Appearance
7.5 — Blood Vessels and the Circulation Routes
If you laid all your blood vessels end to end they would stretch about 100,000 kilometres — two and a half times around the Earth. Almost all of that length is capillaries, which are so fine that a single one is invisible without a microscope, and no cell in your body is more than about 0.1 millimetres from one.
The system has to do two contradictory things. It must deliver blood at high pressure to reach every corner, and it must present that blood to the tissues at a pressure low enough and a speed slow enough for exchange to happen. The vessel types are the sequence of steps between those two requirements.
The vessel types
All vessels except capillaries have three layers: an inner endothelial lining, a middle layer of smooth muscle and elastic tissue, and an outer connective tissue coat. What varies is the proportion.
Elastic arteries — the aorta and its largest branches. The middle layer is dominated by elastic tissue rather than muscle.
That elasticity is not incidental — it converts an intermittent pump into a continuous flow. During systole the aorta stretches, storing about half the ejected volume in its expanded wall. During diastole it recoils, pushing that blood onward. This is why blood flows in the capillaries continuously even though the heart ejects in pulses, and it is called the Windkessel effect, after the air chamber in old fire engines that smoothed the output of a hand pump.
When arteries stiffen with age, this stops working, and the consequences are measurable: systolic pressure rises because the aorta no longer absorbs the ejected volume, and diastolic pressure falls because there is no recoil. The widening gap between them — the pulse pressure — is itself a strong cardiovascular risk marker in older people, and it is why isolated systolic hypertension is the typical pattern after 60.
Muscular arteries — the named arteries supplying organs and limbs. Thick smooth muscle, distributing blood.
Arterioles — small, with a thick muscular wall relative to their tiny lumen.
These are the resistance vessels, and they control almost everything. Because resistance depends on the fourth power of the radius, small changes in arteriolar diameter produce enormous changes in flow. Halving the radius of an arteriole increases its resistance sixteenfold.
R \propto \frac{1}{r^4}
So arterioles are the taps of the circulation. They set total peripheral resistance, and therefore blood pressure; and they decide, organ by organ, who gets the blood.
Capillaries — a single layer of endothelium on a basement membrane, and nothing else. About 5 to 10 micrometres across, so red cells pass in single file, often folding to fit.
This is where the entire purpose of the circulation is achieved. Everything before it is delivery and everything after it is return.
Venules and veins — thin walls, large lumens, and valves in the limb veins to prevent backflow (Chapter 6.6).
Veins are the capacitance vessels. At any moment, roughly 65 percent of your blood volume is in the systemic veins, only about 13 percent in the arteries, 7 percent in the capillaries, and the rest in the heart and lungs.
That reservoir is functional, not incidental. Sympathetic stimulation constricts the veins and shifts blood back to the heart, increasing preload and cardiac output without any change in total blood volume. It is how the body compensates in the first stages of haemorrhage, and it is one reason blood pressure can be normal in someone who has already lost 15 percent of their blood.
Pressure, velocity and area
Three quantities change along the circulation, and understanding why makes the whole system make sense.
Pressure falls continuously, and it falls most steeply across the arterioles, because that is where resistance is concentrated. From about 120/80 mmHg in the aorta, to a mean of about 35 mmHg entering the capillaries, to under 5 mmHg in the vena cava.
Total cross-sectional area rises enormously toward the capillaries. The aorta has a cross-section of about 4.5 cm². The capillary bed's total cross-section is around 4,500 cm² — a thousandfold increase, because although each capillary is tiny, there are billions of them.
And velocity is inversely proportional to total area, because the same volume must pass every second. Blood moves at about 40 cm/s in the aorta and about 0.03 cm/s in the capillaries — over a thousand times slower.
That slowness is the point. A red cell spends about one second crossing a capillary, and that second is what allows oxygen to diffuse out and carbon dioxide in. If blood moved through capillaries at aortic speed there would be no time for exchange, and the whole circulation would be pointless.
This is the same principle as a river widening into a delta — same water, more channels, slower flow.
