12 Lead EKG 101

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					  12 Lead EKG 101

A Basic Overview of How to
Interpret 12 Lead EKGs and
   Treat a Cardiac Patient

 Region IV Pre-Hospital Systems Coordination Committee
            Purpose:

The purpose of this course is to
provide pre-hospital clinicians with the
tools necessary to identify the basic
A&P of the heart, interpret 12 Lead
EKGs, localize and treat AMIs as well
as recognize imposters and potential
complications.
  Basic Cardiac Anatomy &
         Physiology
•Muscular pump about the size of your fist
    •primary function is to pump oxygenated blood to the rest of the
    body.
•Made up of four chambers,
    •right and left atria
    •right and left ventricles
•The septum is a thin muscular wall that separates the right and left
sides of the heart.
•Each contraction of the heart occurs in response to an electrical
impulse that starts in the upper portion of the heart.
•Blood is moved in a closed circuit through the body by the pumping of
the heart.
     Basic Cardiac Anatomy &
            Physiology
•The heart contracts and pumps blood out to the body (systole) and
relaxes to fill with more blood (diastole).

•The heart muscle itself is like all other organs in the body and
requires oxygen to function.
•The oxygen-rich blood is circulated to the heart muscle through the
coronary arteries.
    •There are two main arteries:
        •Right coronary artery
        •Left main coronary artery
             •both start at the aorta
• These vessels then branch off into smaller and smaller vessels
along the surface of the heart.
In order to perform work, the heart
needs oxygen and nutrients.

•There are two main arteries:

    •Right coronary artery (RCA)
    •Left coronary artery (LCA).

•The left coronary artery divides into:
    •Left anterior descending (LAD)
    branch
    •Left circumflex branch(LCX)
•The right coronary artery and the
branches of the left coronary artery
provide numerous smaller branches
which penetrate the heart muscle,         •Both coronary arteries originate
supplying it with blood.                  from the aorta and run along the
                                          surface of the heart.
                                          •In the majority of human hearts,
                                          coronary circulation follows a
                                          predictable pattern.
Left Main Coronary Artery
Branches quickly into the LAD & LCX.
Involves almost 2/3 of the heart muscle

Right Coronary Artery (RCA)
The RCA supplies blood to the bottom
(inferior) portion and part of the back
(posterior) portion of the left ventricle. The
posterior portion of the septum is also
supplied with blood from the RCA.
     •SA Node 55%
     •AV Node 90%
     •AV Blocks

Left Anterior Descending Branch (LAD)             Left Circumflux Branch (LCX)
The LAD supplies blood to the front (anterior)    The LCX supplies blood to the left side
portion of the left ventricle, apical including   (lateral) portion and the back
most of the anterior portion of the septum        (posterior) portion of the left ventricle.
separating the ventricles.                             •SA Node 45%
•Bundle Branch Block, AMI, CHF                         •AV Node 10%
                                                       •Lateral & posterior MI
•Sino-Atrial (SA) Node: natural cardiac
pacemaker. The heartbeat starts here and
spreads throughout the network of
conduction fibers in the two atria causing
them to contract.

•Normally, the heartbeat can only reach the
ventricles (the two lower chambers), after it
has passed through the atrioventricular (AV)
node.

•Atrioventricular (AV) Node: slows down
the electrical signal so that the atrial
contractions can finish filling the ventricles
completely. The AV node also prevents the        •His Bundle, bundle branches, and
lower chambers from beating too fast if the      the Purkinje system : The electrical
atria develops a fast rhythm                     signal finally passes to the ventricles
(tachyarrhythmia).                               causing the ventricles to contract
        Anatomy of an EKG
The EKG, or a measure of this electrical activity of
the heart, is comprised of 3 primary parts...

 1. P wave---electrical depolarization of the
 atria...contraction follows...
 2. QRS COMPLEX---electrical depolarization of the
 ventricles...contraction follows...
 3. T wave---electrical repolarization of the
 ventricles...and thus, relaxation...
P wave: Represents positive and negative deflections of
atrial contraction and relaxation

PR Interval: Distance between the P wave and the R
wave. Should be consistent

QRS Complex
Q wave: First negative deflection
   •Normal in I, aVL, V1, V6
   •Significant or pathologic is one box wide and/or 1/3
   the height of the R wave

R Wave: First positive deflection

S Wave: Next negative deflection
ST Segment: Essentially isoelectric, slopes gentely upward


