Essentials of Internal Medicine Ardhendu Sinha Ray, Abhisekh Sinha Ray
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1CARDIOVASCULAR SYSTEM
  • Electrocardiogram
  • Rheumatic Fever
  • Infective Endocarditis
  • Valvular Heart Disease
  • Heart Failure
  • Hypertension
  • Congenital Heart Diseases
  • Cardiomyopathy
  • Tachyarrhythmias
  • Ischemic Heart Diseases2

ElectrocardiogramChapter 1

 
INTRODUCTION
An electrocardiogram is a graphical record of the change in membrane potential generated during cardiac muscle depolarization and repolarization.
The ECG records the depolarization (stimulation) and repolarization (recovery) potentials generated by atrial and ventricular myocardium and spread all over body.
This electric signals are detected by means of electrode (called lead) attached to the extremities and chest wall and are amplified and recorded on a (millimeter) graph paper.
The graph paper is divided into 1 mm2 grid-like boxes. Since the universal ECG paper speed is 25 mm/sec, the smallest 1 mm horizontal division corresponds to 0.04 second with heavier line at interval of 5 small square which is equal to 0.2 second. Vertically the ECG graph measure the amplitude of a specific wave 1 mV = 10 mm with standard calibration.
The conventional ECG is recorded by 12 lead of which 6 are extremity limb lead and 6 are precordial or chest lead.
Out of 6 limb leads. Three are bipolar lead [lead-I, lead-II, lead-III] and three are unipolar (aVR, aVL, aVF).
Bipolar leads are
  • Lead-I → Left arm potential – Right arm potential
  • Lead-II → Left leg potential – Right arm potential
  • Lead-III → Left leg potential – Left arm potential.
Unipolar limb leads are—aVR, aVL and aVF.
In these unipolar leads potential of right arm, left arm and left leg are recorded against ‘zero’ potential which is made within machine by joining the lead of all four limb and passing it through in resistance.
Standard six precordial lead are V1 – V6. These are unipolar lead and one electrodes is placed on the following position and the second electrode is zero potential.
  • V1 on 4th intercostal space just right of sternum.
  • V2 on 4th intercostal space just left of sternum.
  • V3 on midway between V2–V4.
  • V4 on midclavicular line on 5th space.
  • V5 on anterior axillary line on the same plane of V4.
  • V6 on midaxillary line on the same plane of V4 and V5.
  • V7 on posterior axillary line on the same plane of V4V5V6.
  • V8on posterior scapular line on the same plane of V4V5V6V7.
In case of dextrocardia precordial leads are placed on the corresponding position on the right side of the chest and are called V2R to V6R respectively.
 
ESOPHAGEAL LEADS
Apart from these leads there is special lead called esophageal lead where the recording electrode is placed in esophagus 27 cm down from incisor teeth for recording of the potential from the posterior aspect of heart.
Standard ECG has the following wave and P, Q, R, S, T and U wave, and the following interval PR, QRS and QT interval (Figs 1.1 and 1.2).
During examination of ECG we have to look for following point. (1) Heart rate, (2) rhythm, (3) electrical axis of QRS complex, (4) P-wave, (5) P-R interval, (6) Q-wave, (7) QRS complex, (8) ST-segment, (9) Q-T interval, (10) T-wave and (11) U-wave.
 
HEART RATE
It can easily be calculated from an ECG by counting the number of small square in between two consecutive R-wave. And dividing 1500 by the number of small square in between two R-wave we get the heart rate. 1500 comes from the fact that the paper speed of all ECG machine is 25 mm/sec. So in one minute 1500 small square (25 × 60 = 1500) comes out from the machine.
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Fig. 1.1: Normal ECG
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Fig. 1.2: Sinus bradycardia
 
RHYTHM
If the R-R interval is equal in the rhythm strip (lead-II) and the QRS complexes are preceded by ‘P’—then it is called “regular sinus rhythm”. The R-R interval sometime may vary slightly which is called sinus arrhythmia (which is the respiratory variation of heart rate).
 
AXIS OF QRS COMPLEX
The axis of an ECG means the direction of the mean electrical vector of QRS complex. It is determined from extremity lead. In Enthovean concept the heart is located at the center of a triangle formed by joining right arm, left arm and left leg (Fig. 1.3).
In unipolar limb lead the heart is located at the center like Figure 1.6. If we simplify Figure 1.4 like Figure 1.5 and if we superimpose Figure 1.6 over Figure 1.5 we get the hexaxial picture (Fig. 1.7) which is very clumsy. Out of these six axis, we take only two mutually perpendicular leads one is lead-I and the other is aVF (Fig. 1.8) for determination of QRS axis.
 
