ECG BASICS By Dr Bashir Ahmed Dar Chinkipora Sopore Kashmir Associate Professor Medicine Email [email_address]

From Right to Left Dr.Smitha associate prof gynae Dr Bashir associate professor Medicine Dr Udaman neurologist Dr Patnaik HOD ortho Dr Tin swe aye paeds

From Right to Left

Dr.Smitha associate prof gynae

Dr Bashir associate professor Medicine

Dr Udaman neurologist

Dr Patnaik HOD ortho

Dr Tin swe aye paeds

From RT to Lt Professor Dr Datuk rajagopal N Dr Bashir associate professor medicine Dr Urala HOD gynae Dr Nagi reddy tamma HOD-opthomology Dr Setharamarao Prof ortho

From RT to Lt

Professor Dr Datuk rajagopal N

Dr Bashir associate professor medicine

Dr Urala HOD gynae

Dr Nagi reddy tamma HOD-opthomology

Dr Setharamarao Prof ortho

ELECTROGRAPHY MADE EASY ULTIMATE AIM TO HELP PATIENTS

ULTIMATE AIM TO HELP PATIENTS

ECG machine

Limb and chest leads When an ECG is taken we put 4 limb leads or electrodes with different colour codes on upper and lower limbs one each at wrists and ankles by applying some jelly for close contact. We also put six chest leads at specific areas over the chest So in reality we see only 10 chest leads.

When an ECG is taken we put 4 limb leads or electrodes with different colour codes on upper and lower limbs one each at wrists and ankles by applying some jelly for close contact.

We also put six chest leads at specific areas over the chest

So in reality we see only 10 chest leads.

Position of limb and chest leads Four limb leads Six chest leads V1- 4th intercostal space to the right of sternum V2- 4th intercostal space to the left of sternum V3- halfway between V2 and V4 V4- 5th intercostal space in the left mid-clavicular line V5- 5th intercostal space in the left anterior axillary line V6- 5th intercostal space in the left mid axillary line

Four limb leads

Six chest leads

V1- 4th intercostal space to the right of sternum

V2- 4th intercostal space to the left of sternum

V3- halfway between V2 and V4

V4- 5th intercostal space in the left mid-clavicular line

V5- 5th intercostal space in the left anterior axillary line

V6- 5th intercostal space in the left mid axillary line

Horizontal plane - the six chest leads 6.5 V1 V1 V2 V2 V3 V3 V4 V4 V5 V5 V6 V6 RA LA LV RV

Colour codes given by AHA

ECG Paper: Dimensions 5 mm 1 mm 0.1 mV 0.04 sec 0.2 sec Speed = rate Voltage ~Mass

ECG paper and timing ECG paper speed = 25mm/sec Voltage calibration 1 mV = 1cm ECG paper - standard calibrations each small square = 1mm each large square = 5mm Timings 1 small square = 0.04sec 1 large square = 0.2sec 25 small squares = 1sec 5 large squares = 1sec

ECG paper speed = 25mm/sec

Voltage calibration 1 mV = 1cm

ECG paper - standard calibrations

each small square = 1mm

each large square = 5mm

Timings

1 small square = 0.04sec

1 large square = 0.2sec

25 small squares = 1sec

5 large squares = 1sec

After applying these leads on different positions then these leads are connected to a connector and then to ECG machine. The speed of machine kept usually 25mm/second.calibration or standardization done while machine is switched on.

After applying these leads on different positions then these leads are connected to a connector and then to ECG machine.

The speed of machine kept usually 25mm/second.calibration or standardization done while machine is switched on.

ECG paper 5 Large squares = 1 second Time 1 Large square = 0.2 second 1 Small square = 0.04 second 2 Large squares = 1 cm 6.1

The first step while reading ECG is to look for standardization is properly done. Look for this mark and see that this mark exactly covers two big squares on graph.

The first step while reading ECG is to look for standardization is properly done.

Look for this mark and see that this mark exactly covers two big squares on graph.

STANDARDISATION ECG amplitude scale Normal amplitude 10 mm/mV Half amplitude 5 mm/mV Double amplitude 20 mm/mV

ECG WAVES You will see then base line or isoelectric line that is in line with P-Q interval and beginning of S-T segment. From this line first positive deflection will arise as P wave then other waves as shown in next slide. Small negative deflections Q wave and S wave also arise from this line.

You will see then base line or isoelectric line that is in line with P-Q interval and beginning of S-T segment.

From this line first positive deflection will arise as P wave then other waves as shown in next slide.

Small negative deflections Q wave and S wave also arise from this line.

ECG WAVES

The Normal ECG Normal Intervals: PR 0.12-0.20s QRS duration <0.12s QTc 0.33-0.43s

Simplified normal Position of leads on ECG graph Lead 1# upward PQRS Lead 2# upward PQRS Lead 3# upward PQRS Lead AVR#downward or negative PQRS Lead AVL# upward PQRS Lead AVF# upwards PQRS

Lead 1# upward PQRS

Lead 2# upward PQRS

Lead 3# upward PQRS

Lead AVR#downward or negative PQRS

Lead AVL# upward PQRS

Lead AVF# upwards PQRS

Simplified normal Position of leads on ECG graph Chest lead V1# negative or downward PQRS Chest leads V2-V3-V4-V5-V6 all are upright from base line .The R wave slowly increasing in height from V1 to V6. So in normal ECG you see only AVR and V1 as negative or downward defelections as shown in next slide.

Chest lead V1# negative or downward PQRS

Chest leads V2-V3-V4-V5-V6 all are upright from base line .The R wave slowly increasing in height from V1 to V6.

So in normal ECG you see only AVR and V1 as negative or downward defelections as shown in next slide.

Normal ECG

NSR

P-wave Normal P wave length from beginning of P wave to end of P wave is 2 and a half small square. Height of P wave from base line or isoelectric line is also 2 and a half small square.

Normal P wave length from beginning of P wave to end of P wave is 2 and a half small square.

Height of P wave from base line or isoelectric line is also 2 and a half small square.

P-wave Normal values up in all leads except AVR. Duration. < 2.5 mm. Amplitude. < 2.5 mm. Abnormalities 1. Inverted P-wave Junctional rhythm. 2. Wide P-wave (P- mitrale) LAE 3. Peaked P-wave (P-pulmonale) RAE 4. Saw-tooth appearance Atrial flutter 5. Absent normal P wave Atrial fibrillation

Normal values

up in all leads except AVR.

Duration. < 2.5 mm.

Amplitude.

< 2.5 mm.

Abnormalities

1. Inverted P-wave

Junctional rhythm.

2. Wide P-wave (P- mitrale)

LAE

3. Peaked P-wave (P-pulmonale)

RAE

4. Saw-tooth appearance

Atrial flutter

5. Absent normal P wave

Atrial fibrillation

P wave height 2 and half small squares ,width also 2 and half small square

Shape of P wave The upward limb and downward limbs of P wave are equal. Summit or apex of P wave is slightly rounded.

The upward limb and downward limbs of P wave are equal.

Summit or apex of P wave is slightly rounded.

P pulmonale & P mitrale P pulmonale-Summit or apex of P wave becomes arrow like pointed or pyramid shape,the height also becomes more than two small squares from base line. P waves best seen in lead 2 and V1.

P pulmonale-Summit or apex of P wave becomes arrow like pointed or pyramid shape,the height also becomes more than two small squares from base line.

P waves best seen in lead 2 and V1.

P pulmonale & P mitrale P mitrale- the apex or summit of p wave may become notched .the notch should be at least more than one small square. Duration of P becomes more than two and a half small squares.

P mitrale- the apex or summit of p wave may become notched .the notch should be at least more than one small square.

Duration of P becomes more than two and a half small squares.

Left Atrial Enlargement Criteria P wave duration in II >than 2 and half small squares with notched p wave or Negative component of biphasic P wave in V 1 ≥ 1 “small box” in area

Right Atrial Enlargement Criteria P wave height in II >2 and half small squares and are also tall and peaked. or Positive component of biphasic P wave in V 1 > 1 “small box” in area

Atrial fibrillation P waves thrown into number of small abnormal P waves before each QRS complex The duration of R-R interval varies The amplitude of R-R varies Abnormal P waves don’t resemble one another.

P waves thrown into number of small abnormal P waves before each QRS complex

The duration of R-R interval varies

The amplitude of R-R varies

Abnormal P waves don’t resemble one another.

Atrial flutter The P waves thrown into number of abnormal P waves before each QRS complex. But these abnormal P waves almost resemble one another and are more prominent like saw tooth appearance.

The P waves thrown into number of abnormal P waves before each QRS complex.

But these abnormal P waves almost resemble one another and are more prominent like saw tooth appearance.

Junctional rhythm In Junctional rhythm the P waves may be absent or inverted.in next slide u can see these inverted P waves.

