ECG basic محاضرة الدكتور الكبسي

BASIC ELECTROCARDIOGRAM INTERPRETATION
Mohammed Al-Kebsi, MSc, PhD, FGHA As. Prof of Cardiology Al-Thawra Cardiac Center Sanaa University kibsi@hotmail.com
Learning Modules
ECG Basics How to Analyze a Rhythm Normal Sinus Rhythm Heart Arrhythmias Diagnosing a Myocardial Infarction Advanced 12-Lead Interpretation
Dr Mohammed Alkebsi (kibsi@hotmail.com)
kibsi@hotmail.com
Phases of the EKG
ECG Paper: Dimensions

5 mm 1 mm
Voltage ~Mass
0.1 mV
0.04 sec 0.2 sec
Speed = rate
Dr Mohammed Alkebsi (kibsi@hotmail.com) Dr Mohammed Alkebsi (kibsi@hotmail.com)
ECG Basics
ECG graphs: 1 mm squares 5 mm squares Paper Speed: 25 mm/sec standard Voltage Calibration: 10 mm/mV standard
Frontal Plane Leads:

Standard (bipolar) Leads:
I: RA- to LA+ II: RA- to LL+ III: LA- to LL+
Augmented Vector (Unipolar) Leads

aVR: to RA+ aVL: to LA+ aVF: to LL+
V1 : 4th ICS & Rt sternal border V2 : 4th ICS & Lt sternal border V3 : midway, between V2 & V4 V4 : 5th ICS, mid clavicular line V5 : 5th ICS, anterior axillary line V6 : 5th ICS, mid axillary line
RIGHT
LEFT
Step approach to analyze ECG

Rate Rhythm P wave morphology PR interval QRS interval, QRS complex morphology ST segment T wave Electrical axis U wave QT duration
Inferior II, III, AVF
Antero-Septal V1,V2, V3,V4
Posterior V1, V2, V3

Lateral I, AVL, V5, V6

Cardiac Cycle Basics:

Begins with SA Node depolarization P P = 1 Cycle Heart rate (pulse) is determined by ventricle depolarization/contraction R R = 1 heart beat
R R P P
Calculating Heart Rates

Sinus Rhythm: Each QRS complex is preceded by P wave NSR: Within the intrinsic rate of the SA Node: 60100 bpm Tachycardia: >100 bpm Bradycardia: < 60 bpm
Method 1
Count the number of small squares between R R waves (X): Divide 1500 by X: Example: X = 20 Rate = 1500 / X 1500 / 20 =75 Rate = 75 bpm
Method 2
Count the number of big squares between R R waves (X): Divide 300 by X: Example: X = 4 Rate = 300 / X 300 / 4 =75 Rate = 75 bpm
Paper Speed: 25 mm/ sec 60 seconds / minute 60 X 25 = 1500 mm / minute

Method 3
Method 4
Take 6 sec strip (30 large boxes) Count the R/R waves X 10 When there is irregularity in ECG.
1
R 30 R 30 30 30 10 R 10 10 10 R
2 2 3
4 4
5 5
6 6 7
300
150
100
Interpreting Axis Deviation:

Normal Electrical Axis:
(Lead I + / aVF +)
Left Axis Deviation:

Lead I + / aVF
Right Axis Deviation:

Lead I - / aVF +
No Mans Land Man

- Both I and aVF are
Blue Segment: -30to +90Is normal QRS Dr Mohammed Alkebsi (kibsi@hotmail.com) axis
How do we Determine Axis??

Method 1
Method 2 using the hexaxial diagram
Normal axis Lead I Lead II Lead III Positive Positive Positive or negative
Right axis deviation Negative Positive or negative Positive
Left axis deviation Positive Negative Negative
Method 3 Simplest method

Shaking hands
Check Leads: I and aVF
Rhythm ID: Algorithm

P-Wave: What is the atrial rhythm? < 0.12 sec (3 mm) QRS: What is the ventricular rhythm? <0.10 sec (<3 mm) P-R Interval: Is AV conduction normal? 0.12-0.20 sec (3-5 mm) Any unusual complexes? IS IT DANGEROUS?
P-wave
It is important to remember that the P wave represents the sequential activation of the RA and LA, and it is common to see notched or biphasic P waves of RA and LA activation. P duration < 0.12 sec P amplitude < 2-3 mm
Normal P-Wave P Sinus: Normal, Tachy, Brady
Irregular P wave
Premature Beats: Narrow P waves: PACs
Abnormal shape of P-Wave PP Pulmonale