POSITIVITY OF THE LEADS
As the depolarization wave runs from SA node and move towards apex (downward and to the left) the left hand side of lead-I is considered positive and the lower half of aVF is considered positive and the upper half aVF is negative and right side of lead-I negative, then the simplified picture come out like Figure 1.8.
Degree of each lead and the extent of normal axis, left axis and right axis deviation is determined by an international convention Figure 1.9.
  • Left hand side of lead-I is 0°
  • Right hand side of lead-I is ± 180°
  • Lower half of aVF is + 90°
  • Upper half of aVF is − 90°
  • Normal axis − 30° to + 110° (Fig. 1.10)
  • Left axis − 30° to − 90° (Fig. 1.10)
  • Right axis + 110° to + 180° (Fig. 1.10)
  • Indeterminate axis from − 90°–180° (Fig. 1.10).
Now in a given ECG for determination of mean axis of QRS complex, we have to consider the mean deflection of QRS from the isoelectric line by summation of deflection of QRS complex in lead I and aVF.
For example (Fig. 1.11), suppose in lead-I the summation of deflection of QRS complex in positive and is equal to 6 small square and in lead aVF it is 5. Small square on the 5positive side then we have to give a mark 6 mm away from the center on lead-I and 5 mm away from the center on lead aVF on the positive side of the lead (Fig 1.11) and we have to draw perpendicular at that point on lead-I and aVF respectively. The meeting point of this two perpendiculars is in the left lower quadrant joined with center with a line. This line is the mean electrical axis of the QRS complex (Fig. 1.11).
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Fig. 1.3: Thin complex tachycardia
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Fig. 1.4: Bipolar limb lead
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Fig. 1.5: Simplified bipolar limb lead
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Fig. 1.6: Unipolar limb lead
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Fig. 1.7: Simplified bipolar limb lead superimposed on unipolar limb lead
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Fig. 1.8: Simplified diagram from hexaxial system
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Fig. 1.9: Degree of each lead is allotted by international convention
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Fig. 1.10: Hexaxial lead with allotted degree and axis deviation
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Fig. 1.11: Example of normal axis deviation
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Fig. 1.12: Determination of left axis deviation with the help of lead II'
If in the second example (Fig. 1.12) suppose the summation of deflection of QRS in aVF is negative we have to give point on the negative side of aVF lead and the summation deflection of QRS complex in lead-I is positive then the meeting point of the perpendicular on lead-I and aVF is in the left upper quadrant. Then the picture will be like Figure 1.12. Now in such condition whether actual left axis deviation have occured is to be determined by examining lead-II. As perpendicular on lead II at the center is −30°. If the summation of QRS in lead-II is positive then although the QRS axis has rotated upwards but it has not 7crossed above −30°, i.e. although the QRS axis has rotated leftward but it is within the limit of normal axis (−30°). If the summation of QRS deflection is negative in lead-II. The mean QRS vector has rotated upward and beyond −30° and left axis deviation has taken place.
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Fig. 1.13: Determination of right axis deviation
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Fig. 1.14: Example of indeterminate axis
Suppose the summation of QRS deflection in aVF is positive but in lead-I it is negative then the picture will be like Figure 1.13. Then the meeting point of the perpendiculars are in the lower right quadrant. In this condition whether there is true right axis deviation is present to be determined by compairing the height of R-wave in aVF and lead-III. If the complexes in aVF is taller than lead-III then the mean QRS axis is closer to +90° and it is within normal axis, but if the complex in lead-III is taller than aVF then it is considered that the electrical axis is closer to 120° so right axis deviation is present.
If in both lead-I and aVF the summation of QRS deflexion is negative then the meeting point of the perpendiculars would be like Figure 1.14 in the right upper quadrant. This type of axis deviation is called, indeterminate axis or north-west axis which is rarely seen in congenital heart disease where there is hypertrophy of the extreme superolateral wall of the both ventricle.
 
