R-R Interval
60-100 bpm or Greater than 3 boxes and Less than 5 boxes
Normal
Greater than 5 Boxes and Less than 60 bpm
Bradycardia
Less than 3 boxes AND Greater 100 BPM 
Tachycardia
Regularity
Regular
Irregular
Regularly Irregular
Bigeminy/Trigeminy
Irregularly Irregular
Atrial Fibrillation Likely
Early QRS
Wide
Premature Ventricular Contraction
NArrow
Premature atrial contraction
P waves
Upright in I, II, aVF, V3-V6
Sinus rhythm
Wide Lead I/II, Bifid, negative V1
LAE
​Upgoing >1mm in V1, tall peaked P in II/III/aVF
RAE
Neither
Normal
Non-SinuS
Normal Rate
  • Limb lead reversal (R-L arm or R arm - R leg as described above)
  • Ectopic atrial rhythm or atrial tachycardia with 2:1 A-V conduction
  • Dextrocardia (QRS too is inverted in I; QRS progression is reversed in chest leads)
  • Atrial paced rhythm (usually QRS is also paced)
Tachycardia
  • Ectopic atrial rhythm (P wave morphology abnormal both in limb leads and in chest leads)
  • Atrial tachycardia with 2:1 A-V conduction (twice as many Ps as is apparent)
  • Atrial flutter with 2:1 A-V conduction (twice as many Ps as is apparent; use “halving method" or block down the AV node to find hidden flutter waves)
  • Paced atrial rhythm (pacer spikes; QRS usually also paced; rate regular at 60 or 70)
  • Retrograde P waves (AV junctional rhythm; idioventricular rhythm; ventricular paced rhythm; reentrant SVT): P waves follow the QRS complexes
  • Dextrocardia (both P and QRS downgoing in I; QRS progression is reversed in chest leads)
  • R-L arm lead reversal (lead I as above but normal QRS progression in chest leads)
  • R arm - R leg lead reversal (P downgoing in lead I; and flat line in lead II)
  • Artifact (Parkinsonian tremor [limb leads] and HFOV [chest leads] may mimic atrial flutter)
No P Waves
Irregular
SLow and Narrow
AV junctional Escape
Slow and WIDE
  • Junctional escape with BBB
  • Ventricular escape
Fast and Narrow
SVT
FAst and WIDE
  • Ventricular tachycardia 90% of the time
  • SVT with aberrancy 10% of the time
Regular
PR INTERVALS
Less than 3 boxes (0.12s)
Normal RATE
  • Small AV Node (Congenital)
  • High dose corticosteroids
  • WPW
FAST RATE
Sinus tachycardia lively due to adrenergic activation
  • Fever
  • Shock
  • Thyrotoxicosis
  • Beta-adrenergic agonists
Very Slow
Consider isorhythmic AV dissociation (junctional escape rhythm with
sinus P waves “marching through”)
3-5 Little Boxes
Normal
Greater than 5 boxes (0.20s)
First Degree AV Block
  • Advanced Age
  • Atherosclerotic conduction system
  • Left atrial enlargement
  • Fever/IV drug use
    • Aortic valve endocarditis
  • Drugs
    • Non-dihydropiridine Ca channel (diltiazem/verapamil)
    • Beta blockers
    • DIgoxin
  • Myocarditis
  • Connective tissue disease
    • Ankylosing spondylitis; HLA-B27
  • Cardiomyopathies
Variable PR boxes
Progressive Prolongation
​Mobitz Type I 2nd Degree AV block (Wenckebach)
Random interval
  • Third degree AV block
  • Fluctuating vagal tone
    • Marked sinus arrhythmia (OSA, autonomic dysfunction)
Occaisional Dropped QRS
​Mobitz Type II 2nd Degree AV block
QRS Complex
Wide (>3 little boxes)
P Waves
QRS Predominantly Upgoing in V1
rSr'
RBBB
FASt, no consistent P-QRS relationship
Ventricular tachycardia
Short PR, Delta Wave
Wolff-Parkinson White
Pacer Spikes
BiV paced
QRS Predominantly Downgoing in V1
Qs or rS
LBBB
Short PR INterval, Delta Wave
WPW
Pacer Spikes
RV Paced
Other
Nonspecific Intraventricular conduction delay
  • Does not fit any of the above
  • Frequently coexists with LAE, First degree AV block, atrial fibrillation
Causes of IVCD
  • LVH with QRS widening: when LVH criteria are present
  • “Periinfarction block”: when pathologic Q waves are present
  • Hyperkalemia: when narrow-based peaked T waves are present
