ELECTROCARDIOGRAMs

(ECGs)

May 2019
 LEAD PLACEMENT

Standard 12-lead ECG:

• Limb Leads - 6 in all

- I, II, III, aVL, aVR, aVF
• Chest leads - 6 in all
-V1,V2,V3,V4,V5,V6
 LIMB LEADS

Bipolar Augmented

- -
aVR + aVL
+
- + I

+ +
III II +
aVF
 CHEST LEADS

Along the horizontal plane:

• V1 and V2 - Right side of the heart

• V3 and V4 - Intraventricular septum
• V5 and V6 - Left side of the heart
 PROCESS

SA Node - Heart pacemaker; located in the RA;

initiates next step
 PROCESS

P Wave - Atrial depolarization and contraction

 PROCESS

AV Node - Slows the depolarization of the atria;

connects atria and ventricles electrically
 PROCESS

QRS complex - ventricular depolarization; begins in

Bundle of His
PROCESS
VENTRICULAR DEPOLARIZATION

His Bundle

Left Bundle Branch & Right Bundle Branch

Purkinje Fibers
VENTRICULAR DEPOLARIZATION

• Q Wave - 1st downward wave of the

complex
• R Wave - 1st upward wave of the complex
• S Wave - downward wave preceded by an
upward wave
 PROCESS

ST Segment - Initial plateau phase of

ventricular repolarization
 PROCESS

T wave - Rapid phase of ventricular

repolarization
NORMAL ECG
 RHYTHM

Normal sinus rhythm:

• Each P wave is followed by a QRS
• Regular or irregular
 RATE
• P wave rate 60 - 100 bpm with <10% variation - Normal
• Rate < 60 bpm = Sinus Bradycardia
- Results from:
- Excessive vagal stimulation
- SA nodal ischemia (Inferior MI)
• Rate > 100 bpm = Sinus Tachycardia
- Results from:
- Pain / anxiety
- CHF
- Volume depletion
- Pericarditis
- Chronotropic Drugs (Dopamine)
 RATE
Methods:
• Method 1 = 1500/ # of small boxes between RR

• Method 2
 P WAVE

Normal:
• Height < 2.5 mm in lead II
• Width < 0.11 s in lead II
P WAVE ABNORMALITY
P WAVE ABNORMALITIES

Right atrial hypertrophy:

• A P wave in lead II taller then 2.5 mm

(2.5 small squares)
• The P wave is usually pointed
P WAVE ABNORMALITIES

Left atrial abnormality (dilatation

or hypertrophy):

• M shaped P wave in lead II

• Prominent terminal negative component to
P wave in lead V1
 P WAVE ABNORMALITIES
Premature Atrial Complex (PAC):
• An abnormal P wave (arrowed in figure below)
• As P waves are small and rather shapeless, the difference
in a PAC is usually subtle; the one shown here is a clear
example
• Occurs earlier than expected
• Followed by a compensatory pause - but not a full
compensatory pause
P WAVE ABNORMALITIES

Hyperkalemia:
• The following changes may be seen in hyperkalemia
- Small or absent P waves
- Atrial fibrillation
- Wide QRS
- Shortened or absent ST segment
- Wide, tall and tented T waves
- Ventricular fibrillation
P WAVE ABNORMALITIES

Arrhythmias (will cover later):

• Premature atrial complex (PAC)
• Atrial flutter
• Atrial fibrillation
• Paroxysmal reentrant tachycardia (SVT)
• Multifocal atrial tachycardia
 PR INTERVAL

Normal PR interval:

• 0.12 to 0.20 s (3 - 5 small squares)

PR INTERVAL ABNORMALITIES

Shorter PR interval:
• Wolf-Parkinson-White syndrome
- Short PR interval, less than 3 small squares
(120 ms)
- Slurred upstroke to the QRS indicating pre-
excitation (delta wave)
- Broad QRS
- Secondary ST and T wave changes
PR INTERVAL ABNORMALITIES

Long PR interval (will cover later):

• AV blocks
 QRS COMPLEX

• QRS Axis
• Normal duration of complex is < 0.12 s (3 small
squares)
• NO pathological Q waves
• NO left or right ventricular hypertrophy
 AXIS
• Using leads I and aVF, the axis can be
assigned to one of the four quadrants at a
glance
 AXIS - NORMAL
• Both I and aVF +ve = NORMAL AXIS
• Lead I +ve and aVF -ve
-If the axis is in the "left" quadrant take your
second glance at lead II.
- Lead II +ve = NORMAL AXIS
- Lead II -ve = LEFT AXIS DEVIATION
AXIS - LEFT AXIS DEVIATION
 Left anterior hemiblock
 Left ventricular hypertrophy
 Q waves of inferior myocardial infarction
 Artificial cardiac pacing
 Emphysema
 Hyperkalemia
Wolff-Parkinson-White syndrome - right sided
accessory pathway
 Tricuspid atresia
 Ostium primum ASD
 Injection of contrast into left coronary artery
 AXIS - NORTHWEST TERRITORY

