N 564 EKG Interpretation Lecture Version 2013 Stein

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EKG Interpretation

Kevin Stein, MS, CRNA, APN



2004 Anna Story 2

A Normal 12 Lead ECG



Conduction System





SA Node

• Heart’s dominate pacemaker

• Responsible for ‘sinus rhythm’ of heart

• Located in upper-posterior wall of RA

• Automaticity – ability to generate pacemakingstimuli

• Depolarization spreads outwards from SA node

like the waves created from a pebble dropped ina lake

• Depolarization of SA node produces p-wave





Atrial Conducting System

• Internodal tracts (located in RA)

– Anterior internodal tract

– Middle internodal tract

– Posterior internodal tract

• Conduction tract (innervates LA)

– Bachmann’s Bundle



Atrial Conducting System

• Internodal Tracts

– Course from the SA node to the AV node

• Bachmann’s Bundle

– Originates in SA node and distributes

depolarization to LA

• Results in simultaneous contraction of atria

• Depolarization of right and left atrial

myocardium produces p-wave



AV Node

• When wave of atrial depolarization enters the

AV node, depolarization slows

– Produces brief pause

• Seen with flat baseline following p-wave on EKG

– Allows time for blood to enter ventricles

– Slowed conduction through AV node carried by

calcium ions





Conducting System

• AV valves

– Electrically insulate the ventricles from the atria

• This leaves the AV node as the sole pathway to conduct

stimuli from atria to ventricles



Ventricular Conduction System

• After a slow depolarization through the AV node,depolarization shoots rapidly through the ventricularconduction system

• Ventricular conduction system originates in the Bundle

of His• Bundle of His immediately bifurcates in the

interventricular septum into the RBB and LBB – Ventricular depolarization begins midway down the

interventricular septum, where the LBB produces fine

terminal filaments – The RBB does not produce terminal filaments in the

septum• Left-to-right depolarization of septum





SA Node

AnteriorInternodal

Pathway

MiddleInternodal

Pathway

PosteriorInternodal

Pathway

Anterior interatrialmyocardial band

(Bachmann s Bundle)

Left AtriumAN Region

N Region

NH Region AV Node

Bundle of His

Right Bundle

Branch

Left Bundle

Branch

Anterior

Division

Posterior

Division

RightAtrial

Tracts



P R t



Pacema er Rates

40-60

0-60

SA Node 60-100 BPM

Atrial Cells 55-60 BPM

AV Node 40-60 BPMHis Bundle 40-45 BPM

Bundle Branches 40-45 BPM

Purkinje Fibers 35-40 BPM

Ventricular Cells 30-35 BPM





The EKG Representation of

the Cardiac Cycle

• P-wave

– Atrial depolarization and contraction

– In reality atrial contraction lasts longer than the p-wave

•

PR Interval – Represents the time between the beginning of atrial

contraction and the beginning of ventricular contraction

• QRS Complex

– Ventricular depolarization and contraction

– In reality ventricular contraction lasts longer than the QRScomplex









The EKG Representation of

the Cardiac Cycle

• Repolarization of ventricular myocytes beginimmediately after QRS and persist until end of T-wave

• QT Interval – Represents the duration of ventricular

systole/contraction

– Ventricular contraction begins with the QRS andpersists until the end of the T-wave

– Good indicator of repolarization – Normal QT interval is less that half of the R-to-R

interval• Corrected for heart rate



Depolarization

Repolarization



Ventricular

Systole

QT

Interval



Repolarization

Plateau

Rapid

Repolarization

Phase

ST

Segment



Recording the EKG



Recording the EKG



Recording the EKG

• y-axis – amplitude (mV)

• x-axis – time (sec)

•

1 small square = 1mm x 1mm or 0.1mV x0.04sec

• 1 large square = 5mm x 5mm or 0.5mV x

0.2sec

• 2 large squares = 1mV

• 5 large squares = 1 sec





• Limb Leads

–I

– II

– III

–

AVR – AVL

– AVF

• Chest Leads

–V1

– V2

– V3

–

V4

– V5

– V6



Limb Leads

• Electrodes are placed on the right arm, the leftarm, and the left leg

• A pair of electrodes is used to record one lead

–A different pair is used for each lead

• Einthoven’s triangle

• Bipolar limb leads

– I, II, III

• Unipolar/Augmented limb leads

– aVF, aVR, aVL











Augmented Limb Leads

• aVR, aVL, and aVF intersect at angles different

from leads I, II, and III

• Split the angles formed by leads I, II, and III



Limb Leads



All six limb leads meet to form six

intersecting leads that lie in a flat

“frontal” plane on the patient’s chest!