J point: the point at which the ST Segment takes off from
the QRS complex


T Wave: Upright always in leads I, II, V2-V6. aVR is always
negative. Leads III, aVL, aVF, and V1 can be positive or
negative


U Wave: Seen best in V3, same polarity as T wave, sign of
hypokalemia


QT Interval: One complete ventricular cycle. None are > ½
the preceding R-R
Putting the A&P with the EKG
         Einthoven’s Triangle

Lead I
extends from       -       +
the right to the
left arm
                           -
                               Lead III
                               extends from the left
                               arm to the left foot



Lead II
extends from the
right arm to the
                       +
left foot
Anatomy of a 12-Lead EKG




This is an example a 12-lead EKG.
       Anatomy of a 12-Lead EKG
                (cont.)
•At the bottom of this 12-
lead are rhythm strips
(highlighted).

•Any of the 12-leads can
be shown as rhythm
strips.

•You can configure the
device to show you any
of the six limb leads on
the rhythm strip (I, II, III,
aVR, aVL or aVF).
   Anatomy of a 12 Lead EKG
            (cont.)
The format of the 12-lead EKG is very standard.
While there are a few exceptions, the format you see
here is typical of what you will see in most 12-lead
EKGs done in North America.
        Anatomy of a 12-Lead EKG
                 (cont.)
•The 12-lead can provide a computer generated interpretation.

•When you see “ACUTE MI SUSPECTED” the machine is right about
98% of the time.

•In order to attain specificity, if the computer isn’t absolutely sure that
an AMI is present, it will not say anything about it.

•In other words YOU are the primary interpreter, the computer is your
backup.
 Anatomy of a 12-Lead EKG (cont.)
•The 12-Lead is very good at measuring intervals and durations.

   •It is better at measuring the PR-interval and the QRS width.

•We express these intervals and durations in seconds

   •12-lead expresses them in milliseconds. It is simple to convert
   milliseconds to seconds.
       Anatomy of a 12-Lead EKG
                (cont.)

•When you use an EKG to
determine the cardiac
rate and rhythm, certain
sampling time is required.

12-lead interpretation:
Only one beat from each
lead is needed to make an
interpretation.
          Anatomy of a 12-Lead EKG
                   (cont.)
•There are six positive electrodes on the
chest, yielding six leads.
•There are four electrodes on the limbs
from which the EKG machine makes
another six leads.
    •Each lead has one positive electrode.

    •Positive electrode is a camera.

    •view is from the positive electrode toward
    the negative electrode.

    •The portion of the left ventricle that each
    leads “sees” is determined by the location
    of that positive electrode.

    •Different placements of the electrodes will
    yield different viewpoints.
Anatomy of a 12-Lead EKG
         (cont.)

         Types of Leads
   I      aVR      V1      V4
   II     aVL      V2      V5
   III    aVF      V3      V6

 Limb Leads        Chest Leads
Anatomy of a 12-Lead EKG
         (cont.)

View of Posterior Heart Wall
•Leads V1 & V2
  -Tall R
  -ST Depression
  -Upright T-Wave
Anatomy of a 12-Lead EKG
         (cont.)

View of Inferior Heart Wall
• Leads II, III, aVF
  - Looks at inferior heart wall
   -Looks from the left leg up
Anatomy of a 12-Lead EKG
         (cont.)
View of Lateral Heart Wall
• Leads I and aVL
  – Looks at lateral heart
    wall
  – Looks from the left arm
    toward heart


  *Sometimes known as
  High Lateral*
Anatomy of a 12-Lead EKG
         (cont.)
View of Lateral Heart Wall
• Leads V5 & V6
  – Looks at lateral heart wall
  – Looks from the left lateral
    chest toward heart


  *Sometimes referred
  to as Low Lateral or
  Apical view*
Anatomy of a 12-Lead EKG
         (cont.)
View of Entire Lateral Heart Wall
• Leads I, aVL, V5, V6
  - Looks at the lateral wall of the
  heart from two different perspectives




                       Lateral Wall
Anatomy of a 12-Lead EKG
         (cont.)
View of Anterior Heart Wall
• Leads V3, V4
  – Looks at anterior heart wall
  – Looks from the left anterior
    chest
Anatomy of a 12-Lead EKG
         (cont.)
View of Septal Heart Wall
• Leads V1, V2
  - Looks at septal heart wall
  - Looks along sternal borders
Anatomy of a 12-Lead EKG
         (cont.)




