Ecg

RVH RAD, and V1 R wave > 7mm tall LVH R in V5 (or V6) + S in V1 (or V2) > 35, or avL
R > 13 mm
QRS 1-2.5
RATE RHYTHM AXIS INTERVALS

(P-PR-QRS-QT) HYPERTROPHY
2.52.5 PR
> P 3-5
half of the >A QT RR interval
QRS > 0.12sec Look at V1: Terminal R = RBBB Terminal S = LBBB
MI
lateral
Leads I, aVL, and V5- V6
Inferior Anterior . leads V1-V4

Leads II, III aVF
Pathological Q waves (1)any Q wave in V1&V2&V3 (2) have a height of <25% partner R (3) <0.04 seconds.
QRS Complexes
I + + -
II Axis normal + - left axis deviation + right axis deviation
How TO Understand Arrhythmias

2 keyes to Understand
Arrhythmias
1-impulse formation 2 -impulse conduction
1--impulse formation i.e. the pacemaker

A** Site of origin i.e., where is the abnormal rhythm coming from?
Sinus Node (e.g., sinus tachycardia Atria (e.g., PAC AV junction (e.g., junctional escape rhythm
Ventricles (e.g., PVC
B*Regularity of ventricular or atrial response
Regular (e.g., PSVT Regular irregularity (e.g., ventricular bigeminy Irregular irregularity (e.g., atrial fibrillation or MAT Irregular (e.g., multifocal PVCs
2-Descriptors of impulse conduction i.e., how abnormal rhythm conducts through the heart
Antegrade (forward) vs. retrograde (backward) conduction Conduction delays or blocks: i.e., 1st , 2nd( type I or II), 3rd degree blocks
Supraventricular arrhythmias
Premature atrial complexes Premature junctional complexes Atrial fibrillation Atrial flutter Ectopic atrial tachycardia and rythm Multifocal atrial tachycardia Paroxysmal supraventricular tachycardia Junctional rhythms and tachycardias
ALL ARE NARROW BUT THE DIFFERENCE IS WIDE !!
IT IS TOO WIDE HOW TO NARROW??
IT IS TOO WIDE HOW TO NARROW??
Ventricular arrhythmias
(1)Premature ventricular complexes (2)Ventricular tachycardia (3)Idioventricular rhythm ALL ARE WIDE BUT THE DIFFERENCE IS NARROW!!
Premature atrial complexes These may occur as single or repetitive events and may be (unifocal or multifocal) in origin
Premature atrial contractions, also called occur whenever an ectopic site in the heart's atria produces an electrical impulse early or prematurely in the ECG rhythm strip. Premature contractions are also know as Premature Beats, Ectopics, Premature Systoles and Extra Systoles.
For a premature atrial contraction to be diagnosed, the following qualities must be present.
1. The beat must come early or prematurely in the ECG rhythm strip 2. The premature beat must have a 'P' wave, and that 'P' wave must have a different shape than the sinus 'P' waves in the strip.
3. The 'PR' interval of the premature beat must be as least .12 seconds (3 small boxes) in length.
4. The 'QRS' complex of the premature beat must be the same shape as the other sinus 'QRS' complexes.
The premature P wave differs in contour from the normal sinus wave, which is usually followed by a normal QRST sequence .
Whenever a gap occurs in a rhythm strip, always check the beat at the front of the gap to see if it is different from the other beats in
What are these Games 1- ?1

