Regional circulations

The core idea

Arterioles in each organ set their own tone, so local needs override the central nervous system in most beds. Three local mechanisms do the work:

• Autoregulation: flow stays nearly constant while perfusion pressure changes over a wide range. It is strongest in brain, heart and kidney.
• Myogenic response: stretch of vascular smooth muscle opens stretch-activated cation channels, depolarises the cell and makes it contract. A rise in pressure therefore narrows the arteriole and keeps flow steady.
• Metabolic control: active tissue releases adenosine, CO₂, H⁺, K⁺, lactate and lowers local O₂; these dilate arterioles so that flow follows activity (active hyperaemia). After a period of blocked flow, the accumulated metabolites cause a large rebound (reactive hyperaemia).
• In the kidney a fourth mechanism, tubuloglomerular feedback, adds to the myogenic response: the macula densa senses a high NaCl load in the distal tubule and releases adenosine, which constricts the afferent arteriole and brings GFR back down.

Main controller in each organ

Coronary circulation

• The myocardium extracts about 70–75% of delivered oxygen even at rest, so coronary venous blood is the most desaturated in the body. Extra demand cannot be met by extracting more; it must be met by raising flow.
• During exercise the main signal is local metabolic vasodilatation, with adenosine (from ATP breakdown) the classic mediator, helped by low O₂, CO₂, H⁺, K⁺ and nitric oxide. Sympathetic alpha-constriction is weak and overridden.
• Left ventricular flow is mainly diastolic. The contracting LV wall squeezes intramyocardial vessels, so flow to the LV falls almost to zero (or briefly reverses) in early systole and peaks in early diastole. The subendocardium is compressed most and is the first layer to become ischaemic.
• Right ventricular flow continues through systole and diastole, because RV pressure is low and does not compress its vessels much.
• In a normal heart, a faster heart rate raises total coronary flow because metabolic dilatation outweighs the lost diastolic time. When the vessels are already maximally dilated (fixed stenosis, aortic stenosis, severe LV hypertrophy), tachycardia shortens diastole and cuts LV flow, so angina appears with fast rates even with normal coronary arteries.
• Coronary perfusion pressure is aortic diastolic pressure minus LV end-diastolic pressure. Low diastolic pressure (aortic regurgitation, hypotension) or high LVEDP (heart failure) reduce it.
• A stenosis of about 70% or more uses up the dilator reserve: flow is enough at rest but not on exertion (stable angina).
• Venous drainage: the coronary sinus carries about 75% of coronary venous return (most of the left ventricle's), into the right atrium. Anterior cardiac veins drain much of the RV directly into the right atrium, and small Thebesian veins open straight into the chambers; those entering the left heart add a little to the normal physiological shunt.

Cerebral circulation

• Resting flow is about 750 mL/min, around 15% of cardiac output for an organ that is 2% of body weight; grey matter receives more than white.
• Autoregulation holds flow constant for MAP of about 60–150 mmHg (some texts give 50–150). In chronic hypertension the whole curve shifts to the right, so a sudden drop to "normal" pressure can cause cerebral ischaemia.
• CO₂ is the most powerful regulator. CO₂ crosses the blood–brain barrier and lowers perivascular pH, dilating arterioles. Flow changes by about 2–4% per mmHg change in PaCO₂ (roughly doubling at a PaCO₂ of 80 mmHg). Hyperventilation lowers PaCO₂, constricts vessels and briefly lowers intracranial pressure.
• Hypoxia dilates cerebral vessels only when PaO₂ falls below about 50–60 mmHg (6.7–8 kPa).
• Causes of a raised cerebral blood flow: hypercapnia, severe hypoxia, acidosis, seizures and increased neuronal activity (K⁺, adenosine), fever, anaemia, and drugs such as volatile anaesthetics, ketamine and nitrates. Among volatile agents, halothane dilates cerebral vessels most. Thiopental and propofol reduce flow. Around an infarct, local acidosis and lost autoregulation produce "luxury perfusion".
• Neurovascular coupling: active neurones and astrocytes release K⁺, adenosine, NO and prostaglandins, matching local flow to local activity.
• The Cushing reflex: raised intracranial pressure compresses vessels; brainstem ischaemia drives a strong sympathetic rise in blood pressure, and the baroreflex then slows the heart (hypertension, bradycardia, irregular breathing).
• The blood–brain barrier comes from tight junctions between capillary endothelial cells, supported by a basement membrane and astrocyte foot processes.

