The left ventricle is the heart's main pumping chamber, driving oxygenated blood through the aortic valve into the whole systemic circulation. Its wall is about 9-11 mm thick, roughly three times that of the right ventricle, and it is circular in cross-section. It forms the apex and most of the left border and diaphragmatic surface of the heart.
| Location | Left and posterior part of the heart, forming the apex (normally near the left fifth intercostal space, midclavicular line) and most of the left heart border. |
|---|---|
| Parts |
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| Nerve Supply | Cardiac plexus; Vagus nerves (parasympathetic, slows rate); Sympathetic cardiac nerves from cervical and upper thoracic (T1-T4) ganglia (raise rate and force) |
| Blood Supply | Left anterior descending artery; Left circumflex artery; Posterior descending artery (from the right coronary artery in most people) |
| Venous drainage |
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| Lymphatic drainage |
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Generates systemic arterial pressure, typically around 120 mmHg at peak, to perfuse all organs. Its ejection fraction (normally about 55-70%) is the most widely used single measure of heart pumping performance.
Left ventricular hypertrophy develops with long-standing hypertension or aortic stenosis, and also as a normal adaptation in endurance and strength athletes (athlete's heart), which must be told apart from cardiomyopathy. Most myocardial infarctions involve the left ventricle. Reduced ejection fraction is a key guide to heart failure treatment and to decisions about implantable defibrillators.
Thickening of the ventricular wall due to pressure overload such as hypertension or aortic stenosis. Pathological hypertrophy raises the risk of heart failure and arrhythmias.
A thinned, bulging scar after a large myocardial infarction. It can hold clot, cause arrhythmias and reduce pumping efficiency.
Enlargement and weakening of the ventricle with reduced contraction. Causes include genetic variants, alcohol, viral myocarditis and some chemotherapy drugs.
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