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ECG: Indication and Interpretation
The document provides information about electrocardiography (EKG/ECG). It describes the conduction system of the heart and how electrical signals are conducted to trigger heart contractions. It explains how an EKG works, including electrode placement and what different parts of the EKG waveform represent. It also covers how to interpret an EKG, such as measuring heart rate and identifying abnormalities. Common abnormalities, their causes, and clinical significance are discussed.
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ECG: Indication and Interpretation
- 1. Guide Dr. J. SinghMadam Rakesh Verma
- 2. The electrocardiogram(EKG) is a graphical representation of the electrical events of the cardiac cycle. 1895 - William Einthoven, credited for the invention of EKG 1924 - William Einthoven got the Noble prize for the same
- 5. SA nodeis the pacemaker where the electrical impulse is generated. Located along the posterior wall of the right atrium right beneath the opening of the SVC. It is crescent shaped and about 3 mm wide and 1 cm long. The impulse travels from the SA node through the internodal pathways to the atrioventricular node (AV node).
- 6. The AVnode is responsible for conduction of the impulse from the atria to the ventricles. The impulse is delayed slightly at this point to allow complete emptying of the atria before the ventricles contract. The impulse continues through the AV bundle and down the left and right bundle branches of the Purkinje fibers.
- 7. The Purkinje fibersconduct the impulse to all parts of the ventricles
- 8. Turn onmachine Calibrate to 10mm/ mV Rate at 25mm/ s Record and print Label the tracing - Name, DOB, Hospital number, date and time
- 9. 10 electrodesin total are placed on the patient The 10 leads are lubricated with jelly then placed over the respective sites
- 13. Chest leadsare labelled “V”(vector) and are numbered from 1 to 6. The placement of these electrodes needs to be exact to give the optimum information.
- 14. V1 fourthintercostal space, right sternal edge V2 fourth intercostal space, left sternal edge V4 at the apex (fifth ICS mid clavicular line) V3 midway between V2 and V4 V5 same level as V4 but on the anterior axillary line V6 same level as V4 and V5 but on the mid mid-axillary line
- 15. Electrical impulse(wave of depolarisation) picked up by placing electrodes on patient The voltage change is sensed by measuring the current change across 2 electrodes – a positive electrode and a negative electrode If the electrical impulse travels towards the positive electrode this results in a positive deflection If the impulse travels away from the positive electrode this results in a negative deflection
- 16. P wave:Activation (depolarization) of the right and left atria QRS complex: right and left ventricular depolarization T wave: ventricular repolarization
- 17. PR interval:time interval from onset of atrial depolarization (P wave) to onset of ventricular depolarization (QRS complex) QRS duration: duration of ventricular muscle depolarization QT interval: duration of ventricular depolarization and repolarization RR interval: duration of ventricular cardiac cycle (an indicator of ventricular rate) PP interval: duration of atrial cycle (an indicator of atrial rate)
- 18. Symtoms Palpitation,cyanosis, chest pain, syncope, seizure, poisoning Signs tachycardia, bradycardia, hypothermia, murmur, Shock Evaluation of rheumatic heart disease, congenital heart diseases Evaluation of suspected electrolyte imbalance Evaluation of cases like drowning, electrocution During cardiopulmonary resuscitation (CPR). Evaluation of patients with implanted defibrillators and pacemakers To detect myocardial injury, ischemia, and the presence of prior infarction as well. Effects and side effects of pharmacotherapy Evaluation of metabolic disorders processes among others. Contraindications No absolute contraindications patient refusal, exist. patients allergies to adhesive used to affix the leads
- 20. Limb leads PolesE.g. Bipolar Positive and negative poles I, II, III Unipolar Positive and zero poles aVL, aVR, aVF, chest leads
- 24.