.2- ?!.... 3- ?!
PACs may have three different outcomes : )1)Normal conduction: similar to normal QRS complexes in the ECG . )2)Non-conducted: no QRS complex because the PAC meets the AV node when still refractory . )3)Conducted with aberration: the PAC makes it into the ventricles but finds one or more of the conducting fascicles or bundle branches refractory, hence the resulting QRS is usually wide .
The pause after a PAC is usually incomplete - i.e. the PAC usually enters the sinus node and resets its timing, causing the next sinus P to appear earlier than expected (premature ventricular complexes, by contrast, are usually followed by a complete pause because they do not usually disturb the sinus node(
PACs have 3 different outcomes )1 :) Normal conduction
Atrium
AVN
Ventricle
SAN
)2)Non-conducted: no QRS complex because the PAC meets the AV node when still refractory.
AVN
Ectopic Focus
SAN
SAN
)3)Conducted with aberration: the PAC makes it into the ventricles but finds one or more of bundle branches refractory, hence the resulting QRS is usually wide.
Bundle Branch
Atrium
AVN
Ventricle
SAN
The pause after a PAC is usually incomplete; i.e., the PAC usually enters the sinus node and resets its timing, causing the next sinus P to appear earlier than expected. (PVCs, on the other hand, are usually followed by a complete pause because the PVC does not usually perturb the sinus node;
RVH RAD, and V1 R wave > 7mm tall LVH R in V5 (or V6) + S in V1 (or V2) > 35, or avL R > 13 mm
QRS 1-2.5

2.52.5 PR
> P 3-5
MI
lateral

Leads II, III aVF
QRS Complexes
I + + -
Enter the goose
How to Differentiate Between: (1)PACs Conducted with aberration & (2)PVC ?!!!
Step 1: Is any one of the following present: ischaemic heart disease, or heart failure, or past heart surgery, or cardiac enlargement?
NO YES (VT) Comment: likelihood of VT is so high in patients with previous myocardial infarction (or substantial organic heart disease) that one should manage as for ventricular tachycardia without wasting further time evaluating the ECG! )
Step 2: Are there any RS complexes in the V leads? NO (VT) YES
Comment:. Absence of any RS complex in the precordial leads V1..V6 is 100% specific for VT, but is insensitive (26%).
Step 3: Is the interval from start of R to nadir of S > 100ms? NO YES (VT)
Aduration of over 100ms almost excludes SVT (98% specific for VT).
Step 4: Is there AV dissociation, NO YES (VT)
evidence of AV dissociation is 98% specific for VT.
Whenever one of these two 'QRS' shapes appeared as a single beat or as a run of beats, they were found to be most likely produced from aberrant ventricular conduction
A Word of Warning When there is any doubt whether beats are ventricular or aberrant, it is best to always consider them as ventricular to be on the safe side. Ventricular rhythms are life-threatening, whereas aberrant ones are not.
Supraventricular Tachycardia (SVT)
Supraventricular tachycardia describes any cardiac rhythm where the rate is 150 beats per minute or greater, and there is no evidence of any 'P' waves being present.
When cardiac rates reach 150 beats per minute, the 'P' waves are often lost or buried in the 'T' waves. This makes it impossible to determine whether the rhythms are produced by an ectopic site in the atria, creating an atrial tachycardia, or in the AV node, creating a junctional tachycardia
Supravenricular tachycardia must have the following qualities:

1. The rhythm must be regular and have a rate of 150 beats per minute or more. 2. No 'P' waves can be seen either before or after the 'QRS' complexes. 3. The 'QRS' complexes must be of normal width or duration (under .12 seconds).
Atrial Tachycardia
Atrial tachycardia occurs when a single ectopic site in one of the atria takes over pacing the heart instead of the SA node
An Atrial Tachycardia rhythm will have the following
1. The rate will be regular. 2. A 'P' wave will precede each 'QRS' complex. 3. The 'PR' intervals will all be the same and over .12 seconds in length.
Multifocal Atrial Tachycardia (MAT) Discrete, multifocal P' waves occurring at rates of 100-250/min and with varying P'R intervals (should see at least 3 different P wave morphologies in a given lead).
.
Ventricular response is irregularly irregular (i.e., often confused with A-fib). May be intermittent, alternating with periods of normal sinus rhythm
Multifocal atrial tachycardia will have the following qualities: 1. It will be irregular. 2. It will have a rate of 150 beats per minute or greater. 3. It will have different shape 'P' waves all mixed in with the 'T' wave
Paroxysmal Supraventricular Tachycardia (PSVT)
When a short burst of SVT occurs in a rhythm strip, it is called a run of Paroxysmal Supraventricular Tachycardia PSVT).
QRS 1-2.5

