Cardiac Dysrhythmia
Recognition & Response

Bedside Quick Reference

📋 Version 1.0 📅 February 2026 🏥 Thompson Health — Nursing Education
Section 1

Conduction System & ECG Basics

Cardiac Conduction Pathway

The heart's electrical system triggers each heartbeat in an orderly sequence. Disruption at any level produces a recognizable dysrhythmia pattern.

Normal Conduction Sequence
SA Node (right atrium) → atrial depolarization → AV Node (brief delay — allows ventricular filling) → Bundle of His → Right & Left Bundle Branches → Purkinje Fibers → ventricular depolarization

Key Points at Each Level

Pacemaker Hierarchy

If a higher-level pacemaker fails, a lower-level escape pacemaker takes over — slower but potentially life-saving.

Pacemaker Site Intrinsic Rate QRS Appearance Clinical Significance
SA Node 60 – 100 bpm Narrow (<0.12 s) Normal primary pacemaker
AV Junction 40 – 60 bpm Narrow (<0.12 s) Escape when SA fails; inverted/absent P waves
Ventricles 20 – 40 bpm Wide (≥0.12 s), bizarre Last-resort escape; inadequate CO; prepare to pace

ECG Waveform Reference

Waveform / Interval What It Represents Normal Value Abnormal → Think
P Wave Atrial depolarization (SA node fires → atria contract) Smooth, upright in II; <0.12 s wide, <2.5 mm tall Absent → junctional/AF; inverted → junctional/retrograde
PR Interval Atrial depol + AV nodal delay (P onset → QRS onset) 0.12 – 0.20 s (3–5 small boxes) >0.20 s → AV block; <0.12 s → WPW / junctional
QRS Complex Ventricular depolarization (ventricular contraction follows) <0.12 s (3 small boxes) ≥0.12 s → bundle branch block, ventricular origin, aberrant
ST Segment Early ventricular repolarization (should be isoelectric) At baseline Elevation → ischemia/injury; Depression → ischemia
T Wave Ventricular repolarization Same direction as QRS; asymmetric Peaked (hyperK), inverted (ischemia), tall (hyperK)
QT Interval Total ventricular depol + repol (Q onset → T end) QTc ≤ 0.44 s (varies with rate — use corrected QTc) Prolonged QTc → Torsades risk (drugs, electrolytes)
Small box = 0.04 s · Large box = 0.20 s · 25 mm/sec standard paper speed
📏 ECG Paper Quick Facts
Horizontal (time): 1 small box = 0.04 s · 1 large box = 0.20 s · 5 large boxes = 1 second
Vertical (voltage): 1 small box = 0.1 mV · 10 small boxes (1 large) = 1.0 mV
Section 2

5-Step ECG Analysis Method

Use this systematic approach for every rhythm strip. Consistency prevents missed findings.

  1. 1

    Rate

    Regular rhythm — 300 Method: Count the number of large boxes between two consecutive R waves, then divide 300 by that number.
    Example: 4 large boxes → 300 ÷ 4 = 75 bpm

    Irregular rhythm — 6-Second Count Method: Count the number of QRS complexes in a 6-second strip (30 large boxes) and multiply by 10.
    Example: 8 complexes in 6 s → 80 bpm

    Memorize the sequence: 300 → 150 → 100 → 75 → 60 → 50 (1, 2, 3, 4, 5, 6 large boxes)

  2. 2

    Rhythm

    Compare R-R intervals across the entire strip using calipers or a pen mark.

    • Regular: R-R intervals vary by <0.04 s (less than 1 small box)
    • Regularly irregular: Pattern to the irregularity (e.g., grouped beats in Wenckebach)
    • Irregularly irregular: No pattern — classic for atrial fibrillation
  3. 3

    P Waves

    Ask these questions for every strip:

    • Present? If absent → AF, VF, or junctional rhythm
    • Upright in Lead II? Upright = SA node origin; inverted = retrograde (junctional)
    • One P for every QRS? More P's than QRS = AV block; no relationship = 3rd-degree block
    • All P's look the same? Variable morphology = wandering pacemaker, PACs, or multifocal atrial
  4. 4

    PR Interval

    Measure from the beginning of the P wave to the beginning of the QRS complex.

    • Normal: 0.12 – 0.20 s (3 – 5 small boxes)
    • Short (<0.12 s): Pre-excitation (WPW), junctional rhythm
    • Long (>0.20 s): First-degree AV block
    • Progressive lengthening → dropped QRS: Second-degree Type I (Wenckebach)
    • Fixed PR with sudden drop: Second-degree Type II (Mobitz II)
  5. 5

    QRS Width

    Measure the widest QRS from the beginning of the Q wave (or R if no Q) to the end of the S wave.