 I Lateral         aVR        V1 Septal     V4 Anterior


II Inferior    aVL Lateral    V2 Septal     V5 Lateral


III Inferior   aVF Inferior   V3 Anterior   V6 Lateral
        Anatomy of a 12-Lead EKG -
               ST Segment
•The ST segment is normally iso-
electric (baseline) neither elevated or
depressed.

   •May slope upward toward
   a relatively tall T wave


•The ST segment is probably the
single most important element to
identify on the ECG when looking for
evidence of AMI.
        The Three I’s

   Ischemia
    – lack of oxygenation
    – ST depression or T inversion
   Injury
    – prolonged ischemia
    – ST elevation
   Infarct
    – death of tissue
    – may or may not show in Q wave
     CARDIAC ISCHEMIA
       ( Myocardial ischemia, Ischemic heart
     disease, Ischemia, Myocardium ischemia,
                  Silent ischemia )



Cardiac ischemia is a situation in which the blood
flow within a coronary artery is limited to the
point where the oxygen needs of the heart muscle
cannot be met (hypoxia).
      CARDIAC ISCHEMIA
Minor episodes of cardiac ischemia tend to cause
  little long-term damage to the heart, but these
  episodes can sometimes cause serious effects in
  some patients:
 They can cause arrhythmias, which can lead to
  either syncope or cardiac arrest and sudden
  cardiac death.
 Severe or lengthy episodes can trigger a result in
  myocardial infarction.
 The collective effects of minor episodes of
  cardiac ischemia can potentially lead to
  cardiomyopathy.
Symptoms of Cardiac Ischemia
May be painful
  symptoms of cardiac
  ischemia,
 Pain, pressure or
  discomfort from
  cardiac ischemia is
  angina. Angina may
  feel like a squeezing
  vise or crushing
  pressure deep in the
  chest behind the
  sternum. May also be
  felt in the shoulders,
  arms, back, neck or
  jaw.
     EKG in Acute Ischemia




Tracing taken during an episode of anginal pain
that occurred while the patient was at rest. Marked
ST elevation in leads V2-5 with some ST
depression in aVF.
  EKG after Acute Ischemia




This tracing was taken 30 minutes after the initial.
The patient was pain-free and asymptomatic. The
ST segments are isoelectric, and the ECG is
normal
        Evaluation after Acute
              Ischemia
   Subsequent clinical evaluation
    – serial ECGs
    – enzyme determinations,
    revealed no evidence of acute myocardial
      infarction. Disappearance of the ST elevation
      and     the    absence    of   clinical    and
      electrocardiographic evidence of infarction on
      subsequent examinations indicate that initial
      ECG is representative of severe, acute, and
      reversible ischemia.
Well Perfused Myocardium
                                Epicardial Coronary Artery


                               Lateral Wall of LV
Septum
            Left
         Ventricular
           Cavity




                                          Positive Electrode
                       Interior Wall of LV
Normal ECG
         Ischemia
                                      Epicardial Coronary Artery


                                     Lateral Wall of LV
Septum
                 Left
              Ventricular
                Cavity




                                                  Positive Electrode

                            Interior Wall of LV
          Ischemia


   Inadequate oxygen to tissue
   Subendocardial
   Represented by ST
    depression or T inversion
   May or may not result in
    infarct
ST depression
            Injury

   Prolonged ischemia
   Transmural
   Represented by ST
    elevation
   Usually results in infarct
ST elevation
Injury
      Thrombus




    Ischemia
              Infarct

   Death of tissue

   Represented by Q wave

   Not all infarcts develop Q waves
                   Infarction

                                  Infarcted Area
                                  Electrically Silent




Depolarization

                 Many infarcts do not develop Q waves
Q Waves
                     Thrombus
                  Infarcted Area
                  Electrically Silent




