Lp 03 - ECG in Chamber Enlargement

ECG in chamber enlargements

ECG in chamber enlargementsAtrial EnlargementsCan be caused by: volume-overload (e.g. mitral/tricuspid valve insufficiency) pressure overload (e.g. mitral/tricuspid valve stenosis)

Right Atrial Enlargement (RAE)Etiology: stenosis/ insufficiency of the tricuspid valve; increased pressure in RV; RV failure.

Atrial depolarization: the RA has a larger mass, determines a larger depolarization vector, and the resultant atrial vector is moved downwards (verticalized) or even towards right. The depolarization time of RA is increased, but usually it doesnt increase the total atrial depolarization time (because the left atrium starts to activate later).Right Atrial Enlargement (RAE)On ECG: normal duration of P wave.In frontal plane: Tall P wave in inferior leads (DII, aVF, DIII), with amplitude > 2.5 mm in at least one of these 3 leads; this aspect = P pulmonale P wave axis is deviated downward (around +90). (Sometimes it is even deviated towards right).In horizontal plane: In V1 and/or V2 the first component of the P wave, the positive one, is taller; it is significant for diagnosis is P wave is taller than 2 mm in V1 or V2.

Left Atrial Enlargement (LAE)

Etiology: stenosis (e.g. post-rheumatic), regurgitation of the mitral valve; increased pressure in LV; LV failure.

Atrial depolarization:Normal RA depolarization. LAE generates a larger vector => the global depolarization vector is more horizontal than normal (the electrical axis of atrial depolarization is deviated towards left); also it needs more time for depolarization and because the LA begins its depolarization after the right atrium this determines a longer global atrial depolarization time.

Left Atrial Enlargement (LAE)On ECG: A larger duration of P wave: P wave 0.12

In frontal plane: P wave is positive and bifid in DI, aVL, DII. This aspect and the P wave duration 0.12 = P mitraleP wave axis is oriented towards 0.In horizontal plane:In V1 and/or V2 the second part of the biphasic P wave, the negative one, is larger than the first positive one; it is significant for diagnosis if the negative phase of the P wave has a duration 0.04 and amplitude > 1mm.In V5 and V6 it is a similar aspect with DI.

***In biatrial chamber enlargement the ECG will feature characteristics of LAE in frontal plane and RAE in horizontal plane.Ventricular Enlargements

Can be caused by:pressure overloads (e.g. aortic stenosis); volume overloads usually dilations (eventually) occurs (e.g. aortic regurgitation). primary/secondary cardiomyopathies associated either with hypertrophy, either with dilation.

Left Ventricular Enlargement (Left Ventricular Hypertrophy = LVH)Etiology: aortic stenosis/ insufficiency, mitral regurgitation, high systemic arterial blood pressure.Ventricular depolarization: The LV depolarization vectors are larger than normal. Because there is more LV mass, the depolarization time of the LV (and the total ventricular depolarization time) can be increased.Ventricular repolarization: can be also affected: if the stimulus has a long way from subendocardial to subepicardial cells, the subendocardial cells have the opportunity to repolarize first so the repolarization vector is inverted.

Left Ventricular Hypertrophy = LVHOn ECG: the most important criteria are the voltage criteria; Voltage criteria: In frontal plane:R in aVL > 13 mmWhite-Block index = R in DI + S in DIII - (S in DI + R in DIII) > +17 mmIn horizontal plane: R in V5 or V6 > 25 mmS in V1 or V2 > 25 mmS in V1 + R in V5/V6 > 35 mm (Sokolov-Lyon index)Left Ventricular Hypertrophy = LVHOther criteria: Left QRS axis deviation (usually around -30)QRS duration 0.10 - 0.12 sec.Delayed intrinsicoid deflection > 0.05 sec. in V5, V6 Secondary repolarization changes: depressed ST segment (but with J point on isoelectric line) and negative, asymmetrical T waves in left leads, where the QRS complex is predominantly positive.LA enlargement.The Romhilt-Estes point score system ("diagnostic" >5 points; "probable" 4 points):ECG CriteriaPointsS in V1 or V2 25 (30)mm or R in V5 or V6 25 (30)mm3ST-T vector opposite to QRS in V5, V6, D1, aVL3P mitrale3Left axis deviation (QRS of -30 or more)2QRS duration >0.10 sec1Delayed intrinsecoid deflection in V5 or V6 (>0.05 sec)1Left Ventricular Hypertrophy = LVH

