Coronary perfusion

10 min read Last updated April 8, 2026

Clinical approach: preventing myocardial ischaemia (perioperative)

  • Think in terms of oxygen supply vs demand
    • Supply: coronary perfusion pressure, diastolic time, coronary vascular resistance, arterial oxygen content
    • Demand: heart rate, contractility, wall stress (preload/afterload), LV hypertrophy
  • Key levers in theatre/ICU
    • Avoid tachycardia (shortens diastole; increases demand)
    • Maintain diastolic pressure (esp. in CAD/AS/LVH); treat hypotension early
    • Treat anaemia/hypoxaemia; optimise CaO2
    • Avoid excessive LVEDP (fluid overload, acute LV failure) which reduces CPP
    • Balance coronary vasodilators: may improve supply but can cause hypotension/tachycardia or coronary steal in select settings
  • When is coronary perfusion most vulnerable?
    • LV subendocardium during tachycardia, hypotension, raised LVEDP, LVH, severe aortic stenosis
    • During induction/neuraxial sympathectomy (drop in diastolic pressure) and emergence (tachycardia/hypertension)

Applied scenarios (how physiology explains management)

  • Aortic stenosis
    • LVH + high LVEDP → reduced subendocardial perfusion; coronary flow becomes pressure-dependent
    • Maintain sinus rhythm, avoid tachycardia, maintain diastolic pressure; cautious vasodilation
  • Tachyarrhythmia with hypotension
    • Reduced diastolic time + reduced aortic diastolic pressure → marked fall in LV coronary perfusion
    • Treatment priorities: slow rate, restore perfusion pressure, correct hypoxia/anaemia/acidosis
  • Raised LVEDP (acute LV failure, high PEEP, fluid overload)
    • CPP = Ao diastolic − LVEDP (approx) → raised LVEDP directly reduces CPP
    • Diuresis/vasodilators/inotropes may improve perfusion by lowering LVEDP and/or raising Ao diastolic (careful balance)

Definitions and key equations

  • Coronary perfusion pressure (CPP) is the pressure gradient driving coronary blood flow across the myocardium
  • Left coronary CPP (clinically useful approximation): Aortic diastolic pressure − LV end-diastolic pressure (LVEDP)
    • More exact: inflow pressure at coronary ostium (aortic root diastolic) minus effective back-pressure (LV cavity pressure / intramyocardial pressure / coronary venous pressure depending on layer)
  • Right coronary CPP: often approximated as Aortic diastolic pressure − RVEDP (or right atrial pressure as a surrogate when RVEDP low)
  • Coronary blood flow: Flow = CPP / Coronary vascular resistance (CVR)
  • Subendocardial viability ratio (SEVR) / DPTI:SPTI concept: supply-demand index ≈ (Diastolic pressure–time integral) / (Systolic pressure–time integral)
    • Falls with tachycardia (reduced diastolic time), hypotension (reduced DPTI), LVH/raised LVEDP (reduced effective diastolic gradient), hypertension (increased SPTI)

Phasic nature of coronary blood flow

  • Left coronary flow is predominantly diastolic
    • Systole: high intramyocardial pressure compresses intramural vessels (especially subendocardium) → reduced/briefly reversed flow
    • Diastole: myocardial relaxation reduces extravascular compression → flow rises; peak early diastole
  • Right coronary flow occurs in both systole and diastole (more continuous)
    • Because RV systolic pressure is much lower than LV → less extravascular compression
    • In pulmonary hypertension/RV hypertrophy, RCA flow becomes more diastolic (RV systolic pressure rises)
  • Subendocardium is most at risk
    • Highest wall stress and greatest systolic compression; perfused last and at lowest effective driving pressure
    • Vulnerability increases with LVH, tachycardia, hypotension, raised LVEDP

Determinants of coronary perfusion (supply side)

  • Aortic diastolic pressure
    • Primary determinant of LV coronary inflow pressure
    • Falls with vasodilation, hypovolaemia, reduced SVR; may be supported with vasopressors (e.g., noradrenaline, metaraminol) while controlling HR
  • LVEDP / intramyocardial pressure (back-pressure)
    • Raised LVEDP reduces effective gradient; worsens subendocardial perfusion
    • Raised by LV failure, mitral regurgitation, fluid overload, high afterload, high PEEP (via reduced venous return and altered transmural pressures), diastolic dysfunction
  • Diastolic time (heart rate)
    • Tachycardia disproportionately shortens diastole → reduces time available for LV perfusion
    • Also increases demand (double hit)
  • Coronary vascular resistance (CVR)
    • Determined mainly by arteriolar tone; extravascular compression adds a dynamic component (especially in LV)
    • Autoregulation maintains flow over a range of perfusion pressures by adjusting CVR (limited in severe stenosis/maximal vasodilation)
  • Arterial oxygen content (CaO2)
    • CaO2 = (1.34 × Hb × SaO2) + (0.023 × PaO2); coronary flow can increase to compensate but extraction is already high at baseline