Tall Peaked RA enlargement secondary to PH (COPD)
P-Mitrale
Broad notched LA enlargement secondary to MVD
Absent P-Wave P-
Abnormal shape of P-Wave
Absent P: V-tach, A-fib, Junctional Rhythm
Rate: 4060 bpm Rhythm: Regular P Waves: Absent, inverted, buried, or retrograde retrograde Dr Mohammed Alkebsi (kibsi@hotmail.com) PR Interval: None, short. QRS: Normal (0.060.10 sec)
Irregular P-Wave PIrregular P: A-Flutter
Fibrillation vs. Flutter?

Multi-focal origins chaotic Rate: >400 bpm IRREGULAR-R One focus - organized Rate: 200-400 bpm REGULAR - R
Ventricles: QRS Rhythms

Regular rhythms? R-R intervals equivalent Regular irregular rhythms? R-R intervals equivalent with occasional irregularities Irregular rhythms? R-R intervals irregular
Regular Irregular Irregular

Premature Beats: PVC Widened QRS, not preceded P wave Usually does not disrupt P-wave regularity T wave is inverted after PVC Followed by compensatory ventricular pause
PVC Patterns:
PVC: 1 Isolated beat Couplet: 2 consecutive PVCs Bigeminy: PVC every other beat Non-Sustained VT: >3 beats for less than 1 minute Sustained VT: > 1 minute of ventricular tachycardia
T-wave
The T wave is the most labile wave in the ECG. T wave changes including low-amplitude T waves and abnormally inverted T waves may be the result of many cardiac and non-cardiac conditions. The normal T wave is usually in the same direction as the QRS except in the right precordial leads (V1,V2). Normally; T wave is always upright in leads I, II, V3-6, and always inverted in lead aVR. The other leads are variable depending on the direction of the QRS and the age of the patient. Dr Mohammed Alkebsi (kibsi@hotmail.com)
T-wave
DD of T Wave Inversion
Q wave and non-Q wave MI (e.g., evolving anteroseptal MI). Myocardial ischemia Subacute or old pericarditis Myocarditis Myocardial contusion (from trauma) CNS disease causing long QT interval (subarrachnoid hemorrhage).
Idiopathic apical hypertrophy (a rare form of hypertrophic cardiomyopathy) Mitral valve prolapse Digoxin effect RVH and LVH with "strain" (see below: T wave inversion in leads aVL, V4-6 in LVH)
DD of T Wave Inversion Nice Seeing "U" Again

The normal U wave has the same polarity as the T wave and is usually less than one-third the amplitude of the T wave. Best seen in the right precordial leads especially V2 and V3. U wave is asymmetric with the ascending limb moving more rapidly than the descending limb (just the opposite of the normal T wave).
ECG Intervals
PR Interval: 0.12 - 0.20 sec QRS Duration: 0.06 - 0.10 sec QTc
Men < 0.43
borderline o.43-0.45 prolonged >0.45
Women < 0.43

borderline o.43-0.47 prolonged >0.47
QT interval
Bazett's Formula: QTc = (QT)/SqRoot RR (in Formula: QTc (QT)/SqRoot seconds) Poor Man's Guide to upper limits of QT: For HR = 70 bpm, QT<0.40 sec; for every 10 bpm bpm, QT< increase above 70 subtract 0.02 sec, and for every 10 bpm decrease below 70 add 0.02 sec. For example: If HR=80 QT < 0.38 If HR= 60 QT < 0.42
CONDUCTION ARRHYTHMIAS
Conduction Disturbance?
Ectopic Beats: wide QRS complexes AV Blocks: Prolonged P-R intervals Ventricular: Bundle Branch Blocks Wide QRS / Normal P-R
HEART BLOCK
S-A block occurs in the conduction between the SA node and atria. A-V Blocks occur in the conduction between the atria and ventricles Ventricular Blocks: Occur in the Bundle Branches
S-A block occurs in the conduction between the SA node and atria.
A-V Blocks occur in the conduction between the atria and ventricles
Sinus arrest
Ventricular Blocks: Occur in the Bundle Branches
The SA node fails to discharge and then resumes. Electrical activity resumes either when the SA node resets itself or when a lower latent pacemaker begins to discharge. The pause (arrest) time interval is not a multiple of the normal P-P interval.
SA block

