Electrocardiography

ElectrocardiographySaeed Oraii MD, CardiologistInterventional ElectrophysiologistTehran Arrhythmia Clinic

Tehran Arrhythmia Center

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ECGA graphic recording of electrical potentials generated by the heart

A noninvasive, inexpensive and highly versatile test


Normal Pathway of Electrical Conduction


Normal Impulse ConductionSinoatrial node

AV node

Bundle of His

Bundle Branches

Purkinje fibers


Cardiac Action Potential


Cardiac action potentials from different locations have different shapes


ElectrophysiologyElectric currents that spread through the heart are produced by three componentsCardiac pacemaker cellsSpecialized conduction tissueThe heart muscleECG only records the depolarization and repolarization potentials generated by atrial and ventricular myocardium.


Electrocardiograph 1903


Normal Electrocardiogram


ECG WaveformsLabeled alphabetically beginning with the P waveTehran Arrhythmia Center


The PQRSTP wave - Atrial depolarization T wave - Ventricular repolarization QRS - Ventricular depolarization


QRS-T Cycle Corresponds to Different Phases of Ventricular Action Potential


The PR IntervalAtrial depolarization +delay in AV junction (AV node/Bundle of His)

(delay allows time for the atria to contract before the ventricles contract)


Impulse Conduction & the ECGSinoatrial node

AV node

Bundle of His

Bundle Branches

Purkinje fibers


Limb Leads


Precordial Leads


Position of Precordial Electrodes


Precordial Leads


3-D Representation of Cardiac Electrical Activity


Vector ConceptCardiac depolarization and repolarization waves have direction and magnitude.They can, therefore, be represented by vectors.ECG records the complex spatial and temporal summation of electrical potentials from multiple myocardial fibers conducted to the surface of the body.


Limb Leads Directions


Vector Concept


Ventricular DepolarizationSeptal q wave


QRS Axis


Determination of QRS Axis


Direction of Propagation


Determination of QRS Axis


Main Vector


Normal QRS Axis


Left Axis Deviation


Right Axis Deviation


Timing Intervals


The ECG PaperHorizontallyOne small box - 0.04 sOne large box - 0.20 s VerticallyOne large box - 0.5 mV


The ECG PaperEvery 3 seconds (15 large boxes) is marked by a vertical line.This helps when calculating the heart rate.3 sec3 sec


Major ECG AbnormalitiesTehran Arrhythmia Center


Right Atrial EnlargementP Pulmonale, Amplitude 2.5 mm


Right Atrial EnlargementThe P waves are tall, especially in leads II, III and avF.


Right Atrial EnlargementTo diagnose RAE you can use the following criteria:IIP > 2.5 mm, orV1 or V2P > 1.5 mmRemember 1 small box in height = 1 mmA cause of RAE is RVH from pulmonary hypertension, hence P Pulmonale.> 2 boxes (in height)> 1 boxes (in height)


Left Atrial EnlargementP Mitrale, Duration 120 ms


Left Atrial EnlargementThe P waves in lead II are notched and in lead V1 they have a deep and wide negative component.


Left Atrial EnlargementTo diagnose LAE you can use the following criteria:II> 0.04 s (1 box) between notched peaks, orV1Neg. deflection > 1 box wide x 1 box deepNormalLAEA common cause of LAE has been Mitral Stenosis, hence P Mitrale.


Left Ventricular HypertrophyWhy is left ventricular hypertrophy characterized by tall QRS complexes?LVHEchocardiogramAs the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage.


Left Ventricular Hypertrophy


Left Ventricular HypertrophyCompare these two 12-lead ECGs. What stands out as different with the second one?NormalLeft Ventricular HypertrophyAnswer:The QRS complexes are very tall (increased voltage)


Left Ventricular HypertrophyCriteria exists to diagnose LVH using a 12-lead ECG. For example:The R wave in V5 or V6 plus the S wave in V1 or V2 exceeds 35 mm.


