Basics of ECG leads and recording Electrocardiography. ecg.pdf · Basics of Electrocardiography Dr....

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Basics of Electrocardiography

Dr. Badri Paudel GMC

Outline 1.  Review of the conduction system

2.  ECG leads and recording

3.  ECG waveforms and intervals

4.  Normal ECG and its variants

5.  Interpretation and reporting of an ECG

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Electrocardiography

•  A recording of the electrical activity of the heart over time

•  Gold standard for diagnosis of cardiac arrhythmias

•  Helps detect electrolyte disturbances (hyper- & hypokalemia)

•  Allows for detection of conduction abnormalities

•  Screening tool for ischemic heart disease during stress tests

•  Helpful with non-cardiac diseases (e.g. pulmonary embolism or hypothermia

• Pericarditis and Chamber hypertrophy 11/13/13 badri@gmc 3

What is an ECG? An ECG is the recording (gram)

of the electrical activity (electro)

generated by the cells of the heart(cardio) that reaches the body surface.



Recording ECG

William Einthoven


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Basics

" ECG graphs: – 1 mm squares – 5 mm squares

" Paper Speed: – 25 mm/sec standard

" Voltage Calibration: – 10 mm/mV standard


ECG Graph Paper •  Runs at a paper speed of 25 mm/sec •  Each small block of ECG paper is 1 mm2 •  At a paper speed of 25 mm/s, one small block equals 0.04 s •  Five small blocks make up 1 large block which translates into 0.20 s (200 msec) •  Hence, there are 5 large blocks per second •  Voltage: 1 mm = 0.1 mV between each individual block vertically


ECG Paper: Dimensions 5 mm

1 mm

0.1 mV

0.04 sec 0.2 sec

Speed = rate

Voltage ~Mass


ECG Leads Leads are electrodes which measure the difference in electrical potential between either:

1. Two different points on the body (bipolar leads)

2. One point on the body and a virtual reference

point with zero electrical potential, located in the center of the heart (unipolar leads)

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ECG Leads

The standard ECG has 12 leads:

3 Standard Limb Leads

3 Augmented Limb Leads

6 Precordial Leads

The axis of a particular lead represents the viewpoint from which it looks at the heart.

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Recording of the ECG: Leads used: •  Limb leads are I, II, II. • Each of the leads are bipolar; i.e., it requires two sensors on the skin to make a lead. •  If one connects a line between two sensors, one has a vector. •  There will be a positive end at one electrode and negative at the other. •  The positioning for leads I, II, and III were first given by Einthoven. Form the basis of Einthoven’s triangle.

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Types of ECG Recordings

�  Bipolar leads record voltage between electrodes placed on wrists & legs (right leg is ground)

�  Lead I records between right arm & left arm

�  Lead II: right arm & left leg

�  Lead III: left arm & left leg

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Standard Limb Leads

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Standard Limb Leads

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Augmented Limb Leads

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All Limb Leads

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Where do those chest stickers go?

Ø  Make sure to “feel” for intercostal space – don’t just use your eyes! 11/13/13 badri@gmc 18

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Precordial Leads

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……and the FEMALES �  Not all nipple lines are

created equal

�  Measure intercostal spaces to be accurate in electrode placement �  All 12 leads measured from

same electrode placement

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Lead Placement in the Female �  Avoid placing electrodes on top of breast tissue

�  Use the back of the hand to displace breast tissue out of the way to place electrode �  Avoids perception of “groping” �  Can ask the patient to move left breast out of way.

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Precordial Leads

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Summary of Leads

Limb Leads Precordial Leads

Bipolar I, II, III (standard limb leads)

-

Unipolar aVR, aVL, aVF (augmented limb leads)

V1-V6

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Arrangement of Leads on the EKG

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Anatomic Groups (Septum)

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Anatomic Groups (Anterior Wall)

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Anatomic Groups (Lateral Wall)

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Anatomic Groups (Inferior Wall)

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Anatomic Groups (Summary)

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Heart & 12 – Lead Strip Correlation

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12 – Lead Strips Remember: Every lead is like a “camera angle”

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12 – Lead Strips cont. Imagine your strips broken into groups like this…

I

II

III

aVL

aVF

V1

V2

V3

V4

V5

V6

aVR



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Elements of the ECG: •  P wave

•  Depolarization of both atria; •  Relationship between P and QRS helps distinguish various cardiac arrhythmias

•  Shape and duration of P may indicate atrial enlargement

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•  PR interval: •  From onset of P wave to onset of QRS

•  Normal duration = 0.12-2.0 sec (120-200 ms) (3-4 horizontal boxes)

•  Represents atria to ventricular conduction time (through His bundle)

•  Prolonged PR interval may indicate a 1st degree heart block


• QRS complex:

•  Represents ventricular depolarization

•  Larger than P wave because of greater muscle mass of ventricles

•  Normal duration = 0.08-0.12 seconds

•  Its duration, amplitude, and morphology are useful in diagnosing cardiac arrhythmias, ventricular hypertrophy, MI, electrolyte derangement, etc.

