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EKG Rhythm Interpretation

Strip interpretation, normal sinus to lethal arrhythmias

P Wave: Atrial depolarization. Duration: 0.06–0.12 sec. Normally upright in lead II.
PR Interval: AV conduction time. Measured from P wave onset to QRS onset. Normal: 0.12–0.20 sec (3–5 small boxes).
QRS Complex: Ventricular depolarization. Normal: <0.12 sec (<3 small boxes). Wide QRS suggests bundle branch block or ventricular origin.
ST Segment: Early ventricular repolarization. Should be isoelectric (flat). Elevation or depression >1 mm may indicate ischemia or infarction.
T Wave: Ventricular repolarization. Normally upright in most leads. Inverted T waves may indicate ischemia. Peaked T waves: hyperkalemia.
QT Interval: Total ventricular activity (depolarization + repolarization). Measured from QRS onset to T wave end. Normal: 0.36–0.44 sec, rate-dependent (QTc corrects for heart rate). Prolonged QT → risk of Torsades de pointes.
Grid measurements: 1 small box = 0.04 sec  |  1 large box = 0.20 sec  |  5 large boxes = 1 sec. Voltage: 1 small box = 0.1 mV.
0.04 s1 small0.20 sec1 large box = 5 small← 5 small boxes = 1 large box →

Cardiac Rhythms

Expand each card to review rate, characteristics, clinical significance, and nursing actions.

