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مشاركةبواسطة دكتور كمال سيد » الجمعة نوفمبر 30, 2018 4:07 pm

Type #5: A New Left Bundle Branch Block – Equivalent to a STEMI

This must not be forgotten. At least a couple times, I recall proper treatment for STEMI was not instituted because the clinician either did not recognize that a new left bundle branch block is a STEMI equivalent or assumed the LBBB was old. You can learn the diagnostic criteria for this bundle branch in Left Bundle Branch Block ECG Review.

Sometimes, of course, there is no prior ECG for comparison, and you have to actually use your clinical judgment. Always err on the side of caution, and look out for the patient. It is better to activate the cath lab and find normal coronary arteries than to not and have a patient go into cardiogenic shock — as usually this type of MI indicates left main or proximal LAD involvement.

This is what a LBBB looks like in the precordial leads.

Note: There are criteria such as the Sgarbossa criteria and certain signs such as Chapman’s sign and Cabrera’s sign to diagnose an acute MI in the setting of a prior known left bundle, but the sensitivity is somewhat low.

Here is one last thing when trying to solidify this topic in your brain. A right ventricular infarct frequently accompanies an inferior STEMI; although unheard of to occur isolated, it may be just rare or under-recognized. An RV infarction can be detected with a right-sided ECG. It is a good idea to do a right-sided ECG in all inferior STEMI cases, as RV involvement can change the management approach. Learn the complications of STEMI in STEMI Topic Review.

Alrighty, then! By looking at these — again, and again, and again — you will never miss any type of STEMI on an ECG. This is the most important thing about using your ECG interpretation knowledge in the clinical setting, so I am glad you read all the way to the end. ... cg-pattern

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مشاركةبواسطة دكتور كمال سيد » الجمعة نوفمبر 30, 2018 4:08 pm

Related Content:

Blog: Think Again - ECG Case #1 Blog: 10 Steps to Learn ECG Interpretation Atrial Arrhythmias ECG Quiz Beginner ECG Quiz Chamber Enlargements and Axis ECG Quiz Comprehensive ECG Quiz Expert ECG Quiz Heart Blocks ECG Quiz Infarcts and Ischemia ECG Quiz Miscellaneous ECG Quiz Ventricular Arrhythmias ECG Quiz ECG Cases ... cg-pattern

Learn EKG using the following modules. Each module includes training materials as well as interactive question and answer exercises.

ECG Monitor Quiz ... nitor-quiz


Practical Clinical Skills

Basic Arrhythmia ... rpret.html ... ic_Q_Waves

Normal Electrocardiography (ECG) Intervals

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مشاركةبواسطة دكتور كمال سيد » الجمعة نوفمبر 30, 2018 7:44 pm


EKG Waveform Lesson

EKG Waveform
Letters are used to indicate important points on a typical waveform.

PR Interval
The PR Interval indicates atrioventricular conduction time. The interval is measured from where the P wave begins until the beginning of the QRS complex.

QRS Complex
The QRS complex indicates ventricular depolarization. The QRS interval is measured from the end of the PR interval to the end of the S wave.

QT Interval
The QT interval indicates ventricular activity, both depolarization and repolarization. Measure the QT interval from the beginning of the QRS complex to the end of the T wave.

ST Interval
The ST segment traces the early part of ventricular repolarization. The ST segment begins at the end of the QRS complex and continues to beginning of the T wave.

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مشاركةبواسطة دكتور كمال سيد » الجمعة نوفمبر 30, 2018 9:26 pm


The ST segment represents ventricular repolarization. Repolarization follows upon contraction and depolarization. During repolarization the cardiomyocytes elongate and prepare for the next heartbeat.
This process takes much more time than the depolarization. The elongation that takes place during repolarization is not passive; it is an active process during which energy is consumed. On the ECG, the repolarization phase starts at the junction, or j point, and continues until the T wave. The ST segment is normally at or near the baseline. Minor STT changes are not necessarily associated with cardiac ischemia .

The T wave is usually concordant (corresponding in direction with the planes of ..) with the QRS complex.
Thus if the QRS complex is positive in a certain lead (the area under the curve above the baseline is greater than the area under the curve below the baseline) than the T wave usually is positive too in that lead. Accordingly the T wave is normally upright or positive in leads I, II, AVL, AVF and V3-V6.
The T wave is negative in V1 and AVR. The T wave flips around V2, but there is likely some genetic influence in this as in Blacks the T wave usually flips around V3.