                 Ischemia




Depolarization
                  Summary
 A normal ECG does NOT rule out
  ACS
 ST segment depression represents
  ischemia
    – Possible infarct
 ST segment elevation is evidence of
  AMI
 Q wave MI may follow ST elevation or
  depression
     Pathophysiology of the AMI
•Chronic accumulation of atherosclerotic plaque in
coronary vessels around the heart
•Fibrous plaque prone to rupture, lead to thrombytic
blockage
•Clots form due to damaged tissue and platelets
   •Both release chemicals causing a clot to form
•Forms a substance called fibren that traps cells and
platelets eventually blocking and narrowing
•Tissue damage in AMI results from rupture of plaque on
vessel walls creating a chain reaction that forms a clot in
the coronary artery.
               Process of an AMI
Impaired blood flow:
•Produces varying degrees of
myocardial injury
•Damage dependent on flow reduction
and duration
•Tissue death progress quickly in a
wave pattern
    •Begins with endocardium
    •Ends with epicardium
    •Infarction becomes larger toward
    the surface of the heart.
Ischemia – Shortage of oxygen at
cellular level
Injury – Diminishing supply of oxygen
Infarct – cardiac cells die of anoxia.
  EKG Changes from Infarction

First Detectable Change in EKG
•Tall T-waves
  •increase in height
  •more symmetric
  •may occur in the first few minutes


             *Known as hyper acute phase*
   EKG Changes from Infarction
       “The Acute Phase”
Signs of Myocardial Injury
•ST Segment Elevation
  •Primary indication of injury
  •Occurs in first hour to hours

•ST Segment Elevation in Leads
  •1mm or greater in limb leads
  •2 mm or greater in chest leads
     •Hallmark indication of AMI

              *Known as Acute Phase*
    EKG Changes of Infarction
      “Reciprocal Changes”
 ST elevation in contiguous leads most
  often represents acute infarction
 ST depression in contiguous leads may
  represent acute ischemia
 In acute infarction, ST elevation in
  contiguous leads coupled with
  reciprocal ST depression in non-
  infarcting leads is added evidence of an
  AMI.
Reciprocal ST segment depression



Acute ST segment elevation
    EKG Changes from Infarction
       “T Wave Inversion”
Signs of Myocardial Injury
T wave inversion
   • presence of ischemia
   • May precede ST elevation
•Prominent in precordial chest leads
   • Inversion in limb leads is pathologic
   • T wave inversion can be caused by
   other things than ischemia
    EKG Changes from Infarction
     “The Indeterminate Phase”
Signs of Myocardial Infarction

Pathologic Q-wave
•First indication of tissue death
•First few to several hours
    •Q-wave ¼ size of QRS suggests
    infarct
    •Represent current or past events
•Determine timing through ST elevation
and T-wave inversion
  Natural Progression of EKG in
            Infarction
Over time:
•T-wave regains normal contour
•ST-segment returns to isometric line
•Q-wave remains as evidence of infarct
   •Indicates presence of previous MI



     *ST segment elevation
     provides the strongest
     evidence of early
     recognition of AMI*
      EKG Changes from Infarction
               (cont.)
• All of the changes in the previous slides are: Indicative
Changes
• ST segment elevation is helpful in detecting an MI in its early
stages
• Hyperacute (Tall) T-waves alone are specific enough to
diagnose an MI
• T-wave inversion can occur with simple angina and is therefore
not specific
• Pathological Q-wave is the most accurate recognition of an MI
   • Not in the first few hours
• ST segment elevation provides the strongest evidence for early
recognition of an MI
                  ECG Variants
   Coronary Spasm:
    “Printzmetals angina”
    Injury pattern that resolves
    w/ rest, NTG,O2 etc.


   Early Repolarization:
    elevated “J” point seen
    best in V3,4. Key to Dx
    pt’s are usually young &
    asymptomatic


   Pericarditis: ST elevation
    usually global associated
    w/ fever, pleuritic c/p.
     ECG Variants due to Drugs or
       Electrolytes Imbalances
   Hypokalemia: lg U waves (
    usually taller than T) seen best in
    precordial leads. <2.7
   Hyperkalemia:
     –   Tall peaked T waves > 6.0
     –   PR prolongs, QRS widens
     –   P waves disappear > 8.0
   Hypocalcemia:
     –   Prolonged QT interval
   Hypercalcemia:
     –   Shortened QT interval
   Digitalis effect:
     –   ST depression- downsloping,
         curved ST segments.
     –   “scooping”, “sagging”, flat or
         inverted T’s in lateral leads
     –   PR prolonged
     –   QT shortened
                 Bundle Branch Blocks

“Turn Signal Rule”
    This is a simple method for differentiating right bundle branch block from
       left bundle branch block. V1 will be the only lead you need to view
        1. Locate the terminal (last) force of the QRS complex
        2. Determine if it is pointing up or down.
        3. Compare to the turn signal in your car:
           » Up is for a right turn & RBBB
           » Down is for a left turn and LBBB


Clinical significance:
   Bundle branch is a significant complication of infarction. Since the left anterior descending artery is
   the primary supplier of the bundle branches, BBB is considered a complication of anterior septal
   infarcts.

