Difficulty: Intermediate | Prerequisites: Cardiac output and stroke volume (Part 2 of these notes), basic physics concepts of pressure, flow, and resistance.
This section covers the plumbing side of the cardiovascular system: the different types of blood vessels, how blood flows through them, what determines blood pressure, and how the body regulates pressure both locally and systemically. It also covers capillary exchange (Starling forces) and what happens when regulation fails (oedema, haemorrhage responses). This is where the cardiac pump meets the vascular circuit, and the key linking equation is MAP ≈ CO x TPR. If you understand that equation and the factors feeding into each side, you can reason through most clinical scenarios in this chapter.
Arterioles are the main resistance vessels and the biggest site of pressure drop. Veins are capacitance vessels holding most of the blood volume. Blood flow depends on the pressure gradient divided by resistance, and vessel radius is by far the most powerful determinant of resistance (fourth-power relationship). Mean arterial pressure is set by cardiac output and total peripheral resistance. The baroreceptor reflex adjusts both in real time. At the capillary level, filtration and reabsorption are governed by the balance of hydrostatic and oncotic pressures (Starling forces). When that balance tips, oedema results.
Elastic arteries
The largest arteries (aorta, pulmonary trunk, major branches). Their walls are rich in elastin, allowing them to stretch during systole and recoil during diastole, smoothing pulsatile flow into more continuous flow downstream.
Muscular arteries
Medium-sized arteries with a thick smooth muscle layer. They distribute blood to specific organs and regions.
Arterioles
Small-diameter vessels with substantial smooth muscle relative to their lumen size. They are the primary resistance vessels in the circulation and the major site of pressure drop. Think of them as the taps of the circulatory system: by constricting or dilating, they control how much blood reaches each capillary bed and heavily influence total peripheral resistance.
Capillaries
The smallest, thinnest-walled vessels (single layer of endothelium). They are the major site of exchange of gases, nutrients, and wastes between blood and tissues. They do not contain smooth muscle or cardiac muscle. They do not generate high pressure.
Veins (and venules)
Low-pressure, thin-walled vessels that return blood to the heart. They function as capacitance vessels (blood reservoirs), normally holding roughly 60-70% of total blood volume. Many contain one-way venous valves to prevent backflow. They have the largest total cross-sectional area among vessel types.
Venous valves
One-way flaps inside veins that ensure blood flows toward the heart and does not pool under gravity.
Compliance (vascular)
The ability of a vessel wall to stretch and accommodate volume. Veins have the greatest compliance of any vessel type, which is why they serve as the body's blood reservoir.
Total peripheral resistance (TPR)
The sum of all vascular resistance in the systemic circulation, determined primarily by arteriolar diameter. Also called systemic vascular resistance (SVR).
Resistance vessel
Arterioles. Their smooth muscle tone is the single largest controllable factor in setting TPR.
Capacitance vessel
Veins. Their high compliance allows them to hold large volumes of blood at low pressure.
Mean arterial pressure (MAP)
The average pressure in the arterial system during one cardiac cycle. Determined most directly by cardiac output and total peripheral resistance: MAP ≈ CO x TPR.
Pulse pressure
The difference between systolic and diastolic pressure (systolic minus diastolic). It reflects the volume ejected per beat (stroke volume) and arterial compliance.
Venous return
The flow of blood back to the right atrium. Factors that increase it include the skeletal muscle pump, the respiratory pump, sympathetic venoconstriction (decreasing venous compliance), and gravity (when supine).
Skeletal muscle pump
Contraction of skeletal muscles in the limbs compresses veins, pushing blood toward the heart. Venous valves prevent backflow. This is a major mechanism for increasing venous return during exercise.
Baroreceptors
Stretch-sensitive nerve endings in the walls of the carotid sinus and aortic arch that detect changes in arterial pressure and relay information to the cardiovascular control centre in the medulla.
Baroreceptor reflex
A negative-feedback loop: when arterial pressure falls, baroreceptor firing decreases, the medulla increases sympathetic output and decreases parasympathetic output, resulting in increased heart rate, increased contractility, and vasoconstriction to restore pressure. The opposite occurs when pressure rises.
Nitric oxide (NO)
A potent vasodilator released by vascular endothelial cells. It relaxes underlying smooth muscle, reducing local resistance and increasing blood flow.
Active hyperaemia
An increase in blood flow to a tissue in response to increased metabolic activity. Local metabolites (adenosine, CO2, H+, K+) and reduced O2 cause arteriolar vasodilation.
Reactive hyperaemia
An increase in blood flow to a tissue after a period of temporary ischaemia (reduced blood supply). The same metabolite buildup drives vasodilation when the occlusion is released.
Capillary hydrostatic pressure (Pc)
The blood pressure inside the capillary, which pushes fluid out of the capillary into the interstitial space (favours filtration).