The T wave angle is the result of small differences in the duration of the repolarization between the endocardial and epicardial layers of the left ventricle. The endocardial myocytes need a little more time to repolarize (about 22 msec). This difference causes an electrical current from the endocardium to the epicardium, which reads as a positive signal on the ECG.
ST elevatie is measured at the junctional or j-point.

ST elevation

Myocardial Infarction

schemia occurs when part of the heart muscle, the myocardium, is deprived of oxygen and nutrients.
Common causes of ischemia are:
Narrowing or obstruction of a coronary artery.
A rapid arrhythmia, causing an imbalance in supply and demand for energy.

A short period of ischemia causes reversible effects :
The heart cells will be able to recover. When the episode of ischemia lasts for a longer period of time, heart muscle cells die. This is called a heart attack or myocardial infarction. That is why it is critical to recognize ischemia on the ECG in an early stage.

Severe ischemia results in ECG changes within minutes. While the ischemia lasts, several ECG changes will occur and disappear again. Therefore, it may be difficult to estimate the duration of the ischemia on the ECG, which is crucial for adequate treatment.

Signs and symptoms of myocardial ischemia:

Crushing pain on the chest (angina pectoris), behind the sternum, often radiating to the lower jaw or the left arm
Fear of dying
Shock (manifesting as paleness, low blood pressure, fast weak pulse) shock
Rhythm disturbances (in particular, increasing prevalence of ventricular ectopia, ventricular tachycardia, AV block)
Risk assessment of Cardiovascular disease

Narrowing of the coronary artery, leading to a myocardial infarction, usually develops over several years. An increased risk of cardiovascular disease, which may lead to a myocardial infarction or cerebrovascular accident, can be estimated using SCORE system which is developed by the European Society of cardiology (ESC).
As shown in the figure, the most important risk factors for myocardial infarction are:
Male sex
Diabetes Mellitus

Risk assessment of ischemia
An exercise test such as a bicycle or treadmill test, may be useful in detecting myocardial ischemia after exercise.
In such a test, continuous ECG monitoring is performed during exercise. # The ST-segment,# blood pressure and # clinical status of the patient (i.e. chest complaints) are monitored during and after the test.
An exercise test is positive for myocardial ischemia when the following criteria are met:

Horizontal or downsloping @ ST-depression of >1mm, 60 or 80ms after the J-point
ST @ elevation of > 1.0 mm

The diagnosis of acute myocardial infarction is not only based on the ECG.
A myocardial infarction is defined as:

Elevated# blood levels of cardiac enzymes (CKMB or Troponin T) AND
One of the following criteria are met
The patient has # typical complaints,
The ECG shows# ST elevation or depression.
pathological # Q waves develop on the ECG
A coronary# intervention had been performed (such as stent placement)

So detection of elevated serum cardiac enzymes is more important than ECG changes. However, the cardiac enzymes can only be detected in the serum 5-7 hours after the onset of the myocardial infarction. So, especially in the first few hours after the myocardial infarction, the ECG can be crucial.

ECG Manifestations of Acute Myocardial Ischaemia (in Absence of LVH and LBBB)are

ST elevation#
New ST elevation at the J-point in two contiguous leads with the cut-off points : ≥0.2 m in men or ≥ 0.15 mV in women in leads V2–V3 and/or ≥ 0.1 mV in other leads.
ST depression and T-wave changes.
New horizontal or down-sloping ST depression >0.05 mV in two contiguous leads; and/or T inversion ≥0.1 mVin two contiguous leads with prominent R-wave or R/S ratio ≥ 1

A study using MRI to diagnose myocardial infarction has shown that more emphasis on ST segment depression could greatly improve the yield of the ECG in the diagnosis of myocardial infarction (sensitivity increase from 50% to 84%).[4]

Myocardial infarction diagnosis in left or right bundle branch block can be difficult, but it is explained in these seperate chapters:

MI diagnosis in left bundle branch block or paced rhytm
MI Diagnosis in RBBB

ECG Manifestations of Acute Myocardial Ischaemia (in Absence of LVH and LBBB)are [3]:

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مشاركةبواسطة دكتور كمال سيد » الأحد ديسمبر 02, 2018 10:57 pm



First, the standard 12-lead ECG is a 10-second strip. The bottom one or two lines will be a full “rhythm strip” of a specific lead, spanning the whole 10 seconds of the ECG. Other leads will span only about 2.5 seconds. Each ECG is divided by large boxes and small boxes to help measure times and distances.