•  Q wave greater than 1/3 the height of the R wave, greater than 0.04 sec are abnormal and may represent MI


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T wave: •  Represents repolarization or recovery of ventricles •  Interval from beginning of QRS to apex of T is referred to as the absolute refractory period

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What’s a J point and where is it? �  J point – point to mark end

of QRS and beginning of ST segment �  Evaluate ST elevation 0.04

seconds after J point �  Based on relationship to the

baseline �  Used in assessing ST

elevation

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ST segment: •  Connects the QRS complex and T wave •  Duration of 0.08-0.12 sec (80-120 msec

QT Interval

•  Measured from beginning of QRS to the end of the T wave •  Normal QT is usually about 0.40 sec •  QT interval varies based on heart rate

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�  3 distinct waves are produced during cardiac cycle

�  P wave caused by atrial depolarization

�  QRS complex caused by ventricular depolarization

�  T wave results from ventricular repolarization

ECG

Fig 13.24 13-63

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Elements of the ECG: •  P wave: Depolarization of both atria;

•  Relationship between P and QRS helps distinguish various cardiac arrhythmias •  Shape and duration of P may indicate atrial enlargement

•  PR interval: from onset of P wave to onset of QRS

•  Normal duration = 0.12-2.0 sec (120-200 ms) (3-4 horizontal boxes)

•  Represents atria to ventricular conduction time (through His bundle)

•  Prolonged PR interval may indicate a 1st degree heart block

•  QRS complex: Ventricular depolarization

•  Larger than P wave because of greater muscle mass of ventricles

•  Normal duration = 0.08-0.12 seconds

•  Its duration, amplitude, and morphology are useful in diagnosing cardiac arrhythmias, ventricular hypertrophy, MI, electrolyte derangement, etc.

•  Q wave greater than 1/3 the height of the R wave, greater than 0.04 sec are abnormal and may represent MI

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ST segment: •  Connects the QRS complex and T wave •  Duration of 0.08-0.12 sec (80-120 msec

T wave: •  Represents repolarization or recovery of ventricles •  Interval from beginning of QRS to apex of T is referred to as the absolute refractory period

QT Interval •  Measured from beginning of QRS to the end of the T wave •  Normal QT is usually about 0.40 sec •  QT interval varies based on heart rate

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Time relationships between developed force and the changes in transmembrane potentials in a thin strip of ventricular muscle

Time

Mechanical event

Electrical event

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QRS waveform nomenclature

R r qR qRs Qrs QS

Qr Rs rS qs rSr’ rSR’

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Localising the arterial territory

Inferior II, III, aVF

Lateral I, AVL, V5-V6

Anterior / Septal V1-V4 11/13/13 badri@gmc 53

Standard sites unavailable �  Patient pathology

Amputation or burns or bandagesà should be placed as closely as possible to the standard sites

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Specific cardiac abnormalities

�  Situs inversus dextrocardiaà right & left arm electrodes should be reversed

pre-cordial leads should be recorded from V1R(V2) to V6

�  RVH & RV infarction:V3R & V4R

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Continuous monitoring �  Bed side:

�  Holter monitoring:

�  TMT: Mason Likar system

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Other practical points �  Electrodes should be selected for maximum

adhesiveness and minimum discomfort,electrical noise,and skin-electrode impedance

�  Effective contact between electrode and skin is essential.

�  ECG :calibration

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�  ECG :paper speed

�  Electrical artifacts:external or internal

external can be minimized by straightening the lead wires

internal can be due to muscle tremors,shivering ,hiccoughs .

�  Supine position

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MODERN EKG MACHINE

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Interpretation of an ECG

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Steps involved �  Heart Rate

�  Rhythm

�  Axis

�  Wave morphology

�  Intervals and segments analysis

�  Chamber enlargement

�  Specific changes

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Determining the Heart Rate �  Rule of 300

�  10 Second Rule

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Rule of 300 Take the number of “big boxes” between neighboring QRS complexes, and divide this into 300. The result will be approximately equal to the rate

Although fast, this method only works for regular rhythms.

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What is the heart rate?

(300 / 6) = 50 bpm

www.uptodate.com

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(300 / ~ 4) = ~ 75 bpm

www.uptodate.com

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(300 / 1.5) = 200 bpm

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The Rule of 300 It may be easiest to memorize the following table:

# of big boxes

Rate

1 300

2 150

3 100

4 75

5 60

6 50 11/13/13 badri@gmc 67 11/13/13 badri@gmc 68

10 Second Rule

As most EKGs record 10 seconds of rhythm per page, one can simply count the number of beats present on the EKG and multiply by 6 to get the number of beats per 60 seconds.

This method works well for irregular rhythms.

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33 x 6 = 198 bpm The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/

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The QRS Axis

The QRS axis represents the net overall direction of the heart’s electrical activity.

Abnormalities of axis can hint at:

Ventricular enlargement

Conduction blocks (i.e. hemiblocks)

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The QRS Axis By near-consensus, the normal QRS axis is defined as ranging from -30° to +90°.

-30° to -90° is referred to as a left axis deviation (LAD)

+90° to +180° is referred to as a right axis deviation (RAD)

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Determining the Axis

�  The Quadrant Approach

�  The Equiphasic Approach

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Determining the Axis

Predominantly Positive

Predominantly Negative

Equiphasic

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The Quadrant Approach 1. Examine the QRS complex in leads I and aVF to

determine if they are predominantly positive or predominantly negative. The combination should place the axis into one of the 4 quadrants below.

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The Quadrant Approach 2. In the event that LAD is present, examine lead II to

determine if this deviation is pathologic. If the QRS in II is predominantly positive, the LAD is non-pathologic (in other words, the axis is normal). If it is predominantly negative, it is pathologic.

