Electrocardiogram (ECG) Interpretation - Part 1 of 2

Electrocardiogram (ECG)
Interpretation
Module 1 of 2
Marc Imhotep Cray, M.D.

Learning Objectives
• To recognize normal rhythm of heart 

“Normal Sinus Rhythm (NSR)”
• To recognize 15 most common rhythm
disturbances (3-Lead ECG)
• To Interpret an acute myocardial infarction on
a 12-Lead ECG, including: anterior, lateral,
anterolateral and inferior wall MIs
Marc Imhotep Cray, M.D. 2

Topics Outline
• ECG Basics
• How to Analyze a Rhythm
• Normal Sinus Rhythm
• Cardiac Dysrhythmias
• Diagnosing a Myocardial Infarction

Review of ECG Basics
Normal ECG Morphology
Features include:
 Regular rhythm at 60-100 bpm
 Normal P wave morphology and axis
(upright in I and II, inverted in aVR)
 Narrow QRS complexes (< 100 ms
wide)
 Each P wave is followed by a QRS
complex
 The PR interval is constant

EKG Paper
ECG tracings are recorded on grid paper
 Horizontal axis of EKG paper

records time, w black marks at
top indicating 3 second intervals
o Each second is marked by 5
large grid blocks thus each
large block equals 0.2 second
 Vertical axis records EKG

amplitude (voltage)
o Two large blocks equal 1
millivolt (mV)
o Each small block equals 0.1 Mv
 Within large blocks are 5 small

blocks each representing 0.04
seconds
ECG Paper cont’d.
• Horizontally
– One small box - 0.04 s
– One large box - 0.20 s
• Vertically
– One large box - 0.5 mV

ECG Paper cont’d.
3 sec 3 sec
• Every 3 seconds (15 large boxes) is marked by a

vertical line
• This Helps When Calculating Heart Rate
Note: Strip above and those that follow are not

marked but all are 6 seconds long

Autorhythmicity
• Heart has two types of action potentials (APs)
– Myocardial action potential
– Pacemaker action potential
• Pacemaker cells (SA, AV node , His Bundle & Purkinje
fibers) show automaticity= ability to generate a heart
beat=intrinsic rhythmicity
– Thus, heart does not require nerve or hormonal input to beat
– Ex. Heart transplant pts. nerves are severed but heart beats on

Pacemakers of Heart
• SA Node - Dominant pacemaker with an intrinsic

rate of 60 - 100 beats/ minute
• AV Node - Back-up pacemaker with an intrinsic

rate of 40 - 60 beats/minute
• Ventricular cells - Back-up pacemaker with an

intrinsic rate of 20 - 45 bpm

Normal Impulse Conduction
Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers

Impulse Conduction & the ECG
Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers

“PQRST”

PR Interval
Atrial depolarization + delay in AV

junction (AV node/Bundle of His)
delay allows time for atria to

contract before ventricles contract

Conduction pathway summary
• SA node→ atria → AV node→bundle of His→ right and left
bundle branches→ Purkinje fibers → ventricles
• left bundle branch divides into left anterior and posterior fascicles
• SA node “pacemaker” inherent dominance with slow phase of

upstroke
• AV node—located in posteroinferior part of interatrial septum
• Blood supply usually from RCA
• 100-msec delay allows time for ventricular filling
• Pacemaker rates—SA > AV > bundle of His/ Purkinje/ventricles
• Speed of conduction—Purkinje > atria > ventricles > AV node

Electrocardiogram tracing summary
• P wave—atrial depolarization
o Atrial repolarization is masked by QRS complex
• PR interval—time from start of atrial depolarization to start of
ventricular depolarization (normally < 200 msec)
• QRS complex—ventricular depolarization (normally < 120 msec)
• QT interval—ventricular depolarization, mechanical contraction of
ventricles, ventricular repolarization
• T wave—ventricular repolarization
• T-wave inversion may indicate ischemia or recent MI
• J point—junction between end of QRS complex and start of ST
segment
• ST segment—isoelectric, ventricles depolarized
• U wave—prominent in hypokalemia, bradycardia
Conduction-ECG Relationship
Tao Le T and Bhushan V, Cardiovascular, In: First Aid for the USMLE Step 1 2017. New York, NY: McGraw-Hill ,2017; 271.