    • Narrow (<0.12 s / <3 small boxes): Supraventricular origin (SA, atrial, or AV junctional) — normal conduction through the ventricles
    • Wide (≥0.12 s / ≥3 small boxes): Ventricular origin, bundle branch block, aberrant conduction, or paced rhythm

    Wide + fast + no pulse = VF/VT until proven otherwise → ACLS

⚡ Normal Values Quick Reference
Heart Rate 60 – 100 bpm
PR Interval 0.12 – 0.20 s (3 – 5 small boxes)
QRS Duration <0.12 s (<3 small boxes)
QTc Interval ≤0.44 s (rate-corrected)
Rhythm Regular (R-R varies <0.04 s)
Section 3

Sinus Rhythms

All sinus rhythms originate in the SA node. P waves are upright in Lead II, one-to-one P:QRS relationship, and PR interval is normal. Differences relate to rate and regularity.

Normal Sinus Rhythm (NSR)

60 – 100 bpm
Rate60 – 100 bpm
RhythmRegular
P WavesUpright, uniform, 1:1
PR Interval0.12 – 0.20 s
QRSNarrow <0.12 s
SignificanceNormal cardiac rhythm
Nursing Action: Continue routine monitoring. No intervention required.

Sinus Bradycardia

<60 bpm
Rate<60 bpm
RhythmRegular
P WavesUpright, uniform, 1:1
PR Interval0.12 – 0.20 s
QRSNarrow <0.12 s
SignificanceMay be normal or pathologic

Common Causes

  • Normal variant: athletes, during sleep, vasovagal response
  • Medications: beta-blockers, calcium channel blockers, digoxin, opioids
  • Inferior MI (RCA occlusion → SA node ischemia)
  • Hypothyroidism, hypothermia, increased ICP (Cushing's reflex)
  • Sick sinus syndrome
Nursing Action:
  • Assess for symptoms: hypotension, chest pain, altered mental status, syncope, diaphoresis
  • Symptomatic: Notify provider immediately → Atropine 0.5 mg IV (per order); transcutaneous pacing if refractory
  • Asymptomatic: Increase monitoring frequency; review and report contributing medications; document
  • Obtain 12-lead ECG; check electrolytes if not recent

Sinus Tachycardia

>100 bpm
Rate>100 bpm (usually <180)
RhythmRegular
P WavesUpright, may merge with T at fast rates
PR Interval0.12 – 0.20 s
QRSNarrow <0.12 s
SignificanceAlmost always a secondary response

Common Causes (Treat the Cause!)

  • Pain, anxiety, fever, sepsis (most common on the floor)
  • Hypovolemia / hemorrhage / dehydration
  • Hypoxia, pulmonary embolism, heart failure
  • Medications: atropine, epinephrine, dopamine, albuterol, thyroid supplements
  • Anemia, hyperthyroidism, stimulants, caffeine
Nursing Action: Do NOT slow sinus tach without first identifying the cause.
  • Assess: vital signs, O₂ saturation, pain scale, temperature, fluid status, recent medications
  • Treat underlying cause (fluids, analgesia, antipyretics, anxiolytics as ordered)
  • Notify provider if rate >130 without clear cause, if hemodynamically unstable, or if rate is not responding to treatment
  • Obtain 12-lead ECG to rule out SVT

Sinus Arrhythmia

60 – 100 bpm (varies)
Rate60 – 100 bpm
RhythmIrregular — cycles with breathing
P WavesUpright, uniform
PR Interval0.12 – 0.20 s
QRSNarrow <0.12 s
SignificanceBenign; normal in young adults

Rate speeds up with inspiration (vagal tone decreases) and slows with expiration (vagal tone increases). Normal variant; common in children and young athletes.

Nursing Action: No treatment required. Document as benign finding. Confirm it correlates with respiratory cycle if uncertain.
Section 4

Atrial Rhythms

Atrial rhythms arise from ectopic foci in the atria (not the SA node). P waves are present but may appear early, abnormal in shape, or buried. QRS is usually narrow (normal ventricular conduction).

Premature Atrial Complexes (PACs)

Early beat
RateUnderlying rate + early beat
RhythmIrregular at PAC
P WavesEarly, different morphology (ectopic atrial focus)
PR IntervalMay be short or variable
QRSNarrow (usually); wide if aberrant conduction
PauseIncomplete compensatory pause (SA node resets)

PACs occur when an irritable atrial focus fires before the SA node. Usually benign. Triggers: caffeine, alcohol, stimulants, electrolyte disturbances, emotional stress, hypoxia.

Nursing Action: Usually benign — monitor and document frequency.
  • Assess for triggers: caffeine, medications, electrolytes (K⁺, Mg²⁺)
  • Notify provider if PACs are frequent (>6/min), occur in runs, or patient is symptomatic (palpitations, presyncope)
  • Frequent PACs may precede AF — monitor for rhythm changes

Supraventricular Tachycardia (SVT / PSVT)

150 – 250 bpm
Rate150 – 250 bpm
RhythmRegular (abrupt onset/termination)
P WavesOften buried in T wave or retrograde; may not be visible
PR IntervalNot measurable if P buried
QRSNarrow (<0.12 s) unless aberrant
SignificanceSymptomatic; may reduce CO

Classic mechanism: re-entry circuit within or near the AV node (AVNRT most common). Sudden onset of rapid palpitations, light-headedness, chest tightness. Distinguishing SVT from sinus tach: SVT rate usually >150 with abrupt onset; sinus tach gradual.