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Quadrant Approach: Example 1

Negative in I, positive in aVF à RAD 11/13/13 badri@gmc 78

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Quadrant Approach: Example 2

Positive in I, negative in aVF à Predominantly positive in II à

Normal Axis (non-pathologic LAD) 11/13/13 badri@gmc 79

The Equiphasic Approach 1. Determine which lead contains the most equiphasic

QRS complex. The fact that the QRS complex in this lead is equally positive and negative indicates that the net electrical vector (i.e. overall QRS axis) is perpendicular to the axis of this particular lead.

2. Examine the QRS complex in whichever lead lies 90° away from the lead identified in step 1. If the QRS complex in this second lead is predominantly positive, than the axis of this lead is approximately the same as the net QRS axis. If the QRS complex is predominantly negative, than the net QRS axis lies 180° from the axis of this lead.

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Equiphasic Approach: Example 1

Equiphasic in aVF à Predominantly positive in I à QRS axis ≈ 0° 11/13/13 badri@gmc 81

Equiphasic Approach: Example 2

Equiphasic in II à Predominantly negative in aVL à QRS axis ≈ +150° 11/13/13 badri@gmc 82

-90°-60°

-30°

0°

aVL

I

30°

60°

aVR

II

90°120°

III

150°

180°

-150°

-120°

aVF

Marked RAD

LAD

RAD

Normal Axis

-30° to +100°11/13/13 badri@gmc 83

Using leads I, II, aVF LEAD 1 LEAD 2 LEAD aVF

Normal UPRIGHT UPRIGHT UPRIGHT

Physiological Left Axis UPRIGHT UPRIGHT /

BIPHASIC NEGATIVE

Pathological Left Axis UPRIGHT NEGATIVE NEGATIVE

Right Axis NEGATIVE UPRIGHT BIPHASIC NEGATIVE

UPRIGHT

Extreme Right Axis NEGATIVE NEGATIVE NEGATIVE

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12-Lead ECG




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Common causes of LAD �  May be normal in the elderly and very obese

�  Due to high diaphragm during pregnancy, ascites, or ABD tumors

�  Inferior wall MI �  Left Anterior Hemiblock �  Left Bundle Branch Block �  WPW Syndrome �  Congenital Lesions �  RV Pacer or RV ectopic rhythms �  Emphysema

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Common causes of RAD �  Normal variant

�  Right Ventricular Hypertrophy

�  Anterior MI

�  Right Bundle Branch Block

�  Left Posterior Hemiblock

�  Left Ventricular ectopic rhythms or pacing

�  WPW Syndrome


Genesis of QRS �  Initially there is a small vector from left to right

through the IVS ,followed by a larger vector from right to left through the free wall of the LV


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Effect of left oriented lead �  Small septal vector ,directed away from the positive

pole resulting in a small q wave

�  Larger vector of the free wall ,directed towards the positive pole resulting in a tall R wave


Effect of right oriented lead �  Small septal vector which is directed towards the

positive pole,hence a small r wave

�  Large vector of free LV wall which is directed away from the lead and hence a large s wave


Transition zone

V1 V2

V3 V4

V5 V6

The R wave in the precordial leads must grow from V1 to at least V4///////Transition from rS to qR pattern which is usually seen in V3 /V4

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The Normal ECG

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Normal Sinus Rhythm �  Originates in the sinus node

�  Rate between 60 and 100 beats per min

�  Tallest p waves in Lead II

�  Monomorphic P waves

�  Normal PR interval of 120 to 200 msec

�  Normal relationship between P and QRS

�  Some sinus arrhythmia is normal


Sinus Arrhythmia

ECG Characteristics: Presence of sinus P waves

Variation of the PP interval which cannot be attributed to either SA nodal block or PACs

When the variations in PP interval occur in phase with respiration, this is considered to be a normal variant. When they are unrelated to respiration, they may be caused by the same etiologies leading to sinus bradycardia

(Sinus rate increases during inspiration by >10 bpm.)

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Normal P wave �  Atrial depolarisation

�  Duration 80 to 100 msec

�  Maximum amplitude 2.5 mm

�  Axis +45 to +65

�  Biphasic in lead V1

�  Terminal deflection should not exceed 1 mm in depth and 0.03 sec in duration in V1

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Normal P wave

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P’ wave (inverted P wave) �  Results in negative wave form in leads II,III and avF

�  Axis;-80 to -90

�  Retrograde activation of atria due to impulse arising from or passing through AV node

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Normal QRS complex �  Completely negative in lead aVR , maximum

positivity in lead II

�  rS in right oriented leads and qR in left oriented leads (septal vector)

�  Transition zone commonly in V3-V4

�  RV5 > RV6 normally

�  Normal duration 50-110 msec, not more than 120 msec

�  Physiological q wave not > 0.03 sec


�  ECG showing qR pattern in lead III ,disappears on deep inspiration à q wave not significant

�  Mech:shift in the QRS axis

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QRS Complexes •  Non-pathological Q waves are often

present in leads I, III, aVL, V5, and V6 •  The R wave in lead V6 is smaller than the

R wave in V5 •  The depth of the S wave, generally, should

not exceed 30 mm •  Pathological Q wave > 2mm deep and >

1mm wide or > 25% amplitude of the subsequent R wave

Amplitude of QRS Depends on the following factors

�  1.electrical force generated by the ventricular myocardium

�  2.distance of the sensing electrode from the ventricles

�  3.Body build;a thin individual has larger complexes when compared to obese individuals

�  4.direction of the frontal QRS axis

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Normal T wave �  Same direction as the preceding QRS complex

