This document provides a detailed summary of EKG patterns and abnormalities, including: - Normal EKG measurements and intervals - Alterations in heart rhythm originating from the sinoatrial node - Irregular rhythms caused by a wandering pacemaker or multifocal atrial tachycardia - Premature beats, tachyarrhythmias, and other irregular rhythms originating from different areas of the heart - Specific arrhythmias and conditions like atrial fibrillation, ventricular tachycardia, Wolff-Parkinson-White syndrome, and sick sinus syndrome

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● Lead I + lead III = Lead II (Einthoven’s Law)
○ Lead I ­ LA → RA
○ Lead II ­ LL→ RA
○ Lead III ­ LL → LA
● Kirchoff’s Law –The sum of the potentials of AVR + AVL + AVF = 0
● NORMAL
○ P wave
■ Amplitude normally 0.5 to 2.5 mm (2.5 squares) (in limb
leads)
■ Duration not over 110 msec (3 squares) (in limb leads)
■ In sinus rhythms, P wave is upright in Lead II and inverted in
aVR. If not, SA node is not pacemaker
■ Normal axis (frontal plane) is 0° to +90 °, usually +30 to +60
● Left axis 0 to ­30 °
● Right axis beyond +75 °
○ PR interval
■ Normal value in adults is 0.12 sec to 0.20 sec (ventricular preexcitation < 3­5 squares < 1st degree AV
block)
○ QRS
■ 60­100ish ms (1.5­2.5 squares)
○ ST segment
■ Usually isoelectric, but may normally deviate between –0.5 and +1.0 mm from baseline in standard and
unipolar extremity leads
■ Upward displacement of 2 or 3 mm may be normal particularly in right precordial leads
○ T wave ­ 10% of amplitude of QRS is normal.
○ U wave
■ Polarity usually same as T wave
■ Most prominent in lead V3
■ Maximum amplitude should not exceed 1 mm
● Alterations in automaticity of the SA node
○ Sinus tachycardia ­ sinus rhythm > 100 beats/min
○ Sinus bradycardia ­ sinus rhythm < 60 beats/min
○ Sinus arrhythmia ­ increased sinus rate with inspiration.
■ withdrawal of parasympathetic tone during inspiration
○ Sinus arrest ­ pause. SA node fails to fire.
■ can be caused by increased parasympathetics, hypersensitive carotid sinus, damage to SA node, digitalis
● Irregular Rhythms
○ Wandering Pacemaker ­ pacemaker activity wanders from SA node to nearby atrial automaticity foci

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■ P’ shape varies
■ Atrial rate <100 (if >100 then becomes multifocal atrial tachycardia)
■ Irregular ventricular rhythm
○ Multifocal Atrial Tachycardia ­ Chaotic Atrial Rhythm
■ P’ wave shape varies (Three or more ectopic P­waves with different configurations/morphologies because P
waves come from different areas in the atrium.)
■ Isoelectric line between P­P intervals
■ Frequent occurrence of varying PR intervals
■ Atrial rate >100 (100­250 bpm)
■ Irregular ventricular rhythm
■ Seen in COPD
○ Atrial Fibrillation
■ Irregular rhythm and irregular ventricular rhythm
■ Chaotic atrial spikes
● Escape beat ­ an automaticity focus transiently escapes overdrive suppression to emit one beat (A beat originating from a site
other than the SA node). Long pause followed by escape beat (versus premature beat where there is no pause before)
● Escape Rhythm ­ an automaticity focus escapes overdrive suppression to pace at its inherent rate (another normal pacemaker
takes over) → a sequence of similar ectopic beats (many ectopic beats). When SA node pacemaker activity is impaired
○ Atrial escape rhythm ⇒ 60­80/min
■ P’ waves are not identical to previous P waves which are from the SA node. (The same is for the escape
beat)
○ Junctional escape rhythm ⇒ 40­60/min

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■ Conducts mainly to ventricles → series of lone QRS complexes.
■ Retrograde atrial depolarization leads to an inverted P’
● can be immediately before the QRS
● can be buried in the QRS
● can be after the QRS
○ Ventricular escape rhythm ⇒ 20­40/min
■ large ventricular complexes
■ can be so slow that it causes Stokes­Adams Syndrome where not enough blood reaches the brain.
● Premature Beats ⇒ irritable focus spontaneously fires a single stimulus
○ Premature atrial beat ⇒ early P’ wave which can be hidden in the T wave with normal QRS following.
■ P’ can depolarize the ventricles leading to a wide QRS in the PAC beat only.
■ If not conducted, lone P wave with no QRS following.
■ Irritated by (same for premature junctional beat) ­ epi, increased SNS stimulation, caffeine, amphetamines,
cocaine, other beta1 stimulants, excess digitalis, toxins, etoh (sometimes), hyperthyroid, stretch
○ Premature junctional beat ⇒ premature irritable stimulation from AV junction which depolarizes the ventricles and
sometimes in a retrograde fashion, will depolarize the atria.

