Introduction to Review of | EKG Interpretation w Physiology and Pharmacology of Cardiac Conductivity

8/13/2019 Introduction to Review of | EKG Interpretation w Physiology and Pharmacology of Cardiac Conductivity

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Marc Imhotep Cray, M.D.

The Electrocardiogram

Discussion Outline Propagation of Electrical Activity Through the

Heart

The Cardiac Action Potential

Generation of the Cardiac Pacemaker


Cardiac Vectors

Section I
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Electrical Conductivity in the Heart

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Within the atria and ventriclesmyocardial cells are connected bygap junctions

Gap junctions allow the cardiacaction potential to propagate fromcell to cell through a lowresistance pathway

Thus, along with its

intercalated discarchitecture, cardiac muscleis able to contract as asyncytial unit

The syncytial interconnecting

nature of cardiac muscle


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Electrical Conductivity in the Heart (2)

Electrical activity can pass from cell to cell in atria and ventricles

The atria and ventricles are electrically isolated by the heartsfibrous skeleton theAnnulus fibrosus

The heart has specialized electrically active cells (conductive tissue)in addition to contractile tissue

CONDUCTIVE TISSUE

These cells form the Sinoatrial (SA) node, Atrioventricular (AV)node, Bundle of His and Purkinje Fibres

Electrical activity normally originates in the SA node

The AV node forms the only site of electrical connection betweenthe atria and ventricles

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Specialized Conductive Tissue in the Heart

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See IVMS notes: N-Cardiac Myocyte & Conductive System Chemical-Electrical Events with Clinical

Considerations.pdf

Click graphic for expandable view
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Autorhythmicity

Some heart cells (SA, AV node and Purkinje) show

automaticity, the ability to generate a heart beat

These cells have an intrinsic rhythmicity which generates a

pacemaker potential

The heart does not require nerve or hormonal input to

beat

The heart transplant patients the nerves are severed but

the heart beats on

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Propagation of the Cardiac Action Potential

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Action potential (AP) starts at SA node.

AP conducted through atrial muscle,

interatrial band and internodal

pathways

The AP is delayed at the AV node

before entering the Bundle of His

Conduction through the Bundle of His

and Purkinje fibres is extremely rapid

The ventricles depolarise from endo to

epicardium and from apex to baseTransmission of cardiac impulse through heart showing

time of appearance (in fractions of a second) of impulse in

different parts of heart



The Cardiac Action Potential

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The cardiac action potential has several distinct phases

The cardiac action potential is different in the ventricles, atria

and conductive tissue

Cells in the specialised electoral pathways of the heart

are spontaneously active and show automaticity

These cells do not have a true resting membrane potential



Cardiac versusSkeletal Muscle AP

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The Phases of

the Ventricular AP

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The rapid depolarization is due to theopening of voltage gated Na+channels

Inactivation of the Na+channels and

opening of slow Ca2+channels produces

the plateau

During the cardiac AP K+conductance

falls

Repolarization occurs by a return of the

Ca2+and K+permeability to resting

values



Mechanism of the Pacemaker Potential

11

The rapid depolarization phase of the AP

in cardiac pacemaker cells is due to

opening of slow Ca2+channels

Repolarization after the AP is due toopening of K+channels

Spontaneous depolarization is produced

by a progressive fall in the K+permeability

combined with an inward current if(the

nature of ifis still under investigation)
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Cardiac Pacemakers

The sinoatrial has the fastest pacemaker potential (~90-100 beats/min) and is the normal pacemaker

The atrioventricular node is the next fastest (~40-60

beats/min) followed by cells in the bundle of His (15-30).

The fastest pacemaker normally drives the heart and

suppresses other pacemakers (overdrive suppression).

A beat generated outside the normal pacemaker is an

ectopicbeat.

The site that generates an ectopic beat is known as an

ectopic focus(foci pl.) or ectopic pacemaker.