�  Blunt apex with asymmetric limbs

�  Height < 5mm in limb leads and <10 mm in precordial leads

�  Smooth contours

�  May be tall in athletes

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ST segment �  Merges smoothly with the proximal limb of the T

wave

�  No true horizontality

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Normal u wave �  Best seen in midprecordial leads

�  Height < 10% of preceding T wave

�  Isoelectric in lead aVL (useful to measure QTc)

�  Rarely exceeds 1 mm in amplitude

�  May be tall in athletes (2mm)

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QT interval �  Normally corrected for heart rate

�  Bazett’s formula

�  Normal 350 to 430 msec

�  With a normal heart rate (60 to 100), the QT interval should not exceed half of the R-R interval roughly

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Measurement of QT interval �  The beginning of the QRS complex is best

determined in a lead with an initial q wave

à leads I,II, avL ,V5 or V6

�  QT interval shortens with tachycardia and lengthens with bradycardia

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Normal standardization

�  1 mV=10 mm

�  Will result in perfect right angles at each corner

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The 10 rules for a normal ECG

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

.2 11/13/13 badri@gmc 124

Rule 1

PR interval

Mill

ivol

ts

Milliseconds

0 200 400 600

-0.5

0

0.5

1.0

P"

R

T"

Q"

S

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

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Rule 2

Mill

ivol

ts

Milliseconds

0 200 400 600

-0.5

0

0.5

1.0

QRS

P"

R

T"

Q"

S

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

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Rule 3

I II III aVR aVL aVF

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

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Rule 4

I II III aVR aVL aVF

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

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Rule 5

P

Q

T

S

All waves are negative in lead aVR

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Rule 6

V1 V2

V3 V4

V5 V6

The R wave in the precordial leads must grow from V1 to at least V4

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Rule 7

The ST segment should start isoelectric except in V1 and V2 where it may be elevated 11/13/13 badri@gmc 131

Rule 8


The P waves should be upright in I, II, and V2 to V6 11/13/13 badri@gmc 132

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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 11/13/13 badri@gmc 133

Rule 10


The T wave must be upright in I, II, V2 to V6 11/13/13 badri@gmc 134

Normal Variants in the ECG

�  Sinus arrhythmia

�  Persistent juvenile pattern

�  Early repolarisation syndrome

�  Non specific T wave changes

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Persistent juvenile pattern

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Features of ERPS �  Vagotonia / athletes’ heart

�  Prominent J point

�  Concave upwards, minimally elevated ST segments

�  Tall symmetrical T waves

�  Prominent q waves in left leads

�  Tall R waves in left oriented leads

�  Prominent u waves

�  Rapid precordial transition

�  Sinus bradycardia

Early Recognition Prevents Streptokinase infusion ! 11/13/13 badri@gmc 138

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Reporting an ECG

1. Patient Details “ Whose ECG is it ?!”

2. Standardisation and lead placement

“Is it properly taken ?”

speed

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Speed

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Voltage

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Limb lead misplacement

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Steps involved �  Heart Rate

�  Rhythm

�  Axis

�  Wave morphology

�  Chamber enlargement

�  Intervals and segments analysis

�  Specific changes

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Sinus Rhythms �  Originate in the SA node

�  Normal sinus rhythm (NSR) �  Sinus bradycardia (SB) �  Sinus tachycardia (ST) �  Sinus arrhythmia

�  Inherent rate of 60 – 100

�  Base all other rhythms on deviations from sinus rhythm

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Sinus rhythm

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Sinus Rhythm

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3. Analysis of Rate, Rhythm and Axis

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Analysis of Rate, Rhythm and Axis

�  Complete Heart Block:

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Analysis of Rate, Rhythm and Axis- contd…

�  Complete Heart Block

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Analysis of Rate, Rhythm and Axis contd..

�  OMI/AF/RBBB

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Arrhythmias Detected on ECG

� Arrhythmias are abnormal heart rhythms

� Heart rate <60/min is bradycardia; >100/min is tachycardia

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Sinus Bradycardia

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Bradyarrhythmias �  What is the rhythm?

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Sinus bradycardia (lead III).

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Sinus tachycardia (lead I)

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Sinus Tachycardia

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Sinus Arrhythmia

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Atrial Rhythms �  Originate in the atria

�  Atrial fibrillation (A Fib) �  Atrial flutter �  Wandering pacemaker �  Multifocal atrial tachycardia (MAT) �  Supraventricular tachycardia (SVT) �  PAC’s �  Wolff–Parkinson–White syndrome (WPW)

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Atrial Fibrillation

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A - Fib

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165

Atrial Fibrillation

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166

Atrial Flutter

Heart rate Rhythm P wave PR interval QRS in sec

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A - Flutter

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Wandering Pacemaker

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Multifocal Atrial Tachycardia (MAT) (Rapid Wandering Pacemaker)

•  Similar to wandering pacemaker (< 100) •  MAT rate is >100 •  Usually due to pulmonary issue

•  COPD •  Hypoxia, acidotic, intoxicated, etc.

•  Often referred to as SVT by EMS •  Recognize it is a tachycardia and QRS is narrow

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Tachyarrhythmias �  What is the rhythm?

