/study / lectures / Physiology I
Coronary Circulation and Autoregulation
TEXTPhysiology I · 9 min read
Coronaries fill in diastole. That single fact drives every hemodynamic decision in CAD, AS, and tachycardia.
After this lesson you can
4 min read8 sections- Map ECG territories to coronary artery distribution.
- Explain why coronaries fill in diastole and the implications for HR.
- Recall the LV vs RV myocardial O₂ demand drivers.
- Recognize the high-risk lesions (left main, proximal LAD, triple vessel).
Coronary anatomy + territories
LCx (left circumflex) supplies the lateral LV wall (I, aVL, V5-V6).
RCA (right coronary artery) supplies the RV + inferior LV wall + SA node (~60% of population) + AV node (90% of population) (II, III, aVF).
DOMINANCE refers to which artery gives rise to the posterior descending artery (PDA) — RCA-dominant in ~85% of population (most), LCx-dominant in ~8%, co-dominant in ~7%.
RCA dominance + occlusion is associated with bradyarrhythmias because both nodes are typically in RCA territory.
- left main stenosis ≥50%
- proximal LAD stenosis
- triple-vessel disease
- last-remaining-vessel disease


Diastolic perfusion physiology
During systole the contracting myocardium physically compresses intramyocardial vessels — flow is briefly minimal or even reversed, especially in subendocardium.
Diastole provides 70-80% of total left coronary flow.
RIGHT coronaries get more uniform perfusion across the cardiac cycle because RV pressure is much lower than LV.
- anything that shortens diastole — tachycardia
- AF with RVR
- hypertension that prolongs systole — reduces left-sided perfusion time disproportionately to demand increase
Subendocardium is the most vulnerable layer because it's perfused last and pressure-compressed first.

Coronary perfusion pressure (CPP) formula
CPP = AORTIC DIASTOLIC PRESSURE − LVEDPNormal: 60-80 mmHg.
CPP falls when aortic diastolic drops (vasodilation, aortic regurgitation, severe systemic hypotension, sepsis) OR LVEDP rises (CHF, volume overload, myocardial ischemia diastolic dysfunction high filling pressure).
50 mmHgsubendocardial ischemia even in normal hearts; CPP <60 mmHgischemia in patients with CAD or LVH.PHENYLEPHRINE raises aortic diastolic without raising HR or contractility first-line for CAD hypotension.
Norepinephrine acceptable as second line.

Autoregulation + right shift in disease
Coronary flow stays constant across MAP 60-140 mmHg via metabolic (adenosine, lactate, K+), myogenic (vascular smooth muscle stretch-response), and endothelial (NO, prostacyclin) mechanisms. β-adrenergic dilation and increased demand from exercise/sympathetic activation match flow to demand.
Outside this autoregulatory range, perfusion becomes PRESSURE-PASSIVE.
DIABETIC and chronically HYPERTENSIVE patients have RIGHT-SHIFTED autoregulation curves — they need HIGHER MAPs (often 80-100 mmHg) to maintain perfusion than the normal-curve textbook would suggest.
Intra-op MAP target should be within 10-20% of patient's known awake baseline, not a universal number.

Steal physiology
Classic example: adenosine — used diagnostically in stress testing precisely because it causes steal in CAD.
Isoflurane was historically thought to cause clinically significant steal but modern data show no clinical relevance at typical MAC values.
In severe LV hypertrophy or aortic stenosis where subendocardium is already chronically underperfused, any vasodilator can theoretically worsen subendo perfusion — pick agents that preserve SVR (etomidate over propofol) and use phenylephrine liberally.

Supply-demand balance
SUPPLY factors: HR (longer diastole = more perfusion), aortic diastolic pressure (CPP), hemoglobin (O₂ carrying capacity), SaO₂, vessel patency.
DEMAND factors: HR (more beats per minute = more O₂ used), wall stress (preload × afterload), contractility, basal metabolic rate.
The 'double product' (HR × SBP) is a clinical surrogate for myocardial O₂ demand.
- lower HR (more diastole, less demand)
- maintain MAP (more supply)
- avoid afterload spikes from light anesthesia (more demand)
- normalize Hb + SaO₂ + temperature (more supply, less demand)

Specific anesthetic implications in CAD
GOALS in CAD: HR 50-70 (longer diastole + lower demand), MAP within 20% of awake baseline, avoid hypoxia, anemia (target Hb ≥8 in CAD; ≥9-10 if active ischemia), and hypothermia. β-blocker continuation through the perioperative period is critical — POISE-1 trial showed that initiating de novo high-dose metoprolol pre-op caused harm (hypotension + stroke), but continuing chronic β-blocker is protective.
Phenylephrine 100 mcg boluses for hypotension preserves CPP without HR rise.
Pretreatment with IV fentanyl + IV esmolol blunts laryngoscopy hypertensive response.
Avoid simultaneous steep Trendelenburg + tachycardia (worst combo for subendo perfusion).
AORTIC STENOSIS = same principles but hyper-amplified; severe AS patients tolerate hypotension extremely poorly because the hypertrophied LV is exquisitely CPP-dependent.

Recognizing intraop ischemia
ECG signs (V5 + II monitoring catches ~95% of intra-op ischemia events): ST depression (subendocardial), ST elevation (transmural), new T-wave inversion, new arrhythmia (bigeminy, VT).
- unexplained hypotension
- new wall-motion abnormality on TEE (gold standard for cardiac surgery)
- rising PA wedge pressure (LV dysfunction)
Treat suspected intra-op ischemia: 100% O₂, hold β-blocker if bradycardic but otherwise continue, treat HTN/HR aggressively, phenylephrine for hypotension, nitroglycerin gtt 0.5-5 mcg/kg/min if BP allows, consider deepening anesthesia if light, send postop ECG + troponin, cardiology consult.

⚠ Common pitfalls
- Allowing tachycardia in CAD — shortens diastole, drops coronary supply.
- Aggressive afterload reduction in severe AS — collapses the diastolic pressure that drives coronary flow.
- Treating an inferior MI like an anterior — RV involvement common; preload-dependent, avoid nitro.
- Ignoring NT-proBNP or troponin elevations in pre-op assessment as 'old' findings.
💎 Clinical pearls
- Left main equivalent (proximal LAD + LCx) carries the same operative risk as left main itself.
- DAPT timing: bare-metal 30 days, drug-eluting 6-12 months — non-cardiac surgery decisions hinge on this.
- Ratio rule: keep DBP × HR-recovery-time product favorable — slow HR and decent diastolic = perfusion.
- Right coronary supplies SA + AV nodes in most people — RCA occlusion = bradyarrhythmias, expect it.
Recap
- Left main equivalent (proximal LAD + LCx) carries the same operative risk as left main itself.
- DAPT timing: bare-metal 30 days, drug-eluting 6-12 months — non-cardiac surgery decisions hinge on this.
- Ratio rule: keep DBP × HR-recovery-time product favorable — slow HR and decent diastolic = perfusion.
- Right coronary supplies SA + AV nodes in most people — RCA occlusion = bradyarrhythmias, expect it.
Mark each section done to complete the module.