   When BBB is the result of MI, the incidence of pump failure is 65-70% and the in-hospital mortality
   rate is 40%-60%. The BBB itself is not dangerous, but the high mortality rate is due to the extensive
   amount of tissue death occurring when an infarct is serious enough to cause a BBB. Another
   manifestation of BBB is in the form of AV Block. This is why infranodal AV blocks are more
   serious and have wide QRS complexes.
            Localizing the Area of
                  Infarction
•Indicative changes are not found in every lead
•Only present in leads looking at the infarct
•Indicative changes in two or more leads looking at the same
portion of the heart are anatomically contiguous leads
   •Suspect AMI
•ST segment elevation in two or more leads that are not
contiguous
   •AMI not the suspected cause
       Recognition & Localization
•Recognizing infarct: Know which part of the heart each lead
looks at
•Localizing Infarct: Note which lead is displaying evidence and
which portions of heart they are looking at
            Leads Displaying         Location of Infarct Site
           Indicative Changes
                                    Inferior
        II, III, aVF

        V1 & V2                     Septal

        V3 & V4                     Anterior

        V5, V6, I, and aVL          Lateral

     *Simply knowing the changes to look for and which part
                of the heart each lead looks at*
                Anterior Wall MI

Anterior Wall infarct: Occlusion of the Left Anterior
Descending Artery (LAD)
•2mm ST segment elevation in two or more of leads V1-V4
   •Reciprocal changes in leads II, III, aVF
•Lethal due to large myocardium involvement
Possible conduction defects:
Bundle Branch Block
2nd Degree Block Type II
CHB
Anterior Wall MI
                    Inferior Wall MI
Inferior Wall MI: Occlusion of Right Coronary Artery (RCA)
•At least 1mm ST segment elevation in leads II, III, aVF
•Reciprocal ST depression in leads I & aVL or precordial leads
Conduction defects:
•Sinus bradycardia
•Sinus arrest
•1st degree block
•Accelerated Idoventricular rhythm
Complications:
•Bradyarrhythmias – protective mechanism, 90% of blood supply for
SA & AV nodes from the RCA
•Hypotension – treated with fluids, consider right side involvement
Inferior Wall MI
                 Lateral Wall MI

Lateral Wall MI: results from occlusion of the Left
Circumflex Artery
•At least 1 mm ST segment elevation in leads I, aVL, V5 & V6
and /or 2 mm ST segment elevation in V5 & V6
   •Reciprocal ST depression in V1
   •Sometimes an extension of an Anterior or Inferior MI
•Conduction defects are rare
Anterior/Lateral Wall MI
                Posterior Wall MI
Posterior Wall MI: Occlusion of the Right Coronary Artery
(RCA) or the Posterior Descending Artery
•No leads that look at the posterior wall
   •Leads look at the infarct site from the opposite
   side(backwards)
•ST depression in V1 & V2
•Tall R waves in V1 and/or V2
•Most often associated with Inferior MI
     *Associated with dangerous conduction disturbances*
Posterior Wall MI
            Right Ventricular MI
Right Ventricular MI: caused by proximal occlusion of the
Right Coronary Artery (RCA)
• Associated with Inferior Wall MI
     • Can happen independently
     • Standard 12-Lead does not assess right side of heart
• Infarction is significant
• Indicates large infarction
• Indicates involvement of both ventricles
• If the possibility of RVI exists a set of chest leads can be
applied to the right side of the chest
     • V1-6R leads look at right ventricle
     • Lead V4R most accurate
Right Ventricular MI
                   Septal Wall MI

Septal Wall MI: caused by septal perforation involving the
LAD or the Posterior Descending
•Most often in the setting of an Anterior MI
•Loss of R-wave in leads V1, V2 or V3
   •May have ST segment elevation in V1 & V2
   •No reciprocal changes
            Overview of Infarcts
 Location of      Arterial         Indicative        Reciprocal
   Infarct        Supply            Changes           Changes
Anterior       LAD               V1-V4             II, III, aVF