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Physiology:

Neural Control of Heart Rate (1)

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Norepinephrine (NE) from sympathetic nerves and circulating adrenaline,

increase the heart rate and enhances conduction of the AP

Acetylcholine (ACh) released from parasympathetic nerves reduces the

heart rate and conduction across the AV node



Physiology:


Agents that alter heart rate are chronotropic

Positive chronotropic agents increase heart rate

Epinephrine and Ne act onb-adrenergic receptors on heart

Isoproterenol is b-adrenergic agonist which increases heart rate Propranolol is a b-adrenergic antagonist that blocks the actions of

adrenaline, NA and Isoproterenol

Adrenergic stimulation increases the Na+and Ca2+permeability of

cardiac cells, hypopolarizing them and increasing the pacemakerpotential rise

At rest heart is under weak sympathetic tone

Predominate tone at rest is parasympathetic

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Pharmacology:


Agents with negative chronotropic actions slow the heart

Acetylcholine acts on M-cholinergic (muscarinic) receptors on

the heart

Methacholine, carbachol (carbamylcholine) and muscarine are

pharmacological stimulants of muscarinic receptors Atropine is a muscarinic antagonist that blocks actions of ACh

and other muscarinic receptor agonists

ACh increases K+permeability of cardiac cell hyperpolarizing

them and reducing the rise in the pacemaker potential

AGAIN: At rest the heart is under parasympathetic tone which

slows the natural rhythm of the heart

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Pharmacology:

Resting Autonomic Control of Heart Rate

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At rest heart rate is under

both sympathetic and

parasympathetic tone

Normally the

parasympathetic inhibition

of rate is larger than the

sympathetic stimulation



Pharmacology (2)Some Other Agents

Nifedipine and Verapamil are calcium channel blocking agentsthat reduce heart rate

Increased extracellular K+(hyperkalemia): hyperpolarizes cardiac

myocytes, shortens the AP and slows the heart

Arrhythmia or heart block is often produced with fibrillation athigher level

Only a 5-10mM rise in extracellular K+can cause death

Excessive extracellular Ca2+

(hypercalcemia) can produce spasticcontractions of the heart

Reduced Ca2+(hypocalcemia) concentrations inhibit heart

contraction and can trigger ectopic foci

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(EKG/ECG)

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P wave is due to atrialdepolarization

The QRS complex is due to

ventricular depolarization

T wave is Ventricular

repolarization

U wave is often seen in

hypokalemiaAn atrial T wave is occasionally

seen in complete heart block



Extracellular Action Potential

19

Recording the depolarization

wave and the repolarization wave

from a cardiac muscle fiber



EKG Intervals

20

P-R interval: delay between atrial

and ventricular depolarization

QRS: time for ventricular

depolarization

Q-T: Duration of electrical systole



Normal EKG Intervals

P-R interval is normally 0.12-0.20 sec, most of this time is delay atthe AV node

An increased P-R interval (>0.28 sec) is characteristic of 1stdegree

heart block

QRS complex normally lasts less than 0.10 sec.

Increased width of the complex is a characteristic of defects in

the branch bundles or Purkinje fibres i.e. branch bundle block

Q-T interval varies inversely with heart rate21



The Cardiac Vector

22

The heart is a three dimensionalobject so the mean axis of

polarity in the heart exists as a

vector

A vector has both an orientationand a magnitude

Both the direction and

magnitude of the cardiac vector

change during the heart beat

A mean vector through the

partially depolarized heart


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The Cardiac Vector (2)

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EKG Limb Leads

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Dependence of speed of depolarization on resting potential

ANormal resting potential (RP) and normal rapid -50 rise of phase 0

depolarization.B Less negative RP results in slower rise of phase O, and lower

maximal amplitude of the action potential.


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Normal EKG recorded on the

Bipolar Limb Leads

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Uses of the EKG

Heart Rate

Conduction in the heart

Arrhythmias

Direction of the cardiac vector Damage to the heart muscle

Provides NO (direct) information about pumping

or mechanical events in the heart

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EKG Interpretation

Section II


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The Basics

PQRST

Rate

Rhythm

Axis

Intervals

Ischemia

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PQRST waves

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Name the waves

P T

Q

R

Name the intervals

PR QT


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PQRST waves

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Name the waves

Name the intervals

P

TS

R

PR QT


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RateThe Paper

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Measure the rate by the distance between QRS complexes

300

150

100

75

60

Or look at the right upper corner for the rate

or look at the monitor for the rate


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RateThe Paper

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What are the time intervals between lines?

0.2 sec

200 msec

0.04 sec

40 msec

Normal paper speed is 25 mm/sec


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Rhythm Questions

Is this sinus rhythm?

Are there P waves present?

If notAtrial fibrillation


P before every QRS PR interval the same for every beat

PR less than 0.2 sec (one big box)

Not sinus rhythm

AV block Tachydysrhythmia

Bradydysrhythmia

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1. P in front of every QRS?

