notes on ECG diagnosis (part-2)

[dr_hani]

*Atrial fibrillation :

The activation in the atria may also be fully irregular and chaotic, producing irregular fluctuations in the baseline. A consequence is that the ventricular rate is rapid and irregular, though the QRS contour is usually normal. Atrial fibrillation occurs as a consequence of rheumatic disease, atherosclerotic disease, hyperthyroidism, and pericarditis. (It may also occur in healthy subjects as a result of strong sympathetic activation.)

http://butler.cc.tut.fi/~malmivuo/bem/bembook/19/fi/1902ge.gif
Baseline irregular, ventricular response irregular

*Junctional rhythm :

If the heart rate is slow (40-55/min), the QRS-complex is normal, the P-waves are possibly not seen, then the origin of the cardiac rhythm is in the AV node. Because the origin is in the juction between atria and ventricles, this is called junctional rhythm. Therefore, the activation of the atria occurs retrograde (i.e., in the opposite direction). Depending on whether the AV-nodal impulse reaches the atria before, simultaneously, or after the ventricles, an opposite polarity P-wave will be produced before, during, or after the QRS-complex, respectively. In the second case the P-wave will be superimposed on the QRS-complex and will not be seen.

http://butler.cc.tut.fi/~malmivuo/bem/bembook/19/fi/1902he.gif
P-wave is often inverted, may be under or after QRS complex
Heart rate is slow

*Premature ventricular contraction :

A premature ventricular contraction is one that occurs abnormally early. If its origin is in the atrium or in the AV node, it has a supraventricular origin. The complex produced by this supraventricular arrhythmia lasts less than 0.1 s. If the origin is in the ventricular muscle, the QRS-complex has a very abnormal form and lasts longer than 0.1 s. Usually the P-wave is not associated with it.

http://butler.cc.tut.fi/~malmivuo/bem/bembook/19/fi/1903ae.gif
Time interval between normal R peaks
is a multiple of R-R intervals

*Ventricular tachycardia :

A rhythm of ventricular origin may also be a consequence of a slower conduction in ischemic ventricular muscle that leads to circular activation (re-entry). The result is activation of the ventricular muscle at a high rate (over 120/min), causing rapid, bizarre, and wide QRS-complexes; the arrythmia is called ventricular tachycardia. As noted, ventricular tachycardia is often a consequence of ischemia and myocardial infarction.

http://butler.cc.tut.fi/~malmivuo/bem/bembook/19/fi/1903be.gif
Wide ventricular complexes
Rate> 120/min

*Ventricular fibrillation :

When ventricular depolarization occurs chaotically, the situation is called ventricular fibrillation. This is reflected in the ECG, which demonstrates coarse irregular undulations without QRS-complexes. The cause of fibrillation is the establishment of multiple re-entry loops usually involving diseased heart muscle. In this arrhythmia the contraction of the ventricular muscle is also irregular and is ineffective at pumping blood. The lack of blood circulation leads to almost immediate loss of consciousness and death within minutes. The ventricular fibrillation may be stopped with an external defibrillator pulse and appropriate medication.



http://butler.cc.tut.fi/~malmivuo/bem/bembook/19/fi/1903ce.gif
Rapid, wide, irregular ventricular complexes

*Pacer rhythm :

A ventricular rhythm originating from a cardiac pacemaker is associated with wide QRS-complexes because the pacing electrode is (usually) located in the right ventricle and activation does not involve the conduction system. In pacer rhythm the ventricular contraction is usually preceded by a clearly visible pacer impulse spike. The pacer rhythm is usually set to 72/min..

http://butler.cc.tut.fi/~malmivuo/bem/bembook/19/fi/1903de.gif
Rapid, wide, irregular ventricular complexes

*First-degree atrioventricular block :

When the P-wave always precedes the QRS-complex but the PR-interval is prolonged over 0.2 s, first-degree atrioventricular block is diagnosed.

http://butler.cc.tut.fi/~malmivuo/bem/bembook/19/fi/1904ae.gif
Rapid, wide, irregular ventricular complexes

*Second-degree atrioventricular block :

If the PQ-interval is longer than normal and the QRS-complex sometimes does not follow the P-wave, the atrioventricular block is of second-degree. If the PR-interval progressively lengthens, leading finally to the dropout of a QRS-complex, the second degree block is called a Wenkebach phenomenon.

http://butler.cc.tut.fi/~malmivuo/bem/bembook/19/fi/1904be.gif
Intermittently skipped ventricular beat

*Third-degree atrioventricular block :

Complete lack of synchronism between the P-wave and the QRS-complex is diagnosed as third-degree (or total) atrioventricular block. The conduction system defect in third degree AV-block may arise at different locations such as:
-Over the AV-node
-In the bundle of His
-Bilaterally in the upper part of both bundle branches
-Trifascicularly, located still lower, so that it exists in the right bundle-branch and in the two fascicles of the left bundle-branch.

http://butler.cc.tut.fi/~malmivuo/bem/bembook/19/fi/1904ce.gif
P-P interval normal and constant,
QRS complexes normal, rate constant, 20 - 55 /min

[dr_hani]

*Right bundle-branch block :