- 25. Horizontally ◦ Onesmall box - 0.04 s ◦ One large box - 0.20 s Vertically ◦ One large box - 0.5 mV ◦ 25mm = 1s
- 26. Height 10mm= 1mV Half standardisation 5mm=1mV One fourth standardisation 2.5mm= 1mV (only amplitude is changed not speed) Paper speed = 25mm/ s 25 mm (25 small squares / 5 large squares) equals one second
- 27. If the heartrate is regular Count the number of large squares between R waves i. e. the RR interval in large squares Rate = 300/RR(no. of large boxes) = 1500/RR(no. of small boxes)
- 28. If therhythm is irregular it may be better to estimate the rate using the rhythm strip at the bottom of the ECG (usually lead II) The rhythm strip is usually 25cm long (250mm i. e. 10 seconds) Count the number of R waves on that strip and multiple by 6 you will get the rate Heart rate Regular slow 300/RR (large square) Regular fast 1500/RR (small square) Irregular R wave in rhythm strip X 6
- 29. New born110-150/min 2year 85-125/min 4year 75-125/min 6year 65-100/min > 6 year 60-100/min Tachycardia Sinus tachcardia Supraventrical Ventricular Atrial flutter and fibrillation Bradycardia Sinus bradycardia Heart block
- 30. Normal rhythmmust have a P wave before each QRS complex The easiest way to tell is to take a sheet of paper and line up one edge with the tips of the R waves on the rhythm strip. Mark off on the paper the positions of 3 or 4 R wave tips Move the paper along the rhythm strip so that your first mark lines up with another R wave tip See if the subsequent R wave tips line up with the subsequent marks on your paper If they do line up, the rhythm is regular. If not, the rhythm is irregular
- 31. Absent Pwave – indicate non sinus rhythm SA block AV rhythm (may be present) Atrial fibrillation Idioventricular rhythm Multiple P waves ◦ Atrial flutter ◦ Atrial fibrillation ◦ 2nd ar 3rd degree block Changing P wave shape ◦ Wandering atrial pacemaker
- 33. The axis isthe overall direction of the cardiac impulse or wave of depolarisation of the heart An abnormal axis (axis deviation) can give a clue to possible pathology
- 35.
- 36. Lead I LeadaVF Mean axis
- 38.
- 41. Lead (mm) = R-Samplitude Lead I = 4-0 = 4mm Lead aVF = 13-2 = 11mm Lead I Lead aVF Mean axis
- 42. Lead I Lead aVF LeadI = 5+ (-10)= -5mm Lead aVF = 17-4 = 13mm
- 43. Right AxisDeviation - Right ventricular hypertrophy, Anterolateral MI, Left Posterior Hemi-block, COPD, pulmonary arterial hypertension or large pulmonary embolism Left Axis Deviation- Ventricular tachycardia, Left ventricular hypertrophy, Left Anterior hemi-block Wolff-Parkinson-White syndrome can cause both Left and Right axis deviation
- 44. Normal values 1. upin all leads except aVR. 2. Duration. < 2.5 mm. 3. Amplitude. < 2.5 mm. Abnormalities 1. Inverted P-wave Junctional rhythm. 2. Wide P-wave (P- mitrale) LAE 3. Peaked P-wave (P- pulmonale) RAE 4. Saw-tooth appearance Atrial flutter 5. Absent normal P wave Atrial fibrillation
- 53. Definition: the time intervalbetween beginning of P- wave to beginning of QRS complex. Normal PR interval <3yrs – 0.08sec 3-16 yrs – 0.10sec >16 – 0.12sec Abnormalities 1. Short PR interval WPW syndrome 2. Long PR interval First degree heart block
- 55.
- 56. If thePR interval is constant with a missed QRS complex: 2nd degree heart block, Mobitz type II, each QRS followed after P wave If there is no relationship between the P waves and the QRS complexes: 3rd degree heart block Block Relation Electrical origin 1st degree Each P has QRS SA node 2nd degree Each QRS has P SA node 3rddegree No Relation Fasciular,Ventricular, or other
- 59. Q waves<0.04 second. That’s is less than one small square duration. Present commonly in I,II,III,aVF, and always present in V5 and V6 (lateral leads) Absent in V1 Height < 1/4 of R wave height.
- 62. The widthof the QRS complex should be less than 0.12 seconds (3 small squares) Height of R wave is (V1-V6) >8 mm in at least one of chest leads. Morphology: progression from Short R and deep S (rS) in V1 to tall R and short S in V6 (qRs).
