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ECG Basics Sonia Samtani
7/2017
UCI Resident Lecture Series
Agenda
I. IntroductionII.The Conduction System III.ECG Basics IV.Cardiac Emergencies V.Summary
The Conduction System
Lead Placement
aVF
Precordial Leads
Electrical Leads:
Limb Leads (Frontal): I, II, III, AVF, AVR, AVL
Precordial Leads (Transverse): V1 – V6
Providing a 2-D view of the hearts electrical activity
Depolarization towards lead = + deflection
Depolarization away from lead = - deflection
Anatomy of an ECG:
Interpretation
Develop a systematic approach to reading EKGs and use it every time
The system we will learn is:
Rate
Rhythm (including intervals and blocks)
Axis
Hypertrophy
Ischemia
Rate
Rule of 300- Divide 300 by the number of boxes between each QRS = rate
Number of big boxes
Rate
1 300
2 150
3 100
4 75
5 60
6 50
Start 300 150 100 75 60 50
Rhythm: Normal Sinus Rhythm
Originating from SA node
P wave before every QRS
P wave in same direction as QRS
P wave has same morphology each beat
Upright P wave in I, II
Intervals
PR
0.20 sec (less than one large box)
QRS
0.08 – 0.10 sec (1-2 small boxes)
QT
450 ms in men, 460 ms in women
Based on sex / heart rate
Half the R-R interval with normal HR
Blocks
AV blocks First degree block
PR interval fixed and > 0.2 sec Second degree block, Mobitz
type 1 PR gradually lengthened, then
drop QRS Second degree block, Mobitz
type 2 PR fixed, but drop QRS
randomly Type 3 block
PR and QRS dissociated
QRS Duration
QRS > 0.10sec indicates conduction system disease, usually in the bundles (LAFB, LPFB, Incomplete RBBB)
QRS > 0.12sec indicates Bundle Branch Block, either RBBB, LBBB or IVCD
Right Bundle Branch Block
Look for characteristic R-S-R’ morphology in V1 (aka bunny ears)
Where R’ is larger than R
Look for broad terminal S-waves in V5, V6, I & AVL
Right Bundle Branch Block
Left Bundle Branch Block
Look for wide QRS > 0.12sec
Absence of RBBB
No S-wave or Q-wave in Lead I or V6
Dominate S-wave in V1 with small Q or small R-wave
May see R-S-R’ in V5 or V6
LBBB
QT & QTc Intervals
Normal QT interval represents time to repolarization of ventricles (T-wave)
The QT maybe prolonged with slow heart rates or short with fast heart rates. As a result,use QTc.
Bazett’s Formula: QTc = QT / √RR
Normal is ~0.42sec, concern > 0.46sec and higher, usually >0.5sec at risk for…
The QRS Axis
Overall Direction of Heart’s Electrical Activity.
Axis of –30 to +90 degrees is normal
Extreme Right Axis
Causes of Left Axis Deviation
Left anterior hemiblock – most common!! Not typically caused by LVH Inferior myocardial infarction with Q-
waves 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
Causes of Right Axis Deviation
Normal finding in children and tall thin adults
Right ventricular hypertrophy
Chronic lung disease even without pulmonary hypertension
Lateral wall myocardial infarction with Q-waves
Left posterior hemiblock
Pulmonary embolus (remember S1Q3T3)
Wolff-Parkinson-White syndrome - left sided accessory pathway
Atrial septal defect
Ventricular septal defect
Causes of Extreme Right Axis
Lead transposition – someone placed the leads wrong (happens very commonly)
Artificial cardiac pacing
Ventricular tachycardia
Emphysema
Hyperkalemia
Hypertrophy
Limb Leads
R wave in lead I + S wave in lead III > 25 mm
R wave in aVL > 11 mm
R wave in aVF > 20 mm
S wave in aVR > 14 mm
Precordial Leads
R wave in V4, V5 or V6 > 26 mm
R wave in V5 or V6 plus S wave in V1 > 35 mm
Largest R wave plus largest S wave in precordial leads > 45 mm
Non Voltage Criteria:
Increased R wave peak time > 50 ms in leads V5 or V6
ST segment depression and T wave inversion in the left-sided leads: AKA the left ventricular ‘strain’ pattern
Ischemia: Q-ST-T Changes
Q-waves indicate myocardial infarction, or scar tissue
Pathologic Q waves - usually need to be >0.04 sec wide & > 25% of subsequent R-wave
ST segment elevations represent myocardial infarction
ST segment depression represents myocardial ischemia
Compare ST segment to baseline TP segment
Group Q-ST-T wave changes by groups of leads that correspond to left ventricular walls
Grouped Leads
Cardiac Emergencies
“Mr. Jones is Tachycardic”
History of prior myocardial infarction (MI) has a 98% positive predictive value of VT
History of congestive heart failure and recent angina pectoris has a 100% positive predictive value for VT.
Age greater than 35 has a sensitivity of 92%
Hemodynamic instability can be seen with VT
VT does not respond to carotid sinus massage
Cannon A-waves in presence of AV dissociation strongly suggests VT.
History and Physical Exam:
Atrioventricular Dissociation
Detected in the lead where the p wave is most prominent.
QRS variability can indicate AV dissociation.
“Doctor, the patient is hypotensive with SBP 80s”
HPI/Physical Exam:
Symptoms can be chest pain, shortness of breath, or near syncope
Beck’s Triad:
Hypotension with a Narrowed Pulse Pressure
Jugular Venous Distention
Muffled heart Sounds
Pulsus Paradoxsus
Pulsus Paradoxsus
Treatment:
IV Fluids for Temporizing
Pericardiocentesis
Pericardial Window (not acutely)
”Our patient in Trauma B is having chest pain”
Unstable angina vs. NSTEMI vs. STEMI
Unstable Angina = Normal troponin, CK-MB with nml ECG or non-specific ECG findings. (But will have symptoms).
NSTEMI = +troponin/CKMB, without ECG changes.
STEMI= +troponin/CKMB and ST segment elevation in two or more contiguous leads or ST elevation equivalents (i.e. new LBBB).
ACS
ECG localization of Acute MI
Anatomic Location
ECG leads Coronary
Inferior II, III, aVF RCA
Ateroseptal V1-V3 LAD
Lateral and apical
I, aVL, V4-V6
LAD, left circumflex
Posterior ST depression with tall R waves in V1-V3.
posterior descending artery
“Doctor, our patient who was admitted with UTI has this rhythm strip”.
Torsades de Pointes
Prolonged QT is a risk factor for Torsades de Pointes (turning of points)
Torsades is a polymorphic ventricular tachycardia
POINTS
POINTS
What causes prolonged QT?
Congenital defect in K-channels Hypocalcemia, Hypokalemia, Hypomagnesemia Hypothermia HIV Connective tissue disease: SLE, Sjogren’s Myocardial Ischemia Anorexia Nervosa Intracranial Pathology
QT Prolonging Medication:
Treatment
2 grams IV Magnesium Sulfate
Stop the medication
Defibrillate if torsades deteriorates into ventricular fibrillation or unstable
Keep K+ > 5.0 and Mg2+ > 3.0
Summary:
Work to develop a systematic way of reading ECGs: Rate Rhythm (including intervals and blocks) Axis Hypertrophy Ischemia
Wide based tachycardia is VT until proven otherwise
A New LBBB is a STEMI equivalent
Many, Many medications prolong the QT
Torsades de Pointes is treated with magnesium
Last Word:
You may not be able to change the circumstances of your training but you can change your attitude, it’s the only thing you can control
– Dr. George Ruiz
Thanks so much for your kind attention!