Nursing Action:
  1. Assess hemodynamic stability (BP, LOC, chest pain, diaphoresis)
  2. Stable: Vagal maneuvers (Valsalva, carotid sinus massage — provider order); IV access; 12-lead ECG
  3. Adenosine 6 mg rapid IV push (followed by 20 mL saline flush) — per order; may repeat with 12 mg ×2 if no response
  4. Unstable (hypotension, chest pain, altered LOC): Prepare for synchronized cardioversion — notify provider/activate response team
  5. Continuous monitoring; post-conversion rhythm documentation

Atrial Flutter

Atrial 250 – 350 bpm
Atrial Rate250 – 350 bpm
Ventricular RateDepends on AV conduction (2:1 → ~150; 4:1 → ~75)
RhythmRegular (if fixed block ratio) or regularly irregular
P WavesSawtooth flutter waves (F waves) — best in II, III, aVF
PR/FR IntervalFixed block ratio (2:1, 3:1, 4:1)
QRSNarrow unless aberrant

Key identifier: Characteristic sawtooth (flutter) waves at ~300 bpm. At 2:1 conduction, ventricular rate ≈ 150 bpm — suspect flutter if rate is exactly 150. AV node protects ventricles from very rapid rates.

⚠️ Stroke Risk
Atrial flutter carries similar stroke risk to AF. Anticoagulation should be addressed per provider. If flutter has been present >48 hours, cardioversion requires TEE or adequate anticoagulation first.
Nursing Action:
  • Assess for symptoms and hemodynamic stability
  • Rate control medications per order (beta-blockers, calcium channel blockers, digoxin)
  • Monitor for variable block and abrupt rate changes
  • Anticoagulation assessment with provider
  • Stable with persistent flutter: cardioversion (electrical or pharmacologic) per provider plan

Atrial Fibrillation (AF)

Atrial 350–600 bpm; ventricular variable
Atrial Rate350 – 600 bpm (chaotic)
Ventricular RateIrregularly irregular; 60 – 170+ bpm
RhythmIrregularly irregular (hallmark)
P WavesNone — chaotic fibrillatory (f) waves; undulating baseline
PR IntervalNot measurable
QRSNarrow (unless aberrant or WPW)
🫀 Atrial Kick — Clinical Pearl
Atrial fibrillation eliminates the atrial kick — the active filling contribution of atrial contraction to ventricular preload. This reduces cardiac output by 15–20%, which may be poorly tolerated in patients with CHF, hypertrophic cardiomyopathy, or significant diastolic dysfunction. Assess for signs of decompensation.

Key Clinical Concerns

  • Stroke Risk: Blood pools in the left atrial appendage → thrombus formation → embolic stroke. Use CHA₂DS₂-VASc score to guide anticoagulation.
  • Rate Control: Goal ventricular rate 60–100 bpm at rest. Medications: beta-blockers, calcium channel blockers (diltiazem IV for rapid AF), digoxin.
  • New-onset vs. chronic: New-onset AF within 48 h may be cardioverted safely; >48 h requires anticoagulation or TEE to exclude LA thrombus before cardioversion.
Nursing Action:
  • Assess HR, BP, symptoms (palpitations, dyspnea, chest pain, neurological changes)
  • IV access; 12-lead ECG; cardiac monitoring
  • Rate control medications per order; monitor for response
  • Anticoagulation as ordered (heparin, LMWH, DOACs)
  • New neuro deficits → Stroke protocol immediately
  • Unstable (hypotension, pulmonary edema, chest pain): Prepare for synchronized cardioversion — notify provider stat
Section 5

Junctional Rhythms

Junctional rhythms arise from the AV node/junction when the SA node fails to fire or is suppressed. Key features: inverted or absent P waves, narrow QRS (unless aberrant conduction exists).

Key Concept: Retrograde P Waves
The AV junction depolarizes the atria retrograde (backward). P waves appear:
  • Before QRS — if atria depolarize just before ventricles (short PR <0.12 s)
  • Buried in QRS — if simultaneous depolarization (P waves absent/hidden)
  • After QRS — if atria depolarize after ventricles (P in ST segment, inverted)
In Lead II: retrograde P waves are inverted (negative).

Junctional Escape Rhythm

40 – 60 bpm
Rate40 – 60 bpm
RhythmRegular
P WavesInverted, absent, or after QRS
PR Interval<0.12 s or not measurable
QRSNarrow <0.12 s
SignificanceBackup pacemaker — SA node failed

This is a protective escape mechanism — the AV junction stepping in because the SA node is not functioning. May be seen with increased vagal tone, medication effects (dig toxicity, beta-blockers), inferior MI, or sick sinus syndrome.