In Junctional rhythm the P waves may be absent or inverted.in next slide u can see these inverted P waves.

Paroxysmal atrial tachycardia The P and T waves you cant make out separately The P and T waves are merged in one The R-R intervals do not vary but remain constant and same. The heart rate being very high around 150 and higher.

The P and T waves you cant make out separately

The P and T waves are merged in one

The R-R intervals do not vary but remain constant and same.

The heart rate being very high around 150 and higher.

NORMAL P-R INTERVAL PR interval time 0.12 seconds to 0.2 seconds. That is three small squares to five small squares.

PR interval time 0.12 seconds to 0.2 seconds.

That is three small squares to five small squares.

PR interval Definition: the time interval between beginning of P-wave to beginning of QRS complex. Normal PR interval 3-5mm or 3-5 small squares on ECG graph (0.12-0.2 sec) Abnormalities 1. Short PR interval WPW syndrome 2. Long PR interval First degree heart block

Definition: the time interval between beginning of P-wave to beginning of QRS complex.

Normal PR interval

3-5mm or 3-5 small squares on ECG graph (0.12-0.2 sec)

Abnormalities

1. Short PR interval

WPW syndrome

2. Long PR interval

First degree heart block

Short P-R interval Short P-R interval seen in WPW syndrome or pre- excitation syndrome or LG syndrome P-R interval is less than three small squares. The beginning of R wave slopes gradually up and is slightly widened called Delta wave. There may be S-T changes also like ST depression and T wave inversion.

Short P-R interval seen in WPW syndrome or pre- excitation syndrome or LG syndrome

P-R interval is less than three small squares.

The beginning of R wave slopes gradually up and is slightly widened called Delta wave.

There may be S-T changes also like ST depression and T wave inversion.

Lengthening of P-R interval Occurs in first degree heart block. The P-R interval is more than 5 small squares or > than 0.2 seconds. This you will see in all leads and is same fixed lengthening .

Occurs in first degree heart block.

The P-R interval is more than 5 small squares or > than 0.2 seconds.

This you will see in all leads and is same fixed lengthening .

Q WAVES Q waves <0.04 second. That’s is less than one small square duration. Height <25% or < 1 / 4 of R wave height.

Q waves <0.04 second.

That’s is less than one small square duration.

Height <25% or < 1 / 4 of R wave height.

Normal Q wave

Abnormal Q waves The duration or width of Q waves becomes more than one small square on ECG graph. The depth of Q wave becomes more than 25% of R wave. The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy.

The duration or width of Q waves becomes more than one small square on ECG graph.

The depth of Q wave becomes more than 25% of R wave.

The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy.

Q wave in MI

Q wave in septal hypertrophy

QRS COMPLEX QRS duration <0.11 s That is less than almost three small squares Some books write 2 and a half small squares. Height of R wave is (V1-V6) >8 mm some say >10 mm chest leads (in at least one of chest leads).

QRS duration <0.11 s

That is less than almost three small squares

Some books write 2 and a half small squares.

Height of R wave is (V1-V6) >8 mm some say >10 mm chest leads (in at least one of chest leads).

QRS complex Normal values Duration : < 2.5 mm. Morphology : progression from Short R and deep S (r/s) in V1 to tall R and short S in V6 with small Q in V5-6. Abnormalities : 1. Wide QRS complex Bundle branch block. Ventricular rhythm . 2. Tall R in V1 RVH. RBBB. Posterior MI. WPW syndrome. 3. abnormal Q wave [ > 25% of R wave] MI. Hypertrophic cardiomyopathy. Normal variant.

Normal values

Duration : < 2.5 mm.

Morphology : progression from Short R and deep S (r/s) in V1 to tall R and short S in V6 with small Q in V5-6.

Abnormalities :

1. Wide QRS complex

Bundle branch block.

Ventricular rhythm .

2. Tall R in V1

RVH.

RBBB.

Posterior MI.

WPW syndrome.

3. abnormal Q wave

[ > 25% of R wave]

MI.

Hypertrophic cardiomyopathy.

Normal variant.

Small voltage QRS Defined as < 5 mm peak-to-peak in all limb leads or <10 mm in precordial chest leads. causes — pulmonary disease, hypothyroidism, obesity, cardiomyopathy. Acute causes — pleural and/or pericardial effusions

Defined as < 5 mm peak-to-peak in all limb leads or <10 mm in precordial chest leads.

causes — pulmonary disease, hypothyroidism, obesity, cardiomyopathy.

Acute causes — pleural and/or pericardial effusions

Normal upward progression of R wave from V1 to V6 V 1 V 2 V 3 V 4 V 5 V 6 The R wave in the precordial leads must grow from V1 to at least V4

J point The term J point means Junctional point at the end of S wave between S wave and beginning of S-T segment.

The term J point means Junctional point at the end of S wave between S wave and beginning of S-T segment.

J point Q S ST

L V H-Voltage Criteria In adult with normal chest wall SV1+RV5 >35 mm or SV1 >20 mm or RV6 >20 mm

In adult with normal chest wall

SV1+RV5 >35 mm

or

SV1 >20 mm

or

RV6 >20 mm

Left ventricular hypertrophy-Voltage Criteria Count small squares of downward R wave in V1 plus small squares of R wave in V5 . If it comes to more than 35 small squares then it is suggestive of LVH.

Count small squares of downward R wave in V1 plus small squares of R wave in V5 .

If it comes to more than 35 small squares then it is suggestive of LVH.

LEFT VENTRICULAR HYPERTROPHY

Right ventricular hypertrophy Normally you see R wave is downward deflection in V1.but if you see upward R wave in V1 then it is suggestive of RVH etc.

Normally you see R wave is downward deflection in V1.but if you see upward R wave in V1 then it is suggestive of RVH etc.

Dominant or upward R wave in V1 Causes RBBB Chronic lung disease, PE Posterior MI WPW Type A Dextrocardia Duchenne muscular dystrophy

Causes

RBBB

Chronic lung disease, PE Posterior MI WPW Type A Dextrocardia Duchenne muscular dystrophy

Right Ventricular Hypertrophy WILL SHOW AS Right axis deviation (RAD) Precordial leads In V1, R wave > S wave In V6, S wave > R wave Usual manifestation is pulmonary disease or congenital heart disease

WILL SHOW AS

Right axis deviation (RAD)

Precordial leads

In V1, R wave > S wave

In V6, S wave > R wave

Usual manifestation is pulmonary disease or

congenital heart disease

Right Ventricular Hypertrophy

Right ventricular hypertrophy Right ventricular hypertrophy (RVH) increases the height of the R wave in V1. And R wave in V1 greater than 7 boxes in height, or larger than the S wave, is suspicious for RVH. Other findings are necessary to confirm the ECG diagnosis.

Right ventricular hypertrophy (RVH) increases the height of the R wave in V1. And R wave in V1 greater than 7 boxes in height, or larger than the S wave, is suspicious for RVH. Other findings are necessary to confirm the ECG diagnosis.

Right Ventricular Hypertrophy Other findings in RVH include right axis deviation, taller R waves in the right precordial leads (V1-V3), and deeper S waves in the left precordial (V4-V6). The T wave is inverted in V1 (and often in V2).

Other findings in RVH include right axis deviation, taller R waves in the right precordial leads (V1-V3), and deeper S waves in the left precordial (V4-V6). The T wave is inverted in V1 (and often in V2).

Right Ventricular Hypertrophy True posterior infarction may also cause a tall R wave in V1, but the T wave is usually upright, and there is usually some evidence of inferior infarction (ST-T changes or Qs in II, III, and F).

True posterior infarction may also cause a tall R wave in V1, but the T wave is usually upright, and there is usually some evidence of inferior infarction (ST-T changes or Qs in II, III, and F).

Right Ventricular Hypertrophy A large R wave in V1, when not accompanied by evidence of infarction, nor by evidence of RVH (right axis, inverted T wave in V1), may be benign “counter-clockwise rotation of the heart.” This can be seen with abnormal chest shape.

A large R wave in V1, when not accompanied by evidence of infarction, nor by evidence of RVH (right axis, inverted T wave in V1), may be benign “counter-clockwise rotation of the heart.” This can be seen with abnormal chest shape.

Right Ventricular Hypertrophy Tall R wave in V 1 Right axis deviation Right atrial enlargement Down sloping ST depressions in V 1 -V 3 ( RV strain pattern) Although there is no widely accepted criteria for detecting the presence of RVH, any combination of the following EKG features is suggestive of its presence:

Tall R wave in V 1

Right axis deviation

Right atrial enlargement

Down sloping ST depressions in V 1 -V 3 ( RV strain pattern)

Right Ventricular Hypertrophy

Left Ventricular Hypertrophy

Left Ventricular Hypertrophy

ECG criteria for RBBB •(1) QRS duration exceeds 0.12 seconds or 2 and half small squares roughly in V1 and may also see it in V2. •(2) RSR complex in V1 may extend to V2.

