Evidence-based physiotherapy and rehabilitation resources
Editorial & review policy
Evidence-based physiotherapy and rehabilitation resources
Editorial & review policyHuman Physiology · Cardiovascular system
Blood pressure is held steady by reflexes, local signals and hormones, while each organ adjusts its own share of the flow. This page explains those controls, how the brain, heart, muscle and skin circulations differ, and what happens when control fails on standing up.
Part 3 · Cardiovascular System · Chapter 15 of 47
By the end of this page you should be able to:
Every time you sit a patient up after bed rest, you are testing their cardiovascular control. Some will feel dizzy or faint because the reflexes that hold blood pressure have weakened.
Knowing how each organ protects its own blood supply also explains why blood pressure targets matter after stroke, why exercise helps the coronary arteries, and why heat makes exercise harder.
| Level | Main mechanisms | Speed | Main purpose |
|---|---|---|---|
| Local | Myogenic response, metabolites, endothelial nitric oxide | Seconds | Match flow to each tissue’s needs |
| Neural | Sympathetic and vagal nerves directed by the medulla | Seconds | Hold arterial pressure steady; redistribute flow |
| Hormonal | Adrenaline, angiotensin II, antidiuretic hormone, natriuretic peptides | Minutes to days | Adjust vessel tone and blood volume |
These levels interact. Local signals ask for more flow; neural reflexes decide how much can be given without letting arterial pressure fall. Joyner and Casey describe this as a hierarchy of competing physiological needs [2].
Figure 1 · The baroreceptor reflex
Stretch receptors in the carotid sinus and aortic arch fire faster as arterial pressure rises. The medulla responds by increasing vagal activity and reducing sympathetic activity, so the heart slows and vessels dilate. A fall in pressure produces the opposite.
The reflex is fast and works beat to beat. It is the main defence against the fall in pressure on standing up.
| Reflex or input | Stimulus | Main effect |
|---|---|---|
| Peripheral chemoreceptors | Low oxygen, high carbon dioxide or acid in blood | Raise sympathetic activity and breathing |
| Cardiopulmonary receptors | Stretch of atria and great veins | Adjust sympathetic tone and kidney water handling |
| Exercise pressor reflex | Mechanical and chemical signals from working muscle | Raise heart rate and blood pressure |
| Central command | Signals from motor areas as exercise begins | Raise heart rate immediately, before metabolic change |
Many organs keep their blood flow nearly constant when blood pressure changes. This is autoregulation. Arteriolar smooth muscle contracts when stretched by higher pressure (the myogenic response), and accumulating metabolites dilate it when flow is low [1].
The endothelium adds a third signal. Faster flow along the vessel wall releases nitric oxide, which relaxes smooth muscle. Damage to the endothelium, as in coronary disease, weakens this dilation.
Figure 2 · Brain blood flow autoregulation
In the brain, autoregulation usually holds flow steady between mean pressures of about 60 and 150 mmHg [1]. In long-standing hypertension the range shifts upward, so a sudden drop to ‘normal’ pressure can reduce brain flow [1]. After acute ischaemic stroke or severe head injury, autoregulation may be lost [1].
Why this matters after stroke
Without autoregulation, brain flow follows blood pressure passively [1]. Large swings in pressure during early mobilisation can therefore under- or over-perfuse vulnerable tissue. Follow the team’s blood pressure limits and monitor during first sitting and standing.
| Circulation | Special features | Main controller | Clinical note |
|---|---|---|---|
| Coronary | Flow mainly in diastole in the left ventricle; high oxygen extraction even at rest | Local metabolites | More demand must be met by more flow; fast heart rates shorten diastole |
| Cerebral | Autoregulation; very sensitive to carbon dioxide [1] | Myogenic, metabolic, CO2 | Hyperventilation lowers brain flow |
| Skeletal muscle | Flow can rise more than twentyfold in exercise | Local metabolites versus sympathetic tone [2] | Muscle pump aids venous return |
| Skin | Arteriovenous shunts for heat loss | Sympathetic, temperature | Heat diverts blood from muscle |
| Pulmonary | Low pressure; vessels constrict in low oxygen | Local oxygen | Covered in Part 4 |
| Renal and splanchnic | High resting flow; cut in exercise | Sympathetic, autoregulation | Covered in Parts 5 and 7 |
Figure 3 · Where the blood goes
In heavy exercise, cardiac output may rise fivefold, and working muscle can take most of it. Local metabolites dilate muscle arterioles and blunt the effect of sympathetic nerves there. Elsewhere, sympathetic constriction reduces flow to the gut and kidneys [2].
