SlideShare una empresa de Scribd logo
1 de 140
Descargar para leer sin conexión
Basics of ECG

            Dr. Sreedhar Rao
MD(Rog Nidan), (Ph.D), MBA (Hospital Management)

Asst. Professor, Dept. of Rog Nidan
Module 1 - Objectives


• Define ECG
• Describe heart anatomy and circulation
• Describe the fundamentals of heart
  electrophysiology
What is ECG?


• Electrocardiogram is the
  physical translation of
  the electrical phenomena
  created in the heart
  muscles.
The graph paper recording produced by the machine is termed an electrocardiogram,
                      It is usually called ECG or EKG




                                                         STANDARD
                                                        CALLIBRATION
                                                     Speed = 25mm/s
                                                   Amplitude = 0.1mV/mm

                                                        1mV à10mm high
                                                 1 large square à 0.2s(200ms)
                                                      1 small squareà 0.04s
                                                    (40ms) or 1 mV amplitude
With ECGs we can identify

  •Arrhythmias
  •Myocardial ischemia and infarction
  •Pericarditis
  •Chamber hypertrophy
  •Electrolyte disturbances (i.e.
  hyperkalemia, hypokalemia)
  •Drug toxicity (i.e. digoxin and drugs
  which prolong the QT interval)
THE HISTORY OF ECG MACHINE

1903                              NOW
Willem Einthoven                  Modern ECG machine
A Dutch                           has evolved into compact
doctor and physiologist.          electronic systems that often
He invented the first             include computerized
practical electrocardiogram and   interpretation of the
received the Nobel Prize in       electrocardiogram.
Medicine in 1924 for it
Basic Regions of the heart


This is where the
  blood from the
   body enters
Basic Regions of the heart


The Triscuspid
valve is a three-
  flap valve that
lies between the
right atrium and
  right ventricle
Basic Regions of the heart


 This chamber
   empties its
 content into the
pulmonary artery
   going to the
      lungs.
Basic Regions of the heart


 This chamber
   empties its
 content into the
pulmonary artery
   going to the
      lungs.
Basic Structures inside the heart


Pulmonary artery
 carries blood to
    the lungs
Basic Regions of the heart

 Thicker heart
  muscles of the
left than the right
 ventricle due to
   greater force
     needed to
 circulate blood.
Basic Regions of the heart

Pulmonary veins
   carries blood
 back to the heart.
Basic Structures inside the heart


 Mitral Valve
 prevents the
  reflux of its
content back to
 the left atria.
Basic Structures inside the heart


The Aortic Valve is a
   3-flap, semilunar
 valve that keeps the
  blood from coming
      back to the
     ventricles at
        diastole.
Basic Regions of the heart

The blood from the
   lungs return to
    the body after
  receiving oxygen
    through here.
Basic Structures inside the heart


               The chordae tendinae is a
                   fibrous cartilage like
                 tissue that controls the
                 mechanical movement
                        of the valve.
Basic Structures inside the heart


                The papillary muscles
                 suspends the chordae
                      tendinae.
Basic Structures inside the heart


                The septum divides the
                heart into two. The right
                    side receives the
                unoxygenated blood and
                  the left side send the
                oxygenated blood to the
                        periphery.
The Basics of Electrophysiology
In response to the
  stimulation to the
Vagus nerve, the SA
  node genertes its
    own electrical
      conduction,
  normally, 60 -100
     impulses per
        minute.
The Basics of Electrophysiology
From the SA node the
        electrical
    conduction will
    travel through a
     nodal pathway.
   That is Anterior,
       Middle, and
  Posterior Internodal
        pathway
The Basics of Electrophysiology
Bachmann bundle is
     the SA node
     pathway that
  stimulates the left
        atrium.
The Basics of Electrophysiology
The AV Node generates
       about 40-60
    stimulations per
    minutes, if the SA
  node fails to function.
The Basics of Electrophysiology
The AV Bundle (also
 known as Bungle of
  His) branches into
  two main bundle.
The Basics of Electrophysiology
The Left and Right
 Bundle Branches
 then attach to the
myocardial muscles
  through Purkinje
       fibers.
Module 2 - Objectives


Topic: ECG Calibration, Representation,


          • Describe how the electrophysiological
            property of the heart influences its
            mechanical activity.
          • Describe how ECG is calibrated.
          • Describe the ECG waveforms.
Electrophysiology Property of the heart
Electrical Cells – make up the
   cardiac conduction system.

Properties:
ü Automaticity – the ability to
  spontaneously generate and
  discharge an electric
  impulse.

ü Excitability – the ability of
  the cell to respond to an
  electrical impulse

ü Conductivity – the ability to
  transmit an electrical
  impulse from one cell to the
  next.
Electrophysiology Property of the heart
Myocardial cells – make
  up the muscular walls
  of the atrium and
  ventricles of the heart.

ü Contractility – the
  ability of the cell to
  shorten and lengthen
  its fibers.

ü Extensibility – the
  ability of the cell stretch
HOW TO DO ELECTROCARDIOGRAPHY

1. Place the patient in a supine or
   semi-Fowler's position. If the
   patient cannot tolerate being flat,
   you can do the ECG in a more
   upright position.
2. Instruct the patient to place their
   arms down by their side and to
   relax their shoulders.
3. Make sure the patient's legs are
   uncrossed.
4. Remove any electrical devices,
   such as cell phones, away from          Patient, supine position
   the patient as they may interfere
   with the machine.
5. If you're getting artifact in the
   limb leads, try having the patient
   sit on top of their hands.
6. Causes of artifact: patient
   movement, loose/defective
   electrodes/apparatus, improper
   grounding.                               An ECG with artifacts.
Electrodes
Usually consist of a conducting gel, embedded
in the middle of a self-adhesive pad onto
which cables clip. Ten electrodes are used for a
12-lead ECG.


Placement of electrodes               The limb electrodes
                                      RA - On the right arm, avoiding thick muscle
                                      LA – On the left arm this time.
                                      RL - On the right leg, lateral calf muscle
                                      LL - On the left leg this time.-
                                       The 6 chest electrodes
                                       V1 - Fourth intercostal space, right sternal
                                       border.
                                       V2 - Fourth intercostal space, left sternal border.
                                       V3 - Midway between V2 and V4.
                                       V4 - Fifth intercostal space, left midclavicular
                                       line.
                                       V5 - Level with V4, left anterior axillary line.
                                       V6 - Level with V4, left mid axillary line.
Basics of ECG
PEOPLE USUALLY REFER THE
  ELECTRODES CABLES AS
                           LEADS
LEADS                      should be correctly
                           defined as the tracing
                           of     the    voltage
DUDE, THAT’S               difference   between
                           the electrodes and is
CONFUSING!                 what     is   actually
                           produced by the ECG
                           recorder.
SO, WHERE ARE THE


LEADS?
LEADS I, II, III
THEY ARE FORMED BY VOLTAGE TRACINGS BETWEEN
THE LIMB ELECTRODES (RA, LA, RL AND LL). THESE
ARE THE ONLY BIPOLAR LEADS. ALL TOGETHER THEY
ARE CALLED THE LIMB LEADS OR
THE EINTHOVEN’S TRIANGLE

                                                 RA             I        LA




                                                           II            III


                                                      RL            LL
LEADS aVR, aVL, aVF
THEY ARE ALSO DERIVED FROM THE LIMB ELECTRODES, THEY
MEASURE THE ELECTRIC POTENTIAL AT ONE POINT WITH
RESPECT TO A NULL POINT. THEY ARE THE AUGMENTED LIMB
LEADS




                                                   RA                    LA

                                                        aVR     aVL




                                                              aVF
                                                        RL          LL
LEADS
V1,V2,V3,V4,V5,V6
THEY ARE PLACED DIRECTLY ON THE CHEST. BECAUSE
OF THEIR CLOSE PROXIMITY OF THE HEART, THEY DO
NOT REQUIRE AUGMENTATION. THEY ARE CALLED THE
PRECORDIAL LEADS


                                                 RA                       LA



                                                           V1
                                                                V2
                                                                 V3
                                                                   V4 V6
                                                                     V5


                                                      RL             LL
These leads help to determine heart’s electrical
axis. The limb leads and the augmented limb
leads form the frontal plane. The precordial
leads form the horizontal plane.
The Different Views Reflect The Angles At Which LEADS "LOOK" At
               The Heart And The Direction Of The Heart's Electrical Depolarization.

               Leads                      Anatomical representation of the heart
V1, V2, V3, V4                    Anterior
I, aVL, V5, V6                    left lateral
II, III, aVF                      inferior
aVR, V1                           Right atrium
ECG Calibration

• Horizontally
   • One small box - 0.04 s
   • One large box - 0.20 s
• Vertically
   • One large box - 0.5 mV
ECG Calibration
A NORMAL ECG WAVE
REMEMBER
THE NORMAL SIZE
                              <3 small square




                                          < 2 small square




                  <3-5 small square


                                      < 2 large square
ECG Representation


P wave represents Atrial
     depolarization

Vector is from SA node
       to AV node
ECG Representation

    QRS Complex
represents Ventricular
     depolarization

       Normal
0.06 to 0.10 seconds
ECG Representation


  T wave represents
       Ventricular
     repolarization

Vector is from SA node
       to AV node
ECG Representation
       PR Interval
   0.12 – 0.20 seconds

Time for electrical
  impulse takes to travel
  from sinus node
  through the AV node
  and entering the
  ventricles
ECG Representation
      QT Interval
  0.32 – 0.40 seconds

A prolonged QT interval
  is a risk factor for
  ventrial
  tachyarrhythmias and
  sudden death
ECG Representation
ST segment represents
    the early phase of
        ventricular
      repolarization

    It is Isoelectric
ECG Representation




Isoelectric line
Understanding
ECG Waveform


If a wavefront of
depolarization
travels towards the
positive electrode, a
positive-going
deflection          will
result.       If    the
waveform        travels
away      from      the
positive electrode, a
negative          going
deflection will be
seen.
ECG RULES
• Professor Chamberlains 10 rules of normal:-
RULE 1




 PR interval should be 120 to 200
milliseconds or 3 to 5 little squares
RULE 2




The width of the QRS complex should not
exceed 110 ms, less than 3 little squares
RULE 3




The QRS complex should be
dominantly upright in leads I and II
RULE 4




QRS and T waves tend to have the
same general direction in the limb
leads
RULE 5




All waves are negative in lead aVR
RULE 6




The R wave must grow from V1 to at least V4
The S wave must grow from V1 to at least V3
and disappear in V6
RULE 7




The ST segment should start isoelectric
except in V1 and V2 where it may be
elevated
RULE 8




The P waves should be upright in I,
II, and V2 to V6
RULE 9




There should be no Q wave or only a small
q less than 0.04 seconds in width in I, II, V2
to V6
RULE 10




The T wave must be upright in I,
II, V2 to V6
INTERPRETATION




The More You See, The More You Know
The best way to interpret an ECG is to do it step-by-step

                               Rate
                             Rhythm
                          Cardiac Axis
                             P – wave
                          PR - interval
                         QRS Complex
                          ST Segment
               QT interval (Include T and U wave)
                        Other ECG signs
RATE
CALCULATING RATE

As a general interpretation, look at lead II at the bottom part of the ECG strip. This
lead is the rhythm strip which shows the rhythm for the whole time the ECG is
recorded. Look at the number of square between one R-R interval. To calculate
rate, use any of the following formulas:



                                           300
          Rate =
                    the number of BIG SQUARE between R-R interval


                                          OR

                                          1500
          Rate =
                    the number of SMALL SQUARE between R-R interval
CALCULATING RATE

For example:




                   300                          1500
          Rate =                or     Rate =
                    3                            15


         Rate = 100 beats per minute
CALCULATING RATE

If you think that the rhythm is not regular, count the number of electrical beats in a
6-second strip and multiply that number by 10.(Note that some ECG strips have 3
seconds and 6 seconds marks) Example below:
     1         2         3         4          5        6         7         8




 There are 8 waves in this 6-seconds strip.