Atrio-Ventricular Blocks: AtrioSA Node fires, but conduction is impaired: Degrees of Block: 1 Conduction delayed, but QRS captured : 2 Partial Block: Occasional ventricular : capture 3 Complete: Atria and ventricles completely : dissociated
First Degree Block:

Prolonged P- R interval
Second Degree Block:

Type I: Wenckebach P-R Interval gets progressively longer until the AV conduction is completely blocked: When AV conduction blocked, there is not QRS complex QRS is normal
Second Degree Block:

Type II: Regular ventricular rate slow 2:1, 3:1 or 4:1 P:R waves Only occassional but regular ventricular capture QRS is normal
Third Degree (Complete) AV Block

AV conduction is completely dissociated Ventricles contract at intrinsic rate (30-40 bpm) Normal P waves, but more than QRS waves QRS complexes may be normal or widened
Identifying AV Blocks:
Name Conduction PR-Int R-R Rhythm
Bundle Branch Blocks
1 :
P=R
> .20
Regular
2 :Mobitz I P > R 2 :Mobitz II P > R 3 : P>R
Progressi Irregular ve Constant Grossly Irregular Regular Regular

(20-40 bpm)

Turning our attention to bundle branch blocks Remember normal impulse conduction is SA node AV node Bundle of His Bundle Branches Purkinje fibers
Normal Impulse Conduction

Sinoatrial node AV node Bundle of His Bundle Branches Purkinje fibers

So, depolarization of the Bundle Branches and Purkinje fibers are seen as the QRS complex on the ECG. Therefore, a conduction block of the Bundle Branches would be reflected as a change in the QRS complex.

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).
Right BBB
Look at the V leads to recognize Bundle Branch Blocks


Why does the QRS complex widen?
RBBB
What QRS morphology is characteristic? QRS duration 110ms rSR pattern or notched R wave in V1 rSR Wide S wave in I and V6 V1
Rabbit Ears
LBBB
What QRS morphology is characteristic? QRS duration 120ms Broad R wave in I and V6 Prominent QS wave in V1 Absence of q waves (including physiologic q waves) in I and V6
LBBB
RBBB
Guess: RBBB or LBBB?

Wide QRS Rabbit Ears in V1 and V2
= RBBB!
Guess: RBBB or LBBB?

Wide QRS Mostly down in V1 and V2 Mostly up in lead V6
ST Segment Analysis: Ischemia Diagnosis

Key Reference Points:
Isoelectric line: Use the PR segment as reference J-Point: Point at which QRS complex ends and ST segment begins ST Slope: Downsloping > Horizontal > Upsloping (questionable/angina)
= LBBB!
Recall that in either RBBB or LBBB, the QRS must be wide (> .12 sec) Dr Mohammed Alkebsi (kibsi@hotmail.com)
ST-Depression ST-
Determining Regions of infarction

RCA: Inferior myocardium II, III, aVF LCA: Lateral myocardium I, aVL, V5, V6 LAD: Anterior/Septal myocardium V1-V4
>1.0 mm depression: Downsloping: Very predictive Horizontal: Very predictive Upsloping: Predictive if angina present >2.0 mm depression Usually indicative of ischemia
ECG Changes
Ways the ECG can change include:
ST elevation & depression
ECG Changes & the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is:
inverted
Non-ST Elevation
T-waves peaked Appearance of pathologic Q-waves

ST Elevation
flattened
ST Elevation (Transmural or Q-wave), or Non-ST Elevation (Subendocardial or non-Q-wave)