How to Analyze a Rhythm
Rhythm Analysis
 Step 1: Calculate rate

 Step 2: Determine regularity
 Step 3: Assess the P waves
 Step 4: Determine PR interval
 Step 5: Determine QRS duration

Step 1: Calculate Rate
3 sec 3 sec
Option 1 (6-second x 10 method)

• Count # of R waves in a 6 second
rhythm strip, then multiply by 10
Interpretation? 9 x 10 = 90 bpm

Step 1: Calculate Rate cont’d.
R wave
Option 2 (300, 150, 100, 75, 60, 50 method)

– Find a R wave that lands on a bold line
– Count number of large boxes to next R wave
– If second R wave is 1 large box away rate is 300,
2 boxes - 150, 3 boxes - 100, 4 boxes - 75, etc. (cont.)
Step 1: Calculate Rate
3 1 1
0 5 0 7 6 5
0 0 0 5 0 0
• Option 2 (cont.)
– Memorize the sequence:
300 - 150 - 100 - 75 - 60 - 50
Interpretation? Approx. 1 box less than 100 = 95 bpm

Step 2: Determine regularity
R R
• Look at R-R distances (using a caliper or markings on

a pen or paper)
• Regular (are they equidistant apart)? Occasionally
irregular? Regularly irregular? Irregularly irregular?
Interpretation? Regular

Step 3: Assess the P waves
• Are there P waves?

• Do the P waves all look alike?
• Do the P waves occur at a regular rate?
• Is there one P wave before each QRS?
Interpretation? Normal P waves w 1 P wave for every QRS

Step 4: Determine PR interval
• Normal: 0.12 - 0.20 seconds (3 - 5 sm boxes)

Interpretation? 0.12 seconds

Step 5: QRS duration
• Normal: 0.04 - 0.12 seconds. (1 - 3 sm boxes)

Interpretation? 0.08 seconds

NSR Summary
• Rate 90-95 bpm

• Regularity regular
• P waves normal
• PR interval 0.12 s
• QRS duration 0.08 s
Interpretation? Normal Sinus Rhythm

Normal Sinus Rhythm
Basic Rhythm Analysis
• Rate – too fast or too slow?
• Rhythm – regular or irregular?
• Is there a normal looking QRS? Is it wide
or narrow?
• Are P waves present?
• What is relationship of P waves to QRS
complex?

NSR Parameters
• Rate 60 - 100 bpm

• Regularity regular
• P waves normal
• PR interval 0.12 - 0.20 s
• QRS duration 0.04 - 0.12 s
Any deviation from above is
• Sinus tachycardia
• Sinus bradycardia or
• A dysrhythmia
Normal Sinus Rhythm
12 lead ECG in sinus rhythm

Arrhythmia Formation
Arrhythmias can arise from problems in:

• Sinus node
• Atrial cells
• AV junction
• Ventricular cells

SA Node Problems
SA Node can:
• fire too slow Sinus Bradycardia
• fire too fast Sinus Tachycardia*
*Sinus Tachycardia may be an appropriate response

to stress.

Atrial Cell Problems
Atrial cells can:

• fire occasionally from a focus Premature
Atrial Contractions (PACs)
• fire continuously due to a looping re-

entrant circuit Atrial Flutter

Atrial Cell Problems
Atrial cells can also:

• fire continuously from multiple foci Atrial Fibrillation
or
• fire continuously due to multiple micro re-entrant
“wavelets” Atrial Fibrillation

Key Scientific Point
Atrial tissue
 Multiple micro re-entrant
“wavelets” refers to wandering
small areas of activation which
generate fine chaotic impulses
 Colliding wavelets can, in turn,

generate new foci of activation

AV Junctional Problems
AV junction can:
• fire continuously due to a looping re-entrant circuit
Paroxysmal Supraventricular Tachycardia (PSVT)
• block impulses coming from SA Node AV Junctional

Blocks

Ventricular Cell Problems
Ventricular cells can:
• fire occasionally from 1 or more foci Premature
Ventricular Contractions (PVCs)
• fire continuously from multiple foci Ventricular

Fibrillation (VF)
• fire continuously due to a looping re-entrant circuit 

Ventricular Tachycardia (VT)