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■ P’ wave can be before, during or after the QRS.
■ Upper AV Junctional Rhythm
● AV node not pacemaker.
● Retrograde/inverted P waves precede the QRS complexes by short P­R intervals (start pacemaker
near AV node → travels faster because shorter distance) in leads II, III, and aVF
■ Middle AV Junctional Rhythm
● P waves cannot be identified since they are buried in the QRS complexes. Atrial fibrillation is ruled
out since the base line shows no oscillations.
■ Lower AV Junctional Rhythm
● Retrograde P waves follow QRS complexes. They are best seen in leads II, III, and aVF
● Atria depolarized AFTER the ventricles depolarize.
○ Premature ventricular beat ⇒ irritate the ventricles
■ Wide and tall QRS with opposite polarity of the normal QRS
■ Only depolarizes the ventricles, not the SA node.
■ Irritated by ­ airway obstruction, hypoxia, reduced CO, low potassium, mitral valve prolapse, stretch,
myocarditis
○ Ventricular Parastole ⇒ from an entrance block but not irritable PVC’s coupled to long series of normal cycles
○ Multifocal PVCs ⇒ each focus is own unique identifiable PVC
○ R on T ⇒ PVC falls on a T wave/falls on a vulnerable period and starts shit
■ from hypoxia and low serum potassium.
● Tachyarrhythmias ⇒ rapid ventricular rhythms originating in a very irritable automaticity foci
○ Paroxysmal (sudden) tachycardia ⇒ 150­250 (sinus tachycardia is not sudden like paroxysmal)
■ Paroxysmal Atrial Tachycardia (PAT)
● rapid rate, spike P’ waves
● 2:1 ratio P’:QRS
● (suspect digitalis excess or toxicity ­ digitalis can inhibit the AV node)

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● PAT with AV block → more than one P’ wave for every QRS response
■ Paroxysmal Junctional Tachycardia (PJT) ­ sudden rapid pacing of a very irritable automaticity foci in the
AV junction
● inverted P’ before, during, or after the QRS ­ can depolarize the atria in a retrograde fashion from
below
● Wide QRS from depolarizing left before right
■ Junctional Tachycardia → AV nodal reentry tachycardia

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● continuous reentry circuit → rapidly paces the atria and ventricles. Each pacing stimulus records in
an origin near the coronary sinus.
■ Supraventricular tachycardia → irritable automaticity foci that produce both paroxysmal atrial and
junctional tachycardia (above the ventricles)
■ Paroxysmal Ventricular Tachycardia → resembles a series of PVCs
● SA node still paces atria → independent pacing of the atria and ventricles (AV dissociation)
● Indicates coronary insufficiency leading to poor O2 to the heart.
● Distinguishing wide QRS insufficiency complex SVT from VTach.
SVT VTach
Pt with coronary disease or infarction uncommon very common
QRS width (duration) <0.14s >0.14s
AV dissociation showing captures or
fusions
rare yes
Axis ­ extreme RAD rare yes
●
■ Torsades de Pointes (250­350)
● caused by low potassium, meds that block the K+ channels, congenital abnormalities,
long/lengthened QT segment.
● Possibly from two irritable foci in different ventricular areas.
○ Flutter ⇒ 250­350
■ Atrial flutter ­ saw­tooth shape

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● Originates in the atrial automaticity focus
■ Ventricular Flutter
● single ventricular automaticity focus
● Sine waves of similar amplitude
● Tends to go to VFib.
○ Fibrillation ⇒ 350­450 (multiple foci discharge rapidly)
■ atrial fibrillation
● many irritable parasystolic atrial foci
● causes many irregular spokes on the EKG
● No identifiable P or P’ waves with irregular QRS response.
■ Ventricular Fibrillation
● Many irritable parasystolic ventricular automaticity foci pacing rapidly (entrance block)
■ Wolff­Parkinson­White Syndrome

