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Anaes TopicsApplied cardiovascular & respiratory physiology

Anaes · Applied cardiovascular & respiratory physiology

Microcirculation & control of blood flow

Also known as Microcirculation · Capillary exchange · Starling forces · Autoregulation · Local blood flow control · Hypoxic pulmonary vasoconstriction

The microcirculation — the arterioles, capillaries and venules — is where blood flow is actually distributed and where exchange with the tissues occurs. The framework rests on five exam-critical ideas: local blood flow is controlled chiefly at the arteriolar and precapillary sphincter level, by metabolic feedback (CO2, hydrogen ion, potassium, adenosine, lactate) that matches flow to demand, by myogenic tone, and by endothelial factors (nitric oxide, prostaglandins, endothelin); capillary exchange is governed by the Starling forces — the balance of hydrostatic and oncotic pressures across the capillary wall — with filtration at the arterial end and reabsorption at the venous end; oedema results from a disturbance of one of four factors (raised hydrostatic pressure, low plasma oncotic pressure, raised capillary permeability, lymphatic obstruction); the lung is the exception that proves metabolic control, constricting rather than dilating in response to hypoxia (hypoxic pulmonary vasoconstriction); and microcirculatory dysfunction — a leaky, leaky-flow state with shunting — explains why a normal macroscopic blood pressure does not guarantee tissue oxygenation in sepsis. Built on the microvascular-failure-in-septic-shock review (Popovich 2026), the carbon-dioxide-vasodilator review (Duse 2026), the transvascular-exchange/revised-Starling review (Alamilla-Sanchez 2023), the capillary-hydration study (Pstras 2022), the perioperative-renal-microcirculation review (Li 2026), and the pulmonary-vascular-tone study (Maier 2026).

high6 referencesUpdated 26 July 20267 min readVerification in progress

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Red flags

  • CO2 triple vasodilation (NO/sGC, SKCa/IKCa endothelial, KV/IKCa myogenic) with blunted/delayed diseased responses and carbonic-anhydrase metabolic coupling [2]; metabolite/bed-dominance lists beyond that triple are viva teaching, not in [2].
  • Starling principle correct but incomplete — revised Michel-Weinbaum with glycocalyx subendothelial restricted oncotic gradient and mainly lymphatic refilling (microconstant model) [3]; equation arithmetic and four-mechanism oedema groupings are teaching with that owner.
  • Refilling coefficient Kr falls exponentially in haemodialysis from moving interstitial/other Starling forces, not from falling LpS — do not use Kr to guide removal or assess status [4].
  • Pulmonary metaboreflex plus chemoreflex raise PASP additively (+8.4 mmHg combined; n-15/n-14), not synergistically [6]; HPV direction/volatiles/one-lung specifics are textbook/protocol, not in [6].
  • Haemodynamic incoherence: restored pressure/output with heterogeneous perfusion, low functional capillary density, hyperdynamic shunting — output short of radii-cubed shear demand forces derecruitment [1]; periop AKI triad carries occult hypoxia despite stable macro [5].
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Saved on this device.

Practise this topic16 MCQs with explanations

Target exams

ANZCAFRCAABAEDAICFCAIFCA_SA

Red flags

  • CO2 triple vasodilation (NO/sGC, SKCa/IKCa endothelial, KV/IKCa myogenic) with blunted/delayed diseased responses and carbonic-anhydrase metabolic coupling [2]; metabolite/bed-dominance lists beyond that triple are viva teaching, not in [2].
  • Starling principle correct but incomplete — revised Michel-Weinbaum with glycocalyx subendothelial restricted oncotic gradient and mainly lymphatic refilling (microconstant model) [3]; equation arithmetic and four-mechanism oedema groupings are teaching with that owner.
  • Refilling coefficient Kr falls exponentially in haemodialysis from moving interstitial/other Starling forces, not from falling LpS — do not use Kr to guide removal or assess status [4].
  • Pulmonary metaboreflex plus chemoreflex raise PASP additively (+8.4 mmHg combined; n-15/n-14), not synergistically [6]; HPV direction/volatiles/one-lung specifics are textbook/protocol, not in [6].
  • Haemodynamic incoherence: restored pressure/output with heterogeneous perfusion, low functional capillary density, hyperdynamic shunting — output short of radii-cubed shear demand forces derecruitment [1]; periop AKI triad carries occult hypoxia despite stable macro [5].
The one-line answer

Flow follows driving pressure over resistance with radius the master variable (fourth-power Poiseuille teaching). A one-million-arteriole simulation shows vasodilation raises whole-network flow demand with the sum of radii cubed for a given shear target — when cardiac output cannot meet it, vessels derecruit into heterogeneous perfusion with low functional capillary density despite restored pressure and output (haemodynamic incoherence) [1]. CO2 is a triple vasodilator (endothelial NO/sGC, endothelial SKCa/IKCa, myogenic KV and IKCa) with blunted/delayed responses in diseased arteries [2]. Transvascular exchange follows the Starling principle, correct but incomplete — the revised Michel-Weinbaum model places the glycocalyx subendothelial restricted oncotic gradient centrally, with refilling mainly lymphatic [3]. Perioperative AKI reflects a microcirculatory-hypoxia/mitochondrial/immuno-metabolic triad with occult hypoxia despite stable macro-parameters [5]; chemoreflex and metaboreflex activation raise pulmonary pressure additively, not synergistically [6]. Autoregulation windows, litre Starling numbers, and reflection-coefficient arithmetic are textbook furniture, not in any retrieved abstract.[1][2][3][5][6]

Meet the patient

A septic patient in the ICU has a mean arterial pressure of 75, maintained with noradrenaline. The lactate is rising, the urine output is falling, and the skin is mottled despite a pressure that looks adequate on the monitor.[1]

This is haemodynamic incoherence — heterogeneous capillary perfusion with low functional capillary density persisting despite restored pressure and cardiac output; the model reproduces the hyperdynamic circulation and microvascular shunting of severe sepsis [1]. Endothelial injury states (sepsis, acute inflammation) disturb transvascular exchange, where the glycocalyx subendothelial restricted oncotic gradient limits reabsorption and refilling runs mainly lymphatic [3]. The cuff pressure is necessary but not sufficient — the microcirculation decides whether the cells get oxygen (model interpretation, not a measured MAP target).[1][3]

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References6ShowHide
  1. [1]Popovich I. On the inevitability of microvascular failure in septic shock and other vasodilatory conditions Crit Care, 2026.PMID 42343425
  2. [2]Duse DA, et al. Carbon dioxide is a triple vasodilator Cardiovasc Res, 2026.PMID 42334380
  3. [3]Alamilla-Sanchez ME, et al. Advances in the Physiology of Transvascular Exchange and A New Look At Rational Fluid Prescription Int J Gen Med, 2023.PMID 37408844
  4. [4]Pstras L, et al. Vascular refilling coefficient is not a good marker of whole-body capillary hydraulic conductivity in hemodialysis patients: insights from a simulation study Sci Rep, 2022.PMID 36088359
  5. [5]Li S, et al. Pathological triad of perioperative acute kidney injury: renal microcirculatory hypoxia, mitochondrial damage, and immuno-metabolic reprogramming Front Immunol, 2026.PMID 42338604
  6. [6]Maier LE, et al. The influence of metaboreflex activation on pulmonary pressure with combined chemoreflex activation in acute and chronic hypoxia J Physiol, 2026.PMID 42306962

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