- 63. New born+125 1 month +90 3 years +60 Adult +50 Preterm 0.04s Full term 0.0.5s 1 -3yrs 0.06s >3 years 0.07s Adult 0.08s
- 64. LAD ◦ LVH ◦LBBB ◦ Left anterior hemiblock RAD ◦ RVH ◦ RBBB Superiorly oriented axis ◦ Left anterior hemiblock, particularly with endocardial cushion defect ◦ RBBB Bundle branch block Preexication (WPW) Intraventricular block Idioventricular rhythm Ventricular implanted pacemaker
- 65. Abnormally large deflections(positive or negative) ◦ Ventricular hypertrophy ◦ Ventricular conduction defects like - BBB, preexication,artificial ventricular pacemaker Low voltage complex – limb lead less than 5mm ◦ Myocarditis ◦ Pericardial effusion ◦ Hypothyroidism ◦ Pericarditis
- 67. Right axisdeviation of +110° or more. Dominant R wave in V1 Dominant S wave in V5 or V6 Right atrial enlargement (P pulmonale). Right ventricular strain pattern = ST depression / T wave inversion in the right precordial (V1-4) and inferior (II, III, aVF) leads.
- 69. Left axisdeviation Increased R wave amplitude in the left-sided ECG leads (I, aVL and V4-6) and Increased S wave depth in the right-sided leads (III, aVR, V1-3). The thickened LV wall leads to prolonged depolarisation and delayed repolarisation (ST and T-wave abnormalities) in the lateral leads. Left atrial enlargement (P mitrale). Left ventricular strain pattern = ST depression / T wave inversion in the lateral (I, aVL,V5-V6) leads.
- 71. In RBBB, activationof the right ventricle is delayed as depolarisation has to spread across the septum from the left ventricle. The left ventricle is activated normally, meaning that the early part of the QRS complex is unchanged. The delayed right ventricular activation produces a secondary R wave (R’) in the right precordial leads (V1-3) and a wide, slurred S wave in the lateral leads (V5-6) Delayed activation of the right ventricle also gives rise to secondary repolarization abnormalities, with ST depression and T wave inversion in the right precordial leads (V1-3) QRS duration ≥ 120ms rSR’ pattern or notched R wave in V1-3 along with T wave inversion Wide S wave in I and V6
- 74. Normally theseptum is activated from left to right, producing small Q waves in the lateral leads. In LBBB, the normal direction of septal depolarisation is reversed (becomes right to left), as the impulse spreads first to the RV to the LV via the septum. Eliminates the normal septal Q waves in the lateral leads. . The overall direction of depolarisation (from right to left) produces tall R waves in the lateral leads (I, V5-6) and deep S waves in the right precordial leads (V1-3) As the ventricles are activated sequentially (right, then left) rather than simultaneously, this produces a broad or notched (‘M’-shaped) R wave in the lateral leads. QRS duration ≥ 120ms Broad R wave in I, aVL, and V5-6 Prominent QS wave in V1-3 Absence of q waves (including physiologic q waves) in I and V6
- 77. The STsegment should sit on the isoelectric line (at least in the begining) It is abnormal if there is planar (i.e. flat) elevation or depression of the ST segment
- 78. 1. ST elevation: Morethan one small square Infarcts Angina. Acute pericarditis. Early repolarization ST depression: More than one small square Ischemia. Ventricular strain. BBB. Hypokalemia. Digoxin effect.
- 80.
- 81. T waveis best measured in left precordial leads In V5 <1yr 11mm >1yr 14mm Abnormalities: 1. Peaked T-wave: Posterior wall MI. Hyperkalemia. . 2. T- inversion: Ischemia. Myocardial infarction. Myocarditis Ventricular strain BBB. Hypokalemia. Digoxin effect.
- 84. The normalrange for QT is 0.38-0.42 (≤ 11mm ) Definition: Time interval between beginning of QRS complex to the end of T wave. QT interval varies with heart rate - As the heart rate gets faster, the QT interval gets shorter It is possible to correct the QT interval with respect to rate by using the following formula: Bazzet’s formula QTc = QT/ √RR (QTc = corrected QT)
- 85. Long QTc– causes ◦ Drugs – procanamide, quinidine ◦ Hypocalcemia, ◦ hypomagnesemia, ◦ hypokalemia ◦ Hypothermia ◦ AMI ◦ Congenital Jerwell and Lange-Neilsen syndrome Romano- Ward syndrome Short QT interval: hypercalcemia, digitalis Abnormalities:
- 87. U wavesoccur after the T wave and are often difficult to see They are thought to be due to repolarisation of the atrial septum Prominent U waves can be a sign of hypokalaemia
- 88.