Dysrhythmia Recognition & Response

Clinical Reference & Study Guide  ·  Thompson Health 2026 Edition  ·  19 pages

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Clinical Reference & Study Guide

Dysrhythmia
Recognition
& Response

Bedside Quick Reference Manual
Recognize  →  Assess Stability  →  Act
2026 Edition
19 Pages  ·  Print double-sided for booklet use
Thompson Health  ·  For educational use
Not a substitute for clinical judgment

How to Use This Manual

Thompson Health · Dysrhythmia Recognition & Response · 2026

🎯 Purpose

This manual supports recognition of cardiac dysrhythmias at the bedside. Use it during monitoring, when interpreting telemetry strips, or as an open-book study resource.

Each rhythm section follows the same structure: Recognize → Clinical significance → Act.

⚡ Quick Start

  1. Apply the 5-Step Method (p. 3) to every strip
  2. Identify the rhythm using the appropriate section (p. 5–12)
  3. Assess hemodynamic stability before any intervention
  4. Refer to ACLS algorithms for treatment decisions (p. 13–14)
  5. Verify medications and doses on p. 15
  6. When in doubt — call the provider

⚠ Important Safety Note

This manual is an educational reference tool. It does not replace clinical judgment, provider orders, or institutional protocols. Always assess the patient, not just the monitor.

📚 Table of Contents

Foundations
ECG Fundamentals & 5-Step Method3
Normal Intervals & Conduction System4
Rhythm Recognition
Sinus Rhythms5
Atrial Ectopy (PAC, WAP, MAT)6
Atrial Fibrillation7
Atrial Flutter & SVT8
Junctional Rhythms9
Ventricular Ectopy & PVCs10
Ventricular Tachycardia, Fibrillation & Arrest11
AV Blocks12
Emergency Algorithms
ACLS: Bradycardia With a Pulse13
ACLS: Tachycardia & Cardiac Arrest14
Medications & QTc Reference15
Reference
Notes16

📋 How This Manual Is Organized

Rhythm cards use a consistent 3-column layout:

RECOGNIZE CLINICAL NOTE ACT
Rate, rhythm, P waves, PR, QRS Why it matters, what to watch for Immediate action & escalation

🔗 Online companion course: thompsonhealth.com/dysrhythmia

Thompson Health · For educational use · Not a substitute for clinical judgment
2

ECG Fundamentals & 5-Step Method

Thompson Health · Dysrhythmia Recognition & Response · 2026

5-Step Rhythm Interpretation

Apply this sequence to every strip before making any clinical decision.

1 Rhythm Regular or irregular? Mark two consecutive R waves on scrap paper, slide to the next beat to check regularity. Consistent spacing = regular.
2 Rate 6-Second Method: Count QRS complexes in 6 seconds × 10. Count 30 large boxes, or use the tick marks at the top of the paper. Works for ALL rhythms — regular or irregular.
3 P Waves Present? Upright in Lead II? One P per QRS? Do all P waves look alike? Is every P followed by a QRS?
4 PR Interval Measure from the start of the P wave to the start of the QRS. Normal: 0.12–0.20 sec (3–5 small boxes). Prolonged or absent?
5 QRS Width Narrow <0.12 sec (<3 small boxes) = supraventricular origin. Wide ≥0.12 sec = ventricular origin or aberrant conduction.

ECG Paper Basics

Time (Horizontal)
1 small box0.04 sec (40 ms)
1 large box (5 small)0.20 sec (200 ms)
5 large boxes1.0 second
6-second strip30 large boxes
Amplitude (Vertical)
1 small box0.1 mV
1 large box0.5 mV
Standard calibration10 mm = 1 mV

Rate Estimation — Quick Reference

When counting R-R large boxes for a regular rhythm:

Large boxesApprox. rate
1 box300 bpm
2 boxes150 bpm
3 boxes100 bpm
4 boxes75 bpm
5 boxes60 bpm
6 boxes50 bpm

Use the 6-second method for irregular rhythms (AFib, MAT, etc.)