The ECG paper speed is ordinarily 25 mm/sec. As a result, each 1 mm (small) horizontal box corresponds to 0.04 second (40 ms), with heavier lines forming larger boxes that include five small boxes and hence represent 0.20 sec (200 ms) intervals.
Two large blocks equal 1 millivolt (mV). Each small block equals 0.1 mV. Within the large blocks are 5 small blocks, each representing 0.04 seconds.

The Normal P wave :
The P wave morphology can reveal right or left atrial hypertrophy or atrial arrhythmias and is best determined in leads II and V1 during sinus rhythm.
Characteristics of a normal p wave : # The maximal height of the P wave is 2.5 mm in leads II and / or III.
The p wave is # positive in II and AVF, and biphasic in V1
The # p wave duration is shorter than 0.12 seconds

i.e less than 3 small squares
The @ P wave morphology can reveal right or left atrial hypertrophy or atrial arrhythmias and is best determined in leads II and V1 during sinus rhythm.

An example of normal sinus rhythm.

The Abnormal P wave

Elevation or depression of the# PTa segment (the part between the p wave and the beginning of the QRS complex) can result from atrial infarction or pericarditis.

If the p-wave is enlarged, the atria are enlarged
if # P wave is more than 2.5 small squares (0.1 sec) i.e peaked it indicates Rt atrial enlargement
if # P wave is broad or nocthed i.e width more than 2.5 small squares it indicates Lt atrial enlargement
If the P wave is inverted, it is most likely an ectopic atrial rhythm not originating from the sinus node.

The first measurement is known as the "P-R interval" and is measured from the beginning of the upslope of the P wave to the beginning of the QRS wave. This measurement should be 0.12-0.20 seconds, or 3-5 small squares in duration.
The PR interval may be prolonged when conduction of the electrical wave through the AV node is slow.

QRS Morphology

The basic questions in judging QRS morphology are:

Are there any pathological Q waves as a sign of previous myocardial infarction?
Are there signs of left or right ventricular hypertrophy?
Does the QRS complex show microvoltage (roughly QRS < 5mm)?
Is the conduction normal or prolonged (QRS-interval > 0,12s)?
Is the R wave propagation normal? Normally R waves become larger from V1-V5. At V5 it should be maximal. If the R wave in V2 is larger than in V3, this could be a sign of a (previous) posterior myocardial infarction. Other causes are noted in the chapter Clockwise and Counterclockwise rotation.

If all these items are normal you can go on to the next step: ST morphology.

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مشاركةبواسطة دكتور كمال سيد » الأحد ديسمبر 02, 2018 10:59 pm


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مشاركةبواسطة دكتور كمال سيد » الاثنين ديسمبر 03, 2018 8:41 pm


The term "heart rate" normally refers to the rate of ventricular contractions. However, because there are circumstances in which the atrial and ventricular rates differ (e.g., second and third degree AV block), it is important to be able to determine both atrial and ventricular rates. This is easily done by examining an ECG rhythm strip, which is usually taken from a single lead (e.g., Lead II).
In the example below, there are four numbered R waves, each of which is preceded by a P wave. Therefore, the
atrial and ventricular rates will be the same because there is a one-to-one correspondence.
Atrial rate can be determined by measuring the time intervals between P waves (P-P intervals). Ventricular rate can be determined by measuring the time intervals between the QRS complexes, which is done by looking at the R-R intervals.
Remember, if the heart is in sinus rhythm and there is a one-to-one correspondence between P waves and QRS completes, then the atrial rate will be the same as ventricular rate.

Abnormal Rhythms - Definitions

General Terms:

Normal sinus rhythm - heart rhythm controlled by sinus node at a rate of 60-100 beats/min; each P wave followed by QRS and each QRS preceded by a P wave.

Bradycardia - a heart rate that is lower than normal.

Tachycardia - a heart rate that is higher than normal.

Paroxysmal - an arrhythmia that suddenly begins and ends.

Specific Arrhythmias:

Sinus bradycardia - low sinus rate <60 beats/min.

Sinus tachycardia - high sinus rate of 100-180 beats/min as occurs during exercise or other conditions that lead to increased SA nodal firing rate.