Plasma colloid osmotic pressure (oncotic pressure, πp)
The osmotic pressure exerted by plasma proteins (mainly albumin) that pulls fluid back into the capillary (opposes filtration).
Starling forces
The four pressures governing capillary fluid exchange: capillary hydrostatic pressure, interstitial hydrostatic pressure, plasma colloid osmotic pressure, and interstitial osmotic pressure. Net filtration pressure is determined by their balance.
Oedema
Excess fluid accumulation in the interstitial space. Caused by anything that increases capillary hydrostatic pressure, decreases plasma oncotic pressure, increases capillary permeability, or impairs lymphatic drainage.
Hypoalbuminaemia
Abnormally low plasma albumin concentration (as in liver failure or nephrotic syndrome), which reduces plasma oncotic pressure and leads to oedema.
Elastic arteries: stretch and recoil to smooth pulsatile flow. Pressure is highest here.
Muscular arteries: distribute blood to organs.
Arterioles: main resistance vessels. The largest pressure drop occurs across the arterioles. Small changes in radius produce large changes in resistance (fourth-power relationship).
Capillaries: exchange vessels. Thinnest walls (single endothelial layer). Slowest blood velocity (because total cross-sectional area is largest here). No smooth muscle.
Venules and veins: return blood to the heart. Capacitance vessels holding ~60-70% of blood volume. Contain venous valves.
Veins normally contain the largest percentage of total blood volume (roughly 60-70%).
Capillaries hold a relatively small fraction.
Arterioles and arteries hold the remainder.
Capillaries have the largest total cross-sectional area in the circulation.
Blood velocity is inversely related to total cross-sectional area. Because capillaries collectively have the largest cross-sectional area, blood velocity is slowest there. This is functionally important: slow flow maximises time for exchange.
The aorta has the smallest cross-sectional area (single tube), so velocity is highest there.
Flow = pressure gradient / resistance (analogous to Ohm's law).
Blood flow through an organ is directly proportional to the pressure gradient across it and inversely proportional to vascular resistance.
Resistance depends on vessel length, blood viscosity, and (most powerfully) vessel radius: R ∝ 1/r⁴. A small decrease in radius produces a markedly increased vascular resistance.
The largest pressure drop occurs across the arterioles, because they are the main resistance vessels.
MAP ≈ CO x TPR. This is the most direct relationship.
MAP can also be estimated as: diastolic pressure + 1/3 (pulse pressure).
MAP is determined by cardiac output and total peripheral resistance together, not by heart rate alone, stroke volume alone, or pulse pressure alone.
Pulse pressure = systolic pressure minus diastolic pressure.
It reflects stroke volume and arterial compliance.
Note: pulse pressure is not the same as MAP, and EDV minus ESV gives you stroke volume, not pulse pressure.
Generalised arteriolar vasoconstriction (e.g. by a vasoconstrictor drug) increases TPR most directly. If CO stays constant, MAP rises.
Generalised arteriolar vasodilation decreases TPR. If CO stays constant, MAP falls.
A drug that increases arteriolar radius throughout the body decreases TPR first.
Chronic hypertension results in increased left ventricular afterload, because the ventricle must generate more pressure to eject against chronically elevated arterial pressure.
Increases venous return: skeletal muscle pump activation, respiratory pump, sympathetic venoconstriction (decreases venous compliance, squeezing blood forward), supine position.
Decreases venous return: standing motionless (blood pools in leg veins), increased venous compliance (venodilation), haemorrhage (less total blood volume).
When a patient stands up quickly after lying down, the variable that decreases first is venous return (blood pools in the lower extremities under gravity before any reflex compensation).
Baroreceptors detect stretch in arterial walls, which correlates with pressure.
When pressure drops (e.g. haemorrhage, standing), baroreceptor firing decreases.
Decreased firing leads the medulla to increase sympathetic output and decrease parasympathetic output.
Results: increased heart rate, increased contractility, arteriolar vasoconstriction (increased TPR), venoconstriction (increased venous return).
When pressure rises, the opposite occurs: increased baroreceptor firing leads to parasympathetic dominance, lowering HR and vasodilating.
Acute loss of ~1 litre of blood reduces blood volume, reducing venous return, reducing preload, reducing stroke volume and cardiac output, reducing MAP.
Before compensation: decreased venous return, decreased stroke volume, decreased MAP (the combination is: ↓ venous return, ↓ stroke volume).
Baroreceptor firing decreases (less arterial wall stretch).
Compensatory response: increased sympathetic activity (increased HR, increased contractility, vasoconstriction).
Active hyperaemia: increased metabolic activity produces local metabolites (adenosine, CO2, H+, K+, decreased O2) that cause arteriolar vasodilation, increasing blood flow to match demand.