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● Delta wave = area of preexcitation
● Can have paroxysmal tachycardia
○ rapid conduction ­ SVT (atrial flutter and afib) can be rapidly conducted through the
accessory pathway
○ some bundles have automaticity foci that can initial paroxysmal tachycardia
○ Re­entry ­ ventricular depolarization may immediately re­stimulate the atria in a
retrograde fashion via the accessory pathway causing a theoretical circus reentry loop
■ Lown­Ganong­Levine Syndrome (LGL)
● AV node is bypassed by an extension of the anterior internodal tract (James Bundle) which
conducts atrial depolarizations directly to the Bundle of His without delay
● No significant PR interval delay
● P waves are adjacent to the QRS’s on EKG.
● Sinus Block
○ SA node may temporarily fail to pace for at least one cycle then resumes pacing
○ The pause can induce an escape beat from an automaticity foci
○ Sick Sinus Syndrome
■ seen in the elderly with heart disease
■ Marked sinus bradycardia without normal escape mechanisms or atrial and junctional foci
■ can develop bradycardia­tachycardia syndrome ⇒ intermittent episodes of SVT (a flutter or afib)
○ AV Block
■ First Degree AV block

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● lengthened PR interval > 0.2 s (1 large square)
● No wide QRS
■ Second degree AV block
● Wenckebach → lengthening of PR interval until QRS is dropped.
● Mobitz 2 → 1 normal cycle preceded by a series of paced P waves that fail to conduct through the
AV node
■ Third degree AV block
● block of the conduction of atrial stimuli to ventricles.
● Atria and ventricles pace at different rates.
● Bundle Branch Block/Intraventricular Conduction Delay
○ block of one bundle branch which produces a delay of depolarization of the ventricle it supplies.
○ Wide QRS with rabbit ears (>0.12s) (3 squares or more in any lead) ­­ RSR’
○ RBBB ­ rabbit ears in V1, V2

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● Deep and round S­waves in I, aVL and V4­6
● Secondary S­T, T­wave change in V1­3
● abnormal depolarization and repolarization
● Complete RBBB with RVH > 15 mm. Can Dx only with RBBB.
● LBBB ­ rabbit ears in V5, V6
○ Absence of septal q­waves in V4­6 (small q from septal activation not seen)
○ RSR’ or “M” pattern of QRS in I, aVL and V4­6
○ Secondary S­T, T­wave change in I, aVL and V4­6
○ Septal activation in opposite direction (R→ L)
● If RSR’ of normal QRS duration ⇒ incomplete BBB
● Intermittent mobitz ­ occasional dropped QRS due to permanent BBB with intermittent BBB of other side.
● Hemiblock

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○ Anterior Hemiblock
■ LAD ⇒ usually associated with an MI (or other heart dz)
■ Normal or slightly widened QRS (0.10­0.12s)
■ Q1S3 ⇒ Q in I or wise/deep S in III)
■ Left Anterior block
● Mean and terminal QRS vectors are directed to the left of ­30° in frontal plane
● Initial 0.02­second QRS vector
○ Directed right and inferiorly and produces a small 0.02­second Q­wave in Lead I and
AVL
○ Small 0.02­second R­wave in Leads II, III and AVF
● Other causes of abnormal left axis deviation are ruled out i.e., inferior wall myocardial infarction
○ Anterior hemiblock with RBBB
■ RBBB ­ mean QRS vector is within normal range or shows minimal RAD
■ RBBB + LAD = anterior hemiblock
○ Posterior hemiblock
■ RAD (usually associated with an MI)
■ normal or slightly widened QRS
■ S1Q3 ­ Wide S in I and Q in III
■ Posterior block
● This condition is very difficult to diagnose ­ right ventricular enlargement and lateral infarctions
● Mean and terminal QRS vectors in frontal plane show right axis deviation
● Initial 0.02­second QRS vector
○ Directed slightly leftward and superiorly and produces a small 0.02­second R­wave in
Lead I and AVL (r/o anterolateral infarction)
○ Small 0.02­second Q­wave in Leads II, III and AVF
○ Bifascicular block
■ RBBB + anterior hemiblock
■ RBBB + posterior hemiblock
○ Intermittent block
■ continuous EKG pattern with intermittent wide QRS characteristic of intermittent BBB or with intermittent
changes of QRS axis.
○ Incomplete Trifascicular Block
■ First­degree A­V block plus a right bundle branch block plus either a left anterior hemiblock or posterior
hemiblock
● Axis ­ direction of depolarization as it passes through the heart
○ origin of mean QRS vector is the AV node = tail of the
vector. 0­90 is normal
○ Mean QRS vector will point toward hypertrophy and away
from infarct
○ V1, V2 = rightward rotation
○ V5, V6 = leftward rotation
● Hypertrophy
○ Diphasic wave = atrial enlargement
○ Right atrial enlargement ­ initial large deflection in V1. Tall
P wave