Right Ventricular Hypertrophy


Right Ventricular Hypertrophy

Compare the R waves in V1, V2 from a normal ECG and one from a person with RVH.Notice the R wave is normally small in V1, V2 because the right ventricle does not have a lot of muscle mass.But in the hypertrophied right ventricle the R wave is tall in V1, V2.NormalRVH


Right Ventricular Hypertrophy To diagnose RVH you can use the following criteria:Right axis deviation, andV1R wave > 7mm tall


RVH, RA enlargement


Bundle Branch BlocksWith Bundle Branch Blocks you will see two changes on the ECG.QRS complex widens (> 0.12 sec). QRS morphology changes (varies depending on ECG lead, and if it is a right vs. left bundle branch block).


Bundle Branch BlocksWhy does the QRS complex widen?When the conduction pathway is blocked it will take longer for the electrical signal to pass throughout the ventricles.


Left Bundle Branch Block


Right Bundle Branch Block


Right Bundle Branch BlocksWhat QRS morphology is characteristic?For RBBB the wide QRS complex assumes a unique, virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2). Rabbit Ears


RBBB


RBBB, RAD (Bifascicular Block)


RBBB, LAD (Bifascicular Block)


Myocardial IschemiaECG is the cornerstone in the diagnosis of myocardial ischemiaFindings depend on several factors:Nature of the process, reversible vs. irreversibleDuration, acute vs. chronicExtent, transmural vs. subendocardialLocalization, anterior vs. inferoposteriorOther underlying abnormalities


Evolution of a Myocardial InfarctionWhen myocardial blood supply is abruptly reduced or cut off to a region of the heart, a sequence of injurious events occur beginning with ischemia (inadequate tissue perfusion), followed by necrosis (infarction), and eventual fibrosis (scarring) if the blood supply isn't restored in an appropriate period of time.

The ECG changes over time with each of these events


ST Elevation InfarctionPeaked T-waves, then T-wave inversion, ST depression, The ECG changes seen with a ST elevation infarction are:Before injuryNormal ECGST elevation & appearance of Q-waves ST segments and T-waves return to normal, but Q-waves persist


Acute Ischemia


ST ElevationA great way to diagnose an acute MI is to look for elevation of the ST segment.


ECG ChangesWays the ECG can change include:


ST ElevationElevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction.


ST Elevation InfarctionA. Normal ECG prior to MI

B. Ischemia from coronary artery occlusion results in ST depression (not shown) and peaked T-waves

C. Infarction from ongoing ischemia results in marked ST elevation

D/E. Ongoing infarction with appearance of pathologic Q-waves and T-wave inversion

F. Fibrosis (months later) with persistent Q- waves, but normal ST segment and T- waves Evolving infarction:


Views of the HeartSome leads get a good view of the:

Anterior portion of the heartLateral portion of the heartInferior portion of the heart


Anterior MIRemember the anterior portion of the heart is best viewed using leads V1- V4.Limb LeadsAugmented LeadsPrecordial Leads


Lateral MIThe lateral portion of the heart is best viewed by: Limb LeadsAugmented LeadsPrecordial LeadsLeads I, aVL, and V5- V6


Inferior MIThe inferior portion of the heart by: Limb LeadsAugmented LeadsPrecordial LeadsLeads II, III and aVF


Inferior Wall MINote the ST elevation in leads II, III and aVF.


Anterolateral MIThis persons MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6, I, and aVL)!


Myocardial Infarction


Non-ST Elevation MIThere are two distinct patterns of ECG change depending if the infarction is:

ST Elevation (Transmural or Q-wave), or Non-ST Elevation (Subendocardial or non-Q-wave)Non-ST ElevationST Elevation


Non-ST Elevation InfarctionNote the ST depression and T-wave inversion in leads V2-V6.

ECG of an evolving non-ST elevation MI:Question: What area of the heart is infarcting?Cannot say!


