# Circulation > Circulation for FMGE Physiology: blood pressure = CO x TPR, baroreflex wiring, RAAS, Poiseuille's law, Starling capillary forces and oedema. - Canonical URL: https://prepelephant.com/topics/fmge/physiology/circulation-fmge - Exam / course: FMGE · Subject: Physiology - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-02 - Last updated: 2026-10-02 - How to cite: "Circulation", PrepElephant, https://prepelephant.com/topics/fmge/physiology/circulation-fmge ## Direct answer Mean arterial pressure is cardiac output multiplied by total peripheral resistance — roughly 5 L/min through about 18-20 mmHg of resistance per litre per minute — and it is defended second to second by the baroreceptor reflex: stretch receptors in the carotid sinus (signalling through Hering's nerve to the glossopharyngeal nerve) and the aortic arch (through the vagus) slow the heart and dilate vessels whenever pressure rises. Over hours to days the renin-angiotensin-aldosterone system takes the shift. At the capillary, Starling forces trade hydrostatic filtration against albumin-driven oncotic reabsorption, and disturbing that trade or the lymphatics produces oedema — the clinical end-point this topic keeps returning to. ## What you must remember - Numbers: 120/80 mmHg with pulse pressure 40 and mean arterial pressure near 93, calculated as diastolic plus one-third of pulse pressure; hypertension begins at 140/90. - Poiseuille's law makes resistance vary inversely with the fourth power of radius — which is why arterioles are the resistance vessels. - Baroreflex wiring, verbatim for the exam: carotid sinus via Hering's nerve to the glossopharyngeal (IX), aortic arch via the vagus (X), both converging on the nucleus tractus solitarius of the medulla. - Baroreceptors reset within one to two days, so they buffer minute-to-minute swings but do not set long-term pressure — that role belongs to the kidney through pressure-natriuresis. - Renin release from juxtaglomerular cells on three triggers: falling renal perfusion via beta-1 drive, low sodium chloride at the macula densa, and reduced stretch; angiotensin converting enzyme in the lung then makes angiotensin II. - Angiotensin II does five things at once: vasoconstricts, releases aldosterone (sodium retention, potassium loss), stimulates thirst and ADH, and promotes sympathetic activity — the reason ACE inhibitors cough and hyperkalaemia coexist. - Capillary Starling balance: about 2-4 mL/min of net filtrate is returned as lymph; oedema follows raised capillary pressure (heart failure), low oncotic pressure (nephrotic syndrome, cirrhosis, kwashiorkor), capillary injury (burns, sepsis) or lymphatic blockage (filariasis). ## Approach to a sudden fall in blood pressure A patient stands up, or bleeds, or faints — walk the compensation ladder in time order. Within seconds the baroreceptors sense reduced stretch and unload: sympathetic outflow surges, heart rate climbs, veins constrict to shift reservoir blood centrally, and arterioles clamp to defend mean pressure; the medulla does this before anyone has drawn a blood gas. Within the next half hour, angiotensin II and vasopressin add their vasoconstriction, and capillaries absorb interstitial fluid as precapillary sphincters close — auto-transfusion. Over hours to days aldosterone holds sodium, the kidney reclaims water by ADH, thirst drives intake, and erythropoietin slowly rebuilds the lost red cell mass. Grade the haemorrhage while the ladder runs, because exam stems hide the class in the vital signs: losing up to 15 per cent of blood volume leaves a normal lying blood pressure; class II (15-30 per cent) shows tachycardia with a narrowed pulse pressure; class III (30-40 per cent) brings hypotension with tachycardia and confusion; class IV beyond 40 per cent is immediately life-threatening. A narrowing pulse pressure is the earliest quantitative clue — systolic pressure is stroke-volume dependent and falls before diastolic, which the vasoconstriction actually supports. ## The classic trap The nerve assignment trips candidates every year: Hering's nerve belongs to the carotid sinus and joins the glossopharyngeal; the vagus carries aortic arch signals — swap them and the anatomy question is lost. The second trap is calling baroreceptors long-term controllers: they reset within days, so chronic hypertension persists with normal reflex sensitivity, and the kidney is the organ whose pressure-natriuresis curve has shifted. The Valsalva manoeuvre completes the topic in one question: straining raises intrathoracic pressure, impeding venous return (heart rate rises in phase II), and release causes pressure overshoot with reflex bradycardia (phase IV) — a bedside test of baroreflex integrity that goes flat-line in autonomic neuropathy, a common sequela of long-standing Indian diabetes. ## Frequently asked questions ### What is the full wiring of the baroreceptor reflex? Carotid sinus afferents run in Hering's nerve to the glossopharyngeal nerve, aortic arch afferents in the vagus, both ending in the nucleus tractus solitarius, which adjusts autonomic outflow within seconds. ### Why do baroreceptors not control long-term blood pressure? They reset to the prevailing pressure within one to two days; sustained control rests on renal sodium and water excretion — pressure natriuresis. ### Which four forces govern capillary fluid exchange? Capillary hydrostatic pressure favouring filtration, interstitial hydrostatic pressure opposing it, plasma oncotic pressure (albumin) reabsorbing, and interstitial oncotic pressure filtering — the small net surplus returns as lymph. ### What are the three triggers for renin release? Reduced renal perfusion pressure via beta-1 sympathetic drive, low sodium chloride delivery to the macula densa, and direct baroreceptor stretch release in juxtaglomerular cells. ### What does the Valsalva manoeuvre test? Baroreflex integrity — tachycardia during strain and bradycardia overshoot on release; both patterns are lost in autonomic failure. ### Why does filariasis cause chronic oedema? Lymphatic obstruction by adult worms prevents return of the net capillary filtrate, producing the progressive non-pitting oedema and elephantiasis endemic in parts of India.