Rate: 60–100 BPM
Rhythm: Regular
P Waves: Upright, one P wave before each QRS
PR Interval: 0.12–0.20 sec
QRS: <0.12 sec
Clinical Significance: Normal cardiac rhythm. No intervention needed.
Nursing Actions: Document rhythm strip q shift. Continue routine monitoring. Educate patient on normal findings.
Rate: <60 BPM
Rhythm: Regular
P Waves: Upright, one P wave before each QRS
PR Interval: Normal (0.12–0.20 sec)
QRS: Normal (<0.12 sec)
Clinical Significance: May be normal in athletes. Concerning if symptomatic — decreased cardiac output (↓CO). Causes: beta blockers, CCBs, vagal stimulation, hypothyroidism, ↑ICP.
Nursing Actions: Assess for symptoms: dizziness, hypotension, chest pain, altered LOC. Hold rate-lowering meds if ordered. Atropine 0.5 mg IVP if symptomatic (per ACLS). Prepare for transcutaneous pacing if unstable.
Rate: 100–160 BPM
Rhythm: Regular
P Waves: Upright; may be buried in preceding T wave at higher rates
PR Interval: Normal (may be difficult to measure if P buried in T)
QRS: Normal (<0.12 sec)
Clinical Significance: Compensatory response to stress, pain, fever, hypovolemia, PE, anxiety, stimulants, or CHF. Sustained tachycardia → ↑myocardial O₂ demand → ischemia risk.
Nursing Actions: Identify & treat underlying cause: pain, fever, hypovolemia, anxiety. Assess for symptoms (palpitations, ↓CO). Monitor VS. Administer O₂ if hypoxic.
Rate: Atrial: 350–600 (chaotic); Ventricular: variable (typically 100–160 if uncontrolled)
Rhythm: Irregularly irregular — hallmark finding
P Waves: Absent — replaced by chaotic fibrillatory (f) waves along baseline
PR Interval: Not measurable
QRS: Normal (<0.12 sec) unless pre-existing BBB
Clinical Significance: Loss of atrial kick → 20–30% ↓CO. HIGH stroke risk from atrial thrombus formation (especially LAA). Most common sustained dysrhythmia. Classified as paroxysmal, persistent, or permanent.
Nursing Actions: Assess for stroke symptoms (FAST). Rate control: beta blockers, CCBs, digoxin. Rhythm control: cardioversion, amiodarone, flecainide. Anticoagulation based on CHA₂DS₂-VASc score (warfarin/DOACs). Monitor for s/s of embolic events.
Rate: Atrial: 250–400 BPM; Ventricular: varies by AV block ratio (2:1, 3:1, 4:1)
Rhythm: Atrial: regular. Ventricular: may be regular or irregular depending on block ratio
P Waves: Sawtooth flutter waves (F waves) — best seen in leads II, III, aVF. No isoelectric baseline between waves.
PR Interval: Not measurable
QRS: Normal (<0.12 sec)
Clinical Significance: Similar stroke risk to AFib. Often progresses to AFib over time. May cause 1:1 conduction with severe ↓CO if AV node conduction increases.
Nursing Actions: Same approach as AFib: rate or rhythm control + anticoagulation. Synchronized cardioversion effective at lower energy (50–100 J) compared to AFib. Assess for s/s of decreased CO.
Rate: 100–250 BPM
Rhythm: Usually regular
P Waves: Absent or dissociated from QRS (AV dissociation — P waves march through at independent rate)
PR Interval: None
QRS: Wide (>0.12 sec), bizarre, tombstones appearance
Clinical Significance: LIFE-THREATENING. May be pulseless → treat as cardiac arrest. Sustained monomorphic VT causes severe ↓CO. Torsades de pointes: polymorphic VT with prolonged QT — caused by hypomagnesemia, medications.
Nursing Actions: Pulseless VT: START CPR immediately, defibrillate, follow ACLS algorithm. Pulse present but unstable: synchronized cardioversion. Stable VT: amiodarone 150 mg IV over 10 min, then 1 mg/min infusion. Identify cause: MI, electrolyte imbalance, drug toxicity. For Torsades: magnesium sulfate 2 g IV.
Rate: Unmeasurable — chaotic electrical activity
Rhythm: Chaotic, grossly irregular baseline
P Waves: Absent
PR Interval: Absent
QRS: Absent — chaotic undulating baseline (coarse vs fine VF)
Clinical Significance: LETHAL — NO cardiac output. Patient is unconscious, pulseless, apneic. This is a cardiac arrest rhythm. Defibrillation is the ONLY effective treatment.
Nursing Actions: IMMEDIATE DEFIBRILLATION — call CODE BLUE. High-quality CPR (2 min cycles). Epinephrine 1 mg IV/IO q3–5 min. Identify reversible causes: Hs & Ts — Hypoxia, Hypovolemia, Hydrogen ions (acidosis), Hypo/Hyperkalemia, Hypothermia; Tension pneumothorax, Tamponade (cardiac), Toxins, Thrombosis (PE/MI).
Rate: None — no electrical activity
Rhythm: Flatline (confirm in 2 leads)
P Waves: May see occasional P waves without QRS (P-wave asystole)
PR Interval: Absent
QRS: Absent
Clinical Significance: DEATH — confirm in 2 leads before initiating protocol. Check lead connections — may be a technical problem (lead disconnected). NOT a shockable rhythm.
Nursing Actions: CHECK THE PATIENT FIRST. Confirm asystole in 2 leads. CPR immediately. Epinephrine 1 mg IV/IO q3–5 min. Consider reversible causes (Hs & Ts). Check lead connections & gain settings — artifact or disconnected leads can mimic asystole. Do NOT defibrillate — not a shockable rhythm.
Rate: Underlying rhythm dependent (typically 60–100 BPM if sinus)
Rhythm: Regular (underlying rhythm determines pattern)
P Waves: Upright, one P wave before each QRS — normal morphology
PR Interval: Prolonged >0.20 sec (>5 small boxes), constant
QRS: <0.12 sec (unless pre-existing BBB)
Clinical Significance: Often asymptomatic and discovered incidentally. May be caused by AV nodal disease, increased vagal tone, medications (beta blockers, CCBs, digoxin), electrolyte imbalances, or inferior MI. Usually benign but monitor for progression to higher-grade block.
Nursing Actions: Assess for symptoms (dizziness, fatigue, hypotension). Review medications — hold rate-lowering drugs if PR significantly prolonged. Document PR interval q shift. Monitor for progression to 2nd- or 3rd-degree block. Notify provider if new onset or PR continues to lengthen.
Rate: Atrial: normal; Ventricular: slightly slower due to dropped beats
Rhythm: Atrial: regular. Ventricular: irregular — patterned dropped QRS
P Waves: Normal morphology; one non-conducted P wave before each dropped QRS
PR Interval: Progressively lengthens each cycle until a QRS is dropped, then the cycle resets
QRS: <0.12 sec (narrow, unless pre-existing BBB)
Clinical Significance: Usually benign and often transient. Commonly caused by increased vagal tone, inferior MI, medications (digoxin, beta blockers). Typically does not require treatment unless symptomatic. Rarely progresses to complete heart block.