Tip: Always look at the patient first, then the monitor. A "bad" rhythm in a patient with a normal BP and clear mentation is very different from the same rhythm in a hemodynamically unstable patient.
Thompson Health · For educational use · Not a substitute for clinical judgment
3

Normal Intervals & Conduction System

Thompson Health · Dysrhythmia Recognition & Response · 2026

Normal Interval Ranges

IntervalNormalSignificance
PR Interval 0.12–0.20 s >0.20 = 1st-degree block; <0.12 = preexcitation (WPW)
QRS Duration <0.12 s ≥0.12 = bundle branch block or ventricular origin
QT Interval 0.36–0.44 s Rate-dependent; flag if >500 ms or >60 ms rise from baseline
QTc (corrected) <440 ms (M)
<460 ms (F)		 >500 ms = high Torsades de Pointes risk; stop offending drugs

Pacemaker Hierarchy

SiteIntrinsic RatePrimary Rhythm Name
SA Node 60–100 bpm Normal Sinus Rhythm
AV Junction 40–60 bpm Junctional Rhythm
Ventricles 20–40 bpm Idioventricular Rhythm

Higher pacemakers suppress lower ones. SA node failure → AV junction takes over at its slower rate. AV junction failure → ventricular escape at 20–40 bpm.

Conduction Pathway

SA Node → Atria → AV Node ⏱ → Bundle of His → L & R Bundle Branches → Purkinje Fibers → Ventricles

⏱ The AV node intentionally slows conduction (~120 ms) to allow atrial contraction to complete ventricular filling (atrial kick) before the ventricles contract.

Why PR interval matters:
The AV node delay (PR) allows the atria to squeeze blood into the ventricles before contraction begins. A prolonged PR = slowed AV conduction. A blocked PR = dropped beat (no QRS follows the P wave).

ECG Waveform Anatomy

Wave/SegmentRepresents
P waveAtrial depolarization (SA → AV node)
PR segmentAV node conduction delay
QRS complexVentricular depolarization
ST segmentVentricular plateau (isoelectric baseline normal)
T waveVentricular repolarization
U waveLate repolarization (prominent in hypokalemia)
QT intervalTotal ventricular electrical cycle
Thompson Health · For educational use · Not a substitute for clinical judgment
4

Sinus Rhythms

Thompson Health · Dysrhythmia Recognition & Response · 2026

Normal Sinus Rhythm (NSR)

Rate: 60–100 bpm
Recognize
  • Rate 60–100 bpm
  • Rhythm regular
  • Upright P in Lead II before every QRS
  • PR 0.12–0.20 s (constant)
  • QRS <0.12 s (narrow)
Clinical Note

Normal baseline cardiac rhythm. Document as NSR and use as your comparison point. Any deviation from these criteria requires further evaluation.

Act

No intervention required. Continue monitoring. Document as baseline.

Sinus Bradycardia

Rate: <60 bpm
Recognize
  • Rate <60 bpm, otherwise NSR criteria
  • Regular rhythm
  • Normal P-QRS relationship
  • Normal PR and QRS

Drug causes: beta-blockers, CCBs, digoxin, amiodarone, opioids
Non-drug: athletes, vasovagal, hypothyroidism, inferior/posterior MI, elevated ICP

Clinical Note

Often benign (especially athletes). Concerning when patient is symptomatic.

Symptoms to assess: dizziness, syncope, near-syncope, hypotension, chest pain, altered mental status, acute HF.

Inferior MI can cause vagally-mediated bradycardia — treat aggressively in that context.

Act

Asymptomatic: Observe and monitor.

Symptomatic: ACLS Bradycardia Algorithm (p. 13).

Atropine 1 mg IV push — first-line for symptomatic.

Identify and address reversible causes (hold offending meds, treat ischemia).

Sinus Tachycardia

Rate: >100 bpm (usually 100–150)
Recognize
  • Rate >100 bpm, regular
  • Normal P before each QRS
  • PR and QRS normal
  • P wave may merge into T at high rates

Causes: fever, pain, hypovolemia, anxiety, anemia, hypoxia, PE, hyperthyroidism, sepsis, stimulants, caffeine

Clinical Note

Sinus tachycardia is a compensatory response, not a primary arrhythmia. Treating the rate without addressing the cause is inappropriate and may be harmful.

New sinus tach in a hospitalized patient → assess for deterioration.

Act

Identify and treat the underlying cause.

  • Pain → analgesia
  • Fever → antipyretics
  • Hypovolemia → fluids
  • Hypoxia → O2 / airway

Notify provider for new onset or unexplained rate >130.

Sinus Arrhythmia

60–100 bpm

Recognize: Irregular rhythm that speeds with inspiration, slows with expiration. All NSR criteria otherwise met.

Clinical: Normal variant reflecting vagal (autonomic) modulation. Common in young patients, athletes. Confirm the respiratory correlation if uncertain.

Act: No treatment needed. Document and reassure.

Sinus Pause / Arrest

Variable

Recognize: Sudden pause >2 seconds with no P wave. Underlying rhythm usually NSR. Beat may resume (pause) or recovery may be delayed (arrest).

Clinical: May reflect SA node dysfunction, vagal surge, or drug effect. Prolonged pauses can cause dizziness or syncope.