Nursing Action:
  • Assess for symptoms: dizziness, hypotension, syncope (rate may be too slow for adequate CO)
  • Notify provider — identify and treat underlying cause
  • Review medications (digoxin level, beta-blockers)
  • Symptomatic: Atropine 0.5 mg IV per order; prepare for transcutaneous pacing
  • Do NOT suppress this rhythm — it is keeping the patient alive

Accelerated Junctional Rhythm

60 – 100 bpm
Rate60 – 100 bpm
RhythmRegular
P WavesInverted, absent, or after QRS
PR Interval<0.12 s or not measurable
QRSNarrow <0.12 s
SignificanceEnhanced automaticity of AV junction

Enhanced automaticity of the junction fires at a rate matching the SA node range. The rate is "accelerated" beyond the junction's normal intrinsic rate (40–60). Causes: digoxin toxicity, myocardial ischemia, post-cardiac surgery, electrolyte imbalance.

Nursing Action:
  • Assess for symptoms; hemodynamic stability
  • Monitor for digoxin toxicity if on digoxin
  • Identify and address underlying cause
  • Notify provider; continue monitoring

Junctional Tachycardia

>100 bpm
Rate>100 bpm (usually 100 – 130)
RhythmRegular
P WavesInverted, absent, or after QRS
PR Interval<0.12 s or not measurable
QRSNarrow <0.12 s
SignificanceLess common; may impair CO

Less common than AVNRT (SVT). May be seen with digitalis toxicity, myocarditis, or cardiac surgery. Distinguished from AVNRT by slightly lower rate and clinical context.

Nursing Action: Assess symptoms; notify provider. Manage underlying cause. Hemodynamically unstable → ACLS protocol/cardioversion per provider.
💡 Junctional Rhythm Summary
All junctional rhythms share: inverted/absent P waves + narrow QRS (unless aberrant). The rate classifies them: <40 = junctional escape with poor SA & AV function · 40–60 = junctional escape · 60–100 = accelerated junctional · >100 = junctional tachycardia
Section 6

Ventricular Rhythms

Ventricular rhythms originate below the Bundle of His. Wide, bizarre QRS complexes (≥0.12 s) are the hallmark because impulses travel through ventricular muscle rather than the fast His-Purkinje system. These rhythms range from benign ectopy to immediately life-threatening.

Premature Ventricular Complexes (PVCs)

Early wide beats
RateUnderlying rate + early PVC
RhythmIrregular at PVC
P WavesNo P before PVC; may see retrograde P after
PR IntervalNone for PVC
QRSWide ≥0.12 s, bizarre, opposite T wave direction
PauseFull compensatory pause (SA node NOT reset)

PVC Terminology

TermDefinitionSignificance
UnifocalAll PVCs look identical — same ectopic focusLess concerning than multifocal
MultifocalPVCs with different morphologies — multiple fociMore concerning; may indicate significant irritability
BigeminyEvery other beat is a PVCAssess hemodynamics; frequent ectopy
TrigeminyEvery third beat is a PVCAssess hemodynamics; frequent ectopy
CoupletTwo consecutive PVCsIncreased concern; may precede VT
Run / Salvo3+ consecutive PVCs (<30 s = nonsustained VT)High concern — notify provider
R-on-TPVC falls on T wave (vulnerable period)Can precipitate VT/VF — high risk
Nursing Action:
  • Assess symptoms: palpitations, dizziness, decreased BP with PVCs
  • Identify and treat causes: hypoxia (most common), electrolyte imbalances (K⁺, Mg²⁺), ischemia, medications (digoxin toxicity), stimulants, anxiety
  • Obtain 12-lead ECG; check labs (K⁺, Mg²⁺, troponin if new)
  • Notify provider for: >6 PVCs/min, multifocal PVCs, couplets, runs, R-on-T pattern
  • Continuous monitoring; document frequency and morphology

Idioventricular Rhythm (IVR)

20 – 40 bpm
Rate20 – 40 bpm
RhythmRegular (ventricular escape)
P WavesAbsent or AV dissociation
PR IntervalNone (AV dissociation)
QRSVery wide >0.12 s, bizarre
SignificanceLast-resort pacemaker — critical

The ventricles are functioning as the only pacemaker — SA node and AV junction have both failed. Cardiac output at this rate is severely compromised. Immediate intervention required.

Nursing Action:
  1. Check pulse immediately — if pulseless, this is PEA → start CPR and activate code blue
  2. If pulse present: notify provider STAT; prepare for transcutaneous pacing
  3. IV access; atropine per order (may not be effective as block is below AV node)
  4. Do NOT suppress IVR — it is the only rhythm present
  5. Cardiac consult for transvenous pacing

Accelerated Idioventricular Rhythm (AIVR)

40 – 100 bpm
Rate40 – 100 bpm
RhythmRegular
P WavesAbsent or AV dissociation
QRSWide ≥0.12 s, bizarre
SignificanceOften benign — reperfusion marker

Reperfusion rhythm: Commonly seen after successful thrombolysis or PCI for STEMI. Enhanced automaticity of ventricular cells recently restored from ischemia. Rate is between IVR and VT. Usually self-limiting and benign.

