Coronary circulation
32 named structures.
Draft — not yet clinically reviewed. The structure of this map is checked automatically, but its wording has not been fact-checked against a textbook. Do not rely on it for an exam answer yet.
Hover or tab a structure to trace what it connects to. Some structures reveal further branches.
Clinical detail
- Right (anterior) aortic sinusTachycardia or aortic stenosis shortens diastole and raises LV wall tension1 question
- Left (posterior) aortic sinus and left main stemAcute left main occlusion1 question
- Right coronary arteryRCA occlusion1 question
- Left anterior descending (anterior interventricular) arteryProximal LAD occlusion1 question
- Left circumflex arteryCircumflex occlusion1 question
- Sinoatrial nodal arteryOcclusion of the RCA proximal to the SA nodal branch2 questions
- Right (acute) marginal arteryRCA occlusion proximal to the acute marginal branch1 question
- Posterior descending (posterior interventricular) arteryRight dom. 70-85% Left dom. 5-10% Co-dom. ~10%Inferior MI infarcting the posteromedial papillary muscle, which has a single supply from the PDA1 question
- Atrioventricular nodal arteryRCA occlusion proximal to the AV nodal branch1 question
- Diagonal branches of the LADLAD occlusion proximal to the first diagonal1 question
- Septal perforating branches of the LADAnterior MI with new right bundle branch block and left anterior fascicular block2 questions
- Obtuse marginal branches of the circumflexObtuse marginal occlusion1 question
- Sinoatrial nodeSinus node ischaemia in inferior MI2 questions
- Atrioventricular node and His bundleComplete heart block complicating inferior MI1 question
- Right ventricular free wallRight ventricular infarction1 question
- Anterior left ventricular wall and apexLarge anterior MI1 question
- Anterior two-thirds of the interventricular septumSeptal infarction on day 3 to 71 question
- Lateral left ventricular wallIsolated lateral STEMI1 question
- Inferior (diaphragmatic) left ventricular wall and posterior third of the septumInferior STEMI with ST elevation in III greater than II and ST depression in I or aVL1 question
- Posterior (inferobasal) left ventricular wallPosterior MI1 question
- Septal leads V1 and V2V1 V2ST elevation in V1 and V2 with new right bundle branch block1 question
- Anterior leads V3 and V4V3 V4ST elevation across V1 to V6 with I and aVL1 question
- Lateral leads I, aVL, V5 and V6I aVL V5 V6Isolated ST elevation in I and aVL with depression in III1 question
- Inferior leads II, III and aVFII III aVFInferior STEMI with ST elevation in V1 (or V1 elevation with V2 depression)1 question
- Posterior leads V7 to V9V7 V8 V9Chest pain with ST depression in V1 to V3 and a normal-looking 12-lead elsewhere1 question
- Right-sided lead V4RV4RST elevation in V4R in an inferior STEMI1 question
- Rhythm strip findings of nodal ischaemiaSymptomatic bradycardia or nodal AV block in inferior MI2 questions
- Coronary sinusCannulating the coronary sinus from the right atrium1 question
Common questions
What does coronary dominance mean and which is commonest?
Dominance is decided by which artery gives off the posterior descending artery (and with it the AV nodal artery and posterolateral branches). The right coronary artery does so in about 70 to 85% (right dominant), the circumflex in 5 to 10% (left dominant), and both contribute in the remainder (co-dominant).
Which artery supplies the SA node and the AV node?
The SA nodal artery comes from the proximal RCA in about 60% and from the proximal circumflex in about 40%. The AV nodal artery arises from the dominant artery at the crux, so from the RCA in about 90%. This is why inferior (RCA) infarcts cause sinus bradycardia and nodal AV block.
Which ECG leads map to which artery?
V1 to V2 septal and V3 to V4 anterior are LAD; I, aVL, V5 and V6 lateral are circumflex or diagonal; II, III and aVF inferior are RCA in 80% and circumflex in 18%; ST depression in V1 to V3 with tall R waves is a posterior MI, confirmed by ST elevation in V7 to V9; ST elevation in V4R is right ventricular infarction from a proximal RCA occlusion.
Why are nitrates dangerous in right ventricular infarction?
The infarcted right ventricle cannot generate pressure and depends on high preload to push blood through to the left side. Nitrates, diuretics and morphine drop venous return and cause profound hypotension; the treatment is intravenous fluid.
Why does the myocardium depend on increasing flow rather than extraction?
Coronary sinus blood is already about 30% saturated because the heart extracts 70 to 80% of the oxygen delivered at rest. There is little extraction reserve, so any increase in demand must be met by coronary vasodilation, mainly through adenosine; a fixed stenosis that limits flow therefore produces ischaemia as soon as demand rises.