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Human Physiology 11/12/08 Jeff Weiner Cardio II Objectives- Dr. Brand 1. List six characteristics of cardiac muscle as given in this lecture. a. Branching fibers with gap junctions at intercalated discs b. Electrical syncytium- currents diffuse through gap junctions c. Graded contraction d. Stretch leads to increased force of contraction e. Automaticity & Rhythmicity f. Aerobic metabolism- many mitochondria 2. Explain the role troponin C and troponin I in excitation of the heart muscle. a. Troponin I (inhibitory) blocks myosin binding sites on actin b. Troponin C binds calcium and turns troponin I to move tropomyosin, exposing the actin binding site 3. In cardiac muscle explain the role in excitation-contraction coupling of: a. T-tubules - Extracellular calcium will enter the myocyte via the T-tubules b. Ryanodine receptor - The SR Calcium release channel c. L-type Ca++ channel (dihydropyridine receptor) - Voltage-gated Ca channel on the T-tubule that lets calcium in when stimulated by an action potential d. Intracellular Ca++ concentration - It is the rise in intracellular Ca (From the SR) that causes muscle cell contraction e. Sarcoplasmic reticulum - Store of intracellular calcium f. The SERCA transporter - ATP pump to get Ca BACK to the SR (major mechanism) g. The Na+, Ca++ exchanger in the cell membrane - Another mechanism for removing intracellular calcium 4. Describe the effects of sympathetic stimulation on contractility, the duration of systole, and the rate of relaxation of the myocardium, and explain the intracellular mechanisms that mediate the changes. a. Sympathetic stimulation will increase contractile force and shorten the duration of systole (increases rate of relaxation). It will stimulate L-type channels, more calcium enters and more is released from the SR. It also increases sensitivity of contractile machinery to calcium. Relaxation is sped up by stimulating SERCA faster. 5. Explain what is meant by the “Frank-Starling” mechanism, and describe the intracellular mechanism responsible for the effect. a. Increased venous return leads to increased “stretch” of the ventricle. This will cause an increased force of contraction and a subsequent increase in stroke volume 6. Make a diagram showing a normal cardiac function curve, and show how the curve shifts for increases or decreases in contractility. - NO 7. Define two indicators of cardiac contractility as given in lecture. a. Changes in dP/dt; the rate of change of ventricular pressure during ejection at a given EDV b. Change in ejection fraction; EF = SV/EDV 8. Identify the two determinants of cardiac output. a. Cardiac Output = Heart rate X Stroke Volume Human Physiology 11/12/08 Jeff Weiner 9. Describe the effects of increases or decreases in sympathetic and parasympathetic stimulation on heart rate. a. Increase in sympathetic stimulation will increase heart rate, increase in parasympathetic stimulation will decrease heart rate, and vice versa. 10. Define the term compliance and compare the compliance of arteries versus veins. a. Compliance is the change in unit volume of a structure per unit change in pressure, or “how much the heart fills in a given pressure” i. Walls of veins are thinner and much more compliant than arteries (page 399) 11. Identify the two determinants of stroke volume a. Frank-Starling mechanism (intrinsic) and changes in contractility (catecholamines, extrinsic) 12. Define these terms as they relate to the ventricle: a. Active relaxation - depends on the SERCA transporter that pumps Ca into the SR during relaxation. This is ATP dependent, and is inhibited in ischemia, impairing relaxation of the contractile machinery b. Passive relaxation - refers to the compliance of the myocardial tissue. Fibrosis (scarring) or other cardiomyopathies may decrease compliance 13. Explain the difference between laminar and turbulent flow and identify three factors that can cause turbulence to occur. a. In laminar or streamlined flow, velocity is maximal at the center of the vessel, and there are concentric thin layers of plasma with gradually decreasing velocity towards the walls of the vessel- it is the dominant type of flow in the circulation b. Examples of turbulent flow: Flow across an obstruction, regurgitant flow across an incompetent valve, abnormal shunt from a high to low pressure chamber. i. Caused by increase in velocity, increase in diameter, and lowering of viscosity 14. Describe the effects of changes in hematocrit on viscosity of the blood. a. Higher hematocrit (% red blood cells/plasma) will cause viscosity to increase (polycythemia) and vice versa. 15. Explain the role of the aorta in maintaining blood pressure during diastole. a. Aortic pressure is maintained during diastole by recoil of the aorta as blood flows to the periphery.