Exchange at the capillary
Four routes across the wall:
Diffusion — the main route. Oxygen and carbon dioxide dissolve through the cells directly; water-soluble substances go through gaps between cells.
Filtration and reabsorption — bulk flow of fluid, described below.
Vesicular transport — for large molecules.
Through gaps — in some tissues the capillaries have pores or are frankly discontinuous.
Capillary type varies by organ, and each type is matched to a job.
Continuous capillaries — tight junctions, minimal leak. Muscle, skin, lung, and — most tightly of all — the brain, where they form the blood–brain barrier (Chapter 11.10).
Fenestrated capillaries — with pores. Kidney glomeruli, gut lining, endocrine glands. Anywhere rapid fluid or hormone exchange is needed.
Sinusoidal capillaries — large gaps, allowing whole cells through. Liver, spleen, bone marrow. This is why new blood cells can leave the marrow and enter the circulation, and why the liver can access everything in the blood.
Starling forces
Four pressures decide whether fluid leaves or enters a capillary, and they were described by Ernest Starling in 1896.
Pushing fluid out:
- Capillary hydrostatic pressure — blood pressure inside. About 35 mmHg at the arterial end, 15 mmHg at the venous end.
- Interstitial oncotic pressure, small.
Pulling fluid in:
- Plasma oncotic pressure — from albumin, about 25 mmHg, and constant along the length (Chapter 7.1).
- Interstitial hydrostatic pressure, small.
At the arterial end, 35 mmHg pushing out beats 25 mmHg pulling in, so fluid filters out. At the venous end, 15 mmHg pushing out loses to 25 mmHg pulling in, so fluid is reabsorbed.
Reabsorption does not quite match filtration. Around 20 litres are filtered per day and about 17 litres reabsorbed. The remaining 3 litres are collected by the lymphatic system and returned to the blood (Chapter 7.8).
Oedema — tissue swelling — is any disturbance of this balance, and there are exactly four ways to get it.
Raised capillary pressure — heart failure, venous obstruction, standing still for long periods, pregnancy compressing pelvic veins. Reduced plasma oncotic pressure — liver disease, nephrotic syndrome, malnutrition. Increased capillary permeability — inflammation, burns, sepsis, allergy. Blocked lymphatic drainage — lymphoedema.
And the distribution of the swelling tells you which. Oedema from heart failure or low albumin follows gravity, so it is in the ankles in someone walking and over the sacrum in someone bedbound. Oedema confined to one limb suggests local obstruction — a clot or lymphatic blockage — rather than a systemic cause, and that distinction is made at the bedside before any test.
Controlling flow, organ by organ
The organs are supplied in parallel from the aorta, not in series. Every organ therefore receives blood at the same pressure, and how much it gets depends entirely on the resistance of its own arterioles.
That arrangement is what makes redistribution possible. Constrict the arterioles to the gut and dilate those to the muscle, and blood shifts from one to the other with no change in the total.
Resting distribution, as a percentage of cardiac output:
| Organ | Share of output | Notes |
|---|---|---|
| Liver and gut | ~25% | Rises after a meal |
| Kidneys | ~20% | Far more than they need for themselves |
| Skeletal muscle | ~20% | Rises to 80%+ in exercise |
| Brain | ~15% | Essentially constant, always |
| Heart | ~5% | Rises with demand |
| Skin | ~5% | Rises hugely for heat loss |
Two of those figures need explaining.
The kidneys take 20 percent of cardiac output for organs weighing under 300 grams. They do not need that for their own metabolism. They receive it because their job is to filter the blood, so the volume they process is the whole point (Chapter 10.2).
And the brain's share is essentially fixed. It cannot be reduced to divert blood elsewhere, because neurons have no fuel reserve and no anaerobic capacity (Chapter 1.1). In shock, when the body is shutting down flow to everything it can, cerebral and coronary flow are the last to be sacrificed — and when they go, the person dies.
Local control
Autoregulation — an organ maintaining its own flow despite changes in perfusion pressure. The brain and kidneys do this well over a wide range, which is why cerebral blood flow stays constant between mean arterial pressures of about 60 and 160 mmHg.
