Bundle branch block

80,021views

Bundle branch block

Cardiology

Cardiology

Introduction to the cardiovascular system
Anatomy of the heart
Anatomy of the coronary circulation
Anatomy clinical correlates: Heart
Anatomy of the superior mediastinum
Anatomy of the inferior mediastinum
Anatomy clinical correlates: Mediastinum
Development of the cardiovascular system
Fetal circulation
Cardiac muscle histology
Artery and vein histology
Arteriole, venule and capillary histology
Cardiovascular system anatomy and physiology
Lymphatic system anatomy and physiology
Coronary circulation
Blood pressure, blood flow, and resistance
Pressures in the cardiovascular system
Laminar flow and Reynolds number
Resistance to blood flow
Compliance of blood vessels
Control of blood flow circulation
Microcirculation and Starling forces
Measuring cardiac output (Fick principle)
Stroke volume, ejection fraction, and cardiac output
Cardiac contractility
Frank-Starling relationship
Cardiac preload
Cardiac afterload
Law of Laplace
Cardiac and vascular function curves
Altering cardiac and vascular function curves
Cardiac work
Cardiac cycle
Pressure-volume loops
Changes in pressure-volume loops
Physiological changes during exercise
Cardiovascular changes during hemorrhage
Cardiovascular changes during postural change
Normal heart sounds
Abnormal heart sounds
Action potentials in myocytes
Action potentials in pacemaker cells
Excitability and refractory periods
Cardiac excitation-contraction coupling
Cardiac conduction system
Cardiac conduction velocity
ECG basics
ECG normal sinus rhythm
ECG intervals
ECG QRS transition
ECG axis
ECG rate and rhythm
ECG cardiac infarction and ischemia
ECG cardiac hypertrophy and enlargement
Baroreceptors
Chemoreceptors
Renin-angiotensin-aldosterone system
Arterial disease
Angina pectoris
Stable angina
Unstable angina
Myocardial infarction
Prinzmetal angina
Coronary steal syndrome
Peripheral artery disease
Subclavian steal syndrome
Aneurysms
Aortic dissection
Vasculitis
Behcet's disease
Kawasaki disease
Hypertension
Hypertensive emergency
Renal artery stenosis
Coarctation of the aorta
Cushing syndrome
Conn syndrome
Pheochromocytoma
Polycystic kidney disease
Hypotension
Orthostatic hypotension
Abetalipoproteinemia
Familial hypercholesterolemia
Hypertriglyceridemia
Hyperlipidemia
Chronic venous insufficiency
Thrombophlebitis
Deep vein thrombosis
Lymphedema
Lymphangioma
Shock
Vascular tumors
Human herpesvirus 8 (Kaposi sarcoma)
Angiosarcomas
Persistent truncus arteriosus
Transposition of the great vessels
Total anomalous pulmonary venous return
Tetralogy of Fallot
Hypoplastic left heart syndrome
Patent ductus arteriosus
Ventricular septal defect
Atrial septal defect
Atrial flutter
Atrial fibrillation
Premature atrial contraction
Atrioventricular nodal reentrant tachycardia (AVNRT)
Wolff-Parkinson-White syndrome
Ventricular tachycardia
Brugada syndrome
Premature ventricular contraction
Long QT syndrome and Torsade de pointes
Ventricular fibrillation
Atrioventricular block
Bundle branch block
Pulseless electrical activity
Tricuspid valve disease
Pulmonary valve disease
Mitral valve disease
Aortic valve disease
Dilated cardiomyopathy
Restrictive cardiomyopathy
Hypertrophic cardiomyopathy
Heart failure
Cor pulmonale
Endocarditis
Myocarditis
Rheumatic heart disease
Pericarditis and pericardial effusion
Cardiac tamponade
Dressler syndrome
Cardiac tumors
Acyanotic congenital heart defects: Pathology review
Cyanotic congenital heart defects: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Coronary artery disease: Pathology review
Peripheral artery disease: Pathology review
Valvular heart disease: Pathology review
Cardiomyopathies: Pathology review
Heart failure: Pathology review
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart blocks: Pathology review
Aortic dissections and aneurysms: Pathology review
Pericardial disease: Pathology review
Endocarditis: Pathology review
Hypertension: Pathology review
Shock: Pathology review
Vasculitis: Pathology review
Cardiac and vascular tumors: Pathology review
Dyslipidemias: Pathology review
Cholinergic receptors
Adrenergic receptors
Cholinomimetics: Direct agonists
Cholinomimetics: Indirect agonists (anticholinesterases)
Muscarinic antagonists
Sympathomimetics: Direct agonists
Sympatholytics: Alpha-2 agonists
Adrenergic antagonists: Presynaptic
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
ACE inhibitors, ARBs and direct renin inhibitors
Thiazide and thiazide-like diuretics
Calcium channel blockers
cGMP mediated smooth muscle vasodilators
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
Lipid-lowering medications: Statins
Lipid-lowering medications: Fibrates
Miscellaneous lipid-lowering medications
Positive inotropic medications

