The Heart, the Lungs, and the Blood

TL;DR. A fist-sized muscular pump moves about 5 litres of blood a minute at rest and up to five times that under load, pushing it through roughly 100,000 km of vessels and returning it every minute. The lungs present 70 to 100 square metres of surface, a membrane less than a thousandth of a millimetre thick, across which oxygen enters and carbon dioxide leaves 20,000 times a day. Both systems have enormous reserve and one shared vulnerability: their working parts do not regenerate. Heart muscle lost to a heart attack becomes scar, and alveoli destroyed by smoke are gone permanently. Everything you can do for these organs is protection and capacity-building, because there is no repair option.

Key takeaways

• The heart beats roughly 2.5 to 3 billion times in a lifetime without a single scheduled maintenance stop, and it is the only muscle that generates its own electrical rhythm.
• The heart feeds itself between beats. Coronary arteries fill during relaxation, not contraction, which is why a very fast heart rate can starve the heart muscle.
• Aerobic fitness (VO2max) is one of the strongest predictors of mortality ever measured, outperforming smoking, diabetes, and hypertension in some cohorts.
• The endothelium, a single-cell layer lining every vessel, weighs about a kilogram in total and is where atherosclerosis begins. It is a functioning organ, not a pipe surface.
• Lungs have no way to regrow alveoli. Emphysema is permanent, which is what makes stopping smoking urgent rather than merely advisable.
• Veins hold about two-thirds of your blood volume at any moment, acting as a reservoir the body can draw on.

The heart

In short: A 300-gram pump with its own electrical system and its own blood supply, which fills between beats and cannot repair itself.

What it is

Two pumps side by side in one organ. The right side takes oxygen-poor blood returning from the body and pushes it a short distance to the lungs at low pressure. The left side takes oxygen-rich blood from the lungs and pushes it to the entire body at high pressure, which is why its wall is roughly three times thicker.

Its own electricity

The heart does not need a nerve signal to beat. A cluster of specialised cells, the sinoatrial node, depolarises spontaneously 60 to 100 times a minute and sets the rhythm. The impulse spreads across the atria, pauses at the atrioventricular node (giving the atria time to finish emptying into the ventricles), then races down a fast conduction pathway so both ventricles contract almost simultaneously.

Nerves and hormones modulate this rate but do not create it. A heart removed from the body and supplied with oxygen and nutrients will keep beating, which is what makes transplantation possible.

Three things follow that appear later:

• Damage to the conduction pathway causes heart block, and a pacemaker substitutes for it.
• Chaotic atrial electrical activity is atrial fibrillation (Chapter 21).
• Chaotic ventricular activity is ventricular fibrillation, which pumps no blood at all, and a defibrillator works by depolarising the whole muscle at once so the sinoatrial node can restart in an orderly way.

It feeds itself between beats

The heart receives no oxygen from the blood passing through its chambers. It has its own supply: two coronary arteries branching off the aorta immediately above the aortic valve.

Crucially, they fill during diastole, the relaxation phase, because during contraction the muscle squeezes its own vessels shut. Two consequences:

• A very fast heart rate shortens diastole disproportionately, reducing the heart's own blood supply exactly when its demand is highest. This is why a racing heart can provoke chest pain in someone with narrowed coronaries, and part of why beta blockers help angina.
• Diastolic blood pressure matters for coronary perfusion, which is one reason very low diastolic pressure in someone with stiff arteries is not automatically good.

Reserve and durability

The heart's reserve is in its capacity to increase output, not in spare tissue. A fit person can raise cardiac output fivefold; an unfit or failing heart cannot, which is felt as breathlessness on exertion long before anything is felt at rest.

What ages it:

• Maximum heart rate falls by roughly 0.7 beats per minute per year, regardless of fitness. This is one of the few genuinely fixed declines.
• The ventricle stiffens, filling less easily, which contributes to heart failure with preserved ejection fraction (Chapter 21).
• Valves thicken and calcify, and aortic stenosis becomes common in the eighties.
• Heart muscle does not regenerate meaningfully. Turnover is around 1 percent a year in young adults and lower with age, so any muscle lost is permanently replaced by scar.

What damages it: high blood pressure (making it pump against resistance for decades), blocked coronary arteries, diabetes, smoking, excess alcohol (which can cause cardiomyopathy directly), untreated sleep apnoea, some chemotherapy drugs (anthracyclines cause cumulative, permanent damage), and viral myocarditis.

What protects it: everything in Chapter 63, with blood pressure control, not smoking, and aerobic exercise at the top.

The blood vessels

In short: Not plumbing but an active organ, whose single-cell lining is where cardiovascular disease begins.

The endothelium is the single layer of cells lining the entire system. Laid flat it would cover several thousand square metres and it weighs roughly a kilogram. It is not a passive surface:

• It releases nitric oxide, which relaxes the vessel wall. This is what exercise improves and what smoking, high glucose, and high LDL impair.
• It controls clotting, presenting a non-stick surface until it is injured, then doing the opposite.
• It controls what crosses into tissue, tightly in the brain (the blood-brain barrier) and loosely in the liver.
• Its injury is the first step in atherosclerosis (Chapter 21).

Arterial stiffening is the most consistent vascular change with age. Elastin fragments and is replaced by stiffer collagen, so the aorta stops cushioning each beat. Systolic pressure rises, diastolic often falls, and the gap between them widens. It is not entirely inevitable: populations with low sodium intake and high physical activity show far less of it.

The blood

In short: Five litres carrying oxygen, fuel, heat, hormones, immune cells, and the clotting system, with the marrow replacing 2 million red cells every second.

