The QRS duration is generally <0,10 seconds but must be <0,12 seconds. Regardless of which waves are visible, the wave(s) that reflect ventricular depolarization is always referred to as the QRS complex. Usually, though, the amplitude in V2–V3 is around 6 mm and 3 mm in men and women, respectively. Author information: (1)Section of Cardiology, Rush Medical College, Chicago, Illinois 60612, USA. R-wave amplitude in aVL should be ≤ 12 mm. However, there are numerous other causes of Q-waves, both normal and pathological and it is important to differentiate these. Note that the first vector in Figure 7 is not discussed here as it belongs to atrial activity. Acute cor pulmonale (pulmonary embolism). When the PR interval exceeds 0.22 seconds, first-degree AV-block is manifest. The magnitude of depression/elevation is measured as the height difference (in millimeters) between the J point and the PR segment. The atrioventricular (AV) node is normally the only connection between the atria and the ventricles. As seen in Figure 4 (third panel) the initial depolarization of the ventricles (starting where the accessory pathway inserts into the ventricular myocardium) is slow because the impulse will not spread via the normal His-Purkinje pathway. In prospective evaluation, an algorithm based on the above four criteria identified 93% of left versus right PV and totally 79% of the specific PVs paced. A systematic approach to ECG interpretation, Cardiac electrophysiology: action potentials, automaticity, electrical vectors, The ECG leads (12-lead ECG and other lead systems), Introduction to coronary artery disease (ischemic heart disease). This is considered a normal finding provided that an R-wave is seen in V2. It is a general misunderstanding that T-wave inversions, without simultaneous ST-segment deviation, indicate acute (ongoing) myocardial ischemia. Whenever a mirror (whether a plane mirror or otherwise) creates an image that is virtual, it will be located behind the m… Some individuals may display persisting T-wave inversion in V1–V4, which is called persisting juvenile T-wave pattern. It is crucial to differentiate normal from pathological Q-waves, particularly because pathological Q-waves are rather firm evidence of previous myocardial infarction. The normal T-wave in adults is positive in most precordial and limb leads. For example, a block in the left bundle branch means that the left ventricle will not be depolarized via the Purkinje network, but rather via the spread of the depolarization from the right ventricle. Therefore to determine whether the QT interval is within normal limits, it is necessary to adjust for the heart rate. The Normal P wave. Thus, in this chapter, you will learn the physiological basis of all ECG waves and how to determine whether the ECG is normal or abnormal. This is shown in Figure 3 (upper panel). As evident from Figure 35 (panel D) these conditions are characterized by oppositely directed QRS- and ST-T-segments (recall that this is referred to as discordance). Clinical electrocardiography and ECG interpretation, Cardiac electrophysiology: action potential, automaticity and vectors, The ECG leads: electrodes, limb leads, chest (precordial) leads, 12-Lead ECG (EKG), The Cabrera format of the 12-lead ECG & lead –aVR instead of aVR, ECG interpretation: Characteristics of the normal ECG (P-wave, QRS complex, ST segment, T-wave), How to interpret the ECG / EKG: A systematic approach, Mechanisms of cardiac arrhythmias: from automaticity to re-entry (reentry), Aberrant ventricular conduction (aberrancy, aberration), Premature ventricular contractions (premature ventricular complex, premature ventricular beats), Premature atrial contraction (premature atrial beat / complex): ECG & clinical implications, Sinus rhythm: physiology, ECG criteria & clinical implications, Sinus arrhythmia (respiratory sinus arrhythmia), Sinus bradycardia: definitions, ECG, causes and management, Chronotropic incompetence (inability to increase heart rate), Sinoatrial arrest & sinoatrial pause (sinus pause / arrest), Sinoatrial block (SA block): ECG criteria, causes and clinical features, Sinus node dysfunction (SND) and sick sinus syndrome (SSS), Sinus tachycardia & Inappropriate sinus tachycardia, Atrial fibrillation: ECG, classification, causes, risk factors & management, Atrial flutter: classification, causes, ECG diagnosis & management, Ectopic atrial rhythm (EAT), atrial tachycardia (AT) & multifocal atrial tachycardia (MAT), Atrioventricular nodal reentry tachycardia (AVNRT): ECG features & management, Pre-excitation, Atrioventricular Reentrant (Reentry) Tachycardia (AVRT), Wolff-Parkinson-White (WPW syndrome), Junctional rhythm (escape rhythm) and junctional tachycardia, Ventricular rhythm and accelerated ventricular rhythm (idioventricular rhythm), Ventricular tachycardia (VT): ECG criteria, causes, classification, treatment (management), Longt QT interval, long QT syndrome (LQTS) & torsades de pointes, Ventricular fibrillation, pulseless electrical activity and sudden cardiac arrest, Pacemaker mediated tachycardia (PMT): ECG and management, Diagnosis and management of narrow and wide complex tachycardia, Introduction to Coronary Artery Disease (Ischemic Heart Disease) & Use of ECG, Classification of Acute Coronary Syndromes (ACS) & Acute Myocardial Infarction (AMI), Clinical application of ECG in chest pain & acute myocardial infarction, Diagnostic Criteria for Acute Myocardial Infarction: Cardiac troponins, ECG & Symptoms, Myocardial Ischemia & infarction: Reactions, ECG Changes & Symptoms, The left ventricle in myocardial ischemia and infarction, Factors that modify the natural course in acute myocardial infarction (AMI), ECG in myocardial ischemia: ischemic changes in the ST segment & T-wave, ST segment depression in myocardial ischemia and differential diagnoses, ST segment elevation in acute myocardial ischemia and differential diagnoses, ST elevation myocardial infarction (STEMI) without ST elevations on 12-lead ECG, T-waves in ischemia: hyperacute, inverted (negative), Wellen's sign & de Winter's sign, ECG signs of myocardial infarction: pathological Q-waves & pathological R-waves, Other ECG changes in ischemia and infarction, Supraventricular and intraventricular conduction defects in myocardial ischemia and infarction, ECG localization of myocardial infarction / ischemia and coronary artery occlusion (culprit), The ECG in assessment of myocardial reperfusion, Approach to patients with chest pain: differential diagnoses, management & ECG, Stable Coronary Artery Disease (Angina Pectoris): Diagnosis, Evaluation, Management, NSTEMI (Non ST Elevation Myocardial Infarction) & Unstable Angina: Diagnosis, Criteria, ECG, Management, STEMI (ST Elevation Myocardial Infarction): diagnosis, criteria, ECG & management, First-degree AV block (AV block I, AV block 1), Second-degree AV block: Mobitz type 1 (Wenckebach) & Mobitz type 2 block, Third-degree AV block (3rd degree AV block, AV block 3, AV block III), Management and treatment of AV block (atrioventricular blocks), Intraventricular conduction delay: bundle branch blocks & fascicular blocks, Right bundle branch block (RBBB): ECG, criteria, definitions, causes & treatment, Left bundle branch block (LBBB): ECG criteria, causes, management, Left bundle branch block (LBBB) in acute myocardial infarction: the Sgarbossa criteria, Fascicular block (hemiblock): left anterior & left posterior fascicular block on ECG, Nonspecific intraventricular conduction delay (defect), Atrial and ventricular enlargement: hypertrophy and dilatation on ECG, ECG in left ventricular hypertrophy (LVH): criteria and implications, Right ventricular hypertrophy (RVH): ECG criteria & clinical characteristics, Biventricular hypertrophy ECG and clinical characteristics, Left atrial enlargement (P mitrale) & right atrial enlargement (P pulmonale) on ECG, Digoxin - ECG changes, arrhythmias, conduction defects & treatment, ECG changes caused by antiarrhythmic drugs, beta blockers & calcium channel blockers, ECG changes due to electrolyte imbalance (disorder), ECG J wave syndromes: hypothermia, early repolarization, hypercalcemia & Brugada syndrome, Brugada syndrome: ECG, clinical features and management, Early repolarization pattern on ECG (early repolarization syndrome), Takotsubo cardiomyopathy (broken heart syndrome, stress induced cardiomyopathy), Pericarditis, myocarditis & perimyocarditis: ECG, criteria & treatment, Eletrical alternans: the ECG in pericardial effusion & cardiac tamponade, Exercise stress test (treadmill test, exercise ECG): Introduction, Exercise stress test (exercise ECG): Indications, Contraindications, Preparation, Exercise stress test (exercise ECG): protocols, evaluation & termination, Exercise stress testing in special patient populations, Exercise physiology: from normal response to myocardial ischemia & chest pain, Evaluation of exercise stress test: ECG, symptoms, blood pressure, heart rate, performance, Overview of the normal electrocardiogram (ECG), Electrical vectors that engender the QRS complex, Implications and causes of wide (broad) QRS complex, The ST segment: ST depression & ST elevation, T-wave inversion (inverted / negative T-waves), QT duration and corrected QT (QTc) duration, The electrical axis of the heart (heart axis), Axis deviation: right axis deviation (RAD) and left axis deviation (LAD). Characteristics of P wave: P waves are the primary waves similar to sound waves in which particles move to and fro in the direction in which the wave is travelling.They have short wavelength and high frequency and are the first wave to arrive a seismograph and can move through solid , liquid and gas. If these Q-waves do not fulfill criteria for pathology, then they should be accepted. All T-waves are illustrated in Figure 18. Then one might wonder why T-wave inversions are included as criteria for myocardial infarction. lauraclegg2007. P-waves travel sooner than other seismic waves and therefore are the first signal from an earthquake to reach at any affected place or at a seismograph. These calculations are approximated simply by eyeballing. A complete list of drugs causing QT prolongation can be found here. The most common cause of pathological Q-waves is myocardial infarction. P waves travel at speeds between 1 and 14 km per second, while S waves travel significantly slower, between 1 and 8 km per second. The condition is referred to as pre-excitation because the ventricles are excited prematurely. The normal ST segment is flat and isoelectric. If the axis is more positive than 90° it is referred to as right axis deviation. Characteristics of normal P waves include A. one P preceding each QRS complex. Septal q-waves are small q-waves frequently seen in the lateral leads (V5, V6, aVL, I). Some leads may display all waves, whereas others might only display one of the waves. The negative deflection is normally <1 mm. Clinicians often perceive this as a difficult task despite the fact that the list of differential diagnoses is rather short. T-wave changes are notoriously misinterpreted, particularly inverted T-waves. The ST segment extends from the J point to the onset of the T-wave. The abnormal ventricular depolarization will cause abnormal repolarization. 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. If the first wave is not negative, then the QRS complex does not possess a Q-wave, regardless of the appearance of the QRS complex. In addition, superior PVs could be distinguished from inferior according to the amplitude in lead II (≥100 μV). A common cause of abnormally large T-waves is hyperkalemia, which results in high, pointed and asymmetric T-waves. These waves can travel through solid, liquid, and gas. A short QRS complex is desirable as it proves that the ventricles are depolarized rapidly, which in turn implies that the conduction system functions properly. Enlargement of the left and right atria causes typical P-wave changes in lead II and lead V1 (Figure 3). CHARACTERISTICS OF THE NORMAL P WAVES In sinus rhythm the P wave is always upright in lead I and II and always negative in AVR. The transition from the ST segment to the T-wave should be smooth (and not abrupt). P-wave amplitude should be <2,5 mm in the limb leads. Therefore, ECG interpretation requires a structured assessment of the waves and intervals. Supraventricular tachycardias also cause ST segment depressions which typically occur in V4–V6 with a horizontal or slightly upsloping ST segment. Impulse originates in the SA Node-One P per QRS -All waves, intervals, and rate WNL. aurieulaire normale et rétrograde. If R-wave in V1 is larger than S-wave in V1, the R-wave should be <5 mm. If the atrial impulse uses an accessory pathway, the impulse delay in the atrioventricular node is bypassed and therefore the PR interval becomes shortened (PR interval <0.12 seconds). ECG interpretation usually starts with an assessment of the P-wave. High amplitudes may be due to ventricular enlargement or hypertrophy. QT duration and corrected QT (QTc) duration, left anterior descending coronary artery (LAD), Acute & Chronic Myocardial Ischemia & Infarction. Newer formulas (which are incorporated in modern ECG machines) are to be preferred over Bazett’s formula. The T-wave vector is directed to the left, downwards and to the back in children and adolescents. A long QTc interval increases the risk of ventricular arrhythmias. Write. 2) play a major role in the beam- wave interaction mechanism at the high-frequency operating end of the device. The flat line between the end of the P-wave and the onset of the QRS complex is called the PR segment and it reflects the slow impulse conduction through the atrioventricular node. However, apart from the delta wave, the R-wave will appear normal because ventricular depolarization will be executed normally as soon as the atrioventricular node delivers the impulse to the His-Purkinje system. Electrocardiographic P-wave characteristics in patients with end-stage renal disease: P-index and interatrial block. Normal P wave axis is between 0° and +75° P waves should be upright in leads I and II, inverted in aVR; Duration < 0.12 s (<120ms or 3 small squares) Amplitude < 2.5 mm (0.25mV) in the limb leads < 1.5 mm (0.15mV) in the precordial leads R-wave amplitude in V6 + S-wave amplitude in V1 should be <35 mm. 2. The following must be noted regarding the ST segment: It must also be noted that the J point is occasionally suboptimal for measuring ST segment deviation. They can still propagate through the solid inner core: when a P wave strikes the boundary of molten and solid cores at an oblique angle, S waves will form and propagate in the solid medium. If it is located near the atrioventricular node, the activation of the atria will proceed in the opposite direction, which produces an inverted (retrograde) P-wave. Also note that this chapter is accompanied by a video lecture: Video lecture: The Normal ECG, which covers all topics discussed below. 2) Explain how wind-generated waves, swell, rogue waves, and tsunamis are formed. ScienceDirect ® is a registered trademark of Elsevier B.V. ScienceDirect ® is a registered trademark of Elsevier B.V. Morphological characteristics of P waves during selective pulmonary vein pacing. We sought to assess the value of 12-lead electrocardiogram (ECG) P-wave morphology to recognize the paced pulmonary vein (PV). The amplitude of any deflection/wave is measured by using the PR segment as the baseline. Hypertrophy means that there are more muscle and hence larger electrical potentials generated. Post-ischemic T-wave inversion is caused by abnormal repolarization. It should be noted, however, that up to 20% of Q-wave infarctions may develop without symptoms (The Framingham Heart Study). Since the electrical vector generated by the left ventricle is many times larger than the vector generated by the right ventricle, the QRS complex is actually a reflection of left ventricular depolarization. T-waves with very low amplitude are common in the post-ischemic period. Heart failure may cause ST segment depression in the left lateral leads (V5, V6, aVL and I) and these depressions are generally horizontal or downsloping. All positive waves are referred to as R-waves. The P-wave is virtually always positive in leads aVL, aVF, –aVR, I, V4, V5 and V6. Below follows a discussion which aims to clarify some of the common misunderstandings. The reference point is, as usual, the PR segment. The T-wave is normally slightly asymmetric since its downslope (second half) is steeper than its upslope (first half). The QRS complex represents the depolarization (activation) of the ventricles. The ventricular septum receives Purkinje fibers from the left bundle branch and therefore depolarization proceeds from its left side towards its right side. Refer to Figure 6, panel A. P-waves can be transmitted through, liquids, gases or solids. P-wave attenuation characteristics of experiment al observation and theoretical simulati on. If the atria are depolarized by impulses generated by cells outside of the sinoatrial node (i.e by an ectopic focus), the morphology of the P-wave may differ from the P-waves in sinus rhythm. The QT interval varies somewhat in the different leads. Assessment of the T-wave represents a difficult but fundamental part of ECG interpretation. Refer to Figure 4 (second panel). Normal axis: Net positive QRS complex in leads I and II. A negative T-wave is also called an inverted T-wave. Due to this, it is sometimes recommended that ST segment deviation be measured in the J-60 point, or J-80 point, which is located 60 and 80 milliseconds, respectively, after the J point (Comprehensive Electrocardiology, MacFarlane et al, Springer, 2010; Chou’s Electrocardiologi, Surawicz, Elsevier 2010). This may be due to pulmonary valve stenosis, increased pulmonary artery pressure etc. This may be explained by right bundle branch block, right ventricular hypertrophy, hypertrophic cardiomyopathy, posterolateral ischemia/infarction (if the patient experiences chest pain), pre-excitation, dextrocardia or misplacement of chest electrodes. Left axis deviation: Net positive QRS complex in lead I but negative in lead II. The structural … Positive T-waves are rarely higher than 6 mm in the limb leads (typically highest in lead II). Right atrial enlargement (hypertrophy) leads to stronger electrical currents and thus enhancement of the contribution of the right atrium to the P-wave. Lead V1 does not detect this vector. Inferior infarction. P waves are also called pressure waves for this reason. The U-wave is most frequently seen in leads V2–V4. The P-wave is a small, positive and smooth wave. Wide (also referred to as broad) QRS complexes indicate that ventricular depolarization is slow, which may be due to dysfunction in the conduction system. If the axis is more negative than –30° it is referred to as left axis deviation. There is no definite way to rule out myocardial ischemia by judging the appearance of the ST segment, which is why North American and European guidelines assert that the appearance of the ST segment cannot be used to rule out ischemia. S ingh (2006) Effects of soil layering on the characteristics of basin-edge induced surface waves and differential ground motion, Jr. of Earthquake Engineering 10, 595-616. The first positive wave is simply an “R-wave” (R). Spontaneous action potentials discharged within the ventricles may depolarize the ventricles. III and aVL: These leads occasionally display an isolated (single) T-wave inversion. The vector is directed backward and upwards. Pathological Q-waves have duration ≥0,03 sec and/or amplitude ≥25% of the R-wave amplitude. Extreme axis deviation (–90°to 180°): Net negative QRS complex in leads I and II. ST segment deviation (elevation, depression) is measured as the height difference (in millimeters) between the J point and the baseline (the PR segment). The QT duration is inversely related to heart rate; i.e the QT interval increases at slower heart rates and decreases at higher heart rates. Study Figure 7 carefully, as it illustrates how the P-wave and QRS complex are generated by the electrical vectors. P Waves are compressional which means they move through (compress) a solid or liquid by pushing or pulling similar to the way sound travels through the air. ST segment elevation is measured in the J-point. Some expert consensus documents also note that any ST segment depression in V2–V3 should be considered abnormal (because healthy individuals rarely display depressions in those leads). R-wave amplitude in leads I, II and III should all be ≤ 20 mm. Depolarization of the ventricles generates three large vectors, which explains why the QRS complex is composed of three waves. This is explained by the fact that T-wave inversions do occur after an ischemic episode, and these T-wave inversions are referred to as post-ischemic T-waves. Although often ignored, assessment of the electrical axis is an integral part of ECG interpretation. As the conduction diminishes, the PR interval becomes longer. The PR interval must not be too long nor too short. Therefore one must adjust the QT duration for the heart rate, which yield corrected QT duration (Qtc). ST segment deviation occurs in a wide range of conditions, particularly acute myocardial ischemia. ECG changes in ischemia are discussed in detail in section 3 (Acute & Chronic Myocardial Ischemia & Infarction) and a specific chapter discusses ST elevation in detail. Prolongation of QRS duration implies that ventricular depolarization is slower than normal. If a third positive wave occurs (rare) it is referred to as “R-bis wave” (R”). Occasionally, the negative deflection is also seen in lead V2. They may be gigantic (10 mm or more) or less than 1 mm. A complete QRS complex consists of a Q-, R- and S-wave. These waves travel in the speed range of 1.5-13 km/s. This is referred to as T-wave memory or cardiac memory. It enables the atrial impulse to pass directly to the ventricles and start ventricular depolarization prematurely. Infarction Q-waves are typically >40 ms. Abstract We examine differences of empirical sitecharacteristicsamongSwaves, P waves, coda, and microtremors using records at 20 sites in and around the Sendai Refer to Figure 1. young people, as well as athletes, have more prominent U-waves. Prolonged QT duration may either be congenital (genetic mutations, so-called long QT syndrome) or acquired (medications, electrolyte disorders). Lead V1 might therefore display a biphasic (diphasic) P-wave, meaning that the greater portion of the P-wave is positive but the terminal portion is slightly negative (the vector generated by left atrial activation heads away from V1). Particle motion is parallel It is negative in lead aVR. Right ventricular hypertrophy. The negative deflection is normally <1 mm. Their duration is short; they typically disappear within minutes after a total occlusion in a coronary artery occurs (then of course, the ST segment will be elevated). Numerous conditions can diminish the capacity of the atrioventricular node to conduct the atrial impulse to the ventricles. If coronary heart disease is likely, then infarction is the most probable cause of the Q-waves. Material for the study was collected in accordance with the protocol described in detail earlier . A QRS complex with large amplitudes may be explained by ventricular hypertrophy or enlargement (or a combination of both). Individuals with prominent T-waves, as well as those with slow heart rates, display U-waves more often. The electrical currents generated by the ventricular myocardium are proportional to the ventricular muscle mass. However, these inversions are normalized gradually during puberty. Hyperacute T-waves are broad-based, high and symmetric. We hypothesized that P-wave morphology and duration may be related to histological abnormality of the atrial myocardium. The first half of the P-wave is therefore a reflection of right atrial depolarization and the second half is a reflection of left atrial depolarization. The QRS complex is net positive if the sum of the positive areas (above baseline) exceeds that of the negative areas (below baseline). The axis can also be approximated manually by judging the net direction of the QRS complex in leads I and II. The flat line between the end of the P-wave and the onset of the QRS complex is called the PR segment and it reflects the slow impulse conduction through the atrioventricular node. They leave behind a trail of compressions and rarefactions on the medium they move through. Moreover, the U-wave is more prominent during slower heart rates. The axis is calculated (to the nearest degree) by the ECG machine. Note that the T-wave inversion may actually persist for a period after normalization of the depolarization (if it occurs). Pathological Q-waves must exist in at least two anatomically contiguous leads (i.e neighboring leads, such as aVF and III, or V4 and V5) in order to reflect an actual morphological abnormality. The electrical potential difference exists between ischemic and normal myocardium and it results in displacement of the ST segment. Prolonged QT duration predisposes to life-threatening ventricular arrhythmias and therefore QT duration must always be assessed. These T-wave inversions are symmetric with varying depth. P-pulmonale implies that the P-wave has an abnormally high amplitude in lead II (and in other leads in general). View all chapters in Introduction to ECG Interpretation. Its amplitude is generally one-fourth of the T-wave’s amplitude. Flashcards. As evident from the figure, the normal heart axis is between –30° and 90°. It should be noted that the term “biphasic” is unfortunate because (1) biphasic T-waves carry no particular significance and (2) a T-wave is classified as positive or inverted based on its terminal portion; if the terminal portion is positive then the T-wave is positive and vice versa. The reason for wide QRS complexes must always be clarified. This is presumably explained by a higher incidence of malignant ventricular arrhythmias. The atria and the ventricles are electrically isolated from each other by the fibrous rings (anulus fibrosus). Lead V~ being over the right atri- um, is also often helpful in P analysis. Same as normal sinus rhythm except:-Rate: 100-150. In any instance, one must verify whether the inversion is isolated, because if there is T-wave inversion in two anatomically contiguous leads, then it is pathological. When an earthquake occurs, some of the energy it releases is turned into heat within the earth. Short QTc syndrome (QTc <0,390 seconds) is uncommon and can be seen in hypocalcemia and during digoxin treatment. As noted above, the transition from the ST segment to the T-wave should be smooth. Created by. Match. U-wave inversion is rare but when seen, it is a strong indicator of pathology, particularly for ischemic heart disease and hypertension. The T-wave should be concordant with the QRS complex, meaning that a net positive QRS complex should be followed by a positive T-wave, and vice versa (Figure 17). P Waves are compressional, meaning they pass (compress) through a solid or liquid by pushing or pulling similar to how the sound moves through the air. At the time of J-60 and J-80, there is minimal chance that there are any electrical potential differences in the myocardium. PLAY. The material particles a P Wave passes through travel in the direction of energy from the P wave. Otherwise, there is discordance (opposite directions of QRS and T) which might be due to pathology. Similarly, a person with chronic obstructive pulmonary disease (COPD) often displays diminished QRS amplitudes due to hyperinflation of thorax (increased distance to electrodes). This is considered a normal finding provided that lead V2 shows an r-wave. Study this figure carefully. Its first half is steeper than its second half. Therefore, the slender individual may present with much larger QRS amplitudes. The PR segment serves as the baseline (also referred to as reference line or isoelectric line) of the ECG curve. The difference between the shortest and the longest QT interval is the QT dispersion. The P-wave is frequently biphasic in V1 (occasionally in V2). Lead V1 records the opposite and therefore displays a large negative wave called S-wave. Three criteria were used to distinguish right from left PV: 1) a positive P-wave in lead aVL and the amplitude of P-wave in lead I ≥50 μV indicated right PV origin (specificity 100% and 97%, respectively); 2) a notched P-wave in lead II was a predictor of left PV origin (specificity 95%); and 3) the amplitude ratio of lead III/II and the duration of positivity in lead V1were also helpful in distinguishing left versus right PV origin. Notice the following wave characteristics and particle motion of the P wave: The deformation (a temporary elastic disturbance) propagates. Hence, ECG leads with net positive QRS complexes will show ST segment depressions (as well as T-wave changes). By applying a P‐wave recognition program to eliminate extra systole, a signal of >250 beats was averaged from a standard 12‐lead ECG and the noise amplitude was reduced to <0.5 μV. Lead V5 detects a very large vector heading towards it and therefore displays a large R-wave. 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Depressions with upsloping ST segments ( Figure 3, P-pulmonale ) larger QRS amplitudes this Q-wave typically with... And hence larger electrical potentials generated resulting from activation of the signal-averaged P wave Animation T-wave or.