Ecg Made Easy By Dr Bashir Ahmed Dar Associate Professor Medicine Chinkipora Sopore Kashmir

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

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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

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

ELECTROGRAPHY MADE EASY

 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.

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

     

Horizontal plane - the six chest leads LA RA V1

V2

LV RV

V6

V3 V4 V5 V6 V5 V4 V1

V2

V3

6.5

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 Voltage calibration 1 mV

= 25mm/sec = 1cm

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ECG paper - standard calibrations – each small square = 1mm – each large square = 5mm

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Timings – 1 small square – 1 large square – 25 small squares – 5 large squares

= = = =

0.04sec 0.2sec 1sec 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.

ECG paper 1 Small square = 0.04 second

2 Large squares = 1 cm

1 Large square = 0.2 second 5 Large squares = 1 second

Time

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.

STANDARDISATION ECG amplitude scale

Normal amplitude

Half amplitude

Double amplitude

10 mm/mV

5 mm/mV

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.

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

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.

Normal ECG

Slide 13

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.

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

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

Slide 9

Shape of P wave  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 & 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.

Slide 14

Slide 16

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 V1 ≥ 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 V1 > 1 “small box” in area

Slide 15

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.

Slide 41

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.

Slide 40

Junctional rhythm  In

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

Slide 43

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.

Slide 39

NORMAL P-R INTERVAL  PR

interval seconds.

 That

time 0.12 seconds to 0.2

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

Short P-R interval  Short

P-R interval seen in WPW syndrome or preexcitation 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.

Slide 17

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 .

Slide 44

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.

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.

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 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.

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

Normal upward progression of R wave from V1 to V6 V1

V2

V3

V4

V5

V6

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.

ST

Q

S J point

L V H-Voltage Criteria 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.

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.

Dominant or upward R wave in V1  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

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  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).

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 “counterclockwise rotation of the heart.” This can be seen with abnormal chest shape.

Right Ventricular Hypertrophy

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 V1

 Right

axis deviation  Right atrial enlargement  Down sloping ST depressions in V1-V3 ( 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.

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.

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.

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

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.

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.

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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

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.

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

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.

NORMAL ST- SEGMENT 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.

Abnormalities ST elevation: More than one small square 1.

   

Acute MI. Prinzmetal angina. Acute pericarditis. Early repolarization

ST depression: More than one small square     

Ischemia. Ventricular strain. BBB. Hypokalemia. Digoxin effect.

Slide 11

Slide 12

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

upwards.

lost and convexity appear facing

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

Abnormalities of ST- segment

Q waves in myocardial infarction

T-wave Normal values. 1.amplitude: < 10mm in the chest leads.

. 2. T- inversion:



Abnormalities:



1. Peaked T-wave:  Hyper-acute MI.  Hyperkalemia.  Normal variant



   

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.

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 R

QT interval

R

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

QT interval

R

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

QT interval

R

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

R

QT interval

R

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

R

QT interval

Normal QTc = 0.46 sec

R

Atrioventricular (AV) Heart Block

Classification of AV Heart Blocks Degree 1 Degree Block St

2nd Degree, Mobitz Type I

AV Conduction Pattern Uniformly prolonged PR interval Progressive PR interval prolongation

2nd Degree, Mobitz Type II

Sudden conduction failure

3rd Degree Block

No AV conduction

AV Blocks  First

Degree

– Prolonged AV conduction time – PR interval > 0.20 seconds

1st 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

First Degree Block

prolonged PR interval

Analyze the Rhythm

AV Blocks  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

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Second Degree – 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

2nd degree AV Block (“Mobitz I” also called “Wenckebach”):

• Irregular Rhythm • PRI continues to lengthen until a QRS is missing (non-conducted sinus impulse) • PRI is NOT CONSTANT

PRI = .24 sec

PRI = .36 sec

PRI = .40 sec

QRS is “dropped”

Pause 4:3 Wenckebach (conduction ratio may not be constant)

Pattern Repeats………….

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 

Second Degree AV Block

Mobitz type I or Winckebach Mobitz type II

Type 1 (Wenckebach) Progressive prolongation of the PR interval until a P wave is not conducted.

Type 2

Constant PR interval with unexpected intermittent failure to conduct

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

PRI is CONSTANT

Non-conducted sinus impulses

“2:1 block”

“3:1 block”

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)

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.

Mobitz Type II

Mobitz Type II

Sudden appearance of a single, nonconducted 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

3rd 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.

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

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

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!

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

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

LBB LPIF

Lead I

Left Anterior Hemiblock (LAHB): 2.

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

1.

LASF

2.

Lead III

Lead AVF

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)

Lead I

LBB LPIF

Left Posterior Hemiblock (LPHB): 2.

1.

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%

LASF 2. Lead III

Lead AVF

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 

Trifascicular Block  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

Cardiac Pacemakers  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

Cardiac Pacemakers

Cardiac Pacemakers  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 

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

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

Implanted Defibrillators 

AICD – Automated

Implanted CardioDefibrillator



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

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

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

Sinus block

ARRTHYMIAS AND ECTOPIC BEATS

Recognizing and Naming Beats & Rhythms Atrial Escape Beat

QRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normal

normal ("sinus") 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 "atrial" beat

Recognizing and Naming Beats & Rhythms

Junctional Escape Beat

QRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normal

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 "junctional" or a “nodal” beat

Recognizing and Naming Beats & Rhythms

Ventricular Escape Beat

QRS is wide and much different ("bizarre") 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

there is no p wave, indicating that the beat did not originate anywhere in the atria actually a "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

