9.1 Cardiac Anatomy & Pathophysiology

Cardiac Anatomy & Pathophysiology

ARRT Cardiac-Interventional Procedures 1.A.1–1.A.2.a sit on the Focus of Questions layer for anatomy and pathophysiology. Hemodynamics and native coronary angiography are unreadable if you cannot name the chamber, the valve, the sinus the catheter is in, or whether the inferior wall is even this patient's RCA territory. This section is that map. Typical adult pressures, saturations, cardiac output, and the ~85% right-dominant figure below are cath-lab teaching ranges, not unpublished ARRT cutoffs.

Quick Answer: The right coronary artery (RCA) arises from the right sinus of Valsalva. The left main (LM) arises from the left sinus and usually bifurcates into the left anterior descending (LAD) and left circumflex (LCx). Dominance is which vessel gives the posterior descending artery (PDA) and typically the posterolateral left-ventricular (PLV) branches — about 85% right-dominant in typical adult teaching. Left-dominant PDA from the LCx is the exam trap.

Chambers and valves

Four chambers, four valves, one circuit that diagnostic catheters actually visit.

The right atrium (RA) receives systemic venous return from the superior and inferior venae cavae and the coronary sinus. It empties across the tricuspid valve into the right ventricle (RV). The RV ejects across the pulmonic valve into the pulmonary artery (PA). Pulmonary veins empty into the left atrium (LA), then across the mitral valve into the left ventricle (LV). The LV ejects across the aortic valve into the aorta. The aortic root has right, left, and non-coronary sinuses. Coronary ostia live in the right and left sinuses — not the non-coronary sinus.

For the R.T.(CI), chamber identity is a waveform plus a saturation. A catheter you believe is in the PA that saturates 98% is not in the PA. A tracing labeled LV with a mean of 5 mmHg and a venous saturation is an RA or RV mislabel, not a normal left heart.

Coronary origins, ramus, conus, and dominance

RCA ostium: right sinus of Valsalva. The first RCA branch is often the conus (conus arteriosus) branch to the RV outflow tract. A separate conus ostium from the right sinus is a common variant — a first RCA branch that is not seen on a selective injection is not automatically an occlusion.

LM ostium: left sinus of Valsalva. LM typically bifurcates into LAD (anterior interventricular groove; septal perforators and diagonals) and LCx (left atrioventricular groove; obtuse marginals). A ramus intermedius appears when the LM trifurcates — a third vessel between LAD and LCx. Do not call a ramus a missed diagonal or a high obtuse marginal without seeing the origin.

Dominance is not which coronary looks larger. It is which vessel gives the PDA (posterior interventricular groove, usually inferior septum) and, in typical teaching, the PLV branches to the inferior and posterior LV. Typical adult teaching: about 85% right-dominant (PDA and PLV from RCA), a smaller left-dominant group (PDA and PLV from LCx), and a co-dominant remainder. Exam trap: left-dominant PDA from the LCx. Inferior ST elevation is not automatically an RCA occlusion. If you inject only the RCA and stop, you can miss a left-dominant LCx culprit.

Conduction: RCA versus LAD ischemia and heart block

The sinoatrial (SA) node sits near the superior vena cava–RA junction. The SA nodal artery is often an RCA branch; a sizable minority arise from LCx, so SA node always equals RCA is not a law. The atrioventricular (AV) node sits in the triangle of Koch. The AV nodal artery is an RCA branch in right-dominant anatomy, which is why inferior RCA ischemia classically produces AV block that is often nodal and may respond to atropine or to washout of contrast.

The His bundle penetrates the membranous septum, then the right bundle branch (RBB) and left bundle branch (LBB) (anterior and posterior fascicles) run in the ventricular septum. Basal septum is heavily LAD septal-perforator territory. Proximal LAD ischemia therefore threatens bundle-branch block, bifascicular block, and a wider, less stable infranodal escape — a different emergency from typical RCA–AV nodal block. An RCA injection with transient AV block and a proximal-LAD occlusion with new left bundle-branch block are not interchangeable.

Pathophysiology the diagnostic numbers show

Coronary artery disease. Plaque rupture or erosion with thrombus is the acute coronary syndrome pathway: abrupt flow drop, unstable ST change, a hazy or occlusive culprit. Demand ischemia is supply–demand mismatch without acute thrombosis — anemia, tachyarrhythmia, severe aortic stenosis, hypotension — and the angiogram may show only fixed stenoses that were tolerated at rest. Do not treat every troponin as rupture, and do not dismiss a tight stenosis as not ACS solely because the patient was anemic.

Valves — pressure versus volume overload.

• Aortic stenosis (AS): LV pressure overload. LV systolic pressure exceeds aortic systolic pressure (the pullback gradient in 9.2). Concentric hypertrophy, high end-diastolic pressure, and hypotension if afterload drops suddenly.
• Aortic regurgitation (AR): LV volume overload, wide aortic pulse pressure, elevated LV end-diastolic pressure.
• Mitral stenosis (MS): LA / pulmonary-capillary wedge pressure (PCWP) elevated relative to LV end-diastolic pressure, post-capillary pulmonary hypertension.
• Mitral regurgitation (MR): large v waves in PCWP/LA with LA and LV volume overload.

HFpEF versus HFrEF. Heart failure with preserved ejection fraction (HFpEF): ejection fraction is not low, but the LV is stiff — high LVEDP/PCWP, often hypertensive or concentrically hypertrophied. Heart failure with reduced ejection fraction (HFrEF): dilated, poorly emptying LV, low stroke volume and low cardiac output (CO) / cardiac index (CI). Both can flood the lungs; the ventriculogram and filling pressures tell you which.

Pulmonary hypertension — pre- versus post-capillary. A high mean PA is not one disease. Post-capillary (left-heart) disease: PCWP is high and the lungs sit downstream of a stiff or failing LV or mitral block. Pre-capillary physiology: mean PA is high while PCWP is not — the problem is in the pulmonary arteries. Record both numbers; the diagnosis is the pair.

Chamber / typical teaching pressure / O2 sat

Typical adult cath-lab teaching values — not unpublished ARRT cutoffs. Body size and lab practice move the edges.

A saturation step-up from RA toward PA suggests left-to-right shunt; a step-down on the left heart suggests right-to-left shunt or admixture. The arithmetic is a later chapter. The anatomy is the saturations themselves.

Worked case

Inferior ST elevation and hypotension. The RCA injection looks modest. Do not stop. Identify the PDA: if the LCx gives the PDA, the inferior wall is left-dominant LCx territory. AV block can still appear if the AV nodal artery is RCA-derived, but the culprit may be LCx. Shoot the left system, name the PDA origin, and do not let inferior equals RCA close the case.

Exam traps

• Left-dominant PDA from the LCx — inferior wall is not automatically RCA.
• A ramus is a trifurcating LM branch, not a failed engagement.
• A separate conus ostium is a variant, not always an occluded first RCA branch.
• RCA ischemia often yields AV nodal block; proximal LAD yields bundle-branch / infranodal block.
• High mean PA without PCWP does not distinguish pre- from post-capillary pulmonary hypertension.
• Teaching pressure and saturation ranges are not ARRT-published cutoffs.