Docstoc

12-Lead-EKG-Interpretation

Document Sample
12-Lead-EKG-Interpretation Powered By Docstoc
					12 Lead EKG Interpretation

 Stephanie Roberson NREMT-P, BS
  Virginia College of Osteopathic
             Medicine
                 Disclaimer
• This is intended to simplify some of the
  concepts introduced to us in lecture.
• You should by all means still understand the
  concepts in the lectures provided by the
  faculty.
• At any place should an opinion differ from
  something introduced by the faculty, defer to
  the opinion of the faculty (they write the
  tests).
                        Objectives
• Proper lead placement
• Relevant cardiac anatomy
• Interpreting the 12 lead EKG
  –   Rate
  –   Rhythm
  –   Axis
  –   Bundle branch blocks (BBB)
  –   Ventricular Hypertrophy
  –   Atrial enlargement
  –   ST elevation
       • Ischemia, injury, and infarction
  – Pericarditis
             What is 12 lead?
• Consists of 10 lead cables that generate 12
  different views of the heart
• Limb leads (look at the frontal plane)
  – I, II, III
  – aVR, aVL, aVF
• Precordial leads/Voltage/Modified Chest leads
  (look at the horizontal plane)
  – V1, V2, V3, V4, V5, V6
                 12 Leads
• Leads I, II, and III are bipolar
• aVR, aVL, and aVF are unipolar leads
• Leads V1-V6 are all positive leads with the
  reference point (negative pole) becoming the
  heart
Proper Lead Placement
             Precordial Leads
• V1 – right 4th ICS
• V2 – left 4th ICS
• V3 – between V2 and V4
• V4 – 5th ICS midclavicular
• V5 - between V4 and V6, 5th ICS anterior
  axiallary line
• V6 – horizontal to V4 mid-axillary, 5th ICS
Precordial Leads are Unipolar
Cardiac Conduction System
           Walls of the Heart




                                Anterior/
                                septal


                                       lateral

Inferior
           “I See All Leads”
   I         aVR         V1         V4

Lateral                 Septal    Anterior
   II         aVL        V2         V5

Inferior    Lateral     Septal    Lateral
  III        aVF         V3         V6

Inferior    Inferior   Anterior   Lateral
Coronary Artery Correlation to Leads
   I       aVR       V1        V4

  LCX                LAD       LAD

  II       aVL       V2        V5

 RCA       LCX       LAD       LCX

  III       III      V3        V6

 RCA       RCA       LAD       LCX
       Right Coronary v. Left Coronary

• RCA feeds:                   • LCA feeds:
  – Right ventricle              – Anterior wall LV (LAD)
  – Inferior wall of LV (90%     – Septal wall LV (LAD)
    of population)               – Lateral wall
  – Posterior wall of LV           (LCircumflexA)
    (posterior descending        – Posterior wall LV
    artery)                        (LCircumflexA)
           Putting It All Together
   I            aVR          V1         V4
 LCX                        LAD        LAD
Lateral                    Septal    Anterior

   II           aVL          V2        V5
  RCA           LCX         LAD       LCX
Inferior       Lateral     Septal    Lateral

   III           aVF         V3        V6
  RCA            RCA        LAD       LCX
Inferior       Inferior   Anterior   Lateral
System for Interpreting the 12 Lead
•   Rhythm
•   Axis
•   Bundle Branch Blocks (BBB)
•   Ventricular Hypertrophy
•   ST elevation
          Interpret the Rhythm
• Rate?
• Rhythm?
• P wave?
• PR Interval?
• QRS Interval?
• R-wave progression – R wave should appear
  smaller in V1 steadily progressing to the largest at
  V6 with the transition (equiphasic) at V3.
• S-wave regression – S wave should appear largest
  in V1 steadily regressing to smallest in V6 with
  transition (equiphasic) at V3.
Note that R waves progress nicely, but
   S wave regression is not steady.
              Assess the Axis
• Axis is the term we use to define the net flow
  of electrical activity in the heart.
• Axis deviation is when the net flow of
  electricity in the heart is not going in the
  normal direction due to either a physiological
  or pathological change.
• Axis is used to help diagnose a hemiblock (Dr.
  Rawlins said he will not be teaching
  hemiblocks…so moving on)
         Assessing the Axis
Lead I         Lead aVF   Interpretation


 Up              Up           All good!