Analyzing a Rhythm Table
Component Characteristics
Rate bpm is commonly ventricular rate. If atrial and ventricular rates
differ, as in a 3rd-degree block, measure both rates. Normal: 60–100
bpm. Slow (bradycardia): <60 bpm. Fast (tachycardia): >100 bpm
Regularity Measure R-R intervals and P-P intervals. Regular: Intervals consistent.
Regularly irregular: Repeating pattern. Irregular: No pattern
P Waves If present: Same in size, shape, position? Does each QRS have a P
wave? Normal: Upright (positive) and uniform
PR Interval Constant: Intervals are same. Variable: Intervals differ.
Normal: 0.12–0.20 sec and constant
QRS Interval Normal: 0.06–0.10 sec. Wide: >0.10 sec. None: Absent
QT Interval Beginning of R wave to end of T wave Varies with HR. Normal: Less
than half the R-R interval
Dropped Occur in AV blocks. Occur in sinus arrest.
beats
Cardiac Dysrhythmias
Dysrhythmias
• Sinus Rhythms
• Premature Beats
• Supraventricular Arrhythmias
• Ventricular Arrhythmias
• AV Junctional Blocks

Sinus Rhythms
• Sinus Bradycardia
• Sinus Tachycardia
• Sinus Arrest
• Normal Sinus Rhythm

Rhythm #1
• Rate? 30 bpm
• Regularity? regular
• P waves? normal
• PR interval? 0.12 s
• QRS duration? 0.10 s
Interpretation? Sinus Bradycardia
Sinus Bradycardia
• Deviation from NSR

- Rate < 60 bpm

Sinus Bradycardia cont’d.
• Etiology: SA node is depolarizing slower

than normal, impulse is conducted normally
(i.e. normal PR and QRS interval)

Rhythm #2
• Rate? 130 bpm

• P waves? normal
Interpretation? Sinus Tachycardia
Sinus Tachycardia

- Rate > 100 bpm

Sinus Tachycardia cont’d.
• Etiology: SA node is depolarizing faster than

normal, impulse is conducted normally
• Remember: sinus tachycardia is a response
to physical or psychological stress, not a
primary arrhythmia.

Sinus Arrest
• Etiology: SA node fails to depolarize and no
compensatory mechanisms take over
• Sinus arrest is usually a transient pause in sinus
node activity

Premature Beats
• Premature Atrial Contractions
(PACs)
• Premature Ventricular Contractions
(PVCs)

Rhythm #3
• Rate? 70 bpm
• Regularity? occasionally irreg.
• P waves? 2/7 different contour
• PR interval? 0.14 s (except 2/7)
Interpretation? NSR w PAC
Premature Atrial Contractions
(PACs)

– These ectopic beats originate in atria (but not
in SA node) therefore, contour of P wave, PR
interval, and timing are different than a
normally generated pulse from SA node

PAC cont’d.
• Etiology: Excitation of an atrial cell forms an

impulse that is then conducted normally
through AV node and ventricles

• When an impulse originates anywhere in atria

(SA node, atrial cells, AV node, Bundle of His)
and then is conducted normally through
ventricles QRS will be narrow (0.04 - 0.12 s)

Rhythm #4
• Rate? 60 bpm
• Regularity? occasionally irreg.
• P waves? none for 7th QRS
• QRS duration? 0.08 s (7th wide)
Interpretation? Sinus Rhythm with 1 PVC
Premature ventricular
contractions (PVCs)

– Ectopic beats originate in ventricles resulting
in wide and bizarre QRS complexes
– When there are more than 1 premature beats
and they look alike, called “uniform”
– When they look different, called “multiform”

PVCs cont’d.
• Etiology: One or more ventricular cells are

depolarizing and impulses are abnormally
conducting through ventricles

• When an impulse originates in a ventricle,
conduction through ventricles will be
inefficient and QRS will be wide and bizarre

Ventricular Conduction
Normal Abnormal
Signal moves rapidly Signal moves slowly
through ventricles through ventricles
Supraventricular dysrhythmias
• Atrial Fibrillation
• Atrial Flutter
• Paroxysmal Supraventricular Tachycardia
(PSVT)

Rhythm #5
• Rate? 100 bpm

• Regularity? irregularly irregular
• P waves? none
• PR interval? none
Interpretation? Atrial Fibrillation
Atrial Fibrillation cont’d.

