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Review ECG (2nd year)

body fluids are good conductors>fluctuations in potential that represent the algebraic sum of the action potentials of myocardial fibers can be recorded extracellularly>electrocardiogram ECG recording: bipolar standard limb leads I, II, III

unipolar augmented extremity leads avL avR avF unipolar precordial leads v123456 note:
upward deflection is written when the active electrode becomes positive relative to the indifferent electrode, and a downward deflection is written when the active electrode becomes negative. The P wave is produced by atrial depolarization, the QRS complex by ventricular depolarization, T wave by ventricular repolarization. (ventricular hyperpolarization) The U wave is an inconstant finding, believed to be due to slow repolarization of the papillary muscles. The intervals between the various waves of the ECG and the events in the heart that occur during these intervals are shown in

Normal Durations Intervals PR intervala QRS duration QT interval ST interval (QT minus QRS) Average Range 0.18b 0.08 0.40 0.32 Events in the Heart during Interval 0.120.20 Atrial depolarization and conduction through AV node to 0.10 to 0.43 ... Ventricular depolarization and atrial repolarization Ventricular depolarization plus ventricular repolarization Ventricular repolarization (during T wave)

PR interval: Time needed to transmit impuls from SA node to AV node2 . Normal 0.12 0.22 sec Short PR interval= preeksitasion syndrome Prolonged PR interval= think about A-V block. QRS complex: Describe activation of left and right ventrikel2. Duration 0.05 0.10 sec

Measure usually in limbs lead amplitudo less than 10 mm in all leads = low voltage Abnormal complex QRS seen in conduction defect Q wave: Normal Q wave seen in lead I, aVL, and V5-6 describe activation of septum left to right Q wave in V1-2 is abnormal Pathologic Q : duration > 0,04 sec and/ or height > dari 1/3 complex QRS ST segment: Usually isoelectric, elevation < 1 mm in extremity still normal Depression < 0.5 mm T wave : Describe repolarization of ventricle Normal positive in leads I,II and V3-V6 Normal negative in lead III QT duration: D e s c r i b e t o t a l s y s t o l i c t i m e Normal QT correction 0.44 + 0.02 sec

Normal ecg the position of the heart: The atria are located posteriorly in the chest. The ventricles form the base and anterior surface of the heart, and the right ventricle is anterolateral to the left. So, aVR waves are therefore all negative (downward) deflections aVL and aVF look at the ventricles, and the deflections are therefore predominantly positive or biphasic. Depolarization initiated in the SA node spreads radially through the atria, then converges on the AV node. Atrial depolarization is complete in about 0.1 s. Because conduction in the AV node is

slow, a delay of about 0.1 s (AV nodal delay) occurs before excitation spreads to the ventricles. It is interesting to note here that when there is a lack of contribution of INa in the depolarization (phase 0) of the action potential, a marked loss of conduction is observed. In humans, depolarization of the ventricular muscle starts at the left side of the interventricular septum and moves first to the right across the mid portion of the septum. The wave of depolarization then spreads down the septum to the apex of the heart. It returns along the ventricular walls to the AV groove, proceeding from the endocardial to the epicardial surface. The last parts of the heart to be depolarized are the posterobasal portion of the left ventricle, the pulmonary conus, and the uppermost portion of the septum. ventricular depolarization first moves across the midportion of the septum from left to right toward the exploring electrode so, NO Q wave in V1 and V2, and the initial portion of the QRS complex is a SMALL upward deflection. The wave of excitation then moves down the septum and into the left ventricle away from the electrode, producing a LARGE S wave. The wave moves back along the ventricular wall toward the electrode, producing the return to the isoelectric line. Conversely, in the left ventricular leads (V4V6) there may be an initial small Q wave (left to right septal depolarization), and there is a large R wave (septal and left ventricular depolarization) followed in V4 and V5 by a moderate S wave (late depolarization of the ventricular walls moving back toward the AV junction).

ECG of Acute Coronary Syndrome&MI


pathogenesis

Table 303 Summary of the Three Major Abnormalities of Membrane Polarization Associated with Acute Myocardial Infarction. Defect in Infarcted Cells Rapid repolarization Delayed depolarization Current Flow Resultant ECG Change in Leads Over Infarct Out of infarct ST segment elevation TQ segment depression (manifested as ST segment elevation) Out of infarct ST segment elevation

Decreased resting membrane potential Into infarct

The first changeabnormally rapid repolarization after discharge of the infarcted muscle fibers as a result of accelerated opening of K+ channelsdevelops seconds after occlusion of a coronary artery in experimental animals. It lasts only a few minutes, but before it is over the resting membrane potential of the infarcted fibers declines because of the loss of intracellular K+. Starting about 30 min later, the infarcted fibers also begin to depolarize more slowly than the surrounding normal fibers. Because of the rapid repolarization in the infarct, the membrane potential of the area is greater than it is in the normal area during the latter part of repolarization, making the normal region negative relative to the infarct. Extracellularly, current therefore flows out of the infarct into the normal area (since, by convention, current flow is from positive to negative). This current flows toward electrodes over the injured area, causing increased positivity between the S and T waves of the ECG. Similarly, the delayed

depolarization of the infarcted cells causes the infarcted area to be positive relative to the healthy tissue during the early part of repolarization, and the result is also ST segment elevation. The remaining changethe decline in resting membrane potential during diastolecauses a current flow into the infarct during ventricular diastole. The result of this current flow is a depression of the TQ segment of the ECG. However, the electronic arrangement in electrocardiographic recorders is such that a TQ segment depression is recorded as an ST segment elevation. Thus, the hallmark of acute myocardial infarction is elevation of the ST segments in the leads overlying the area of infarction. Leads on the opposite side of the heart show ST segment depression.