  • Hypothermia: when Osborne waves, bradycardia, ST-T abnormalities, long QT are present
  • Drug toxicities: when QT prolongation is present (TCA: deep S in I; tall R’ in aVR)
  • Infiltrative heart disease and connective tissue disease (e.g., amyloidosis, PSS)
No P Waves Present
Rate Less than 60
Ventricular escape (usually 35-40/min)
  • Sinus arrest or AV block
Rate 60-120
Accelerated Idioventricular rhythm
  • Reperfusion arrhythmia
  • Cocaine
  • Electrolytes
Rate Greater than 125
Ventricular Tachycardia
Axis
Lead I positive
AVF Positive
Normal Axis
AVF Negative
Left axis deviation
  • Advanced age
  • LVH
  • Inferior MI (loss of inferior forces)
  • Left anterior fasicular block
Lead I Negative
AVF Positive
Right Axis Deviation
  • Young age
  • RVH, pulmonary hypertension, COPD, secundum ASD
  • Lateral MI (loss of lateral forces)
  • Left posterior fascicular block
AVF Negative
Extreme axis deviation
Amplitude
S1 + R in V5 or V6  greater than 35mm
Sensitive, but not specific for Left Ventricular Hypertrophy
Check amplification (r/o 20 mm/mV)
R in avl Greater than 13mm
Specific, but not sensitive for LVH
​Check amplification (r/o 20 mm/mV)
R in I + S in III Greater than 27mm
Intermediate sensitivity-specificity for LVH
​Check amplification (r/o 20 mm/mV)
​
QRS Less than 5 mm Limb Leads
Low Voltage
  • First, check amplification is 5 mm/mV
  • Decreased muscle mass
  • Obesity
  • Remote MI
  • Emphysema
  • Amyloidosis
  • Scleroderma
  • Pericardial effusion
  • ​Anasarca
Chest Leads Less then 10 mm
Low Voltage
  • First, check amplification is 5 mm/mV
  • Decreased muscle mass
  • Obesity
  • Remote MI
  • Emphysema
  • Amyloidosis
  • Scleroderma
  • Pericardial effusion
  • ​Anasarca
Variable QRS
  • Respirophasic: extensive diaphragmatic excursions (diaphragm. paralysis, severe COPD)
  • Electrical alternans (every other beat taller): suggestive of large pericardial effusion
  • Electrical pseudo-alternans: bigeminal PVCs, intermittent WPW
R Wave Progression
Upgoing in V1 R/S Greater than 1
QRS Narrow (Less than 0.11S)
RVH: T will also be negative in V1 (strain)
  • Right axis deviation
  • Deep S waves in V5-V6
  • V1 may start with narrow Q (qR)
  • Clinical picture (emphysema)

Posterior MI
  • T upright in V1 (mirror image)
  • Inverted Ts in lateral leads
  • Inverted Ts in inferior leads
  • Clinical picture (chest pain)
​
No other signs of RVH, MI, WPW
  • Normal Variant
QRS Wide (Greater than  0.12s)
rSr'
RBBB
FASt, no consistent P-QRS relationship
Ventricular tachycardia
Short PR, Delta Wave
Wolff-Parkinson White
Pacer Spikes
BiV paced
R WAVE REGRESSION FROM V1-V3
V1-V3 Lead Reversal
  • R wave regression from V1 to V3
  • Computer may read it as anterior MI
  • P wave biphasic in V3
Downgoing V1
QRS Narrow (less than .11s)
QRS Wide (Greater than .12S)
Qs or rS
LBBB
Short PR INterval, Delta Wave
WPW
Pacer Spikes
RV Paced
Upgoing V5-V6
Normal
Downgoing V5-V6
QRS Narrow (Less than 0.11S)
  • Emphysema
  • RVH
  • LAFB
  • Lateral MI
QRS Wide (Greater than 0.12S)
  • Paced rhythm
  • WPW
  • VT
Regression of r/s in Chest leads
  • Possible anterior MI
  • Severe emphysema, RVH
  • Morbid obesity
  • RBBB
  • Dextrocardia
  • Incorrect electrode placement
Q >0.03S + >1/3 of QRS in Neighboring Leads
Pathological Q waves
Vessel Specific Distribution
Previous MI
Noninfarction
  • LBBB
  • WPW
  • LVH
  • Infiltrative processes (amyloidosis, scleroderma, cardiac metastases)
  • Cardiomyopathies
  • PE
  • Hyperkalemia
ST Segments
ST Elevation
VASCULAR DISTRIBUTION
II, III, aVF
​Inferior MI-RCA (or LCX)
V1-V4
​Anteroseptal-LAD
V1-V6 (+/- I, avl)
Extensive anterior- LAD
V3-V6 (+/- I, avl)
​Lateral-LCX
I, avL, V2
​High lateral- LAD, D1
avr
Possible left main obstruction
Mirror Image V1-V2: Posteriorlateral-LCX
TRANSIENT ST ELEVATION WITHOUT Q OR T CHANGES