Nursing Action:
  • Assess pulse and hemodynamics — if stable, this is typically benign and self-limited
  • Notify provider (especially if occurring post-thrombolysis or post-PCI — document as possible reperfusion rhythm)
  • Do not treat unless hemodynamically compromised — suppressing may cause worse rhythm
  • Monitor closely; document onset and duration

Ventricular Tachycardia (VT)

>100 bpm · Wide QRS
Rate>100 bpm (usually 150 – 250)
RhythmRegular (monomorphic) or irregular (polymorphic)
P WavesAV dissociation — P waves may be seen but unrelated to QRS
QRSWide ≥0.12 s, bizarre, uniform (mono) or varying (poly)
SubtypesMonomorphic, Polymorphic, Torsades de Pointes
DurationNonsustained <30 s; Sustained ≥30 s
🚨 PRIORITY ACTION: Check for Pulse First
VT with a pulse is treated differently from pulseless VT. Always check for pulse before initiating treatment. Pulseless VT → CPR + Defibrillation (unsynchronized). Pulse present → see algorithm below.

VT with Pulse — Stable vs. Unstable

StatusSignsTreatment
Unstable Hypotension, chest pain, altered LOC, signs of shock Synchronized cardioversion (200 J biphasic) → ACLS
Stable Normotensive, alert, no chest pain Antiarrhythmic therapy per order: Amiodarone 150 mg IV over 10 min; Lidocaine 1–1.5 mg/kg IV; consider elective cardioversion
Nursing Action:
  1. Check pulse immediately
  2. Call for help; activate response team / code blue if pulseless
  3. Pulseless VT → CPR; defibrillate 200 J unsynchronized; ACLS epinephrine 1 mg IV q3-5 min
  4. Pulse present, unstable → synchronized cardioversion; O₂; IV access; antiarrhythmics per order
  5. Pulse present, stable → 12-lead ECG; notify provider; antiarrhythmics per order
  6. Prepare crash cart, defibrillator, suction

Ventricular Fibrillation (VF)

No organized rhythm — DEFIBRILLATE NOW
RateNo identifiable rate — chaotic
RhythmCompletely chaotic, no pattern
P WavesNone
QRSNo identifiable QRS complexes — coarse or fine fibrillatory waves
PulseABSENT — cardiac arrest
COZero — no effective cardiac output
🚨 CARDIAC ARREST — CODE BLUE
VF produces no cardiac output. Every minute without defibrillation decreases survival by 7–10%. Start CPR immediately and defibrillate as soon as possible. Early defibrillation is the single most important intervention.
Nursing Action — IMMEDIATE:
  1. Confirm unresponsive, no pulse, no normal breathing
  2. Call code blue / activate rapid response
  3. Start high-quality CPR (100–120/min, 2 in. depth, allow full recoil)
  4. Apply defibrillator pads; charge to 200 J (biphasic)
  5. DEFIBRILLATE — clear all personnel, deliver shock
  6. Resume CPR immediately for 2 minutes
  7. IV/IO access; Epinephrine 1 mg IV q3-5 min; Amiodarone 300 mg IV after 3rd shock
  8. Continue 2-minute CPR cycles; check rhythm/pulse every 2 min
  9. Search for reversible causes: H's and T's
Section 7

AV Blocks

AV blocks represent impaired or absent conduction through the AV node or infranodal conduction system. Classified by degree (how complete the block is) and location (AV node vs. bundle branches). Location matters: nodal blocks respond to atropine; infranodal (His-Purkinje) blocks do not.

First-Degree AV Block

All beats conduct — prolonged PR
RateNormal (underlying rate)
RhythmRegular
P WavesNormal, 1:1 P:QRS
PR Interval>0.20 s (prolonged, constant)
QRSNarrow <0.12 s
Dropped BeatsNone — all P waves conduct

Every P wave conducts to the ventricles, but with a delay longer than normal. The AV node conducts slowly but completely. Causes: inferior MI, medications (beta-blockers, digoxin, CCBs), myocarditis, increased vagal tone, fibrosis.

Nursing Action: Monitor only. No treatment required for isolated first-degree block. Document and notify provider. Watch for progression to higher-degree block, especially with new inferior MI.

Second-Degree AV Block — Type I (Wenckebach / Mobitz I)

Progressive PR → dropped QRS
RateAtrial: normal · Ventricular: slightly slower
RhythmRegularly irregular (grouped beats)
P WavesRegular; more P waves than QRS
PR IntervalProgressive lengthening → suddenly dropped QRS
QRSNarrow (AV node level)
Pattern"Grouped beating" — repeating cycles

The AV node becomes progressively fatigued with each impulse until it fails to conduct once — then the cycle resets. Location: AV node. Usually benign, especially inferior MI (transient, often resolves). Atropine generally effective.