Red cells are unusual. They eject their nucleus and mitochondria during development, which frees space for haemoglobin and means they cannot repair themselves or use oxygen for their own metabolism. They survive about 120 days of being squeezed through capillaries narrower than they are, then are removed by the spleen and liver, and their iron is recycled. That 120-day lifespan is why HbA1c averages three months of blood glucose.

Haemoglobin is four protein chains, each holding an iron atom that binds one oxygen molecule. Its binding is cooperative: picking up the first oxygen makes the next easier, which produces an S-shaped curve that loads oxygen efficiently in the lungs and unloads it efficiently in tissue. Warm, acidic, carbon-dioxide-rich conditions, exactly what an exercising muscle produces, shift the curve so haemoglobin releases more oxygen precisely where it is needed. It is an elegant piece of automatic control, and Chapter 48 is about what happens when one amino acid in it is wrong.

Clotting is a cascade: a dozen factors activating each other in sequence, so that a small trigger produces a large, fast response. It is deliberately positive feedback, restrained by an equally elaborate anticlotting system. Nearly every anticoagulant drug blocks one specific step in that cascade (Chapter 56).

The lungs

In short: A hundred square metres of gas-exchange surface with a self-cleaning conveyor belt, and the alveoli never grow back.

What it is

Air travels down the trachea, through roughly 23 generations of branching tubes, and ends in alveoli: 300 to 500 million tiny sacs with a combined surface area of 70 to 100 square metres, about half a tennis court, wrapped in capillaries.

Breathing is driven by the diaphragm, a dome of muscle that flattens on contraction, enlarging the chest and drawing air in by suction. Exhalation at rest is passive: the lungs recoil elastically. That elastic recoil is exactly what emphysema destroys (Chapter 45), which is why COPD patients struggle to breathe out.

Surfactant is a detergent-like substance lining the alveoli that stops them collapsing under surface tension. Premature babies have not yet made enough, which causes respiratory distress syndrome, and giving artificial surfactant is one of the great advances in neonatal care.

The self-cleaning system

You inhale roughly 11,000 litres of air a day, carrying dust, pollen, microbes, and pollution. The airways handle it with a mucociliary escalator: a layer of sticky mucus riding on a bed of cilia that beat 1,000 or more times a minute, moving the sheet upward at roughly a centimetre a minute to the throat, where it is swallowed.

Cigarette smoke paralyses and then destroys those cilia. The escalator stops. Mucus pools, bacteria colonise, and the smoker coughs because coughing is now the only clearance mechanism left. That single fact explains chronic bronchitis, why smokers get pneumonia more often, and why a "smoker's cough" is not benign (Chapter 45).

Reserve and durability

Lung reserve is large: you can lose an entire lung and function normally at rest.

What ages it:

• FEV1, the volume you can force out in one second, peaks in the mid-twenties and declines by roughly 25 to 30 mL a year afterwards. In a susceptible smoker it declines two to three times faster, which is the Fletcher-Peto curve in Chapter 45.
• The chest wall stiffens and respiratory muscles weaken.
• Alveolar walls are lost gradually even without smoking, reducing surface area.

The two-sided lesson from that decline curve: the height of your peak matters as much as the rate of your decline. Childhood respiratory infections, prematurity, and maternal smoking all lower the peak, so a person can reach the disease threshold decades earlier with an entirely normal rate of decline.

What damages the lungs: tobacco smoke above all, then household smoke from cooking fires (affecting billions of people, mostly women and children), outdoor particulate pollution, occupational dusts (silica, coal, asbestos), and repeated severe infection including tuberculosis.

What protects them: not smoking and not being around smoke, clean cooking fuel, ventilation and filtration indoors, respiratory protection at work, vaccination against influenza, pneumococcus, COVID-19, and RSV, and aerobic exercise, which does not increase lung capacity much but improves everything downstream of it.

Reading the warning signs

In short: Six symptoms from these systems mean urgent assessment, and knowing which is which is genuinely useful.

The numbers worth knowing about yourself

In short: Five measurements describe the state of these systems better than any symptom.

Don't be confused: a low resting heart rate is usually good and occasionally a problem. In a fit person, a rate in the 40s or 50s reflects a strong heart ejecting more per beat. In someone unfit, or with dizziness, fainting, or fatigue, the same number can mean the conduction system is failing. The number alone does not distinguish them; symptoms do.

Sources and notes

Cardiac and respiratory physiology figures are standard (Guyton and Hall, Textbook of Medical Physiology; West, Respiratory Physiology: The Essentials). Alveolar number and surface area estimates: Ochs et al., American Journal of Respiratory and Critical Care Medicine, 2004 (approximately 480 million alveoli on average). Cardiomyocyte turnover: Bergmann et al., Science, 2009. Maximum heart rate decline with age: Tanaka, Monahan, and Seals, JACC, 2001. FEV1 decline: Fletcher and Peto, BMJ, 1977. Cardiorespiratory fitness and mortality: Mandsager et al., JAMA Network Open, 2018, which found no upper limit to the benefit of higher fitness in a cohort of over 122,000. Endothelial mass and surface estimates vary by method and are given as approximations. Mucociliary clearance rates: standard respiratory physiology. Sex differences in heart attack presentation: multiple registry analyses cited in Chapter 21.

Open questions. Whether adult human cardiomyocyte renewal can be therapeutically increased is unresolved. The extent to which arterial stiffening is an inevitable consequence of ageing versus a consequence of lifetime sodium intake and inactivity continues to be debated.

Next: the organs that process everything you swallow and everything your cells discard. 👉