Act: Monitor. Frequent or symptomatic pauses → notify provider. Evaluate for sick sinus syndrome; consider EP referral.

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5

Atrial Ectopy

Thompson Health · Dysrhythmia Recognition & Response · 2026

Premature Atrial Contraction (PAC)

Single ectopic beat
Recognize
  • Early beat with abnormal or different P wave morphology
  • QRS usually narrow (normal ventricular conduction)
  • Non-compensatory pause follows (resets SA node)
  • QRS may be absent (blocked PAC) or wide (aberrant conduction)
Clinical Note

Usually benign. Common triggers: caffeine, stress, electrolyte disturbance, alcohol, stimulant medications.

⚠ Frequent PACs (>10/hr, runs, or PAC bigeminy) are an independent predictor of new-onset atrial fibrillation — document and report to provider.

Act

Isolated: Reduce triggers. Reassure patient.

Frequent: Document frequency. Notify provider.

Check electrolytes (K+, Mg2+). Review medication list for stimulants.

Wandering Atrial Pacemaker (WAP)

Rate: <100 bpm
Recognize
  • ✅ ≥3 different P wave morphologies
  • Rate <100 bpm
  • Irregular rhythm
  • Varying PR intervals
  • QRS usually narrow
Clinical Note

Pacemaker site shifts between SA node, atria, and AV junction. Common with increased vagal tone, COPD, digitalis effect, and underlying heart disease.

Key distinction from AFib: distinct, identifiable P waves are present in WAP.

Act

Usually benign. Observe and monitor.

Treat underlying cause (COPD exacerbation, hypoxia, drug effect).

Multifocal Atrial Tachycardia (MAT)

Rate: >100 bpm
Recognize
  • ✅ ≥3 different P wave morphologies
  • Rate >100 bpm
  • Irregular rhythm (looks like AFib)
  • Distinct, identifiable P waves between QRS complexes
  • PR and P-P intervals vary
Clinical Note

Strongly associated with COPD, hypoxia, hypomagnesemia, hypokalemia, heart failure, and sepsis. Distinguish from AFib by finding distinct P waves.

Often challenging to rate-control; addressing the underlying cause is the priority.

Act

Treat the cause first:

  • Supplemental O2 / bronchodilators for COPD
  • Correct K+ and Mg2+
  • Rate control if needed: metoprolol, verapamil, or diltiazem

Atrial Tachycardia

Rate: 100–250 bpm
Recognize
  • Rate 100–250 bpm, usually regular
  • P waves present but abnormal morphology
  • Isoelectric line visible between P waves (key: not sawtooth)
  • QRS usually narrow
  • PR may be prolonged
Clinical Note

Triggered by ectopic atrial focus firing rapidly. May be caused by catecholamines, digoxin toxicity, structural heart disease, or prior ablation.

Adenosine may transiently slow rate (unmask P waves) but rarely terminates atrial tachycardia.

Act

Unstable: Synchronized cardioversion.

Stable: Rate control (beta-blocker, CCB). Treat underlying cause. Check digoxin level if applicable. Specialist referral for recurrent episodes.

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6

Atrial Fibrillation

Thompson Health · Dysrhythmia Recognition & Response · 2026

Atrial Fibrillation (AFib)

Ventricular rate: variable (often 110–180 uncontrolled)
Recognize
  • Irregularly irregular ventricular rhythm (hallmark)
  • No discrete P waves — chaotic fibrillatory baseline (f-waves)
  • Atrial rate 350–600 bpm (unmeasurable)
  • QRS usually narrow; wide if bundle branch block or WPW
  • PR interval: not measurable
Clinical Note

Stroke risk: Chaotic atrial activity → blood pools in the left atrial appendage → thrombus → embolism → stroke. AFib accounts for ~15–20% of all ischemic strokes.

Atrial kick loss: Coordinated atrial contraction contributes ~25–30% to cardiac output. AFib eliminates this — clinically significant in patients with diastolic dysfunction, HFrEF, or hypertrophic cardiomyopathy.

Act

Unstable (hypotension, AMS, chest pain, acute HF): Immediate synchronized cardioversion (120–200J biphasic).

Stable: Rate control first; then anticoagulation decision; consider rhythm control with specialist involvement.

🎯 Stroke Risk — CHA₂DS₂-VASc

Risk FactorPoints
Congestive heart failure1
Hypertension1
Age ≥75 years2
Diabetes mellitus1
Stroke / TIA history2
Vascular disease (prior MI, PAD, aortic plaque)1
Age 65–74 years1
Sex category (female)1

Score ≥2 (men) or ≥3 (women) = anticoagulation recommended. DOACs preferred over warfarin for most patients.