          Rate      = (Number of waves in 6-second strips) x 10
                    = 8 x 10
                    = 80 bpm
CALCULATING RATE

You can also count the number of beats on any one row over the ten-second strip
(the whole lenght) and multiply by 6. Example:




         Rate     = (Number of waves in 10-second strips) x 6
                  = 13 x 6
                  = 78 bpm
CALCULATING RATE



           Interpretation     bpm                       Causes


           Normal           60-99   -

           Bradycardia      <60     hypothermia, increased vagal tone (due to
                                    vagal stimulation or e.g. drugs), atheletes (fit
                                    people) hypothyroidism, beta blockade, marked
                                    intracranial hypertension, obstructive jaundice,
                                    and even in uraemia, structural SA node
                                    disease, or ischaemia.


           Tachycardia      >100    Any cause of adrenergic stimulation (including
                                    pain); thyrotoxicosis; hypovolaemia; vagolytic
                                    drugs (e.g. atropine) anaemia, pregnancy;
                                    vasodilator drugs, including many hypotensive
                                    agents; FEVER, myocarditis
RHYTHM
RHYTHM

Look at p waves and their relationship to QRS complexes.
Lead II is commonly used
Regular or irregular?
If in doubt, use a paper strip to map out consecutive beats and see whether the rate
is the same further along the ECG.
Measure ventricular rhythm by measuring the R-R interval and atrial rhythm by
measuring P-P interval.
RHYTHM




Normal Sinus Rhythm




 ECG rhythm characterized by a usual rate of anywhere between 60-99 bpm,
 every P wave must be followed by a QRS and every QRS is preceded by P
 wave. Normal duration of PR interval is 3-5 small squares. The P wave is
 upright in leads I and II
RHYTHM




Sinus Bradycardia




Rate < 60bpm, otherwise normal
RHYTHM




Sinus Tachycardia




 Rate >100bpm, otherwise, normal
RHYTHM




Sinus pause




 In disease (e.g. sick sinus syndrome) the SA node can fail in its pacing
 function. If failure is brief and recovery is prompt, the result is only a missed
 beat (sinus pause). If recovery is delayed and no other focus assumes
 pacing function, cardiac arrest follows.
RHYTHM




Atrial Fibrillation




 A-fib is the most common cardiac arrhythmia involving atria.
 Rate= ~150bpm, irregularly irregular, baseline irregularity, no visible p waves,
 QRS occur irregularly with its length usually < 0.12s
RHYTHM




Atrial Flutter




Atrial Rate=~300bpm, similar to A-fib, but have flutter waves, ECG baseline
adapts ‘saw-toothed’ appearance’. Occurs with atrioventricular block (fixed
degree), eg: 3 flutters to 1 QRS complex:
RHYTHM




Ventricular Fibrillation




A severely abnormal heart rhythm (arrhythmia) that can be life-threatening.
Emergency- requires Basic Life Support
Rate cannot be discerned, rhythm unorganized
RHYTHM



Ventricular tachycardia




fast heart rhythm, that originates in one of the ventricles- potentially life-
threatening arrhythmia because it may lead to ventricular fibrillation, asystole,
and sudden death.
Rate=100-250bpm
RHYTHM




Torsades de Pointes




 literally meaning twisting of points, is a distinctive form of polymorphic
 ventricular tachycardia characterized by a gradual change in the
 amplitude and twisting of the QRS complexes around the isoelectric
 line. Rate cannot be determined.
RHYTHM


Supraventricular Tachycardia




SVT is any tachycardiac rhythm originating above the ventricular tissue.
Atrial and ventricular rate= 150-250bpm
Regular rhythm, p is usually not discernable.

*Types:
    •Sinoatrial node reentrant tachycardia (SANRT)
    •Ectopic (unifocal) atrial tachycardia (EAT)
    •Multifocal atrial tachycardia (MAT)
    •A-fib or A flutter with rapid ventricular response. Without rapid ventricular
    response both usually not classified as SVT
    •AV nodal reentrant tachycardia (AVNRT)
    •Permanent (or persistent) junctional reciprocating tachycardia (PJRT)
    •AV reentrant tachycardia (AVRT)
RHYTHM




Atrial Escape




 a cardiac dysrhythmia occurring when sustained suppression of sinus
 impulse formation causes other atrial foci to act as cardiac pacemakers.
 Rate= 60-80bpm, p wave of atrial escape has abnormal axis and different
 from the p wave in the sinus beat. However QRS complexes look exactly
 the same.
RHYTHM



Junctional Escape




 Depolarization initiated in the atrioventricular junction when one or more
 impulses from the sinus node are ineffective or nonexistent. Rate: 40-60
 bpm, Rhythm: Irregular in single junctional escape complex; regular in
 junctional escape rhythm, P waves: Depends on the site of the ectopic
 focus. They will be inverted, and may appear before or after the QRS
 complex, or they may be absent, hidden by the QRS. QRS is usually
 normal
RHYTHM




Ventricular escape




 The depolarization wave spreads slowly via abnormal pathway in the
 ventricular myocardium and not via the His bundle and bundle
 branches.
RHYTHM




Atrial premature beat (APB)




 Arises from an irritable focus in one of the atria. APB produces different
 looking P wave, because depolarization vector is abnormal. QRS complex
 has normal duration and same morphology .
RHYTHM




Junctional Premature Beat




 Arises from an irritable focus at the AV junction. The P wave associated with
 atrial depolarization in this instance is usually buried inside the QRS complex
 and not visible. If p is visible, it is -ve in lead II and +ve in lead aVR and it it
 may occur before or after QRS.
RHYTHM




Premature Ventricular Complexes (PVCs)




 is a relatively common event where the heartbeat is initiated by the heart
 ventricles(arrow) rather than by the sinoatrial node, Rate depends on
 underlying rhythm and number of PVCs. Occasionally irregular rhythm,
 no p-wave associated with PVCs. May produce bizarre looking T wave.
RHYTHM




Asystole




 a state of no cardiac electrical activity, hence no contractions of the
 myocardium and no cardiac output or blood flow.
 Rate, rhythm, p and QRS are absent
RHYTHM




Pulseless Electrical Activity (PEA)




 Not an actual rhythm. The absence of a palpable pulse and myocardial
 muscle activity with the presence of organized muscle activity (excluding
 VT and VF) on cardiac monitor. Pt is clinically dead.
RHYTHM




   Artificial pacemaker




    Sharp, thin spike. Rate depends on pacemaker, p wave
    maybe absent or present
    Ventricular paced rhythm shows wide ventricular pacemaker
    spikes
Basics of ECG
CARDIAC AXIS
CARDIAC AXIS
The cardiac axis refers to the general direction of the heart's depolarization wavefront
(or mean electrical vector) in the frontal plane. With a healthy conducting system the
cardiac axis is related to where the major muscle bulk of the heart lies.




                     Electrical impulse that travels towards the electrode produces an
                     upright (positive) deflection (of the QRS complex) relative to the
                     isoelectric baseline. One that travels away produces negative
                     deflection. And one that travels at a right angle to the lead,
                     produces a biphasic wave.
CARDIAC AXIS

    To determine cardiac axis look at QRS complexes of lead , II, III.
     Axis           Lead I             Lead II             Lead III
     Normal         Positive           Positive            Positive/Negative
     Right axis     Negative           Positive            Positive
     deviation
     Left axis      Positive           Negative            Negative
     deviation
     Remember, positive(upgoing) QRS omplex means the impulse travels towards
                      the lead. Negative means moving away.
CARDIAC AXIS




Positive



Positive



Positive




                 Normal Axis Deviation
CARDIAC AXIS




Positive



Negative



Negative




                  Left Axis Deviation
CARDIAC AXIS




 Negative


 Positive



 Positive




               Right Axis Deviation
CARDIAC AXIS




    Cardiac Axis                             Causes
Left axis deviation    Normal variation in pregnancy, obesity; Ascites,
                       abdominal distention, tumour; left anterior
                       hemiblock, left ventricular hypertrophy, Q Wolff-
                       Parkinson-White syndrome, Inferior MI

Right axis deviation   normal finding in children and tall thin adults,
                       chronic lung disease(COPD), left posterior
                       hemiblock, Wolff-Parkinson-White syndrome,
                       anterolateral MI.
North West             emphysema, hyperkalaemia. lead transposition,
                       artificial cardiac pacing, ventricular tachycardia
P- WAVE
P -WAVE




          Normal P- wave
          3 small square wide, and 2.5 small square high.
          Always positive in lead I and II in NSR
          Always negative in lead aVR in NSR
          Commonly biphasic in lead V1
P -WAVE

          P pulmonale
          Tall peaked P wave. Generally due to enlarged
          right atrium- commonly associated with congenital
          heart disease, tricuspid valve disease, pulmonary
          hypertension and diffuse lung disease.




          Biphasic P wave
          Its terminal negative deflection more than 40 ms
          wide and more than 1 mm deep is an ECG sign of
          left atrial enlargement.