– No organized atrial depolarization so no normal P
waves (impulses are not originating from SA node)
– Atrial activity is chaotic (resulting in an irregularly
irregular rate)
– Common, affects 2-4%, up to 5-10% if > 80 years old

Atrial Fibrillation cont’d.
• Etiology: due to multiple re-entrant wavelets

conducted betw R & L atria and impulses are formed
in a totally unpredictable fashion
• AV node allows some of impulses to pass through at
variable intervals (so rhythm is irregularly irregular)

Rhythm #6
• Rate? 70 bpm
• P waves? flutter waves
Interpretation? Atrial Flutter
Atrial Flutter

– No P waves Instead flutter waves (note
“sawtooth” pattern) are formed at a rate of 250
- 350 bpm
– Only some impulses conduct through AV node
(usually every other impulse)

Atrial Flutter cont’d.
• Etiology: Reentrant pathway in right atrium with

every 2nd, 3rd or 4th impulse generating a QRS
(others are blocked in AV node as node repolarizes)

Rhythm #7
• Rate? 74 148 bpm

• Regularity? Regular  regular
• P waves? Normal  none
• PR interval? 0.16 s  none
Interpretation? Paroxysmal Supraventricular
Tachycardia (PSVT) 66
Paroxysmal Supraventricular
Tachycardia (PSVT)

– heart rate suddenly speeds up, often
triggered by a PAC (not seen here) and
P waves are lost

AV Nodal Blocks
• 1st Degree AV Block
• 2nd Degree AV Block, Type I
• 2nd Degree AV Block, Type II
• 3rd Degree AV Block

Rhythm # 8
• Rate? 60 bpm
• P waves? normal
Interpretation? 1st Degree AV Block
1st Degree AV Block

– PR Interval > 0.20 s

1st Degree AV Block cont’d.
• Etiology: Prolonged conduction delay in AV

node or Bundle of His

Rhythm # 9
• Rate? 50 bpm
• Regularity? regularly irregular
• P waves? nml, but 4th no QRS
• PR interval? lengthens
Interpretation? 2nd Degree AV Block, Type I
2nd Degree AV Block, Type I
Mobitz type I (Wenckebach)

– PR interval progressively lengthens, then impulse
is completely blocked (P wave not followed by
QRS)

2nd Degree AV Block, Type I cont’d.
• Etiology: Each successive atrial impulse

encounters a longer and longer delay in AV
node until one impulse (usually 3rd or 4th)
fails to make it through AV node

Rhythm # 10
• Rate? 40 bpm
• P waves? nml, 2 of 3 no QRS
Interpretation? 2nd Degree AV Block, Type II
2nd Degree AV Block, Type II
Mobitz type II

– Occasional P waves are completely blocked (P
wave not followed by QRS)
– Progressive lengthening of PR interval until a QRS
is dropped
– Consistent ratio of conducted to dropped QRS
complexes
NB: Requires a pacemaker
Rhythm #11
• Rate? 40 bpm
• P waves? no relation to QRS
• QRS duration? wide (> 0.12 s)
Interpretation? 3rd Degree AV Block
3rd Degree AV Block

– P waves are completely blocked in AV junction
QRS complexes originate independently from
below junction
– Complete dissociation between atrial and
ventricular rates
NB: Requires a pacemaker

3rd Degree AV Block cont’d.
• Etiology: There is complete block of conduction in

AV junction atria and ventricles form impulses
independently of each other
• Without impulses from atria, ventricles own
intrinsic pacemaker kicks in at around 30 - 45 bpm

Remember
• When an impulse originates in a ventricle, conduction

through ventricles will be inefficient and QRS will be
wide and bizarre

#12 Ventricular Tachycardia
• Ventricular cells fire continuously due to a looping re-entrant circuit
• Rate usually regular, 100 - 250 bpm
• P wave: may be absent, inverted or retrograde
• QRS: complexes bizarre, > .12
• Rhythm: usually regular

#13 Ventricular Fibrillation
• Rhythm: irregular-coarse or fine, wave form varies in size & shape
• Fires continuously from multiple foci
• No organized electrical activity
• No cardiac output
• Causes: MI, ischemia, untreated VT, underlying CAD, acid base
imbalance, electrolyte imbalance, hypothermia etc.