Sick sinus syndrome - a disturbance of SA nodal function that results in a markedly variable rhythm (cycles of bradycardia and tachycardia).
Atrial tachycardia - a series of 3 or more consecutive atrial premature beats occurring at a frequency >100/min; usually due to abnormal focus within the atria and paroxysmal in nature, therefore appearance of P wave is altered in different ECG leads. This type of rhythm includes paroxysmal atrial tachycardia (PAT).

Atrial flutter - sinus rate of 250-350 beats/min.

Atrial fibrillation - uncoordinated atrial depolarizations.

Junctional escape rhythm - SA node suppression can result in AV node-generated rhythm of 40-60 beats/min (not preceded by P wave).
AV nodal blocks - a conduction block within the AV node (or occasionally in the bundle of His) that impairs impulse conduction from the atria to the ventricles.

First-degree AV nodal block -
the conduction velocity is slowed so that the PR interval is increased to greater than 0.20 seconds. In the tracing below, the PR interval is 0.24 sec (6 small squares instead of 3 - 5 small squares). Rate is not altered by the presence of the prolonged PR interval because it is still being controlled by the SA node. This type of block can be caused by @ enhanced vagal tone,@ digitalis,@ beta-blockers,@ calcium channel blockers, or@ ischemic damage to the nodal tissue.
in 1st deg AV block the P R interval is regularly (fixed) prolonged i.e <one large box (5 small squares i.e < 0.2 sec)

Second-degree AV nodal block -
the conduction velocity is slowed to the point where some impulses from the atria cannot pass through the AV node. This results in P waves that are not followed by QRS complexes.
There are two subtypes of second-degree AV blocks : Mobitz Type I and Mobitz Type II.

In Mobitz I (also called "Wenkebach"), the PR interval gradually increases over several beats until it is sufficiently prolonged (that is, AV conduction is sufficiently impaired) that the impulse fails to pass into the ventricles (i.e., a QRS will not follow the P wave).
In the first tracing below, the PR interval for the first beat is 0.16 sec and increases to 0.24 sec by the third beat. In the fourth beat, the P wave is not followed by a QRS; therefore, the ventricular beat is dropped.
The fifth beat starts this cycle over again.
Mobitz II occurs is when the P-R interval is fixed in duration, but some P waves are not followed by a QRS as illustrated in the second tracing below. This is an example of a 2:1 rhythm because there are 2 P waves for each QRS. Other ratios (e.g., 3:2) may occur. In either type of second-degree block, the ventricular rate will be less than the normal sinus rhythm (indicated by green arrows in figures).
Also note that the QRS complexes appear normal in shape and duration because they are still being triggered by impulses from the atria passing through the AV node.

Third-degree AV nodal block -

conduction through the AV node is completely blocked so that no impulses are able to be transmitted from the atria to the ventricles. QRS complexes still occur (escape rhythm), but they originate from within the AV node, bundle of His, or other ventricular regions.
Therefore, QRS complexes will not be preceded by P waves. Furthermore, there will be complete asynchrony between the P wave and QRS complexes. Atrial rate and rhythm may be completely normal (green arrows indicate P waves, although in the last beat it is obscured by the QRS ), but ventricular rate will be greatly reduced the extent of which depends on the location of the site generating the ventricular rhythm. Ventricular rates typically range from 30 to 40 beats/min if the ventricular foci generating ventricular rhythm is below the bundle of His. .
The following figure shows QRS complexes having an abnormal shape and prolonged duration because ventricular depolarization is not following normal conduction pathways

Supraventricular tachycardia (SVT) -
usually caused by reentry currents within the atria or between ventricles and atria producing high heart rates of 140-250; the QRS complex is usually normal width, unless there are also intraventricular conduction blocks (e.g., bundle branch block).
Ventricular premature beats (VPBs) -
caused by ectopic ventricular foci; characterized by widened QRS; often referred to as a premature ventricular complex, or PVC.
Ventricular tachycardia (VT) -
high ventricular rate caused by aberrant ventricular automaticity (ventricular foci) or by intraventricular reentry; can be sustained or non-sustained (paroxysmal); usually characterized by widened QRS (>0.14 sec); rates of 100 to 280 beats/min; life-threatening.
Ventricular flutter -
very rapid ventricular depolarizations >250/min; sine wave appearance; leads to fibrillation.