          P mitrale
          Wide P wave, often bifid, may be due to mitral
          stenosis or left atrial enlargement.
PR- INTERVAL
PR INTERVAL

                  NORMAL PR INTERVAL




                                                     Long PR interval
                                                     may indicate heart
                                                     block

                                                     Short PR interval
                                                     may disease like
                                                     Wolf-Parkinson-
          PR-Interval 3-5 small square (120-200ms)   White
PR-INTERVAL


First degree heart block




 P wave precedes QRS complex but P-R intervals prolong (>5 small
 squares) and remain constant from beat to beat
PR-INTERVAL


Second degree heart block


 1. Mobitz Type I or Wenckenbach




 Runs in cycle, first P-R interval is often normal. With successive beat, P-R
 interval lengthens until there will be a P wave with no following QRS complex.
 The block is at AV node, often transient, maybe asymptomatic
PR-INTERVAL


Second degree heart block


 2. Mobitz Type 2




 P-R interval is constant, duration is normal/prolonged. Periodically, no
 conduction between atria and ventricles- producing a p wave with no
 associated QRS complex. (blocked p wave).
 The block is most often below AV node, at bundle of His or BB,
 May progress to third degree heart block
PR-INTERVAL


Third degree heart block (Complete heart block)




 No relationship between P waves and QRS complexes
 An accessory pacemaker in the lower chambers will typically activate
 the ventricles- escape rhythm.
 Atrial rate= 60-100bpm. Ventricular rate based on site of escape
 pacemaker. Atrial and ventricular rhythm both are regular.
PR-INTERVAL

Wolff–Parkinson–White syndrome

                                 Wolf Parkinson White Syndrome
                                 One beat from a rhythm strip in V2
                                 demonstrating characteristic findings in
                                 WPW syndrome. Note the characteristic
                                 delta wave (above the blue bar), the short
                                 PR interval (red bar) of 0.08 seconds, and
                                 the long QRS complex (green) at 0.12
                                 seconds


                                 Accessory pathway (Bundle of Kent)
                                 allows early activation of the ventricle
                                 (delta wave and short PR interval)
QRS-COMPLEX
QRS COMPLEX

                        NORMAL QRS COMPLEX


                                                 S amplitude in V1 + R
                                                 amplitude in V5 < 3.5
Q wave amplitude less than                       Increased amplitude
1/3 QRS amplitude(R+S) or                        indicated cardiac hypertrophy
< 1 small square




                 QRS complex< 3 small square (0.06 - 0.10 sec)
                  Prolonged indicates hyperkalemia or
                  bundle branch block
QRS COMPLEX

Left Bundle Branch Block (LBBB)                     Right bundle branch block (RBBB)
indirect activation causes left ventricle contracts indirect activation causes right ventricle
later than the right ventricle.                     contracts later than the left ventricle

QS or rS complex in V1 - W-shaped                   Terminal R wave (rSR’) in V1 - M-shaped
RsR' wave in V6- M-shaped                           Slurred S wave in V6 - W-shaped




Mnemonic: WILLIAM                                   Mnemonic: MARROW
ST- SEGMENT
ST SEGMENT

                      NORMAL ST SEGMENT




                                               ST segment is isoelectric
                                               and at the same level as
                                               subsequent PR-interval




ST segment < 2-3 small square (80 to 120 ms)
ST SEGMENT

                    OK, WE GONNA TALK ABOUT
                   MYOCARDIAL INFARCTION (MI)


                   THERE ARE 2 TYPES OF MI


 ST-ELEVATION MI (STEMI)        AND        NON ST-ELEVATION MI (NSTEMI)



    WE DECIDE THIS BY LOOKING AT THE ST SEGMENT IN ALL LEADS


                           Flat (isoelectric) ± Same level with subsequent PR
                           segment
  NORMAL
ST SEGMENT                 Elevation or depression of ST segment by 1 mm or
                           more, measured at J point is abnormal.
                           J point is the point between QRS and ST segment
Ischaemic change can be attributed to
         ST-SEGMENT
                                                    different coronary arteries supplying the
                                                    area.
Localizing MI
                                                    Location of Lead with  Affected
Look at ST changes, Q wave in all leads. Grouping
                                                    MI          ST changes coronary
the leads into anatomical location, we have this:
                                                                           artery
    I            aVR     V1         V4              Anterior       V1, V2, V3,    LAD
                                                                   V4
   II            aVL    V2         V5               Septum         V1, V2         LAD

   III           aVF    V3         V6               left lateral   I, aVL, V5,    Left
                                                                   V6             circumflex
                                                    inferior       II, III, aVF   RCA

                                                    Right atrium aVR, V1          RCA

                                                    *Posterior     Posterior      RCA
                                                                   chest leads
         (RCA)
                                                    *Right         Right sided    RCA
                                                    ventricle      leads

                                  (LAD)
                                                    *To help identify MI, right sided and
                                                    posterior leads can be applied
DIAGNOSING MYOCARDIAL INFARCTION (STEMI)

                                      Criteria:
                                      ST elevation in > 2 chest leads > 2mm elevation
                                      ST elevation in > 2 limb leads > 1mm elevation
                                      Q wave > 0.04s (1 small square).


                                    *Be careful of LBBB
                                    The diagnosis of acute myocardial infarction should be
                                    made circumspectively in the presence of pre-existing
                                    LBBB. On the other hand, the appearance of new LBBB
                                    should be regarded as sign of acute MI until proven
                                    otherwise

     Pathologic Q waves are a sign of previous myocardial infarction.

Definition of a pathologic Q wave
Any Q-wave in leads V2–V3 ≥ 0.02 s or QS complex in leads V2 and V3
Q-wave ≥ 0.03 s and > 0.1 mV deep or QS complex in leads I, II, aVL, aVF, or V4–V6 in any two
       leads of a contiguous lead grouping (I, aVL,V6; V4–V6; II, III, and aVF)
R-wave ≥ 0.04 s in V1–V2 and R/S ≥ 1 with a concordant positive T-wave in the absence of a
       conduction defect.
A little bit troublesome to remember? I usually take pathological Q wave as >1 small square deep
ST SEGMENT

ST-ELEVATION MI (STEMI)
  0 HOUR                  Pronounced T Wave initially
                          ST elevation (convex type)



                          Depressed R Wave, and Pronounced T Wave. Pathological Q waves
  1-24H                   may appear within hours or may take greater than 24 hr.- indicating full-
                          thickness MI. Q wave is pathological if it is wider than 40 ms or deeper
                          than a third of the height of the entire QRS complex


  Day 1-2                 Exaggeration of T Wave continues for 24h.




  Days later               T Wave inverts as the ST elevation begins to resolve. Persistent ST
                           elevation is rare except in the presence of a ventricular aneurysm.



  Weeks later              ECG returns to normal T wave, but retains
                           pronounced Q wave. An old infarct may look like this
ST SEGMENT

Let’s see this




                                               >2mm




                                                   Pathological Q wave
   Check again!
      I          aVR   V1        ST elevation in > 2 chest leads > 2mm
                            V4
                                 Q wave > 0.04s (1 small square).
     II          aVL   V2   V5
                                      Yup, It’s acute
                                      anterolateral MI!
     III         aVF   V3   V6
ST SEGMENT


How about this one?




 Check again!
    I       aVR       V1   V4
                                Inferior MI!
   II       aVL       V2   V5

   III      aVF       V3   V6
ST SEGMENT


NON ST-ELEVATION MI (NSTEMI)
NSTEMI is also known as subendocardial or non Q-wave MI.
In a pt with Acute Coronary Syndrome (ACS) in which the ECG does not show ST
elevation, NSTEMI (subendocardial MI) is suspected if

              •ST Depression (A)
              •T wave inversion with or without ST depression (B)
              •Q wave and ST elevation will never happen




                  To confirm a NSTEMI, do Troponin test:
                      •If positive - NSTEMI
                      •If negative – unstable angina pectoris
ST SEGMENT


NON ST-ELEVATION MI (NSTEMI)




   N-STEMI: acute coronary syndrome (with troponin increase). Arrows
   indicate ischemic ST segment changes. Without appropriate treatment
   in many cases STEMI infarction will occur.
ST SEGMENT

                            MYOCARDIAL ISCHEMIA
                            1mm ST-segment depression
                            Symmetrical, tall T wave
                            Long QT- interval

A ST depression is more suggestive of myocardial ischaemia than infarction
ST SEGMENT



             PERICARDITIS
             ST elevation with
             concave shape, mostly
             seen in all leads
ST SEGMENT



             DIGOXIN
             Down sloping ST segment depression
             also known as the "reverse tick" or
             "reverse check" sign in
             supratherapeutic digoxin level.
ST SEGMENT

                          Now, moving to




LEFT VENTRICULAR               AND
                                           RIGHT VENTRICULAR
HYPERTROPHY                                HYPERTROPHY

        So, we have to start looking at the S waves and R waves
ST SEGMENT

Left ventricular hypertrophy (LVH)
To determine LVH, use one of the following Criteria:
  Sokolow & Lyon Criteria: S (V1) + R(V5 or V6) > 35mm
  Cornell Criteria: S (V3) + R (aVL) > 28 mm (men) or > 20 mm (women)
  Others: R (aVL) > 13mm
   Example:




               S (V1) + R(V5) = 15 + 25 = 40mm
               S(V3) + R (aVL)= 15 + 14 =29mm
               R(aVL) =14 mm                           LVH!
ST SEGMENT


Let’s see another example of LVH




                                                                  LVH strain pattern




 Tall R waves in V4 and V5 with down sloping ST segment depression and T
 wave inversion are suggestive of left ventricular hypertrophy (LVH) with strain
 pattern. LVH with strain pattern usually occurs in pressure overload of the left
 ventricle as in systemic hypertension or aortic stenosis.
ST SEGMENT

Right ventricular hypertrophy (RVH)
                 Right axis deviation (QRS axis >100o)
                           V1(R>S), V6 (S>R)
                Right ventricular strain T wave inversion

Example:




                           So, it’s RVH!
ST SEGMENT



               Common Causes of LVH and RVH


                LVH                                  RVH
  Hypertension (most common cause)   Pulmonary hypertension
  Aortic stenosis                    Tetralogy of Fallot
  Aortic regurgitation               Pulmonary valve stenosis
  Mitral regurgitation               Ventricular septal defect (VSD)
  Coarctation of the aorta           High altitude
  Hypertrophic cardiomyopathy        Cardiac fibrosis
                                     COPD
                                     Athletic heart syndrome
QT- INTERVAL
QT- INTERVAL

QT interval decreases when heart rate increases.
A general guide to the upper limit of QT interval. For HR = 70 bpm, QT<0.40 sec.
    •For every 10 bpm increase above 70 subtract 0.02s.
    •For every 10 bpm decrease below 70 add 0.02 s