Left Ventricular Hypertrophy = LVHDD:LBBB (left bundle branch block)Left anterior fascicular blockAnterior MIWPW syndrome type BLeft positional axis without cardiac pathologies (horizontalised heart)

** In V1 the QRS aspect can be QS

Repolarization changes:

In ventricular hypertrophies, intraventricular conduction blocks, WPW syndrome secondary to the depolarization abnormalities there can be present repolarization changes; they are called secondary repolarization changes. Typically secondary repolarization changes are: ST and T are opposed to QRS (= where QRS complex is predominantly positive, ST is depressed and T is negative); j point is isoelectric; the depressed ST is descending; T wave is asymmetrical.We name ECG primary repolarization changes those that appear as a result as a primary repolarization abnormality : ST depression or elevation, and T symmetrical negative or positive (as it happens in ischemic heart disease: the earliest affected are the repolarization processes).Sometimes the patient has multiple cardiac modifications: e.g. LVH and ischemic heart disease; and the changes of repolarization are so-called mixed repolarization changes.Right Ventricular Enlargement (Right Ventricular Hypertrophy = RVH)Etiology: pulmonary hypertension primary/secondary (e.g. long-standing mitral stenosis with narrow orifice); tricuspid regurgitation, stenosis of pulmonary artery; congenital heart defects; cardiomyopathies.

Ventricular depolarization: larger RV vectors that counterbalance the left normal ones; usually the enlarged mass of RV is smaller than the normal mass of left ventricle, so although the depolarization time for RV is longer, the total ventricular depolarization time is normal.

Ventricular repolarization can be affected secondary to depolarization disturbances: secondary modifications of ST-T.

Right Ventricular Hypertrophy = RVHVoltage criteria (can be present 1 criterion or more):

In frontal plane: White-Block index = R in DI + S in DIII - (S in DI + R in DIII) < - 14 mm

Horizontal plane: R in V1 > 7 mmR in V1 + S in V5 or V6 > 11 mm (Sokolov-Lyon index)R/S ratio > 1 in V1 and/or V2R/S ratio < 1 in V5 and/or V6

Right Ventricular Hypertrophy = RVHOther criteria: if there are present, they are additional criteria for diagnosis; but their absence doesnt exclude the LVH diagnosis based on voltage criteria!Right QRS electrical axis deviation between 90and 150TIDI 0.04 sec in V1 and/or V2Secondary repolarization changes. (ST and T wave in opposition to QRS complex).P pulmonaleRight Ventricular Hypertrophy = RVHDD: Left posterior fascicular blockPosterior wall MIWPW syndrome type A

**Usually QRS duration is normal.

Right Ventricular Hypertrophy = RVH

Cor Pulmonale= alteration in structure and function of the RV secondary to a respiratory disease/affliction that determines an increase in the pressure in pulmonary circulatory system.Cor pulmonale can be acute (e.g. in pulmonary thromboembolism = PTE) or chronic (e.g. in COPD).In cor pulmonale some aspects of ECG can be suggestive, but arent highly specific or sensitive:S1Q3T3 pattern = deeper S wave in DI, q wave in DIII, negative T wave in DIII (+/- ST segment slightly elevated in DIII) DD with inferior MIT wave inversion (= negative T waves) in anterior precordial leadsRV overload, incomplete/complete RBBB, RA overloadSinusal tachycardia; other arrhythmias.Right/extreme right axis deviation for QRS electrical axisS1S2S3 pattern = preeminent S waves in DI, DII, DIIIOther repolarization changes: nonspecific ST-T changes; ST elevation in DIII, aVF, V1