•(1) QRS duration exceeds 0.12 seconds or 2 and half small squares roughly in V1 and may also see it in V2.

•(2) RSR complex in V1 may extend to V2.

ECG criteria for RBBB • ST/T must be opposite in direction to the terminal QRS(is secondary to the block and does not mean primary ST/T changes). It you meet all above criteria it is then complete right bundle branch block. In incomplete bundle branch block the duration of QRS will be within normal limits.

• ST/T must be opposite in direction to the terminal QRS(is secondary to the block and does not mean primary ST/T changes).

It you meet all above criteria it is then complete right bundle branch block.

In incomplete bundle branch block the duration of QRS will be within normal limits.

RBBB & MI If abnormal Q waves are present they will not be masked by the RBBB pattern. •This is because there is no alteration of the initial part of the complex RS (in V1) and abnormal Q waves can still be seen.

If abnormal Q waves are present they will not be masked by the RBBB pattern.

•This is because there is no alteration of the initial part of the complex RS (in V1) and abnormal Q waves can still be seen.

Significance of RBBB RBBB is seen in :- (1) occasional normal subjects (2) pulmonary embolus (3) coronary artery disease (4) ASD (5) active Carditis (6) RV diastolic overload

RBBB is seen in :-

(1) occasional normal subjects

(2) pulmonary embolus

(3) coronary artery disease

(4) ASD

(5) active Carditis

(6) RV diastolic overload

Partial / Incomplete RBBB is diagnosed when the pattern of RBBB is present but the duration of the QRS does not exceed 0.12 seconds or roughly 2 and a half small squares.

is diagnosed when the pattern of RBBB is present but the duration of the QRS does not exceed 0.12 seconds or roughly 2 and a half small squares.

In next slide you will see ECG characteristics of a typical RBBB showing wide QRS complexes with a terminal R wave in lead V1 and slurred S wave in lead V6. Also you see R wave has become upright in V1.QRS duration has also increased making it complete RBBB.

ECG characteristics of a typical RBBB showing wide QRS complexes with a terminal R wave in lead V1 and slurred S wave in lead V6.

Also you see R wave has become upright in V1.QRS duration has also increased making it complete RBBB.

ECG criteria for LBBB (1)Prolonged QRS complexes, greater than 0.12 seconds or roughly 2 and half small squares in all leads almost. (2)Wide, notched QRS (M shaped) V5, V6 (3)Wide, notched QS complexes are seen in V1 (due to spread of activation away from the electrode through septum + LV) (4)In V2, V3 small r wave may be seen due to activation of para septal region

(1)Prolonged QRS complexes, greater than 0.12 seconds or roughly 2 and half small squares in all leads almost.

(2)Wide, notched QRS (M shaped) V5, V6

(3)Wide, notched QS complexes are seen in V1 (due to spread of activation away from the electrode through septum + LV)

(4)In V2, V3 small r wave may be seen due to activation of para septal region

ECG criteria for LBBB So look in all leads for QRS duration to make it complete LBBB or incomplete LBBB as u did in RBBB. Look in V5 and V6 for M shaped pattern at summit or apex of R wave. Look for any changes as S-T depression and T wave in inversion if any.

So look in all leads for QRS duration to make it complete LBBB or incomplete LBBB as u did in RBBB.

Look in V5 and V6 for M shaped pattern at summit or apex of R wave.

Look for any changes as S-T depression and T wave in inversion if any.

Significance of LBBB LBBB is seen in :- (1) Always indicative of organic heart disease (2) Found in ischemic heart disease (3) Found in hypertension. MI should not be diagnosed in the presence of LBBB ->Q waves are masked by LBBB pattern Cannot diagnose the presence of MI with LBBB

LBBB is seen in :-

(1) Always indicative of organic heart disease

(2) Found in ischemic heart disease

(3) Found in hypertension.

MI should not be diagnosed in the presence of LBBB ->Q waves are masked by LBBB pattern

Cannot diagnose the presence of MI with LBBB

Partial / Incomplete LBBB is diagnosed when the pattern of LBBB is present but the duration of the QRS does not exceed 0.12 seconds or roughly 2 and half small squares.

is diagnosed when the pattern of LBBB is present but the duration of the QRS does not exceed 0.12 seconds or roughly 2 and half small squares.

NORMAL ST- SEGMENT it's isoelectric. [i.e. at same level of PR or PQ segment at least in the beginning]

it's isoelectric.

[i.e. at same level of PR or PQ segment at least in the beginning]

NORMAL CONCAVITY OF S-T SEGMENT It then gradually slopes upwards making concavity upwards and not going more than one small square upwards from isoelectric line or one small square below isoelectric line. In MI this concavity may get lost and become convex upwards called coving of S-T segment.

It then gradually slopes upwards making concavity upwards and not going more than one small square upwards from isoelectric line or one small square below isoelectric line.

In MI this concavity may get lost and become convex upwards called coving of S-T segment.

Abnormalities ST elevation: More than one small square Acute MI. Prinzmetal angina. Acute pericarditis. Early repolarization ST depression: More than one small square Ischemia. Ventricular strain. BBB. Hypokalemia. Digoxin effect.

ST elevation:

More than one small square

Acute MI.

Prinzmetal angina.

Acute pericarditis.

Early repolarization

ST depression:

More than one small square

Ischemia.

Ventricular strain.

BBB.

Hypokalemia.

Digoxin effect.

Stress test ECG – note the ST Depression

Note the arrows pointing ST depression

ST depression & Troponin T positive is NON STEMI

Coving of S-T segment Concavity lost and convexity appear facing upwards.

Concavity lost and convexity appear facing upwards.

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

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

Abnormalities of ST- segment acute MI pericarditis early repolariz. ischemia

Q waves in myocardial infarction

T-wave Normal values. 1.amplitude: < 10mm in the chest leads. Abnormalities: 1. Peaked T-wave: Hyper-acute MI. Hyperkalemia. Normal variant . 2. T- inversion: Ischemia. Myocardial infarction. Myocarditis Ventricular strain BBB. Hypokalemia. Digoxin effect.

Normal values.

1.amplitude:

< 10mm in the chest leads.

Abnormalities:

1. Peaked T-wave:

Hyper-acute MI.

Hyperkalemia.

Normal variant

.

2. T- inversion:

Ischemia.

Myocardial infarction.

Myocarditis

Ventricular strain

BBB.

Hypokalemia.

Digoxin effect.

QT- interval Definition : Time interval between beginning of QRS complex to the end of T wave. Normally: At normal HR: QT ≤ 11mm (0.44 sec) Abnormalities : Prolonged QT interval: hypocalcemia and congenital long QT syndrome. Short QT interval: hypercalcemia.

Definition : Time interval between beginning of

QRS complex to the end of T wave.

Normally: At normal HR: QT ≤ 11mm (0.44 sec)

Abnormalities :

Prolonged QT interval: hypocalcemia and congenital long QT syndrome.

Short QT interval: hypercalcemia.

QT Interval - Should be < 1/2 preceding R to R interval -

QT Interval - Should be < 1/2 preceding R to R interval - QT interval

QT Interval - Should be < 1/2 preceding R to R interval - QT interval

QT Interval - Should be < 1/2 preceding R to R interval - QT interval R R

QT Interval - Should be < 1/2 preceding R to R interval - QT interval R R

QT Interval - Should be < 1/2 preceding R to R interval - QT interval R R

QT Interval - Should be < 1/2 preceding R to R interval - QT interval 65 - 90 bpm R R

QT Interval - Should be < 1/2 preceding R to R interval - QT interval 65 - 90 bpm Normal QT c = 0.46 sec R R

Atrioventricular (AV) Heart Block

Classification of AV Heart Blocks Degree AV Conduction Pattern 1 St Degree Block Uniformly prolonged PR interval 2 nd Degree, Mobitz Type I Progressive PR interval prolongation 2 nd Degree, Mobitz Type II Sudden conduction failure 3 rd Degree Block No AV conduction

AV Blocks First Degree Prolonged AV conduction time PR interval > 0.20 seconds

First Degree

Prolonged AV conduction time

PR interval > 0.20 seconds

1 st Degree AV Block Prolongation of the PR interval, which is constant All P waves are conducted

1st degree AV Block : Regular Rhythm PRI > .20 seconds or 5 small squares and is CONSTANT Usually does not require treatment PRI > .20 seconds

1st degree AV Block :

Regular Rhythm

PRI > .20 seconds or 5 small squares and is CONSTANT

Usually does not require treatment

First Degree Block prolonged PR interval

prolonged PR interval

Analyze the Rhythm

AV Blocks Second Degree Definition More Ps than QRSs Every QRS caused by a P

Second Degree

Definition

More Ps than QRSs

Every QRS caused by a P

Second-Degree AV Block There is intermittent failure of the supraventricular impulse to be conducted to the ventricles Some of the P waves are not followed by a QRS complex.The conduction ratio (P/QRS ratio) may be set at 2:1,3:1,3:2,4:3,and so forth