AFib vs Flutter: Quick Comparison

AFib Flutter
Regularity Irregularly irregular Regular or regularly irregular
Atrial activity Chaotic f-waves Organized sawtooth F-waves
Atrial rate 350–600 bpm 250–350 bpm (~300 typical)
Ventricular rate Variable 150 (2:1), 100 (3:1), 75 (4:1)
Stroke risk High Similar — same anticoag rules

Rate Control vs Rhythm Control

Rate control (most patients): Slow the ventricular response — don't necessarily restore sinus rhythm.

  • Beta-blocker (metoprolol) — first-line in most patients
  • CCB (diltiazem, verapamil) — avoid in HFrEF
  • Digoxin — adjunct in HF, limited rate control during activity
  • Target: HR <110 bpm at rest

Rhythm control (selected patients): Restore and maintain sinus rhythm.

  • Synchronized electrical cardioversion (if <48 hrs or anticoagulated)
  • Chemical cardioversion: amiodarone, flecainide, propafenone
  • Catheter ablation for paroxysmal AFib
  • Specialist involvement required
🚨 New-onset AFib with rapid ventricular response + hemodynamic instability:
Do not delay. Prepare for immediate synchronized cardioversion. Sedate if possible. Do not wait for rate control to work.
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7

Atrial Flutter & Supraventricular Tachycardia

Thompson Health · Dysrhythmia Recognition & Response · 2026

Atrial Flutter

Atrial: ~300 bpm  |  Ventricular: depends on block ratio
Recognize
  • Sawtooth flutter waves (F-waves) — most visible in leads II, III, aVF, and V1
  • Atrial rate typically ~300 bpm
  • No isoelectric baseline between flutter waves
  • Ventricular rate determined by AV conduction ratio:
RatioVentricular Rate
2:1~150 bpm ⚠
3:1~100 bpm
4:1~75 bpm
Clinical Note

Classic clue: Regular rate of ~150 bpm with no clear P waves = flutter until proven otherwise. Apply vagal maneuver or give adenosine to slow ventricular rate and unmask flutter waves.

Organized macro-reentrant circuit around the tricuspid annulus in the right atrium. Catheter ablation is highly effective (>90% cure rate).

Stroke risk is similar to AFib — apply the same anticoagulation rules (CHA₂DS₂-VASc).

Act

Unstable: Synchronized cardioversion 50–100J biphasic.

Stable:

  • Rate control: beta-blocker or CCB
  • Anticoagulation per CHA₂DS₂-VASc
  • Refer for ablation if recurrent
  • Digoxin: less effective for flutter than AFib

Supraventricular Tachycardia (SVT / AVNRT)

Rate: 150–250 bpm
Recognize
  • Rate 150–250 bpm, regular
  • Abrupt onset and termination ("paroxysmal")
  • QRS usually narrow (<0.12 s)
  • P waves often hidden in or just after QRS
  • May see "pseudo-r'" in V1 (retrograde P in QRS)
  • Wide QRS possible if aberrant conduction or WPW (antidromic)
Clinical Note

Most common: AVNRT (reentrant circuit within AV node, ~60%) and AVRT (accessory pathway, ~30%).

Patients describe sudden palpitations, "fluttering," dizziness, chest pressure, or dyspnea. Rarely causes hemodynamic collapse in structurally normal hearts.

⚠️ In WPW, antidromic SVT is a wide-complex tachycardia — avoid AV nodal blockers.

Act

Unstable: Synchronized cardioversion 50–100J.

Stable (stepwise):

  1. Vagal maneuvers (Valsalva, carotid massage)
  2. Adenosine 6 mg rapid IV push + 20 mL NS flush; if no effect → 12 mg (may repeat once)
  3. If adenosine fails: IV diltiazem or metoprolol

Adenosine Administration — Critical Points

  • Initial dose: 6 mg rapid IV push
  • If no effect: 12 mg rapid IV push (may give a second 12 mg dose)
  • Site: Antecubital or more proximal — do not use hand veins
  • Flush: Immediately follow with 20 mL NS flush, fast
  • Half-life: <10 seconds — speed of administration is critical

Warn the patient before administration:

  • Brief chest tightness / pressure
  • Flushing and warmth
  • Transient sense of doom or "impending death"
  • All sensations last only 10–30 seconds
Do not use adenosine in: WPW with irregular wide-complex tachycardia, known sick sinus syndrome without pacemaker, or severe asthma.
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8

Junctional Rhythms

Thompson Health · Dysrhythmia Recognition & Response · 2026
Origin: All junctional rhythms originate in the AV junction (AV node / Bundle of His). Because ventricular conduction uses the normal pathway, the QRS is usually narrow. The key feature is the absent, inverted, or retrograde P wave.