Each camera position

represents the positive

electrode of a standard limb

lead. Each limb lead records

from a different angle to

provide a different view of

the same cardiac activity.



Limb Leads

• Lateral leads

– Have positive electrode positioned laterally (left arm)

– I and aVL

•Inferior leads – Have a positive electrode positioned inferiorly (left

foot)

– II, III, aVF

• Allows you to determine if depolarization ismoving toward/away from the patient’s left sideand inferiorly toward the left foot



Chest Leads

• Also called precordial leads

• Six chest leads are all positive electrodes

• Numbered V1 to V6 from right to left around chest

•

Depolarization moving toward chest lead producespositive deflection on EKG

• Look at heart in horizontal plane

– Cuts body into top and bottom halves

•Each lead (positive) is oriented through AV node andprojects through the patient’s back (negative)



Horizontal View with Chest Leads





Chest Leads

• Waves in the six chest leads show progressivechanges from V1-V6

– Normally QRS in V1 is mainly negative

–Normally QRS in V6 is mainly positive• Why?

• Leads V1 & V2 are oriented over the right side of theheart

•

Leads V3 & V4 are oriented over the interventricularseptum

• Leads V5 & V6 are oriented over the left side of theheart





Limb andChest Leads





EKG Interpretation

1. RATE

2. Rhythm

3. Axis

4. Hypertrophy

5. Infarction



Rate

• First step in EKG interpretation

• Measured in cycles/min

• SA node



Automaticity Foci

• Also called eptopic foci

• Focal areas of automaticity in heart

• Potential pacemakers

• Capable of taking over pacemakingresponsibilities from SA node in an emergency

• Under normal circumstances, these foci areelectrically silent

• Can be found in the atria, ventricles, and the AVJunction



Automaticity Foci

• Level

– Atria

• Atrial automaticity foci

– AV Junction

• Junctional automaticity

foci

– Ventricles

• Ventricular automaticity

foci

• Inherent Rate Range

– 60-80/min

– 40-60/min

– 20-40/min



Overdrive Suppression

SA Node

Atrial Foci (60-80 bpm)

Junctional Foci (40-60 bpm)

Ventricular Foci (20-40 bpm)

Overdrive Suppression

Any automaticity center willoverdrive-suppress all others

that have a slower inherent

pacemaking rate.

Emergency failsafe pacing at 3

separate levels.



Determine the Rate

1. Find an R-wave that peaks on a heavy black

line (start line)

2. Count off ‘300, 150, 100’ for the three thick

lines that follow the start line

3. Count off the next three lines as ‘75, 60, 50’

4. Where the next R-wave falls, determines the

rate





Determine the Rate - Bradycardia

• On the top margin of EKG strip, there are

small marks that identify 3 second intervals

• Taking two of these gives us a 6 second strip

• Count the number of complete R-wave to R-

wave cycles in the strip

• Find the rate by multiplying by 10



Determine the Rate - Bradycardia

• Count the # of R waves in a 6 second rhythm

strip, then multiply by 10.

• Reminder: all rhythm strips in the Modules are

6 seconds in length.

Interpretation?9 x 10 = 90 bpm

3 sec 3 sec





Determine the Rate

• Say “300, 150, 100” …“75, 60, 50”

• But for bradycardia: rate = cycles/6 sec. strip

✕ 10



EKG Interpretation

1. Rate

2. RHYTHM

3. Axis

4. Hypertrophy

5. Infarction







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 with 1 P

wave for every QRS



Determine PR interval

• Normal: 0.12 - 0.20 seconds

(3 - 5 boxes)

• Prolonged = some kind of AV block present

Interpretation? 0.12 seconds



QRS duration

•

Normal: 0.04 - 0.12 seconds(1 - 3 boxes)

• Prolonged = Look for Bundle Branch Block

Interpretation?