Nursing Action:
  • Assess for symptoms — usually asymptomatic; may cause mild bradycardia
  • Notify provider; document PR pattern (show progressive lengthening on strip)
  • Monitor for progression to higher-degree block
  • Symptomatic: Atropine 0.5 mg IV per order (usually effective)
  • Hold QT-prolonging or AV-nodal blocking medications if implicated (per provider)

Second-Degree AV Block — Type II (Mobitz II)

Fixed PR → sudden dropped QRS — HIGH RISK
RateAtrial: normal · Ventricular: bradycardic
RhythmIrregular (dropped beats unpredictable)
P WavesRegular; more P waves than QRS
PR IntervalFIXED and constant → suddenly dropped QRS (no warning)
QRSOften wide (bundle branch involvement)
LocationBundle of His or bundle branches (infranodal)
⚠️ HIGH-RISK BLOCK — Pacing Required
Mobitz II indicates disease in the His-Purkinje system. It can progress suddenly and unpredictably to complete (third-degree) block or asystole. Transcutaneous pacing should be prepared. Atropine is often ineffective (block is infranodal).
Nursing Action:
  1. Notify provider IMMEDIATELY
  2. Prepare transcutaneous pacemaker at bedside and ensure it is functional
  3. IV access; continuous monitoring; 12-lead ECG
  4. Atropine 0.5 mg IV per order (may not respond — do not delay pacing for atropine)
  5. Anticipate transvenous pacing placement (cardiology/EP consult)
  6. Do not leave patient unattended

Third-Degree AV Block (Complete Heart Block)

Complete AV dissociation — EMERGENCY
Atrial RateNormal (SA node firing independently)
Ventricular RateDepends on escape pacemaker: junctional 40–60; ventricular 20–40
RhythmBoth regular, but completely independent
P WavesPresent and regular but no relationship to QRS
PR IntervalCompletely variable — no constant PR
QRSNarrow if junctional escape; Wide if ventricular escape
🚨 EMERGENCY — Transcutaneous Pacing NOW
No impulses conduct from atria to ventricles. The ventricles rely on an escape pacemaker — slow and unreliable. Patient will be hemodynamically compromised. Cardiac output is severely reduced. This is a medical emergency requiring immediate pacing.
Nursing Action:
  1. Activate rapid response / call provider STAT
  2. Apply transcutaneous pacemaker pads if not already placed
  3. Initiate transcutaneous pacing (see Section 8 — Pacemakers for technique)
  4. Atropine 0.5 mg IV (unlikely to work but may buy time in nodal block)
  5. Dopamine or epinephrine drip may be needed to support BP during pacing setup
  6. Prepare patient for transvenous pacemaker insertion (EP/cardiology)
  7. If pulseless → CPR, code blue, ACLS

AV Block Comparison: Type I vs. Type II

Feature 2° Type I (Wenckebach) 2° Type II (Mobitz II)
PR Pattern Progressive lengthening before dropped QRS Constant/fixed PR — sudden dropped QRS (no warning)
QRS Width Typically narrow (<0.12 s) Often wide (≥0.12 s) — bundle branch involvement
Block Location AV Node (supranodal) Bundle of His / Bundle Branches (infranodal)
Atropine Response Usually effective Usually NOT effective
Risk of Progression Low (usually transient) HIGH — may progress suddenly to complete block
Pacing Urgency If symptomatic, prepare pacer Transcutaneous pacer at bedside ALWAYS
Common Causes Inferior MI, medications, vagal tone Anterior MI, fibrosis/sclerosis of conduction system
Section 8

Pacemakers

Pacemakers deliver electrical stimuli to maintain an adequate heart rate when the native conduction system fails. Understanding normal pacemaker function is essential to recognizing malfunction.

Pacemaker Nomenclature (NBG Code — First 3 Positions)

Position I — Chamber Paced II — Chamber Sensed III — Response to Sensing
A Atrium Atrium Triggered
V Ventricle Ventricle Inhibited
D Dual (A + V) Dual (A + V) Dual (T + I)
O None None None
Example: VVI = Pace ventricle, Sense ventricle, Inhibit pacing when native beat sensed. DDD = Dual chamber pacing/sensing with dual response.

Common Pacemaker Modes

VVI — Single-Chamber Ventricular Demand Pacing

  • Paces: Ventricle only
  • Senses: Ventricle — detects native QRS complexes
  • Response: Inhibited — pacing is suppressed when native beat sensed at or above programmed rate
  • Use: Chronic AF with slow ventricular response; backup for bradycardia
  • Limitation: No AV synchrony — loses atrial kick; "pacemaker syndrome" possible
On strip: Pacing spike immediately before QRS (wide, paced QRS). No atrial pacing spike.