#14 Asystole
• Ventricular standstill, no electrical activity, no cardiac output
– no pulse!
• Cardiac arrest, may follow VF or PEA (Pulseless electrical
activity)
• Remember! No defibrillation with Asystole
• Rate: absent due to absence of ventricular activity
Occasional P wave may be identified

#15 Idioventricular Rhythm
• Escape rhythm (safety mechanism) to prevent vent. standstill
• His/purkinje system takes over as heart’s pacemaker
• Treatment: pacing
• Rhythm: regular
• Rate: 20-40 bpm
• P wave: absent
• QRS: > .12 seconds (wide and bizarre)

Diagnosing a Myocardial Infarction
Diagnosing a myocardial infarction
To Dx a MI you need to go beyond looking at a rhythm
strip and obtain a 12-Lead ECG
Rhythm Strip

The 12-Lead ECG
• 12-Lead ECG sees heart from 12 different views helps you
see what is happening in different portions of heart
– rhythm strip is only 1 of these 12 views
12 lead ECG in sinus rhythm

Which coronary artery?
 Site of infarct can be determined by correlating ECG
findings w knowledge of coronary circulation
o However, nml coronary vasculature varies widely from
individual to individual so only possible to make
generalizations
 Idea is you should be able to look at a 12 lead ECG

pattern of ischemia or infarction and predict
coronary lesion location that will show at cardiac
catheterization

Two main coronary arteries are right coronary artery
and left anterior descending coronary artery
 SA and AV nodes are supplied
by branches of RCA
• Infarct may cause nodal
dysfunction (bradycardia or
heart block)
 Right-dominant circulation
(85%) = PDA arises from RCA
 Left-dominant circulation
(8%) = PDA arises from LCX
 Codominant circulation (7%)
= PDA arises from both LCX
and RCA
 Coronary artery occlusion
most commonly in LAD
 Coronary blood flow peaks in Tao Le T and Bhushan V, Cardiovascular, In: First Aid for the USMLE Step 1 2017.
New York, NY: McGraw-Hill ,2017; 271.
early diastole
Correlating ECG findings w knowledge of coronary circulation
Taylor GJ. 150 practice ECGs: Interpretation and Review, 3rd ed. Malden, Mass: Blackwell Publishing, 2006.
Correlating ECG findings w knowledge of coronary circulation
The 12-Leads
12-leads include:
–3 Limb leads
(I, II, III)
–3 Augmented leads
(aVR, aVL, aVF)
–6 Precordial leads
(V1- V6)

Views of the Heart
Some leads get a good view of: Lateral portion of heart
Anterior portion of heart
Inferior portion of heart

Where do you see ST-T wave changes for
following areas of ischemia or infarction?
Diagram showing the contiguous leads in same color

ST Elevation
• One way to diagnose an
acute MI is to look for
elevation of ST segment

ST Elevation cont’d.
• Elevation of ST segment
(greater than 1 small box)
in 2 leads is consistent w a
myocardial infarction

Anterior View of Heart
• Anterior portion of heart is best viewed
using leads V1- V4

Anterior Myocardial Infarction
• If you see changes in leads V1 - V4 that are

consistent w a MI you can conclude
that it is an anterior wall myocardial
infarction

Putting it all Together
Do you think this person is having a MI If so, where?

Interpretation
Yes, this person in previous slide is having an
acute anterior wall myocardial infarction

Other MI Locations
Now that you know where to look for an anterior
wall MI let’s look at how you would determine if
MI involves lateral wall or inferior wall of heart

Other MI Locations
 Remember 12-leads of ECG look at different portions of heart
– limb and augmented leads “see” electrical activity moving inferiorly (II, III
and aVF), to left (I, aVL) and to right (aVR)
– Whereas, precordial leads “see” electrical activity in posterior to anterior
direction
Limb Leads Augmented Leads Precordial Leads

Other MI Locations
• Now, using these 3 diagrams let’s figure where to
look for a lateral wall and inferior wall MI

Anterior MI
• Remember anterior portion of the heart is best

viewed using leads V1- V4

Lateral MI
• So what leads do you think lateral portion of
heart is best viewed? Leads I, aVL, and V5- V6

Inferior MI
Now how about inferior portion of heart?
Leads II, III and aVF

Now, where do you think this person is having a MI?

