EKG BBB + Hypertrophy

The left bundle branch has

left anterior fascicle

left posterior fascicle

A blocked bundle branch is a

slow and chaotic way to innervate the myocardium = wide, bizarre complex

distinction between a PVC and a BBB

The PVC is aberrantly conducted from inception.

The BBB is normally conducted until it hits the block.

In a blocked right bundle 

impulse transmitted normally by left bundle to most of left ventricle

RBBB results in slow impulse that shows

QRS interval ≥ 0.12 second

can manifest as additional wave

a RBBB may have

RSR’ (bunny ears) in precordial leads V1 and Vs

RSR’ in RBBB (V1 and V2)

Main criteria for RBBB

1.QRS prolongation
≥ 0.12 seconds

2.Slurred S wave in leads I and V₆

3.RSR′ pattern in lead V₁, with R′ taller than R

3 major criteria for RBBB

1.QRS ≥ 0.12 second

*Even one lead with a QRS complex ≥ 0.12 seconds

2. Slurred S wave in leads I and V₆

*S wave can have various morphologies, but all are prolonged and slow

3. RSR′ pattern in V₁

*Can have various presentations

*Some call them “rabbit ears”

*Key point: All predominantly positive in lead V₁If you see an ECG with wide QRS complexes, slurred S waves, and a positive complex in lead V₁, you have made a diagnosis of RBBB.

MOST important diagnostic criterion for RBBB is

slurring of the s wave

If you see an ECG with wide QRS complexes, slurred S waves, and a positive complex in lead V₁, you have

made a diagnosis of RBBB 

RBBB

another finding suggestive of a RBBB is a

QR’ wave

QR′ wave occurs when the ECG shows characteristic changes of

anteroseptal myocardial infarction.

*Q waves in leads V₁ and RBBB

*ECG will show Q wave in place of the

initial R wave of the RSR′ pattern.

Because the Q wave takes the place of the R wave, next positive wave is

an R′ wave; hence QR′.

When looking for a RBBB, don’t make the mistake of

only looking for rabbit ears

QR’ wave too!

in lead 1 and lead 2

in a RBBB, leads V₁ and V₂ should have an increased R:S ratio and some semblance of an RSR′ or QR′ complex.

A LBBB shows

QRS complex always 0.12 seconds wide or more.

Usually composed of monomorphic complexes (all positive or all negative)

Have ST-segment depression or elevation

Have broad T waves

*The result of all these findings is an ugly ECG.

an LBBB can be due to

one of two conditions:

*Block of left bundle

*Block of both fascicles of left bundle

Complexes in a LBBB are

not as sharp as in RBBB = broad, monomorphic complexes

LBBB gives rise to complexes

negative in leads V₁ and V₂ and positive in leads I, V₅, and V₆

left bundle branch block pattern is like a rock thrown up in the air: It goes either all up or all down

criteria for diagnosing LBBB

1.Duration ≥ 0.12 seconds wide

2.Broad, monomorphic R waves in I and V₆; no Q wave

3.Broad, monomorphic S waves in V₁; may have small r wave

Other LBBB criteria

*Can be some variation in R wave size in V₁

*R wave can be narrow (<0.03 second) or notched

*Wider R waves can be sign of posterior AMI

common causes of RBBB

*Congenital birth defect+ atrial septal defect

*Myocardial infarction

*Myocarditis

*Cardiomyopathy

*Hypertension

Pulmonary embolism

common causes of LBBB

*Hypertension

*Coronary artery disease (CAD)

*Dilated cardiomyopathy

*Rheumatic heart disease

*Infiltrative diseases of the heart

*Benign or idiopathic causes

Vast majority due to hypertension, CAD, or both

in a LBBB it is not

possible to diagnose LVH or RVH

summary of LBBB

*Complexes are conducted aberrantly.

*True sizes of complexes cannot be calculated.

*Most LBBBs have normal axis or left axis

in a RBBB, you can diagnose

LVH by normal criteria

summary of RBBB 

*RVH cannot be diagnosed.

*Ischemia: Remember concept of concordance.

*Atrial enlargement: Use usual criteria.

the left anterior fascicle is

Organized, thin bundle of fibers off left bundle

Gives rise to Purkinje fibers

These then innervate anterior and lateral walls of LV

the left posterior fascicle originates from

left bundle

Not organized into tight fascicle—disperse loosely and fan out

Origin of fibers that innervate inferior and posterior walls of left ventricle

Hemiblock means “half” of LBBB is

blocked after it splits into left anterior and left posterior fascicles.

Blocked left anterior fascicle is

left anterior hemiblock (or left anterior fascicular block).

Blocked left posterior fascicle is

left posterior hemiblock (or left posterior fascicular block).