There is intermittent failure of the supraventricular impulse to be conducted to the ventricles

Some of the P waves are not followed by a QRS complex.The conduction ratio (P/QRS ratio) may be set at 2:1,3:1,3:2,4:3,and so forth

Second Degree Types Type I Wenckebach phenomenon Type II Fixed or Classical

Types

Type I

Wenckebach phenomenon

Type II

Fixed or Classical

Type I Second-Degree AV Block: Wenckebach Phenomenon ECG findings 1.Progressive lengthening of the PR interval until a P wave is blocked

ECG findings

1.Progressive lengthening of the PR interval until a P wave is blocked

2nd degree AV Block (“Mobitz I” also called “Wenckebach”) : Pattern Repeats…………. PRI = .24 sec PRI = .36 sec PRI = .40 sec QRS is “dropped” Irregular Rhythm PRI continues to lengthen until a QRS is missing (non-conducted sinus impulse) PRI is NOT CONSTANT Pause 4:3 Wenckebach (conduction ratio may not be constant)

Irregular Rhythm

PRI continues to lengthen until a QRS is missing (non-conducted sinus impulse)

PRI is NOT CONSTANT

Type II Second-Degree AV Block: Mobitz Type II ECG findings 1.Intermittent or unexpected blocked P waves you don’t know when QRS drops 2.P-R intervals may be normal or prolonged,but they remain constant 4. A long rhythm strip may help

ECG findings

1.Intermittent or unexpected blocked P waves you don’t know when QRS drops

2.P-R intervals may be normal or prolonged,but they remain constant

4. A long rhythm strip may help

Second Degree AV Block Mobitz type I or Winckebach Mobitz type II

Mobitz type I or Winckebach

Mobitz type II

Type 1 (Wenckebach) Progressive prolongation of the PR interval until a P wave is not conducted. Constant PR interval with unexpected intermittent failure to conduct Type 2

Mobitz Type I

MOBITZ TYPE 1

2nd degree AV Block (“Mobitz II”) : Irregular Rhythm QRS complexes may be somewhat wide (greater than .12 seconds) Non-conducted sinus impulses appear at unexpected irregular intervals PRI may be normal or prolonged but is CONSTANT and fixed Rhythm is somewhat dangerous May cause syncope or may deteriorate into complete heart block (3rd degree block) It’s appearance in the setting of an acute MI identifies a high risk patient Cause: anterioseptal MI, Treatment: may require pacemaker in the case of fibrotic conduction system Non-conducted sinus impulses “ 2:1 block ” “ 3:1 block” PRI is CONSTANT

2nd degree AV Block (“Mobitz II”) :

Irregular Rhythm

QRS complexes may be somewhat wide (greater than .12 seconds)

Non-conducted sinus impulses appear at unexpected irregular intervals

PRI may be normal or prolonged but is CONSTANT and fixed

Rhythm is somewhat dangerous May cause syncope or may deteriorate into complete heart block (3rd degree block)

It’s appearance in the setting of an acute MI identifies a high risk patient

Cause: anterioseptal MI,

Treatment: may require pacemaker in the case of fibrotic conduction system

Analyze the Rhythm

Second Degree Mobitz Characteristics Atrial rate > Ventricular rate QRS usually longer than 0.12 sec Usually 4:3 or 3:2 conduction ratio (P:QRS ratio)

Characteristics

Atrial rate > Ventricular rate

QRS usually longer than 0.12 sec

Usually 4:3 or 3:2 conduction ratio (P:QRS ratio)

Analyze the Rhythm

Mobitz II Definition: Mobitz II is characterized by 2-4 P waves before each QRS. The PR pf the conducted P wave will be constant for each QRS . EKG Characteristics:Atrial and ventricular rate is irregular. P Wave: Present in two, three or four to one conduction with the QRS. PR Interval constant for each P wave prior to the QRS. QRS may or may not be within normal limits.

Definition: Mobitz II is characterized by 2-4 P waves before each QRS. The PR pf the conducted P wave will be constant for each QRS

. EKG Characteristics:Atrial and ventricular rate is irregular. P Wave: Present in two, three or four to one conduction with the QRS. PR Interval constant for each P wave prior to the QRS. QRS may or may not be within normal limits.

Mobitz Type II

Mobitz Type II Sudden appearance of a single, non-conducted sinus P wave...

Sudden appearance of a single, non-conducted sinus P wave...

Advanced Second-Degree AV Block Two or more consecutive nonconducted sinus P waves

Complete AV Block Characteristics Atrioventricular dissociation Regular P-P and R-R but without association between the two Atrial rate > Ventricular rate QRS > 0.12 sec

Characteristics

Atrioventricular dissociation

Regular P-P and R-R but without association between the two

Atrial rate > Ventricular rate

QRS > 0.12 sec

3 rd Degree (Complete) AV Block EKG Characteristics: No relationship between P waves and QRS complexes Relatively constant PP intervals and RR intervals Greater number of P waves than QRS complexes

Complete heart block P waves are not conducted to the ventricles because of block at the AV node. The P waves are indicated below and show no relation to the QRS complexes. They 'probe' every part of the ventricular cycle but are never conducted.

P waves are not conducted to the ventricles because of block at the AV node. The P waves are indicated below and show no relation to the QRS complexes. They 'probe' every part of the ventricular cycle but are never conducted.

3rd degree AV Block (“Complete Heart Block”) : Irregular Rhythm QRS complexes may be narrow or broad depending on the level of the block Atria and ventricles beat independent of one another (AV dissociation) QRS’s have their own rhythm, P-waves have their own rhythm May be caused by inferior MI and it’s presence worsens the prognosis Treatment: usually requires pacemaker QRS intervals P-wave intervals – note how the P-waves sometimes distort QRS complexes or T-waves

3rd degree AV Block (“Complete Heart Block”) :

Irregular Rhythm

QRS complexes may be narrow or broad depending on the level of the block

Atria and ventricles beat independent of one another (AV dissociation)

QRS’s have their own rhythm, P-waves have their own rhythm

May be caused by inferior MI and it’s presence worsens the prognosis

Treatment: usually requires pacemaker

Third-Degree (Complete) AV Block

Third-Degree (Complete) AV Block The P wave bears no relation to the QRS complexes, and the PR intervals are completely variable

The P wave bears no relation to the QRS complexes, and the PR intervals are completely variable

30 AV Block AV dissociation atria and ventricles beating on their own no relation between P’s & QRS’s Atrial rate is different from ventricular ventricular rate: 30-60 bpm Rhythm is regular for both QRS can be narrow or wide depends on site of pacemaker!

AV dissociation

atria and ventricles beating on their own

no relation between P’s & QRS’s

Atrial rate is different from ventricular

ventricular rate: 30-60 bpm

Rhythm is regular for both

QRS can be narrow or wide

depends on site of pacemaker!

Key points Wenckebach look for group beating & changing PR Mobitz II look for reg. atrial rhythm & consistent PR 3o block atrial & ventricular rhythm regular 􀂾 rate is different!!! no consistent PR

Wenckebach

look for group beating & changing PR

Mobitz II

look for reg. atrial rhythm & consistent PR

3o block

atrial & ventricular rhythm regular

􀂾 rate is different!!!

no consistent PR

Left Anterior Fascicular Block Left axis deviation , usually -45 to -90 degrees QRS duration usually <0.12s unless coexisting RBBB Poor R wave progression in leads V1-V3 and deeper S waves in leads V5 and V6 There is RS pattern with R wave in lead II > lead III S wave in lead III > lead II QR pattern in lead I and AVL,with small Q wave No other causes of left axis deviation

Left axis deviation , usually -45 to -90 degrees

QRS duration usually <0.12s unless coexisting RBBB

Poor R wave progression in leads V1-V3 and deeper S waves in leads V5 and V6

There is RS pattern with R wave in lead II > lead III

S wave in lead III > lead II

QR pattern in lead I and AVL,with small Q wave

No other causes of left axis deviation

Left Anterior Hemiblock (LAHB) : Left axis deviation (> -30 degrees) will be noted and there will be a prominent S-wave in Leads II, and III LPIF LASF LBB 1. 2. Lead III Lead I Lead AVF

Left Anterior Hemiblock (LAHB) :

Left axis deviation (> -30 degrees) will be noted and there will be a prominent S-wave in Leads II, and III

Left Posterior Fascicular Block Right axis deviation QR pattern in inferior leads (II,III,AVF) small q wave RS patter in lead lead I and AVL(small R with deep S)

Right axis deviation

QR pattern in inferior leads (II,III,AVF) small q wave

RS patter in lead lead I and AVL(small R with deep S)

Left Posterior Hemiblock (LPHB) : Right axis deviation and there will be a prominent S-wave in Leads I. Q-waves may be noted in III and AVF. Notes on (LPHB) : QRS is normal width unless BBB is present If LPHB occurs in the setting of an acute MI, it is almost always accompanied by RBBB and carries a mortality rate of 71% LPIF LASF LBB 1. 2. Lead III Lead I Lead AVF

Left Posterior Hemiblock (LPHB) :

Right axis deviation and there will be a prominent S-wave in Leads I. Q-waves may be noted in III and AVF.