0.08 seconds



Sinus Rhythm

• Origin is the SA Node (“Sinus Node”)

• Normal sinus rate is 60 to 100/minute

• Rate more than 100/min. = Sinus Tachycardia

• Rate less than 60/min. = Sinus Bradycardia



Arrhythmias

• Irregular rhythms

• Escape

• Premature beats

• Tachy-arrhythmias



Irregular Rhythms

• Sinus Arrhythmia

• Wandering Pacemaker

• Multifocal Atrial Tachycardia

• Atrial Fibrillation

Usually caused by multiple, active automaticity

sites!



Escape

• Escape Rhythm – an automaticity focus escapesoverdrive suppression to pace at its inherent rate

– Atrial Escape Rhythm

– Junctional Escape Rhythm

– Ventricular Escape Rhythm

• Escape Beat – an automaticity focus transientlyescapes overdrive suppression to emit one beat

– Atrial Escape Beat – Junctional Escape Beat

– Ventricular Escape Beat



Premature Beats

• Premature Beat – an irritable focus

spontaneously fires a single stimulus

– Premature Atrial Beat

– Premature Junctional Beat

– Premature Ventricular Contraction (PVC)



Tachyarrhythmias



Blocks

• Sinus Block

• AV Block

• Bundle Branch Block

• Hemiblock



Bundle Branch Block

• Caused by a block of conduction in the Right orLeft Bundle Branch

• Delays depolarization to the ventricle that itsupplies

• Ordinarily both ventricles depolarizesimultaneously

• With BBB, one ventricle depolarizes slightly laterthan the other – RBBB – Right ventricular depolarization is delayed – LBBB – Left ventricular depolarization is delayed



Bundle Branch Block



Bundle Branch Block

• Widened QRS

– Greater than 3 small squares or 0.12 sec

• Look for two R-waves

– R and R’

• Look for wide S



Bundle Branch Block

• Always check: Is QRS within 3 tiny squares?

– If No, suspect BBB. Is there a R,R’?

• Find R, R' in right (V1 or V2) or left (V6 or V6) chest leads – If there is a R,R’ in V1/V2 there is probably a RBBB

– If there is a R,R’ in V5/V6 there is probably a LBBB





Right Bundle Branch Block



f dl h l k



Left Bundle Branch Block

dl h l k



Bundle Branch Block

• The mean axis can’t be determined in the

presence of a BBB

• Ventricular hypertrophy can’t be determined

accurately in presence of BBB

ibl k



Hemiblock

• Block of Anterior or Posterior Fasicle of theLeft Bundle Branch

• Commonly associated with infarction

• Always check: Has Axis shifted outside normalrange?

• Anterior Hemiblock:

–

Axis shifts leftward > L.A.D. Look for Q 1S3

• Posterior Hemiblock:

– Axis shifts rightward > R.A.D. Look for S1Q 3

H ibl k



Hemiblock

• Commonly due to loss of blood supply to theanterior or posterior division of the left bundlebranch – Anterior hemiblock

•Often associated with anterior infarction

• Results from occlusion of supply through branches of – LAD

– Posterior hemiblock• Rare d/t collateral circulation

• Results from occlusion of supply through branches of – RCA

– LCA

» LAD

A i H ibl k



Anterior Hemiblock

• Block of the Anterior Division of the LeftBundle Branch

• Evidenced by

– Left Axis Deviation

– Normal or slightly widened QRS

– A Q-wave in lead I and a wide and/or deep S in

lead III



P t i H ibl k



Posterior Hemiblock

• Block of the Posterior Division of the LeftBundle Branch

• Evidenced by

– Right Axis Deviation

– Normal or slightly widened QRS

– Deep or unusually wide S in lead I and a Q-wave in

lead III

Bif i l Bl k



Bifasciular Blocks

• Two fasicles are blocked – RBBB + Anterior Hemiblock

– RBBB + Posterior Hemiblock

•The following are not generally recognized asbifasicular blocks

– Anterior Hemiblock + Posterior Hemiblock

• This is a LBBB

– RBBB + LBBB

• This is a complete AV Block

Ch k f th EKG



Check for these on every EKG

• Rate

• Rhythm

• AXIS

• Hypertrophy

• Infarction

Using Vectors to Represent Electrical



g p

Potentials

• A vector is an arrow that points in the direction of theelectrical potential generated by current flow