ST Elevation Infarction
The ECG changes seen with a ST elevation infarction are:
Heres a diagram depicting an evolving infarction:
A. Normal ECG prior to MI B. Ischemia from coronary artery occlusion results in ST depression (not shown) and peaked T-waves C. Infarction from ongoing ischemia results in marked ST elevation D/E. Ongoing infarction with appearance of pathologic Q-waves and T-wave inversion F. Fibrosis (months later) with persistent Qwaves, but normal ST segment and Twaves Dr Mohammed Alkebsi (kibsi@hotmail.com)
Before injury Normal ECG Ischemia Infarction Fibrosis ST depression, peaked T-waves, then T-wave inversion ST elevation & appearance of Q-waves ST segments and T-waves return to normal, but Q-waves persist
Heres an ECG of an acute MI: Heres an ECG of an inferior wall MI later in time:
Now what do you see in the inferior leads? Question: What ECG changes do you see? ST elevation, Q-waves and T-wave inversion
Extra credit:
What is the rhythm? Atrial fibrillation (irregularly irregular with narrow QRS)! Dr Mohammed Alkebsi (kibsi@hotmail.com)
Non-ST Elevation Infarction

The ECG changes seen with a non-ST elevation infarction are:
Non-ST Elevation Infarction

Heres an ECG of an evolving non-ST elevation MI:
Note the ST depression and T-wave inversion in leads V2-V6.
Before injury Normal ECG Ischemia Infarction Fibrosis ST depression & T-wave inversion ST depression & T-wave inversion ST returns to baseline, but T-wave inversion persists
Question:
What area of the heart is infarcting?
Anterolateral
Left Ventricular Hypertrophy

Many sets of criteria for diagnosing LVH have been proposed:
Sensitivity The sum of the S wave in V1 and the R wave in either V5 or V6 > 35 mm Sum of the largest precordial R wave and the largest precordial S wave > 45 mm Romhilt-Estes Point System Specificity
43%
95%
45% 50-54%
93% 95-97%
Romhilt-Estes Point System for LVH

Criterion Amplitude (any of the following: Largest R or S wave in any limb lead 20mm S in V1 or V2 30mm R in V5 or V6 30mm ST depressions or T wave inversions in lateral precordial leads, I, and/or aVL Left atrial enlargement Left axis deviation QRS duration 90 ms Intrinsicoid deflection in V5 or V6 50 ms
Dr Mohammed Alkebsi (kibsi@hotmail.com) 4 points Probable LVH
Points 3

Compare these two 12-lead ECGs. What stands out as different with the second one?
3 3 2 1 1
Normal
5 points
Definite LVH
Answer: The QRS complexes are very tall (increased voltage) Dr Mohammed Alkebsi (kibsi@hotmail.com)
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: Right axis deviation Right atrial enlargement Downsloping ST depressions in V1-V3 (RV strain pattern) Tall R wave in V1
Everything is clear?
Summary
Dont worry too much right now about trying to remember all the details. Youll focus more on advanced ECG interpretation in your clinical years!
Summary TAILORED ECG
QRS Axis
QRS Axis
QRS Axis
QRS Axis
Frontal Plane QRS Axis = +75 degrees-KH
Frontal Plane QRS Axis = +15 degrees-KH Frontal Plane QRS Axis = -45 degrees-KH
Right Axis Deviation
QRS Axis
Sinus Pause or Arrest

Frontal Plane QRS Axis = +150 degrees (RAD)-KH
Long QT Interval-KH The QT interval duration is greater than 50% of the RR interval, a good indication that it is prolonged in this patient. Although there are many causes for the long QT, patients with this are at risk for malignant ventricular arrhythmias, syncope, and sudden death.
Hyperkalemia and Old Inferior MI The T waves are tall, peaked and have a narrow base, making them very uncomfortable to sit on! These changes are characteristic of hyperkalemia. The QRS is also slightly widened, another feature of hyperkalemia. Q waves in III and aVF indicate an old inferior MI.
Left Atrial Abnormality & 1st degree AV Block-KH

Right Ventricular Hypertrophy
The rhythm is sinus rhythm with a rate of about 75/minute. There is first degree atrioventricular block demonstrated by a PR interval of 300 milliseconds. An inferolateral infarction is indicated by the Q waves in leads II, III, aVF (inferior) and there are Q waves as well as I, aVL, V5 and V6 . The poor R wave progression in the precordial leads and the marked posterior rotation of the QRS axis suggests an anterior infarction as well.
The rhythm is sinus rhythm with at 50/minute. The PR interval is 180 ms. The QRS axis is normal Q waves are seen in lead II, III and aVF as well as V2 V4. There is STsegment elevation in the inferior leads and precordial leads V1-V4. This suggests an anterior myocardial infarction of undetermined age and a possibly inferior infarction (the q wave in AVF is boarder-line). The T waves are also inverted in the lateral leads.