• Both I and aVF -ve = axis in the NORTHWEST TERRITORY

• Causes of “No man’s land”
- Emphysema
- Hyperkalemia
- Lead transposition
- Artificial cardiac pacing
- Ventricular tachycardia
 AXIS - RIGHT AXIS DEVIATION
• Lead I -ve and aVF +ve = RIGHT AXIS DEVIATION
• Causes:
- Normal finding in children and tall thin adults
- Right ventricular hypertrophy
- Chronic lung disease even without pulmonary
hypertension
- Anterolateral myocardial infarction
- Left posterior hemiblock
- Pulmonary embolus
- Wolff-Parkinson-White syndrome - left sided
accessory pathway
- Atrial septal defect
- Ventricular septal defect
 WIDE QRS COMPLEX
Right Bundle Branch Block:
• Wide QRS, more than 120 ms (3 small squares)
• Secondary R wave in lead V1 (RSR)
•Other features include slurred S wave in lateral leads
and T wave changes in the septal leads
WIDE QRS COMPLEX
 WIDE QRS COMPLEX
Left Bundle Branch Block:
• Wide QRS, more than 120 ms (3 small squares)
• M shape QRS , R’R’
WIDE QRS COMPLEX
 WIDE QRS
Hyperkalemia:
• Changes that can be seen:
- Small or absent P waves
- Atrial fibrillation
- Wide QRS
- Shortened or absent ST segment
- Wide, tall and tented T waves
- Ventricular fibrillation
 WIDE QRS

Ventricular rhythm (will cover later):

 PATHOLOGICAL Q WAVES
• Q waves > 1mm
• Their depth > 25% of the height of the QRS
• Q waves in V6 and aVL (not pathological…small)
• Look for anatomical site, ignore aVR

Anatomical Site Lead with Abnormal EKG complexes Coronary Artery most often responsible
Inferior II, III, aVf RCA
Antero Septal V1-V2 LAD
Antero Apical V3-V4 LAD (distal)
Antero Lateral V5-V6, I, aVL CFX
Posterior V1-V2 (Tall R, Not Q) RCA
PATHOLOGICAL Q WAVES
 NON Q WAVE MI
• Not all MIs develop Q waves (up to 1/3 never do or
they develop and resolve)

• WHY?
• Infarct was not complete (transmural)
• Infarct occurred in a electrically “silent” area of
the heart, where an EKG cannot record the injury
• Acute Infarct (Q waves will eventually appear)
 RIGHT VENTRICULAR
HYPERTROPHY (RVH)

• Right axis deviation

• Deep S waves in the lateral leads
• A dominant R wave in lead V1
 LEFT VENTRICULAR
HYPERTROPHY (LVH)
 Sokolow + Lyon (Am Heart J, 1949;37:161)
 S in V1+ R in V5 or V6 > 35 mm

 Cornell criteria (Circulation, 1987;3: 565-72)

 S in V3 + R in aVL > 28 mm in men
 S in V3 + R in aVL > 20 mm in women

 Framingham criteria (Circulation,1990; 81:815-820)

 R in aVL > 11mm, R in V4-6 > 25mm
 S in V1-3 > 25 mm,
 S in V1 or V2 + R in V5 or V6 > 35 mm,
 R in I + S in III > 25 mm
 LVH
• Increased amplitude in height and depth
 QT INTERVAL

• Calculate the corrected QT interval

- QTc = QT / RR = 0.42
- Normal = 0.42 s
 LONG QT INTERVAL

Causes:
• Myocardial infarction, myocarditis, diffuse
myocardial disease
• Hypocalcemia, Hypercalcemia (Short QT),
hypothyrodism
• Subarachnoid hemorrhage, intracerebral
hemorrhage
• Drugs (e.g. Sotalol, Amiodarone)
• Heredity
 ST SEGMENT

Normal ST segment:
• No elevation or depression
 ST ELEVATION

Causes of elevation include:

• Acute MI (eg. Anterior, Inferior, Lateral).
• LBBB
• Acute pericarditis
• Normal variants (e.g. athletic heart, high-take off),
 ACUTE MI
• ST elevation in leads where MI occurs
• Look for reciprocal changes
(e.g. Ant MI look for ST depression in inferior leads)

Anatomical Site Lead with Abnormal EKG complexes Coronary Artery most often responsible
Inferior II, III, aVf RCA
Antero Septal V1-V2 LAD
Antero Apical V3-V4 LAD (distal)
Antero Lateral V5-V6, I, aVL CFX
Posterior V1-V2 (Tall R, Not Q) RCA
LOCATING THE DAMAGE
LOCATION: 12 LEAD
 ST DEPRESSION

Causes of depression include:

• Myocardial ischemia
• Digoxin Effect
• Ventricular Hypertrophy
• Acute Posterior MI
• Pulmonary Embolus
• LBBB
 DIGOXIN EFFECT

• Shortened QT interval
• Characteristic down-sloping ST depression
• Dysrhythmias
- Ventricular / atrial premature beats
- PAT (paroxysmal atrial tachycardia) with
variable AV block
- Ventricular tachycardia and fibrillation
- Many others
 ACUTE POSTERIOR MI
• The mirror image of acute injury in leads V1 - 3
• (Fully evolved) tall R wave, tall upright T wave in leads
V1 -V3
• Usually associated with inferior and/or lateral wall MI

Mirror Test: Once you have determined an inferior (or other) MI has
occurred, you begin looking for reciprocal changes. If there is ST
depression in V1, V2, and V3, flip the EKG over and hold it up to the
light. Now read those leads flipped over. Are there significant Q
waves? Is the ST segment elevated with a coved appearance? Are
the T waves inverted? Answering yes tells you, there is a posterior
infarct as well.
 ST DEPRESSION

In diagnosis with ischemia:

• Looking for at least 1mm (1 square)
• This can be
1. Upsloping
2. Horizontal (can be combined w/ 1 or 3)
3. Downsloping
 T WAVES

• Repolarization of the ventricles is signaled by

the T wave
 TALL T WAVES

Causes:
• Hyperkalemia
• Hyperacute MI
• LBBB
 SMALL, FLATTENED OR
INVERTED T WAVES
Causes are plenty:
• Ischemia, age, race, hyperventilation, anxiety
• LVH, drugs, pericarditis, I-V conduction delay (RBBB),
• Electrolyte disturbances
• The most important thing to consider is INVERTED T waves
associated with Ischemia
 COMMON ARRHYTHMIAS
Location Bradyarrythmia Tacharrythmia
SA node Sinus Bradycardia Sinus tachycardia
Sick Sinus Syndrome
Atria Atrial Premature Beats
Atrial Flutter
Atrial Fibrillation
Paroxysmal SVT
Multifocal Atrial Tachycardia
AV node Conduction Blocks (1,2 and 3)
Jxal escape rhythm
Ventricles Ventricular escape rhytm Ventricular premature Beats
VT
Torsades de pointes
Ventricular Fibrillation
 SINUS BRADYCARDIA

• Less than 60 bpm

• If profound, could have decreased cardiac output
• Treatment:
- None if uncomplicated
- Atropine
- Pacing
 SINUS TACHYCARDIA

• Greater than 100 bpm

•  Myocardial oxygen demand and may  coronary
artery perfusion resulting in angina in CAD
• Decreased cardiac output could be exhibited
SSS (SICK SINUS SYNDROME)

•Deceased cardiac output, related to

periods of excessive bradycardia, AV block
and/or tachycardia

• Treatment:
- Pacemaker
- Anti coagulation therapy
 ATRIAL PREMATURE BEAT

• Can be in a healthy heart or with CAD

• They are well tolerated because cardiac output is not altered
 ATRIAL FLUTTER

• Saw toothed pattern; 200-350bpm atrial rate

• Can convert to atrial fibrillation
ATRIAL FLUTTER (CONT’D)

• People can feel flutter sensation… if short lived then no

complication; however, with an increased ventricular rate,
people can experience decreased cardiac output.
• Treatment:
- Veramapril, vagal stimulation
- Digoxin (perhaps in combo with other drugs)
- Cardioversion or pacing
 ATRIAL FIBRILLATION

• Chaotic atrial dysrhythmia; atrial rate can be 350+ bpm

• Higher ventricular response = cardiac output

• Treatment:
- Drugs (Digitalis, Verapamil, Beta blocker)
- Anticoagulation therapy
- Cardioversion
 PAROXYSMAL ATRIAL TACHYCARDIA
OR SUPRAVENTRICULAR TACHYCARDIA