Metabolic control — active tissue produces carbon dioxide, adenosine, potassium and hydrogen ions, all of which dilate local arterioles. The tissue that needs blood most is the tissue that automatically gets it, with no central involvement at all.
Reactive hyperaemia is the demonstration: block the blood supply to an arm for a minute, then release it, and the limb flushes red as accumulated metabolites open every arteriole at once.
Endothelial control. The endothelium is not passive lining; it is an active organ.
Nitric oxide is the key molecule. Endothelial cells release it in response to increased flow, and it relaxes the smooth muscle beneath (Chapter 1.8). So a vessel dilates in response to more blood passing through it — flow-mediated dilation, another self-regulating loop.
Endothelial dysfunction — reduced nitric oxide production — is the earliest measurable step in atherosclerosis, appearing years before any plaque. Chapter 18.1.
Sympathetic control — noradrenaline constricting most arterioles. Note there is no significant parasympathetic supply to most blood vessels, so vasodilation is usually achieved by reducing sympathetic tone rather than by an opposing nerve.
The special circulations
Coronary — Chapter 7.7.
Cerebral — the brain is supplied by two internal carotid arteries at the front and two vertebral arteries at the back, which join in a ring at the base of the brain — the circle of Willis. The ring means that if one vessel narrows or occludes, blood can reach its territory from another route. The circle is complete and functional in only about half of people, which is part of why identical arterial blockages produce very different strokes in different people (Chapter 11.10).
Pulmonary — low pressure, and it does one thing backwards. In every other organ, low oxygen dilates the arterioles. In the lung, low oxygen constricts them.
That reversal is correct. In a lung region that is poorly ventilated, sending more blood would waste it — the blood would leave still deoxygenated. So the lung diverts blood away from poorly ventilated regions toward well-ventilated ones, which is called hypoxic pulmonary vasoconstriction and is exactly the right behaviour (Chapter 8.4).
Its downside appears at altitude and in chronic lung disease, where the whole lung is hypoxic, so the whole pulmonary circulation constricts, pressure rises, and the right ventricle strains.
Hepatic portal — blood from the gut does not go straight back to the heart. It drains into the portal vein and passes through the liver first, so everything absorbed from food is processed before reaching the rest of the body.
This is why some drugs cannot be given by mouth. The liver metabolises a large fraction on the first pass, so the dose reaching the circulation is a fraction of the dose swallowed. It is why glyceryl trinitrate is given under the tongue — that region drains directly into the systemic veins, bypassing the liver entirely — and why some drugs are given by injection or patch instead. Chapter 22.2.
Aneurysm and dissection
An aneurysm is a localised dilation of an artery, and the physics of why it is dangerous is worth stating.
Laplace's law says wall tension rises with radius:
T \propto P \times r
So a wider vessel has higher wall tension at the same pressure, which stretches it further, which raises the tension further. This is positive feedback (Chapter 4.7), and it is why aneurysms enlarge at an accelerating rate and why rupture risk rises steeply with diameter.
Abdominal aortic aneurysm — normal aorta about 2 cm; an aneurysm is over 3 cm. Rupture risk is low below 5.5 cm and rises sharply above it, which is why that figure is the usual threshold for repair.
Usually completely silent until rupture, at which point mortality is around 80 percent overall. Screening men at 65 with a single ultrasound has been shown to reduce deaths, and it is a national programme in several countries.
Aortic dissection is different: the inner layer of the wall tears and blood tracks into the wall itself, splitting it lengthwise. The classic description is sudden severe tearing chest pain radiating to the back, and it can present with unequal blood pressures in the two arms.
It is one of the most dangerous conditions in medicine — mortality rises by roughly 1 to 2 percent per hour untreated. And it is a diagnosis that must be made before giving clot-busting drugs for a suspected heart attack, because thrombolysis in a dissection is catastrophic.
What the next page fixes
The vessels distribute blood at a pressure the heart generates. Chapter 7.6 covers how that pressure is regulated — the second-to-second reflexes, the hormone systems that set it over days, why hypertension is the leading modifiable cause of death worldwide, and why almost every effective treatment for it works on the kidney.