The factor that most strongly promotes active hyperaemia: increased local adenosine (and other metabolites).
Increased O2 is the local factor least likely to promote vasodilation, because high oxygen tends to cause local vasoconstriction.
Reactive hyperaemia: increased blood flow after a period of temporary ischaemia. During the occlusion, metabolites accumulate; upon release, they cause robust vasodilation.
Nitric oxide (NO): released by endothelial cells, causes vasodilation of underlying smooth muscle. A key paracrine regulator of local flow.
Forces favouring filtration (fluid out of the capillary): capillary hydrostatic pressure (the dominant force driving filtration) and interstitial osmotic pressure.
Forces opposing filtration (fluid into the capillary): plasma colloid osmotic pressure (oncotic pressure, the dominant force pulling fluid back in) and interstitial hydrostatic pressure.
Net filtration = (forces favouring filtration) minus (forces opposing filtration).
At the arteriolar end of the capillary, filtration dominates. At the venular end, reabsorption dominates (though not completely, with the lymphatics picking up the excess).
Reduced plasma protein concentration (hypoalbuminaemia, as in liver failure) decreases plasma colloid osmotic pressure, so less fluid is pulled back in, and oedema results.
Increased capillary hydrostatic pressure (as in heart failure or venous obstruction) pushes more fluid out.
When both factors are present simultaneously (decreased plasma proteins AND increased capillary hydrostatic pressure), the result is markedly increased oedema formation, because filtration is promoted while reabsorption is impaired.
Relationship | Formula |
|---|---|
Blood flow | Flow = ΔP / R |
Resistance (Poiseuille) | R ∝ (η × L) / r⁴ |
Mean arterial pressure | MAP ≈ CO × TPR |
MAP estimate | MAP ≈ diastolic + 1/3 (systolic - diastolic) |
Pulse pressure | PP = systolic - diastolic |
Where ΔP = pressure gradient, R = resistance, η = viscosity, L = vessel length, r = vessel radius.
The fourth-power relationship of radius to resistance is the single most important thing to remember about vascular physics.
This is why your doctor measures blood pressure: systolic and diastolic readings let them estimate MAP and pulse pressure, which reflect cardiac output and arterial compliance. Antihypertensive drugs target the very mechanisms in these notes: ACE inhibitors and ARBs reduce arteriolar tone (lowering TPR), beta-blockers reduce cardiac output, and diuretics reduce blood volume (lowering venous return and preload). Compression stockings work by opposing venous pooling, exactly the principle of the skeletal muscle pump and venous compliance.
Patients with liver cirrhosis develop oedema (ascites, peripheral swelling) because the failing liver cannot produce enough albumin, reducing plasma oncotic pressure. This is a direct clinical application of Starling forces.
Students often confuse resistance vessels (arterioles) with capacitance vessels (veins). Arterioles control resistance; veins store volume. They are different roles for different vessels.
A common error is thinking capillaries generate high pressure. They do not. Pressure is highest in the aorta and elastic arteries, drops steeply across the arterioles, and is low in capillaries and veins.
Students sometimes think blood velocity is slowest in the smallest individual vessel. Velocity depends on total cross-sectional area, not individual vessel size. Because there are billions of capillaries, their combined cross-sectional area is the largest, and velocity is the slowest.
"Increased O2 causes vasodilation" is a common exam trap. High local O2 actually causes vasoconstriction. It is decreased O2 (and increased CO2, H+, adenosine) that causes vasodilation.
Students confuse pulse pressure with MAP. Pulse pressure = systolic minus diastolic. MAP ≈ CO x TPR.
⚠️ Arterioles = resistance vessels. Veins = capacitance vessels. The largest pressure drop occurs across the arterioles.
⚠️ Veins contain the largest percentage of total blood volume.
⚠️ Blood velocity is slowest in capillaries (largest total cross-sectional area). Capillaries are the site of exchange.
⚠️ Decreased vessel radius markedly increases resistance (fourth-power relationship).
⚠️ MAP is most directly determined by CO and TPR together.
⚠️ Pulse pressure = systolic minus diastolic.
⚠️ Baroreceptor firing decreases when arterial pressure drops. The compensatory response is increased sympathetic activity.
⚠️ Increased local O2 is the factor least likely to promote vasodilation. Adenosine, CO2, and H+ all promote vasodilation.
⚠️ Plasma colloid osmotic pressure is the force that most strongly opposes capillary filtration. Capillary hydrostatic pressure is the force that most strongly favours filtration.
⚠️ Hypoalbuminaemia (e.g. liver failure) causes oedema by decreasing plasma colloid osmotic pressure.
⚠️ Standing up quickly from supine decreases venous return first (before any reflex compensation).