Notes on (LPHB) :

QRS is normal width unless BBB is present

If LPHB occurs in the setting of an acute MI, it is almost always accompanied by RBBB and carries a mortality rate of 71%

Bifascicular Bundle Branch Block RBBB with either left anterior or left posterior fascicular block Diagnostic criteria 1.Prolongation of the QRS duration to 0.12 second or longer 2.RSR’ pattern in lead V1,with the R’ being broad and slurred 3.Wide,slurred S wave in leads I,V5 and V6 4.Left axis or right axis deviation

RBBB with either left anterior or left posterior fascicular block

Diagnostic criteria

1.Prolongation of the QRS duration to 0.12 second or longer

2.RSR’ pattern in lead V1,with the R’ being broad and slurred

3.Wide,slurred S wave in leads I,V5 and V6

4.Left axis or right axis deviation

Trifascicular Block The combination of RBBB, LAFB and long PR interval Implies that conduction is delayed in the third fascicle

The combination of RBBB, LAFB and long PR interval

Implies that conduction is delayed in the third fascicle

Indications For Implantation of Permanent Pacing in Acquired AV Blocks 1.Third-degree AV block, Bradycardia with symptoms Asystole e.Neuromuscular diseases with AV block (Myotonic muscular dystrophy) 2.Second-degree AV block with symptomatic bradycardia

1.Third-degree AV block, Bradycardia with symptoms

Asystole

e.Neuromuscular diseases with AV block (Myotonic muscular dystrophy)

2.Second-degree AV block with symptomatic bradycardia

Cardiac Pacemakers Definition Delivers artificial stimulus to heart Causes depolarization and contraction Uses Bradyarrhythmias Asystole Tachyarrhythmias (overdrive pacing)

Definition

Delivers artificial stimulus to heart

Causes depolarization and contraction

Uses

Bradyarrhythmias

Asystole

Tachyarrhythmias (overdrive pacing)

Cardiac Pacemakers Types Fixed Fires at constant rate Can discharge on T-wave Very rare Demand Senses patient’s rhythm Fires only if no activity sensed after preset interval (escape interval) Transcutaneous vs Transvenous vs Implanted

Types

Fixed

Fires at constant rate

Can discharge on T-wave

Very rare

Demand

Senses patient’s rhythm

Fires only if no activity sensed after preset interval (escape interval)

Transcutaneous vs Transvenous vs Implanted

Cardiac Pacemakers

Cardiac Pacemakers Demand Pacemaker Types Ventricular Fires ventricles Atrial Fires atria Atria fire ventricles Requires intact AV conduction

Demand Pacemaker Types

Ventricular

Fires ventricles

Atrial

Fires atria

Atria fire ventricles

Requires intact AV conduction

Cardiac Pacemakers Demand Pacemaker Types Atrial Synchronous Senses atria Fires ventricles AV Sequential Two electrodes Fires atria/ventricles in sequence

Demand Pacemaker Types

Atrial Synchronous

Senses atria

Fires ventricles

AV Sequential

Two electrodes

Fires atria/ventricles in sequence

Cardiac Pacemakers Problems Failure to capture No response to pacemaker artifact Bradycardia may result Cause: high “threshold” Management Increase amps on temporary pacemaker Treat as symptomatic bradycardia

Problems

Failure to capture

No response to pacemaker artifact

Bradycardia may result

Cause: high “threshold”

Management

Increase amps on temporary pacemaker

Treat as symptomatic bradycardia

Cardiac Pacemakers Problems Failure to sense Spike follows QRS within escape interval May cause R-on-T phenomenon Management Increase sensitivity Attempt to override permanent pacer with temporary Be prepared to manage VF

Problems

Failure to sense

Spike follows QRS within escape interval

May cause R-on-T phenomenon

Management

Increase sensitivity

Attempt to override permanent pacer with temporary

Be prepared to manage VF

Implanted Defibrillators AICD Automated Implanted Cardio-Defibrillator Uses Tachyarrhythmias Malignant arrhythmias VT VF

AICD

Automated Implanted Cardio-Defibrillator

Uses

Tachyarrhythmias

Malignant arrhythmias

VT

VF

Implanted Defibrillators Programmed at insertion to deliver predetermined therapies with a set order and number of therapies including: pacing overdrive pacing cardioversion with increasing energies defibrillation with increasing energies standby mode Effect of standby mode on Paramedic treatments

Programmed at insertion to deliver predetermined therapies with a set order and number of therapies including:

pacing

overdrive pacing

cardioversion with increasing energies

defibrillation with increasing energies

standby mode

Effect of standby mode on Paramedic treatments

Implanted Defibrillators Potential Complications Fails to deliver therapies as intended worst complication requires Paramedic intervention Delivers therapies when NOT appropriate broken or malfunctioning lead parameters for delivery are not specific enough Continues to deliver shocks parameters for delivery are not specific enough and device senses a reset may be shut off (not standby mode) with donut-magnet

Potential Complications

Fails to deliver therapies as intended

worst complication

requires Paramedic intervention

Delivers therapies when NOT appropriate

broken or malfunctioning lead

parameters for delivery are not specific enough

Continues to deliver shocks

parameters for delivery are not specific enough and device senses a reset

may be shut off (not standby mode) with donut-magnet

Sinus Exit Block Due to abnormal function of SA node MI, drugs, hypoxia, vagal tone Impulse blocked from leaving SA node usually transient Produces 1 missed cycle can confuse with sinus pause or arrest

Due to abnormal function of SA node

MI, drugs, hypoxia, vagal tone

Impulse blocked from leaving SA node

usually transient

Produces 1 missed cycle

can confuse with sinus pause or arrest

Sinus block

ARRTHYMIAS AND ECTOPIC BEATS

normal (&quot;sinus&quot;) beats sinus node doesn't fire leading to a period of asystole (sick sinus syndrome) p-wave has different shape indicating it did not originate in the sinus node, but somewhere in the atria. It is therefore called an &quot;atrial&quot; beat QRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normal Atrial Escape Beat Recognizing and Naming Beats & Rhythms

there is no p wave, indicating that it did not originate anywhere in the atria, but since the QRS complex is still thin and normal looking, we can conclude that the beat originated somewhere near the AV junction. The beat is therefore called a &quot;junctional&quot; or a “nodal” beat Junctional Escape Beat QRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normal Recognizing and Naming Beats & Rhythms

actually a &quot;retrograde p-wave may sometimes be seen on the right hand side of beats that originate in the ventricles, indicating that depolarization has spread back up through the atria from the ventricles QRS is wide and much different (&quot;bizarre&quot;) looking than the normal beats. This indicates that the beat originated somewhere in the ventricles and consequently, conduction through the ventricles did not take place through normal pathways. It is therefore called a “ventricular” beat Ventricular Escape Beat there is no p wave, indicating that the beat did not originate anywhere in the atria Recognizing and Naming Beats & Rhythms

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

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

Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery 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) The “Re-Entry” Mechanism of Ectopic Beats & Rhythms

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

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 Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery Cardiac Conduction Tissue The “Re-Entry” Mechanism of Ectopic Beats & Rhythms

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

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 Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery Cardiac Conduction Tissue The “Re-Entry” Mechanism of Ectopic Beats & Rhythms

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

Recognizing and Naming Beats & Rhythms Premature Ventricular Contractions (PVC’s, VPB’s, extrasystoles) : A ventricular ectopic focus discharges causing an early beat Ectopic beat has no P-wave (maybe retrograde), and QRS complex is &quot;wide and bizarre&quot; QRS is wide because the spread of depolarization through the ventricles is abnormal (aberrant) In most cases, the heart circulates no blood (no pulse because of an irregular squeezing motion PVC’s are sometimes described by lay people as “skipped heart beats”

Premature Ventricular Contractions (PVC’s, VPB’s, extrasystoles) :

A ventricular ectopic focus discharges causing an early beat

Ectopic beat has no P-wave (maybe retrograde), and QRS complex is &quot;wide and bizarre&quot;

QRS is wide because the spread of depolarization through the ventricles is abnormal (aberrant)

In most cases, the heart circulates no blood (no pulse because of an irregular squeezing motion

PVC’s are sometimes described by lay people as “skipped heart beats”

