EKG Interpretation

Kevin Stein, MS, CRNA, APN

A Normal 12 Lead ECG

2004 Anna Story

Conduction System

SA Node
Hearts dominate pacemaker Responsible for sinus rhythm of heart Located in upper-posterior wall of RA Automaticity ability to generate pacemaking stimuli Depolarization spreads outwards from SA node like the waves created from a pebble dropped in a 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)

Bachmanns Bundle

Atrial Conducting System

Internodal Tracts
Course from the SA node to the AV node

Bachmanns 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 ventricular conduction 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

Ventricular Conduction System

Ventricular conduction system made up of Purkinje fibers
Use fast-moving sodium ions for conduction of depolarization

Terminal filaments of Purkinje fibers rapidly distribute depolarization to ventricular myocytes

Initiate ventricular contraction

Depolarization of ventricular myocardium produces QRS complex on EKG

SA Node

Right Atrial Tracts

Anterior Internodal Pathway

Middle Internodal Pathway

Posterior Internodal Pathway

Anterior interatrial myocardial band (Bachmanns Bundle)

AV Node

AN Region N Region NH Region Bundle of His

Left Atrium

Right Bundle Branch

Left Bundle Branch

Anterior Division

Posterior Division

Pacemaker Rates
SA Node Atrial Cells AV Node His Bundle Bundle Branches Purkinje Fibers Ventricular Cells
40-60

60-100 BPM 55-60 BPM 40-60 BPM

0-60

40-45 BPM 40-45 BPM 35-40 BPM 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 QRS complex

The EKG Representation of the Cardiac Cycle

ST Segment
Horizontal baseline that follows the QRS Normally level with other areas of baseline Represents the plateau or initial phase of ventricular repolarization

T-wave
Follows the horizontal baseline after the QRS Represents the final rapid phase of ventricular repolarization Repolarization occurs so ventricular myocytes can recover their interior, resting negative charge
Accomplished by potassium ions leaving the myocytes

The EKG Representation of the Cardiac Cycle

Repolarization of ventricular myocytes begin immediately after QRS and persist until end of Twave QT Interval
Represents the duration of ventricular systole/contraction Ventricular contraction begins with the QRS and persists 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

QT Interval

Ventricular Systole

Repolarization

ST Segment

Plateau

Rapid Repolarization Phase

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 x 0.04sec 1 large square = 5mm x 5mm or 0.5mV x 0.2sec 2 large squares = 1mV 5 large squares = 1 sec

Recording the EKG

Deflections below baseline are negative
When depolarization advances away from a positive skin electrode

Deflections above baseline are positive

When depolarization advances toward a positive skin electrode

EKG always reads from negative to positive (electrode) and from left to right on an axis

 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 left arm, and the left leg A pair of electrodes is used to record one lead
A different pair is used for each lead

Einthovens triangle Bipolar limb leads

I, II, III

Unipolar/Augmented limb leads

aVF, aVR, aVL

Bipolar Limb Leads

Recorded using two electrodes Bipolar one lead is positive and one lead is negative

Augmented Limb Leads

Unipolar
Electrode is positive Two remaining electrodes serve as a common ground (negative)

aVF
(A)ugmented/amplified, (V)oltage, left (F)oot Left foot electrode is positive Combination of leads II and III

aVR
Right arm electrode is positive

aVL
Left arm electrode is positive

Augmented Limb Leads

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 patients 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 is moving toward/away from the patients left side and 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 produces positive deflection on EKG Look at heart in horizontal plane
Cuts body into top and bottom halves

Each lead (positive) is oriented through AV node and projects through the patients back (negative)

Horizontal View with Chest Leads

Chest Lead Placement

Chest Leads
Waves in the six chest leads show progressive changes 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 the heart Leads V3 & V4 are oriented over the interventricular septum Leads V5 & V6 are oriented over the left side of the heart

Limb and Chest Leads

EKG Interpretation
1. 2. 3. 4. 5. RATE Rhythm Axis Hypertrophy 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 pacemaking responsibilities from SA node in an emergency Under normal circumstances, these foci are electrically silent Can be found in the atria, ventricles, and the AV Junction

