Left ventricle

What it normally does

• Its wall is two to three times thicker than the right ventricle's — roughly 6 to 10 mm at end-diastole, against an RV free wall of 3 to 5 mm — because it ejects into a high-pressure circuit. The aortic valve opens once left ventricular pressure climbs above aortic diastolic pressure, about 80 mmHg, and ventricular pressure then peaks around 120 mmHg in ejection; the right ventricle opens its valve at a pulmonary artery diastolic pressure of about 10 mmHg and peaks at only about 25 mmHg. Built for pressure, the left ventricle answers a pressure load by thickening its wall and a volume load by dilating its cavity.

  the same organ gives two opposite pictures — hypertension or aortic stenosis thickens the wall inwards onto a small cavity, while a leaking valve or lost muscle stretches the cavity out.

• It holds about 120 mL at end-diastole and ejects about 70 mL of that each beat. The fraction it ejects (ejection fraction, EF) is normally about 55 to 70%, and it is a ratio, not a volume — a big floppy ventricle can eject a near-normal volume with a poor fraction, and a small stiff one can eject a small volume with a high fraction.

  the ejection fraction alone never tells you whether the patient is in heart failure, and a falling stroke volume — not a falling EF — is what the body misreads as blood loss and answers with neurohormonal activation.

• Filling is active work, not passive dropping-in: the muscle has to relax and untwist, which consumes ATP, and it can only happen in diastole. Left ventricular myocardium is also perfused almost entirely in diastole, when the muscle is relaxed and not squeezing its own vessels. Anything that stiffens the muscle or shortens diastole (a fast heart rate) therefore cuts both filling and coronary supply, and roughly a fifth to a quarter of end-diastolic volume in a stiff ventricle comes from atrial contraction.

  tachycardia and the loss of the atrial kick in atrial fibrillation both tip a stiff ventricle into pulmonary oedema, and a thick ventricle can develop angina on exertion with unobstructed coronary arteries.

• Wall stress rises with chamber pressure and with chamber radius and falls with wall thickness (Laplace: stress is proportional to pressure × radius, divided by twice the wall thickness). Of the three terms, thickening the wall is the only one the myocardium itself can change — lowering pressure or radius takes treatment or a smaller load. Dilating does the opposite and drives stress up.

  hypertrophy is the wall's own answer to pressure overload, while dilatation is self-feeding — a bigger radius raises wall stress, wall stress raises oxygen demand, and an ischaemic ventricle dilates further.

What goes wrong

• Thickened wall from pressure overload (concentric hypertrophy)← from “Its wall is two to three times thicker than th…”

  Chronic high pressure — usually hypertension, sometimes a narrowed aortic valve — means the ventricle must generate more pressure with every beat. New sarcomeres are laid down side by side (in parallel), so the wall thickens inwards and the cavity gets smaller. By Laplace, the thicker wall brings wall stress back down, but the price is a stiff muscle with a small chamber and more myocardium to perfuse.

  Pressure load adds sarcomeres in parallel: thick wall, small cavity, S4, undisplaced heaving apex, normal EF.

  You would find: A forceful, sustained apex beat that has NOT moved from the fifth intercostal space in the midclavicular line, a fourth heart sound, tall QRS voltages on the ECG (Sokolow-Lyon: S in V1 plus R in V5 or V6 above about 35 mm), and a wall thickness above about 11 mm on echocardiography.

• Failure to fill (diastolic heart failure, HFpEF)← from “Filling is active work, not passive dropping-i…”

  A thick, stiff ventricle cannot relax and accept its normal filling volume without the pressure inside it rising. That raised diastolic pressure passes back into the left atrium, then the pulmonary veins, and fluid is forced into the lung interstitium. Squeezing looks adequate — the ejection fraction is preserved — but the pump has failed on the filling side. Tachycardia and the loss of atrial contraction in atrial fibrillation both make it acutely worse because both steal filling time and filling volume.

  Normal EF, high filling pressure: stiff ventricle, atrial fibrillation or tachycardia as the trigger, congestion without a dilated chamber.

  You would find: Breathlessness on exertion, crackles at the lung bases and raised natriuretic peptides (an NT-proBNP below about 125 ng/L makes chronic heart failure unlikely) in someone whose echocardiogram shows an EF of 50% or more, usually an older patient with long-standing hypertension. A normal EF does not exclude heart failure.

• Failure to empty with a dilated chamber (systolic heart failure, HFrEF)← from “Wall stress rises with chamber pressure and wi…”

  Muscle is lost or damaged — most often by myocardial infarction, otherwise by alcohol, viral myocarditis, chemotherapy, or chronic volume overload from a leaking mitral or aortic valve. Stroke volume falls, blood is left behind at the end of each beat, and the chamber stretches. Sarcomeres are added end to end (in series) and the ventricle dilates. By Laplace the bigger radius raises wall stress, which raises oxygen demand and damages more muscle, so the dilatation feeds itself. Ejection fraction falls: at 40% or below this is HFrEF, the group in which the disease-modifying drugs have their clearest mortality evidence, while 41 to 49% is the mildly reduced band (HFmrEF).

  Volume load adds sarcomeres in series: dilated chamber, displaced diffuse apex, S3, EF 40% or less, and Laplace makes it self-perpetuating.

  You would find: An apex beat displaced laterally and downwards and diffuse rather than sharp, a third heart sound, and an EF of 40% or less on echocardiography. In Australia, chronic valve leak from rheumatic heart disease is a real cause of this picture in young Aboriginal and Torres Strait Islander patients, among whom rates remain among the highest reported in the world — do not assume a dilated ventricle means an old infarct.

• The neurohormonal vicious cycle← from “It holds about 120 mL at end-diastole and ejec…”

  When stroke volume falls, the body reads it as blood loss. The sympathetic nervous system and the renin-angiotensin-aldosterone system switch on, holding onto salt and water and constricting arterioles. More volume means more stretch on an already dilated ventricle; tighter arteries mean more pressure to eject against. Angiotensin II and aldosterone also drive fibrosis in the ventricular wall directly, and sustained catecholamine exposure downregulates myocardial beta-1 receptors. Short-term rescue, long-term destruction — which is why the drugs that prolong life in heart failure block these systems rather than whipping the heart harder.

  Falling stroke volume is misread as haemorrhage; RAAS and sympathetic activation buy hours and cost years, so the survival drugs are blockers, not stimulants.

  You would find: Ankle oedema, a raised jugular venous pressure (visible more than about 3 cm vertically above the sternal angle with the patient reclined at 45 degrees), resting tachycardia and weight gain over days. It also explains why long-term oral inotropic therapy makes people feel better and die sooner — short courses of intravenous inotropes in cardiogenic shock are a different situation — while beta blockade feels worse for the first weeks and prolongs life.

• Angina with a thick ventricle← from “Filling is active work, not passive dropping-i…”

  The left ventricle is perfused in diastole, when the muscle is relaxed. A hypertrophied wall has more muscle to feed, higher intramural pressure squeezing its own vessels, capillary density that has not kept pace with the added muscle, and a shorter diastole once the rate climbs on exertion. The innermost layer, the subendocardium, is last in line and starves first.

  Supply-demand angina without coronary stenosis: thick wall, short diastole, subendocardium first to go.

  You would find: Exertional chest tightness in someone with aortic stenosis or long-standing hypertension, sometimes with angiographically normal coronary arteries; ECG changes are typically deepest in the leads facing the thickest wall.

What we give, and how it works

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