Left Branch Block: Anatomy, Physiology, Clinical Table, Diagnosis and Treatment

It is usual to see these abnormal ventricular conducts with heart failure since they share the exact etiology.

Left bundle branch block (LBBB) alters ventricular conduction, leading to ventricular asynchrony and heart failure.

Approximately one-third of patients with this modality has a BIB identified by their criteria during vector analysis of the QRS complex (Electrocardiogram waves). In most cases, there is an associated left bundle branch block (LBB).

Anatomy and physiology

It is well known that the intraventricular septum contains its beam, which is the most common, divided into three original fascicles: the right path, with a branch; and the left bundle with two lanes, the left anterior fascicle, and the left posterior fascicle.

The left bundle branch (RHI) and the right bundle branch (RHD) do not exchange stimuli by a mechanism between the right and left pathways: a “physiological barrier.”

This barrier is significant to maintain synchronism between the left and right ventricles and for the role of the LBB.

When ventricular activation is established, it occurs first on the opposite side of the blocked pathway, initiating the depolarization in its septum and the ventricular mass.


Then, before ultimately activating the ventricle of the unblocked beam, the depolarized wave surpasses the physiological barrier of the septum by the normal myocardial cells and reaches the Purkinje system and the septum, activating the remaining ventricle abnormally and with a delay of 0.02. -0.04s in the BRD and more than 0.06s for the BRI.

Clinical picture

The Hematoencephalic Barrier (BH) usually arises from a degenerative process of the heart conduction system. It is justified by its close relationship with cardiovascular diseases that degenerate any of the ventricles.

Although it can also occur in patients without underlying heart diseases.

Common causes of LBB include myocardial infarction (MI), hypertensive heart disease, and lung diseases, such as pulmonary embolism and chronic obstructive pulmonary disease.

In patients with pulmonary embolism, LBB can be found in 6% -67% of cases; a new BRD is usually associated with a larger anterior myocardial infarction and occurs in 3% -7% of MI cases.

In BRI, the most common causes include coronary artery disease, hypertension, and cardiomyopathy.

BRI can also be observed during cardiac stimulation.

The pacemaker lead generally rests on the right ventricle and induces a morphology similar to the BRI on the ECG.

Among patients with chest pain and suspected myocardial infarction, BRI ranges from 1% to 9%; these mostly obscure the diagnosis of acute MI in the ECG criteria, masking the ST-segment elevation.

BRI also has a close relationship with Heart Failure (IC), associated with approximately 25% of cases, and is known as a worsening factor of ejection of the left ventricular fraction.


The ECG is considered the gold standard for the non-invasive diagnosis of conduction disturbances and arrhythmias.

Its sensitivity and specificity are more significant for diagnosing arrhythmias and conduction disorders than structural or metabolic changes.

BRI is most commonly caused by coronary artery disease, hypertensive heart disease, or dilated cardiomyopathy.

It is unusual for BRI to exist in the absence of organic disease.

Therefore, to fully assess the patient due to suspicions of associated anomalies that may cause the Hematoencephalic Barrier (BH), physicians can perform other tests, such as physical examination, chest x-ray, and echocardiography.

Left BH has also been associated with more complications from cardiovascular disease than from correct branch block.

LBB causes some damage to the mechanical function of the LV secondary to asynchronous myocardial activation, which sequentially can trigger ventricular remodeling and a poor prognosis.

It has been shown that dyssynchrony accelerates the progression of the disease in heart failure. The more pronounced the asynchrony is, the higher the mortality in individuals with heart failure.

In addition, recent studies have shown that sudden death was the first manifestation of the disease, being diagnosed ten times more in male individuals with LBB than in those without this condition.

BRI and an abnormal Q wave are risk factors for cardiovascular mortality in end-stage hypertrophic cardiomyopathy and provide new evidence for early intervention.

Some new studies have shown associations between LBBB and adverse prognosis in patients with preserved LV systolic function after myocardial infarction.

Recently, it was shown that LBBB is an independent predictor of mortality in long-term (1 year) follow-up patients without severe heart failure after acute heart failure hospital admission.

The excess mortality in the LBB group was mainly caused by an increase in fatal cardiovascular events, indicating that this could be caused by heart failure (induced by asynchrony).


Cardiac Resynchronization Therapy (CRT) has proven to be a very effective treatment for patients with:
  • Left ventricular function (LVF) depressed.
  • Symptomatic congestive heart failure (ICCS).
  • Ancho QRS anormal.

It can induce inverse remodeling of the IVF with improved function and reduction of the symptoms of heart failure, increasing not only the quality of life and cardiac function but also a remarkable change in prognosis, reducing hospitalization and mortality related to the IC.

The study of individuals with LBBB and their mechanisms of intraventricular conduction abnormalities led to the idea of ​​CRT as the number one therapy for symptomatic patients.

Some predictable changes in the sequence of IVF activation, such as abnormal activation of the septum and markedly delayed activation of the lateral LV with synchronic electromechanical activation, lead to an increase in cardiac work, a less efficient cardiac contraction, and a lower cardiac output.