2.52.5 PR
> P 3-5
MI
lateral

Leads II, III aVF
QRS Complexes
I + + -
Paroxysmal Supraventricular Tachycardia (PSVT) These arrhythmias occur due to circus movements, thus utilising the mechanism of reentry. The onset and resolution are sudden and usually initiated by a premature beat, thus the term "paroxysmal".
They are generally narrowQRS tachycardias (unless there is pre-existing bundle branch block or aberrant ventricular conduction).
The Re-Entry Mechanism of Ectopic Beats & Rhythms.

Electrical Impulse
Cardiac Conduction Tissue

Electrical Impulse
Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery

Premature Beat Impulse
Repolarizing Tissue (long refractory period) 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

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 reenters the pathway and continues in a circular movement. This creates the re-entry circuit
There are several types of PSVT, depending on the location of the reentry circuit
AV nodal reentrant tachycardia (AVNRT) This is the most common form of PSVT accounting for approximately 50% of all symptomatic PSVTs. It is the most common cause of SVT in patients with structurally normal hearts.
It is accompanied by the following features:

1) ECG shows normal regular QRS complexes with a rate of 140-240 bpm. 2) QRS complexes may sometimes show typical bundle branch block/aberration. 3) P waves are either not visible or are seen immediately before or after the QRS complex. 4) An attack may be spontaneously triggered but exertion, tea, coffee or alcohol may trigger an AVNRT. 5) Vagal manoeuvres may terminate an acute attack. 6) Beta-blockers or calcium channel blockers may help to suppress recurrent attacks.
Wolff-Parkinson-White Syndrome
This is the second most common form of PSVT and is seen in patients with Wolff-ParkinsonWhite (WPW) syndrome. The WPW ECG, seen in the diagram, shows a short PR, delta wave and a somewhat widened QRS.
Premature junctional complexes

Similar to PAC's in clinical implications, but occur less frequently. The PJC focus, located in the AV junction, captures the atria (retrograde) and the ventricles (antegrade). The retrograde P wave may appear before, during, or after the QRS complex;
Junctional Escape Complexes

If no stimulus reaches the AV node, the cells assume that the SA node never fired. The AV junction will reach it's automatic threshold and generate an action potential. Unlike PJCs, the escape complexes will appear late in the rhythm
Atrial Fibrillation (A-fib)

may see course or fine undulations or no atrial activity at all. If atrial activity is seen, it resembles an old saw (when compared to atrial flutter that often resembles a new saw).
Atrial Flutter (A-flutter):
Ventricular Arrhythmias
For a premature ventricular contraction to be diagnosed,
1. The beat must come early or prematurely in the ECG rhythm strip. 2. The 'QRS' complex of the early beat will be wide and bizarre. It will not look anything like the sinus 'QRS' complexes. 3. The 'QRS' complex of the early beat will be over .12 seconds in width. 4. Usually no 'P' wave will precede the 'QRS' complex of the PVC. 5. PVC's usually have compensatory pauses
QRS 1-2.5

2.52.5 PR
> P 3-5
MI
lateral

Leads II, III aVF
QRS Complexes
I + + -
Ventricular Escape Beats (VEB's) Ventricular escape beats occur when there is a missed beat or pause in the normal ECG rhythm strip, and a ventricular beat appears at the end of the pause in the rhythm.
Ventricular Escaped beats must have

1. They must occur at the end of a pause. 2. The 'QRS' complex of this late beat must be over .12 seconds in width. 3. No 'P' wave will precede the ventricular beat.
Ventricular Tachycardia
Whenever the rate of a ventricular rhythm is 100 beats per minute or greater, it is called ventricular tachycardia.
VENTRICULAR TACHYCARDIA IS OFTEN A LIFETHREATENING ARRHYTHMIA AND MUST BE CORRECTED IMMEDIATELY.
'R' on 'T' Phenomenon