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Tachyarrhythmias �  AV nodal reentrant tachycardia

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Fast Conduction Path Slow Recovery

Slow Conduction Path Fast Recovery

The “Re-Entry” Mechanism of Ectopic Beats & Rhythms

Electrical Impulse

Cardiac Conduction

Tissue

Tissues with these type of circuits may exist: •  in microscopic size in the SA node, AV node, or any type of heart tissue •  in a “macroscopic” structure such as an accessory pathway in WPW

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Premature Beat Impulse

Cardiac Conduction

Tissue

1. An arrhythmia is triggered by a premature beat 2. The beat cannot gain entry into the fast conducting pathway because of its long refractory period and

therefore travels down the slow conducting pathway only

Repolarizing Tissue (long refractory period)


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3. The wave of excitation from the premature beat arrives at the distal end of the fast conducting pathway, which has now recovered and therefore travels retrogradely (backwards) up the fast pathway



Cardiac Conduction

Tissue


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30

4. On arriving at the top of the fast pathway it finds the slow pathway has recovered and therefore the wave of excitation ‘re-enters’ the pathway and continues in a ‘circular’ movement. This creates the re-entry circuit



Cardiac Conduction

Tissue


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Atrial Re-entry •  atrial tachycardia •  atrial fibrillation •  atrial flutter

Atrio-Ventricular Re-entry •  Wolf Parkinson White •  supraventricular tachycardia

Ventricular Re-entry •  ventricular tachycardia

Atrio-Ventricular Nodal Re-entry •  supraventricular tachycardia

Re-entry Circuits as Ectopic Foci and Arrhythmia Generators

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SVT

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PAC’s

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Wolff–Parkinson–White - WPW

�  Caused by an abnormal accessory pathway (bridge) in the conductive tissue

�  Mainly non-symptomatic with normal heart rates

�  If rate becomes tachycardic (200-300) can be lethal �  May be brought on by

stress and/or exertion 11/13/13 badri@gmc 182

Tachycardia circuits in Wolff-Parkinson-White syndrome

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Wolff–Parkinson–White (AKA - Preexcitation Syndrome)

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Short PR Interval � WPW (Wolff-

Parkinson-White) Syndrome

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

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WPW

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Ventricular preexcitation (WPW)

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AV/Junctional Rhythms

�  Originate in the AV node �  Junctional rhythm rate 40-60 �  Accelerated junctional rhythm rate 60-100 �  Junctional tachycardia rate over 100 �  PJC’s

�  Inherent rate of 40 - 60

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Junctional Rhythm

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ECGs, Normal and Abnormal

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Accelerated Junctional

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Junctional Tachycardia Often difficult to pick out so often identified as “SVT”

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PJC’s

Flat or inverted P Wave or P wave after the QRS

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Ventricular Rhythms

�  Originate in the ventricles / purkinje fibers �  Ventricular escape rhythm (idioventricular) rate 20-40 �  Accelerated idioventricular rate 42 - 100 �  Ventricular tachycardia (VT) rate over 102

�  Monomorphic – regular, similar shaped wide QRS complexes �  Polymorphic (i.e. Torsades de Pointes) – life threatening if

sustained for more than a few seconds due to poor cardiac output from the tachycardia)

�  Ventricular fibrillation (VF) �  Fine & coarse

�  PVC’s

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Idioventricular

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Accelerated Idioventricular

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Arrhythmias Detected on ECG � In flutter contraction rates can be 200-300/min

� In fibrillation contraction of myocardial cells is uncoordinated & pumping ineffective � Ventricular fibrillation is life-threatening

�  Electrical defibrillation resynchronizes heart by depolarizing all cells at same time

13-81 11/13/13 badri@gmc 197

VT (Monomorphic)

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Monomorphic VT

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200

Ventricular Tachycardia

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VT (Polymorphic)

Note the “twisting of the points”

This rhythm pattern looks like ribbon in it’s fluctuations

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V1

Polymorphic VT

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“Torsade de Pointes” (Polymorphic VT Associated with Prolonged Repolarization)

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Ventricular Flutter

•  VT > 250 beats/min, without clear isoelectric line •  Note “sine wave”-like appearance

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VF

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Ventricular Fibrillation (VF)

•  Totally chaotic rapid ventricular rhythm •  Often precipitated by VT •  Fatal unless promptly terminated (DC shock)

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Sustained VT: Degeneration to VF

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Atrial Fibrillation with Rapid Conduction Via Accessory Pathway: Degeneration to VF

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ECGs, Abnormal

No pumping action occurs 11/13/13 badri@gmc 209

PVC’s

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ECGs, Abnormal

Extrasystole : note inverted QRS complex, misshapen QRS and T and absence of a P wave preceding this contraction.

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R on T PVC’s

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R on T PVC’s cont. � Why is R on T so bad?

�  Downslope of T wave is the relative refractory period �  Some cells have repolarized and can be stimulated again to

depolarize/discharge

� Relatively strong impulse can stimulate cells to conduct electrical impulses but usually in a slower, abnormal manner � Can result in ventricular fibrillation

�  Absolute refractory period is from the beginning of the QRS complex through approximately the first half of the T wave

� Cells not repolarized and therefore cannot be stimulated

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Synchronized Cardioversion �  Cardioversion is synchronized to avoid the refractory period

of the T wave

�  The monitor “plots” out the next refractory period in order to shock at the right moment – the safer R wave �  With a QRS complex & T wave present, the R wave can

be predicted (cannot work in VF – no wave forms present)

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AV Heart Blocks

�  1st degree �  A condition of a rhythm, not a true rhythm �  Need to always state underlying rhythm

�  2nd degree �  Type I - Wenckebach �  Type II – Classic – dangerous to the patient

� Can be variable (periodic) or have a set conduction ratio (ex. 2:1)

�  3rd degree (Complete) – dangerous to the patient 11/13/13 badri@gmc 215

Atrioventricular (AV) Blocks �  Delay or interruption in impulse conduction in AV

node, bundle of His, or His/Purkinje system

�  Classified according to degree of block and site of block �  PR interval is key in determining type of AV block �  Width of QRS determines site of block