Transcript

Watch video only

Each heartbeat starts with the heart’s pacemaker cells in the sinoatrial node, sometimes called the SA node, in the right atrium. The SA node sends out an electrical signal that propagates out and contracts both upper chambers. The signal then moves through the atrioventricular node, or AV node, down into the lower chambers. Here it reaches the bundle of His and splits into the left and right bundle branches, which serve the left and the right ventricles. The signal then goes on to each ventricles’ Purkinje fibers, which leads to ventricular contraction.

Now, a “bundle branch block” describes when that electrical signal gets completely blocked or held up along one of the bundle branches. In most cases, this block, or delay, is caused by fibrosis, or scarring, that either occurs acutely or chronically. Acute causes can be things like ischemia, heart attack, or myocarditis, the inflammation of the heart tissue. Chronic conditions might lead to fibrosis of the heart tissue, because they all can cause slow and steady remodeling of the heart muscle; these include: hypertension, coronary artery disease, and cardiomyopathies.
If the block happens on the right side, it’s referred to as a right bundle branch block. With this type, the electrical signal starts at the SA node, contracts the atria, moves through the AV node, splits at the bundle of His, and then moves down the left bundle branch, but is blocked on the right bundle branch. This causes the left ventricle to contract first. The signal then spreads from the purkinje fibers of the left ventricle over to the right ventricle, which causes the right ventricle to contract after the left has contracted. So, with right bundle branch block, the right ventricle contracts late. If the block happened to be on the left side instead, which is called a left bundle branch block, the signal would be delayed on that side, and so the right ventricle would contract first, and then the left ventricle would contract late.

Now, on electrocardiogram or ECG, normally you have the characteristic P wave, which corresponds to the atria contracting, then the QRS complex, which corresponds to both ventricles contracting and is usually between 80 and 100 ms long. If there’s a delay in depolarization of one of the ventricles, the QRS complex gets wider because depolarization starts on time but ends later than usual. Because now one of the ventricles is contracting late, a QRS complex longer than 120 ms is common to see in a bundle branch block. Okay, so far we’ve been looking a relatively common view of the heart, called lead two, which is a type of “limb lead,” since we get it by attaching leads to two limbs: the right arm and left leg.

Even though this lead can provide some solid information, it’s often helpful to use other leads as well, especially when differentiating between left and right bundle branch block. The chest leads, or precordial leads, are really useful for doing just that. Chest leads look at the heart’s electrical activity when viewed from a slice parallel with the ground, whereas limb leads look at the heart in the frontal plane, which is perpendicular to the ground.

For chest leads, they go from V1, coming straight out the front of the chest, to V6, going out the left side of the chest. Each of these is like looking at the heart from a different perspective, right? V1 and V6 are particularly helpful since they’re the farthest apart from each other, and therefore have the most contrast between views. Normally, the first thing to depolarize is the septum, and the wave of depolarization moves from the left bundle branch toward the right ventricle, so toward V1 but away from V6. This means you’ll get a positive deflection on V1, and a negative deflection on V6. Next, that wave moves to the ventricles themselves, and since the left ventricle is usually more massive, you’ll get a large depolarization directed away from V1 but toward V6, so negative on V1 and positive on V6. Let’s say there’s a block along the left bundle branch, so now the overall direction of depolarization comes from the right side and moves toward the left, so away from V1 and toward V6, meaning negative in V1 and positive in V6. V6 will also often be notched from the left ventricle, depolarizing late. So, when it’s all said and done, V1 usually has a QS or “little r”-S complex, because QS means an absent R wave, and “little r”-S means a small R wave, either of which give it a “W” shape. On V6, the large “notched” R wave gives it an “M” shape.

Sources

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  4. "Left bundle branch block: from cardiac mechanics to clinical and diagnostic challenges" EP Europace (2017)
  5. "Left Bundle Branch Block" Circulation: Arrhythmia and Electrophysiology (2020)
  6. "Diagnosis of right bundle branch block: a concordance study" BMC Family Practice (2019)