⚠️ Skeletal muscle pump activation is the factor that most increases venous return.
True or false: Arterioles are the primary capacitance vessels. ___
Fill in the blank: MAP ≈ ___ x ___. ___
True or false: Increased O2 promotes local vasodilation. ___
Fill in the blank: The force that most strongly opposes capillary filtration is plasma ___ osmotic pressure. ___
True or false: After haemorrhage, baroreceptor firing increases. ___
Answers: 1. False (arterioles are resistance vessels; veins are capacitance vessels). 2. CO x TPR. 3. False (increased O2 tends to cause vasoconstriction). 4. colloid (oncotic). 5. False (baroreceptor firing decreases when pressure drops).
Q: Which blood vessel normally contains the largest percentage of total blood volume?
A: Veins.
Q: Which vessel type is the major resistance vessel?
A: Arterioles.
Q: Blood flow through an organ is directly proportional to what?
A: The pressure gradient (across the organ's vascular bed).
Q: A decrease in vessel radius produces what effect on vascular resistance?
A: Markedly increased vascular resistance (fourth-power relationship).
Q: Blood velocity is slowest in which vessel type?
A: Capillaries (largest total cross-sectional area).
Q: Which vessel experiences the largest decrease in pressure?
A: Arterioles (the main site of resistance and pressure drop).
Q: Mean arterial pressure is most directly determined by what?
A: Cardiac output and total peripheral resistance.
Q: Pulse pressure equals what?
A: Systolic pressure minus diastolic pressure.
Q: A drug causes generalised arteriolar vasoconstriction. Which variable increases most directly?
A: Total peripheral resistance.
Q: Generalised arteriolar vasodilation (with CO constant) causes what change in MAP?
A: Decreased MAP.
Q: A patient stands up quickly. Which variable decreases first?
A: Venous return.
Q: After a patient suddenly loses 1 litre of blood, baroreceptor firing will do what?
A: Decrease (less arterial wall stretch due to lower pressure).
Q: Following that haemorrhage, which compensatory response occurs?
A: Increased sympathetic activity (raising HR, contractility, and TPR).
Q: Which Starling force most favours filtration?
A: Capillary hydrostatic pressure.
Q: Which factor most strongly opposes capillary filtration?
A: Plasma colloid osmotic (oncotic) pressure.
Q: A patient with liver failure and severe hypoalbuminaemia develops oedema. What is the primary cause?
A: Decreased plasma colloid osmotic pressure (less albumin means less oncotic pull to reabsorb fluid).
Q: A patient has reduced plasma protein concentration. Which complication is most likely?
A: Oedema.
Q: Which local factor is least likely to promote vasodilation?
A: Increased O2 (high oxygen tends toward vasoconstriction, not vasodilation).
Q: What primarily causes active hyperaemia?
A: Local metabolite accumulation (adenosine, CO2, H+) causing arteriolar vasodilation.
Q: Which statement best describes reactive hyperaemia?
A: Increased blood flow after temporary ischaemia (metabolites accumulated during the occlusion drive vasodilation on release).
Q: Nitric oxide released from vascular endothelium primarily causes what?
A: Vasodilation.
Q: Which blood vessel has the greatest compliance?
A: Veins.
Q: Which structure ensures one-way blood flow within veins?
A: Venous valves.
Q: Which change would most increase venous return?
A: Skeletal muscle pump activation.
Q: Which statement about capillaries is correct?
A: They are the major site of exchange (thin walls, slow velocity, no smooth muscle).
Q: Which statement regarding veins is correct?
A: They function as capacitance vessels (blood reservoirs).
Q: The largest total cross-sectional area is found in which part of the circulation?
A: Capillaries.
Q: A patient has chronic hypertension. Which adaptation is most likely?
A: Increased left ventricular afterload (the ventricle must work harder against chronically elevated arterial pressure).
Q: Which combination is most likely during acute haemorrhage before compensation?
A: Decreased venous return, decreased stroke volume.
Q: A patient has decreased plasma protein AND increased capillary hydrostatic pressure. What is the most likely consequence?
A: Markedly increased oedema formation (filtration is promoted and reabsorption is impaired simultaneously).
This material directly extends the cardiac output concepts from Part 2: MAP = CO x TPR, so anything that changes CO (from Part 2) or TPR (from this section) changes blood pressure. The baroreceptor reflex uses the autonomic pathways covered in Part 2 (sympathetic and parasympathetic effects on the heart) plus the arteriolar vasoconstriction and venoconstriction covered here. Capillary exchange connects to renal physiology (filtration at the glomerulus uses similar Starling forces) and to the lymphatic system (which handles excess filtered fluid). If your course covers exercise physiology, the interplay between increased CO and decreased TPR during exercise is a direct application of this material.
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