Muscle cannot take everything. If all muscle beds dilated fully, the heart could not supply them and blood pressure would fall. Sympathetic restraint of muscle flow protects arterial pressure [2].
The heart extracts most of the oxygen from coronary blood even at rest. When demand rises, the only way to supply more oxygen is to increase flow. Narrowed or poorly dilating coronary arteries therefore cause angina during effort.
Figure 4 · Exercise repairs coronary vessel function
Hambrecht and colleagues randomised 19 patients with coronary disease to exercise training or usual care. After four weeks, coronary flow reserve rose by 29% and abnormal constriction to acetylcholine fell by 54% [3]. This is one way cardiac rehabilitation helps.
On standing, about half a litre of blood pools in the legs and abdomen. Venous return, stroke volume and blood pressure fall briefly. The baroreflex raises heart rate and constricts vessels, and the muscle pump helps return blood, so pressure recovers within seconds.
Figure 5 · Standing up: normal and abnormal
| Condition | Consensus definition [4] |
|---|---|
| Orthostatic hypotension | Sustained fall of at least 20 mmHg systolic or 10 mmHg diastolic within 3 minutes of standing or head-up tilt |
| Postural tachycardia syndrome | Sustained heart rate rise of at least 30 beats/min within 10 minutes of standing, without orthostatic hypotension, with symptoms |
| Neurally mediated (reflex) syncope | Brief loss of consciousness from a reflex fall in heart rate and vessel tone |
Bed rest, dehydration, blood pressure drugs, diabetes, Parkinson disease and spinal cord injury all weaken orthostatic control. Older adults and patients after long stays in intensive care are at particular risk.
Practical skill · first time up
Measure lying blood pressure, then sit and stand in stages, rechecking at one and three minutes [4]. Ask about dizziness and watch for pallor. Ankle pumps, leg crossing and buttock squeezing raise venous return. Stop and lie the patient down if symptoms appear.
| Finding | Likely meaning | Action |
|---|---|---|
| Systolic falls 25 mmHg after 2 minutes standing with dizziness | Orthostatic hypotension [4] | Sit or lie down; graded mobilisation; inform team |
| Heart rate rises 35 beats/min on standing, pressure stable | Possible postural tachycardia [4] | Record; refer for assessment |
| Angina during brisk walking | Coronary flow cannot meet demand | Stop; follow cardiac protocol; review training intensity |
| Dizziness after a hot shower and exercise | Skin vasodilation plus low venous return | Cool down, fluids, sit |
Describe the regulation of arterial blood pressure. Add a note on the cerebral circulation.
Muscle blood flow in exercise is presented as controlled by local metabolites alone, and exercise is said to help the heart mainly by slowing the heart rate.
Muscle flow reflects a balance between local dilation and sympathetic restraint that protects blood pressure [2].
Exercise training directly improves coronary endothelial function and flow reserve within weeks [3].
Blood pressure is a shared resource. Each organ asks for flow; reflexes decide how much can be given. Standing up is the everyday test of that system.
10 questions on this page. Tap one to see the answer and the reasoning.
Answer: (B) Cerebral autoregulation typically operates between mean pressures of about 60 and 150 mmHg [1].
Answer: (A) The autoregulatory range shifts toward high blood pressure [1].
Answer: (B) Autoregulation is lost in severe head injury or acute ischaemic stroke [1].
Answer: (A) Changes in arterial carbon dioxide tension shift cerebral flow and its autoregulatory limits [1].
Answer: (A) Muscle hyperaemia competes with the need to maintain arterial pressure in a hierarchy of needs [2].
Answer: (B) Flow reserve rose from 2.8 to 3.6, an increase of 29% [3].
Answer: (B) Exercise improved endothelium-dependent vasodilation in epicardial and resistance vessels [3].
Answer: (C) The consensus definition uses 20 mmHg systolic or 10 mmHg diastolic within 3 minutes [4].
Answer: (C) A rise of 30 beats/min or more within 10 minutes, without orthostatic hypotension [4].
Answer: (B) This reflex response normally prevents the sustained falls that define orthostatic hypotension [4].
Key takeaways
| Source | Why it earns its place |
|---|---|
| Paulson OB et al. — Cerebrovasc Brain Metab Rev, 1990 | Classic account of cerebral autoregulation [1] |
| Joyner MJ, Casey DP — Physiological Reviews, 2015 | Muscle blood flow in exercise [2] |
| Hambrecht R et al. — NEJM, 2000 | Exercise and coronary endothelial function [3] |
| Freeman R et al. — Clin Auton Res, 2011 | Definitions of orthostatic syndromes [4] |
Reviewed by the Physiotherapist India Team. · Human Physiology contents