Inferior       RCA               II, III, aVF      I, aVL

Lateral        Circumflex        I, aVL, V5, V6    V1

Posterior      Posterior         None              V1, V2
               Descending
               (RCA)
Septal         Septal Perforating Loss of R wave in None
               (LAD)              V1, V2, or V3
               Posterior
               Descending (RCA
              Overview of Infarcts
• Suspect infarction when there are indicative changes in at
least two anatomically contiguous leads
• Indicative changes in many leads suggests larger infarct
• With Inferior Wall MI suspect Right Ventricular Wall Infarct
• Signs of possible Right Ventricular Wall Infarct:
    • Hypotension
    • JVD
    • Clear lung sounds
• Causes of ST segment depression include digitalis, ischemia
and reciprocal changes
• Suspect Posterior Wall Infarctions when an Inferior Wall
Infarction has ST depression in Leads V1-V3
    Complications of Myocardial
            Infarction
Chest Pain: Most common complication
   • Treatment:
   •Oxygen and ASA (162 to 325)mg
   •NTG initially with Morphine if pain persists
   • Usually very effective
Right Ventricular Wall Infarct:
   • Reduces output of right ventricle decreasing left ventricular
   filling (decreased preload)
   • NTG and Morphine can worsen conditions
   • Decrease in blood pressure will worsen area of injury
   • Presence of Inferior Wall Infarction with no EKG or clinical
   evidence of right side infarct does not merit any extra caution
   when using NTG and Morphine
     Complications of Myocardial
             Infarction
AV Block Location: indicates electrical impulse from atrium
is blocked from depolarizing the ventricles
   • Most common block is in the AV Node (nodal block)
   • Second most common block is in the Bundle Branches
   (infranodal)
   • Infarct frequently produces AV Block due to increase in
   parasympathetic tone
   • Local ischemia around node can produce the block
   • Less serious than block caused by tissue injury or death
   • Blocks in AV node produce narrow QRS complex
   • Bundle Branches produce wide complexes
      Complications of Myocardial
              Infarction
     Determining the type of QRS presented with is a
     useful tool in determining the location of the block

                    Nodal Block           Infranodal Block
Coronary Supply     Right Coronary        Left Coronary Artery
                    Artery
QR Width            Narrow                Wide
Stability           Generally Stable      Often Unstable

Atropine Response Usually improves        Often does not
                                          respond
     Complications of Myocardial
             Infarction
Hypotension: A common treatment for hypotension
which is secondary to the infarct is to administer fluid
boluses and inotropic drugs (dopamine)
Hypotension in the setting of an inferior wall infarction is
most likely secondary to right ventricular involvement.
Although RV Infarcts may require significant boluses to
offset loss of preload, continuously monitor the patient for
signs and symptoms of developing left sided failure.
Hypotension in the setting of an anterior wall infarction
may not tolerate fluid boluses and may require a
dopamine infusion.
       Complications of Myocardial
               Infarction
                     Left Coronary Artery         Right Coronary Artery
                     Occlusions                   Occlusions
Leads Showing        V1-V6, I, aVL                II, III, aVF, V4R-V6R
Indicative Changes
Localization         Septal, Anterior, Lateral,   Inferior, Posterior, Right
                     Posterior                    Ventricular
Pain Control         NTG & Morphine as            NTG & Morphine used
                     appropriate                  with caution if RVI
                                                  present
AV Block             Infrequent, usually wide     Frequent, usually
                     ORS, often unstable,         narrow QRS, Generally
                     Atropine may be              stable, Atropine often
                     ineffective, use standby     effective, May not
                     pacing                       require treatment
Hypotension          200-250 cc fluid bolus,      Vigorous fluid therapy if
                     inotropic medications        RVI present, inotropic
                                                  medications
                     Clinical Pearls
• Suspect infarction when there are indicative changes in at
least two anatomically contiguous leads
• Indicative changes in a greater number of contiguous leads
suggests a more extensive infarction
• RV or Posterior infarcts should be considered in setting of
Inferior Wall MI
   •RV: ST segment elevation in rV4
    •Posterior: ST depression +/or Tall Rwave in V1 & V2
• Other clinical signs of RV Infarct may include:
    • Hypotension and JVD in the setting of clear lung sounds
• Other causes of ST segment depression besides ischemia
include digitalis effects and ventricular hypertrophy
• Suspect Posterior Wall Infarctions when an Inferior Wall
Infarction has ST depression in Leads V1-V3
Questions

				
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