Automaticity Foci
Level
Atria
Atrial automaticity foci

Inherent Rate Range

60-80/min
40-60/min

AV Junction
Junctional automaticity foci

Ventricles
Ventricular automaticity foci

20-40/min

Overdrive Suppression

SA Node Overdrive Suppression Atrial Foci (60-80 bpm) Any automaticity center will overdrive-suppress all others that have a slower inherent pacemaking rate. Junctional Foci (40-60 bpm) Ventricular Foci (20-40 bpm) 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 Rwave cycles in the strip Find the rate by multiplying by 10

Determine the Rate - Bradycardia

3 sec 3 sec

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

Determine the Rate

Say 300, 150, 100 75, 60, 50 But for bradycardia: rate = cycles/6 sec. strip 10

EKG Interpretation
1. 2. 3. 4. 5. Rate RHYTHM Axis Hypertrophy Infarction

Rhythm
Identify the basic rhythm, then scan tracing for prematurity, pauses, irregularity, and abnormal waves
Check for: Regularity Check for: P before each QRS Check for: QRS after each P (2 or 3 AV block) Check: PR intervals (for AV Blocks) Check: QRS interval (for Bundle Branch Block)

Determine Regularity
R R

Look at the 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

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 escapes overdrive suppression to pace at its inherent rate
Atrial Escape Rhythm Junctional Escape Rhythm Ventricular Escape Rhythm

Escape Beat an automaticity focus transiently escapes 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 or Left Bundle Branch Delays depolarization to the ventricle that it supplies Ordinarily both ventricles depolarize simultaneously With BBB, one ventricle depolarizes slightly later than 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

Left Bundle Branch Block

Bundle Branch Block

The mean axis cant be determined in the presence of a BBB Ventricular hypertrophy cant be determined accurately in presence of BBB

Hemiblock
Block of Anterior or Posterior Fasicle of the Left Bundle Branch Commonly associated with infarction Always check: Has Axis shifted outside normal range? Anterior Hemiblock:
Axis shifts leftward > L.A.D. Look for Q1S3

Posterior Hemiblock:
Axis shifts rightward > R.A.D. Look for S1Q3

Hemiblock
Commonly due to loss of blood supply to the anterior or posterior division of the left bundle branch
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

Anterior Hemiblock
Block of the Anterior Division of the Left Bundle 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

Left Anterior Hemiblock

Posterior Hemiblock
Block of the Posterior Division of the Left Bundle 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

Bifasciular Blocks
Two fasicles are blocked
RBBB + Anterior Hemiblock RBBB + Posterior Hemiblock

The following are not generally recognized as bifasicular blocks

Anterior Hemiblock + Posterior Hemiblock
This is a LBBB

RBBB + LBBB
This is a complete AV Block

Check for these on every EKG

Rate Rhythm AXIS Hypertrophy Infarction

Using Vectors to Represent Electrical Potentials

A vector is an arrow that points in the direction of the electrical 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

Mean QRS Vector

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

Axis Deviation & Rotation

Envision the AV Node as the center of a sphere surrounding the heart This sphere is first analyzed in the frontal plane and the limb leads are used to determine the axis deviation of the mean QRS vector Next the sphere will be analyzed in the horizontal plane and we will use the chest leads to determine the axis rotation of the mean QRS vector

Bipolar Limb Leads

Augmented Limb Leads

Limb Leads

All six limb leads meet to form six intersecting leads that lie in a flat frontal plane on the patients chest!

Normal Axis

Normal Ventricular Conduction

ECG

Normal Ventricular Conduction

ECG

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 is pointing somewhere into the left half of the sphere If QRS complex in lead I is mainly negative, the vector points to the patients right side
Right Axis Deviation

Lead I is the best lead for detecting RAD

Determining Axis Deviation

Picture sphere surrounding the patient with the AV Node 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 mean QRS vector points downward into the positive half of the sphere If QRS is negative in lead aVF, then the vector points upward 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

Determining the Axis in Degrees

1. Locate the mean QRS vector in an axis quadrant (as previously discussed) 2. Find the isoelectric lead
Equal magnitudes of upward/downward deflection

3. Move 90 away from the isoelectric lead into the predetermined quadrant (step 1)

All six limb leads meet to form six intersecting leads that lie in a flat frontal plane on the patients chest!

