1. Invited Guest Speaker: Dr. Tim Gilbertson Nov. 11 Thursday 11 AM Olin Theater Sensory Cues for Fat and their Role in Fat Intake Dr. Gilbertson is Professor & Associate Department Head of Biology and serves as the Associate Director of the Center for Advanced Nutrition at Utah State University. Dr. Gilbertson's research is focused on the investigation of the mechanisms the body uses to recognize nutrients & how this process is regulated by nutritional need. His lab studies the way nutrients including fats, carbohydrates and minerals are detected by chemosensory cells in the oral cavity and in several nutrient-sensitive, post-ingestive organs. The research spans from genes through behavior with expertise in molecular biology, proteomics, electrophysiology, imaging, biochemistry and analysis of behavior.

2. 10 November 2010 Cardiovascular Physiology The Cardiac Cycle Control of HR and SV MAP and TPR Blood Vessels Lab this week: Frog Heart Physiology Arrive early if you want to pith.

3. 1QQ # 26 for 8:30 am 1.How do action potentials in cardiac myofibers differ from action potentials in skeletal myofibers? a) Cardiac APs are shorter b) Cardiac APs involve Ca++ influx c) Cardiac APs permit summation d) Cardiac APs do not rely on Na+ influx e) Cardiac APs are conducted from myofiber to myofiber via gap junctions of intercalated disks. 2.As blood passes from the left atrium to the left ventricle, it passes through a)the tricuspid valve b)an atrioventricular valve c)a semilunar valve

4. 1QQ # 26 for 9:30 am 1.How do action potentials in cardiac myofibers differ from action potentials in skeletal myofibers? a) Cardiac APs are longer b) Cardiac APs involve Ca++ influx c) Cardiac APs prevent summation d) Cardiac APs do not rely on Na+ influx e) Cardiac APs are conducted from cell to cell via gap junctions of intercalated disks. 2.As blood passes from the right atrium to the right ventricle, it passes through a)the tricuspid valve b)an atrioventricular valve c)a semilunar valve

5. Figure 12.14 Pacemaker Cells in Conducting System: SA Node and Bundle of His Ectopic Pacemaker Locations other than SA Node S 1

6. Figure 12.22 Intrinsic Rate = 100 beat/min S 2

7. Figure 12.23 Effect of “Beta blockers” NEEPIACh mAChR Effect of atropine Beta-adrenergic receptors S 3

8. Figure 12.18 1 st Heart Sound = Closure of Atrioventricular (AV) valves at beginning of Ventricular Systole 2nd Heart Sound = Closure of Semilunar valves at beginning of Ventricular Diastole S 4

9. Figure 12.20 Systolic Diastolic Ejection Fraction = SV/EDV Atrial Fibrillation Ventricular Fibrillation & Defibrillation Stroke Volume Animation S 5

10. Events are same for Cardiac Cycle for Right Side of Heart; only difference is lower systolic pressures in right atrium and right ventricle. S 6

11. Frank-Starling Law of the Heart FS LoH = SV is proportional to EDV Ventricular Function Curve Does not depend on hormones or nerves Assures that the heart adjusts its output based on VENOUS RETURN Ways to enhance Venous Return: 1) muscle contractions 2) “respiratory pump” 3) venoconstriction S 7 Who Cares? Heart transplant patients

12. Fig. 09.21 Low EDV High EDV Length-tension “curve” for Cardiac muscle Overinflation of ventricles leads to less effective pumping S 8

13. Overinflation of ventricles results in reduction in stroke volume S 9 Treatments? …..diuretics

14. Figure 12.25 Contractility NE from Symp postganglionics & EPI from Adrenal medulla Note: cardiac myofibers NOT innervated by parasympathetic division Increase Ejection Fraction S 10

15. 3 Effects of Sympathetic Stimulation 1: Increase rate of contraction 2: Increase peak tension 3: Decrease twitch duration S 11 Why does this happen?

16. Control of Stroke Volume End diastolic volume (preload) Contractility (strength of ventricular contraction due to adrenergic stimulation) Pressure in arteries that must be overcome = Afterload FS LoH S 12

17. Afterload is analogous to trying to pump more air into a tire that is already fully inflated (heart contracting to overcome diastolic pressure.) High blood pressure increases the workload of the heart….. Cardiac hypertrophy….increase chance of irregular conduction of AP through heart S 13 Hypertrophic cardiomyopathy