Occasionally the 'QRS' complex of a PVC will fall on top of a sinus 'T' wave. When this occurs, it is often called an 'R' on 'T' phenomenon. This situation is often considered more dangerous to the patient than other PVC's because it can often lead to long runs of ventricular tachycardia.
Torsades de Pointes (TDP)

Torsade de pointes is a special classification of ventricular tachycardia that was first discovered in France. The name is French and means twisting or turning points.
The 'QRS' complexes of this rhythm are wide and bizarre as in other forms of ventricular rhythms, but the 'QRS' complexes will first be in one direction from the ECG baseline, such as positive or above the baseline, then rotate so that they become negative or below the baseline
The rhythm is regular, and the main feature that sets it off from other ventricular rhythms is that the height or amplitude of 'QRS' complexes varies.
My Brother Answer Me Please
QRS 1-2.5

2.52.5 PR
> P 3-5
MI
lateral

Leads II, III aVF
QRS Complexes
I + + -
Intraventricular Blocks
Bundle Branch Blocks

With Bundle Branch Blocks you will see two changes on the ECG.
1. QRS complex widens (> 0.12 sec). 2. QRS morphology changes (varies depending on ECG lead, and if it is a right vs. left bundle branch block).
If the QRS Complex is Wide

If the rhythm is supraventricular and QRS winding is not due to WPW there are only 3 possibilities: 1. There may be typical RBBB 2. There may be typical LBBB 3. IVCD (IntraVentricular Conduction Delay).
Note: The 3 key leads (and the only 3 leads needed) to determine the type of conduction defect (RBBB, LBBB, or IVCD) are leads I, V1, and V6.
ECG Diagnosis of Bundle Branch Block
QRS > 0.12sec Look at V1:

Terminal R = RBBB as excitation spreading from left to right Terminal S = LBBB as excitation spreading away from right
Right Bundle Branch Blocks

What QRS morphology is characteristic? For RBBB the wide QRS complex assumes a unique, virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2). V1
Rabbit Ears
RBBB and the "r's" -- rSR' complex with the taller right rabbit ear (the R') in a right-sided lead (i.e., V1).
Confirm LI & V6 Terminal wide S = RBBB as excitation going away from left side
ECG Diagnosis of Bundle Branch Block
QRS > 0.12sec Look at V1:

Terminal R = RBBB as excitation spreading from left to right Terminal S = LBBB as excitation spreading away from right
Confirm LI & V6 Terminal R = LBBB as excitation heading towards left
Left Bundle Branch Blocks

What QRS morphology is characteristic? For LBBB the wide QRS complex assumes a characteristic change in shape in V1 and V2).
Normal
Broad, deep S waves
"Incomplete" RBBB has a QRS duration of 0.10 - 0.12s with the same terminal QRS features. This is often a normal variant
"Incomplete" LBBB looks like LBBB but QRS duration = 0.10 to 0.12s, with less ST-T change. This is often a progression of LVH.
Criteria of left anterior fascicular block I. QRS duration < 0.10 sec. II. left axis deviation
Criteria of posterior fascicular block I. QRS duration < 0.10 sec. II. Righy axis deviation
Bifascicular Blocks RBBB plus either LAFB (common) orLPFB (uncommon) Features of RBBB plus features of the fascicular block (axis deviation, etc.)
Trifasicular' block
The combination of
RBBB, LAFB and long PR interval

a permanent pacemaker may be needed.
75 beats/minute Regular Present; negative P waves precede each QRS complex 0.08 sec 0.08 sec Accelerated junctional rhythm
31 beats/minute Irregular Present; a QRS follows 1st, 5th, and 10th P waves. AV conduction ratios are 4:1 and 5:1 0.34 sec 0.16 sec Sinus rhythm with second-degree, high-degree AV block and BBB
84 beats/minute Regular None; atrial flutter waves are present None 0.08 sec Atrial flutter
QRS 1-2.5