Determinants of myocardial oxygen demand

  • Heart rate
    • Major determinant of MVO2; also reduces supply by shortening diastole
  • Contractility
    • Inotropes increase MVO2; may improve perfusion if they raise diastolic pressure and reduce LVEDP, but can worsen ischaemia if tachycardic
  • Wall stress (Laplace): stress ∝ (Pressure × Radius) / (2 × Wall thickness)
    • Increased afterload (pressure) and preload (radius) increase MVO2; LVH (increased thickness) reduces stress but impairs subendocardial perfusion and increases muscle mass

Coronary autoregulation and metabolic control

  • At rest, myocardium extracts a high proportion of delivered oxygen (~60–80%), so increased demand is met mainly by increased coronary blood flow
  • Metabolic vasodilators: adenosine (key), CO2, H+, K+, lactate; hypoxia promotes vasodilation
  • Endothelial factors: nitric oxide (vasodilator), prostacyclin; endothelin (vasoconstrictor)
  • Neural/humoral influences are usually secondary to metabolic control
    • Sympathetic stimulation: α causes vasoconstriction; β2 causes vasodilation; net effect often increased flow due to increased metabolic demand overriding direct vasoconstriction
  • Autoregulation range is reduced/abolished distal to a critical stenosis (arterioles already maximally dilated at rest) → flow becomes pressure-dependent

Coronary steal and redistribution

  • Concept: vasodilation in non-ischaemic territories can divert flow away from an ischaemic region supplied by a stenosed artery with maximally dilated arterioles
    • More likely with potent arteriolar vasodilators (e.g., adenosine, dipyridamole) and in presence of collateral-dependent myocardium
    • Clinical relevance perioperatively is variable; hypotension and tachycardia are often more important drivers of ischaemia than steal per se
  • Transmural distribution: subendocardium is disadvantaged when perfusion pressure falls or LVEDP rises; vasodilation may preferentially increase epicardial flow unless driving pressure is adequate

Effects of common drugs/physiological changes on coronary perfusion

  • Volatile agents
    • Reduce BP (↓diastolic pressure) and may cause tachycardia (agent-dependent) → can reduce CPP; also reduce MVO2 via reduced afterload/contractility
  • Propofol
    • Vasodilation and reduced sympathetic tone → ↓aortic diastolic pressure; usually also ↓MVO2; watch in fixed coronary stenosis/AS where pressure dependence is marked
  • Ketamine
    • Sympathomimetic: ↑HR/↑BP/↑contractility → ↑MVO2; may improve CPP via ↑diastolic pressure but tachycardia can reduce diastolic time
  • Vasopressors
    • Noradrenaline/phenylephrine can increase aortic diastolic pressure (↑CPP) but may increase afterload and reflex bradycardia (phenylephrine) which can be beneficial for diastolic time
    • Excessive vasoconstriction can increase LV work; aim for adequate perfusion pressure without undue tachycardia
  • Nitrates
    • Venodilation → ↓preload and LVEDP → can improve CPP gradient and reduce wall stress (↓MVO2)
    • May cause hypotension and reflex tachycardia (reduce CPP/diastolic time) if not controlled
  • Beta-blockers
    • ↓HR and ↓contractility → ↓MVO2 and ↑diastolic time; can improve supply-demand balance
  • Intra-aortic balloon pump (IABP)
    • Inflation in diastole augments aortic diastolic pressure (↑CPP); deflation before systole reduces afterload (↓MVO2)
Define coronary perfusion pressure (CPP). How would you estimate it for the left ventricle and why is it clinically useful?

CPP is the driving pressure gradient for coronary blood flow; for LV it is mainly a diastolic phenomenon.

  • CPP is the pressure gradient between coronary arterial inflow and the effective downstream/back-pressure.
  • LV approximation: CPP ≈ Aortic diastolic pressure − LVEDP.
  • Useful because it links common perioperative problems to ischaemia risk: hypotension (↓Ao diastolic) and LV failure/overfilling (↑LVEDP) both reduce CPP.
  • Coronary flow then depends on Flow = CPP/CVR; in severe coronary stenosis distal arterioles may be maximally dilated so flow becomes pressure-dependent.
Why is left coronary blood flow predominantly diastolic whereas right coronary flow is more evenly distributed through the cardiac cycle?

The key difference is the magnitude of systolic extravascular compression.

  • During LV systole, intramyocardial pressure is high and compresses intramural vessels → markedly reduced (sometimes reversed) left coronary flow.
  • During diastole, LV relaxes → extravascular compression falls → left coronary flow rises and peaks early diastole.
  • RV systolic pressure is much lower → less compression of RCA branches → RCA flow persists in systole and diastole.
  • If RV pressure rises (pulmonary hypertension/RV hypertrophy), RCA flow becomes more diastolic, mirroring LV behaviour.
Explain why tachycardia is particularly harmful to coronary perfusion and myocardial oxygen balance.

Tachycardia reduces supply and increases demand simultaneously.