Prinzmetal angia
PERSISTENT ST ELEVATION WITH Q OR T CHANGES
Cardiac trauma
WIDE QRS
​Coved ST-Ts in leads with downgoing QRS
  • LBBB
  • WPW
  • Paced rhythm
upward concave ST elevation and upright Ts in V1-V2
LVH
TERMINAL NOTCH, HAMMOCK ST ELEVATION
Bradycardia
Hypothermia
Tachycardia
Pericarditis
Normal Rate
Benign early repolarization
PEAKED TS
Hyperkalemia
COVED ST ELEVATION, NO TS IN ANTEROSEPTAL
Hypercalcemia
V1-V2: RSR', COVED ST ELEVATION, T WAVE INVERSION
  • Brugada syndrome
  • Na-Channel blocker toxicity
CHANGES WITH CYCLE
Artifact
RATE GREATER THAN 150 PER MINUTE
May be atrial flutter
OTHER
  • LV Aneurysm
  • Myocarditis
  • Acute adrenergic stress
  • SAH, ICH, Acute CNS disorder
  • Following high energy cardioversion
  • Subacute cardiac rupture
ST DEPRESSION
Horizontal or downsloping ST with upright Ts
Probable Ischemia
  • ​“Someone stepped on the ST segment”
  • May be diffuse or localized
  • Diffuse ST depression with ST elevation in aVR: possible left main obstruction
  • ST depression during PSVT is not diagnostic
Downsloping ST with inverted Ts
Probable LV Strain
  • Usually in association with LVH
  • LVH, strain and chest pain: ECG not very useful
Upsloping ST with J point depression
Nonspecific
  • ST usually back to baseline 2 mm after the end of QRS
  • Causes: anemia, metabolic abnormalities, MVP, normal variant
Scooped ST
Digitalis or Hypercalcemia
  • Usually seen in left leads (I, V5-V6)
  • QT interval may be shortened
  • May be associated with other markers of digitalis effect:
    • Bradycardia, 1o AV block, atrial fibrillation with slow
    • Ventricular response, digitalis-toxic tachyarrhythmias
T WAVES
Flat, Bifid, or Notched
  • ​Hypokalemia
  • Drugs (antiarrhythmics)
  • Acute CNS disorder (SAH, CVA, trauma)
  • Liver failure
  • Congenital long QT syndrome
Inverted
Deep, symmetrical (V-shaped)
Consider ischemia
Vascular Localization
Consider ischemia
Biphasic T WAVE
Consider ischemia
Upsloping depression with non-symmetrical T wave inversion
I, aVL, V5-V6
  • LV Strain
V1-V3
  • RV Strain
  • Anterior ischemia
Diffuse, shallow
Nonspecific
​WPW, LBBB, other wide complex rhythms
​Cardiac memory
Normal
  • T wave axis usually follows the QRS axis
  • Ts are always inverted in aVR; usually inverted in V1; upright in most other leads
  • Isolated T wave inversion in lead III is normal
  • With vertical QRS axis, T wave inversion in aVL is normal
  • If T axis is normal but T waves are narrow based and peaked: consider hyperkalemia
  • T waves are usually smooth; sharp notches or “shoulders” on the upslope or downslope of Ts are suggestive of superimposed Ps (or artifact)
QT Intervals
Less than 0.44s
Short QT
Lower limit is uncertain
  • Congenital short QT syndrome
  • Hypercalcemia
Clinical significance: May increase risk of VT/VF
More than 0.44S
Prolonged QT
  • Drug Effects
    • Digitalis
    • Antiarrhythmics
      • quinidine
      • procainamide
      • disopyramide
      • sotalol
      • amiodarone, dofetilide, ibutilide
    • Psychotropic Agents
      • haloperidol, TCAs, SSRIs, phenothiazines
    • Antihistamines
    • Anitbiotics
      • macrolides
      • quinolones
      • azoles
    • Many, many more
  • Metabolic Abnormalities
    • Alkalosis
    • Hypomagnesemia
    • Hypokalemia
    • Hypocalcemia
    • Hypothermia
    • Liver failure
  • Acute myocardial injury and/or catecholamine effect
    • ischemia
    • pulmonary edema (usually ~24 hrs after resolution)
    • stress-induced cardiomyopathy (including Tako-Tsubo syndrome)
    • massive PE
    • beta-adrenergic agonists (inotropes, inhalers)
    • pheochromocytoma
  • Acute CNS Disorders
    • Closed head injury
    • Status epilepticus
    • SAH
    • CVA, especially Thalamic stroke
    • Brain Tumore
  • Congenital Long QT Syndrome