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■ if height > 2.5mm in II and >0.12s, suspect right atrial enlargement
■ pointed P wave greater than 2.5 mm, which is best seen in leads perpendicular to the heart bottom wall (II,
III, aVF) and chest leads V1 and V2
○ Left atrial enlargement ­ large terminal deflection in V1. Long P wave
● P wave is a prolonged and biphasic (bifid). It is best seen in leads I, II and aVL and sometimes possibly in
leads V5 and V6. (http://www.health­tutor.com/p­mitrale­ecg.html )
● Right ventricular hypertrophy

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○ Large R wave in V1, S wave is much smaller
○ The large R wave in V1 progressively becomes smaller in V2, V3, V4
○ RVH causes RAD + rightward shift.
● Left ventricular hypertrophy
○ QRS complexes are exaggerated in amplitude eps. in chest leads.
○ Very tall R waves in V5
○ Height/depth of S in V1 + height of R in V5 > 35 mm ⇒ LVH.

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○ Can see an asymmetrical inverted T wave (ideal leads V5/V6)
○ ventricular strain
○ V1 provides the most information regarding hypertrophy ­­ diphasic waves, R wave in V1, S wave in V1, R
wave in V5
○ Accompanied by
■ left atrial abnormality
● >0.11s
■ Left axis deviation 0­30
■ ST segment T wave changes → left ventricular strain pattern (systolic overload)
○ Extremity leads
■ Amplitude of R­wave in Lead I and/or AVL > 15 mm
■ Amplitude of R­wave in AVF > 21 mm
■ Sum of R­wave in Lead I plus S­wave in
■ Lead III > 25 mm
○ Precordial leads
■ SV1 + RV5 or SV1 + RV6 > 35 mm
■ R­wave in V5 or V6 > 26 mm
■ R­wave in V6 taller than R­wave in Lead V5
● Infarction
○ Ischemia ­ reduced blood supply
■ characterized by symmetric inverted T waves
■ Leads V2­V6 is pathological
■ Marked T wave inversion in leads V2, V3 is Wellen’s Syndrome ⇒ Stenosis of anterior descending
artery.
○ Injury ­ acute or recent
■ if no Q waves, can be non­Q wave infarction
■ ST elevation is infarct. Depression in reciprocal changes.
○ Pericarditis

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■ ST segment is elevated (diffuse) and usually flat or concave (middle sags down).
■ Entire T wave may be elevated off baseline
○ Subendocardial infarction

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○ Necrosis ­ dead tissue
■ Q wave indicates necrosis → can Dx infarction
■ Insignificant Q waves < 0.04s (1mm)
■ Significant Q waves > 0.04s (or ⅓ QRS amplitude ­ old criterion)
○ Anterior Infarct

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■ elevated ST segments and Q waves in V1, V2, V3, V4 ⇒ anterior descending of left coronary
artery
○ Posterior Infarct
■ Mirror image of anterior infarct
■ ST depression in V1, V2
■ Large R waves, maybe Q in V6
○ Lateral infarct

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■ I, AVL Q waves
■ Circumflex left coronary artery
○ Inferior Infarct
■ II, III, AVF Q waves
■ right/left coronary artery
○ Cannot Dx infarction with LBBB

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● hyperkalemia
○ wide, flat P
○ peaked T
○ wide QRS
● Hypokalemia
○ T/U wave fusion.
○ Flat T wave
○ Prominent U wave
● Hypercalcemia
○ short QT interval

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● Hypocalcemia
○ prolonged QT interval
● Digitalis
○ positive inotrope ­ Improve contractility of the failing heart (mechanical effect)
○ Prolong the refractory period of the AV node in patients with supraventricular arrhythmias (electrical effect)
○ inhibits the cell membrane sodium­potassium ATPase pump
○ Therapeutic use for treating Atrial fibrillation
○ Salvador Dali’s mustache
○ Toxicity ­ Sinus bradycardia, AV block, VTach secondary to ectopic beats
● Quinidine
○ Class IA antiarrhythmic (blocks Na and K channels)
○ retards and repolarizes
○ Long QT interval → can lead to Torsades
○ Wide, notched P
○ Wide QRS
○ depression ST
○ U wave