P-WAVE
It is due to depolarization of atria and in normal ECG P-wave is upright is lead-II negative in aVR and biphasic in V1. Ascending limb of P is due to right atrial depolarization and the descending limb of P is due to left atrial depolarization.
  • Abnormalities in P-wave
    • Absent P-wave—In atrial fibrillation, instead of P-wave there will be an uneven baseline with varying R-R interval (Fig. 1.15).
    • Tall peaked P-wave in lead-II—It is called “P-pulmonale”, where the height of P-wave is more than 2 mm and is due to right atrial hypertrophy (Fig. 1.16).
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      Fig.1.15: Atrial flutter with fibrillation
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      Fig. 1.16: P-pulmonale
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      Fig. 1.17: P-mitrale
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      Fig. 1.18: High junctional rhythm
    • Broad with notched P-wave in lead-II— It is called P-mitrale. P-wave is more than 2 mm broad seen in left atrial hypertrophy. The notch may or may not be present (seen in mitral stenosis) and usually there is deep negative P-wave in V1 (Fig. 1.17).
    • Shaw tooth P-wave with fixed R-R interval —Seen in atrial flutter (Fig. 1.15).
    • P-wave with different configuration seen in MAT (multifocal atrial tachycardia) (Fig. 1.18).
 
P-R INTERVAL
It is the time interval between beginning of atrial depolarization to beginning of ventricular depolarization normally it ranges from 0.12–0.2 sec (3–5 small division of the paper).
Short P-R interval < 0.12 sec is seen in WPW and LGL syndrome (Figs 1.19. and 1.20).
It is due to the presence of aberrant conduction pathway known as bundle of Kent which bypasses AV node. If the bundle of Kent end in cardiac musculature it will produce WPW syndrome and if the bundle of Kent ends in His bundle it will produce LGL syndrome.
In WPW syndrome, there will be short P-R interval and QRS will start just after P-wave but as the initial part of ventricular depolarization spread through musculature, it will produce a slow gradual upstroke in the initial part of QRS but the later part of ventricular depolarization takes place through His bundle and the conducting tissue so the 9later part of QRS will be sharp. This initial slow upstroke in QRS is called delta wave (Figs 1.20 to 1.22).
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Fig. 1.19: WPW syndrome with short P-R interval with delta wave
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Fig.1.20: WPW syndrome with short P-R interval with delta wave
In LGL syndrome there will be also short P-R interval and QRS will start just after P-wave as the bundle of Kent reenter His bundle after bypassing AV node (Figs 1.23A and B).
  • The ventricular depolarization will start just after atrial depolarization. Creating a sharp upstroke of QRS.
Long P-R interval—Seen in 1st degree heart block.
1st degree heart block—In this condition all the atrial depolarization wave is conducted to ventricle but with some delay in AV node due to long refractory period. In this condition P-R interval is >0.2 second or greater than 5 small square (Fig. 1.40).
2nd degree heart block—In this condition not all atrial depolarization wave is conducted to ventricle. There is some drop of beat (impulse) in the AV node. Depending 10on the dropping fashion of ventricular depolarization it is subdivided into Mobitz type-I and type-II.
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Fig. 1.21A: Dx: WPW syndrome
Clues: Short P-R interval and delta waves are obvious in the precordial leads. This tracing illustrates that not every lead will have a short P-R interval and a delta have in WPW syndrome if the delta wave is isoelectric in that lead (see lead-I specially). RVH should accompany RAD and S-waves in the left precordial leads, which this tracing does not have
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Fig. 1.21B: Dx: WPW syndrome
Clues: At first glance, it appears to be posterolateral MI with pathologic Q-waves in lead-I and aVL. However, the P-R interval is short in the precordial leads and slurred upstroke of typical delta wave is present. This delta wave is directed from the patient's left to right, registering as a negative delta wave in lead-I and aVL, simulating lateral wall MI. In lead-II, the P-R interval is normal and no delta wave is seen because the delta wave is isoelectric in that lead
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Fig. 1.22: WPW syndrome
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Fig. 1.23A: LGL syndrome
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Fig. 1.23B: Schematic diagram of the conducting tissue of heart with aberrant path (bundle of Kent)
Mobitz type-I block (Wenckebach block)—In this condition there is gradual prolongation of P-R interval in the successive beat followed by a drop of QRS complex (ventricular depolarization) following a P-wave, called Mobitz type-I block Figure 1.24.
Mobitz type-II block—In this condition due to disease or ischemia AV node cannot conduct all depolarization wave to ventricle. There is a fixed block in AV node and every 2nd or 3rd or 4th atrial depolarization wave is blocked in the AV node. Accordingly they are called 2 : 1, 3 : 1 or 4 : 1 heart block.
Complete heart block (Fig. 1.25)—In complete heart block none of the atrial impulse is conducted to ventricle. All atrial depolarization wave in blocked at AV node and the ventricle is excited from a focus anywhere from the lower part of the conducting system (AV node, His bundle, bundle branch, anterior or posterior, fascicle, Purkinje's fiber) or from ventricular musculature.
 
QRS INTERVAL
It is the time taken for ventricular depolarization. Normal interval is 0.1–0.12 second. If it is more than 0.12 second or 3 small square then either LBBB or complete RBBB in present.
 
Q-T INTERVAL
It is the total time of ventricular depolarization and repolarization and is measured from onset of Q-wave to end of T-wave.13
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Fig. 1.24: In these three channel rhythm strips, P-waves occur regularly at a rate of about 85/min. Occasionally, the P-waves failed to result in a QRS. Prior to that, the P-R interval progressively lengthens; a typical type-I 2nd degree AV block
Dx: Type-I 2nd degree AV block (AV Wenckebach phenomenon)
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Fig.1.25: Complete heart block with AV dissociation
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Fig. 1.26A: Physiological Q-wave. In the septal wall electrical vector moves away from the lead-I, aVL V5, V6 creating physiological Q-wave is the lead I, aVL, V5, V6. It is called physiological Q-wave
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Fig. 1.26B: In postmyocardial infarction state, lead facing the infarcted wall (which is electrically neutral) actually looks towards the opposite wall where the electrical vector moves away from the corresponding lead creating a broad and wide Q-wave
Q-T interval varies with heart rate and must be corrected (called QTC). The normal QTC is 0.42 second in men and 0.43 second in female. Person with prolong QT are susceptible to ventricular ectopic beat and arrhythmia.
 
Q-WAVE
It is the first negative deflection in the QRS complex.
Physiological Q-wave (Fig. 1.26A): In normal ECG it is seen in the left-sided chest lead V5, V6, and aVL and lead-I which is due to intraventricular septal depolarization. venticular septum is the first structure to depolarize during ventricular depolarization. As the septal depolarization vector moves from left to right (moves away from the lead) which originates from a twig from left bundle branch creating Q-wave in the left-sided lead-I, aVL, V5, V6 (Fig. 1.26A).
Criteria for physiological Q-wave
  • Thin Q-wave less than one small square duration.
  • Depth of Q-wave less than 1/3rd of the following Rwave.
Pathological Q-wave: In postmyocardial infarction state Q-wave is seen in the lead facing the wall of infarction.
The respective lead looks towards the opposite wall of the ventricular cavity (through the infarcted zone which is electrically neutral) where the electrical vector moves away from the corresponding lead creating Q-wave (Fig. 1.26B).
Criteria for pathological Q-wave
  • Must be more than 1 small square width.
  • 15Depth of Q is more than 1/3rd of the following R wave. In anteroseptal wall infarction Q-wave is seen in lead V2–V4 (Figs 1.39, 1.42 and 1.43).
In anterolateral wall infarction Q-wave is seen in lead V4–V6, aVL and lead-I.
In inferior wall infarction Q-wave is seen in lead-II, III and aVF (Figs 1.40 to 1.44).
 
R-WAVE
From the height of R-wave we can have an idea about ventricular hypertrophy.
Criteria of LVH, —R taller than 25 mm in V5 /V6
RV5 /RV6> 25 mm or RV6 + SV1 > 35 mm (Figs 1.27 and 1.28).
Criteria of RVH is R > S in V1
 
QRS COMPLEX
From QRS complex we can conclude about bundle branch block.
In right bundle branch block (RBBB) (Figs 1.29 to 1.33) we see RSR’ pattern in V1 lead. The initial positive R-wave in V1 is due to septal depolarization which occurs from left to right. Where the vector is running towards the lead. Then left ventricle is activated and the S-wave is due to left ventricular depolarization which occurs from right to left vector running away from the lead. After that right ventricle is depolarized from left to right creating a R-wave.
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Fig.1.27: LVH with left axis deviation
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Fig.1.28: Narrow QRS tachycardia at a rate of 129/min. The P-waves are inverted in the inferior leads, suggesting either junctional rhythm or low atrial rhythm. The P-R interval of 120 milliseconds favors junctional tachycardia. Voltage criteria and ST-T changes favor LVH is present
Dx: 1. Probable junctional tachycardia
2. LVH
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Fig.1.29: An example of typical RBBB
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Fig.1.30: Right bundle branch block (RSR’ pattern in V1)
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Fig. 1.31: Right bundle branch block
The late positive vector, i.e. R-wave is due to late right ventricular depolarization which produces right ward vector. In this situation when the duration of QRS is less than 12 second (< 3 small division), it is called incomplete RBBB and when the duration of QRS is more than 0.12 second (> 3 small division) it is called complete RBBB.
In left bundle branch block (LBBB) (Figs 1.34 to 1.36) In the left sided lead (V5, V6, aVL and lead-I). There will be no Q-wave at the beginning as the septal depolarization in LBBB occurs from right to left (instead of normal left to right). So it will produce a initial positive R-wave followed by a notch or a short duration negative wave which is due to right ventricular depolarization vector (which moves towards right, away from in V5, V6) (Fig. 1.36) and in the late part of QRS there is a positive deflection which is due to late depolarization of left ventricle where vector moves towards left creating a late positive deflection in V5, V6.18
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Fig. 1.32: An example of typical right bundle branch block
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Fig. 1.33: RBBB (RSR’ in V1 and slurring of S-wave in lead-I) and left axis deviation (negative QRS in aVF and II reflect BIFB. Acute anteroseptal STEMI is present (deep Q with ST elevation and inverted T in V2 V3 V4)
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Fig. 1.34: Broad and notched QRS complex of right bundle branch block
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Fig. 1.35: LBBB broad or wide QRS complex of right bundle branch block
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Fig. 1.36: Irregularly irregular rhythm at a rate of 129/min with no definite P-waves indicating atrial fibrillation. The QRS is wide and has a typical LBBB pattern. If the rate is faster one could easily be mistaken the tracing for a run of VT.
Dx: 1. Atrial fibrillation with a ventricular response of 129/min
2. LBBB
 
ST-SEGMENT
ST-segment gives us information about ischemia and infarction.
In STEMI (ST-elevated myocardial infarction) there will be elevation of ST-segment with convexity upward which incorporate T-wave within it and is seen in the early hours of STEMI (Fig. 1.37) but as the times passes (Fig. 1.38)—The following changes in ECG gradually appear
  • The ST-segment gradually comes down
  • T-wave gradually become inverted
  • Deep and wide Q-wave gradually appear
  • Height of R gradually comes down (Fig. 1.38).
All these four changes begins to appear simultaneously or sequentially within few hours after the onset of acute myocardial infarction (Figs 1.40 to 1.43).
Reciprocal change—In STEMI the lead facing the opposite wall of infarction usually have ST-segment depression which is called reciprocal changes. In case of inferior wall infarction. ST elevation is seen in II, III, aVF but reciprocal changes (ST-depression) are seen 21in V2,V3 and V4. In true posterior wall infarction reciprocal changes are seen in V2,V3 and V4. In anteroseptal wall infarction reciprocal changes are seen in lead-II, III aVF.
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Fig. 1.37: Early stage of STEMI
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Fig. 1.38: Late stage of STEMI
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Fig. 1.39: STEMI (involving anteroseptal wall)
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Fig. 1.40: Sinus rhythm at 66/min with 1st degree AV block.
ST elevation in inferolateral leads with horizontal ST depression in V1–V3 is diagnostic of STEMI of inferoposterolateral wall. ST is reciprocally depressed only in aVL, not in lead-I indicating RV is not involeved and the culprit lesion must be not in proximal RCA but either RCA not proximal or circumflex coronary artery
Dx: 1. Sinus rhythm with 1st degree AV block; 2. STEMI of inferoposterolateral wall
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Fig. 1.41: The ‘sawtooth’ pattern of atrial flutter is obvious in the rhythm strip of lead-II. The flutter rate is somewhat slow at 240/min. Antiarrhythmics are well-known to slow the flutter rate down to 200/min very easily. Complete RBBB is also present. Q-waves in lead-III aVF indicate inferior infaract as well
Dx: 1. Atrial flutter with 2:1 AV conduction
2. RBBB
3. Inferior wall myocardial infarction (MI), probably old
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Fig. 1.42: Irregularly irregular rhythm with no visible P-waves indicates atrial fibrillation. Significant, coved ST elevation in the precordial leads as well as in lead-I and aVL indicate acute extensive anterior myocardial infarction (MI). Lead-I and aVL represents high lateral wall which often is perfused by diagonal branch which takes off very proximaly in LAD. Therefore infarction pattern involving precordial lead-I and aVL means the culprit lesion is in the proximal LAD. If lead-I and aVL are not involved, the lesion is in the LAD not proximal. If only lead-I and aVL are involved without precordial leads, the lesion is in the diagonal branch. The ST depression in the inferior leads is the reciprocal change of the ST elevation in aVL
Dx: 1. Atrial fibrillation with a ventricular response of 85 min
2. Acute, extensive anterior infarct
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Fig. 1.43: Normal sinus rhythm at a rate of 74/min. QS pattern in the right precordial leads with a slight elevation of the ST-segment and a terminal T-wave inversion reflect recent AMI
Dx: 1. Normal sinus rhythm
2. Recent anteroseptal infarct of some duration
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Fig. 1.44: Inferior wall STEMI with reciprocal changes in the anterior wall
In non-ST elevated myocardial infarction (NSTEMI)—Three changes are seen—
  • Depression of ST-segment (<1 mm).
  • Transient elevation of ST-segment (<20 minutes duration).
  • Deep isometric inversion of T-wave (Figs 1.45 and 1.52).
In myocardial ischemia, three classic changes are seen in ST-segment not associated with chest pain.
The ischemic changes in ST-T segment are—
  • Down slopping of ST-segment with inversion of T-wave (Fig. 1.46). With unequal length of the ascending and descending limb of T-wave (sensitivity 95%).
  • Horizontal depression of ST-segment > 2 mm and longer >2 small division (Fig. 1.47). Sensitivity (80–85%).
  • J point is the junction of end ventricular depolarization and beginning of ventricular repolarization.
  • Upslopping ST-segment (Fig. 1.48) is also seen in ischemia but sensitivity is (60–65%).
Rarely there may be elevation of ST-segment with convexity downward and present in the adjacent leads seen in pericardial diseases (Figs 1.49A and B). Also called early repolarization.
 
T-WAVE
Tall peaked T-wave commonly seen in two conditions— (a) hyperkalemia and (b) early stage of acute myocardial infarction STEMI. The differentiating point between these two conditions are—26
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Fig. 1.45: Deep isometric inversion of T-wave is V4, V5, V6 suggestive of NSTEMI
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Fig. 1.46: Down slopping ST with inversion of T-wave seen in ischemia with unequal length of the ascending and descending limb of T-wave
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Fig. 1.47: Horizontal depression of ST-segment seen in ischemia
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Fig. 1.48: Upslopping ST-segment seen in ischemia
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Fig. 1.49A: Elevated ST with convexity downward known as early repolarization seen in pericardial disease and may be seen as a normal varient
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Fig. 1.49B: Normal sinus rhythm at a rate of 80/min. QRS voltage for LVH is present. There is about 4 mm ST elevation in V3–V4, and to a lesser degree in other precordial leads. The notching in the junction in V4 and upward concavity of the ST-segment are all diagnostic of early repolarization pattern as a normal variant. The PR-segment is slightly depressed which is also part of this condition. Sometimes these findings may be mistaken for an acute MI or pericarditis
Dx: 1. NSR
2. LVH by voltage
3. Early repolarization pattern as a normal variant
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Fig. 1.50: Tall peaked T-wave with J point below isoelectric line seen in hyperkalemia (P-R interval is considered isoelectric line)
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Fig. 1.51: Tall peaked T-wave with ‘J’ point above isoelectric line (P-R interval) seen in very early stage of acute myocardial infarction
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Fig. 1.52: Isometric inversion of T-wave seen in NSTEMI and UA ascending and descending limb of T-wave are of equal length
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Fig. 1.53: Flattening or depression of T-wave without chest pain seen in chronic ischemia
  1. In case of hyperkalemia the J point is much below the isoelectric line (Fig. 1.50).
  2. In case of early stage acute myocardial infarction the ‘J’ point in much above the isoelectric line (Fig. 1.51) followed by tall peaked T wave.
Isolated inversion of T-wave may be seen in (a) NSTEMI (non-ST elevated myocardial infarction and (b) old infarction or ischemia (Figs 1.45 and 1.52).
 
U-WAVE
It is rare and is due to repolarization of conducting tissue of heart. It is prominent in hypocalcemia (Fig. 1.53).