2.52.5 PR
> P 3-5
MI
lateral

Leads II, III aVF
QRS Complexes
I + + -
26 beats/minute Regular Present; the 1st, 3rd, and 5th P waves are followed by QRS complexes 0.19 sec 0.10 sec Sinus rhythm with second-degree, 2:1 AV block
89 beats/minute Irregular Present; precede all QRS complexes exept 2nd and 8th 0.18 sec 0.08 sec (all except 2nd and 8th); 0.12 sec (2nd and 8th) Normal sinus rhythm with isolated unifocal PVCs
182 beats/minute Irregular Present; precede each QRS complex 0.08 sec 0.09 sec Atrial tachycardia

41 beats/minute Irregular Present; precede each QRS complex 0.16 sec 0.08 sec Sinus bradycardia with sinus arrhythmia
33 beats/minute Irregular Present; the 1st, 2nd, and 4th P waves are followed by QRS complexes .22 to .36 sec. The PR intervals increase until the QRS complex fails to follow the P wave 0.10 sec Sinus rhythm with second degree, type I AV block (Wenckebach)
126 beats/minute Irregular None; fine atrial fibrillation waves are present None 0.10 sec Atrial fibrillation
-21year-old female with a history of "seizure" disorder. She is on no medications and her electrolytes are normal. This ECG is most consistent with? a )Wolff-Parkinson-White pre-excitation syndrome (WPW) b )Long QT syndrome c )Hypokalemia d )Tricyclic overdose e )Hypothyroidism
QRS 1-2.5

2.52.5 PR
> P 3-5
MI
lateral

Leads II, III aVF
QRS Complexes
I + + -
b Long QT syndrome
Dx: Congenital long QT syndrome. Note the broad T waves with notching (or possibly U waves) in the precordial leads. This characteristic may identify patients with long QT syndrome at increased risk for torsade de pointes and syncope and sudden death.
Patients at high risk of recurrent syncope or sudden death are usually considered for implantable cardioverter defibrillator therapy .along with beta-blockade
Limb lead reversal. The left and right arm leads are reversed. The clue is inversion of the P wave and QRS complex in lead I. Whenever you see a negative P wave and QRS complex in lead I the likely diagnosis is limb lead reversal. Dextrocardia is another possibility, but in dextrocardia there is loss of R wave progression in the left chest leads which is not seen in this tracing. Another clue is the dissimilarity of the morphology of the QRS complexes in lead I and V6.
History: 36-year-old male with hypertension and hypercholesterolemia presents to the emergency room with chest pain and the following ECG. How would you manage this patient? a) Thrombolytics b) Emergency cardiac catheterization with angioplasty standby c) Conservative management
c) "Conservative" management.
This patient has acute pericarditis. don't forget the differential diagnosis of ST elevations not only includes 1) ischemic heart disease but also 2) pericarditis, 3) left bundle branch block (LBBB) normal In this EKG two features point to pericarditis: The diffuseness of the ST elevations (I, II, III, aVF, V3-V6). In myocardial infarction the ST elevations tend to be localized (inferior, anterior, posterior, lateral), often, but not always with reciprocal ST depressions.
SINUS BRADYCARDIA
EKG Criteria Rate: <60 bpm. Rhythm: Regular generally. Pacemaker: SA node P wave: Present, all originating from SA node, all look the same. PRI: <.20 seconds and constant. QRS: Normal, .08-.12 seconds
SINUS TACHYCARDIA
EKG Criteria Rate: >100 bpm. Rhythm: Regular, generally. Pacemaker: SA node. P wave: Present and normal, may be buried in T waves in rapid tracings. PRI: .12-.20 seconds, generally closer to .12
QRS: Normal.
1 Acute Inferior wall MI with first degree block
Advanced AV block in setting of Atrial Tachycardia or Atrial Flutter
Acute Anterior wall MI
QRS 1-2.5