Acute Pericarditis


Metabolic Abnormalities


Hyper-kalemia K 6.9


Same patient

K 3.9


Hypothermia, Osborn Wave


Hypothermia, Corrected


Right Axis Deviation (Left Posterior Hemiblock)Tehran Arrhythmia Center


Anterior MITehran Arrhythmia Center


RBBB and Inferior MITehran Arrhythmia Center


LA Enlargement and Prolonged PR IntervalTehran Arrhythmia Center


LBBBTehran Arrhythmia Center


Acute Inferior MITehran Arrhythmia Center


Left Anterior Hemiblock, Prolonged PR intervalTehran Arrhythmia Center


LVH and LA EnlargementTehran Arrhythmia Center


Anterior MITehran Arrhythmia Center


Old Inferior MI and Atrial FibrillationTehran Arrhythmia Center


RA EnlargementTehran Arrhythmia Center


RBBB, LAH, Prolonged PR (Trifascicular Block)Tehran Arrhythmia Center


Tehran Arrhythmia [email protected]


Atria and ventricles can be considered as two distinct syncitia as the cells are closely connected to each other. The two syncitia are separated by an insulated barrier that consists of the valves and central fibrous trigone. No impulse can normally pass this barrier except through the penetrating bundle of His. Left bundle branch is divided into left anterior and left posterior fascicles and possibly a septal fascicle. Sinus node and AV nodal cells depolarize mainly through activation of slow Ca channels. So the upstroke of the phase 0 of action potential is less steep.PR interval is normally 120-200 ms. QRS duration is normally 100 ms or less. QT interval varies inversely with heart rate and should be corrected by rate. It is normally 440 ms or less. U wave is a small rounded deflection that is sometimes recorded after the T wave, usually with the same polarity as T wave. An abnormal increase in U wave amplitude is most commonly due to drugs or electrolyte abnormalities and may indicated susceptibility to ventricular arrhythmias (Torsade de Pointes).QRS wave corresponds to ventricular depolarization and T wave to ventricular repolarization. QT interval includes both ventricular depolarization and repolarization times.I, II and III are bipolar limb leads. VR, VL and VF are unipolar leads. The positive pole of these leads are connected to the corresponding limb and zero pole is created by connecting all the three angles of the Einthoven triangle to negative pole. Unipolar leads aVR, aVL and aVF are simply augmented leads by excluding the corresponding lead from zero pole.Limb leads record electrical signals spread in frontal plane. Precordial leads are created to record signals in transverse plane too.Precordial leads are unipolar leads.One may record the signals from the right side of the chest by positioning the electrodes as mirror images of the left sided electrodes. An R is added to the end of the name of the lead to show that they are recorded from the right side.Limb leads record electrical signals spread in frontal plane. Precordial leads record signals in transverse plane.Each lead has a vector. If the signal is parallel to the vector of that lead, it will record the largest positive signal. If it goes right in the opposite direction, a large negative deflection is recorded. And if the electrical signal goes perpendicular to the vector of the lead it will not record anything i.e. an isoelectric or equiphasic line is depicted.The first part of the ventricles to be depolarized is the left side of interventricular septum. The electrical current goes from the left toward the right side. Therefore a small positive deflection is depicted by right precordial leads (V1 and V2) and a small initial q wave called septal q wave is depicted by left precordial leads (V5 and V6).You may determine an axis for each part of the QRS (instantaneous vector) for example the initial 40 ms of the QRS. A main axis is determined by considering the whole QRS (main vector).Some consider an axis to be normal from -30 degrees to 100 degrees.Heart Rate can be readily calculated by from the interbeat (R-R) interval by dividing the number of large (0.2 s) time units between consecutive R waves into 300 or the number of small (0.04 s) units into 1500.Tall P waves (2.5 mm or more) usually best recorded in inferior leads. Also called P Pulmonale.Broad (120 ms or more) biphasic P waves in inferior leads. Increase terminal negative portion of P wave in V1. Also called P Mitrale. This pattern may also occur with atrial conduction delays without enlargement. Therefore, the more general term left atrial abnormality is frequently used.Tall left precordial R waves and deep right precordial S waves. ST segment depression and T inversion in left precordial leads. Left axis deviation.There are a number of Voltage Criteria for the diagnosis of LVH including (S in V1+ R V5 or R in V 6 equal or more than 35 mm) or ( R in V5 or V6 equal or more than 25 mm).Tall R wave in lead V1 (R larger or equal to S) usually with right axis deviation. ST depression and T inversion in precordial leads.With severe RVH there may be a qR pattern in V1.Broad, bizzare QRS of 120 ms or more in duration. Positive (R) complexes in left precordial leads and negative (QS) complexes in right precordials. ST-T changes.The initial portion of the QRS and the septal q waves are preserved.

Electrocardiography

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