Diagrammatic illustration of serial electrocardiographic patterns in anterior infarction. A) Normal tracing. B) Very early pattern (hours after infarction): ST segment elevation in I, aVL, and V36; reciprocal ST depression in II, III, and aVF. C) Later pattern (many hours to a few days): Q waves have appeared in I, aVL, and V56. QS complexes are present in V34. This indicates that the major transmural infarction is underlying the area recorded by V34; ST segment changes persist but are of lesser degree, and the T waves are beginning to invert in the leads in which the ST segments are elevated. D) Late established pattern (many days to weeks): The Q waves and QS complexes persist, the ST segments are isoelectric, and the T waves are symmetric and deeply inverted in leads that had ST elevation and tall in leads that had ST depression. This pattern may persist for the remainder of the patient's life. E) Very late pattern: This may occur many months to years after the infarction. The abnormal Q waves and QS complexes persist. The T waves have gradually returned to normal.

After some days or weeks, the ST segment abnormalities subside. The dead tisue>silent. The infarcted area is therefore negative relative to the normal myocardium during systole, and it fails to contribute its share of positivity to the electrocardiographic complexes.

Common changes include the appearance of a Q wave in some of the leads in which it was not previously present and an increase in the size of the normal Q wave in some of the other leads, (although so-called non-Q-wave infarcts are also seen). Another finding in infarction of the anterior left ventricle is "failure of progression of the R wave"; that is, the R wave fails to become successively larger in the precordial leads as the electrode is moved from right to left over the left ventricle. If the septum is infarcted, the conduction system may be damaged, causing bundle branch block or other forms of heart block. Myocardial infarctions are often complicated by serious ventricular arrhythmias, with the threat of ventricular fibrillation and death. In experimental animals, and presumably in humans, ventricular arrhythmias occur during three periods. During the first 30 min of an infarction, arrhythmias due to reentry are common. There follows a period relatively free from arrhythmias, but, starting 12 h after infarction, arrhythmias occur as a result of increased automaticity. Arrhythmias occurring 3 d to several weeks after infarction are once again usually due to reentry. It is worth noting in this regard that infarcts that damage the epicardial portions of the myocardium interrupt sympathetic nerve fibers, producing denervation super-sensitivity to catecholamines in the area beyond the infarct. Alternatively, endocardial lesions can selectively interrupt vagal fibers, leaving the actions of sympathetic fibers unopposed.???? - review anatomy of coronary a.

LCA>

LAD>

ant. LV Ant.(med) RV Post(lower) RV

LC>

lat. LV Post(lower/apex) LV

RCA> supply other sites Note SA node has a dual blood supply from branches of RCA and LC AV node receive its major supply from LAD Determine the stage of infarction (norm>subendocardial injury>transmural injury>necrosis>necrosiswithfibrosis>fibrosis)

4 form

1. subendocardium Subendocardium close to ecg lead >> more negative >> St segment depression

2. transmural Injury site will be early repolarization so positive normal site negative >> st segment elevation

3. st elevation < non st elevation myocardial infarction , non transmural or subendocardial infarction> Normal direction of repolarization but slow repolarization >> long qt interval and /or high t wave 4. st elevation < st elevation myocardial infarction, transmural infarction> q wave Hyperacute t wave>> st segment elevation>>abnormal Q wave >> t wave inversion Ischemic site has slow repolarization >> inverse repolarization >> inverse t wave and wide Qt interval

Myocardial infarction<myocardial necrosis> >> abnormal or pathological Q wave >>wide and deep Q wave

Q wave >=0.02 second >>v2-v3 Q wave >=0.03 s and deep>=0.1mv >> lead I II avl avf v4-v6 R wave >=0.04s >>v1-v2 Q wave that have r wave follow>> have normal site Q wave that have only qs wave >> all necrosis St segment elevate 1. Acute myocardial infarction 2. Prinzmetal s angina<variant angina> 3. Ventricular wall motion abnormality and ventricular aneurysm

St segment depression 1. Subendocardial injury 2. Myocardial infarction with st elevation 3. Myocardial infarction with st elevation

Deep t inversion 1. Evoving <subacute,chronic>stage of Q wave infarction 2. Myocardial infarction no st elevation 3. Non infarction ischemia

Determine site of infarction: (forcus on LV infarction) Ant. Wall Inf. Wall Lat. Wall Post. Wall leads that reflect the infarct: v2-6 leads that reflect the infarct: avF, II, III leads that reflect the infarct: avL, I, V6 leads that reflect the infarct: v1-2 , esophageal leads

Note RV infarction associate with inf. Wall of LV infarction OR post. Wall of LV infarction due to RCA occlusion. Dx by the presence of ST elevation in RIGHT precordial leads: v1, v3R, v4R Type of ant wall infarction: Anteroseptal infarction Anteroapical infarction Anterolateral infarction Apical infarction Summary: early stage: leads that reflect the infarct: v1-3 leads that reflect the infarct: v3-5 leads that reflect the infarct: v4-7, avL, I leads that reflect the infarct: v2-4, II, III, avF ST elevation in more than one lead from v3-6 (area of infarction) persist up to 2 wks ST depression in leads at opposite wall Late stage: T wave (deep , symmetric) inversion from v3-6 (area of infarction)

Note QS complexes or abnormal Q waves (on the initial 0.04s of ventricular depo + Q:R ratio>25%) may appear very early or late. Gradually disappear after several mo, sometimes, persist for year note! lead III commonly record abnormal Q waves Lead aVL (Px with vertical heart position) may record abnormal Q waves Lead v2(other conditions that mimic MI) may record QR or QRS complex both Inf wall and ant wall infarction can be found at the same time but pattern of inf wall infarction may be a result of backward replacement of the apex(ant wall overlie the left diaphragm)> DDx by nuclear wall motion or thallium test