Junctional P Wave — Three Patterns

⬆
Absent P Wave
P hidden within QRS complex
⬇
Inverted P Wave
Inverted in II, III, aVF; before QRS with short PR <0.12 s
↩
Retrograde P Wave
P follows QRS — atria depolarize after ventricles

Junctional Escape Rhythm

Rate: 40–60 bpm
Recognize
  • Rate 40–60 bpm, regular
  • Absent, inverted, or retrograde P waves
  • Narrow QRS (<0.12 s)
  • SA node not functioning as primary pacemaker
Clinical Note

Occurs when SA node fails or rate slows enough for the AV junction to "escape" as a protective backup pacemaker. Common causes: vagal stimulation, sick sinus syndrome, inferior MI, drug effect (digoxin, beta-blockers).

Act

Assess hemodynamics. If symptomatic → ACLS Bradycardia algorithm (p. 13). Identify and treat underlying cause. Consider pacemaker evaluation for recurrent episodes.

Accelerated Junctional Rhythm

Rate: 60–100 bpm
Recognize
  • Rate 60–100 bpm (exceeds intrinsic junctional rate)
  • Same P wave features as junctional escape
  • Narrow QRS, regular
Clinical Note

Rate is abnormally fast for the AV junction. Associated with digoxin toxicity, post-cardiac surgery, inferior MI with reperfusion, and excess catecholamines.

Check digoxin level if clinically indicated.

Act

Usually benign and self-limited. Monitor. Identify and treat underlying cause. Hold digoxin if toxicity suspected; notify provider.

Junctional Tachycardia

Rate: >100 bpm
Recognize
  • Rate >100 bpm, regular
  • Narrow complex (usually)
  • Inverted or retrograde P waves
  • May be confused with SVT
Clinical Note

Distinguish from SVT by identifying the P/QRS relationship and response to adenosine. Junctional tachycardia is typically caused by enhanced automaticity (not reentry), so adenosine may slow it transiently but not terminate it.

Act

Unstable: Cardioversion.

Stable: Treat underlying cause. Rate control with beta-blockers or CCBs if symptomatic. Digoxin toxicity → digoxin-specific Fab fragments (Digibind).

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9

Ventricular Ectopy & PVCs

Thompson Health · Dysrhythmia Recognition & Response · 2026

Premature Ventricular Contraction (PVC)

Early beat from ventricular focus
Recognize
  • Wide, bizarre QRS (≥0.12 s) — different from normal beats
  • No preceding P wave
  • T wave deflects opposite to QRS direction
  • Usually followed by a compensatory pause
  • Uniform (unifocal = one shape) vs. multifocal (multiple shapes)
Clinical Note

Common and often benign in structurally normal hearts. Triggers: electrolyte disturbance, ischemia, hypoxia, stimulants, caffeine, anxiety, medication toxicity.

Concerning with: frequent PVCs, runs, multifocal morphology, R-on-T, new-onset in acute MI.

In acute MI: New PVCs require immediate provider notification — risk of degeneration to VF.

Act

Isolated, rare, asymptomatic: Monitor. Reduce triggers. Check electrolytes.

Frequent, symptomatic, or in setting of MI: Notify provider. Correct K+/Mg2+. Antiarrhythmics if directed.

⚠ PVC Warning Patterns — Notify Provider

PatternDefinitionRisk
Bigeminy PVC every other beat Moderate — effective ventricular rate may be halved
Trigeminy PVC every third beat Moderate
Couplet 2 PVCs in a row Moderate-high
Triplet / VT run 3 or more PVCs = ventricular tachycardia High ⚠
R-on-T Phenomenon: PVC falls on the T wave (vulnerable period of repolarization). The myocardium is partially repolarized — at highest risk for sustaining a lethal dysrhythmia. May trigger VT or VF.
Multifocal PVCs: PVCs with different QRS morphologies indicate multiple irritable ventricular foci — more concerning than unifocal PVCs. Document morphologies and report.

Idioventricular Rhythm

20–40 bpm

Recognize: Wide QRS (≥0.12 s), regular, rate 20–40 bpm. No P waves or AV dissociation. Ventricular escape pacemaker in control.

Clinical: Cardiac emergency if symptomatic. Occurs when SA and AV junctional pacemakers fail.

Act: Assess perfusion immediately. ACLS Bradycardia algorithm. Transcutaneous pacing. Identify reversible causes.

