Ventricular Enlargement and Hypertrophy

Objectives:

• LVH
• RVH
• PE

EKG of LVH

Several EKG criteria have been used in the diagnosis of LVH. These include:

CHANGES IN THE PRECORDIAL LEADS

• Abnormalities in the QRS complex
• Increased amplitude or voltage of the QRS complex
• Limb leads
• R wave in any limb lead measuring ≥20 mm
• S wave in any limb lead measuring  ≥20 mm
• R wave in aVL >11 mm
• R in lead I +S in III  >25 mm
• Precordial leads
• S wave in V1 or V2 ≥30 mm
• R wave in V5 or V6 ≥30 mm
• R wave in V5 or V6 >26 mm
• S wave in V1, V2 or V3 ≥25 mm
• R wave in V4, V5 or V6 ≥25 mm
• SV1 + RV5 or V6 > 35 mm
• Tallest S + tallest R in V1 to V6 >45 mm
• R wave in V6 > R wave in V5
• Limb + Precordial leads
• R wave in aVL + S wave in V3 >20 mm in females
• R wave in aVL + S wave in V3  >28 mm in males
• Total QRS voltage from all 12 ECG leads >175 mm
• Increased duration of the QRS complex
• Delayed onset of intrinsicoid deflection ≥ 0.05 seconds in V5 or V6
• Increased duration of the QRS complex ≥ 0.09 seconds

• Abnormalities in the ST segment and T wave
• ST segment depression and T wave inversion in V5 or V6 indicating left ventricular strain

CHANGES IN THE LIMB LEADS

• Abnormalities in P wave
• Terminal negativity of the P wave in V1 measuring ≥1 mm x1 mm

• Left axis deviation
• ≥–30 °
• ≥–15 °

There are many criteria used for diagnosing LVH (which include various combinations of the above points), I am not mentioning them here for now to avoid complicating the learning process. Just know that in LVH:

• increased voltage of QRS complex
• increased duration of QRS complex (prolonged VAT and delayed onset of intrinsicoid deflection)
• LAE
• LAD ≥30°
• ST and T wave changes

Ventricular activation time and intrinsicoid deflection

• VAT
• measured from the onset of the QRS complex to the top of the R wave
• VAT of leads overlying the left ventricle (V5 or V6) is prolonged (>0.05 seconds).
• represents the time it takes for the impulse to activate the myocardium below the recording electrode. The thicker the mycocardium, the longer it takes for the electrical impulse to travel from endocardium to epicardium.
• Intrinsicoid deflection 
• represented by the immediate downward deflection of the R wave toward the baseline
• represents that impulse has reaches the epicardium and is represented by downward deflection of R wave towards the baseline
• onset of intrinsicoid deflection signals that the whole myocardium below the recording electrode has been fully activated
• Because the VAT is prolonged when there is LVH, the onset of intrinsicoid deflection in V5 V6 is also delayed

Abnormalities in the ST segment and T wave

• Pressure overload
• The ECG shows tall R waves in V5 and V6 associated with depression of the ST segment and inversion of the T wave. These ST-T changes are often described as due to left ventricular “strain” 
• Volume overload
• The ECG shows prominent Q waves, tall R waves, and tall and upright T waves in V5 and V6
• LVH associated with Left ventricular strain is more common than LVH from volume overload because hypertension is the most common cause of LVH

Cause of ST segment depression and T wave inversion?