Recognizing and Naming Beats & Rhythms Characteristics of PVC's PVC’s don’t have P-waves unless they are retrograde (may be buried in T-Wave) T-waves for PVC’s are usually large and opposite in polarity to terminal QRS Wide (> .16 sec) notched PVC’s may indicate a dilated hypokinetic left ventricle Every other beat being a PVC (bigeminy) may indicate coronary artery disease Some PVC’s come between 2 normal sinus beats and are called “interpolated” PVC’s Interpolated PVC – note the sinus rhythm is undisturbed The classic PVC – note the compensatory pause

Characteristics of PVC's

PVC’s don’t have P-waves unless they are retrograde (may be buried in T-Wave)

T-waves for PVC’s are usually large and opposite in polarity to terminal QRS

Wide (> .16 sec) notched PVC’s may indicate a dilated hypokinetic left ventricle

Every other beat being a PVC (bigeminy) may indicate coronary artery disease

Some PVC’s come between 2 normal sinus beats and are called “interpolated” PVC’s

PVC's are Dangerous When : They are frequent (> 30% of complexes) or are increasing in frequency The come close to or on top of a preceding T-wave (R on T) Three or more PVC's in a row (run of V-tach) Any PVC in the setting of an acute MI PVC's come from different foci (&quot;multifocal&quot; or &quot;multiformed&quot;) These dangerous phenomenon may preclude the occurrence of deadly arrhythmias: Ventricular Tachycardia Ventricular Fibrillation Recognizing and Naming Beats & Rhythms sinus beats Unconverted V-tach r V-fib V-tach “ R on T phenomenon” time The sooner defibrillation takes place, the increased likelihood of survival

PVC's are Dangerous When :

They are frequent (> 30% of complexes) or are increasing in frequency

The come close to or on top of a preceding T-wave (R on T)

Three or more PVC's in a row (run of V-tach)

Any PVC in the setting of an acute MI

PVC's come from different foci (&quot;multifocal&quot; or &quot;multiformed&quot;)

These dangerous phenomenon may preclude the occurrence of deadly arrhythmias:

Ventricular Tachycardia

Ventricular Fibrillation

Recognizing and Naming Beats & Rhythms Notes on V-tach : Causes of V-tach Prior MI, CAD, dilated cardiomyopathy, or it may be idiopathic (no known cause) Typical V-tach patient MI with complications & extensive necrosis, EF<40%, d wall motion, v-aneurysm) V-tach complexes are likely to be similar and the rhythm regular Irregular V-Tach rhythms may be due to to: breakthrough of atrial conduction atria may “capture” the entire beat beat an atrial beat may “merge” with an ectopic ventricular beat (fusion beat) Fusion beat - note p-wave in front of PVC and the PVC is narrower than the other PVC’s – this indicates the beat is a product of both the sinus node and an ectopic ventricular focus Capture beat - note that the complex is narrow enough to suggest normal ventricular conduction. This indicates that an atrial impulse has made it through and conduction through the ventricles is relatively normal.

Notes on V-tach :

Causes of V-tach

Prior MI, CAD, dilated cardiomyopathy, or it may be idiopathic (no known cause)

Typical V-tach patient

MI with complications & extensive necrosis, EF<40%, d wall motion, v-aneurysm)

V-tach complexes are likely to be similar and the rhythm regular

Irregular V-Tach rhythms may be due to to:

breakthrough of atrial conduction

atria may “capture” the entire beat beat

an atrial beat may “merge” with an ectopic ventricular beat (fusion beat)

Recognizing and Naming Beats & Rhythms Premature Atrial Contractions (PAC’s) : An ectopic focus in the atria discharges causing an early beat The P-wave of the PAC will not look like a normal sinus P-wave (different morphology) QRS is narrow and normal looking because ventricular depolarization is normal PAC’s may not activate the myocardium if it is still refractory (non-conducted PAC’s) PAC’s may be benign: caused by stress, alcohol, caffeine, and tobacco PAC’s may also be caused by ischemia, acute MI’s, d electrolytes, atrial hypertrophy PAC’s may also precede PSVT PAC Non conducted PAC Non conducted PAC distorting a T-wave

Premature Atrial Contractions (PAC’s) :

An ectopic focus in the atria discharges causing an early beat

The P-wave of the PAC will not look like a normal sinus P-wave (different morphology)

QRS is narrow and normal looking because ventricular depolarization is normal

PAC’s may not activate the myocardium if it is still refractory (non-conducted PAC’s)

PAC’s may be benign: caused by stress, alcohol, caffeine, and tobacco

PAC’s may also be caused by ischemia, acute MI’s, d electrolytes, atrial hypertrophy

PAC’s may also precede PSVT

Premature Junctional Contractions (PJC’s) : An ectopic focus in or around the AV junction discharges causing an early beat The beat has no P-wave QRS is narrow and normal looking because ventricular depolarization is normal PJC’s are usually benign and require not treatment unless they initiate a more serious rhythm Recognizing and Naming Beats & Rhythms PJC

Premature Junctional Contractions (PJC’s) :

An ectopic focus in or around the AV junction discharges causing an early beat

The beat has no P-wave

QRS is narrow and normal looking because ventricular depolarization is normal

PJC’s are usually benign and require not treatment unless they initiate a more serious rhythm

Recognizing and Naming Beats & Rhythms Multifocal Atrial Tachycardia (MAT) : Multiple ectopic focuses fire in the atria, all of which are conducted normally to the ventricles QRS complexes are almost identical to the sinus beats Rate is usually between 100 and 200 beats per minute The rhythm is always IRREGULAR P-waves of different morphologies (shapes) may be seen if the rhythm is slow If the rate < 100 bpm, the rhythm may be referred to as “wandering pacemaker” Commonly seen in pulmonary disease, acute cardiorespiratory problems, and CHF Treatments: Ca ++ channel blockers,  blockers, potassium, magnesium, supportive therapy for underlying causes mentioned above (antiarrhythmic drugs are often ineffective) Note IRREGULAR rhythm in the tachycardia Note different P-wave morphologies when the tachycardia begins

Multifocal Atrial Tachycardia (MAT) :

Multiple ectopic focuses fire in the atria, all of which are conducted normally to the ventricles

QRS complexes are almost identical to the sinus beats

Rate is usually between 100 and 200 beats per minute

The rhythm is always IRREGULAR

P-waves of different morphologies (shapes) may be seen if the rhythm is slow

If the rate < 100 bpm, the rhythm may be referred to as “wandering pacemaker”

Commonly seen in pulmonary disease, acute cardiorespiratory problems, and CHF

Treatments: Ca ++ channel blockers,  blockers, potassium, magnesium, supportive therapy for underlying causes mentioned above (antiarrhythmic drugs are often ineffective)

Recognizing and Naming Beats & Rhythms Paroxysmal (of sudden onset) Supraventricular Tachycardia (PSVT) : A single reentrant ectopic focuses fires in and around the AV node, all of which are conducted normally to the ventricles (usually initiated by a PAC) QRS complexes are almost identical to the sinus beats Rate is usually between 150 and 250 beats per minute The rhythm is always REGULAR Possible symptoms: palpitations, angina, anxiety, polyuruia, syncope ( d Q ) Prolonged runs of PSVT may result in atrial fibrillation or atrial flutter May be terminated by carotid massage u carotid pressure r u baroreceptor firing rate r u vagal tone r d AV conduction Treatment: ablation of focus, Adenosine ( d AV conduction), Ca ++ Channel blockers Note REGULAR rhythm in the tachycardia Rhythm usually begins with PAC

Paroxysmal (of sudden onset) Supraventricular Tachycardia (PSVT) :

A single reentrant ectopic focuses fires in and around the AV node, all of which are conducted normally to the ventricles (usually initiated by a PAC)

QRS complexes are almost identical to the sinus beats

Rate is usually between 150 and 250 beats per minute

The rhythm is always REGULAR

Possible symptoms: palpitations, angina, anxiety, polyuruia, syncope ( d Q )

Prolonged runs of PSVT may result in atrial fibrillation or atrial flutter

May be terminated by carotid massage

u carotid pressure r u baroreceptor firing rate r u vagal tone r d AV conduction

Treatment: ablation of focus, Adenosine ( d AV conduction), Ca ++ Channel blockers

Sinus arrest or exit block

PAC

Junctional Premature Beat single ectopic beat that originates in the AV node or Bundle of His area of the condunction system – Retrograde P waves immediately preceding the QRS – Retrograde P waves immediately following the QRS – Absent P waves (buried in the QRS)

single ectopic beat that originates in the AV node or

Bundle of His area of the condunction system

– Retrograde P waves immediately preceding the QRS

– Retrograde P waves immediately following the QRS

– Absent P waves (buried in the QRS)

Junctional Escape Beat

Junctional Rhythm Rate : 40 to 60 beats/minute (atrial and ventricular) • Rhythm : regular atrial and ventricular rhythm • P wave : usually inverted, may be upright; may precede, follow or be hidden in the QRS complex; may be absent • PR interval : not measurable or less than .20 sec.