Hemiblocks cause ventricles to be

innervated asynchronously and aberrantly.

When left anterior fascicle is blocked:

depolarization of left ventricle has to progress from interventricular septum, inferior wall, and posterior wall toward anterior and lateral walls

gives rise to unopposed vector pointed superior and leftward

a left anterior hemiblock produces changes in the 

net axis of ventricles toward left, producing left axis deviation

Electrical axis between –30° and –90 °

criteria for diagnosing left anterior hemiblock

1.Left axis deviation with axis at –30˚ to –90˚

2.Either a qR complex or an R wave in lead I

3.An rS complex in lead III, and probably leads II and aVF

left anterior hemiblock = QRS complex should be positive in lead I, negative in leads aVF and II

a left posterior hemiblock is

Rare because:

*Left posterior fascicle is difficult to block; fibers are not organized as a discrete bundle

*Lesion that could cause this type of block would have to be very large

criteria for diagnosing left posterior hemiblock 

1.Axis of 90 ° to 180 °in right quadrant

2.s wave in lead I and q wave in lead III

Right atrial enlargement (generally more dilatation than hypertrophy) is usually caused by

increased pressure in the right atrium. This is referred to as right atrial overload.

Right atrial enlargement may be due to

Pulmonary valve stenosis

Tricuspid valve stenosis and insufficiency = (relatively rare)

Pulmonary hypertension from various causes, such as the following:

*COPD

*Status asthmaticus

*Pulmonary embolism

*Pulmonary edema

*Mitral valve stenosis or insufficiency

*Congenital heart disease

right atrial enlargement

The typical result of right atrial enlargement is a

tall, symmetrically peaked P wave.

*Leads II, III, and aVF

*This waveform is referred to as P pulmonale.

Left atrial enlargement (generally more dilatation than hypertrophy) is usually caused

by increased pressure in the left atrium

A condition referred to as left atrial overload

left atrial enlargement can occur in

*Mitral valve stenosis and insufficiency

*Acute myocardial infarction (AMI)

*Left heart failure

LVH from various causes, such as the following:

*Aortic stenosis or insufficiency

*Systemic hypertension

*Hypertrophic cardiomyopathy

on ECG in left atrial enlargement you will see

A broad, positive P wave in any lead

A wide, notched P wave with two humps that appear 0.04 second or more apart

*The first hump represents the depolarization of the right atrium.

*The second hump represents the depolarization of the distended left atrium.

left atrial enlargement

left ventricular hypertrophy can be caused by

Pressure overload develops when ventricle has to pump harder against resistance:

*Systemic hypertension

*Aortic stenosis

*Mitral insufficiency

*Hypertrophic cardiomyopathy

Volume or dilation problem: volume overload

*The heart becomes larger in an effort to:

become stronger, pump more blood

in LVH on ECG…

Creates a larger vector and increased amplitude, especially true in precordial leads

*The more mass or cells in the heart, the more action potentials are generated.

in identifying LVH step by step

1. Look in V1 and V2, pick the deepest negative deflection, count small boxes of negative deflection in that lead = remember that number

2. Look in V5 and V6, pick the tallest positive deflection; count small boxes of positive deflection = remember that number

3. Add the two numbers together, suspect LVH if the sum equals 35 or more

4. The product of R and S waves determines LVH.

   Remember: Final product must be ≥ 35 mm.

   The sum is important, not which of the two parts is greater

LVH is often mistaken for AMI because of the

ST-segment elevation and depression associated with it.

*Pay attention to how the tallest or deepest waves have the most ST-segment variations.

right ventricular hypertrophy is usually seen in

RV pressure overload

Potential causes:

*Pulmonary valve stenosis

*Pulmonary emboli

*Pulmonary hypertension

*COPD

signs of RVH on ECG

first thing you should see is a large R wave on the QRS complex.

*Result of adding energy generated by the initial QRS vector to the larger vector generated by the enlarged RV

RVH

*Figure A shows a typical pattern for RVH in V₁.

*In Figure B, the R:S ratio is still greater than 1, but the ST segment and T waves look different (strain pattern).

RVH is diagnosable/likely if

the R:S ratio is greater than or equal to 1 in leads V₁ and/or V₂.

in RVH on an ECG, the R wave is a 

 tall R wave is present in leads II, III, and V1 

• R wave is usually 7 mm or more in height in lead V1.

• It is equal to or greater than the S wave in depth in this lead.

• A relatively tall R wave is also present in the adjacent precordial leads V2 to V3.

in RVH on an ECG, the S wave is

• relatively deeper-than-normal S wave is present in lead I and the left precordial leads V4 to V5.

• in lead V6, the depth of the S wave may be greater than the height of the R wave.