  • Supply: tachycardia disproportionately shortens diastole, reducing time available for LV coronary perfusion.
  • Demand: increases MVO2 by increasing the number of contractions per minute and often increasing contractility via sympathetic activation.
  • Also reduces SEVR/DPTI:SPTI (reduced DPTI, increased SPTI), worsening subendocardial perfusion.
A patient becomes hypotensive after induction. Describe the physiological mechanisms by which this can precipitate myocardial ischaemia, and how you would correct it in principle.

Hypotension reduces coronary driving pressure; management aims to restore CPP while avoiding tachycardia and excessive LV work.

  • ↓Aortic diastolic pressure → ↓CPP → ↓coronary flow (especially if distal arterioles already maximally dilated in CAD).
  • If hypotension triggers tachycardia (pain/light anaesthesia), diastolic time falls and MVO2 rises.
  • Correction principles: treat cause (depth, vasodilation, hypovolaemia), restore diastolic pressure with vasopressor, maintain oxygenation and Hb, control HR.
    • Phenylephrine may raise diastolic pressure and slow HR (reflex), potentially improving supply-demand balance; noradrenaline supports pressure with less reflex bradycardia.
Describe the concept of coronary autoregulation and its relevance to coronary artery disease.

Autoregulation maintains flow by changing resistance, but it has limits—especially distal to a stenosis.

  • Within a physiological pressure range, coronary arterioles adjust tone to keep flow relatively constant (metabolic control predominates).
  • Distal to a significant stenosis, arterioles may be maximally dilated at rest to maintain flow → loss of reserve.
  • Therefore flow becomes pressure-dependent: small drops in aortic diastolic pressure or rises in LVEDP can cause large reductions in flow and ischaemia.
What is the subendocardial viability ratio (SEVR) / DPTI:SPTI? What factors reduce it?

It is a pressure–time surrogate of subendocardial supply-demand balance.

  • SEVR ≈ (Diastolic pressure–time integral, DPTI) / (Systolic pressure–time integral, SPTI).
  • Reduced by: tachycardia (↓diastolic time), hypotension (↓diastolic pressure), raised LVEDP (↓effective gradient), hypertension (↑SPTI), LVH (higher demand and impaired subendocardial perfusion).
  • Clinically: interventions that slow HR and maintain diastolic pressure tend to improve SEVR.
Explain why anaemia and hypoxaemia can precipitate myocardial ischaemia even if coronary perfusion pressure is maintained.

Oxygen delivery depends on content as well as flow; coronary extraction is already high.

  • Myocardial oxygen delivery = coronary blood flow × arterial oxygen content (CaO2).
  • CaO2 falls with low Hb or low SaO2; myocardium has high baseline O2 extraction so there is limited capacity to increase extraction further.
  • Compensation relies mainly on increasing coronary flow; in CAD, flow reserve is limited, so ischaemia can occur despite normal CPP.
What is coronary steal? Give a physiological explanation and a clinical example.

Steal is redistribution of flow away from an ischaemic bed that cannot dilate further.

  • In a stenosed territory, distal arterioles may already be maximally dilated to maintain resting flow.
  • If a vasodilator dilates arterioles in non-ischaemic regions, resistance there falls further, diverting flow away from the stenosed/collateral-dependent region.
  • Classically associated with adenosine or dipyridamole (pharmacological stress testing); perioperatively, hypotension/tachycardia often dominate risk.
How do nitrates improve myocardial oxygen balance? Include effects on CPP and MVO2.

Nitrates mainly reduce preload and LVEDP, which can improve the effective coronary perfusion gradient and reduce demand.

  • Venodilation → ↓preload → ↓LVEDP → can increase effective CPP gradient (Ao diastolic − LVEDP).
  • ↓LV radius and wall stress → ↓MVO2.
  • Potential downsides: hypotension (↓Ao diastolic) and reflex tachycardia (↓diastolic time, ↑MVO2) if not controlled.
Describe how an intra-aortic balloon pump (IABP) improves coronary perfusion and reduces myocardial oxygen demand.

IABP improves supply in diastole and reduces demand in systole.

  • Balloon inflates in diastole → augments aortic diastolic pressure → ↑CPP and coronary blood flow.
  • Balloon deflates just before systole → reduces aortic end-diastolic pressure and afterload → ↓LV wall stress and ↓MVO2.
A viva theme: compare determinants of coronary blood flow with determinants of cerebral blood flow.

Both have autoregulation, but coronary flow is tightly linked to metabolism and is strongly phasic in the LV.

  • Both: Flow ≈ perfusion pressure / vascular resistance; both have autoregulation and CO2/H+ effects.
  • Coronary: metabolic control dominates (adenosine); high baseline O2 extraction; LV flow mainly diastolic and affected by extravascular compression and LVEDP.
  • Cerebral: flow is more continuous; strong CO2 reactivity; intracranial pressure acts as downstream pressure (CPPbrain = MAP − ICP).

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