As a general guide the QT interval should be 0.35- 0.45 s,(<2 large square) and
should not be more than half of the interval between adjacent R waves (R-R
interval)




:




                                 < 2 large square
Calculation of QT interval

 1.Use lead II. Use lead V5 alternatively if lead II cannot be read.
 2.Draw a line through the baseline (preferably the PR segment)
 3.Draw a tangent against the steepest part of the end of the T wave. If the T
 wave has two positive deflections, the taller deflection should be chosen. If the
 T wave is biphasic, the end of the taller deflection should be chosen.
 4.The QT interval starts at the beginning of the QRS interval and ends where
 the tangent and baseline cross.
 5.If the QRS duration exceeds 120ms the amount surpassing ,120ms should be
 deducted from the QT interval (i.e. QT=QT-(QRS width-120ms) )

To calculate the heart rate-corrected QT interval QTc. Bazett's formula is used
QT = 0.04 x 10 small square= 0.4s
                       18 small square
                                                     RR = 0.04 x 18 small square= 0.72s




             10 small square



If abnormally prolonged or shortened, there is a risk of developing ventricular
arrhythmias
The QT interval is prolonged in congenital long QT syndrome, but QT
prolongation can also occur as a consequence of
     •Medication (anti-arrhythmics, tricyclic antidepressants, phenothiazedes)
     •Electrolyte imbalances
     •Ischemia.
QT prolongation is often treated with beta blockers.
LONG QT SYNDROME


LQT is a rare inborn heart condition in
which repolarization of the heart is delayed
following a heartbeat. Example: Jervell and
Lange-Nielsen Syndrome or Romano-Ward
Syndrome




T-WAVE

Normal T wave
Asymmetrical, the first half having more gradual slope
than the second half
>1/8 and < 2/3 of the amplitude of corresponding R wave
Amplitude rarely exceeds 10mm
Abnormal T waves are symmetrical, tall, peaked, biphasic,
or inverted.
U-WAVE

The U wave is a wave on an electrocardiogram that is not always seen. It is
typically small, and, by definition, follows the T wave. U waves are thought to
represent repolarization of the papillary muscles or Purkinje fibers

Normal U waves are small, round and symmetrical and positive in lead II. It is
the same direction as T wave in that lead.




  Prominent U waves are most often seen in hypokalemia, but may be present
  in hypercalcemia, thyrotoxicosis, or exposure to digitalis,epinephrine, and Class 1A and
  3 antiarrhythmics, as well as in congenital long QT syndrome, and in the setting of
  intracranial hemorrhage.
  An inverted U wave may represent myocardial ischemia or left ventricular volume overload
OTHER ECG SIGNS
HYPERKALAEMIA




Narrow and tall peaked T wave (A) is an early sign
PR interval becomes longer
P wave loses its amplitude and may disappear
QRS complex widens (B)
When hyperkalemia is very severe, the widened QRS complexes merge with their
corresponding T waves and the resultant ECG looks like a series of sine waves (C).
If untreated, the heart arrests in asystole


HYPOKALAEMIA

                 T wave becomes flattened together with appearance of a prominent U
                 wave.
                 The ST segment may become depressed and the T wave inverted.
                 these additional changes are not related to the degree of hypokalemia.
HYPERCALCEMIA/HYPOCALCEMIA




Usually, signs are not obvious
Hypercalcemia is associated with short QT interval (A) and
Hypocalcemia with long QT interval (B).
Interval shortening or lengthening is mainly in the ST segment.
PULMONARY EMBOLISM




Tachycardia and incomplete RBBB differentiated PE from no PE.
SIQIIITIII = deep S wave in lead I, pathological Q wave in lead III, and inverted
T wave in lead III.
The ECG is often abnormal in PE, but findings are not sensitive, not specific
Any cause of acute cor pulmonale can cause the S1Q3T3 finding on the ECG.
Thanks for your
  attention!
 Now, find some ECG practice!

Más contenido relacionado

La actualidad más candente

La actualidad más candente (20)

Left Bundle Branch Block (LBBB)
Left Bundle Branch Block (LBBB)Left Bundle Branch Block (LBBB)
Left Bundle Branch Block (LBBB)
 
Ecg for beginners
Ecg for beginnersEcg for beginners
Ecg for beginners
 
Ventricular tachycardia
Ventricular tachycardiaVentricular tachycardia
Ventricular tachycardia
 
Electrophysiologic Study
Electrophysiologic StudyElectrophysiologic Study
Electrophysiologic Study
 
Basics of ecg
Basics of ecgBasics of ecg
Basics of ecg
 
Holter
HolterHolter
Holter
 
Treadmill test (TMT)
Treadmill test (TMT)Treadmill test (TMT)
Treadmill test (TMT)
 
Shortcut to ECG
Shortcut to ECGShortcut to ECG
Shortcut to ECG
 
Stroke volume and cardiac output
Stroke volume and cardiac outputStroke volume and cardiac output
Stroke volume and cardiac output
 
Atrial Flutter
Atrial FlutterAtrial Flutter
Atrial Flutter
 
Stress echocardiography
Stress echocardiographyStress echocardiography
Stress echocardiography
 
Pacemaker basics
Pacemaker basicsPacemaker basics
Pacemaker basics
 
Stress echocardiography/Dobutamine stress echocardiography
Stress echocardiography/Dobutamine stress echocardiographyStress echocardiography/Dobutamine stress echocardiography
Stress echocardiography/Dobutamine stress echocardiography
 
Basics of ecg interpretation by dr sai
Basics of ecg interpretation by dr saiBasics of ecg interpretation by dr sai
Basics of ecg interpretation by dr sai
 
ECG ARTIFACTS AND PITFALLS
ECG ARTIFACTS AND PITFALLS  ECG ARTIFACTS AND PITFALLS
ECG ARTIFACTS AND PITFALLS
 
Tmt protocol
Tmt protocolTmt protocol
Tmt protocol
 
Cardiac resynchronization therapy
Cardiac resynchronization therapyCardiac resynchronization therapy
Cardiac resynchronization therapy
 
Bundle branch blocks by Dr Sujith Chadala
Bundle branch blocks by Dr Sujith ChadalaBundle branch blocks by Dr Sujith Chadala
Bundle branch blocks by Dr Sujith Chadala
 
ECG, step by step approach (Updated)
ECG, step by step approach (Updated)ECG, step by step approach (Updated)
ECG, step by step approach (Updated)
 
Basic pacing concepts
Basic pacing conceptsBasic pacing concepts
Basic pacing concepts
 

Similar a Basics of ECG (20)

ECG1.pptx
ECG1.pptxECG1.pptx
ECG1.pptx
 
BASICS OF ECG pptx.pptx
BASICS OF ECG pptx.pptxBASICS OF ECG pptx.pptx
BASICS OF ECG pptx.pptx
 
ECG
ECGECG
ECG
 
Electrocardiogram
ElectrocardiogramElectrocardiogram
Electrocardiogram
 
ECG
ECGECG
ECG
 
Electrocardiography (ecg)
Electrocardiography (ecg)Electrocardiography (ecg)
Electrocardiography (ecg)
 
ECG Basics 1.pptx
ECG Basics 1.pptxECG Basics 1.pptx
ECG Basics 1.pptx
 
ecg machine
ecg machineecg machine
ecg machine
 
Basics of electrocardiogram
Basics of electrocardiogramBasics of electrocardiogram
Basics of electrocardiogram
 
Ecg lecture
Ecg lectureEcg lecture
Ecg lecture
 
Apps of electrostatistics
Apps of electrostatisticsApps of electrostatistics
Apps of electrostatistics
 
Defibrillation
DefibrillationDefibrillation
Defibrillation
 
8101222.ppt
8101222.ppt8101222.ppt
8101222.ppt
 
Fundamentals of Electrocardiography
Fundamentals of Electrocardiography Fundamentals of Electrocardiography
Fundamentals of Electrocardiography
 
Electrophysiology of heart
Electrophysiology of heartElectrophysiology of heart
Electrophysiology of heart
 
BASICS OF ECG.pptx
BASICS OF ECG.pptxBASICS OF ECG.pptx
BASICS OF ECG.pptx
 
basics of ecg
 basics of ecg basics of ecg
basics of ecg
 
IVMS-CV-Basic Electrocardiography Notes
IVMS-CV-Basic Electrocardiography NotesIVMS-CV-Basic Electrocardiography Notes
IVMS-CV-Basic Electrocardiography Notes
 
Electrocardiography
ElectrocardiographyElectrocardiography
Electrocardiography
 
ECG [electrocardiogram].pptx
ECG [electrocardiogram].pptxECG [electrocardiogram].pptx
ECG [electrocardiogram].pptx
 

Más de Dr. Sreedhar Rao

academicperformanceindicatorsapi-190123081235.pdf
academicperformanceindicatorsapi-190123081235.pdfacademicperformanceindicatorsapi-190123081235.pdf
academicperformanceindicatorsapi-190123081235.pdfDr. Sreedhar Rao
 
Assessment & Accreditation Process of NAAC in Revised Accreditation Framework...
Assessment & Accreditation Process of NAAC in Revised Accreditation Framework...Assessment & Accreditation Process of NAAC in Revised Accreditation Framework...
Assessment & Accreditation Process of NAAC in Revised Accreditation Framework...Dr. Sreedhar Rao
 
CCIM Regulation 18 July 2012
CCIM Regulation 18 July 2012CCIM Regulation 18 July 2012
CCIM Regulation 18 July 2012Dr. Sreedhar Rao
 
AYUSH-Report of Steering Committee on AYUSH for 12th Five Year Plan
AYUSH-Report of Steering Committee on AYUSH for 12th Five Year PlanAYUSH-Report of Steering Committee on AYUSH for 12th Five Year Plan
AYUSH-Report of Steering Committee on AYUSH for 12th Five Year PlanDr. Sreedhar Rao
 
AYUSH Funding Opportunities
AYUSH Funding OpportunitiesAYUSH Funding Opportunities
AYUSH Funding OpportunitiesDr. Sreedhar Rao
 
Fundamentals of chest radiology
Fundamentals of chest radiologyFundamentals of chest radiology
Fundamentals of chest radiologyDr. Sreedhar Rao
 

Más de Dr. Sreedhar Rao (10)

Ethical Guidelines.pptx
Ethical Guidelines.pptxEthical Guidelines.pptx
Ethical Guidelines.pptx
 
academicperformanceindicatorsapi-190123081235.pdf
academicperformanceindicatorsapi-190123081235.pdfacademicperformanceindicatorsapi-190123081235.pdf
academicperformanceindicatorsapi-190123081235.pdf
 
Assessment & Accreditation Process of NAAC in Revised Accreditation Framework...
Assessment & Accreditation Process of NAAC in Revised Accreditation Framework...Assessment & Accreditation Process of NAAC in Revised Accreditation Framework...
Assessment & Accreditation Process of NAAC in Revised Accreditation Framework...
 
CCIM Regulation 18 July 2012
CCIM Regulation 18 July 2012CCIM Regulation 18 July 2012
CCIM Regulation 18 July 2012
 
AYUSH-Report of Steering Committee on AYUSH for 12th Five Year Plan
AYUSH-Report of Steering Committee on AYUSH for 12th Five Year PlanAYUSH-Report of Steering Committee on AYUSH for 12th Five Year Plan
AYUSH-Report of Steering Committee on AYUSH for 12th Five Year Plan
 
AYUSH Funding Opportunities
AYUSH Funding OpportunitiesAYUSH Funding Opportunities
AYUSH Funding Opportunities
 
Basics of Ultrasound
Basics of UltrasoundBasics of Ultrasound
Basics of Ultrasound
 
Basics of MRI
Basics of MRIBasics of MRI
Basics of MRI
 
Basics of CT Scan
Basics of CT ScanBasics of CT Scan
Basics of CT Scan
 
Fundamentals of chest radiology
Fundamentals of chest radiologyFundamentals of chest radiology
Fundamentals of chest radiology
 

Último

Employability skills, work experience presentation
Employability skills, work experience presentationEmployability skills, work experience presentation
Employability skills, work experience presentationmarwaahmad357
 
AI in Action: Elevating Patient Insights
AI in Action: Elevating Patient InsightsAI in Action: Elevating Patient Insights
AI in Action: Elevating Patient InsightsEmily Kunka, MS, CCRP
 
Pharmacokinetic Models by Dr. Ram D. Bawankar.ppt
Pharmacokinetic Models by Dr. Ram D.  Bawankar.pptPharmacokinetic Models by Dr. Ram D.  Bawankar.ppt
Pharmacokinetic Models by Dr. Ram D. Bawankar.pptRamDBawankar1
 
Adenomyosis or Fibroid- making right diagnosis
Adenomyosis or Fibroid- making right diagnosisAdenomyosis or Fibroid- making right diagnosis
Adenomyosis or Fibroid- making right diagnosisSujoy Dasgupta
 
Trustworthiness of AI based predictions Aachen 2024
Trustworthiness of AI based predictions Aachen 2024Trustworthiness of AI based predictions Aachen 2024
Trustworthiness of AI based predictions Aachen 2024EwoutSteyerberg1
 
Different drug regularity bodies in different countries.
Different drug regularity bodies in different countries.Different drug regularity bodies in different countries.
Different drug regularity bodies in different countries.kishan singh tomar
 
Transport across cell membrane (passive, active, vesicular)
Transport across cell membrane (passive, active, vesicular)Transport across cell membrane (passive, active, vesicular)
Transport across cell membrane (passive, active, vesicular)MedicoseAcademics
 
Role of Soap based and synthetic or syndets bar
Role of  Soap based and synthetic or syndets barRole of  Soap based and synthetic or syndets bar
Role of Soap based and synthetic or syndets barmohitRahangdale
 
Basic structure of hair and hair growth cycle.pptx
Basic structure of hair and hair growth cycle.pptxBasic structure of hair and hair growth cycle.pptx
Basic structure of hair and hair growth cycle.pptxkomalt2001
 
CPR.nursingoutlook.pdf , Bsc nursing student
CPR.nursingoutlook.pdf , Bsc nursing studentCPR.nursingoutlook.pdf , Bsc nursing student
CPR.nursingoutlook.pdf , Bsc nursing studentsaileshpanda05
 
ayurvedic formulations herbal drug technologyppt
ayurvedic formulations herbal drug technologypptayurvedic formulations herbal drug technologyppt
ayurvedic formulations herbal drug technologypptPradnya Wadekar
 
Generative AI in Health Care a scoping review and a persoanl experience.
Generative AI in Health Care a scoping review and a persoanl experience.Generative AI in Health Care a scoping review and a persoanl experience.
Generative AI in Health Care a scoping review and a persoanl experience.Vaikunthan Rajaratnam
 
Physiology of Smooth Muscles -Mechanics of contraction and relaxation
Physiology of Smooth Muscles -Mechanics of contraction and relaxationPhysiology of Smooth Muscles -Mechanics of contraction and relaxation
Physiology of Smooth Muscles -Mechanics of contraction and relaxationMedicoseAcademics
 
Understanding AIDS:a roadmap to well ess
Understanding AIDS:a roadmap to well essUnderstanding AIDS:a roadmap to well ess
Understanding AIDS:a roadmap to well essAbhishekKumar524514
 
blood bank management system project report
blood bank management system project reportblood bank management system project report
blood bank management system project reportNARMADAPETROLEUMGAS
 
Arthroscopic Surgery in Indore : A Minimally Invasive Guide to Joint Health
Arthroscopic Surgery in Indore : A Minimally Invasive Guide to Joint HealthArthroscopic Surgery in Indore : A Minimally Invasive Guide to Joint Health
Arthroscopic Surgery in Indore : A Minimally Invasive Guide to Joint HealthGokuldas Hospital
 
CONNECTIVE TISSUE (ANATOMY AND PHYSIOLOGY).pdf
CONNECTIVE TISSUE (ANATOMY AND PHYSIOLOGY).pdfCONNECTIVE TISSUE (ANATOMY AND PHYSIOLOGY).pdf
CONNECTIVE TISSUE (ANATOMY AND PHYSIOLOGY).pdfDolisha Warbi
 

Último (20)

Employability skills, work experience presentation
Employability skills, work experience presentationEmployability skills, work experience presentation
Employability skills, work experience presentation
 
AI in Action: Elevating Patient Insights
AI in Action: Elevating Patient InsightsAI in Action: Elevating Patient Insights
AI in Action: Elevating Patient Insights
 
Pharmacokinetic Models by Dr. Ram D. Bawankar.ppt
Pharmacokinetic Models by Dr. Ram D.  Bawankar.pptPharmacokinetic Models by Dr. Ram D.  Bawankar.ppt
Pharmacokinetic Models by Dr. Ram D. Bawankar.ppt
 
Adenomyosis or Fibroid- making right diagnosis
Adenomyosis or Fibroid- making right diagnosisAdenomyosis or Fibroid- making right diagnosis
Adenomyosis or Fibroid- making right diagnosis
 
Trustworthiness of AI based predictions Aachen 2024
Trustworthiness of AI based predictions Aachen 2024Trustworthiness of AI based predictions Aachen 2024
Trustworthiness of AI based predictions Aachen 2024
 
Different drug regularity bodies in different countries.
Different drug regularity bodies in different countries.Different drug regularity bodies in different countries.
Different drug regularity bodies in different countries.
 
Transport across cell membrane (passive, active, vesicular)
Transport across cell membrane (passive, active, vesicular)Transport across cell membrane (passive, active, vesicular)
Transport across cell membrane (passive, active, vesicular)
 
How to master Steroid (glucocorticoids) prescription, different scenarios, ca...
How to master Steroid (glucocorticoids) prescription, different scenarios, ca...How to master Steroid (glucocorticoids) prescription, different scenarios, ca...
How to master Steroid (glucocorticoids) prescription, different scenarios, ca...
 
Role of Soap based and synthetic or syndets bar
Role of  Soap based and synthetic or syndets barRole of  Soap based and synthetic or syndets bar
Role of Soap based and synthetic or syndets bar
 
Basic structure of hair and hair growth cycle.pptx
Basic structure of hair and hair growth cycle.pptxBasic structure of hair and hair growth cycle.pptx
Basic structure of hair and hair growth cycle.pptx
 
CPR.nursingoutlook.pdf , Bsc nursing student
CPR.nursingoutlook.pdf , Bsc nursing studentCPR.nursingoutlook.pdf , Bsc nursing student
CPR.nursingoutlook.pdf , Bsc nursing student
 
GOUT UPDATE AHMED YEHIA 2024, case based approach with application of the lat...
GOUT UPDATE AHMED YEHIA 2024, case based approach with application of the lat...GOUT UPDATE AHMED YEHIA 2024, case based approach with application of the lat...
GOUT UPDATE AHMED YEHIA 2024, case based approach with application of the lat...
 
ayurvedic formulations herbal drug technologyppt
ayurvedic formulations herbal drug technologypptayurvedic formulations herbal drug technologyppt
ayurvedic formulations herbal drug technologyppt
 
Generative AI in Health Care a scoping review and a persoanl experience.
Generative AI in Health Care a scoping review and a persoanl experience.Generative AI in Health Care a scoping review and a persoanl experience.
Generative AI in Health Care a scoping review and a persoanl experience.
 
Physiology of Smooth Muscles -Mechanics of contraction and relaxation
Physiology of Smooth Muscles -Mechanics of contraction and relaxationPhysiology of Smooth Muscles -Mechanics of contraction and relaxation
Physiology of Smooth Muscles -Mechanics of contraction and relaxation
 
American College of physicians ACP high value care recommendations in rheumat...
American College of physicians ACP high value care recommendations in rheumat...American College of physicians ACP high value care recommendations in rheumat...
American College of physicians ACP high value care recommendations in rheumat...
 
Understanding AIDS:a roadmap to well ess
Understanding AIDS:a roadmap to well essUnderstanding AIDS:a roadmap to well ess
Understanding AIDS:a roadmap to well ess
 
blood bank management system project report
blood bank management system project reportblood bank management system project report
blood bank management system project report
 
Arthroscopic Surgery in Indore : A Minimally Invasive Guide to Joint Health
Arthroscopic Surgery in Indore : A Minimally Invasive Guide to Joint HealthArthroscopic Surgery in Indore : A Minimally Invasive Guide to Joint Health
Arthroscopic Surgery in Indore : A Minimally Invasive Guide to Joint Health
 
CONNECTIVE TISSUE (ANATOMY AND PHYSIOLOGY).pdf
CONNECTIVE TISSUE (ANATOMY AND PHYSIOLOGY).pdfCONNECTIVE TISSUE (ANATOMY AND PHYSIOLOGY).pdf
CONNECTIVE TISSUE (ANATOMY AND PHYSIOLOGY).pdf
 

Basics of ECG

  • 1. Basics of ECG Dr. Sreedhar Rao MD(Rog Nidan), (Ph.D), MBA (Hospital Management) Asst. Professor, Dept. of Rog Nidan
  • 2. Module 1 - Objectives • Define ECG • Describe heart anatomy and circulation • Describe the fundamentals of heart electrophysiology
  • 3. What is ECG? • Electrocardiogram is the physical translation of the electrical phenomena created in the heart muscles.
  • 4. The graph paper recording produced by the machine is termed an electrocardiogram, It is usually called ECG or EKG STANDARD CALLIBRATION Speed = 25mm/s Amplitude = 0.1mV/mm 1mV à10mm high 1 large square à 0.2s(200ms) 1 small squareà 0.04s (40ms) or 1 mV amplitude
  • 5. With ECGs we can identify •Arrhythmias •Myocardial ischemia and infarction •Pericarditis •Chamber hypertrophy •Electrolyte disturbances (i.e. hyperkalemia, hypokalemia) •Drug toxicity (i.e. digoxin and drugs which prolong the QT interval)
  • 6. THE HISTORY OF ECG MACHINE 1903 NOW Willem Einthoven Modern ECG machine A Dutch has evolved into compact doctor and physiologist. electronic systems that often He invented the first include computerized practical electrocardiogram and interpretation of the received the Nobel Prize in electrocardiogram. Medicine in 1924 for it
  • 7. Basic Regions of the heart This is where the blood from the body enters
  • 8. Basic Regions of the heart The Triscuspid valve is a three- flap valve that lies between the right atrium and right ventricle
  • 9. Basic Regions of the heart This chamber empties its content into the pulmonary artery going to the lungs.
  • 10. Basic Regions of the heart This chamber empties its content into the pulmonary artery going to the lungs.
  • 11. Basic Structures inside the heart Pulmonary artery carries blood to the lungs
  • 12. Basic Regions of the heart Thicker heart muscles of the left than the right ventricle due to greater force needed to circulate blood.
  • 13. Basic Regions of the heart Pulmonary veins carries blood back to the heart.
  • 14. Basic Structures inside the heart Mitral Valve prevents the reflux of its content back to the left atria.
  • 15. Basic Structures inside the heart The Aortic Valve is a 3-flap, semilunar valve that keeps the blood from coming back to the ventricles at diastole.
  • 16. Basic Regions of the heart The blood from the lungs return to the body after receiving oxygen through here.
  • 17. Basic Structures inside the heart The chordae tendinae is a fibrous cartilage like tissue that controls the mechanical movement of the valve.
  • 18. Basic Structures inside the heart The papillary muscles suspends the chordae tendinae.
  • 19. Basic Structures inside the heart The septum divides the heart into two. The right side receives the unoxygenated blood and the left side send the oxygenated blood to the periphery.
  • 20. The Basics of Electrophysiology In response to the stimulation to the Vagus nerve, the SA node genertes its own electrical conduction, normally, 60 -100 impulses per minute.
  • 21. The Basics of Electrophysiology From the SA node the electrical conduction will travel through a nodal pathway. That is Anterior, Middle, and Posterior Internodal pathway
  • 22. The Basics of Electrophysiology Bachmann bundle is the SA node pathway that stimulates the left atrium.
  • 23. The Basics of Electrophysiology The AV Node generates about 40-60 stimulations per minutes, if the SA node fails to function.
  • 24. The Basics of Electrophysiology The AV Bundle (also known as Bungle of His) branches into two main bundle.
  • 25. The Basics of Electrophysiology The Left and Right Bundle Branches then attach to the myocardial muscles through Purkinje fibers.
  • 26. Module 2 - Objectives Topic: ECG Calibration, Representation, • Describe how the electrophysiological property of the heart influences its mechanical activity. • Describe how ECG is calibrated. • Describe the ECG waveforms.
  • 27. Electrophysiology Property of the heart Electrical Cells – make up the cardiac conduction system. Properties: ü Automaticity – the ability to spontaneously generate and discharge an electric impulse. ü Excitability – the ability of the cell to respond to an electrical impulse ü Conductivity – the ability to transmit an electrical impulse from one cell to the next.
  • 28. Electrophysiology Property of the heart Myocardial cells – make up the muscular walls of the atrium and ventricles of the heart. ü Contractility – the ability of the cell to shorten and lengthen its fibers. ü Extensibility – the ability of the cell stretch
  • 29. HOW TO DO ELECTROCARDIOGRAPHY 1. Place the patient in a supine or semi-Fowler's position. If the patient cannot tolerate being flat, you can do the ECG in a more upright position. 2. Instruct the patient to place their arms down by their side and to relax their shoulders. 3. Make sure the patient's legs are uncrossed. 4. Remove any electrical devices, such as cell phones, away from Patient, supine position the patient as they may interfere with the machine. 5. If you're getting artifact in the limb leads, try having the patient sit on top of their hands. 6. Causes of artifact: patient movement, loose/defective electrodes/apparatus, improper grounding. An ECG with artifacts.
  • 30. Electrodes Usually consist of a conducting gel, embedded in the middle of a self-adhesive pad onto which cables clip. Ten electrodes are used for a 12-lead ECG. Placement of electrodes The limb electrodes RA - On the right arm, avoiding thick muscle LA – On the left arm this time. RL - On the right leg, lateral calf muscle LL - On the left leg this time.- The 6 chest electrodes V1 - Fourth intercostal space, right sternal border. V2 - Fourth intercostal space, left sternal border. V3 - Midway between V2 and V4. V4 - Fifth intercostal space, left midclavicular line. V5 - Level with V4, left anterior axillary line. V6 - Level with V4, left mid axillary line.
  • 32. PEOPLE USUALLY REFER THE ELECTRODES CABLES AS LEADS LEADS should be correctly defined as the tracing of the voltage DUDE, THAT’S difference between the electrodes and is CONFUSING! what is actually produced by the ECG recorder.
  • 33. SO, WHERE ARE THE LEADS?
  • 34. LEADS I, II, III THEY ARE FORMED BY VOLTAGE TRACINGS BETWEEN THE LIMB ELECTRODES (RA, LA, RL AND LL). THESE ARE THE ONLY BIPOLAR LEADS. ALL TOGETHER THEY ARE CALLED THE LIMB LEADS OR THE EINTHOVEN’S TRIANGLE RA I LA II III RL LL
  • 35. LEADS aVR, aVL, aVF THEY ARE ALSO DERIVED FROM THE LIMB ELECTRODES, THEY MEASURE THE ELECTRIC POTENTIAL AT ONE POINT WITH RESPECT TO A NULL POINT. THEY ARE THE AUGMENTED LIMB LEADS RA LA aVR aVL aVF RL LL
  • 36. LEADS V1,V2,V3,V4,V5,V6 THEY ARE PLACED DIRECTLY ON THE CHEST. BECAUSE OF THEIR CLOSE PROXIMITY OF THE HEART, THEY DO NOT REQUIRE AUGMENTATION. THEY ARE CALLED THE PRECORDIAL LEADS RA LA V1 V2 V3 V4 V6 V5 RL LL
  • 37. These leads help to determine heart’s electrical axis. The limb leads and the augmented limb leads form the frontal plane. The precordial leads form the horizontal plane.
  • 38. The Different Views Reflect The Angles At Which LEADS "LOOK" At The Heart And The Direction Of The Heart's Electrical Depolarization. Leads Anatomical representation of the heart V1, V2, V3, V4 Anterior I, aVL, V5, V6 left lateral II, III, aVF inferior aVR, V1 Right atrium
  • 39. ECG Calibration • Horizontally • One small box - 0.04 s • One large box - 0.20 s • Vertically • One large box - 0.5 mV
  • 41. A NORMAL ECG WAVE REMEMBER
  • 42. THE NORMAL SIZE <3 small square < 2 small square <3-5 small square < 2 large square
  • 43. ECG Representation P wave represents Atrial depolarization Vector is from SA node to AV node
  • 44. ECG Representation QRS Complex represents Ventricular depolarization Normal 0.06 to 0.10 seconds
  • 45. ECG Representation T wave represents Ventricular repolarization Vector is from SA node to AV node
  • 46. ECG Representation PR Interval 0.12 – 0.20 seconds Time for electrical impulse takes to travel from sinus node through the AV node and entering the ventricles
  • 47. ECG Representation QT Interval 0.32 – 0.40 seconds A prolonged QT interval is a risk factor for ventrial tachyarrhythmias and sudden death
  • 48. ECG Representation ST segment represents the early phase of ventricular repolarization It is Isoelectric
  • 50. Understanding ECG Waveform If a wavefront of depolarization travels towards the positive electrode, a positive-going deflection will result. If the waveform travels away from the positive electrode, a negative going deflection will be seen.
  • 51. ECG RULES • Professor Chamberlains 10 rules of normal:-
  • 52. RULE 1 PR interval should be 120 to 200 milliseconds or 3 to 5 little squares
  • 53. RULE 2 The width of the QRS complex should not exceed 110 ms, less than 3 little squares
  • 54. RULE 3 The QRS complex should be dominantly upright in leads I and II
  • 55. RULE 4 QRS and T waves tend to have the same general direction in the limb leads
  • 56. RULE 5 All waves are negative in lead aVR
  • 57. RULE 6 The R wave must grow from V1 to at least V4 The S wave must grow from V1 to at least V3 and disappear in V6
  • 58. RULE 7 The ST segment should start isoelectric except in V1 and V2 where it may be elevated
  • 59. RULE 8 The P waves should be upright in I, II, and V2 to V6
  • 60. RULE 9 There should be no Q wave or only a small q less than 0.04 seconds in width in I, II, V2 to V6
  • 61. RULE 10 The T wave must be upright in I, II, V2 to V6
  • 62. INTERPRETATION The More You See, The More You Know
  • 63. The best way to interpret an ECG is to do it step-by-step Rate Rhythm Cardiac Axis P – wave PR - interval QRS Complex ST Segment QT interval (Include T and U wave) Other ECG signs
  • 64. RATE