 Up             Down          Left Axis
                              Deviation
Down             Up         Right Axis
                            Deviation
Down            Down      Extreme Right
                               Axis
                                   20
                    • P231 Dubin
Quadrant Approach
           Bundle Branch Blocks
• A new onset BBB indicates a severe MI carrying a
  40-60% increase in mortality….however we do
  not always know if it is new. We need an old 12
  lead to compare to. In the absence of an old 12
  lead, we assume the worst and gain additional
  information via blood work and what the patient
  is telling us.
• The bundle branches are supplied by the LAD
• Bundle branches are divided into right and left,
  with the left further divided into anterior and
  posterior fascicles
Cardiac Conduction System


                                     Anterior
                                     Fascicle




                Posterior Fascicle
           Bundle Branch Blocks
• The bundle branches see to it that the ventricles are
  supplied with syncytium (or that they generate
  contractions at the same time)
• A BBB causes the ventricles to contract out of sync
  either reducing preload (for the right) or force of
  contraction (for the left)
• You cannot determine an MI in the presence of a LBBB
  by traditional means (but it can be done…way more
  advanced. For now, at this level, you cannot make the
  diagnosis)
                Recognizing a BBB
•   Different method than shown by Dr. Rawlins.
•   Defining a BBB must be done in V1
•   Complex must be atrial in origin
•   QRS must be wide (> 0.12 sec)
•   Determine right or left BBB
    – Turn signal method
       • Find the J-point
       • Determine the direction of the deflection immediately
         preceding the J point
       • Use your “turn signal” to determine left or right
• Notching of the QRS complex in V5 or V6 is
  additional proof of a LBBB
                      J Point
• Point on the EKG tracing
  where the S wave
  transitions to the ST
  segment
• Not always easy to
  identify.
                Turn Signal???
• After identification of the J point, look at the
  deflection of the wave immediately preceding it.
• Is it up or down?
• Think about the turn signal on a car
  – Push down to signal left
  – Push up to signal right
• If the wave immediate preceding the J point:
  – deflects downward  left BBB
  – deflects upwards  right BBB
         Right BBB

Upward deflection    J Point
Left BBB
J Point    Downward deflection




                             Notched
                                 QRS
         Bundle Branch Blocks
• The turn signal method of determining BBB is
  different from Dr. Rawlin’s method.
• BY ALL MEANS understand Dr. Rawlin’s way as
  well, but this is meant to show you another
  way to assist you in identifying a BBB.
 Why is it important to assess axis and
                 BBB?
• This is not a testable point per Dr. Rawlins. If you don’t
  care why, skip ahead to ventricular hypertrophy.
• But since I’ve heard people asking why this is
  important….
• RBBB  only the left bundle branch is providing an
  electrical pathway to the ventricles
• What happens when one of the fascicles of the LBB is
  also blocked (ie, bifascicular block)?
• Important point because bifascicular block leaves only
  one fascicle of the bundle branches left to depolarize
  both ventricles.
       Bifascicular Block
                                 Only this guy works




RBBB
                                 Left posterior
        Only these guys   RBBB
                                 fascicle
        work
                                 blocked
             Bifascicular Block
• When only one fascicle of the ventricles is
  providing an electrical current, the ventricles
  will still contract, as the signal will propagate
  from the functioning fascicle through
  functioning ventricular cells.
• However, contraction of the ventricles will not
  be coordinated as the electrical signal is
  delayed due to the distance it has to travel.
• Synctium is lost.
        Ventricular Hypertrophy
• Right VH                  • Left VH
  – Occurs when there is      – Occurs when there is
    increased pressure or       prolonged back pressure
    volume on the RV            or increased volume on
  – Typically caused by         the LV
    respiratory diseases      – Caused by prolonged
  – Why?                        HTN, mitral or aortic
                                valve problems, MI,
                                cardiomyopathy
            Determining RVH
• Right axis deviation
• R-wave in V1 > 7mm tall
• Again, Dr. Rawlins teaches a different
  technique. Still know his technique for the
  test.
Right Ventricular Hypertrophy
                     15-16 mm high
                Determining LVH
• This is one of three of the techniques Dr. Rawlins
  teaches. I find this one the easiest.
• Measure the deeper of the S-waves of V1 or V2
• Measure the taller of the R-waves in V5 and V6
• Add the amplitudes of the deepest S-wave of V1 or V2
  to that of the tallest R-wave of V5 or V6
• If the sum is >= 35 mm, then you have LVH.
• Above criteria not applicable in presence of LBBB
Left Ventricular Hypertrophy
                                   15 mm + 22 mm = 37 mm  LVH
                 Approximately 22 mm




    Approximately 15 mm
         Right Atrial Enlargement
• Look in Lead II, III, or aVF (Dr. Rawlins says just Lead II)
• Tall, pointed P wave greater than 2.5 mm high.
• 3 P’s
   – Pointed
   – Prominent
   – Pulmonary
• Causes of RAE
   – Congenital heart disease
   – Tricuspid or pulmonary valve disease
   – Pulmonary HTN
• Clinical Implications
   – Frequently seen with RVH
   – Pulmonary implications
            Right Atrial Enlargement




P wave greater than 2.5 mm tall
            Left Atrial Enlargement
• Lead II shows a widened (> 0.12 sec) P wave with a
  notched or m-shaped appearance (the “golden arches”
  McD’s sign) or the P wave is mooning you (use your
  imagination)
• Lead V1 shows a broad, inverted P wave of > 0.4 sec
  wide
• Causes of LAE
   –   HTN
   –   Pumonary Edema
   –   Nitral or aortic valve stenosis
   –   LVH
   –   AMI
• Clinical Implications
   – Clue to underlying disease process (see causes)
              Left Atrial Enlargement