Inferior Wall MI
This is an inferior MI. Note ST elevation in leads II, III
and aVF

How about now?

Anterolateral MI
This person’s MI involves both the anterior wall (V2-V4) and
lateral wall (V5-V6, I, and aVL)!

Next Module:
“Reading 12-Lead ECGs”
 Best way to read 12-lead ECGs is to develop a step-by-
step approach (just as we did for analyzing a rhythm
strip)
 In next Module we present a 6-step and 9-step approaches:
1. Calculate Rate
2. Determine Rhythm
3. Determine QRS axis
4. Calculate Intervals
5. Assess for Hypertrophy
6. Look for evidence of Infarction

THE END
See next slide for links to tools and resources for further study.
Companion study tools
Video Playlist:
ECG Interpretation
Strong Medicine ECG Video Edu. , Dr. Eric Strong
Reading:
Olivieri , B et al. Ch. 28 ECG (Pgs. 820-28). In: USMLE Step 1
Secrets 3rd. Ed. (Eds. Brown TA and Shah SJ) Saunders, 2013.
ECG eBook:
Shade B. Pocket ECGs: A Quick Information Guide. New York, NY:

McGraw-Hill, 2008. (A good one for beginners.)

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Electrocardiogram (ECG) Interpretation - Part 1 of 2

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Electrocardiogram (ECG)

Marc Imhotep Cray, M.D.

• To recognize normal rhythm of heart 

Marc Imhotep Cray, M.D. 2

Marc Imhotep Cray, M.D. 3

Marc Imhotep Cray, M.D.

 Horizontal axis of EKG paper

 Vertical axis records EKG

 Within large blocks are 5 small

Marc Imhotep Cray, M.D. 6

• Every 3 seconds (15 large boxes) is marked by a

Note: Strip above and those that follow are not

Marc Imhotep Cray, M.D. 7

Marc Imhotep Cray, M.D.

• SA Node - Dominant pacemaker with an intrinsic

• AV Node - Back-up pacemaker with an intrinsic

• Ventricular cells - Back-up pacemaker with an

Marc Imhotep Cray, M.D. 9

Marc Imhotep Cray, M.D. 10

Marc Imhotep Cray, M.D. 11

Marc Imhotep Cray, M.D. 12

Atrial depolarization + delay in AV

delay allows time for atria to

Marc Imhotep Cray, M.D. 13

• SA node “pacemaker” inherent dominance with slow phase of

• Pacemaker rates—SA > AV > bundle of His/ Purkinje/ventricles

• Speed of conduction—Purkinje > atria > ventricles > AV node

Marc Imhotep Cray, M.D. 14

Marc Imhotep Cray, M.D. 16

 Step 1: Calculate rate

Marc Imhotep Cray, M.D. 18

Option 1 (6-second x 10 method)

Marc Imhotep Cray, M.D. 19

Option 2 (300, 150, 100, 75, 60, 50 method)

Marc Imhotep Cray, M.D. 21

• Look at R-R distances (using a caliper or markings on

Marc Imhotep Cray, M.D. 22

• Are there P waves?

Marc Imhotep Cray, M.D. 23

• Normal: 0.12 - 0.20 seconds (3 - 5 sm boxes)

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• Normal: 0.04 - 0.12 seconds. (1 - 3 sm boxes)

Marc Imhotep Cray, M.D. 25

• Rate 90-95 bpm

Marc Imhotep Cray, M.D. 26

Marc Imhotep Cray, M.D.

• Rate 60 - 100 bpm

12 lead ECG in sinus rhythm

Marc Imhotep Cray, M.D. 30

Arrhythmias can arise from problems in:

Marc Imhotep Cray, M.D. 31

*Sinus Tachycardia may be an appropriate response

Marc Imhotep Cray, M.D. 32

Atrial cells can:

• fire continuously due to a looping re-

Marc Imhotep Cray, M.D. 33

Atrial cells can also:

Marc Imhotep Cray, M.D. 25

 Colliding wavelets can, in turn,

Marc Imhotep Cray, M.D. 35

• block impulses coming from SA Node AV Junctional

Marc Imhotep Cray, M.D. 36

• fire continuously from multiple foci Ventricular

• fire continuously due to a looping re-entrant circuit 

Marc Imhotep Cray, M.D. 37

Marc Imhotep Cray, M.D. 40