Nursing Actions: Assess for symptoms (lightheadedness, bradycardia, hypotension). Identify reversible causes (review meds, check electrolytes). If asymptomatic: monitor with serial EKGs. If symptomatic: atropine 0.5 mg IVP per ACLS; prepare for pacing if unresponsive. Educate patient that this is typically self-limiting.
Rate: Atrial: regular. Ventricular: slower — dependent on conduction ratio (2:1, 3:1)
Rhythm: Atrial: regular. Ventricular: regular or regularly irregular (patterned dropped QRS)
P Waves: Normal morphology; more P waves than QRS complexes; non-conducted P waves occur at predictable intervals
PR Interval: Constant on conducted beats (does NOT progressively lengthen — key differentiator from Type I)
QRS: Often wide (>0.12 sec) — block is usually below the Bundle of His
Clinical Significance: MORE DANGEROUS than Type I. Indicates structural damage to the His-Purkinje system. HIGH RISK of progressing to complete (3rd-degree) heart block and asystole. Associated with anterior MI and structural heart disease. Requires immediate intervention.
Nursing Actions: URGENT — notify provider immediately. Prepare for transcutaneous pacing (apply pads). Atropine may be ineffective (block is infranodal). Prepare for transvenous pacing or permanent pacemaker. Continuous cardiac monitoring. Assess for signs of decreased cardiac output (hypotension, altered LOC, chest pain). Hold AV nodal blocking medications.
Rate: Atrial: 60–100 BPM (sinus). Ventricular: 30–40 BPM (ventricular escape) or 40–60 (junctional escape)
Rhythm: Atrial: regular. Ventricular: regular — but P waves and QRS fire independently
P Waves: Present but completely dissociated from QRS — P waves 'march through' at independent rate; no relationship between P and QRS
PR Interval: No PR interval — AV dissociation (P waves and QRS have no fixed relationship)
QRS: Wide if ventricular escape (>0.12 sec); narrow if junctional escape (<0.12 sec)
Clinical Significance: LIFE-THREATENING EMERGENCY. Complete AV dissociation — atria and ventricles beat independently. Severely decreased cardiac output (loss of atrial kick + bradycardia). Common causes: MI (especially inferior), digoxin toxicity, Lyme carditis, post-cardiac surgery, degenerative conduction disease.
Nursing Actions: EMERGENCY — call rapid response / code if patient unstable. Transcutaneous pacing: apply pads NOW — do not wait. If pacing delayed: atropine 0.5 mg IVP (may be ineffective if block is infranodal). Prepare for transvenous pacemaker. Continuous VS and SpO₂ monitoring. Identify reversible causes: check digoxin level, electrolytes, troponin. Patient will likely need permanent pacemaker.
Rate: 40–60 BPM (junctional escape); 60–100 (accelerated junctional); >100 (junctional tachycardia)
Rhythm: Regular
P Waves: Absent, inverted (retrograde), or buried within QRS. If present, may appear before, during, or after QRS (depending on retrograde conduction timing).
PR Interval: Short or absent (if P wave present, PR <0.12 sec)
QRS: Narrow (<0.12 sec) — rhythm originates above ventricles in AV junction
Clinical Significance: Junctional escape rhythm occurs when SA node fails to fire — AV junction takes over as backup pacemaker. Causes: sick sinus syndrome, increased vagal tone, inferior MI, digoxin toxicity, post-cardiac surgery. Accelerated junctional rhythm may indicate digoxin toxicity or ischemia.
Nursing Actions: Assess for symptoms of decreased cardiac output (loss of atrial kick → ↓CO). Check digoxin level if patient on digoxin (toxicity is common cause). Monitor VS and cardiac rhythm. If symptomatic bradycardia: atropine 0.5 mg IVP, consider pacing. If junctional tachycardia: identify and treat underlying cause (pain, fever, hypoxia, digoxin toxicity).
Rate: Underlying rate is sinus (or other baseline); PVCs are early, ectopic beats
Rhythm: Underlying rhythm is regular; PVCs make rhythm irregular — compensatory pause after PVC
P Waves: Absent before PVC (ectopic beat originates in ventricles, not conducted through atria); sinus P waves may be seen independently
PR Interval: None before PVC
QRS: Wide (>0.12 sec), bizarre, premature — not preceded by P wave. Compensatory pause: full R-R interval maintained around PVC.
Clinical Significance: PVCs are common — may be benign in healthy individuals. Concerning when: frequent (>6/min), multifocal (different QRS morphologies), R-on-T phenomenon (PVC falls on T wave → risk of VTach/VFib), or couplets/triplets (2-3 PVCs in a row = runs of VTach). Patterns: bigeminy (every other beat), trigeminy (every 3rd beat). Causes: electrolyte imbalances (hypokalemia, hypomagnesemia), hypoxia, stimulants (caffeine), stress, MI, cardiomyopathy.
Nursing Actions: Assess frequency and pattern (document on rhythm strip). Check electrolytes — K⁺ and Mg²⁺ (replace if low). Review medications (bronchodilators, stimulants). Assess for symptoms: palpitations, decreased CO if frequent. If stable and isolated: monitor. If frequent, multifocal, or with chest pain: notify provider, obtain 12-lead EKG, evaluate for ischemia.
Rate: Ventricular: 150–300 BPM
Rhythm: Irregular — polymorphic, twisting QRS axis
P Waves: Absent or dissociated
PR Interval: Not measurable
QRS: Wide (>0.12 sec), polymorphic — QRS amplitude and axis 'twist' around the isoelectric baseline (classic spindle pattern). Prolonged QT interval (QTc >0.47 sec) on baseline EKG.
Clinical Significance: LIFE-THREATENING polymorphic VT. Associated with prolonged QT interval (congenital Long QT Syndrome or acquired — medications, electrolyte disturbances). May degenerate into VFib if untreated. Classic trigger: hypomagnesemia. Common offending medications: antiarrhythmics (sotalol, amiodarone, procainamide), antipsychotics, macrolide antibiotics, fluoroquinolones, methadone.
Nursing Actions: If pulseless: START CPR — defibrillate per ACLS. Emergency treatment: MAGNESIUM SULFATE 2 g IV push over 1–2 minutes (first-line, even with normal Mg²⁺ level). Correct hypokalemia aggressively (K⁺ goal 4.0–5.0 mEq/L). Overdrive pacing or isoproterenol to increase heart rate (shortens QT). Discontinue all QT-prolonging medications. Review medication history for causative agents. Monitor serial QT/QTc intervals.
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📋 Step-by-Step Rhythm Interpretation