Rate : 40 to 60 beats/minute (atrial and ventricular)

• Rhythm : regular atrial and ventricular rhythm

• P wave : usually inverted, may be upright; may precede,

follow or be hidden in the QRS complex; may

be absent

• PR interval : not measurable or less than .20 sec.

Junctional Rhythm

MaligMalignant PVC patterns Frequent PVCs Multiform PVCs Runs of consecutive PVCs R on T phenomenon – PVC that falls on a T wave PVC during acute MI

Frequent PVCs

Multiform PVCs

Runs of consecutive PVCs

R on T phenomenon – PVC that falls on a T

wave

PVC during acute MI

Types of PVCs Uniform Multiform PVC rhythm patterns – Bigeminy – PVC occurs every other complex – Couplets – 2 PVCs in a row – Trigeminy – Two PVCs for every three complexes

Uniform

Multiform

PVC rhythm patterns

– Bigeminy – PVC occurs every other complex

– Couplets – 2 PVCs in a row

– Trigeminy – Two PVCs for every three complexes

Junctional Escape Rhythm

Ventricular tachycardia (VTach) 3 or more PVCs in a row at a rate of 120 to 200 bts/min-1 Ventricular fibrillation (VFib) No visible P or QRS complexes. Waves appear as fibrillating waves

3 or more PVCs in a row at a rate of 120 to 200 bts/min-1

Ventricular fibrillation (VFib)

No visible P or QRS complexes. Waves appear as fibrillating waves

Torsades de Pointes Type of VT known as “twisting of the points.” Usually seen in those with prolonged QT intervals caused by

Type of VT known as “twisting of the points.”

Usually seen in those with prolonged QT intervals caused by

Why “1500 / X”? Paper Speed: 25 mm/ sec 60 seconds / minute 60 X 25 = 1500 mm / minute Take 6 sec strip (30 large boxes) Count the P/R waves X 10 OR

Paper Speed: 25 mm/ sec

60 seconds / minute

60 X 25 = 1500 mm / minute

Take 6 sec strip (30 large boxes)

Count the P/R waves X 10

Atrial Fibrillation :

Regular “Irregular” Premature Beats: PVC Widened QRS, not associated with preceding P wave Usually does not disrupt P-wave regularity T wave is “inverted” after PVC Followed by compensatory ventricular pause

Premature Beats: PVC

Widened QRS, not associated with preceding P wave

Usually does not disrupt P-wave regularity

T wave is “inverted” after PVC

Followed by compensatory ventricular pause

Notice a Pattern in the PVC’s?

Identifying AV Blocks: Name Conduction PR-Int R-R Rhythm Regular (20-40 bpm) Grossly Irregular P > R 3°: Regular Constant P > R 2°:Mobitz II Irregular Progressive P > R 2°:Mobitz I Regular > .20 P = R 1°:

Most Important Questions of Arrhythmias What is the mechanism? Problems in impulse formation? (automaticity or ectopic foci) Problems in impulse conductivity? (block or re-entry) Where is the origin? Atria, Junction, Ventricles?

What is the mechanism?

Problems in impulse formation? (automaticity or ectopic foci)

Problems in impulse conductivity? (block or re-entry)

Where is the origin?

Atria, Junction, Ventricles?

QRS Axis Check Leads: 1 and AVF

Check Leads:

1 and AVF

Interpreting Axis Deviation: Normal Electrical Axis: (Lead I + / aVF +) Left Axis Deviation: Lead I + / aVF – Pregnancy, LV hypertrophy etc Right Axis Deviation: Lead I - / aVF + Emphysema, RV hypertrophy etc.

Normal Electrical Axis:

(Lead I + / aVF +)

Left Axis Deviation:

Lead I + / aVF –

Pregnancy, LV hypertrophy etc

Right Axis Deviation:

Lead I - / aVF +

Emphysema, RV hypertrophy etc.

NW Axis (No Man’s Land) Both I and aVF are – Check to see if leads are transposed (- vs +) Indicates: Emphysema Hyperkalemia VTach

Both I and aVF are –

Check to see if leads are transposed (- vs +)

Indicates:

Emphysema

Hyperkalemia

VTach

Determining Regions of CAD: ST-changes in leads… RCA: Inferior myocardium II, III, aVF LCA: Lateral myocardium I, aVL, V5, V6 LAD: Anterior/Septal myocardium V1-V4

RCA: Inferior myocardium

II, III, aVF

LCA: Lateral myocardium

I, aVL, V5, V6

LAD: Anterior/Septal myocardium

V1-V4

Regions of the Myocardium: Inferior II, III, aVF Lateral I, AVL, V5-V6 Anterior / Septal V1-V4

Sinus Arrhythmia

Sinus Arrest/Pause

Sinoatrial Exit Block

Premature Atrial Complexes (PACs)

Wandering Atrial Pacemaker (WAP)

Supraventricular Tachycardia (SVT)

Wolff-Parkinson-White Syndrome (WPW)

Atrial Flutter

Atrial Fibrillation (A-fib)

Premature Junctional Complexes (PJC)

Junctional Rhythm

Junctional Rhythm

Accelerated Junctional Rhythm

Junctional Tachycardia

Premature Ventricular Complexes (PVC's) Note – Complexes not Contractions

PVC’s Uniformed/Multiformed Couplets/Salvos/Runs Bigeminy/Trigeminy/Quadrageminy

Uniformed/Multiformed

Couplets/Salvos/Runs

Bigeminy/Trigeminy/Quadrageminy

Uniformed PVC’s

R on T Phenomena

Multiformed PVC’s

PVC Couplets

PVC Salvos and Runs

Bigeminy PVC’s

Trigeminy PVC’s

Quadrageminy PVC’s

Ventricular Escape Beats

Idioventricular Rhythm

Ventricular Tachycardia (VT) Rate: 101-250 beats/min Rhythm: regular P waves: absent PR interval: none QRS duration: > 0.12 sec. often difficult to differentiate between QRS and T wave Note: Monomorphic - same shape and amplitude

Rate: 101-250 beats/min

Rhythm: regular

P waves: absent

PR interval: none

QRS duration: > 0.12 sec. often difficult to differentiate between QRS and T wave

Note: Monomorphic - same shape

and amplitude

Ventricular Tachycardia (VT)

V Tach

Torsades de Pointes (TdeP) Rate: 150-300 beats/min Rhythm: regular or irregular P waves: none PR interval: none QRS duration: > 0.12 sec. gradual alteration in amplitude and direction of the QRS complexes

Rate: 150-300 beats/min

Rhythm: regular or irregular

P waves: none

PR interval: none

QRS duration: > 0.12 sec. gradual alteration in amplitude and direction of the QRS complexes

Torsades de Pointes (TdeP)

Ventricular Fibrillation (VF) Rate: CNO as no discernible complexes Rhythm: rapid and chaotic P waves: none PR interval: none QRS duration: none Note: Fine vs. coarse?

Rate: CNO as no discernible complexes

Rhythm: rapid and chaotic

P waves: none

PR interval: none

QRS duration: none

Note: Fine vs. coarse?

Ventricular Fibrillation (VF)

Ventricular Fibrillation (VF)

Asystole (Cardiac Standstill) Rate: none Rhythm: none P waves: none PR interval: not measurable QRS duration: absent

Rate: none

Rhythm: none

P waves: none

PR interval: not measurable

QRS duration: absent

Asystole (Cardiac Standstill)

Asystole The Mother of all Bradycardias

Atrial Pacemaker (Single Chamber) pacemaker Capture?

Capture?

Ventricular Pacemaker (Single Chamber) pacemaker

Dual Paced Rhythm pacemaker

Pulseless Electrical Activity (PEA) The absence of a detectable pulse and blood pressure Presence of electrical activity of the heart as evidenced by ECG rhythm, but not VF or VT = 0/0 mmHg +

The absence of a detectable pulse and blood pressure

Presence of electrical activity of the heart as evidenced by ECG rhythm, but not VF or VT

ventricular bigeminy The ECG trace below shows ventricular bigeminy, in which every other beat is a ventricular ectopic beat. These beats are premature, wider, and larger than the sinus beats.

The ECG trace below shows ventricular bigeminy, in which every other beat is a ventricular ectopic beat. These beats are premature, wider, and larger than the sinus beats.

ventricular bigeminy

ventricular trigeminy ; The occurrence of more than one type of ventricular ectopic impulse morphology is evidence of multifocal ventricular ectopics. In this example, the ventricular ectopic beats are both wide and premature, but differ considerably in shape

The occurrence of more than one type of ventricular ectopic impulse morphology is evidence of multifocal ventricular ectopics. In this example, the ventricular ectopic beats are both wide and premature, but differ considerably in shape

ventricular trigeminy

ventricular trigeminy

MYOCARDIAL INFARACTION

Diagnosing a MI To diagnose a myocardial infarction you need to go beyond looking at a rhythm strip and obtain a 12-Lead ECG. Rhythm Strip 12-Lead ECG

To diagnose a myocardial infarction you need to go beyond looking at a rhythm strip and obtain a 12-Lead ECG.