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AV Blocks cont. �  Clinical significance dependent on:

ü Degree or severity of the block ü Rate of the escape pacemaker site � Ventricular pacemaker site will be a slower

heart rate than a junctional site ü Patient’s response to that ventricular rate � Evaluate level of consciousness /

responsiveness & blood pressure

�  Assume a patient presenting in Mobitz II or 3rd degree heart block to have an AMI until proven otherwise

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Arrhythmias Detected on ECG �  AV node block occurs when node is damaged

�  First–degree AV node block is when conduction thru AV node > 0.2 sec �  Causes long P-R interval

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1st Degree Block

<

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Prolonged P-R interval caused by first degree heart block (lead II)

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� Second-degree AV node block is when only 1 out of 2-4 atrial APs can pass to ventricles �  Causes P waves with no QRS

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2nd Degree Type I

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2nd Degree Type II (constant)

P Wave PR Interval QRS Characteristics Uniform .12 - .20 Narrow & Uniform Missing QRS after

every other P wave (2:1 conduction)

Note: Ratio can be 3:1, 4:1, etc. The higher the ratio, the “sicker” the heart. (Ratio is P:QRS)

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2nd Degree Type II (periodic)

P Wave PR Interval QRS Characteristics Uniform .12 - .20 Narrow & Uniform Missing QRS after

some P waves

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Arrhythmias Detected on ECG continued

� In third-degree or complete AV node block, no atrial activity passes to ventricles � Ventricles are driven slowly by bundle of His or Purkinjes

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3rd Degree (Complete)

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Complete AV block

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Arrhythmia: conduction failure at AV node


� AV node block occur when node is damaged

�  First–degree AV node block is when conduction through AV node > 0.2 sec �  Causes long P-R interval

� Second-degree AV node block is when only 1 out of 2-4 atrial APs can pass to ventricles �  Causes P waves with no QRS

�  In third-degree or complete AV node block no atrial activity passes to ventricles �  Ventricles driven slowly by bundle of His or Purkinjes

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AV Block �  What are the rhythms?


What are the rhythms?

AV Block �  What is the rhythm?

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AV Block n What is the rhythm?

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235

How Can I Tell What Block It Is?

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Helpful Tips for AV Blocks �  Second degree Type I

�  Think Type “I” drops “one” �  Wenckebach “winks” when it drops one

�  Second degree Type II �  Think 2:1 (knowing it can have variable block like 3:1,

etc.)

�  Third degree - complete �  Think completely no relationship between atria and

ventricles

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237 237

Implanted Pacemaker �  Most set on demand

�  When the heart rate falls below a preset rate, the heart “demands” the pacemaker to take over

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Paced Rhythm - 100% Capture

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4. Chamber enlargements

Left Atrial Enlargement

•  Prominent terminal P negativity (biphasic) in lead V1 (i.e., "P-terminal force") duration >0.04s, depth >1 mm

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Left Atrial Enlargement

•  Notched/bifid (‘M’ shaped) P wave (P ‘mitrale’) in limb leads with the inter-peak duration > 0.04s (1 mm)

P Pulmonale and P Mitrale

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QRS In Hypertrophy

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RVH Changes

•  A tall positive (R) wave –  instead of the rS complex normally seen in

lead V1 – an R wave exceeding the S wave in lead V1 –  in adults the normal R wave in lead V1 is

generally smaller than the S wave in that lead •  Right axis deviation (RAD) •  Right ventricular "strain" T wave inversions

Conditions with Tall R in V1

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Left Ventricular Hypertrophy •  Sokolow & Lyon Criteria (Am Heart J,

1949;37:161) – S in V1+ R in V5 or V6 > 35 mm

•  An R wave of 11 to 13 mm (1.1 to 1.3 mV) or more in lead aVL is another sign of LVH

•  Others: Cornell criteria (Circulation, 1987;3: 565-72) – SV3 + R aVL > 28 mm in men – SV3 + R aVL > 20 mm in women

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5. Segment and wave form analysis

RBBB and LBBB

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LEFT BUNDLE BRANCH BLOCK LBBB

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LEFT BUNDLE BRANCH BLOCK LBBB

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Hemiblocks

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Le> Anterior Hemiblock

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Le> Posterior Hemiblock

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Ischemic Heart Disease

�  Is most commonly due to atherosclerosis in coronary arteries

�  Ischemia occurs when blood supply to tissue is deficient �  Causes increased lactic acid from anaerobic metabolism

�  Often accompanied by angina pectoris (chest pain)

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CHEST PAIN

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259

ST Segment

•  Normal ST Segment is flat (isoelectric) – Same level with subsequent PR segment

•  Elevation or depression of ST segment by 1 mm or more, measured at J point IS ABNORMAL

•  “J” (Junction) point is the point between QRS and ST segment

What’s a J point and where is it? •  J point – point to

mark end of QRS and beginning of ST segment – Evaluate ST elevation

0.04 seconds after J point

– Based on relationship to the baseline

– Used in assessing ST elevation

Ischemic Heart Disease

�  Detectable by changes in S-T segment of ECG

� Myocardial infarction (MI) is a heart attack �  Diagnosed by high levels of creatine phosphate (CPK) &

lactate dehydrogenase (LDH)

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Measuring for ST Elevation •  Find the J point •  Is the ST segment

>1mm above the isoelectric line in 2 or more contiguous leads?