         Lead II                                  Lead V1




                                  Broad, negative P wave > 0.4 sec wide
M-shaped P wave > 0.12 sec wide
          Myocardial Infarction
• Proceeds along a continuum:
  – Ischemia – temporary hypoxia in the cells
  – Injury – prolonged oxygen deprivation in the cells;
    cells will die if not corrected
  – Infarction – cell death from lack of oxygen; dead
    cells cannot generate or pass along electrical
    energy or provide mechanical pumping power
        Recognizing the Three I’s
• Ischemia is represented on a 12 lead by peaked T-
  waves, however this in itself is not enough to confirm
  the beginnings of an MI
• Early ischemia can also be recognized by T-wave
  inversion
• ST segment depression can be either a reciprocal
  change for elevation or ischemia
• Injury and early infarction is represented by ST
  segment elevation
Progressive EKG Changes During an MI
• Normal EKG
• ST depression/peaked T-waves (seen in first hours)
• ST elevation
• Development of Q-wave (in some but not all MI’s); ST
  elevation may begin to decrease; this is typically seen in the
  first or second day of MI
• Q-wave present (may or may not be significant); R-wave may
  be diminished or nonexistent; ST often baseline; possible T-
  wave inversion
• Return of R-wave; Q-wave may or may not be present
• Q-wave typically represents transmural infarction
               ST Elevation
• The ST segment is considered elevated if the J
  point is > 1 mm above the isoelectric line in the
  limb leads (criteria from Dr. Power’s lecture)
• the ST elevation must be >= 2 mm above the
  isoelectric line in precordial leads (criteria from
  Dr. Power’s lecture)
• ST elevation must be present in 2 or more
  anatomically contiguous leads to definitively
  deduce infarction
• ST elevation is often seen but not always
  indicative of MI resulting from hypoxia of
  cardiac cells
           “I See All Leads”
   I         aVR         V1         V4

Lateral                 Septal    Anterior
   II         aVL        V2         V5

Inferior    Lateral     Septal    Lateral
  III        aVF         V3         V6

Inferior    Inferior   Anterior   Lateral
Where is the ST Elevation?
           “I See All Leads”
   I         aVR         V1         V4

Lateral                 Septal    Anterior
   II         aVL        V2         V5

Inferior    Lateral     Septal    Lateral
  III        aVF         V3         V6

Inferior    Inferior   Anterior   Lateral
Where is the ST Elevation?
           “I See All Leads”
   I         aVR         V1         V4

Lateral                 Septal    Anterior
   II         aVL        V2         V5

Inferior    Lateral     Septal    Lateral
  III        aVF         V3         V6

Inferior    Inferior   Anterior   Lateral
• So, can the previous 12 lead be called a septal MI
  as well as an anterior MI?
• By definition, no. To diagnose septal MI, the ST
  elevation MUST be in V1 AND V2.
• HOWEVER, both the septal and anterior walls are
  fed by the LAD, thus it is logical that we would
  see changes in the septal leads as well. After all,
  the “walls” of the heart aren’t actual walls
  separate from one another. Anterior and septal
  MI’s often have what is termed “extension” into
  the wall sharing the same blood supply, the LAD.
• The previous EKG would often be called an
  anterioseptal MI
Where is the ST Elevation?
           “I See All Leads”
   I         aVR         V1         V4

Lateral                 Septal    Anterior
   II         aVL        V2         V5

Inferior    Lateral     Septal    Lateral
  III        aVF         V3         V6

Inferior    Inferior   Anterior   Lateral
Where is the ST Elevation?
           “I See All Leads”
   I         aVR         V1         V4

Lateral                 Septal    Anterior
   II         aVL        V2         V5

Inferior    Lateral     Septal    Lateral
  III        aVF         V3         V6

Inferior    Inferior   Anterior   Lateral
                  Pericarditis
• Signs and symptoms:
  – Chest pain alleviated by leaning forward,
    exacerbated by lying back.
  – Described as sharp and severe, often radiating to
    back
  – Friction rub on auscultation
• Diffuse ST elevation that appears concave (like
  a soup ladle) in all leads except aVR and V1.
“soup ladle” concavity
                         Pericarditis




                         Diffuse ST elevation
      OTHER Causes of ST Elevation
•   Electrolyte changes   • Rhythms of ventricular
•   Hypothermia             origin
•   Increased ICP         • Left Ventricular
•   LBBB                    Hypertrophy
                          • Early Repolarization
Treat the Patient, Not the Monitor!
• Remember, all of these findings are relative to the
  presentation of the patient.
• BBB, hemiblocks, and axis deviations can be
  established changes in an individual’s 12 lead.
• These findings are only significant when they are
  new onset, or more importantly when they are
  accompanied by S&S (typical or atypical) of an MI.
• Treat the patient, not the test!
• Your patient will often tell you their diagnosis in their
  own way if you only take the time to listen to them.

				
DOCUMENT INFO