– Used to show the overall direction of the movement of

depolarization throughout the heart

• The arrowhead of the vector is in the positive direction

– Flow proceeds from negative pole to positive pole

• The length of the arrow is drawn proportional to the

voltage of the potential





M QRS V t



Mean QRS Vector

Causes of Axis Deviation



Causes of Axis Deviation

• Change of the position of the heart in the chest – Obesity results in increased intrabdominal pressure

which places a horizontal displacement on the heart

– A tall slender pt may have a more vertical

displacement• Hypertrophy of one ventricle

– Axis deviates towards the hypertrophied muscle

• Myocardial infarction –

Axis deviated away from the damaged muscle• Bundle branch block

– Axis unreliable











Limb Leads



Limb Leads



All six limb leads meet to form six

intersecting leads that lie in a flat






ECG



Normal Ventricular Conduction

Determining Axis Deviation




•Picture sphere surrounding heart with AV Node as center

• Lead I – Proceeds form right (-) to left (+) through center of sphere

transecting AV Node

– Now consider sphere in two halves

• Right half of sphere is negative, left half is positive – As depolarization moves toward a positive electrode (left arm)

there is a positive deflection on the EKG

– If QRS complex in lead I is mainly upright, the mean vector ispointing somewhere into the left half of the sphere

–

If QRS complex in lead I is mainly negative, the vector points tothe patient’s right side • Right Axis Deviation

– Lead I is the best lead for detecting RAD





• Picture sphere surrounding the patient with the AVNode as the center

• Lead aVF – Left foot has positive electrode

–

Lower half of the sphere is now positive – Upper half of sphere is now negative

– If the QRS is mainly positive in lead aVF, then the meanQRS vector points downward into the positive half of thesphere

–If QRS is negative in lead aVF, then the vector pointsupward into the negative half of the sphere

• Either LAD or extreme RAD



If QRS is positive in lead I and aVF, the vector will point downward and to the left.

This is the normal axis range.

Axis Deviation



Axis Deviation



Determining the Axis in Degrees



Determining the Axis in Degrees

1. Locate the mean QRS vector in an axisquadrant (as previously discussed)

2. Find the isoelectric lead

– Equal magnitudes of upward/downwarddeflection

3. Move 90° away from the isoelectric lead into

the predetermined quadrant (step 1)





All six limb leads meet to form sixintersecting leads that lie in a flat








Chest Leads in the Horizontal Plane



Chest Leads in the Horizontal Plane

Chest Leads on EKG



Chest Leads on EKG

• Orientation of V2 makes it most informativelead for determination of both anterior and

posterior infarction of the left ventricle

• QRS is mainly negative in lead V1 andprogresses until it is mainly positive in lead V6

• Leads V3 and V4 are usually isoelectric

(transitional zone)

Axis Rotation in the Horizontal Plane



Axis Rotation in the Horizontal Plane





• Rate

• Rhythm

• Axis

• HYPERTROPHY

• Infarction

Hypertrophy



Hypertrophy

• Examine p-wave for Atrial Hypertrophy

• Examine R-wave for Right Ventricular

Hypertrophy

• Examine S-wave depth in V1 and R-wave

height in V5 for Left Ventricular Hypertrophy

Atrial Hypertrophy



Atrial Hypertrophy

• Examine p-wave – Normal amplitude is 2-3 mm

– Normal duration is <0.11 sec

• Abnormal p-waves

– P – Pulmonale

• Tall peaked

• Right atrial enlargement r/t pulmonary HTN (COPD)

– P – Mitrale

• Broad notched

• LA enlargement r/t mitral valve dx

i h i l h



Right Atrial Hypertrophy

• Large, diphasic (both positive and negative) p-

wave with tall initial component

• Seen in lead V1

• Suspect if p-wave >2.5mm in any lead

L f A i l H h



Left Atrial Hypertrophy

• Large, diphasic (both positive and negative) p-

wave with wide terminal component

• Seen in lead V1

• Seen with mitral valve stenosis and systemic htn

Right Ventricular Hypertrophy



Right Ventricular Hypertrophy

• R > S wave in V1 – In RVH wall of RV is very thick so more

depolarization occurs towards V1 electrode

• R wave gets progressively smaller from V1-V6

– Enlarged RV adds more vectors toward right sideso rightward rotation of QRS seen

– Rightward rotation in the horizontal plane

• S wave persists in V5-V6• RAD with slightly widened QRS



Left Ventricular Hypertrophy



yp p y

• Left ventricular wall is very thick

• Exaggerated amplitude of QRS in chest leads

– Very deep S-wave in V1

– Large R in V5

• LAD





HypertrophyL ft V t i l d L ft At i



Left Ventricle and Left Atrium




y

• Rate

• Rhythm

• Axis

• Hypertrophy

• INFARCTION (and Ischemia)