Right Bundle Branch Block

Right Atrial Enlargement

Left Bundle Branch Block Left Atrial Enlargement

Left Ventricular Hypertrophy Right Ventricular Hypertrophy

(with frequent PVCs)

Everything is clear?
The rhythm is sinus tachycardia at approximately 120/minute. The P waves are biphasic in V1. The PR interval is 140 ms. There is an M shaped QRS complex (rSR' variant) in leads V1 to V3. In addition there are deep and slurred S waves in leads I, aVL, V5 and V6. There are also prominent S waves proceeded by small r waves in II, III and aVF as well as left axis deviation of the first part of the QRS. Together, these phenomena indicate the presence of a bifascicular block: right bundle branch block and left anterior hemiblock.. The ST elevation seen in leads II, III and aVF and ST depression in leads I and aVL suggest acute inferior injury/infarction. There is also slight ST elevation in V1. The ST elevation in V1 suggests acute anterior ischemia/injury/infarction.
Four days later, the sinus rhythm has slowed down (approximately 80/minute) and the degree of ST changes have diminished. This indicates that the acute process of infarction/ischemia is evolving.
The rhythm is sinus rhythm at approximately 70/min. The deep S waves in the inferior leads and a left axis deviation indicates left anterior hemiblock. There is poor R wave progression in the anterior precordial leads with a QS complex in V4. There is ST segment elevation in leads V1 to V4. There are very small or R waves leads II, III and aVF. All of these phenomena point towards the presence of an anterior wall and possible inferior wall infarction.
This tracing shows sinus rhythm at 70/minute and supraventricular trigeminy (ie., every third beat is premature). The mean ventricular rate is about 80. There are Q waves in leads II, III and aVF indicating the presence of an inferior infarction. There is no significant ST deviation so the infarction is probably old.
Six weeks later, the premature atrial beats have resolved. There is sinus rhythm with a rate of about 75/minute. The PR interval has widened to 232ms which indicates a first degree atrioventricular block. There is a new right bundle branch block as demonstrated by the rSR' complex in V1 and V2 as well as the wide, slurred S waves in I and V6.
This tracing shows sinus rhythm at 82/minute. The PR interval is 180 ms. The QRS interval duration of 260 ms indicates a conduction defect. There is an M shaped QRS complex (rSR' variant) in leads V1 to V3. In addition there are S waves in leads I, aVL, V5 and V6. There are also prominent S waves proceeded and small r waves in II, III and aVF . The QRS has as a left axis deviation. These findings indicate the presence of a bifascicular block, right bundle branch and left anterior hemiblock.. The inverted T waves in V1 and V2 are probably due to the conduction disturbance and not ischemia.
This tracing shows sinus tachycardia at 112/minute. The PR interval is 140 ms. Right atrial enlargement is suggested by the tall P waves in lead II and left artrial abnormality by the negative P wave deflection in V1. There is a slight rSR' morphology in V1 and V2 but no deep S waves in I or V6. This could indicate the presence of a partial right bundle branch block. Narrow but large Q waves are present without ST segment deviation in leads II, III and aVF suggesting an old inferior infarction. The deep QS wave in V3 suggest an anterior infaction. The peaked T waves in V3-V6 suggest the presence of acute anterior ischemia. Q waves usually evolve later in a Q wave infarction. Here, the Q waves and peaked T waves coexist. An explanation for this is that the Q waves represent an old or remote infarction while the peaked T waves represent an active ischemic process, or that the Q waves have appeared more radily than expected. Dr Mohammed Alkebsi (kibsi@hotmail.com)
This tracing shows sinus tachycardia at a rate of 120/minute. The PR interval is 175 ms. The third beat of the tracing is probably a ventricular premature beat. There is significant ST elevation in the inferior leads III and aVF showing an acute inferior infarction. The ST depression in the lateral leads may be reciprocal to this inferior infarction. Deep Q waves are seen in V1-V4 along with a poor R wave progression suggest a an old anterior infarction.
The rhythm is complete (3rd degree) atrioventricular block with a nodal escape and a ventricular rate of 50/minute. There is a small but significant ST elevation inferior leads II, III and avF indicating an acute inferior injury. Deep Q waves in V1-V3 show an anterior infarction which is probably old. The ST elevation in leads V5 and V6 suggest latteral wall acute injury.
This tracing shows sinus tachycardia at a rate of 115/minute. The PR interval is120ms. There are large R waves in the anterior leads V1-V3. This could be the reciprocal equivalent of Q waves posteriorly. These leads also show slight anterior ST segment depression and peaked, inverted T waves which can be interpreted as posterior injury and ischemia (i.e., reciprocal ST segment elevation and peaked T waves). Although true posterior wall infarctions are usually associated with an inferior infarction (not seen in this tracing), this tracing does suggest a possible acute true posterior Q wave infarction. The use of posterior EKG electrodes can be helpful cases of suspected true posterior Q wave infarction. Dr Mohammed Alkebsi (kibsi@hotmail.com)
This tracing shows sinus bradycardia. The rate is 45/minute. The PR interval is 200ms. There is high voltage R waves in V2 and V5 which could suggest biventricular hypertrophy. The peaked T waves in V2 and V3 along with slight ST segment elevation in those leads suggest the early stages of an acute anterior infarction although similar findings can be found with what is called "early replarization". There are deep but narrow Q waves in II, II and aVF suggesting a remote inferior infarction.
This tracing shows sinus rhythm at a rate of 87/minute. The PR interval is 175 ms. The small r waves or QS deflections in III and aVF suggest a possible old inferior infarction..
This tracing shows sinus rhythm. The rate is 60/minute. There is an M shaped QRS complex (rSR' variant) in leads V1 to V3. In addition there are deep and slurred S waves in V6. There are also prominent S waves proceeded by very small r waves in II, III and aVF as well as a left axis deviation of -60. Together, these findings suggest bifascicular block: right bundle branch and left anterior hemiblock (The left axis deviation could also represent an old inferior infarction with regenerated R waves in the inferior leads). There is ST segment depression in leads V1 to V3. This probably indicates reciprocal changes due to the conduction disturbance and is not subendocardial ischemia of the anterior wall or an acute transmural injury of the posterior wall