• The ST segment and T wave represent ventricular repolarization corresponding to phases 2 and 3 of the transmembrane action potential, respectively. Normally, when the ventricles are activated, repolarization begins immediately. During phase 2, corresponding to the ST segment, the electrical potential is normally maintained at almost 0 potential for a sustained duration; thus, there is no deflection recorded in the ECG. The T wave is inscribed only when sufficient potential is generated during repolarization corresponding to the downslope or phase 3 of the transmembrane action potential.
• ST depression: When there is LVH, ventricular activation is prolonged. Repolarization begins in some areas of the ventricle even before the whole myocardium is completely depolarized. This allows repolarization to occur relatively earlier than usual, which can reach sufficient magnitude to cause downward deviation of the ST segment in leads with tall R waves.
• T wave inversion: The T wave in LVH is inverted and is opposite in direction to that of the QRS complex. This implies that depolarization and repolarization of the myocardium occur in the same direction, which is the opposite of normal. The prolonged activation time of the thickened left ventricle allows the endocardium to recover earlier, even before the whole thickness of the myocardium is completely depolarized. Thus, repolarization proceeds from endocardium to epicardium, resulting in depression of the ST segment and inversion of the T waves in leads with tall R waves. Additionally, when the left ventricle is thickened, the myocardium may outstrip its normal blood supply even in the absence of occlusive coronary disease. Thus, the whole thickness of the left ventricle becomes relatively ischemic. The endocardium, which is the first to be depolarized, will recover earlier because it had a longer time to recover.

Left atrial enlargement

• LVH is frequently associated with LAE
• When there is LVH, there is increased left ventricular end-diastolic pressure or volume. This will also increase left atrial pressure or volume because the left atrium and left ventricle behave as common chambers when the mitral valve is open during diastole.
• EKG findings of LAE
• The duration of the P wave is increased in leads I, II, or aVF. The P waves are often notched with M shape pattern measuring >2.5 mm in width or >100 milliseconds in duration.
• Terminally inverted P waves in V1 measuring ≥1 mm in depth and ≥1 mm in duration.

Left axis deviation ≥30°

• axis of QRS complex shift more horizontally as the LV mass is increased
• additionally, LVH is frequently associated with LAFB or incomplete LBBB, which shift the axis more markedly to left

EKG of RVH

In adult patients, the thickness of the right ventricle seldom exceeds that of the left ventricle even when RVH is present. Because both ventricles are activated simultaneously, the forces generated by the right ventricle are masked by the forces generated by the left ventricle. Thus, the diagnosis of RVH by ECG may be difficult unless the right ventricle is severely hypertrophied.

CHANGES IN THE PRECORDIAL LEADS

• Abnormalities in the QRS complex
• Right axis deviation of approximately ≥90°. This should always be present before the diagnosis of RVH is considered.
• qR complex in V1
• R wave measuring ≥7 mm in V1
• R wave taller than the S wave in V1 (R/S ratio ≥1)
• Delayed onset of the intrinsicoid deflection in V1 >0.03 seconds
• rS complex from V1 to V6 with right axis deviation
• S1 S2 S3 pattern in adults

• Prolonged ventricular activation time with delayed onset of intrinsicoid deflection in V1 V2
• VAT of the RV normally measures ≤ 0.03 seconds and is increased to ≥ 0.04 seconds when there is RVH
• prolongation of the QRS complex usually does not occur when there is RVH because the thickness of the RV usually does not exceed that of the LV, even when RVH is present.

• Abnormalities in ST segment and T waves
• ST segment depression and T wave inversion in the right-sided precordial leads (V1 and V2)

CHANGES IN THE LIMB LEADS

• Abnormalities in the P wave
• Peaked P waves in leads II, III, and aVF (P-pulmonale)

• Right Axis deviation 
• Right axis deviation of approximately ≥90°. This should always be present before the diagnosis of RVH is considered.

S1S2S3 pattern

• S1 S2 S3 pattern implies that S waves are present in leads I, II, and III. When the S1 S2 S3 pattern is present, the direction of the mean QRS axis is superior and to the right (causing a tall R wave in aVR), away from leads II and aVF. This brings the main axis of the QRS complex to the northwest quadrant. 
• S1 S2 S3 pattern is not specific for RVH because it can occur normally in young children without any evidence of RVH or cardiac disease. In older individuals, this pattern is suggestive of RVH, especially when other signs of RVH such as right atrial enlargement (P-pulmonale) or prominent R waves are present in V1. Additionally, the size of the S waves in leads I, II, and III are usually deeper than the size of the R waves.

rS complex from V1 to V6 with LAD

• This is also called clockwise rotation or delayed transition. Deep S waves or rS complex from V1 to V6 may be due to RVH or LVH. 
• For RVH to be present there should also be right axis deviation. When RVH is present, the right ventricle rotates anteriorly, causing the left ventricle to rotate in a more posterior orientation. If the ventricles are viewed from below looking upward, the rotation of both ventricles will be clockwise when there is right ventricular enlargement. Because the precordial leads are recorded in their standard location from V1 to V6, the transition zone is not crossed unless the electrodes are moved to the left and more posteriorly. 
• This type of RVH is frequently associated with chronic lung disease (type C RVH).