2. PR interval > 0.12 and < 0.20 sec?

3. P upright in I, II, and III?

Yes to all 3 indicates sinus rhythm

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The AV Blocks

1stDegree AVB

PR interval fixed

PR interval > 200 msec

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Note: A TRACINGS INTERPRATION REVIEW AND QUIZ IS PROVIDED IN THE LAST

(HIGH- YIELD ) SECTION OF THIS PRESENTATION


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The AV Blocks

Type 1 Second Degree Block

Wenkebach

Watch for grouped beating

PR lengthens

RR shortens

Dropped beat

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The AV Blocks

Type 2 Second Degree Block

PR interval fixed

P without QRS

Dropped beat often in a fixed ratio

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The AV Blocks

Third Degree Block AV dissociation

Escape beat

AV nodalrate normal Narrow complex

Junctionalrate 40-60s

Narrow complex

Ventricularrate 30-40s Wide complex, bizarre shape

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Fill in the table with the correct

rhythms (Ans. next slide)

Narrow Wide

Regular

Irregular

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Filled in the Table

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Narrow Wide

Regular

Sinus rhythmSupraventricular tachy (SVT)

Re-entrant tachycardia

(WPW)

Ventriculartachycardia

SVT with BBB

SVT with aberrancy

Irregular

Atrial fibrillation (AF)Multifocal Atrial Tachy (MAT)

AF with BBBAF with aberrancy

Torsade du Pointes

The Normal Axis


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The Normal Axis

-30to 90

-30

90

Note: You will not be able to appreciate the full learning impact of the following slides unless youhave the PowerPoint, as I am sequencing activity moving forward via slide transition


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The AxisLead I

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0


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The AxisLead II

60


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The AxisLead III

120


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The AxisLead aVF

90


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The AxisLead aVL

-30


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Marc Imhotep Cray, M.D.48

The AxisLead aVR

-150


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0I

60II120III

90aVF

-30aVL-150aVR

The Axis


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How to find the axis

Find the most isoelectric limb lead (R=S)

The mean axis is perpendicular to this lead

If the QRS is positive then the axis is in that direction

If the QRS is negative then the axis is away from thatlead

50

A i P i Wh i h i ?


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Axis PracticeWhat is the axis?

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Most isoelectric lead? Lead aVF

Positive or negative? Positive

aVF is 90 The axis is perpendicular to this and is 0

A i P i Wh i h i ?


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Most isoelectric lead?

Positive or negative?

and is -30

Lead II

Positive

II is +60 The axis is perpendicular to this

A i P i Wh i h i ?


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Positive or negative?

Lead aVR

Negative

aVR is -150 The axis is perpendicular to this

Most isoelectric lead?

and is -60

SUMMARY SHEET


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SUMMARY SHEET


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Intervals

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PR interval

Normal range0.12 to 0.20 sec

QT interval

Normal range


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QT interval

The normal QT interval will

vary with heart rate and acorrected score is the most

accurate measure.

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QTc = QT preceding RR interval

RR interval


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Bundle Branch Blocks

Left (LBBB)

Right (RBBB)

Left Anterior Fascicular Block (LAFB)

Left Posterior Fascicular Block (LPFB)

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Wide QRS = Bundle Branch Block

RBBB Rabbit ears in V1

Tall R in V6 with slurred S

Normal or right axis (90 to 110)

LBBB

V1small R and deep, wide S

V6Tall, wide, slurred R Normal or left axis (-30 to -90)

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Fascicular Blocks

LAFB Left axis (-30 to -90)

I and aVL = small Q

II, III, aVF = small R and deep S

q1r3

LPFB

Right axis (110 to 180)

I, aVL, V5-6 = no Q, small R, deep S

II, III, aVF = small Q, tall R

q3r1

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Ischemia or Infarction

ST segment = depression Infarction

ST segment = elevation Ischemia

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Wh d EKG h f th


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Where do you see EKG changes for the

following areas of ischemia? (1)

Anterior

Septal

Anteroseptal

Inferior

Lateral

PosteriorRight ventricular

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Anterior Ischemia

ST segment elevation

V3 and V4

Reciprocal changes (ST depression)

II, III, AVF

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Septal Ischemia


V1 and V2

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Anteroseptal


V1 through V4


II, III, AVF

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Inferior Ischemia


II, III, aVF


V1 through V4

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Lateral Ischemia


I, aVL, V5 and V6

Often associated with anterior ischemia


II, III, AVF

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Posterior Ischemia

Easy to miss!

Tall R wave in V1 and V2

ST segment depression in V1 through V4

If you hold the EKG up to a bright light and

turn it over you will see the classic ST

elevation.

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Right Ventricular

ST segment elevation II, III, aVF

Tall R

II, III, aVF


I and aVL

Check right sided leads

Expect hypotension with nitroglycerine or morphine

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Which coronary artery?