This tracing shows sinus tachycardia. The rate is 123/min. The PR interval is normal at 120ms. The Q waves in II, III and aVF suggest an inferior infarction. The slight ST elevation in the inferior leads and more pronounced elevation in leads V2-V3 suggest acute injury or infarction.
This tracing shows sinus rhythm. The rate is 80/minute. Beat #11 and #14 are premature ventricular beats (as suggested by the wide QRS complex, the compensatory pause {first beat} and the absence of a preceding P wave). An inferior infarction (possibly acute) is suggested by the presence of slight ST segment elevation and Q waves in leads II, III and aVF. Q waves are also seen in precordial leads V1-V4 suggestive of an old anterior infarction. The tracing would have to be compared to an old one to determine if the infarctions are new or old.
The recording shows sinus tachycardia with a rate of 110/minute, the eight beat is an atrial premature beat. The PR interval is 180 ms. There is a left axis deviation of -70 degrees. There is a left anterior hemiblock. There is ST segment elevation in V2-V5 which indicates acute anterior injury/infarction. This is most likely an acute anterior infarction. There is also poor R wave progression which is probably related to the left anterior hemiblock.
I. The recording shows sinus rhythm with a rate of 80/minute. The PR interval is 160 ms. There are relatively tall T waves in the anterior leads suggesting the presence of early anterior wall ischemia/injury. The Q waves in III are not significant as there are no significant Q waves in the other inferior leads.
II. This recording taken 1 hour and 15 minutes later, now shows ST segment elevation, signifying the evolution of an acute anterior infarction.
A 55 year old man with 4 hours of "crushing" chest pain
This patient has a very ominous ECG. There is widespread ST elevation and evolving Q waves in multiple leads including the inferior leads (II, III, and aVF) and the precordial leads (V1 to V6). This patient is having an extensive myocardial infarction. It is possible that she has had a previous inferior MI and is now having an anterior MI (or, the opposite is also possible). Another explanation is that the LAD (left anterior descending artery) was serving as a collateral vessel to a totally occluded right coronary artery. In any case, there is extensive myocardial damage, there must be severe systolic left ventricular dysfunction, and the cardiogenic shock is probably due to pump failure.
The ECG shows "pre-excitation" and is consistent with the Wolff-Parkinson-White syndrome. The preexcitation of the ventricles occurs due to a bypass tract which bypasses the delay inherent in the AV node. The PR interval is short due to ventricular preexcitation, which also causes a Delta wave to be present. This ECG shows a Type B bypass tract resulting from a right-sided accessory pathway. Bypass tracts may be associated with AV reciprocating tachycardias, rapid conduction during atrial fibrillation, and sudden cardiac death.
This patient has ECG criteria for left ventricular hypertrophy "with strain." He meets voltage criteria for LVH. The "sagging" ST depression respresents the "strain" pattern which is typical of severe left ventricular hypertrophy. About 80% of patients with aortic stenosis will have ECG criteria for left ventricular hypertrophy. Multiple criteria have been proposed for the ECG diagnosis of LVH. The Estes Criteria include: 1. Amplitude: 3 points Any one of the following: Largest R or S wave in the limb leads >20 mm S wave in V1 or V2 greater than or equal to 30 mm R wave on V5 or V6 greater than or equal to 30 mm 2. ST-T wave changes of LVH Without digoxin: 3 points With digoxin: 1 point 3. Left atrial enlargement: 3 points 4. Left axis deviation of 30 degrees or more: 2 points 5. QRS duration longer than 0.09 seconds 6. Intrinsicoid deflection in V5 or V6 greater than or equal to 0.05 seconds: 1 point
This patient with mitral stenosis has marked left atrial enlargement as reflected in the P wave in lead V1. The "P terminal force" (the state negative portion of the P wave) is greater than one box by one box. There is marked right axis deviation from right ventricular hypertrophy - probably resulting from secondary pulmonary hypertension. The elevated left atrial pressure resulting from the mitral valve obstruction has led to pulmonary artery hypertension. The right ventricular hypertrophy results as a response to the pulmonary hypertension. Atrial fibrillation typically occurs in such patients, but this patient remarkably is still in sinus rhythm. Shortness of breath, orthopnea, and exercise intolerance are typical. Patients may develop thrombo-embolic strokes from mitral stenosis and these patients require warfarin anticoagulation - particularly if they are in atrial fibrillation.
This patient has a narrow complex tachycardia. Narrow complex tachycardias are essentially always supra-ventricular in origin. Conversely, wide complex tachycardias can be either supraventricular or ventricular in origin. In general, the differential diagnosis of narrow complex tachycardia includes: Sinus tachycardia Atrial fibrillation Atrial flutter Multifocal atrial tachycardia AV nodal re-entry tachycardia AV reciprocating tachycardia SA nodal re-entry tachycardia Atrial tachycardia
The patient has developed very rapid ventricular tachycardia and the cardiovascular collapse is related to the rapid rate. He requires immediate cardioversion. Ventricular tachycardia can occur during the first several days of acute myocardial infarction and is the most common cause of out-of-hospital, sudden death complications of acute myocardial infarctions. Coronary care units (CCUs) were originally developed to treat ventricular tachycardia and ventricular fibrillation in such patients - the original CCUs had little else to offer. VT occurring during the first 24 hours of myocardial infarction does not require specific, longterm evaluation.
Sinus rhythm Normal axis Small Q waves in leads II, III, VF Biphasic T waves in leads II, V6; inverted T waves in leads III, VF Markedly peaked T waves in leads V1V2
Complete heart block Ventricular rate 45/min