DDD — Dual-Chamber Atrioventricular Pacing

  • Paces: Both atria and ventricles
  • Senses: Both atria and ventricles
  • Response: Dual — triggered (atrial sensing triggers ventricular pace) and inhibited (native beats inhibit pacing)
  • Use: AV block with intact sinus node; sick sinus syndrome; most physiologic mode
  • Advantage: Maintains AV synchrony and atrial kick
On strip: Atrial spike before P wave + ventricular spike before QRS (when both are paced). May show only atrial pacing if AV conduction intact.

Normal Pacemaker Function

What You SeeWhat It MeansNormal?
Spike → P wave Atrial pacing — stimulates atrial depolarization ✓ Normal atrial capture
Spike → Wide QRS Ventricular pacing — stimulus travels through muscle (slow), produces wide QRS ✓ Normal ventricular capture
No spike when native beat occurs at/above rate Pacemaker sensed native beat and inhibited (demand mode working) ✓ Normal sensing and inhibition

Pacemaker Malfunction

Failure to Capture

Spike without depolarization

Definition: Pacemaker spike is present but not followed by a P wave (atrial) or QRS (ventricular). The stimulus fails to depolarize the myocardium.

Causes: Lead displacement, fibrosis at lead tip, output too low, metabolic derangement (hyperkalemia, acidosis), battery depletion, myocardial infarction at lead site

Nursing Action: Notify provider. Increase output if programmable. Check lead connections. Prepare transcutaneous pacing as backup. Check electrolytes. Position patient left lateral if capture improves (repositions lead).

Failure to Sense (Undersensing)

Pacer fires when it shouldn't

Definition: Pacemaker does not detect native cardiac activity and fires when it shouldn't — competes with native rhythm. Pacing spikes fall at random points in the cycle.

Danger: A pacing spike during the T wave (relative refractory period) can trigger VT or VF (R-on-T equivalent).

Causes: Lead displacement, low sensitivity setting, electromagnetic interference, lead fracture, fibrosis

Nursing Action: Notify provider immediately. Increase sensitivity setting if temporary pacer. Avoid triggers (electromagnetic sources). If spike falls on T wave → high risk — prepare for VT/VF intervention.

Failure to Pace (Output Failure)

No spike when expected

Definition: No pacemaker spike is generated when one should be — the pacemaker fails to fire when the rate falls below the programmed lower rate limit.

Causes: Battery depletion, lead fracture/disconnection, oversensing (misinterpreting noise as native beats), electromagnetic interference

Nursing Action: Check lead connections and cable connections. Check battery. Notify provider. Assess patient for symptoms. Prepare transcutaneous pacing. Identify and remove sources of electromagnetic interference.

Transcutaneous Pacing (TCP)

When to Use Transcutaneous Pacing
  • Symptomatic bradycardia unresponsive to atropine
  • Second-degree Type II or third-degree AV block
  • Hemodynamically unstable bradycardia of any cause
  • Bridge to transvenous pacing

TCP Procedure (Quick Reference)

  1. Explain to patient — TCP is painful; sedation/analgesia required (midazolam + fentanyl per order)
  2. Apply pads: Anterior-posterior placement preferred (anterior: left precordium / posterior: left subscapular). Ensure good pad contact; shave if needed.
  3. Set pacing rate: Start at 60–80 bpm (or as ordered)
  4. Set output (mA): Start low (begin at 20 mA); increase in 10 mA increments until capture
  5. Confirm capture:
    • Electrical capture: pacing spike followed by wide QRS on monitor
    • Mechanical capture: palpable pulse with each QRS (femoral or carotid — do NOT use radial); BP improves
  6. Set output 10 mA above threshold (safety margin)
  7. Reassess patient; document settings; arrange transvenous pacing
⚠️ TCP Notes
  • Pacing artifact can look like electrical capture — always confirm mechanical capture by palpating a pulse
  • Patient will feel muscle twitching — ensure adequate analgesia
  • Do not delay pacing while titrating medications
  • TCP is a bridge — arrange definitive transvenous pacing promptly
Section 9

Quick Reference & Clinical Decision Aids

Is This Rhythm Dangerous? Decision Tree

NEW RHYTHM DETECTED
↓
CHECK PULSE
↓
NO PULSE
CARDIAC ARREST
CPR + Code Blue NOW
↓
Shockable?
VF/Pulseless VT → Defibrillate
PEA/Asystole → CPR + Epi
PULSE PRESENT
Assess: Rate, BP, LOC, Symptoms
↓
UNSTABLE SIGNS
(hypotension, AMS, chest pain, shock)
UNSTABLE
Notify MD STAT
Tachycardia → Cardiovert
Bradycardia → Pace
STABLE
ASSESS FURTHER
QRS narrow or wide?
Rate fast or slow?
See algorithm below