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Where do you see EKG changes for


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y g

the following areas of ischemia? (2)

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The idea is that you should be able to look at an EKG pattern of ischemia or

infarction and know the coronary lesion location that will show at cardiac cath.

Of course this means you must memorize the previous slides information

The next slide provides more details related to this graphic

Source: Tao Le T and Bhushan V,

Cardiovascular, In First Aid for the USMLE

Step 1 The McGraw-Hill 2013; 2013:253



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following areas of ischemia? (3)

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SA and AV nodes a re usually supplied by RCA

Right-dominant circulation = 8 5 %= PD arises from RCA

Left-dominant circulation = 8 % = PD arises fro m LCX.

Codominant circulation = 7% = PD arises from both LCX and RCA.

Coronary artery occlusion most commonly occurs in the LADCoronary arteries fill during diastole

The most posterior part of the heart is the left atrium ; enlargement can cause dysphagia

(due to compression of the esophagus) or hoarseness (clue to compression of the left

recurrent laryngeal nerve, a branch of the vagusTransesophageal echocardiography is useful for diagnosing left atrial enlargement, aortic

dissection , and thoracic aortic aneurysm

Modified after Tao Le T and Bhushan V, Cardiovascular, In First Aid for the

USMLE Step 1, The McGraw-Hill 2013; 2013:253

Section III


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High Yield Summary Data,

ECG Tracings andGreat External Resources

For more on slides 73-81 see:

Tao Le T and Bhushan V, Cardiovascular, In First Aid for the USMLE Step 1, The McGraw-Hill 2013; 2013:260-65

Further study resources at the end of this presentation


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For more on slides 73-81 see:

Tao Le T and Bhushan V, Cardiovascular, In First Aid for the USMLE Step 1, The McGraw-

Hill 2013; 2013:260-65

Further study resources at the end of this presentation

MAKE THE DIAGNOSIS


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MAKE THE DIAGNOSISYou should go back to determine the answers if you are not sure.

Or *click here to view the source graphic which includes interpretations and explanations.

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* ONCE YOU LAND DOUBLE TO EXPAND, HOLD LEFT MOUSE AND DRAG TO NAVIGATE

MAKE THE DIAGNOSIS (2)
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MAKE THE DIAGNOSIS (2)

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THE END THANK YOU FOR YOUR ATTENTION


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THE END, THANK YOU FOR YOUR ATTENTION

Electrocardiogram, EKG, or ECGExplanation of what an ECG is, who needs one, what to

expect during one, etc. Written by the National Heart Lung and Blood Institute (a division of

the NIH)

University of Maryland School of Medicine Emergency Medicine Interest GroupIntroduction to EKG's as written by a medical student and a cardiologist

ECGpedia: Course for interpretation of ECG

12-lead ECG library

Simulation tool to demonstrate and study the relation between the electric activity of the

heart and the ECG

EKG Review: ArrhythmiasA guide to reading ECG's written by a college (not medical school)professor

CyberHeartTutorial to experiment with cardiac function... (but try to avoid causing cardiac

arrest!)

Resources for Further Study: remarkable and challenginglearning tools. Just dont have a Cardiac Arrest
http://www.nhlbi.nih.gov/health/dci/Diseases/ekg/ekg_what.htmlhttp://davidge2.umaryland.edu/~emig/ekgtu01.htmlhttp://en.ecgpedia.org/http://www.ecglibrary.com/http://www.ecgsim.org/http://www.ecgsim.org/http://www.gwc.maricopa.edu/class/bio202/cyberheart/ekgqzr0.htmhttp://www.gwc.maricopa.edu/class/bio202/cyberheart/cybrhart49.htmhttp://www.gwc.maricopa.edu/class/bio202/cyberheart/cybrhart49.htmhttp://www.gwc.maricopa.edu/class/bio202/cyberheart/ekgqzr0.htmhttp://www.gwc.maricopa.edu/class/bio202/cyberheart/ekgqzr0.htmhttp://www.ecgsim.org/http://www.ecgsim.org/http://www.ecglibrary.com/http://www.ecglibrary.com/http://www.ecglibrary.com/http://en.ecgpedia.org/http://en.ecgpedia.org/http://davidge2.umaryland.edu/~emig/ekgtu01.htmlhttp://www.nhlbi.nih.gov/health/dci/Diseases/ekg/ekg_what.htmlhttp://www.imhotepvirtualmedsch.com/

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Introduction to Review of | EKG Interpretation w Physiology and Pharmacology of Cardiac Conductivity