If the right bundle-branch is defective so that the electrical impulse cannot travel through it to the right ventricle, activation reaches the right ventricle by proceeding from the left ventricle. It then travels through the septal and right ventricular muscle mass. This progress is, of course, slower than that through the conduction system and leads to a QRS-complex wider than 0.1 s. Usually the duration criterion for the QRS-complex in right bundle-branch block (RBBB) as well as for the left brundle- branch block (LBBB) is >0.12 s.
With normal activation the electrical forces of the right ventricle are partially concealed by the larger sources arising from the activation of the left ventricle. In right bundle-branch block (RBBB), activation of the right ventricle is so much delayed, that it can be seen following the activation of the left ventricle. (Activation of the left ventricle takes place normally.)
RBBB causes an abnormal terminal QRS-vector that is directed to the right ventricle (i.e., rightward and anterior). This is seen in the ECG as a broad terminal S-wave in lead I. Another typical manifestation is seen in lead V1 as a double R-wave. This is named an RSR'-complex.



http://butler.cc.tut.fi/~malmivuo/bem/bembook/19/fi/1905a.gif
QRS duration greater than 0.12 s
Wide S wave in leads I, V5 and V6

*Left bundle-branch block :

The situation in left bundle-branch block (LBBB) is similar, but activation proceeds in a direction opposite to RBBB. Again the duration criterion for complete block is 0.12 s or more for the QRS-complex. Because the activation wavefront travels in more or less the normal direction in LBBB, the signals' polarities are generally normal. However, because of the abnormal sites of initiation of the left ventricular activation front and the presence of normal right ventricular activation the outcome is complex and the electric heart vector makes a slower and larger loop to the left and is seen as a broad and tall R-wave, usually in leads I, aVL, V5, or V6.

http://butler.cc.tut.fi/~malmivuo/bem/bembook/19/fi/1905b.gif
QRS duration greater than 0.12 s
Wide S wave in leads V1 and V2, wide R wave in V5 and V6

*Right atrial hypertrophy :

Right atrial hypertrophy is a consequence of right atrial overload. This may be a result of tricuspid valve disease (stenosis or insufficiency), pulmonary valve disease, or pulmonary hypertension (increased pulmonary blood pressure). The latter is most commonly a consequence of chronic obstructive pulmonary disease or pulmonary emboli.
In right atrial hypertrophy the electrical force due to the enlargened right atrium is larger. This electrical force is oriented mainly in the direction of lead II but also in leads aVF and III. In all of these leads an unusually large (i.e., 0.25 mV) P-wave is seen.

http://butler.cc.tut.fi/~malmivuo/bem/bembook/19/fi/1906a.gif
Tall, peaked P wave in leads I and II

*Left atrial hypertrophy :

Left atrial hypertrophy is a consequence of left atrial overload. This may be a result of mitral valve disease (stenosis or insufficiency), aortic valve disease, or hypertension in the systemic circulation.
In left atrial hypertrophy the electrical impulse due to the enlargened left atrium is strengthened. This electrical impulse is directed mainly along lead I or opposite to the direction of lead V1. Because the atrial activation starts from the right atrium, the aforementioned left atrial activation is seen later, and therefore, the P-wave includes two phases. In lead I these phases have the same polarities and in lead V1 the opposite polarities. This typical P-wave form is called the mitral P-wave. The specific diagnostic criterion for left atrial hypertrophy is the terminal portion of the P-wave in V1, having a duration 0.04 s and negative amplitude 0.1 mV..

http://butler.cc.tut.fi/~malmivuo/bem/bembook/19/fi/1906b.gif
Wide, notched P wave in lead II
Diphasic P wave in V1

*Right ventricular hypertrophy :

Right ventricular hypertrophy is a consequence of right ventricular overload. This is caused by pulmonary valve stenosis, tricuspid insufficiency, or pulmonary hypertension (see above). Also many congenital cardiac abnormalities, such as a ventricular septal defect, may cause right ventricular overload.
Right ventricular hypertrophy increases the ventricular electrical forces directed to the right ventricle - that is, to the right and front. This is seen in lead V1 as a tall R-wave of 0.7 mV.

http://butler.cc.tut.fi/~malmivuo/bem/bembook/19/fi/1907a.gif
Large R wave in leads V1 and V3
Large S wave in leads V5 and V6

*Left ventricular hypertrophy :

Left ventricular hypertrophy is a consequence of left ventricular overload. It arises from mitral valve disease, aortic valve disease, or systemic hypertension. Left ventricular hypertrophy may also be a consequence of obstructive hypertrophic cardiomyopathy, which is a sickness of the cardiac muscle cells.
Left ventricular hypertrophy increases the ventricular electric forces directed to the left ventricle - that is, to the left and posteriorly. Evidence of this is seen in lead I as a tall R-wave and in lead III as a tall S-wave (2.5 mV). Also a tall S-wave is seen in precordial leads V1 and V2 and a tall R-wave in leads V5 and V6, (3.5 mV).

http://butler.cc.tut.fi/~malmivuo/bem/bembook/19/fi/1907b.gif
Large S wave in leads V1 and V2
Large R wave in leads V5 and V6

[Cardiac Arrest]

great :)


i really like this :)


i will put this topic in my favorite & read it after i finish my exams


:)



thanx



:)

[Dr.wrood2004]

its so geat ...Dr.hani ..
keep going ..
حفظك الله ..

[reda0007]

Well done dr hani ,
the wxplanation is very clear
and i loved the figures also
thanx again
waiting for nor :12:

[dr_hani]

Thx dr.reda0007 , Dr.wrood and dr.cardiac arrest for wt u said

Hope for all the best