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EARLY REPOLARIZATION

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Characteristic changes in AMI

�  ST segment elevation over area of damage

�  ST depression in leads opposite infarction

�  Pathological Q waves

�  Reduced R waves

�  Inverted T waves

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Myocardial Insult •  Ischemia

–  lack of oxygenation – ST depression or T wave inversion – permanent damage avoidable

•  Injury – prolonged ischemia – ST elevation – permanent damage avoidable

•  Infarct – death of myocardial tissue; damage

permanent; may have Q wave 11/13/13 badri@gmc 266

ST elevation

R

P

Q

ST

•  Occurs in the early stages

•  Occurs in the leads facing the infarction

•  Slight ST elevation may be normal in V1 or V2

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Variable Shapes Of ST Segment Elevations in AMI

Goldberger AL. Goldberger: Clinical Electrocardiography: A Simplified Approach. 7th ed: Mosby Elsevier; 2006. 11/13/13 badri@gmc 268

269

Deep Q wave

R

P

Q

T

ST

•  Only diagnostic change of myocardial infarction

•  At least 0.04 seconds in duration

•  Depth of more than 25% of ensuing R wave

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T wave changes

R

P

Q

T

ST

•  Late change

•  Occurs as ST elevation is returning to normal

•  Apparent in many leads

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Bundle branch block

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

Anterior wall MI Left bundle branch block

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Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q!

R!

P!

Q!T!

ST R!

P!

Q!

ST

P!

Q!T!

ST

R!

P!

S

T

P!

Q!T!

ST

R!

P!

Q!

T!

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Evolution of AMI A - pre-infarct (normal) B - Tall T wave (first few

minutes of infarct) C - Tall T wave and ST

elevation (injury) D - Elevated ST (injury),

inverted T wave (ischemia), Q wave (tissue death)

E - Inverted T wave (ischemia), Q wave (tissue death)

F - Q wave (permanent marking) 11/13/13 badri@gmc 274

EVOLUTION OF MI

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Diagnostic criteria for AMI

•  Q wave duration of more than 0.04 seconds

•  Q wave depth of more than 25% of ensuing r wave

•  ST elevation in leads facing infarct (or depression in opposite leads)

•  Deep T wave inversion overlying and adjacent to infarct

•  Cardiac arrhythmias

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ACUTE INFARCTION

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Location of infarct combinations

aVR V1 V4 I

II

III

LATERAL

INFERIOR

ANT POST ANT

SEPTAL

ANT

LAT

aVL

aVF

V2

V3

V5

V6

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Lateral View – I, aVL, V5, V6

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Lateral infarction Lateral infarction


Left circumflex coronary artery 11/13/13 badri@gmc 280

Complications of Lateral Wall MI I, aVL, V5, V6

•  Monitor for lethal heart blocks

– Second degree type II – classical – Third degree heart block – complete

• Treat with TCP – Consider sedation for patient comfort – Monitor for capture – Monitor for improvement by measuring level

of consciousness and blood pressure 11/13/13 badri@gmc 281

Inferior View – II, III, aVF

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Inferior infarction Inferior infarction


Right coronary artery 11/13/13 badri@gmc 283

Complications of Inferior Wall MI II, III, aVF

•  May see Mobitz type I – Wenckebach –  Due to parasympathetic stimulation & not injury to conduction

system

•  Hypotension –  Right ventricle may lose some pumping ability

•  Venous return exceeds output, blood accumulates in right ventricle

–  Less blood being pumped to lungs to left ventricle and out to body

– Develop hypotension, JVD, with clear lung sounds •  Treated with additional fluid administered cautiously •  Ems to contact Medical Control prior to NTG administration

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Septal View – V1 & V2

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Complications of Septal Wall MI V1 & V2

•  Monitor for lethal heart blocks – Second degree type II – classical – Third degree heart block – complete

•  Treat with TCP

•  Rare to have a septal wall MI alone – Often associated with anterior and/or lateral

wall involvement

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Anterior View – V3 & V4

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Anterior infarction Anterior infarction


Left coronary artery

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Complications of Anterior Wall MI V3 & V4

•  Occlusion of left main coronary artery – the “widow maker” –  Cardiogenic shock and death without prompt reperfusion

•  Second degree AV block type II –  Often symptomatic –  Often progress to 3rd degree heart block –  Prepare to initiate TCP

•  Third degree heart block – complete –  Rhythm usually unstable –  Rate usually less than 40 beats per minute –  Prepare to initiate TCP

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ST T changes- MI anteroseptal/// axis???

�  ST T in V1-V5/ aVL

�  Axis

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291 11/13/13 badri@gmc 292

ST DEPRESSION

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�  ST in V1-V4

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ISCHEMIC T WAVES LAHB RBBB

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INFEROLATERAL ISCHEMIA

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Hypertrophy Strain Pattern vs. ACS

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DIGOXIN EFFECT

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PERICARDITIS

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Patient Presenting with Coronary Chest Pain – AMI Until Proven Otherwise

•  Oxygen –  May limit ischemic injury –  New trends/guidelines coming out in 2011 SOP’s

•  Aspirin - 324 mg chewed (PO) –  Blocks platelet aggregation (clumping) to keep

clot from getting bigger –  Chewing breaks medication down faster & allows

for quicker absorption –  Hold if patient allergic

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•  Nitroglycerin - 0.4 mg SL every 5 minutes –  Dilates coronary vessels to relieve vasospams –  Increases collateral blood flow –  Dilates veins to reduce preload to reduce

workload of heart •  Watch for hypotension •  If inferior wall MI (II, III, aVF), contact Medical

Control prior to administration –  If pain persists, move to Morphine –  Check for recent male enhancement drug use

(ie: viagra, cialis, levitra) •  Side effect could be lethal hypotension

Acute Coronary Syndrome Medications cont.

