Makindo Medical Notes

Related Subjects: |Cardiac Anatomy and Physiology |Coronary Artery Anatomy

Left Coronary Artery (LCA)

• Origin: Arises from the left aortic sinus of the ascending aorta.
• Branches:
  • Left Anterior Descending (LAD) Artery: Gives off septal and diagonal branches.
  • Left Circumflex (LCx) Artery: Gives off obtuse marginal branches.
• Supplied Areas:
  • LAD: Anterior wall of the left ventricle, anterior two-thirds of the interventricular septum, and the apex.
  • LCx: Lateral wall of the left ventricle and part of the posterior wall.

Right Coronary Artery (RCA)

• Origin: Arises from the right aortic sinus of the ascending aorta.
• Branches:
  • Posterior Descending Artery (PDA): Typically arises from the RCA in right-dominant circulation.
  • Right Marginal Artery: Runs along the right margin of the heart.
• Supplied Areas:
  • RCA: Right atrium, right ventricle, sinoatrial (SA) node, and atrioventricular (AV) node.
  • PDA (from RCA): Posterior third of the interventricular septum and the inferior wall of the left ventricle.

Coronary anatomy

Coronary Arteries and ECG Changes

Coronary blood flow

The coronary circulation is the network of blood vessels that supply oxygen and nutrients to the heart muscle (myocardium). The coronary arteries arise from the aorta and branch into smaller vessels that penetrate the heart muscle.

Blood Flow Dynamics

• Diastolic Dominance: Unlike most arteries, coronary blood flow is greatest during diastole (when the heart muscle is relaxed) because the coronary vessels are compressed during systole (heart contraction).
• Autoregulation: Coronary arteries can adjust their diameter to maintain a constant blood flow despite changes in blood pressure. This ensures that the myocardium receives adequate oxygen at all times.
• Myocardial Oxygen Demand: The coronary blood flow is directly proportional to the oxygen demands of the myocardium. During physical exertion, the demand increases, leading to a corresponding increase in coronary blood flow.

Factors Influencing Coronary Blood Flow

• Coronary Resistance: The resistance to blood flow in coronary arteries is influenced by vessel diameter, blood viscosity, and the phase of the cardiac cycle.
• Metabolic Control: Local metabolic factors like adenosine, potassium ions, and carbon dioxide cause vasodilation, increasing blood flow in response to increased myocardial activity.
• Neural and Hormonal Control: Sympathetic stimulation causes vasoconstriction of coronary vessels, while parasympathetic activity leads to vasodilation. Additionally, hormones like epinephrine can also affect coronary blood flow.
• Atherosclerosis: The build-up of plaques in the coronary arteries reduces blood flow, leading to ischaemia and conditions like angina and myocardial infarction.

Clinical Significance

Coronary blood flow is critical to maintaining heart function. Any disruption, such as a blockage in the coronary arteries, can lead to severe consequences like myocardial infarction. Understanding the regulation and dynamics of coronary blood flow is essential for diagnosing and treating cardiovascular diseases.

Coronary Artery Constrictors

• Norepinephrine and Epinephrine: Released during sympathetic activation, these catecholamines cause vasoconstriction by stimulating alpha-adrenergic receptors on the coronary arteries. However, they also have a dilatory effect via beta-adrenergic receptors.
• Endothelin-1: A potent vasoconstrictor produced by endothelial cells. It plays a significant role in coronary artery disease and can lead to vasospasm.
• Angiotensin II: Part of the renin-angiotensin-aldosterone system (RAAS), angiotensin II causes vasoconstriction by acting on angiotensin receptors on the coronary vessels.
• Thromboxane A2: A substance released by platelets during aggregation that promotes vasoconstriction and contributes to the progression of coronary artery disease.
• Serotonin (5-HT): Released by platelets and causes vasoconstriction through stimulation of serotonin receptors, particularly in diseased vessels.

Coronary Artery Dilators

• Nitric Oxide (NO): produced by endothelial cells. NO diffuses into smooth muscle cells, causing relaxation and dilating the coronary arteries.Prostacyclin (PGI₂): produced by endothelial cells that inhibits platelet aggregation and relaxes smooth muscle in coronary vessels.
• Adenosine: released during hypoxia or increased myocardial activity. It binds to A2 receptors on coronary vessels, causing vasodilation.
• Bradykinin: promotes vasodilation by stimulating the release of NO and prostacyclin from endothelial cells.
• Beta-Adrenergic Agonists (e.g., Isoproterenol): stimulate beta-adrenergic receptors on coronary vessels, leading to vasodilation.
• Calcium Channel Blockers: inhibit the entry of calcium into smooth muscle cells, reducing contraction and promoting vasodilation in coronary arteries.