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UNC-Chapel Hill BIOL 252 - Cardiovascular System Part 2

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BIOL 252 1st Edition Lecture 18 Outline of Last Lecture I. B cellsII. Antigen presenting cellsIII. Cellular immunityIV. Humoral ImmunityV. Immunological MemoryVI. Forms of ImmunityVII. Heart PhysiologyVIII. Cardiac RhythmIX. Pacemaker cells has unstable RMPX. Comparison of Cardiac and Skeletal Muscle APsOutline of Current LectureI. Poll EverywhereII. ECG/EKGIII. Principles of Pressure and FlowIV. Heart SoundsV. Phase of Cardiac CycleVI. How much blood does the heart pumpCurrent LectureI. Poll Everywherea. Verapamil is a calcium channel blocker used to treat hypertension. It selectively blocks “slow calcium channels.” How does it lower blood pressure? It is a…1. Positive chronotropic agent2. Negative chronotropic agent3. Positive inotropic agent4. Negative inotropic agent: negatively affects contraction strengtha. How does it lower blood pressure?b. Less calcium, less contraction strength ii. Pacemaker cells – modulate heart rate (SA node cells) iii. Inotropic- group of cells affected by contractility = cardiomyocytesiv. Contractile cells responsible for producing blood pressure v. Slow calcium channels = cardiomyocytes 1. Gives plateau phaseThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.2. 3. If blocking slow calcium channel, what is the missing step?4. Calcium coming in to cardiac muscle cells = part of calcium that triggers contractiona. In skeletal muscle, comes from sarcomereb. In cardiac muscle, comes from SR and extracellular fluid vi. Refractory period: ensures unidirectional AP, build in space so heart cannot receive another AP (prolongs period of AP) II. ECG/EKGa. Two electrodes plus a third groundb. P wave: atrial depolarization (top to bottom)i. Goes from one cell to the next via gap junctionc. QRS complex: atrial repolarization and ventricular depolarization (bottom to top)i. Atria stimulation from SA nodeii. Ventricles stimulated by Purkinje fibers – reason direction is bottom to top => time delay (benefit)d. T wave: ventricular repolarizationIII. Principles of Pressure and Flowa. Pressure = force / area i. Exerted in all directions (omnidirectional) ii. Hydrostatic pressure = fluid pressure b. Flowi. Proportional to pressureii. Small difference in pressure = small movement in fluidc. Pattern of blood moving through the hearti. Atria = low pressure1. Atria contract (systole)ii. At same time, ventricles are relaxed (diastole) iii. Difference in pressure moves blood to ventricles iv. => Atria relax (diastole) while ventricles contract (systole)v. Both sides of heart do that same thingvi. Blood pushes AV valves closed (atrioventricular valves) 1. How we pressurize blood vii. To move blood out of the heart…1. Ventricles continue contracting (systole)2. Semilunar valves pushed opena. Aortic and pulmonary trunk3. Difference in pressure moves blood out of ventricles viii. Ventricles relax and atria relax 1. Blood pushes semilunar vales closed 2. Pressure drives blood throughout entire bodyIV. Heart Soundsa. Valves closing makes noiseb. S1: AV valve closingc. S2: semilunar valve closing d. Valvular insufficiencyi. Causes: 1. Stenosis (narrowed opening surrounded by scar tissue)2. Valvular prolapse (sticking out in wrong direction)3. Congenital malformation e. Phillip was diagnosed with AV Valvular prolapse. Which would you NOT predict?i. His ventricles would be enlargedii. Atria would be enlarged1. Atria pumping against greater pressure, must work harder iii. Heart rate would be greater than normal1. If not able to pump as much blood as normal person, must compensate iv. Blood pressure in his aorta would be within a normal range 1. If heart is compensating (beating faster) to move same amount of blood, expect that the blood pressure would come up as normalV. Phase of Cardiac Cyclea. ESV: end systolic volumei. Volume of blood in ventricle at the end of its contraction ii. Not zero! ~70 mLb. Diastole: contraction, blood volume increasingi. Blood coming from atriumii. iii. Blood volume increases passively until atria contracts iv. EDV: end diastolic volume (~130 mL)v. Ventricle contracts and volume goes down1. Blood goes to aorta (for left ventricle)2. Stroke volume (SV): EDV – ESV 3. Ejection fraction = SV/EDV a. In this case, ~50% VI. How much blood does the heart pumpa. Heart rate x stroke volume = cardiac outputi. Heart rate depends on SA node cells ii. Stroke Volume depends on cardiomyocytes b. mL per minutec. At rest, cardiac output ~5 L/minuted. At max, cardiac output ~25 L/minute i. Increase during exercise to use oxygen more readily ii. If an athlete, can increase cardiac reserve e. How does heart rate change?i. Chronotropic agents affects on nodal cells1. Increase: Sympathetic NS (NE); hormones (NE and TH)2. Decrease: Parasympathetic NS (ACh)3. Tachycardia and bradycardia are abnormal heart rates ii. When body becomes active, proprioceptors in muscles and joints provide info on movementiii. When blood chemistry changes, chemoreceptors provide info on pH and CO21. High CO2 = acidic pH iv. When your brain tells it tov. When blood pressure changes, baroreceptors provide info on blood pressure1. High BP, slow heart


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