Pulmonary circulation

• Pressure about 25/10 mmHg (mean about 15), resistance about one-tenth of systemic, yet it carries the entire right ventricular output.
• When cardiac output rises, pulmonary resistance falls further by recruitment of closed capillaries and distension of open ones, so pressure barely rises.
• Hypoxic pulmonary vasoconstriction: low alveolar PO₂ (more than arterial PO₂) inhibits oxygen-sensitive K⁺ channels in pulmonary arteriolar smooth muscle; the cell depolarises, Ca²⁺ enters and the vessel constricts. This diverts blood away from poorly ventilated alveoli and improves V/Q matching.
• When hypoxia is generalised (altitude, COPD), the same response raises pulmonary pressure, causing pulmonary hypertension and cor pulmonale. Giving high-flow oxygen in COPD releases this constriction in poorly ventilated areas, worsening V/Q mismatch and contributing to CO₂ retention.
• In the fetus, hypoxic constriction keeps pulmonary resistance high; with the first breaths alveolar PO₂ rises, pulmonary resistance falls, left atrial pressure rises and the foramen ovale closes.
• The lung tissue itself is supplied by the bronchial arteries (from the descending thoracic aorta). Some bronchial venous blood drains into the pulmonary veins, another part of the normal shunt.

Skin and skeletal muscle

• Skin flow serves temperature, not metabolism. Fingers, toes, palms, ears and nose contain arteriovenous anastomoses with dense sympathetic (alpha-adrenergic) innervation. In heat, sympathetic tone falls, the anastomoses open and skin flow can rise many times above its metabolic need, delivering heat to the surface. Cutaneous vasodilatation in heat also needs active sympathetic cholinergic dilator fibres linked to sweating (with bradykinin). In cold, the anastomoses close.
• A large skin flow in a hot climate raises cardiac output and can strain a failing heart.
• Raynaud phenomenon is an exaggerated cold- or emotion-induced vasospasm of digital arteries (white, then blue, then red). After warmth and stopping smoking, first-line drug treatment is a dihydropyridine calcium-channel blocker such as nifedipine. Digital ulcers point to secondary Raynaud (for example systemic sclerosis).
• Skeletal muscle at rest is under sympathetic alpha tone; adrenaline at low doses dilates via beta-2 receptors. During exercise local metabolites (K⁺, adenosine, H⁺, CO₂, lactate, low O₂, raised osmolality) override sympathetic constriction ("functional sympatholysis"), while skin, gut and kidney constrict to redirect flow.
• Muscle tolerates complete ischaemia only for a limited time. Under a pneumatic limb tourniquet, prolonged ischaemia and pressure damage muscle and nerve, so upper-limb tourniquet time is usually kept to about 1.5–2 hours; release produces reactive hyperaemia.

Where the blood is

Remember Heart runs on metabolites and fills in diastole; brain answers to CO₂; lung shuts down where oxygen is low; skin is a radiator under sympathetic control.

Exam trap Hypoxia constricts pulmonary arterioles but dilates systemic arterioles, including coronary and cerebral ones.

Exam trap Right coronary flow continues in systole; only left ventricular flow is mainly diastolic.

How FCPS asks about this

• Main regulator of coronary flow in exercise: local metabolites, especially adenosine, because O₂ extraction is already near maximal.
• When does left coronary flow peak: early diastole; tachycardia hurts the subendocardium when vessels are already maximally dilated.
• Coronary sinus drainage: about 75% of coronary venous blood, emptying into the right atrium.
• Cerebral blood flow: about 750 mL/min, 15% of cardiac output; autoregulation range MAP about 60–150 mmHg; most sensitive to PaCO₂.
• Raised cerebral flow: hypercapnia, severe hypoxia, volatile anaesthetics (halothane most), ketamine, seizures.
• Mechanism of hypoxic pulmonary vasoconstriction: low alveolar PO₂ closes K⁺ channels, depolarises smooth muscle; diverts blood to ventilated alveoli.
• Huge skin flow in heat: arteriovenous anastomoses open as sympathetic tone falls; Raynaud first-line drug is nifedipine.