• High ventricular rate

• Inadequate ventricular filling time, decreased cardiac output, and
inadequate myocardial perfusion time
• Treatment:
- Prevent CHF
- Carotid sinus massage to stimulate vagal response
- Cardioversion
- Drugs (Verapamil, Propranolol, and Digoxin)
MULTIFOCAL ATRIAL TACHYCARDIA
• Irregular rhythm with multiple (at least 3) P wave
morphologies in same lead with an irregular and
usually rapid ventricular response.
• Pulmonary disease, hypoxia.
• Rate is greater than 100 bpm.
• Treatment:
- Verapamil
- Resolve causative disorder
 1ST DEGREE AV BLOCK

• PR greater than 120 msec

• No hemodynamic complications
• Could progress to higher AV blocks
 2ND DEGREE AV BLOCK
MOBITZ TYPE 1
(WENCKEBACH)

• PR interval progressively lengthens with each beat until it is

completely blocked
• If bradycardic, could have decreased cardiac output
• Treatment:
- Only if brady (Atropine)
- Rare pacemaker
 2ND DEGREE AV BLOCK
MOBITZ TYPE 2

• Rare, occurs with large ant MI

• PR interval fixed and p waves occur in a regular ratio to QRS
(atrial rate is regular) until conduction is blocked
 2ND DEGREE AV BLOCK
MOBITZ TYPE 2 (CONT’D)

• Symptoms of decreased cardiac output occur with

slowing ventricular rate
- Could progress to complete block
• Treatment:
- Atropine initially
- Permanent pacemaker
 3RD DEGREE AV BLOCK
(COMPLETE)

• Atria and ventricles are independent of each other;

no relationship present
• Symptoms could include lightheadedness or syncope from
decreased rate
 3RD DEGREE AV BLOCK
(COMPLETE) (CONT’D)

• Decreased cardiac output, compromised

coronary perfusion
• Treatment:
- Emergency
- Atropine
- Pacemaker
 JUNCTIONAL ESCAPE RHYTHM

• QRS complexes are not preceded by normal P

waves, because the impulse originate below the SA
node
• Can cause a missed P wave, inverted or in the
QRS
 VENTRICULAR ESCAPE RHYTHM

• Wide QRS complex (> 120ms)

• Decreased cardiac output , lightheadedness and syncope due to
decreased heart rate
• Treatment:
- Atropine
- Electronic pacemaker
 PREMATURE VENTRICULAR
CONTRACTION (PVC)

• Occasional PVC’s have minimal consequences

• Increased frequency or multifocal PVCs can lead to
ventricular tachycardia
• Make sure it does not progress to more PVCs
• Couplet is 2 PVCs in a row
• Triplet is 3 PVCs in a row
 VENTRICULAR BIGEMINY

• Premature Ventricular contraction (PVC) in a bigeminal pattern

• Can be trigeminy (every third is a PVC), quadrigeminy
• Can be multifocal - increased irritability of the ventricle could
lead to more severe dysrhythmia
VENTRICULAR TACHYCARDIA
(VT)
•More than 3 PVC’s in a row > 100bpm

• Wide QRS, AV dissociation, QRS complex does not

resemble typical bundle branch block
• Irritable ventricle
• Sustained VT is an emergency rhythm and could
convert to ventricular fibrillation
 VT
• Decreased cardiac output , irritable ventricle

• Treatment:
- Cardioversion
- Lidocaine or Procainamide to get NSR
- Emergent care
- Long term care: ICD (implantable
cardioverter defibrillator)
 TORSADES DE POINTES

• Form of VT – “twisting of the points”

• People with prolonged QT interval are susceptible
 VENTRICULAR FIBRILLATION

• Chaotic activity of the ventricles

• No effective cardiac output or coronary perfusion
• Associated with severe myocardial ischemia.
• Life-threatening - death occurs within 4 min.
• Treatment:
- Immediate defibrillation
- CPR
- Lidocaine, bretylium. epinephrine
SINUS ARREST
 How to read the ECG
– Look at the whole tracing.

Rhythm: Is there a P wave before each QRS complex?

− Yes: sinus rhythm No: AV junctional or heart block
Rate: Count boxes; use caliper, ruler
PR interval: Normal - 0.20 sec. or less
QRS complex: Skinny (0.10 sec. or less) or broad (BBB or
ventricular)
ST segment: Isoelectric (normal), elevated or depressed
T wave: Upright, flat or inverted

Interpretation: Normal or abnormal.

− Is the rhythm dangerous?