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

Slow Conduction Path Fast Recovery

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

The “Re-Entry” Mechanism of Ectopic Beats & Rhythms Premature Beat Impulse Cardiac Repolarizing Tissue Conduction (long refractory period) Tissue Fast Conduction Path Slow Recovery

Slow Conduction Path Fast Recovery

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

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

Slow Conduction Path Fast Recovery

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

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

Slow Conduction Path Fast Recovery

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 "wide and bizarre" • 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”

R on T phenom em on

M u lt if o c a l P V C 's

C o m p e n s a to ry p a u s e a fte r th e o c c u ra n c e o f a P V C

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

The classic PVC – note the compensatory pause

Interpolated PVC – note the sinus rhythm is undisturbed

Recognizing and Naming Beats & Rhythms 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 ("multifocal" or "multiformed") These dangerous phenomenon may preclude the occurrence of deadly arrhythmias:

• Ventricular Tachycardia • Ventricular Fibrillation

The sooner defibrillation takes place, the increased likelihood of survival

“R on T phenomenon” time

sinus beats

V-tach

Unconverted V-tach r V-fib

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 pwave 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.

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

Recognizing and Naming Beats & Rhythms 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

PJC

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 different P-wave morphologies when the tachycardia begins

Note IRREGULAR rhythm in the tachycardia

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

Rhythm usually begins with PAC

Note REGULAR rhythm in the tachycardia

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)

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.

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

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 

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

Torsades de Pointes  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

OR  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

Notice a Pattern in the PVC’s?

Identifying AV Blocks: Name

1°:

Conduction

P=R

2°:Mobitz P > R I 2°:Mobitz P > R II 3°: P>R

PR-Int

> .20

R-R Rhythm

Regular

Progressive Irregular Constant

Regular

Grossly Irregular

Regular (20-40 bpm)

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?

QRS Axis 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.

NW Axis (No Man’s Land) 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

Regions of the Myocardium: Lateral I, AVL, V5-V6 Inferior II, III, aVF

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 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: P

regular

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: P

regular or irregular

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: P

rapid and chaotic

waves: none

 PR

interval: none

 QRS

duration: none Note: Fine vs. coarse?

Ventricular Fibrillation (VF)

Ventricular Fibrillation (VF)

Asystole (Cardiac Standstill)  Rate:

none

 Rhythm: P

none

waves: none

 PR

interval: not measurable

 QRS

duration: absent

Asystole (Cardiac Standstill)

Asystole The Mother of all Bradycardias

Atrial Pacemaker (Single Chamber)

pacemaker

•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

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.

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

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. 12-Lead ECG

Rhythm Strip

ST Elevation 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.

Anterior Myocardial Infarction If you see changes in leads V1 - V4 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?

Interpretation 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?

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

Putting it all Together How about now?

Anterolateral MI This person’s MI involves both the anterior wall (V2V4) and the lateral wall (V5-V6, I, and aVL)!

I II III

aVR aVL aVF

V1 V2 V3

V4 V5 V6

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

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 elevation hyperacute phase • Occurs in the early stages

R ST P

Q

• Occurs in the leads facing the infarction • Slight ST elevation may be normal in V1 or V2

Deep Q wave • Only diagnostic change of myocardial infarction

R ST

• At least 0.04 seconds in duration

P T Q

• Depth of more than 25% of ensuing R wave

T wave changes • Late change R

• Occurs as ST elevation is returning to normal

ST

P

• Apparent in many leads T Q

Bundle branch block Anterior wall MI I II III

aVR aVL aVF

V1 V2 V3

Left bundle branch block V4 V5 V6

I II III

aVR aVL aVF

V1 V2 V3

V4 V5 V6

Sequence of changes in evolving AMI R

R T

R

ST

ST

P

P

P

QS

T

Q

1 minute after onset

Q

1 hour or so after onset

A few hours after onset

R ST

P

P T

Q

A day or so after onset

ST

T

P T

Q

Later changes

Q

A few months after AMI

Anterior infarction Anterior infarction

I II III

Left coronary artery

aVR aVL aVF

V1 V2 V3

V4 V5 V6

Inferior infarction Inferior infarction

I II III

Right coronary artery

aVR aVL aVF

V1 V2 V3

V4 V5 V6

Lateral infarction Lateral infarction

I II III

Left circumflex coronary artery

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

Surfaces of the Left Ventricle 

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

Inferior Leads – 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

Anterior Leads – 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

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

RIGHT

Inferior II, III, AVF

Posterior V1, V2, V3

LEFT

Antero-Septal V1,V2, V3,V4

Lateral I, AVL, V5, V6

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

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

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)

The Chronic Stabilised Phase  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

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

Changes in NSTEMI

+ + + + _ _ _ _ _ _ _ _ _ + + + +

+ + +

+ + _ + __ + +

Action potentials and electrophysiology +

Na

_ _ _ _ _

_ _ + + + + + _ + + _ _ + + + + + _ _ _ _ _ _ +

_ _ _ + + + + + _ + + _ + + + + + _ _ _ _ _ _

+

K

_ _ _ _ _

+ + _ _ + _ + +

+ + + + _ _ _ _ _ _ _ _ _ + + + +

+ + +

K

Resting

Depolarised

Ca +

Na

++ in(slow)

in

K

++

Ca

+ out

Plateau

Repolarised

3.2

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

Non-ischaemic ST segment changes: in patient taking digoxin (top) and in patient with left ventricular hypertrophy (bottom)

Channer, K. et al. BMJ 2002;324:1023-1026 Copyright ©2002 BMJ Publishing Group Ltd.

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).

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?

I hope you have found this session useful.