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Join Dr. Jim Stallworth and USC School of Medicine guests for a presentation on admissions and opportunities for medical school. Earn up to 5 points for Test #2, covering topics such as cardiac regulation and survival strategies for in vitro organs. Engage in discussions on physiological concepts and clinical applications.
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For sophomores and juniors interested in medical school at: • A visit by Dr. Jim Stallworth and other guests from USC School of Medicine in Columbia, SC. • In RMSC 122 (The Pit) starting at 6:30pm, Tuesday Nov 13th. • Presentation and discussion on admissions and opportunities.
Abstracts and Test 2 • Earn up to 5 points for Test # 2 based on topics of Frog Heart Lab: • Regulation of pacemaker cells by temperature, hormones, neurotransmitters, antagonists • Heart block: 1st, 2nd, and 3rd degree • The conducting system • Strategies for prolonging survival of in vitro organs Cardiac Cycle Animation
1QQ #25 for 10:30Write the number of the one you choose to answer. • Which is more serious and why: atrial fibrillation or ventricular fibrillation? • Explain the Frank-Starling Law of the Heart in terms of what happens in cardiac myofiber sarcomeres as end-diastolic volume exceeds 400 ml. • What are three ways by which stroke volume can be increased?
1QQ #25 for 11:30Write the number of the one you choose to answer. • What is potentially dangerous about cardiac hypertrophy that accompanies rigorous physical training? • Explain the Frank-Starling Law of the Heart in terms what happens in cardiac myofiber sarcomeres as venous return increases. • What are the effects of sympathetic stimulation on cardiac myofibers?
S 11 CO = HR x SV5L/min = 72 beat/min x 70 ml/beat 35L/min = ? beat/min x ? ml/beat Factors that control Cardiac Output by changing heart rate and stroke volume. Afterload (MAP) VR and EDV (FSLoH) + sympathetic Contractility (catecholamines) - parasympathetic
Summary of Factors that Regulate Cardiac Output S 12 Fig. 12.28 Even persons with heart transplants can adjust CO in the absence of innervation of heart. Exercise………increase CO
S 13 Heart is pump that generates pressure gradient. Blood flows through vessels, which have resistance. Arterioles have greatest resistance and create “backpressure” in the arteries and aorta. Mean Arterial Pressure = diastolic +1/3(systolic – diastolic) = 70 + 1/3(120-70) = 70 + 17 = 87 mm Hg
S 14 MAP = CO x TPR Hypertension MAP = (HR x SV) x TPR Mean Arterial Pressure = Cardiac Output x Total Peripheral Resistance Hypotension Who Cares? Hemorrhage Diagram from memory on Friday November 30th.
Name _________________________________________ On the back side of this page, create a diagram for the following. Your response must be confined to the reverse side of this page and you must write legibly. Your response will count 15-20% of the grade on Test 3 and should require no more than 15 minutes to complete at the beginning of class on Friday November 30th. Beginning with a loss of about 1 liter of blood from a vein, diagram the early events associated with hemorrhage and the negative feedback responses to hemorrhage in a well-organized diagram. Write legibly! Completeness, accuracy, and detail, together with the proper sequence earn maximal points. The following abbreviations can be used: AI, AII, JGA, mAChR, Hct, Q, SV, EF, RBC, HR, EDV, ACh, ANH, ADH, CO, TPR, EPO, VR, MAP, EPI, NE, SAN, aAdR , bAdR, Symp (sympathetic), Parasymp (parasympathetic), PV, r (radius), Pc, fAP (frequency of action potentials.) Any other abbreviations must be defined. "If in doubt, write it out!" Use single headed arrows (→) to indicate sequential relationships and doubled-stemmed arrows to indicate increases or decreases.
Velocity in systemic vessels Why is velocity slowest in capillaries and venules?
Flow =ml/min = Riders/min past a location Velocity = m/sec for each rider Velocity slows for exchange
Cumulative cross sectional area of vessels by type Why is velocity slowest in capillaries and venules?
Exchange S 1 Properties of Blood Vessels All vessels and heart chambers lined with ENDOTHELIAL cells (simple squamous) • Arteries • Arterioles • Capillaries • Venules • Veins Elastic, low compliance, large diameter, low resistance vessels Variable Resistance vessels Wall = simple squamous endothelium No smooth muscle; cannot change diameter Capacitance vessels, high compliance, low pressure, valves for unidirectional flow
S 4 Fig. 12.30 Stretching elastic connective tissue Elastic recoil of stretched arterial walls during ventricular systole maintains arterial pressure during diastole as blood drains into arterioles. Atherosclerosis Recoil of elastic connective tissue Point of Confusion: Smooth muscles in arterial walls DO NOT rhythmically contract, do not pump!
Elastic recoil maintains internalpressure without expending energy Arteries are a pressure reservoir to maintain pressure between during ventricular diastole and to keep blood flowing to arterioles during diastole.
S 5 Arteries and Arterial PressureMean Arterial Pressure Arterioles have two main functions: 1) regulate flow to tissues and organs and 2) responsible for Total Peripheral Resistance which influences Mean Arterial Pressure. Arteriole MAP = CO x TPR Poiseulle’s Equation
S 6 Fig. 12.50 CardiacOutput Heart Arteries MeanArterialPressure Arterioles Totol Peripheral Resistance CNS Kidneys Sk. Muscle Skin Gut
What regulates the smooth muscle of arterioles? Extrinsic controls: Intrinsic controls:
S 8 Fig. 12.36 Metabolic vasodilators No parasympathetic innervation of arterioles! Importance of sympathetic “tone.” Metabolic autoregulation, flow autoregulation, myogenic autoregulation
Who Cares? Migraine headaches and sumatriptans (agonists for 5-HT1 receptors)to stimulate vasoconstriction.