2.52.5 PR
> P 3-5
MI
lateral

Leads II, III aVF
QRS Complexes
I + + -
Frequent PVCs in a pattern of bigeminy
Supraventricular Tachycardia
Intermittant Right Bundle Branch Block
Left Anterior Fasicular Block
a) Mid-site idio-junctional rhythm b) Bigeminal PAC's c) Trigeminal PAC's d) Trigeminal PVC's
a) Mid-site idio-junctional rhythm b) Bigeminal PAC's c) Trigeminal PAC's d) Trigeminal PVC's
a) Mobitz Type-I b) Mobitz Type-II c) Sinus Rhythm d) Atrial Fibrillation
a) Supraventricular Tacycardia b) Torsade de Pointes c) Ventricular Tachycardia d) Idio-ventricular Rhythm
QRS 1-2.5

2.52.5 PR
> P 3-5
MI
lateral

Leads II, III aVF
QRS Complexes
I + + -

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RVH RAD, and V1 R wave > 7mm tall LVH R in V5 (or V6) + S in V1 (or V2) > 35, or avL

RATE RHYTHM AXIS INTERVALS

half of the >A QT RR interval

QRS > 0.12sec Look at V1: Terminal R = RBBB Terminal S = LBBB

Inferior Anterior . leads V1-V4

II Axis normal + - left axis deviation + right axis deviation

How TO Understand Arrhythmias

1-impulse formation 2 -impulse conduction

1--impulse formation i.e. the pacemaker

Ventricles (e.g., PVC

B*Regularity of ventricular or atrial response

ALL ARE NARROW BUT THE DIFFERENCE IS WIDE !!

IT IS TOO WIDE HOW TO NARROW??

IT IS TOO WIDE HOW TO NARROW??

What are these Games 1- ?1

PACs have 3 different outcomes )1 :) Normal conduction

RATE RHYTHM AXIS INTERVALS

half of the >A QT RR interval

QRS > 0.12sec Look at V1: Terminal R = RBBB Terminal S = LBBB

Inferior Anterior . leads V1-V4

II Axis normal + - left axis deviation + right axis deviation

Enter the goose

Step 2: Are there any RS complexes in the V leads? NO (VT) YES

Step 4: Is there AV dissociation, NO YES (VT)

evidence of AV dissociation is 98% specific for VT.

Supraventricular Tachycardia (SVT)

Supravenricular tachycardia must have the following qualities:

An Atrial Tachycardia rhythm will have the following

Paroxysmal Supraventricular Tachycardia (PSVT)

RATE RHYTHM AXIS INTERVALS

half of the >A QT RR interval

QRS > 0.12sec Look at V1: Terminal R = RBBB Terminal S = LBBB

Inferior Anterior . leads V1-V4

II Axis normal + - left axis deviation + right axis deviation

The Re-Entry Mechanism of Ectopic Beats & Rhythms.

The Re-Entry Mechanism of Ectopic Beats & Rhythms.

The Re-Entry Mechanism of Ectopic Beats & Rhythms.

Cardiac Conduction Tissue

The Re-Entry Mechanism of Ectopic Beats & Rhythms.

The Re-Entry Mechanism of Ectopic Beats & Rhythms.

It is accompanied by the following features:

Premature junctional complexes

Junctional Escape Complexes

Atrial Fibrillation (A-fib)

Atrial Flutter (A-flutter):

RATE RHYTHM AXIS INTERVALS

half of the >A QT RR interval

QRS > 0.12sec Look at V1: Terminal R = RBBB Terminal S = LBBB

Inferior Anterior . leads V1-V4

II Axis normal + - left axis deviation + right axis deviation

Ventricular Escaped beats must have

VENTRICULAR TACHYCARDIA IS OFTEN A LIFETHREATENING ARRHYTHMIA AND MUST BE CORRECTED IMMEDIATELY.

'R' on 'T' Phenomenon

Torsades de Pointes (TDP)

My Brother Answer Me Please

RATE RHYTHM AXIS INTERVALS

half of the >A QT RR interval

QRS > 0.12sec Look at V1: Terminal R = RBBB Terminal S = LBBB

Inferior Anterior . leads V1-V4

II Axis normal + - left axis deviation + right axis deviation

Bundle Branch Blocks

If the QRS Complex is Wide

ECG Diagnosis of Bundle Branch Block

QRS > 0.12sec Look at V1: