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![Developmental Changes
• Neonates: RV larger than LV(right ventricular dominance)
• Right axis deviation(mean QRS frontal plane axis +60 to +180 degrees)
• Large precordial R waves(forces) (tall R waves in aVR and the right precordial leads [ V1,
and V2]
• Upright T waves in the right precordial leads (V1).
• Deep S waves in lead I and the left precordial leads ( V5 and V6).
• Upright T waves that persist in leads V1 beyond 1 week of life – indicate RVH or strain, even
in the absence of QRS voltage criteria.
• By age 6 years, pediatric ECGs resemble those of the adult](https://image.slidesharecdn.com/ecg-190714134524/75/Ecg-in-children-13-2048.jpg)
![QRS Axis
• Normal QRS Axis in neonates
: +30 to +180 degrees
In adults : -30 to +110
• LAD
• LVH, LBBB, and left anterior
hemiblock
• Superior QRS axis (S>r in Avf)
• Characteristically seen with
endocardial cushion defect [ECD] and
tricuspid atresia)
• RAD
• RVH and RBBB.](https://image.slidesharecdn.com/ecg-190714134524/75/Ecg-in-children-49-2048.jpg)
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Ecg in children
- 1. READING ECG INCHILDREN • Presenter- Dr. Nivedita Mishra • Duration : 1hr 30 mins
- 2. Objectives • To discussconducting system of heart and techniques of obtaining pediatric ECG • To enumerate indication of ECG in children • To enumerate the age related changes in the pediatric ECG • To enumerate the steps involved in interpreting the ECG • To discuss the common ECG abnormalities associated with commonly encountered conditions in children.
- 3. Introduction ECG Electrocardiogram • Recordingof the electrical activity of the heart. Electrocardiograph • Sophisticated galvanometer – detects changes in electromagnetic potential. Lead Axis • Theoretical straight line joining the paired electrodes (Vector measurement)
- 4. Conducting system ofthe heart No mechanical activity of the heart takes place in the absence of a preceeding electrical activity.
- 5. About current vectorsof the Heart: • Heart = moving dipole • Generates current (action potential) between excited (Depol.= in +ve, out -ve) and non excited (pol./repol/resting = in –ve , out +ve) state. • Direction of electric current (by convention): direction in which the +ve charge would move , i.e towards –ve terminal. • Current flows from endocardial surface to epicardial surface to reach the recording electrode placed on the skin. • ECG like a Galvanometer records electric potentials between 2 points on the body surface. • Surface last to Depolarise is the first to Repolarise. • Depolarisation current is +ve current (towards electrode) • Repolarisation current is –ve current (away from electrode)
- 7. ECG – Leads Thehexaxial reference system • Leads I, II, and III (sup,inf/ rt,lt) - bipolar limb leads (Frontal projection) • Leads aVR, aVL, and aVF (sup,inf/ rt,lt) - unipolar limb leads (Frontal projection) • Leads V1–V6 (ant,post/ Rt to Lt) - unipolar precordial leads (Horizontal projection)
- 8. Chest Leads –Electrode Placement Leads Positive Electrode Placement View of Heart •V1 4th Intercostal space to right of sternum Septum •V2 4th Intercostal space to left of sternum Septum •V3 Directly between V2 and V4 Anterior •V4 5th Intercostal space at left midclavicular line Anterior •V5 Level with V4 at left anterior axillary line Lateral •V6 Level with V5 at left midaxillary line Lateral
- 10. By combining scalar(only magnitude, no direction) leads that represent the frontal projections and horizontal projections of vector( magnitude as well as direction) we can derive the direction of force from scalar ECG. I / AVF II / AVL III/ AVR
- 11. Indications for aPediatric ECG • Tachyarrhythmia • Bradyarrhythmia • Electrolyte disturbance • Syncope/seizure • Congenital heart diseases • Cyanotic episodes • Heart Failure • Kawasaki disease • Pericarditis • Drug ingestions • Post cardiac surgery • Rheumatic fever • Myocarditis ABC of clinical electrocardiography Paediatric electrocardiography Clinical review BMJ , 2002
- 12. Pediatric ECG isdifferent than adult • The pediatric ECG characteristics: • The heart rate is faster than in the adult. • All the durations and intervals (PR interval, QRS duration, and QT interval) are shorter than in the adult. • Inferior and lateral Q waves • RSR’ pattern in V1 • Marked sinus arrhythmia • The RV dominance of the neonate and infant • 15 leads instead of 12 leads in adults( V7, V3R, V4R) to better evaluate RV
- 13. Developmental Changes • Neonates:RV larger than LV(right ventricular dominance) • Right axis deviation(mean QRS frontal plane axis +60 to +180 degrees) • Large precordial R waves(forces) (tall R waves in aVR and the right precordial leads [ V1, and V2] • Upright T waves in the right precordial leads (V1). • Deep S waves in lead I and the left precordial leads ( V5 and V6). • Upright T waves that persist in leads V1 beyond 1 week of life – indicate RVH or strain, even in the absence of QRS voltage criteria. • By age 6 years, pediatric ECGs resemble those of the adult
- 14. Normal ECG references Thepediatric ECG, Em Med Clin N Am 24 (2006)
- 16. Steps of ECGinterpretation • Standardization, • Age of the child • Rate • Rhythm • QRS axis • Intervals • P wave morphology • QRS Complex abnormalities • ST and T wave abnormalities • U waves if present
- 17. MOST IMPORTANT!!!! • NEVERdiagnose only on ECG • Should be interpreted keeping in mind the clinical context
- 18. ECG Conventions &Intervals • Depolarisation towards electrode : +ve deflection • Depolarisation away from electrode : - ve deflection • Sensitivity : 10mm = 1 mv • Paper speed : 25mm/sec • Each large square (5mm) = 0.2 sec • Each small square (1mm) = 0.04 sec • Heart rate = 300/ no. of large squares between each R-R interval
- 19. The ECG Paper-Standardisation Amplitude Full standard 10mm/mV Time
- 20.
- 21. Electrical Components Deflection Description Pwave Ht= <2.5 mm (2.5 sm sq) Width= <2.5 mm (0.10sec) First wave, rounded, upright in all leads except aVR Atrial depolarization PR interval 0.12-0.20 sec 3- 5 sm.sq From beginning of P wave to beginning of QRS Depolarization reaches from atria to the ventricles QRS Complex Axis = -30* to +110* 0.10 sec Three deflections following P wave Ventricular depolarization Q Wave: First negative deflection R Wave: First positive deflection S Wave: First negative deflection after R wave
- 22. Electrical components Deflection Description ST segment Fromend of S wave to beginning of T wave Time between ventricular depolarization and beginning of repolarization T wave Rounded upright wave following QRS Represents ventricular repolarization QT interval 0.40 sec QTc=0.44 From beginning of QRS to end of T wave Total ventricular activity U wave Small rounded, upright wave following T wave Repolarization of Purkinje fibers.
- 23. Rate • Both atrialand ventricular rates should be measured • Fast HR: • 1500/No. of small boxes • Slow HR: • 300/No. of large boxes • For irregular Heart rate: • No. of R waves in a 6 sec strip(30 large boxes) X 10 • Countdown method: Find a QRS on thick line, countdown 300, 150, 100, 75, 60, 50 for each thick line till next QRS
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- 25.
- 26. Rhythm Sinus rhythm • Depolarizationoriginating from SA node. • Two characteristics • P wave preceding each QRS complex , with a constant PR interval. • The P axis between 0 and +90 degrees(P wave upright in leads I and aVF.) Normal rate of SAN= 60 to 100 / min Non-sinus rhythm • Some have p waves in front of every QRS but with an abnormal P axis (inverted in lead II).
- 27. Rhythm disturbances • Alteredautomaticity (heart rate) • Altered conductivity • To recognise arrythmias,look at: 1.Presence and Rate of P waves 2.QRS COMPLEX (0.12 sec) – wide (ventricular) narrow (supraventricular) 3. Relationship between P & QRS ORIGIN : SAN/ Atria/ AV Junction/ Ventricles
- 28. Abnormalities in theRhythm 1. Nonventricular arrhythmias • Sinus tachycardia • Sinus bradycardia • Sinus arrythmia • Sinus node dysfunction • Junctional rhythm/low atrial rhythm • Supraventricular Arrythmias(narrow complex tachycardia) • Premature atrial Contraction • Atrial Fibrillation • Atrial Flutter • SVT 2. Ventricular arrythmias (wide complex) • Premature Ventricular contraction • Ventricular Tachycardia • Ventricular fibrillation 3. Nonventricular conduction disturbances 1st degree,2nd degree and complete heart block 4. Ventricular conduction disturbances RBBB,LBBB, WPW
- 29. Sinus Rhythms Sinus Bradycardia- <60/min Sinus Tachycardia – 100 -150/ min in exercise,fear,pain,haemorrhage,thyrotoxicosis Sinus Arrythmia- H.R goes up and down with phases of inspiration (vagal inhibition) and expiration respectively. Beat to beat variability seen. Common in 3-12 yrs olds. Reduces with exercise.
- 34. Atrial Rhythms • Atrialectopics : normal QRS complex following an abnormal P wave (morphologically different from the other sinus P waves present in the same lead) • Atrial tachycardia (150-250/min) : >3 atrial ectopics occuring in a row. • Atrial Flutter : “Saw toothed appearance” of P waves with no isoelectric segments in between them. Associated with AV BLOCK at rates > 180-200. • Atrial fibrillation (>350/min): irregularly irregular RR interval.P waves of variable shapes and sizes throughout ECG.
- 38. JUNCTIONAL RHYTHM • AVNcontrolling atrial and ventricular depolarisation. • AVN discharges when SAN dead (intrinsic junctional rhythm @ 50/min) or AVN is abnormally excitable e.g hypoxia.(1.Accelerated junctional rhythm @ 50- 100/min, 2. Junctional tachycardia @>100/min) • ABSENT P • Seen in: Digoxin toxicity (the classic cause of AJR) Beta-agonists, e.g. isoprenaline, adrenaline Myocardial ischaemia, Myocarditis
- 39. What is therhythm?
- 40. Ventricular Rhythms • Ventriculartachycardia: Rate= >100/min TYPES: 1. Monomorphic VT – all ventricular complexes look the same 2. Polymorphic VT – variant : TORSADES DE POINTES risk of V- Fib. • Ventricular Fibrillation: no definite QRS. Immediately requires Asynchronised D.C shock • Ventricular Flutter: only QRS complexes seen. Rate= 200- 250/min
- 45. QRS axis • Representsthe mean vector of ventricular depolarization process in the vertical plane. • Successive approximation method using hexaaxial reference system • Measured from zero reference point (Lead I) • Direction of QRS complex in leads I and aVF determines the axis quadrant in relation to the heart • Step 1. Locate a quadrant using leads I and aVF • Step 2. Find a lead with equiphasic QRS complex (in which the height of the R wave and the depth of the S wave are equal).The QRS axis is perpendicular to the lead with equiphasic QRS complex. • Inspect the QRS complexes in leads adjacent to the equiphasic lead.If lead to its left side is +ve then axis is 90*to the equiphasic lead towards the left • QRS axis is normally positive in aVF
- 46.
- 47.
- 48. Conditions for whichaxis determination is helpful: • Conduction defects: RBBB,LBBB,hemiblocks • Chamber Enlargements: RVH,LVH • Broad complex tachycardias – bizzare axis s/o ventricular origin • Congenital heart disease – ASD • Pre excited conduction syndromes – WPW/ LGL • Pulmonary embolism = “S1Q3T3 syndrome” marker of Pulmonary HTN/pul infarction
- 49. QRS Axis • NormalQRS Axis in neonates : +30 to +180 degrees In adults : -30 to +110 • LAD • LVH, LBBB, and left anterior hemiblock • Superior QRS axis (S>r in Avf) • Characteristically seen with endocardial cushion defect [ECD] and tricuspid atresia) • RAD • RVH and RBBB.
- 50. P wave- Amplitudeand duration Absent in junctional rhythms, A- FIB • Normal P wave amplitude - less than 3 mm. The duration of the P waves – children <0.09 seconds infants < 0.07 seconds • Atrial hypertrophy: • Tall Peaked P waves – RAH = P PULMONALE • Wide P wave ( height is normal ) – LAH = P-mitrale • Biphasic P wave is normal in V1 • Bifid P wave normal in lead II IF ECG machine is very sensitive
- 52. Progression of Rwave • R-wave progression: Generally a normal increase in R-wave size and decrease in S-wave size from leads V1 to V6 • Represents dominance of left ventricular forces • Reversed in RVH
- 56. Criteria for RVH a.RAD for the patient’s age b. Increased rightward and anterior QRS voltages in the presence of normal QRS duration (1) R in V1, V2, or aVR greater than the upper limits of normal (2) S in I and V6 greater than the upper limits of normal c. Abnormal R/S ratio (1) R/S ratio in V1 and V2 “greater”than upper limit for age (2) R/S ratio in V6 < 1, after 1 month of age. d. Upright T wave in V1 in patients more than 7 days of age, provided that the T is upright in the LPLs (V5, V6). e. A Q wave in V1 (qR or qRs pattern) - severe RVH
- 57. LVH Criteria for LVH a.LAD for the patient’s age b. QRS voltages in favor of the LV in the presence of normal QRS Duration (1) R in I, II, III, aVL, aVF, V5, or V6 greater than the upper limits of normal (2) S in V1 or V2 greater than the upper limits of normal c. Abnormal R/S ratio: An R/S ratio in V1 and V2 “less” than the lower limits of normal for the patient’s age d. Q in V5 and V6, 5 mm or more, coupled with tall symmetric T waves in the same leads e. Inverted T waves in lead I or aVF.
- 58. Ventricular hypertrophy vsventricular conduction delay
- 59.
- 61. • A prolongedQRS Ventricular conduction disturbances • Bundle branch blocks (BBBs) • WPW preexcitation • Low QRS amplitudes: • Pericarditis • Myocarditis • Hypothyroidism • Normal newborns intraventricular block
- 62. Wolff Parkinson WhiteSyndrome
- 63. PR Interval • PRinterval-measured from the onset of the P wave to the beginning of the QRS complex. • Prolonged PR interval (first-degree AV block) • Myocarditis (viral, rheumatic, or diphtheric) • Digitalis or quinidine toxicity • CHDs (ECD, ASD, Ebstein anomaly) • Hyperkalemia • Otherwise normal hearts. • A short PR interval is present in • Wolff-Parkinson-White (WPW) preexcitation • Duchenne muscular dystrophy • Glycogen storage disease • Otherwise normal children. • Variable PR intervals are seen in • Wenckebach (Mobitz type I) second-degree AV block
- 64. PR INTERVALS (AGESPECIFIC)
- 65. QT interval • Normallyvaries primarily with heart rate. • The heart rate–corrected QT interval (QTc) Bazett formula: QTc = QT/√RR interval • Normal QTc interval (mean± SD) is 0.40 (± 0.04) seconds with the upper limit of normal 0.44 seconds in children 6 month and older • Short QT interval(QTc is ≤300 milliseconds) - hypercalcemia , digitalis effect. • Prolong QT interval- • Hypocalcaemia • Myocarditis • Long QT syndromes • Head injury • Drugs
- 66. ST segment • Elevationor depression of up to 1 mm in the limb leads and up to 2 mm in the precordial leads is within normal limits. • Non-pathologic ST segment shift • J depression and • Early repolarization
- 67. Pathological ST depression/elevation (sustained>0.08 ms)
- 68. T wave • Theprecordial T-wave configuration changes over time • Tall, peaked T waves are seen in • Hyperkalemia • LVH (volume overload) • Benign early repolarization
- 69. Abnormalities of Twave • Flat T waves are seen in: • Normal newborns • Hypothyroidism • Hypokalaemia • Digitalis • Pericarditis • Myocarditis • Myocardial ischaemia • Large, deeply inverted T waves are seen with: • Raised intracranial pressure (e.g. intracranial haemorrhage, traumatic brain injury)
- 70. ECG features ofhypokalemia & hyperkalemia
- 72. DIGOXIN: Effects onECG • m/c side effect : AV Block (all types except Mobitz type 2) • Most characteristic side effect : Bidirectional V- Tach (i.e changing axis in alternate cycle) • Most toxic effect: ventricular ectopics (bigemini) • Inverted tick sign,QT shortening
- 73. Summary • Pediatric ECGshould be interpreted based on clinical context. • Be aware of age related differences, the normal ranges for electrocardiographic variables, and the typical abnormalities in infants and children. • Normal ECG is the most important one to learn. • The ECG should always be evaluated systematically to avoid the possibility of overlooking a minor, but important, abnormality. • No substitute to repeated practice of actually interpreting from REAL LIFE ECGs.Mere understanding of principles will not help!
- 74. References • Paediatric Electrocardiographyby Steve Goodacre and Karen McLeod, from the BMJ’s “ABC of Clinical Electrocardiography” series • ECG Made Easy: John R.Hampton 6TH Edn. • Guyton’s textbook of Medical Physiology • The Harriet Lane handbook • A primer of ECG: Simple deductive approach by K.P Misra • Nelsons Textbook of Pediatrics, 21st edition
- 75.
Editor's Notes
- #4 An ECG is a recording of a series of waves and deflections from the body surface of the electrical changes that occur within a heart from a certain “view” during the cardiac cycle.
- #5 Direction of atrial depol.= rt to lt Direction of atrial to ventricular depol. = sup to inf
- #6 Normally, inside of the cells in resting state is more –ve than outside. Cells lose their internal negativity by depolarisation and restore their resting polarity by repolarisation,this is accomplished by membrane pumps which reverse the flow of ions. Galvanometer only measures the magnitude of potential difference, not the direction. More negative the current, more is the potential difference, more is the amplitude recorded by the galvanometer. Direction is told by lead placement: towards +ve electrode=+ ve deflection, away from +ve electrode = _ve deflection, perpendicular to electrodes = biphasic
- #7 Lead = combination of 2 wires with their electrodes to make a complete circuit with the ECG machine. Bipolar lead = 2 electrodes on different sides of the heart. +ve electrode on Lt side & LOWER LT. FOOT Largest P wave in lead II as it is exactly along the current of atrial depolarisation.
- #8 Leads I, II, and III are bipolar leads, which consist of two electrodes of opposite polarity (positive and negative).The third (ground) electrode minimizes electrical activity from other sources. Leads aVR, aVL, and aVF unipolar limb leads -positive electrode and indifference electrode with very high resistance d/t which it remains at zero potential thus making a reference point at the center of the heart’s electrical field. The augmented unipolar leads are of low elrctrical potential and are thus instrumentally augmented. Chest leads are near the heart (on the chest wall) so no augmentation needed. Augmented leads are perpendicular to limb leads.
- #10 One lead looking at heart @ every 30* interval. Low amplitude complexes are recorded d/t more body fat. V1 + V2 = septum + Post. Wall(-ve deflections) V3 + V4 = Ant. Wall V5 + V6 = Lat. Wall
- #11 I, II, AVL = left lateral III, AVF = Inferior AVR = Rt atrium
- #13 Slightly peaked P waves (< 3mm in height is normal if ≤ 6 months) Slightly long QTc (≤ 490ms in infants ≤ 6 months) Q waves in the inferior and left precordial leads.
- #14 At birth, the right ventricle is larger and thicker than the left ventricle, reflecting the greater physiological stresses placed upon it in utero (i.e. pumping blood through the relatively high-resistance pulmonary circulation). This produces an ECG picture reminiscent of right ventricular hypertrophy in the adult: marked rightward axis, dominant R wave in V1 and T-wave inversions in V1-3. Conduction intervals (PR interval, QRS duration) are shorter than adults due to the smaller cardiac size.
- #20 Signal with amplitude of 1mV moves the recording stylus vertically by 1cm. 0.1 mV=1mm=1 small square. ECG paper moves @ 25 mm/sec. 1 min is represented on ECG Paper by 25* 60= 1500 mm 1 large square= 0.2 sec 5 large squares/sec & 300 large squares/min. Each RR Interval represents 1 cardiac cycle.
- #21 All intervals in ECG contain some waves, whereas segments do not!
- #28 In supraventricular rhythms, the wave of depolarisation spreads to ventricles via normal way i.e BOH so narrow QRS. In ventricular rhythms, the wave of depolarisation spreads through the ventricles by abnormal slower pathway through purkinje fibres so broad QRS.
- #40 Accelerated junctional rhythm (AJR) occurs when the rate of an AV junctional pacemaker exceeds that of the sinus node. This situation arises when there is increased automaticity in the AV node coupled with decreased automaticity in the sinus node. Digoxin toxicity (= the classic cause of AJR) Beta-agonists, e.g. isoprenaline, adrenaline Myocardial ischaemia Myocarditis Cardiac surgery Junctional rhythms are arbitrarily classified by their rate: Junctional Escape Rhythm: 40-60 bpm Accelerated Junctional Rhythm: 60-100 bpm Junctional Tachycardia: > 100 bpm They may also be classified by aetiology: Automatic Junctional Rhythms (e.g. AJR) = Due to enhanced automaticity in AV nodal cells Re-entrant Junctional Rhythms (e.g. AVNRT) = Due to re-entrant loop involving AV node Narrow complex rhythm; QRS duration < 120ms (unless pre-existing bundle branch block or rate-related aberrant conduction). Ventricular rate usually 60 – 100 bpm. Retrograde P waves may be present and can appear before, during or after the QRS complex. Retrograde P waves are usually inverted in the inferior leads (II, III, aVF), upright in aVR + V1. AV dissociation may be present with the ventricular rate usually greater than the atrial rate. There may be associated ECG features of digoxin effect or digoxin toxicity. Rapid AJR may be difficult to distinguish from re-entrant junctional tachycardias such as AVNRT or AVRT. Irregularity of rhythm and heart-rate variability are suggestive of automatic junctional tachycardia. Automatic junctional tachycardia is typically non-responsive to vagal manoeuvres — there may be some transient slowing of the ventricular rate but reversion to sinus rhythm will not occur. AJR with aberrant conduction may be difficult to distinguish from accelerated idioventricular rhythm. The presence of fusion or capture beats indicates a ventricular rather than junctional focus. This occurs when the site below the SA node usurps control from the SA node by accelerating its own automaticity, or because the SA node abdicates its role by decreasing its automaticity. The conduction to the SA node is retrograde while to the AV node it is in an antegrade fashion.
- #43 QR FIRST INCREASES THEN DECREASES.
- #45 1*=One p wave per qrs complex.PR interval prolonged. 2*=Progressive PR Prolongation ultimately following with faliure of conduction of atrial beat.recovery with a conducted beat with shorter PR interval in a cyclical pattern. 3*=PR interval is constant in each beat, but some beats don’t get through. 4*=No relationship between p and qrs.atria and ventricles beat at their own rate independently.
- #49 S1Q3T3= Deep S in lead 1,presence of q wave in LEAD 3, T wave inversion in lead 3
- #50 A superior QRS axis is present when the S wave is greater than the R wave in aVF. It includes the left anterior hemiblock (in the range of −30 degrees to −90 degrees) and extreme RAD(LAD-with the QRS axis less than the lower limits of normal) (RAD-with the QRS axis greater than the upper limits of normal)
- #51 The P wave in V1 is often biphasic. Morris index= depth*width >0.04mm-sec indicates left atrial enlargement.
- #52 RSr in V1= RBBB, M PATTERN in V5/V6=LBBB
- #53 (with dominant S waves in right precordial leads and dominant R waves in left precordial leads),
- #54 R-wave progression: Generally a normal increase in R-wave size and decrease in S-wave size from leads V1 to V6 (with dominant S waves in right precordial leads and dominant R waves in left precordial leads), representing dominance of left ventricular forces.
- #57 R Wave prominence >7mm in V1 is a significant change for Rt. Ventricle.
- #58 R Wave in V5/V6 >25 mm S wave depth (in V1) + R wave height (in V5/V6) >35 mm
- #63 Short pr interval <0.12sec d/t bypassing AVN by fast conducting accessory pathway presence of delta wave(slurring on the upstroke of r wave) Broad qrs= wpw (BUNDLE OF KENT joining atria to ventricles) depolarisation of venticles is not simultaneous.so slurring of upstroke of r and broadening of qrs seen. Normal qrs = lown ganong levine syndrome ( JAMES PATHWAY joining atria to bundle of his) PR SHORTENING=DIASTOLIC DYSFUNCTION=PULMONARY CONGESTION IMMEDIATELY AFTER SVT.
- #64 The lower limits of normal PR interval are as follows: (a) <3 years, 0.08 seconds (b) 3–16 years, 0.1 seconds (c) >16 years, 0.12 seconds PR interval Infants and younger children : approx 100 milliseconds Childhood to normal adults : approx 150 milliseconds QRS duration Infants and young children : 50 to 80 milliseconds Childhood to normal adults : 80 to 100 milliseconds QTc Infants younger than 6 months : upto 490 milliseconds More than 6 months : 440 milliseconds
- #66 (average 3 measurements taken from same lead)a familial cause of sudden death by ventricular tachycardia The duration of the Q-T interval varies with the cardiac rate; a corrected Q-T interval (Q-Tc) can be calculated by dividing the measured Q-T interval by the square root of the preceding R-R interval.
- #67 J depression is a shift of the junction between the QRS complex and the ST segment (J point) without sustained ST segment Depression.J POINT IS ELEVATED IN HYPOTHERMIA,HYPOTHYROIDISM. In early repolarization, all leads with upright T waves have elevated ST segments, and leads with inverted T waves have depressed ST segments. This condition, seen in healthy adolescents and young adults, resembles the ST segment shift seen in acute pericarditis; in the former, the ST segment is stable, and in the latter, the ST segment returns to the isoelectric line.
- #68 Pathologic ST segment shift. Abnormal shifts of the ST segment often are accompanied by T wave inversion. A pathologic ST segment shift assumes one of the following forms. • Downward slant followed by a diphasic or inverted T wave (see Fig. 2-20, B). • Horizontal elevation or depression sustained for >0.08 seconds (see Fig. 2-20, C). Examples of pathologic ST segment shifts and T wave changes include LVH or RVH with strain; digitalis effects; pericarditis; myocarditis; and myocardial infarction
- #69 (more than 5mm in limb leads and >15 mm in chest lead)
- #70 In severe ventricular hypertrophy with relative ischemia of the hypertrophied myocardium, the T axis changes. In the presence of criteria of ventricular hypertrophy, a wide QRS-T angle (90 degrees or greater) with the T axis outside the normal range indicates a strain pattern. When the T axis remains in the normal quadrant (0 to +90 degrees), a wide QRS-T angle indicates a possible strain pattern
- #71 Hypokalemia = Prolongation of the PR interval T wave flattening and inversion ST depression Prominent U waves (best seen in the precordial leads)