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Anaes TopicsApplied cardiovascular & respiratory physiology

Anaes · Applied cardiovascular & respiratory physiology

Coronary & cerebral circulation

Also known as Coronary blood flow · Cerebral blood flow · Cerebral autoregulation · Coronary perfusion pressure · CO2 reactivity · Special circulations

The coronary and cerebral circulations are the two most vital special circulations, and each is defended by its own tightly-regulated autoregulation. The framework rests on five exam-critical ideas: the coronary circulation is unusual in that flow occurs predominantly in DIASTOLE, because the contracting myocardium in systole compresses the intramural vessels, so coronary perfusion pressure is diastolic blood pressure minus the left-ventricular end-diastolic pressure; coronary flow is matched to myocardial oxygen demand chiefly by metabolic vasodilation (the heart extracts oxygen near-maximally at rest, so increased demand must be met by increased flow); the cerebral circulation autoregulates, holding cerebral blood flow constant across a cerebral perfusion pressure range of roughly 50 to 150 mmHg, with the curve shifted right in chronic hypertension; cerebral blood flow is exquisitely sensitive to arterial carbon dioxide (hypercarbia increases, hypocarbia decreases it); and cerebral perfusion pressure equals mean arterial pressure minus intracranial pressure, so raised intracranial pressure threatens cerebral perfusion. Built on the cerebrovascular-autoregulation study (Soule 2026), the cerebrovascular-function MRI study (Walsh 2026), the intraoperative cerebral zero-flow-pressure study (Murakami 2026), the flow-mediated epicardial-vasodilation study (Tribhuvan 2026), the perioperative LVAD study (Bottiroli 2026), and the coronary-flow-interventions study (Shah 2026).

high6 referencesUpdated 26 July 20266 min readVerification in progress

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Red flags

  • Coronary blood flow occurs mainly in diastole, and coronary perfusion pressure equals diastolic blood pressure minus left ventricular end-diastolic pressure — so tachycardia (shortened diastole), diastolic hypotension and a high LVEDP all threaten myocardial perfusion, producing subendocardial ischaemia.
  • The heart extracts around 75 percent of the oxygen from coronary blood at rest, so increased demand cannot be met by greater extraction — it MUST be met by greater flow; any failure of metabolic coronary vasodilation causes ischaemia.
  • Cerebral autoregulation holds cerebral blood flow constant from about 50 to 150 mmHg cerebral perfusion pressure, but the curve shifts right in chronic hypertension — so a normotensive target may under-perfuse the hypertensive patient's brain.
  • Cerebral blood flow is linearly sensitive to arterial carbon dioxide: each kPa (or mmHg) change in PaCO2 moves cerebral blood flow several percent — the basis of hyperventilation to lower intracranial pressure, and of the danger of prolonged hypocapnia.
  • Cerebral perfusion pressure equals mean arterial pressure minus intracranial pressure; raised intracranial pressure erodes cerebral perfusion even when mean arterial pressure is preserved.
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Practise this topic8 MCQs with explanations

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ANZCAFRCAABAEDAICFCAIFCA_SA

Red flags

  • Coronary blood flow occurs mainly in diastole, and coronary perfusion pressure equals diastolic blood pressure minus left ventricular end-diastolic pressure — so tachycardia (shortened diastole), diastolic hypotension and a high LVEDP all threaten myocardial perfusion, producing subendocardial ischaemia.
  • The heart extracts around 75 percent of the oxygen from coronary blood at rest, so increased demand cannot be met by greater extraction — it MUST be met by greater flow; any failure of metabolic coronary vasodilation causes ischaemia.
  • Cerebral autoregulation holds cerebral blood flow constant from about 50 to 150 mmHg cerebral perfusion pressure, but the curve shifts right in chronic hypertension — so a normotensive target may under-perfuse the hypertensive patient's brain.
  • Cerebral blood flow is linearly sensitive to arterial carbon dioxide: each kPa (or mmHg) change in PaCO2 moves cerebral blood flow several percent — the basis of hyperventilation to lower intracranial pressure, and of the danger of prolonged hypocapnia.
  • Cerebral perfusion pressure equals mean arterial pressure minus intracranial pressure; raised intracranial pressure erodes cerebral perfusion even when mean arterial pressure is preserved.
The one-line answer

Coronary perfusion pressure = DBP − LVEDP (flow is predominantly diastolic); cerebral perfusion pressure = MAP − ICP (flow autoregulates and tracks PaCO2). Both organs are taught as near-maximal resting extractors, so increased demand must be met by increased flow. Tachycardia threatens the heart; raised ICP threatens the brain. Standard-teaching anchors carried with note: the equations, the 50–150 range, the 2–4%/mmHg reactivity and the extraction fractions are not stated verbatim in any retrieved abstract.[1][5][6]

Meet the patient

A 78-year-old with severe aortic stenosis presents for emergency bowel obstruction surgery. On induction she develops rapid atrial fibrillation at 140. The MAP drops to 50. The ST segments depress in the lateral leads. The trainee asks: what is happening to her heart and brain right now?[5]

The tachycardia shortened diastole — coronary perfusion time collapsed. The low MAP plus her already-elevated LVEDP from a stiff ventricle crushed coronary perfusion pressure. Her cerebral perfusion pressure fell as MAP dropped. Two vital circulations failed from the same haemodynamic insult, by different equations.[1][5]

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References6ShowHide
  1. [1]Soulé Z, Wang S, Cao M, et al. Microcirculation and Cerebrovascular Autoregulation in Patients With Mechanical Circulatory Support Devices J Stroke, 2026.PMID 42237618
  2. [2]Walsh HJ, et al. Multi-modal magnetic resonance imaging to assess cerebrovascular function in patients with atrial fibrillation J Cereb Blood Flow Metab, 2026.PMID 42345329
  3. [3]Murakami S, et al. In Reply to: Comment on Effect of intraoperative position on the zero flow pressure of the cerebral circulation under propofol anesthesia: a prospective observational study J Anesth, 2026.PMID 42313123
  4. [4]Tribhuvan M, et al. Comment on Prevalence of impaired flow-mediated epicardial vasodilation among different types of coronary flow regulation Int J Cardiovasc Imaging, 2026.PMID 42337215
  5. [5]Bottiroli M, et al. Perioperative Management of Patients With Durable and Temporary Left Ventricular Assist Devices Undergoing Non-Cardiac Surgery: A Comprehensive Review J Cardiothorac Vasc Anesth, 2026.PMID 42350177
  6. [6]Shah S, et al. Effects of pharmacologic, non-pharmacologic and exercise-based interventions on coronary collateral circulation: A scoping review Cardiology, 2026.PMID 42319860

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