  • 65. CALCULATING RATE As a general interpretation, look at lead II at the bottom part of the ECG strip. This lead is the rhythm strip which shows the rhythm for the whole time the ECG is recorded. Look at the number of square between one R-R interval. To calculate rate, use any of the following formulas: 300 Rate = the number of BIG SQUARE between R-R interval OR 1500 Rate = the number of SMALL SQUARE between R-R interval
  • 66. CALCULATING RATE For example: 300 1500 Rate = or Rate = 3 15 Rate = 100 beats per minute
  • 67. CALCULATING RATE If you think that the rhythm is not regular, count the number of electrical beats in a 6-second strip and multiply that number by 10.(Note that some ECG strips have 3 seconds and 6 seconds marks) Example below: 1 2 3 4 5 6 7 8 There are 8 waves in this 6-seconds strip. Rate = (Number of waves in 6-second strips) x 10 = 8 x 10 = 80 bpm
  • 68. CALCULATING RATE You can also count the number of beats on any one row over the ten-second strip (the whole lenght) and multiply by 6. Example: Rate = (Number of waves in 10-second strips) x 6 = 13 x 6 = 78 bpm
  • 69. CALCULATING RATE Interpretation bpm Causes Normal 60-99 - Bradycardia <60 hypothermia, increased vagal tone (due to vagal stimulation or e.g. drugs), atheletes (fit people) hypothyroidism, beta blockade, marked intracranial hypertension, obstructive jaundice, and even in uraemia, structural SA node disease, or ischaemia. Tachycardia >100 Any cause of adrenergic stimulation (including pain); thyrotoxicosis; hypovolaemia; vagolytic drugs (e.g. atropine) anaemia, pregnancy; vasodilator drugs, including many hypotensive agents; FEVER, myocarditis
  • 71. RHYTHM Look at p waves and their relationship to QRS complexes. Lead II is commonly used Regular or irregular? If in doubt, use a paper strip to map out consecutive beats and see whether the rate is the same further along the ECG. Measure ventricular rhythm by measuring the R-R interval and atrial rhythm by measuring P-P interval.
  • 72. RHYTHM Normal Sinus Rhythm ECG rhythm characterized by a usual rate of anywhere between 60-99 bpm, every P wave must be followed by a QRS and every QRS is preceded by P wave. Normal duration of PR interval is 3-5 small squares. The P wave is upright in leads I and II
  • 73. RHYTHM Sinus Bradycardia Rate < 60bpm, otherwise normal
  • 74. RHYTHM Sinus Tachycardia Rate >100bpm, otherwise, normal
  • 75. RHYTHM Sinus pause In disease (e.g. sick sinus syndrome) the SA node can fail in its pacing function. If failure is brief and recovery is prompt, the result is only a missed beat (sinus pause). If recovery is delayed and no other focus assumes pacing function, cardiac arrest follows.
  • 76. RHYTHM Atrial Fibrillation A-fib is the most common cardiac arrhythmia involving atria. Rate= ~150bpm, irregularly irregular, baseline irregularity, no visible p waves, QRS occur irregularly with its length usually < 0.12s
  • 77. RHYTHM Atrial Flutter Atrial Rate=~300bpm, similar to A-fib, but have flutter waves, ECG baseline adapts ‘saw-toothed’ appearance’. Occurs with atrioventricular block (fixed degree), eg: 3 flutters to 1 QRS complex:
  • 78. RHYTHM Ventricular Fibrillation A severely abnormal heart rhythm (arrhythmia) that can be life-threatening. Emergency- requires Basic Life Support Rate cannot be discerned, rhythm unorganized
  • 79. RHYTHM Ventricular tachycardia fast heart rhythm, that originates in one of the ventricles- potentially life- threatening arrhythmia because it may lead to ventricular fibrillation, asystole, and sudden death. Rate=100-250bpm
  • 80. RHYTHM Torsades de Pointes literally meaning twisting of points, is a distinctive form of polymorphic ventricular tachycardia characterized by a gradual change in the amplitude and twisting of the QRS complexes around the isoelectric line. Rate cannot be determined.
  • 81. RHYTHM Supraventricular Tachycardia SVT is any tachycardiac rhythm originating above the ventricular tissue. Atrial and ventricular rate= 150-250bpm Regular rhythm, p is usually not discernable. *Types: •Sinoatrial node reentrant tachycardia (SANRT) •Ectopic (unifocal) atrial tachycardia (EAT) •Multifocal atrial tachycardia (MAT) •A-fib or A flutter with rapid ventricular response. Without rapid ventricular response both usually not classified as SVT •AV nodal reentrant tachycardia (AVNRT) •Permanent (or persistent) junctional reciprocating tachycardia (PJRT) •AV reentrant tachycardia (AVRT)
  • 82. RHYTHM Atrial Escape a cardiac dysrhythmia occurring when sustained suppression of sinus impulse formation causes other atrial foci to act as cardiac pacemakers. Rate= 60-80bpm, p wave of atrial escape has abnormal axis and different from the p wave in the sinus beat. However QRS complexes look exactly the same.
  • 83. RHYTHM Junctional Escape Depolarization initiated in the atrioventricular junction when one or more impulses from the sinus node are ineffective or nonexistent. Rate: 40-60 bpm, Rhythm: Irregular in single junctional escape complex; regular in junctional escape rhythm, P waves: Depends on the site of the ectopic focus. They will be inverted, and may appear before or after the QRS complex, or they may be absent, hidden by the QRS. QRS is usually normal
  • 84. RHYTHM Ventricular escape The depolarization wave spreads slowly via abnormal pathway in the ventricular myocardium and not via the His bundle and bundle branches.
  • 85. RHYTHM Atrial premature beat (APB) Arises from an irritable focus in one of the atria. APB produces different looking P wave, because depolarization vector is abnormal. QRS complex has normal duration and same morphology .
  • 86. RHYTHM Junctional Premature Beat Arises from an irritable focus at the AV junction. The P wave associated with atrial depolarization in this instance is usually buried inside the QRS complex and not visible. If p is visible, it is -ve in lead II and +ve in lead aVR and it it may occur before or after QRS.
  • 87. RHYTHM Premature Ventricular Complexes (PVCs) is a relatively common event where the heartbeat is initiated by the heart ventricles(arrow) rather than by the sinoatrial node, Rate depends on underlying rhythm and number of PVCs. Occasionally irregular rhythm, no p-wave associated with PVCs. May produce bizarre looking T wave.
  • 88. RHYTHM Asystole a state of no cardiac electrical activity, hence no contractions of the myocardium and no cardiac output or blood flow. Rate, rhythm, p and QRS are absent
  • 89. RHYTHM Pulseless Electrical Activity (PEA) Not an actual rhythm. The absence of a palpable pulse and myocardial muscle activity with the presence of organized muscle activity (excluding VT and VF) on cardiac monitor. Pt is clinically dead.
  • 90. RHYTHM Artificial pacemaker Sharp, thin spike. Rate depends on pacemaker, p wave maybe absent or present Ventricular paced rhythm shows wide ventricular pacemaker spikes
  • 93. CARDIAC AXIS The cardiac axis refers to the general direction of the heart's depolarization wavefront (or mean electrical vector) in the frontal plane. With a healthy conducting system the cardiac axis is related to where the major muscle bulk of the heart lies. Electrical impulse that travels towards the electrode produces an upright (positive) deflection (of the QRS complex) relative to the isoelectric baseline. One that travels away produces negative deflection. And one that travels at a right angle to the lead, produces a biphasic wave.
  • 94. CARDIAC AXIS To determine cardiac axis look at QRS complexes of lead , II, III. Axis Lead I Lead II Lead III Normal Positive Positive Positive/Negative Right axis Negative Positive Positive deviation Left axis Positive Negative Negative deviation Remember, positive(upgoing) QRS omplex means the impulse travels towards the lead. Negative means moving away.
  • 97. CARDIAC AXIS Negative Positive Positive Right Axis Deviation
  • 98. CARDIAC AXIS Cardiac Axis Causes Left axis deviation Normal variation in pregnancy, obesity; Ascites, abdominal distention, tumour; left anterior hemiblock, left ventricular hypertrophy, Q Wolff- Parkinson-White syndrome, Inferior MI Right axis deviation normal finding in children and tall thin adults, chronic lung disease(COPD), left posterior hemiblock, Wolff-Parkinson-White syndrome, anterolateral MI. North West emphysema, hyperkalaemia. lead transposition, artificial cardiac pacing, ventricular tachycardia
  • 100. P -WAVE Normal P- wave 3 small square wide, and 2.5 small square high. Always positive in lead I and II in NSR Always negative in lead aVR in NSR Commonly biphasic in lead V1
  • 101. P -WAVE P pulmonale Tall peaked P wave. Generally due to enlarged right atrium- commonly associated with congenital heart disease, tricuspid valve disease, pulmonary hypertension and diffuse lung disease. Biphasic P wave Its terminal negative deflection more than 40 ms wide and more than 1 mm deep is an ECG sign of left atrial enlargement. P mitrale Wide P wave, often bifid, may be due to mitral stenosis or left atrial enlargement.
  • 103. PR INTERVAL NORMAL PR INTERVAL Long PR interval may indicate heart block Short PR interval may disease like Wolf-Parkinson- PR-Interval 3-5 small square (120-200ms) White
  • 104. PR-INTERVAL First degree heart block P wave precedes QRS complex but P-R intervals prolong (>5 small squares) and remain constant from beat to beat
  • 105. PR-INTERVAL Second degree heart block 1. Mobitz Type I or Wenckenbach Runs in cycle, first P-R interval is often normal. With successive beat, P-R interval lengthens until there will be a P wave with no following QRS complex. The block is at AV node, often transient, maybe asymptomatic
  • 106. PR-INTERVAL Second degree heart block 2. Mobitz Type 2 P-R interval is constant, duration is normal/prolonged. Periodically, no conduction between atria and ventricles- producing a p wave with no associated QRS complex. (blocked p wave). The block is most often below AV node, at bundle of His or BB, May progress to third degree heart block
  • 107. PR-INTERVAL Third degree heart block (Complete heart block) No relationship between P waves and QRS complexes An accessory pacemaker in the lower chambers will typically activate the ventricles- escape rhythm. Atrial rate= 60-100bpm. Ventricular rate based on site of escape pacemaker. Atrial and ventricular rhythm both are regular.
  • 108. PR-INTERVAL Wolff–Parkinson–White syndrome Wolf Parkinson White Syndrome One beat from a rhythm strip in V2 demonstrating characteristic findings in WPW syndrome. Note the characteristic delta wave (above the blue bar), the short PR interval (red bar) of 0.08 seconds, and the long QRS complex (green) at 0.12 seconds Accessory pathway (Bundle of Kent) allows early activation of the ventricle (delta wave and short PR interval)
