IV every 3-5 minutes to a maximum of 3 mg. If atropine fails, use transcutaneous pacing and/or a chronotropic infusion (dopamine or epinephrine).

Heart blocks reflect delayed or failed AV conduction:

Atropine is often ineffective in Mobitz II and complete block because the lesion is below the AV node — go to pacing. Pacing modalities include transcutaneous (fastest, emergency, requires sedation/analgesia for capture discomfort), transvenous (temporary, more reliable), and epicardial wires placed after cardiac surgery. Always confirm electrical capture (a pacer spike followed by a wide QRS) and mechanical capture (a corresponding palpable pulse) — a spike without a pulse is failure to capture.

ACLS Drug Quick Reference

A final trap: adenosine and cardioversion are for stable versus unstable SVT, but neither belongs in a pulseless rhythm — a patient with no pulse always follows the VF/pVT or PEA/asystole arrest algorithm.