ST Elevation One way to diagnose an acute MI is to look for elevation of the ST segment.

One way to diagnose an acute MI is to look for elevation of the ST segment.

ST Elevation (cont) Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction.

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction.

Anterior Myocardial Infarction If you see changes in leads V 1 - V 4 that are consistent with a myocardial infarction, you can conclude that it is an anterior wall myocardial infarction.

If you see changes in leads V 1 - V 4 that are consistent with a myocardial infarction, you can conclude that it is an anterior wall myocardial infarction.

Putting it all Together Do you think this person is having a myocardial infarction. If so, where?

Do you think this person is having a myocardial infarction. If so, where?

Interpretation Yes , this person is having an acute anterior wall myocardial infarction.

Yes , this person is having an acute anterior wall myocardial infarction.

Putting it all Together Now, where do you think this person is having a myocardial infarction?

Now, where do you think this person is having a myocardial infarction?

Inferior Wall MI This is an inferior MI. Note the ST elevation in leads II, III and aVF.

This is an inferior MI. Note the ST elevation in leads II, III and aVF.

Putting it all Together How about now?

How about now?

Anterolateral MI This person’s MI involves both the anterior wall (V 2 -V 4 ) and the lateral wall (V 5 -V 6 , I, and aVL)!

This person’s MI involves both the anterior wall (V 2 -V 4 ) and the lateral wall (V 5 -V 6 , I, and aVL)!

The ST segment should start isoelectric except in V1 and V2 where it may be elevated I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

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

ST segment elevation over area of damage

ST depression in leads opposite infarction

Pathological Q waves

Reduced R waves

Inverted T waves

ST elevation hyperacute phase Occurs in the early stages Occurs in the leads facing the infarction Slight ST elevation may be normal in V 1 or V 2 R P Q ST

Occurs in the early stages

Occurs in the leads facing the infarction

Slight ST elevation may be normal in V 1 or V 2

Deep Q wave Only diagnostic change of myocardial infarction At least 0.04 seconds in duration Depth of more than 25% of ensuing R 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

T wave changes Late change Occurs as ST elevation is returning to normal Apparent in many leads R P Q T ST

Late change

Occurs as ST elevation is returning to normal

Apparent in many leads

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

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

Anterior infarction Anterior infarction Left coronary artery I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Inferior infarction Inferior infarction Right coronary artery I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Lateral infarction Lateral infarction Left circumflex coronary artery I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

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

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

Surfaces of the Left Ventricle Inferior - underneath Anterior - front Lateral - left side Posterior - back

Inferior - underneath

Anterior - front

Lateral - left side

Posterior - back

Inferior Surface Leads II, III and avF look UP from below to the inferior surface of the left ventricle Mostly perfused by the Right Coronary Artery

Leads II, III and avF look UP from below to the inferior surface of the left ventricle

Mostly perfused by the Right Coronary Artery

Inferior Leads II III aVF

II

III

aVF

Anterior Surface The front of the heart viewing the left ventricle and the septum Leads V2 , V3 and V4 look towards this surface Mostly fed by the Left Anterior Descending branch of the Left artery

The front of the heart viewing the left ventricle and the septum

Leads V2 , V3 and V4 look towards this surface

Mostly fed by the Left Anterior Descending branch of the Left artery

Anterior Leads V2 V3 V4

V2

V3

V4

Lateral Surface The left sided wall of the left ventricle Leads V5 and V6, I and avL look at this surface Mostly fed by the Circumflex branch of the left artery

The left sided wall of the left ventricle

Leads V5 and V6, I and avL look at this surface

Mostly fed by the Circumflex branch of the left artery

Lateral Leads V5, V6, I, aVL

Posterior Surface Posterior wall infarcts are rare Posterior diagnoses can be made by looking at the anterior leads as a mirror image. Normally there are inferior ischaemic changes Blood supply predominantly from the Right Coronary Artery

Posterior wall infarcts are rare

Posterior diagnoses can be made by looking at the anterior leads as a mirror image. Normally there are inferior ischaemic changes

Blood supply predominantly from the Right Coronary Artery

Inferior II, III, AVF Antero-Septal V1,V2, V3,V4 Lateral I, AVL, V5, V6 Posterior V1, V2, V3 RIGHT LEFT

ST Segment Elevation The ST segment lies above the isoelectric line: Represents myocardial injury It is the hallmark of Myocardial Infarction The injured myocardium is slow to repolarise and remains more positively charged than the surrounding areas Other causes to be ruled out include pericarditis and ventricular aneurysm

The ST segment lies above the isoelectric line:

Represents myocardial injury

It is the hallmark of Myocardial Infarction

The injured myocardium is slow to repolarise and remains more positively charged than the surrounding areas

Other causes to be ruled out include pericarditis and ventricular aneurysm

ST-Segment Elevation

T wave inversion in an evolving MI

The ECG in ST Elevation MI

The Hyper-acute Phase Less than 12 hours “ ST segment elevation is the hallmark ECG abnormality of acute myocardial infarction” (Quinn, 1996) The ECG changes are evidence that the ischaemic myocardium cannot completely depolarize or repolarize as normal Usually occurs within a few hours of infarction May vary in severity from 1mm to ‘tombstone’ elevation

Less than 12 hours

“ ST segment elevation is the hallmark ECG abnormality of acute myocardial infarction” (Quinn, 1996)

The ECG changes are evidence that the ischaemic myocardium cannot completely depolarize or repolarize as normal

Usually occurs within a few hours of infarction

May vary in severity from 1mm to ‘tombstone’ elevation

The Fully Evolved Phase 24 - 48 hours from the onset of a myocardial infarction ST segment elevation is less (coming back to baseline). T waves are inverting. Pathological Q waves are developing (>2mm)

24 - 48 hours from the onset of a myocardial infarction

ST segment elevation is less (coming back to baseline).

T waves are inverting.

Pathological Q waves are developing (>2mm)

The Chronic Stabilised Phase Isoelectric ST segments T waves upright. Pathological Q waves. May take months or weeks.

Isoelectric ST segments

T waves upright.

Pathological Q waves.

May take months or weeks.

Reciprocal Changes Changes occurring on the opposite side of the myocardium that is infarcting

Changes occurring on the opposite side of the myocardium that is infarcting

Reciprocal Changes ie S-T depression in some leads in MI

Non ST Elevation MI Commonly ST depression and deep T wave inversion History of chest pain typical of MI Other autonomic nervous symptoms present Biochemistry results required to diagnose MI Q-waves may or may not form on the ECG

Commonly ST depression and deep T wave inversion

History of chest pain typical of MI

Other autonomic nervous symptoms present

Biochemistry results required to diagnose MI

Q-waves may or may not form on the ECG

Changes in NSTEMI

Action potentials and electrophysiology + + + + _ _ _ _ 3.2 Ca in(slow) ++ K out + Na in + Resting Depolarised Repolarised Plateau + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + Ca ++ K + K + Na + _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _

LVH and strain pattern Ventricular Strain Strain is often associated with ventricular hypertrophy Characterized by moderate depression of the ST segment.

Copyright ©2002 BMJ Publishing Group Ltd. Channer, K. et al. BMJ 2002;324:1023-1026 Non-ischaemic ST segment changes: in patient taking digoxin (top) and in patient with left ventricular hypertrophy (bottom)

Examples of T wave abnormalities Copyright ©2002 BMJ Publishing Group Ltd. Channer, K. et al. BMJ 2002;324:1023-1026

Sick Sinus Syndrome Sinoatrial block (note the pause is twice the P-P interval) Sinus arrest with pause of 4.4 s before generation and conduction of a junctional escape beat Severe sinus bradycardia

Bundle Branch Block

Left Bundle Branch Block Widened QRS (> 0.12 sec, or 3 small squares) Two R waves appear – R and R’ in V5 and V6, and sometimes Lead I, AVL. Have predominately negative QRS in V1, V2, V3 (reciprocal changes).

Widened QRS (> 0.12 sec, or 3 small squares)

Two R waves appear – R and R’ in V5 and V6, and sometimes Lead I, AVL.

Have predominately negative QRS in V1, V2, V3 (reciprocal changes).

Right Bundle Branch Block

Where’s the MI?

Where’s the MI?

Where’s the MI?

Final one…

Which one is more tachycardic during this exercise test?

Any Questions?

Thanks for paying attention. I hope you have found this session useful.