Bradycardia Action Guide (HR < 60 bpm)

Bradycardia Algorithm (Simplified — Per ACLS)
  1. Is the patient symptomatic?
    Signs of poor perfusion: hypotension, altered mental status, ischemic chest discomfort, acute heart failure, shock
  2. If YES → Immediate treatment:
    • O₂ if SpO₂ <94%; IV access; 12-lead ECG; monitor
    • Atropine 0.5 mg IV — may repeat every 3–5 min to max 3 mg total
    • If atropine ineffective: Transcutaneous pacing (preferred over drugs if available)
    • Dopamine 2–10 mcg/kg/min IV or Epinephrine 2–10 mcg/min IV while awaiting pacing
  3. If NO (asymptomatic):
    • Identify and treat underlying cause (medications, electrolytes, ischemia)
    • Observe; increase monitoring; notify provider
  4. If Mobitz II or 3rd-degree block: Prepare pacemaker regardless of symptoms — these can deteriorate without warning

Tachycardia Action Guide (HR > 100 bpm)

Tachycardia Algorithm (Simplified — Per ACLS)
  1. Is the patient unstable? (hypotension, chest pain, altered LOC, signs of shock)
  2. UNSTABLE → Immediate synchronized cardioversion
    • Regular narrow-complex: 50–100 J biphasic
    • Regular wide-complex: 100 J biphasic
    • Irregular (AF with RVR): 120–200 J biphasic
    • Sedate if time permits; notify provider; apply pads
  3. STABLE → Identify rhythm type:
    • Narrow QRS, regular: Vagal maneuvers → Adenosine 6 mg rapid IV push → 12 mg if no response
    • Narrow QRS, irregular (AF/Flutter): Rate control (diltiazem, metoprolol, digoxin) per order; anticoagulation assessment
    • Wide QRS, regular: Presume VT; Amiodarone 150 mg IV over 10 min; prepare for cardioversion
    • Wide QRS, irregular: May be pre-excited AF, polymorphic VT, Torsades; avoid AV nodal blockers in WPW; Torsades → Mg²⁺ 1–2 g IV, defibrillate if unstable

Emergency Drug Quick Reference

Drug Indication Adult Dose Notes
ATROPINE Symptomatic bradycardia; AV block (nodal level) 0.5 mg IV bolus; repeat q3–5 min; max 3 mg Anticholinergic — accelerates SA node rate. NOT effective for Mobitz II or 3rd-degree block (infranodal). <0.5 mg may worsen bradycardia.
ADENOSINE Stable SVT (narrow QRS, regular); diagnostic for wide-complex tachycardia 6 mg rapid IV push with 20 mL saline flush; may repeat 12 mg ×2 if no response Very short half-life (~10 s) — must give via large antecubital or central IV rapidly. Causes transient asystole (warn patient). Contraindicated in WPW + AF/Flutter, sick sinus without pacemaker, 2°/3° AV block.
AMIODARONE VT with pulse (stable); refractory VF/pulseless VT (cardiac arrest); rate control AF Stable VT: 150 mg IV over 10 min, then 1 mg/min × 6 h, then 0.5 mg/min × 18 h
Cardiac arrest: 300 mg IV/IO push; second dose 150 mg		 Prolongs QT interval — monitor QTc. Multiple drug interactions. Hypotension with rapid infusion. Phlebitis with peripheral line — use central if possible. Long half-life (weeks).
LIDOCAINE VT with pulse; refractory VF/pulseless VT (alternative to amiodarone) 1–1.5 mg/kg IV bolus (max 3 mg/kg loading); maintenance 1–4 mg/min infusion Class Ib antiarrhythmic. CNS toxicity: tinnitus, tremor, seizures at toxic levels. Reduce dose in liver failure and elderly. Less effective than amiodarone for refractory VF in most studies.

When to Activate Rapid Response vs. Code Blue

Response Activate When Examples
Rapid Response Team Patient has pulse; acutely deteriorating; you are concerned but not in arrest New hemodynamically significant dysrhythmia; Mobitz II or 3rd-degree block; SVT/VT with BP drop; acute mental status change; respiratory distress
Code Blue Unresponsive; pulseless; no normal breathing VF; pulseless VT; PEA; asystole; sudden collapse; monitor shows VF and patient unresponsive
🚨 Trust Your Assessment
If the patient looks bad — call for help. Don't wait for a "perfect" rhythm diagnosis before activating a rapid response. An early call is always better than a late code. Your assessment of clinical deterioration is valid even if you're uncertain of the exact rhythm.
✅ The H's and T's — Reversible Causes of Cardiac Arrest
H's:
  • Hypovolemia
  • Hypoxia
  • Hydrogen ion (acidosis)
  • Hypo/Hyperkalemia
  • Hypothermia
T's:
  • Tension pneumothorax
  • Tamponade (cardiac)
  • Toxins
  • Thrombosis — pulmonary
  • Thrombosis — coronary (MI)