Ventricular fibrillation -
uncoordinated ventricular depolarizations; leads to death if not quickly converted to a normal rhythm or at least a rhythm compatible with life.

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مشاركةبواسطة دكتور كمال سيد » الاثنين ديسمبر 03, 2018 10:56 pm


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مشاركةبواسطة دكتور كمال سيد » الثلاثاء ديسمبر 04, 2018 10:35 pm

Ischemia, Injury & Infarction

12-Lead Ischemia - Views

Inferior wall of left ventricle@
Right Coronary Artery@
Marginal branch@

V1 & V2
Left Coronary@
Septal branch@

V3 & V4
Left Coronary@
Anterior Descending and Diagonal arteries@

I, aVL, V5 & V6
Left Coronary@
Circumflex & Obtuse marginal@

Labeled Views

12-Lead Ischemia - Ischemia, Injury Infarction
Think of the process of ischemia, injury and infarction as a worsening continuum.
If immediate, aggressive and effective care is not provided, ischemia will worsen (or progress) to injury and ultimately infarction (tissue death)
Ischemia, injury and infarction each impact the cardiac complex in unique ways.

12-Lead Analysis requires we follow these steps of analysis.
ST segment for presence of deviation@
T wave morphology changes@
Q wave morphology changes@

The changes we have been referring to must occur in anatomically contiguous leads. This refers to 2 or more leads “looking” at (viewing) the same part of the heart or numerically consecutive chest leads

Examples Include:

II, III, aVF (2 of the 3 leads must show changes. It does not have to be all three)@
I, aVL can show changes and not effect V5 and V6 to still be clinically significant!@
Numerically consecutive chest leads@

We always recall that V1 is next to V2, but do not forget that V2 is also contiguous with (next to) V3…if V2 & V3 are showing changes, this is clinically significant too. See the next slide for an illustration.

12-Lead Ischemia - Ischemia
Ischemia causes a # delay in repolarization and causes specific changes to either or both the ST segment and T wave.
Ischemia is evidenced when# ST segment depression of 1 mm or more or T wave inversion is seen in two or more anatomically contiguous leads
S T segment depression
It is often a sign of myocardial ischemia, of which coronary insufficiency is a major cause. Other ischemic heart diseases causing ST depression include: Subendocardial ischemia or even infarction. Subendocardial means non full thickness ischemia. In contrast, ST elevation is transmural (or full thickness) ischemia.

T Wave Inversion
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

12Lead Ischemia - Injury
Ischemia delayed for even a few minutes can progress (worsen) to myocardial injury@.
Injury is evidenced when@ ST segment elevation of 1 mm or more is seen in two or more anatomically contiguous leads
injury Examples.
Note: ST Elevation in both examples
to me 2nd example?? needs explain

12-12Lead Ischemia - Infarction

A normal (physiologic) “Q” wave measures less than 0.04 second@
Depth measures less than 1/3 height of R wave@


Once an MI is completed, the ST segment will # return to the baseline and the # T wave will return to its normal orientation,# but “Q” waves are often the one remaining change to a cardiac complex as evidence that tissue necrosis or tissue death (infarction) has occurred.

the term used that refers to @ direct changes seen on a 12-Lead ECG is Indicative changes
the term used that refers to @ reverse or indirect changes seen on a 12-Lead ECG because the ECG is looking at that surface of the heart indirectly is Reciprocal changes
12-12Lead Ischemia - AMI Location Practice 1 **********************

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مشاركةبواسطة دكتور كمال سيد » الاثنين ديسمبر 31, 2018 11:26 pm


Which of the following best describes first-degree heart block?

A A fixed prolonged PR interval with irregularly dropped QRS complexes
B A fixed prolonged PR interval (>200 ms)
C A slowly increasing PR interval with regularly dropped QRS complexes

ans = B
First-degree heart block involves a fixed prolonged PR interval (>200 ms). In first-degree AV block, the impulse that conducts from atria to the ventricles through the atrioventricular node (AV node) is delayed and travels slower than normal.

Common causes include:

AV nodal disease
Enhanced vagal tone (for example in athletes)
Acute myocardial infarction(especially acute inferior MI)
Electrolyte disturbances
The drugs that most commonly cause first-degree heart block are those that increase the refractory time of the AV node:

Calcium channel blockers
Cardiac glycosides
Cholinesterase inhibitors



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