Use this systematic approach every time you interpret a rhythm strip.

  1. 1

    Calculate the Rate

    Method 1: Count large boxes between R waves → 300 ÷ # boxes = BPM. Method 2: Count QRS complexes on a 6-second strip × 10. Quick check: if R-R is 3 large boxes → ~100 BPM; 5 large → ~60 BPM.

  2. 2

    Determine Regularity

    Measure R-R intervals — are they consistent? Calipers or marking pen on paper help. Irregularly irregular = AFib. Regularly irregular = may be sinus arrhythmia or patterned block.

  3. 3

    Assess P Waves

    Are P waves present? Upright in lead II? One P wave before each QRS? Sawtooth pattern = atrial flutter. Chaotic baseline = AFib. P waves marching through QRS = AV dissociation (VTach).

  4. 4

    Measure PR Interval

    Normal: 0.12–0.20 sec (3–5 small boxes). Prolonged PR = 1st-degree AV block. Progressively lengthening = 2nd-degree Type I (Wenckebach). Constant prolonged with dropped QRS = 2nd-degree Type II.

  5. 5

    Measure QRS Width

    Normal: <0.12 sec (<3 small boxes). Wide QRS (>0.12): bundle branch block, ventricular rhythm, hyperkalemia, or paced rhythm. Be suspicious of VTach until proven otherwise.

  6. 6

    Interpret & Act

    Put it all together: What is the rhythm called? Is it stable or unstable? What is the clinical significance? What are your immediate nursing actions? Document findings and notify provider per protocol.