Narrow-complex tachycardia, rate about 200/min No P waves visible Normal axis Regular QRS complexes Normal QRS complexes, ST segments and T waves Clinical interpretation This is a supraventricular tachycardia, and since no P waves are visible this is a junctional, or atrioventricular nodal, tachycardia.
Sinus rhythm Peaked P waves, best seen in lead II Right axis deviation Dominant R waves in lead V1 Deep S waves in lead V6 Inverted T waves in leads II, III, VF, V1V3 Severe right ventricular hypertrophy.
Atrial fibrillation with a ventricular rate of about 40/min Left axis Left bundle branch block
ECG Quiz 6
The heart rate is 120/min and the QRS complex durations is 150 ms. There is a conspicuous lack of clearly seen P waves. Ventricular tachycardia is possible with the QRS complex duration of 150 ms but is unlikely as the r in V1 is small, the R/S ratio in lead V6 is less than one and there is no sign of AV dissociation or of capture beats. The rhythm is probably a sinus tachycardia with first degree heart block (P waves falling on the T waves) or a junctional tachycardia. Right bundle branch block is indicated by rSR' variant morphology in V1-V3 and wide, slurred S waves in I and V6. There is a left axis deviation. Inferior infarction is indicated by the qs complexes in III and aVF. It is probably old.
78 year old man, baseline ECG.
A-Fib, PVC, LBBB
82 year old man with respiratory distress. Cath emergently? Sinus tachycardia and LVH with secondary repolarization abnormality Emergent cath revealed no significant CAD.
ECG 6 months later, with chest pain.
The new ECG shows LBBB with inferolateral ST elevations. No cath was performed. (The patient was DNR/DNI with severe dementia and his HCPOA did not want invasive procedures.) Dr Mohammed Alkebsi (kibsi@hotmail.com) Peak CK 1242, CK-MB 171.5, Troponin T 6.560.
66 year old woman with chest pressure and abnormal troponin. 59 year old woman h/o CABG with N/V and diaphoresis. Cath emergently?
Sinus rhythm with SI, QIII, TIII, and anterior T wave inversions. Cardiac cath revealed no significant CAD. CT revealed massive PE.
Sinus tachycardia and LVH with secondary repolarization abnormality. Emergent cath was deferred. Serial cardiac biomarkers were negative. Elective cath revealed no culprit CAD.
18 year old man with palpitations. What is the rhythm? His subsequent ECG:
66 year old man with sudden CP followed by syncope. What is the diagnosis? Sinus tachycardia with P pulmonale and inferior injury pattern. However, with the widespread ST depressions (> 7 leads), LM or 3-vessel disease is possible.
The first ECG shows ectopic atrial tachycardia. Note the inverted P waves in leads II, III, and AVF Alkebsi (kibsi@hotmail.com) Dr Mohammed and compare to the second ECG, when the patient is in sinus rhythm.
Cath revealed severe 3-vessel disease.