Accelerated Idioventricular (AIVR)

40–100 bpm

Recognize: Wide QRS, regular, rate 40–100. Same features as idioventricular but faster than intrinsic rate.

Clinical: Commonly occurs post-reperfusion (after thrombolytics or primary PCI) — can be a sign of successful reperfusion. Usually transient and self-limiting.

Act: Observe. Do not suppress — it may be the only functioning rhythm. If hemodynamically unstable, treat with atropine.

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10

Ventricular Tachycardia, Fibrillation & Arrest Rhythms

Thompson Health · Dysrhythmia Recognition & Response · 2026

Ventricular Tachycardia (VT) — Monomorphic

Rate: >100 (usually 150–250 bpm)
Recognize
  • Rate >100 bpm, usually regular
  • Wide QRS (≥0.12 s) with consistent morphology
  • ≥3 consecutive PVCs
  • AV dissociation may be visible (P waves march through independently)
  • Fusion beats and capture beats are diagnostic if present
Clinical Note

ALWAYS check for a pulse first. VT can occur with or without a pulse — treatment is completely different.

Treat all wide-complex tachycardia as VT until proven otherwise.

Sustained VT (>30 seconds) is a medical emergency regardless of hemodynamics.

Act

Pulseless VT: Immediate CPR + defibrillation (120–200J biphasic).

Pulse + unstable: Synchronized cardioversion 100J biphasic. Sedate if possible.

Pulse + stable: Amiodarone 150 mg IV over 10 min; or procainamide; prepare for cardioversion.

Torsades de Pointes (Polymorphic VT)

Rate: 150–300 bpm
Recognize
  • Polymorphic VT — QRS axis twists around the isoelectric line ("turning on the axis")
  • Rate 150–300 bpm
  • Often preceded by prolonged QT or short-long-short cycle
  • Episodes may be self-terminating or degenerate to VF
Clinical Note

Triggers: Hypokalemia, hypomagnesemia, QT-prolonging medications, congenital long QT syndrome, bradycardia-dependent QT prolongation.

Standard antiarrhythmics (amiodarone) may worsen Torsades. Magnesium is the treatment of choice.

Act

Pulseless: Defibrillate immediately.

With pulse: Magnesium sulfate 2g IV over 15 min. Correct K+ >4.0 mEq/L and Mg2+ >2.0. Discontinue offending drugs. Overdrive pacing for refractory cases.

Ventricular Fibrillation (VF)

Unmeasurable

Recognize: Chaotic, disorganized electrical activity. No organized QRS complexes. No pulse. No cardiac output.

Act: Immediate CPR + defibrillation 120–200J (biphasic). Epinephrine 1 mg IV q3–5 min. Amiodarone 300 mg after 2nd shock. See cardiac arrest algorithm (p. 14).

Asystole

None

Recognize: Flat line (or near-flat). No electrical activity. Confirm in ≥2 leads before treating — "flatline" may be lead artifact.

Act: CPR + epinephrine 1 mg q3–5 min. Non-shockable — do not defibrillate. Poorest prognosis; identify reversible causes (H's & T's) urgently.

PEA — Pulseless Electrical Activity

Organized — no pulse

Recognize: Organized rhythm on monitor. No palpable pulse. No cardiac output.

Clinical: Always has a reversible cause — find it and fix it.

Act: CPR + epinephrine. Immediately identify H's & T's (see p. 14). Non-shockable.

H's & T's — Reversible Causes of Cardiac Arrest: Hypovolemia · Hypoxia · H+ ion (acidosis) · Hypo/Hyperkalemia · Hypothermia  |  Tension pneumothorax · Tamponade (cardiac) · Toxins · Thrombosis (pulmonary or coronary)
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11

AV Blocks

Thompson Health · Dysrhythmia Recognition & Response · 2026

AV Block — Recognition & Risk Summary

Block Type PR Interval Dropped Beats Risk Level Treatment
1st Degree >0.20 s, fixed None — every P conducts Low Observe; treat underlying cause
2nd Degree
Type I (Wenckebach)		 Progressive lengthening, then drops Periodic — after PR peaks Moderate Atropine if symptomatic; usually transient
2nd Degree
Type II (Mobitz II) ⚠️		 Fixed — QRS drops suddenly without warning Sudden, unpredictable High Prepare for pacing; atropine often ineffective
3rd Degree (Complete) 🚨 None — P and QRS independent AV dissociation (all beats) Emergency Transcutaneous pacing immediately