Infarction



• Results from the occlusion of a coronaryartery

• Infarcted area can become necrotic so it can’tdepolarize or contract

• Ventricular foci in the hypoxic area around theinfarct become very irritable

– Can produce deadly ventricular arrhythmias

• Diagnosable with EKG

– Will tell us which coronary artery is occluded



Infarction



• Since most critical problems originate in theLV, myocardial infarction is usually

conceptualized in terms of the left ventricle

–When we describe location of the infarct, we arespeaking of an area within the LV

Coronary Anatomy



y y



Blood Supply



pp y

•

Two main coronary arteries – Left coronary artery

• Two major branches – Left anterior descending

» Supplies blood to the anterior portion of the LV

» Occlusion results in an anterior infarction

–Circumflex

» Distributes blood to the lateral portion of the LV

» Occlusion results in a lateral infarction

– Right coronary artery• Wraps around the RV posteriorly to supply the posterior portion of the

LV

•Usually provides supply to SA node, AV node, and the Bundle of His

• Occlusion of a branch of the RCA results in a posterior infarction

• Associated with serious arrhythmias





Infarction



• Ischemia• Injury

• Necrosis

Evolving MI and Hallmarks of AMI



2004 Anna Story 137

Evolving MI and Hallmarks of AMI

1 year

Q wave

ST Elevation

T wave inversion

Ischemia



• Decreased blood supply• Produces angina

• Characterized by transient inverted t-waves

– Usually symmetrically inverted – Inverted t-waves are most pronounced in the chest

leads

– Inverted t-waves in V2-V6 always pathological

– Inverted t-waves in V2-V3 alert us to stenosis of LAD

• Can also be seen at the periphery of an infarct

Ischemia



= T wave inversion

• Inverted T wave (of

ischemia) is symmetrical

– Normally T wave is upright

when QRS is upright, and

vice versa

• Usually in the same leads

that demonstrate signs of

acute infarction (Q wavesand ST elevation)

Injury



• Acute infarct• ST segment elevation

• Elevation of > 1mm above the baseline

• Usually the earliest EKG sign of an infarction

• With time the ST segment returns to baseline

• Prinzmetal’s angina can cause transient ST

elevation at rest in the absence of an

infarction

Injury



= ST elevation

• Signifies an acute process

• ST elevation associatedwith significant Q wavesindicates an acute (or

recent) infarct – If ST elevation w/o Q-

waves, non-Q-waveinfarction must be r/o

• ST depression (persistent)

may represent a“subendocardialinfarction”

Depressed ST Segment



•

Depressed ST segment > 1 mm from baseline in leadswhere QRS is upright indicates compromised coronaryblood flow until proven otherwise – Requires complete workup

• Possible causes –

Angina• Chest pain caused by diminished coronary blood flow without

infarction

– Subendocardial infarction• An infarction that does not extend through the full thickness of the LV

– Positive stress test• With exercise the myocardium demands more blood than the

narrowed coronaries can deliver

– Digitalis



Necrosis



• Dead tissue• Diagnostic Q-wave

– First downward stroke of QRS

•

Significant Q-waves are absent in normal tracings

Necrosis



= Q wave (significant Q ’s only)

• Significant Q wave: – One mm wide (0.04

sec in duration/onesmall box) or

– 1/3 the amplitude (ormore) of the QRS

• Omit lead AVR whenlooking for significantQ ’s

• Old infarcts: Q wavesremain for a lifetime

The Q-wave



•Infarct is necrotic

• Can’t depolarize

• Has no vectors

•

Positive electrode nearest the infarction detectsno ‘toward’ vector

• Positive electrode only sees ‘away’ vector fromthe opposite wall (through necrotic void)

• Therefore Q-wave is inscribed on EKG in thoseleads

Infarction Review



• Scan all leads for: – Q waves

– Inverted T waves

–ST segment elevation or depression

– Find the location of the pathology and then

identify the occluded coronary artery



Location Leads Vessel

Posterior V1, V2 Right coronary artery

Inferior II, III, aVF Right or left coronary

arteryLateral I, aVL, V5, V6 Left circumflex artery

Anterior V1, V2, V3, V4 Left anterior descending

artery



Anterior Infarction



•

Occlusion of the LAD• Characterized by poor R-wave progression

• Anterior infarction – Q-waves in V1, V2, V3, or V4

• Antero-septal infarction – Q-waves in V1 and V2

– ST elevation will be seen in acute infarct

• Antero-lateral – Q-waves in V3 and V4

• Remember q-waves are normal in V5 and V6!