ECG basic محاضرة الدكتور الكبسي

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ECG basic محاضرة الدكتور الكبسي

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BASIC ELECTROCARDIOGRAM INTERPRETATION

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Phases of the EKG

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Dr Mohammed Alkebsi (kibsi@hotmail.com)

ECG Paper: Dimensions

0.04 sec 0.2 sec

Frontal Plane Leads:

Augmented Vector (Unipolar) Leads

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Step approach to analyze ECG

Inferior II, III, AVF

Antero-Septal V1,V2, V3,V4

Posterior V1, V2, V3

Lateral I, AVL, V5, V6

Cardiac Cycle Basics:

Calculating Heart Rates

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Paper Speed: 25 mm/ sec 60 seconds / minute 60 X 25 = 1500 mm / minute

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Interpreting Axis Deviation:

Left Axis Deviation:

Right Axis Deviation:

No Mans Land Man

Dr Mohammed Alkebsi (kibsi@hotmail.com)

How do we Determine Axis??

Method 2 using the hexaxial diagram

Right axis deviation Negative Positive or negative Positive

Left axis deviation Positive Negative Negative

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Method 3 Simplest method

Rhythm ID: Algorithm

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Normal P-Wave P Sinus: Normal, Tachy, Brady

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Abnormal shape of P-Wave PP Pulmonale

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Abnormal shape of P-Wave

Absent P: V-tach, A-fib, Junctional Rhythm

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Irregular P-Wave PIrregular P: A-Flutter

Fibrillation vs. Flutter?

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Ventricles: QRS Rhythms

Regular Irregular Irregular

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Dr Mohammed Alkebsi (kibsi@hotmail.com)

Dr Mohammed Alkebsi (kibsi@hotmail.com)

DD of T Wave Inversion Nice Seeing "U" Again