AV Block Identification Flowchart

AV BLOCK IDENTIFICATION FLOWCHART ───────────────────────────────────────────────────────────────────── Is the PR interval FIXED or VARIABLE? │ ├── FIXED ──► Does every P wave conduct to a QRS? │ │ │ ├── YES (every P → QRS, PR just prolonged) ──► 1ST DEGREE │ │ All P waves conduct. PR >0.20 s but consistent. │ │ │ └── NO (some P waves not followed by QRS) ──► 2ND DEGREE TYPE II ⚠️ │ Fixed PR. QRS drops suddenly without warning. │ Block below AV node (infra-Hisian). HIGH RISK. │ └── VARIABLE ──► Is the PR progressively lengthening before a dropped beat? │ ├── YES (PR gets longer → longer → drop → cycle repeats) ──► 2ND DEGREE TYPE I │ Wenckebach / Mobitz I. Block at AV node level. Usually transient. │ └── NO (P waves and QRS completely independent) ──► 3RD DEGREE 🚨 Complete AV dissociation. Atria and ventricles beat independently. Escape pacemaker controls ventricles. EMERGENCY. ───────────────────────────────────────────────────────────────────── LOCATION DETERMINES RESPONSE: AV node level (1°, Type I) → Atropine may improve conduction Below AV node (Type II, 3°) → Atropine often INEFFECTIVE or worsens → PACE

Type I vs Type II — Quick Differentiation

Type I (Wenckebach) Type II (Mobitz II)
PR Pattern Progressive lengthening Fixed (constant)
QRS Width Usually narrow Often wide (BBB pattern)
Block Location AV node Below AV node (His/bundle branches)
Atropine Usually improves Often no effect or worsens
Progression risk Lower High → may progress to 3rd degree

🚨 Third-Degree Block: Key Points

  • Atria and ventricles beat completely independently (AV dissociation)
  • Ventricular rate set by escape pacemaker:
Narrow QRS escape Junctional (40–60 bpm) — more stable
Wide QRS escape Ventricular (20–40 bpm) — less stable, higher risk
  • Atrial rate will always be faster than ventricular rate in 3rd degree
  • Transcutaneous pacing is the immediate intervention
  • Prepare for transvenous pacing; obtain urgent cardiology consultation
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12

ACLS Algorithm: Bradycardia With a Pulse

Thompson Health · Dysrhythmia Recognition & Response · 2026

Adult Bradycardia Algorithm (AHA 2020)

Identify & Assess
HR <50 bpm WITH symptoms?
Hypotension · Altered mental status · Signs of shock · Ischemic chest pain · Acute HF
↓ NO — Asymptomatic
Identify and treat underlying cause.
Monitor and observe.
Hold contributing medications (beta-blockers, CCBs, digoxin, antiarrhythmics).
Check electrolytes, thyroid, ECG for ischemia.
↓ YES — Symptomatic
✓ IV access   ✓ O₂   ✓ Monitor   ✓ 12-lead ECG
↓
Atropine — First Line
1 mg IV push q3–5 min   ·   Max: 3 mg total
↓ If atropine ineffective or not appropriate
Second-Line Options (choose one or combine)
▼ Transcutaneous pacing (TCP)
▼ Dopamine infusion: 5–20 mcg/kg/min
▼ Epinephrine infusion: 2–10 mcg/min
↓
Consider transvenous pacing.
Expert/cardiology consultation.

Transcutaneous Pacing (TCP) — Key Points

  • Apply pads (anterior-posterior preferred) before initiating
  • Start rate at 60–80 bpm; titrate to patient tolerance
  • Increase milliamps (mA) until electrical capture — widened QRS following pacing spike
  • Confirm mechanical capture — palpate pulse, check BP
  • Sedate and analgese the patient — TCP is painful
  • Typical capture threshold: 40–80 mA (varies by patient)

Atropine — When It May Not Work

Atropine works by blocking vagal (parasympathetic) input to the AV node. It is less effective or ineffective when:

  • The block is below the AV node (Type II, 3rd degree with wide QRS) — the block is not vagally mediated
  • Following cardiac transplantation (denervated heart)
  • Some cases of inferior MI with vagal component already treated
In Type II and 3rd degree blocks with wide QRS escape: proceed to pacing — do not rely on atropine.
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ACLS Algorithms: Tachycardia & Cardiac Arrest

Thompson Health · Dysrhythmia Recognition & Response · 2026

Adult Tachycardia With a Pulse (AHA 2020)

Assess Stability
Unstable = Hypotension · AMS · Signs of shock · Ischemic chest pain · Acute HF
↓ UNSTABLE
Synchronized Cardioversion
Sedate if possible
Narrow regular: 50–100 J   |   AFib: 120–200 J
Flutter/regular SVT: 50–100 J   |   Wide: 100 J
Escalate energy if no conversion
↓ STABLE
Assess QRS Width
Narrow (<0.12 s)
Regular? → Vagal → Adenosine
Irregular? → Rate control (AFib/Flutter)
Wide (≥0.12 s)
Treat as VT until proven otherwise
Amiodarone 150 mg IV over 10 min
Or procainamide

Adult Cardiac Arrest Algorithm (AHA 2020)

Unresponsive / No normal breathing
Activate EMS/code · Start CPR · Attach monitor/defibrillator
→
Rhythm Check
Shockable or non-shockable?
SHOCKABLE
VF / Pulseless VT
  • ⚡ Shock (biphasic 120–200 J)
  • Immediately resume CPR ×2 min
  • Epinephrine 1 mg IV/IO q3–5 min (after 2nd shock)
  • ⚡ Shock → CPR 2 min → rhythm check
  • Amiodarone 300 mg (then 150 mg) after 3rd shock; or Lidocaine 1–1.5 mg/kg if amiodarone unavailable
  • Continue CPR cycles
NON-SHOCKABLE
Asystole / PEA
  • Start CPR ×2 min
  • Epinephrine 1 mg IV/IO ASAP
  • Continue high-quality CPR
  • Epinephrine 1 mg q3–5 min
  • Rhythm check every 2 min
  • Search for & treat H's and T's (see p. 11)
High-Quality CPR Reminders: Rate 100–120/min  ·  Depth ≥2 inches (5 cm)  ·  Full chest recoil  ·  Minimize interruptions  ·  Rotate compressors q2 min  ·  Avoid excessive ventilation
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ACLS Medications & QTc Reference

Thompson Health · Dysrhythmia Recognition & Response · 2026

ACLS Medication Quick Reference

MedicationIndicationDoseNotes
Epinephrine Cardiac arrest 1 mg IV/IO q3–5 min Give ASAP for non-shockable rhythms
Epinephrine Symptomatic bradycardia 2–10 mcg/min infusion Titrate to effect; if atropine ineffective
Atropine Symptomatic bradycardia 1 mg IV push q3–5 min (max 3 mg) Ineffective in Type II / 3° block below AV node
Amiodarone VF / pulseless VT (refractory) 300 mg IV push, then 150 mg After 2nd–3rd shock in cardiac arrest
Amiodarone Stable wide-complex tachycardia 150 mg IV over 10 min May repeat; max 2.2 g/24 hr; ⚠️ prolongs QT
Adenosine Stable regular narrow-complex SVT 6 mg rapid IV push → 12 mg → 12 mg Follow each dose immediately with 20 mL NS flush
Dopamine Symptomatic bradycardia 5–20 mcg/kg/min infusion Alternative to epinephrine infusion
Magnesium sulfate Torsades de Pointes 2 g IV over 15 min First-line for Torsades; correct K+ and Mg2+
Lidocaine VF/pVT (amiodarone alternative) 1–1.5 mg/kg IV, then 0.5–0.75 mg/kg Use if amiodarone unavailable
Procainamide Stable VT or wide-complex tachy 20–50 mg/min until terminated; max 17 mg/kg Avoid in prolonged QT or HF; stop if QRS widens >50%

📈 QTc Quick Reference

QTc Normal<440 ms (men)   /   <460 ms (women)
⚠ Flag>500 ms   OR   >60 ms rise from baseline
🚨 High RiskTorsades de Pointes

Torsades treatment: Magnesium sulfate 2g IV over 15 min. Defibrillate if pulseless. Correct K+ >4.0 and Mg2+ >2.0.

Risk factors: Hypokalemia, hypomagnesemia, bradycardia, female sex, multiple QT-prolonging medications, congenital long QT.

Check interactions at: CredibleMeds.org

Common QT-Prolonging Medications

Cardiac

  • Amiodarone
  • Sotalol
  • Dofetilide
  • Flecainide
  • Quinidine

Non-Cardiac

  • Haloperidol
  • Azithromycin
  • Ciprofloxacin
  • Ondansetron
  • Methadone
  • Hydroxychloroquine

Energy Guide (Biphasic)

Defibrillation (VF/pVT)120–200 J (or manufacturer spec)
Cardioversion: narrow regular50–100 J initial
Cardioversion: AFib / wide120–200 J initial
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Notes

Thompson Health · Dysrhythmia Recognition & Response · 2026
Use this page for key takeaways, clinical pearls, and personal reminders. Name: _____________________________   Date: ____________
Thompson Health
Nursing Education & Professional Development
F.F. Thompson Hospital  ·  Canandaigua, NY
Dysrhythmia Recognition & Response
2026 Edition  ·  For educational use only
Not a substitute for clinical judgment
16