Anterior Infarction



Antero-septal Infarction



Anteroseptal MI: Fully Evolved

The QS complexes, resolving ST segmentelevation and T wave inversions in V1-2 are

evidence for a fully evolved anteroseptal MI.

The inverted T waves in V3-5, I, aVL are also

probably related to the MI.

Antero-lateral Infarction



Extensive Anterior/Anterolateral MI: Recent

Significant pathologic Q-waves (V2-6, I, aVL)plus marked ST segment elevation are

evidence for this large anterior/anterolateral

MI. The exact age of the infarction cannot be

determined without clinical correlation and

previous ECGs, but this is likely a recent MI.



Lateral Infarction



• Occlusion of the circumflex• Q-waves in the lateral leads

– I

– aVL



Lateral MI



2004 Anna Story 160

Lateral Infarction



Inferior Infarction



• Occlusion of the RCA or LCA• Q-waves in the inferior leads

– II, III, aVF

– ST segment changes seen in an acute MI

• One-third of inferior infarctions also include

portions of the RV





Inferior MI



2004 Anna Story 165

Inferior Infarction



Inferior Infarction(+ LBBB)



Posterior Infarction



•Occlusion of a branch of the RCA

• Large R-wave in V1 and V2

– Large R-wave in V1 can also be seen with right

ventricular hypertrophy• ST depression in V1 and V2

– With acute infarction

•These are opposite changes compared to whatis seen in an anterior infarction

Posterior MI



2004 Anna Story 169

Posterior Infarction



Postero-lateral Infarction



Acute Infero-posterior Infarction





2004 Anna Story 173

•A combination of infarcts such as: – Anterolateral yellow and red

– Inferoposterior blue and green

–

Anteroseptal yellow and green

Putting it ALL together



2004 Anna Story 174



2004 Anna Story 175

Locating Infarct or Ischemic Area



•Important because treatment and prognosisdepend on location

• Four general areas within the LV

–Lateral

– Inferior

– Anterior

–

Posterior• Infarct may include more than one area



EKG Distributions



• Anteroseptal: V1, V2, V3, V4

• Anterior: V1 –V4

• Anterolateral: V4 –V6, I, aVL

• Lateral: I and aVL

• Inferior: II, III, and aVF

• Inferolateral: II, III, aVF, and V5

and V6

Warning



•EKG diagnosis of infarction is generally notvalid in the presence of a LBBB

– LV depolarizes after RV with LBBB

–

Any Q-waves originating in the LV would fall in themiddle of the QRS complex

– Difficult to detect Q-waves

COPD



•Often produces low voltage amplitude in allleads

• Usually RAD

• Multifocal Atrial Tachycardia is also seen withCOPD



This ECG demonstrates many of the features of chronic pulmonary disease:

Rightward QRS axis (+90 degrees).Peaked P waves in the inferior leads > 2.5 mm (P pulmonale) with a rightward P-wave

axis (inverted in aVL)

Clockwise rotation of the heart with a delayed R/S transition point (transitional lead =

V5).

Absent R waves in the right precordial leads (SV1-SV2-SV3 pattern).

Pulmonary Embolism



•S1Q 3T3

– Wide S-wave in Lead I

– Large Q-wave in lead III

–

Inverted t-wave in Lead III• Acute transient Right Bundle Branch Block

• R.A.D. and clockwise rotation

• Inverted t-waves in V1 – V4• ST depression in Lead II



Pulmonary Embolism



Hyperkalemia



•P-wave flattens down

• QRS complex widens

• T-wave becomes peaked

Hyperkalemia



Hypokalemia



•Flattened or inverted t-waves

• Appearance of a u-wave

• Low serum potassium can initiate Torsades de

Pointes and V-tach

Calcium



•Hypercalcemia – QT interval shortens

• Hypocalcemia

–QT interval is prolonged



Documents

N 564 EKG Interpretation Lecture Version 2013 Stein