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Acute Coronary Syndrome Region X EMS Medications cont.

•  Morphine - 2 mg slow IVP – Decreases pain & apprehension – Mild venodilator & arterial dilator

• Reduces preload and afterload – Given if pain level not changed after

nitroglycerin – Give 2mg slow IVP repeated every 2 minutes

as needed – Max total dose 10 mg

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T wave •  The normal T wave is asymmetrical, the

first half having a more gradual slope than the second half

•  The T wave should generally be at least 1/8 but less than 2/3 of the amplitude of the corresponding R wave

•  T wave amplitude rarely exceeds 10 mm •  Abnormal T waves are symmetrical, tall,

peaked, biphasic or inverted.

T wave

•  As a rule, the T wave follows the direction of the main QRS deflection. Thus when the main QRS deflection is positive (upright), the T wave is normally positive.

•  Other rules – The normal T wave is always negative in lead

aVR but positive in lead II. – Left-sided chest leads such as V4 to V6

normally always show a positive T wave. 306

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HYPERKALEMIA: PEAKED T WAVES

See a normal EKG…

HYPOKALEMIA: PROMINENT U WAVES

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 0.02

sec. –  For every 10 bpm decrease below 70 add 0.02 sec

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

QT Interval

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Long QT Syndrome

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Prolonged QTc

•  During sleep •  Hypocalcemia •  Ac myocarditis •  AMI •  Drugs like

quinidine,procainamide,tricyclic antidepressants

•  Hypothermia •  HOCM

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•  Advanced AV block or high degree AV block

•  Jervell-Lange –Neilson syndrome •  Romano-ward syndrome

Shortened QT

•  Digitalis effect •  Hypercalcemia •  Hyperthermia •  Vagal stimulation

QT Interval

•  The QT interval increases slightly with age and tends to be longer in women than in men.

•  Bazett's correction is used to calculate the QT interval corrected for heart rate (QTc): QTc = QT/ Sq root [R-R in seconds]

U wave •  Normal U waves are small, round, symmetrical

and positive in lead II, with amplitude < 2 mm (amplitude is usually < 1/3 T wave amplitude in same lead)

•  U wave direction is the same as T wave direction in that lead

•  More prominent at slow heart rates and usually best seen in the right precordial leads.

•  Origin of the U wave is thought to be related to afterdepolarizations which interrupt or follow repolarization

Final Impression “ Does the ECG correlate with the clinical scenario ?”

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Rhythm Identification Practice

�  Review the following rhythm strips

�  On mouse click, the answer will show

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Sinus w/ 1st degree Block No symptoms are due to the first degree heart

block; symptoms would be related to the underlying rhythm

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Junctional Tachycardia Note: Inverted P waves; heart rate 140

How is the patient tolerating the heart rate?

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2nd Degree Type 1 – Wenckebach PR getting longer and finally 1 QRS drops;

patient generally asymptomatic; can be normal rhythm for some patients

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WPW Syndrome Slurring at beginning of QRS (delta wave) Better diagnosed on 12 lead EKG; patient asymptomatic unless heart rate becomes

tachycardic

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2nd Degree Type II (2:1 conduction) Should be preparing the TCP for this patient

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3rd degree heart block (complete) with narrow QRS

Symptoms usually based on overall heart rate – the slower the heart rate the more

symptomatic the patient. Prepare the TCP.

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NSR to Torsade des Pointes If torsades is long lasting, patient may

become unresponsive and arrest. Prepare for defibrillation followed immediately with CPR

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Intermittent 2nd Degree Type II (Long PR intervals; periodic dropped beat)

Consider need to apply TCP and then turn on if patient symptomatic

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Why would this patient have symptoms of a stroke?

�  Atrial fibrillation puts patient at risk from clots in the atria breaking loose and lodging in a vessel in the brain

�  Rhythm irregularly irregular

�  Patient most likely on Coumadin and digoxin 11/13/13 badri@gmc 328

Ventricular Tachycardia �  What 2 questions should you ask for all tachycardias?

�  Is the patient stable or unstable? �  If stable, then you have time to determine if the QRS is

narrow or wide

�  What’s this strip?

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Paroxysmal Supraventricular Tachycardia (PSVT) into sinus rhythm

Evidence of abrupt stopping of the SVT

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Sinus Arrhythmia Common in the pediatric patient and influenced by

respirations. Treatment is not indicated

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Sinus with unifocal PVC’s in trigeminy

Often PVC’s go away after administration of oxygen

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Multifocal Atrial Tachycardia (MAT)

Rapid Wandering Pacemaker Identification can be SVT and treatment would

be based on patient symptoms

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ST elevation in V2 – V5 (Anterior wall)

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No ST elevation but peaked T waves (Hyperkalemia)

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ST elevation in II, III & aVF (Inferior wall with LBBB)

Watch for hypotension

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ST Elevation Inferior Wall – II, III, aVF


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ST elevation in II, III, aVF (Inferior wall - note reciprocal changes)


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ST elevation in V1 – V6, I & aVL (Anteroseptal with lateral extension)

Extensive anteroseptal Watch for heart block

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ST elevation V2-V5 Watch for heart block

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Thank You!!! 11/13/13 badri@gmc 342

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