Lead I sign

• When there is chronic obstructive pulmonary disease such as emphysema or chronic bronchitis, the overinflated lungs push the diaphragm downward, causing the heart to become vertically oriented. 
• When this occurs, the axes of the P wave, QRS complex, and T wave are all shifted rightward and inferiorly toward lead aVF (90°), resulting in the so called “lead I sign” (where all the deflections in lead I become conspicuous by their diminutive appearance). Because lead I (0°) is perpendicular to lead aVF, lead I and often V6 will conspicuously show small deflections  because the P, QRS, and T waves become isoelectric in these leads.
• The ventricles also rotate in a clockwise fashion, causing poor R wave progression and delay in the transition zone. 
• EKG changes in COPD is an example of type C RVH

Types of RVH

Type A RVH

• This is the most recognizable type of RVH. The R waves are tall in V1, often in V2 and V3. The R wave is usually monophasic (no S wave) in V1. If an S wave is present, the R wave is always taller than the height of the S wave with an R/S ratio >1. V5 and V6 may show deeper S waves than R waves. 
• In type A RVH, the thickness of the right ventricle is greater than the thickness of the left ventricle, and the right ventricle is the dominant ventricle. 
• Axis: axis of the QRS complex is significantly deviated to the right at approximately +120°
• Seen in: This type of RVH is the most commonly recognized and is seen in severe pulmonic stenosis, primary pulmonary hypertension, or mitral stenosis with severe pulmonary hypertension. 

Type B RVH

• The R wave in V1 is slightly taller than the S wave or the ratio between the R wave and S wave is ≥1. V1 may also exhibit an rsr’ pattern. The QRS complex in V5 and V6 is not different from normal. 
• Axis:  frontal axis is vertical at approximately 90°
• Seen in: this type of RVH is usually due to atrial septal defect or mitral stenosis with mild to moderate pulmonary hypertension

Type C RVH

• This type of RVH is difficult to recognize and is frequently missed because the R wave in V1 is not tall and is smaller than the S wave. Instead, a deep S wave is present in V1 and in V2 that extends up to V6. Thus, V1 to V6 will show rS complexes. In V6, the R wave continues to be smaller in amplitude than the S wave. 
• Axis: axis of the QRS complex is approximately 90° or less. 
• Seen in:  type of RVH is usually due to COPD but could also occur acutely as a manifestation of acute pulmonary embolism

EKG changes in Acute Pulmonary Embolism

Sinus tachycardia and incomplete right bundle branch block are the most frequent ECG findings.

• Rhythm:
• Sinus tachycardia, atrial flutter, or atrial fibrillation
• Changes in the QRS complex:
• Right axis deviation of approximately ≥90°
• S1 Q3 T3 pattern (S wave in lead I, Q with inverted T wave in 
• rSR’ pattern in V1 usually of acute onset
• V1 may also show QS, qR, or R >S pattern
• Clockwise rotation with persistent S in V6 similar to type C RVH
• Changes in the P wave:
• P-pulmonale with peaking of the P waves in leads II, III, and aVF
• Ta waves become exaggerated in leads II, III, and aVF, causing 1 mm of ST depression in the inferior leads
• Changes in the ST segment and T waves
• ST elevation in V1
• Inverted T waves in V1 to V3 or up to V6

The electrocardiogram shows sinus tachycardia, right axis deviation ≥90° , S1 Q3 T3 pattern, rR' pattern in V1, and persistent S in the precordial leads extending to V6. These findings are usually acute in onset due to acute right heart strain.

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