Cardiology Physiology and Blood Flow

• What causes angina?

  The increased oxygen consumption requirement is not met by the amount of coronary blood flow, which is decreased.
• Vasospasm, fixed stenosis, and thrombus are ways to decrease coronary blood flow.
• Increased heart rate, contractility, afterload, and preload can lead to increased oxygen consumption.
• Coronary Vascular Reserve: difference in coronary blood flow while at rest compared to during exercise with maximum vasodilation
• At rest the smooth muscle cells are constricted and only allowing as much blood flow that is needed based on the needs of the myocardium. With exercise the smooth muscle cells relax and vasodilation occurs. At maximum vasodilation there is typically about a 5 fold increase in blood flow to the heart compared to while at rest.
• What is the Fick Principle?

  The Fick Principle is a method used to calculate cardiac output by measuring the amount of oxygen consumed by the body.
• Prostacyclin (PGI2) is a vasoactive substance synthesized and released by the vascular endothelium.
• Vascular endothelium is an important source for synthesis and release of vasoactive substances.
• Nitric oxide (NO) is a vasoactive substance synthesized and released by the vascular endothelium.
• Endothelium-derived hyperpolarizing factor (EDHF) is a vasoactive substance synthesized and released by the vascular endothelium.
• Endothelin-1 (ET-1) is a vasoactive substance synthesized and released by the vascular endothelium.
• Variant (Printzmetal's) Angina is generally believed to be due to coronary artery vasospasm, and pain often occurs at rest but can be induced by stress (“supply ischemia”).
• Unstable Angina is generally caused by spontaneous thrombus formation, and the pain can occur at rest or during exercise (“supply ischemia”).
• Myocardial Oxygen Balance is determined by the balance between oxygen supply and oxygen demand.
• Decreasing demand (reducing cardiac workload) is another way to increase oxygenation.
• Hypoxia results from a decreased ratio of oxygen supply/oxygen demand.
• With limited Flow Reserve, additional O2 demand with exertion results in coronary O2 supply/O2 demand imbalance and ischemia.
• Afterload, Heart Rate, Inotropy, Stroke Volume are factors that increase cardiac workload.
• Flow is impeded during systole due to extravascular compression.
• Flow is greatest during diastole and driven by aortic pressure.
• Coronary Flow is reduced during Systole due to extravascular compression.
• Vascular Steal in the Coronary Circulation is a phenomenon that occurs when the heart muscle is ischemic.
• Decreased Heart Rate provides proportionally more diastolic time for coronary perfusion and reduces MVO2.
• The three components of resistance to coronary blood flow are the epicardial arteries (normally very low resistance without CAD), the coronary resistance arterioles and small arteries, and Extravascular Compression (the vessels get squeezed when the heart contracts).
• Coronary Pressure and Coronary Flow are inversely related.
• Coronary Flow Reserve is reduced with Stenosis.
• Local Metabolic Control of Coronary Flow is a mechanism that regulates Coronary Flow.
• Atherosclerosis, Thrombosis, Vasospasm, Hypoxemia/Anemia are factors that reduce blood flow.
• Cardiac Output = Total Oxygen Uptake / Arterio-Venous Difference
• Fick's principle states that the product of cardiac output (CO) and arterio-venous O2 content difference equals the total oxygen uptake (VO2).
• Ischemia is most likely to occur in the subendocardial tissue because there is where pressure changes are felt the most during systole and diastole.
• What are some ways that coronary blood flow can be decreased?

  Atherosclerosis, vasoconstriction, thrombosis, vasospasm, stenosis
• What are some parameters in that oxygen consumption can be increased?


  Heart rate, contractility, afterload, preload
• The conflict between decreased coronary blood flow and increased oxygen consumption is what causes angina.
• Coronary Vascular Reserve: difference in coronary blood flow while at rest compared to during exercise with maximum vasodilation.
• Stimulation of the sympathetic nerve’s releases norepinephrine at the sympathetic nerve endings; Norepinephrine stimulates beta 1 adrenergic receptors, which mediates the effects on the heart rate and Increasing the permeability of the fiber membrane to sodium and calcium ions.
• Acetylcholine is released at the vagal endings decreasing the rate of rhythm of the sinus node and decreasing the excitability of the AV junctional fibers between the atrial musculature and the AV node.
• Atrioventricular valves include mitral and tricuspid valves.
• Semilunar valves include the aortic and pulmonic valves.
• A blood clot is formed by platelets and can also be called a thrombus. A thrombus traveling through veins until it reaches a point where it can't progress forward is called an embolism.