Chest Leads in the Horizontal Plane

Chest Leads on EKG

Orientation of V2 makes it most informative lead for determination of both anterior and posterior infarction of the left ventricle QRS is mainly negative in lead V1 and progresses until it is mainly positive in lead V6 Leads V3 and V4 are usually isoelectric (transitional zone)

Axis Rotation in the Horizontal Plane

Check for these on every EKG

Rate Rhythm Axis HYPERTROPHY Infarction

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
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

Right Atrial Hypertrophy

Large, diphasic (both positive and negative) pwave with tall initial component Seen in lead V1 Suspect if p-wave >2.5mm in any lead

Left Atrial Hypertrophy

Large, diphasic (both positive and negative) pwave with wide terminal component Seen in lead V1 Seen with mitral valve stenosis and systemic htn

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 side so 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

Left ventricular wall is very thick Exaggerated amplitude of QRS in chest leads
Very deep S-wave in V1 Large R in V5

LAD

Left Ventricular Hypertrophy

mm of S in V1

+
mm of R in V5

Total: If more than 35 mm there is LVH

Left Ventricular Hypertrophy

LAD with slightly widened QRS Leftward rotation in the horizontal plane Inverted T wave in V5 and V6
Slants downward gradually, but up rapidly

Hypertrophy
Left Ventricle and Left Atrium

Check for these on every EKG

Rate Rhythm Axis Hypertrophy INFARCTION (and Ischemia)

Infarction
Results from the occlusion of a coronary artery Infarcted area can become necrotic so it cant depolarize or contract Ventricular foci in the hypoxic area around the infarct 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 the LV, myocardial infarction is usually conceptualized in terms of the left ventricle
When we describe location of the infarct, we are speaking of an area within the LV

Coronary Anatomy

Blood Supply
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

Q wave ST Elevation

1 year
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T wave inversion
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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 waves and 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 Prinzmetals angina can cause transient ST elevation at rest in the absence of an infarction

Injury
= ST elevation
Signifies an acute process ST elevation associated with significant Q waves indicates an acute (or recent) infarct
If ST elevation w/o Qwaves, non-Q-wave infarction must be r/o

ST depression (persistent) may represent a subendocardial infarction

Depressed ST Segment
Depressed ST segment > 1 mm from baseline in leads where QRS is upright indicates compromised coronary blood 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 Qs only)
Significant Q wave:
One mm wide (0.04 sec in duration/one small box) or 1/3 the amplitude (or more) of the QRS

Omit lead AVR when looking for significant Q s Old infarcts: Q waves remain for a lifetime

The Q-wave
Infarct is necrotic Cant depolarize Has no vectors Positive electrode nearest the infarction detects no toward vector Positive electrode only sees away vector from the opposite wall (through necrotic void) Therefore Q-wave is inscribed on EKG in those leads

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 Posterior

Leads V1, V2

Vessel Right coronary artery

Inferior
Lateral Anterior

II, III, aVF

I, aVL, V5, V6 V1, V2, V3, V4

Right or left coronary artery

Left circumflex artery 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 MI

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Anterior Infarction

Antero-septal Infarction

Anteroseptal MI: Fully Evolved The QS complexes, resolving ST segment elevation 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

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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

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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 what is seen in an anterior infarction

Posterior MI

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Posterior Infarction

Postero-lateral Infarction

Acute Infero-posterior Infarction

 A combination of infarcts such as:

Anterolateral yellow and red Inferoposterior blue and green Anteroseptal yellow and green

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Putting it ALL together

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Locating Infarct or Ischemic Area

Important because treatment and prognosis depend on location Four general areas within the LV
Lateral Inferior Anterior Posterior

Infarct may include more than one area

Dominant Coronary Artery

The base of the LV receives its blood supply from branches of the dominant coronary artery
Right coronary artery
Most common

Left coronary artery

Diagnosis of inferior infarction does not necessarily identify the artery branch that is occluded

EKG Distributions
Anteroseptal: V1, V2, V3, V4 Anterior: V1V4 Anterolateral: V4V6, 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 not valid in the presence of a LBBB
LV depolarizes after RV with LBBB Any Q-waves originating in the LV would fall in the middle of the QRS complex Difficult to detect Q-waves

COPD
Often produces low voltage amplitude in all leads Usually RAD Multifocal Atrial Tachycardia is also seen with COPD

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
S1Q3T3
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

Sources
Dubin, D. (2000). Rapid Interpretation of EKGs: Dr. Dubins Classic, Simplified Methodology for Understanding EKGs. (6th Ed.) Valley Stream: C.o.v.e.r Publishing Various Google image searches Various definitions from wiki.com