  • 110. QRS COMPLEX NORMAL QRS COMPLEX S amplitude in V1 + R amplitude in V5 < 3.5 Q wave amplitude less than Increased amplitude 1/3 QRS amplitude(R+S) or indicated cardiac hypertrophy < 1 small square QRS complex< 3 small square (0.06 - 0.10 sec) Prolonged indicates hyperkalemia or bundle branch block
  • 111. QRS COMPLEX Left Bundle Branch Block (LBBB) Right bundle branch block (RBBB) indirect activation causes left ventricle contracts indirect activation causes right ventricle later than the right ventricle. contracts later than the left ventricle QS or rS complex in V1 - W-shaped Terminal R wave (rSR’) in V1 - M-shaped RsR' wave in V6- M-shaped Slurred S wave in V6 - W-shaped Mnemonic: WILLIAM Mnemonic: MARROW
  • 113. ST SEGMENT NORMAL ST SEGMENT ST segment is isoelectric and at the same level as subsequent PR-interval ST segment < 2-3 small square (80 to 120 ms)
  • 114. ST SEGMENT OK, WE GONNA TALK ABOUT MYOCARDIAL INFARCTION (MI) THERE ARE 2 TYPES OF MI ST-ELEVATION MI (STEMI) AND NON ST-ELEVATION MI (NSTEMI) WE DECIDE THIS BY LOOKING AT THE ST SEGMENT IN ALL LEADS Flat (isoelectric) ± Same level with subsequent PR segment NORMAL ST SEGMENT Elevation or depression of ST segment by 1 mm or more, measured at J point is abnormal. J point is the point between QRS and ST segment
  • 115. Ischaemic change can be attributed to ST-SEGMENT different coronary arteries supplying the area. Localizing MI Location of Lead with Affected Look at ST changes, Q wave in all leads. Grouping MI ST changes coronary the leads into anatomical location, we have this: artery I aVR V1 V4 Anterior V1, V2, V3, LAD V4 II aVL V2 V5 Septum V1, V2 LAD III aVF V3 V6 left lateral I, aVL, V5, Left V6 circumflex inferior II, III, aVF RCA Right atrium aVR, V1 RCA *Posterior Posterior RCA chest leads (RCA) *Right Right sided RCA ventricle leads (LAD) *To help identify MI, right sided and posterior leads can be applied
  • 116. DIAGNOSING MYOCARDIAL INFARCTION (STEMI) Criteria: ST elevation in > 2 chest leads > 2mm elevation ST elevation in > 2 limb leads > 1mm elevation Q wave > 0.04s (1 small square). *Be careful of LBBB The diagnosis of acute myocardial infarction should be made circumspectively in the presence of pre-existing LBBB. On the other hand, the appearance of new LBBB should be regarded as sign of acute MI until proven otherwise Pathologic Q waves are a sign of previous myocardial infarction. Definition of a pathologic Q wave Any Q-wave in leads V2–V3 ≥ 0.02 s or QS complex in leads V2 and V3 Q-wave ≥ 0.03 s and > 0.1 mV deep or QS complex in leads I, II, aVL, aVF, or V4–V6 in any two leads of a contiguous lead grouping (I, aVL,V6; V4–V6; II, III, and aVF) R-wave ≥ 0.04 s in V1–V2 and R/S ≥ 1 with a concordant positive T-wave in the absence of a conduction defect. A little bit troublesome to remember? I usually take pathological Q wave as >1 small square deep
  • 117. ST SEGMENT ST-ELEVATION MI (STEMI) 0 HOUR Pronounced T Wave initially ST elevation (convex type) Depressed R Wave, and Pronounced T Wave. Pathological Q waves 1-24H may appear within hours or may take greater than 24 hr.- indicating full- thickness MI. Q wave is pathological if it is wider than 40 ms or deeper than a third of the height of the entire QRS complex Day 1-2 Exaggeration of T Wave continues for 24h. Days later T Wave inverts as the ST elevation begins to resolve. Persistent ST elevation is rare except in the presence of a ventricular aneurysm. Weeks later ECG returns to normal T wave, but retains pronounced Q wave. An old infarct may look like this
  • 118. ST SEGMENT Let’s see this >2mm Pathological Q wave Check again! I aVR V1 ST elevation in > 2 chest leads > 2mm V4 Q wave > 0.04s (1 small square). II aVL V2 V5 Yup, It’s acute anterolateral MI! III aVF V3 V6
  • 119. ST SEGMENT How about this one? Check again! I aVR V1 V4 Inferior MI! II aVL V2 V5 III aVF V3 V6
  • 120. ST SEGMENT NON ST-ELEVATION MI (NSTEMI) NSTEMI is also known as subendocardial or non Q-wave MI. In a pt with Acute Coronary Syndrome (ACS) in which the ECG does not show ST elevation, NSTEMI (subendocardial MI) is suspected if •ST Depression (A) •T wave inversion with or without ST depression (B) •Q wave and ST elevation will never happen To confirm a NSTEMI, do Troponin test: •If positive - NSTEMI •If negative – unstable angina pectoris
  • 121. ST SEGMENT NON ST-ELEVATION MI (NSTEMI) N-STEMI: acute coronary syndrome (with troponin increase). Arrows indicate ischemic ST segment changes. Without appropriate treatment in many cases STEMI infarction will occur.
  • 122. ST SEGMENT MYOCARDIAL ISCHEMIA 1mm ST-segment depression Symmetrical, tall T wave Long QT- interval A ST depression is more suggestive of myocardial ischaemia than infarction
  • 123. ST SEGMENT PERICARDITIS ST elevation with concave shape, mostly seen in all leads
  • 124. ST SEGMENT DIGOXIN Down sloping ST segment depression also known as the "reverse tick" or "reverse check" sign in supratherapeutic digoxin level.
  • 125. ST SEGMENT Now, moving to LEFT VENTRICULAR AND RIGHT VENTRICULAR HYPERTROPHY HYPERTROPHY So, we have to start looking at the S waves and R waves
  • 126. ST SEGMENT Left ventricular hypertrophy (LVH) To determine LVH, use one of the following Criteria: Sokolow & Lyon Criteria: S (V1) + R(V5 or V6) > 35mm Cornell Criteria: S (V3) + R (aVL) > 28 mm (men) or > 20 mm (women) Others: R (aVL) > 13mm Example: S (V1) + R(V5) = 15 + 25 = 40mm S(V3) + R (aVL)= 15 + 14 =29mm R(aVL) =14 mm LVH!
  • 127. ST SEGMENT Let’s see another example of LVH LVH strain pattern Tall R waves in V4 and V5 with down sloping ST segment depression and T wave inversion are suggestive of left ventricular hypertrophy (LVH) with strain pattern. LVH with strain pattern usually occurs in pressure overload of the left ventricle as in systemic hypertension or aortic stenosis.
  • 128. ST SEGMENT Right ventricular hypertrophy (RVH) Right axis deviation (QRS axis >100o) V1(R>S), V6 (S>R) Right ventricular strain T wave inversion Example: So, it’s RVH!
  • 129. ST SEGMENT Common Causes of LVH and RVH LVH RVH Hypertension (most common cause) Pulmonary hypertension Aortic stenosis Tetralogy of Fallot Aortic regurgitation Pulmonary valve stenosis Mitral regurgitation Ventricular septal defect (VSD) Coarctation of the aorta High altitude Hypertrophic cardiomyopathy Cardiac fibrosis COPD Athletic heart syndrome
  • 131. QT- INTERVAL QT interval decreases when heart rate increases. A general guide to the upper limit of QT interval. For HR = 70 bpm, QT<0.40 sec. •For every 10 bpm increase above 70 subtract 0.02s. •For every 10 bpm decrease below 70 add 0.02 s As a general guide the QT interval should be 0.35- 0.45 s,(<2 large square) and should not be more than half of the interval between adjacent R waves (R-R interval) : < 2 large square
  • 132. Calculation of QT interval 1.Use lead II. Use lead V5 alternatively if lead II cannot be read. 2.Draw a line through the baseline (preferably the PR segment) 3.Draw a tangent against the steepest part of the end of the T wave. If the T wave has two positive deflections, the taller deflection should be chosen. If the T wave is biphasic, the end of the taller deflection should be chosen. 4.The QT interval starts at the beginning of the QRS interval and ends where the tangent and baseline cross. 5.If the QRS duration exceeds 120ms the amount surpassing ,120ms should be deducted from the QT interval (i.e. QT=QT-(QRS width-120ms) ) To calculate the heart rate-corrected QT interval QTc. Bazett's formula is used
  • 133. QT = 0.04 x 10 small square= 0.4s 18 small square RR = 0.04 x 18 small square= 0.72s 10 small square If abnormally prolonged or shortened, there is a risk of developing ventricular arrhythmias The QT interval is prolonged in congenital long QT syndrome, but QT prolongation can also occur as a consequence of •Medication (anti-arrhythmics, tricyclic antidepressants, phenothiazedes) •Electrolyte imbalances •Ischemia. QT prolongation is often treated with beta blockers.
  • 134. LONG QT SYNDROME LQT is a rare inborn heart condition in which repolarization of the heart is delayed following a heartbeat. Example: Jervell and Lange-Nielsen Syndrome or Romano-Ward Syndrome T-WAVE Normal T wave Asymmetrical, the first half having more gradual slope than the second half >1/8 and < 2/3 of the amplitude of corresponding R wave Amplitude rarely exceeds 10mm Abnormal T waves are symmetrical, tall, peaked, biphasic, or inverted.
  • 135. U-WAVE The U wave is a wave on an electrocardiogram that is not always seen. It is typically small, and, by definition, follows the T wave. U waves are thought to represent repolarization of the papillary muscles or Purkinje fibers Normal U waves are small, round and symmetrical and positive in lead II. It is the same direction as T wave in that lead. Prominent U waves are most often seen in hypokalemia, but may be present in hypercalcemia, thyrotoxicosis, or exposure to digitalis,epinephrine, and Class 1A and 3 antiarrhythmics, as well as in congenital long QT syndrome, and in the setting of intracranial hemorrhage. An inverted U wave may represent myocardial ischemia or left ventricular volume overload
  • 137. HYPERKALAEMIA Narrow and tall peaked T wave (A) is an early sign PR interval becomes longer P wave loses its amplitude and may disappear QRS complex widens (B) When hyperkalemia is very severe, the widened QRS complexes merge with their corresponding T waves and the resultant ECG looks like a series of sine waves (C). If untreated, the heart arrests in asystole HYPOKALAEMIA T wave becomes flattened together with appearance of a prominent U wave. The ST segment may become depressed and the T wave inverted. these additional changes are not related to the degree of hypokalemia.
  • 138. HYPERCALCEMIA/HYPOCALCEMIA Usually, signs are not obvious Hypercalcemia is associated with short QT interval (A) and Hypocalcemia with long QT interval (B). Interval shortening or lengthening is mainly in the ST segment.
  • 139. PULMONARY EMBOLISM Tachycardia and incomplete RBBB differentiated PE from no PE. SIQIIITIII = deep S wave in lead I, pathological Q wave in lead III, and inverted T wave in lead III. The ECG is often abnormal in PE, but findings are not sensitive, not specific Any cause of acute cor pulmonale can cause the S1Q3T3 finding on the ECG.
  • 140. Thanks for your attention! Now, find some ECG practice!