1 / 32

S

S. S 1. Secretion. Reabsorption. Filtration. S 2. Circulatory System Circulates. Nutrients: glucose, amino acids, fatty acids, ketones, etc Wastes: Hormones: bound & free Gases: CO 2 and O 2 Formed Elements: Cells and Cell Fragments

jhurley
Download Presentation

S

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. S S 1 Secretion Reabsorption Filtration

  2. S 2 Circulatory System Circulates • Nutrients: glucose, amino acids, fatty acids, ketones, etc • Wastes: • Hormones: bound & free • Gases: CO2 and O2 • Formed Elements: Cells and Cell Fragments • Erythrocytes, Leukocytes, Thrombocytes = Platelets Other roles of the Cardiovascular System Thermoregulation Blood Clotting Reproduction (ex: penile erection)

  3. Formed elements Blood volume ~ 5 liters S 3 Figure 12.01 Serum = plasma – clotting factors Entering and Exiting the blood Components…… EPO and “The Scoop on Tissie” Discontinuous capillaries in bone marrow, spleen, & liver permit erythrocytes to enter and exit blood. Hct = percentage of blood volume occupied by RBCs Anemia Blood doping & erythropoietin (hormone that stimulates erythrocyte production in bone marrow) to increase hematocrit

  4. Fig. 12.02 When left heart can’t pump all the blood it receives from pulmonary circuit (due to high aortic pressure and/or damage to left ventricle) blood accumulates in pulmonary circuit. This is congestive heart failure. Symptom: shortness of breath. S 4 Arteries..away from heartVeins..return to heart Regional blood flow determined by arteries and arterioles. Resting Cardiac Output = 5L/min for each side!

  5. Figure 12.04 S 5 CO = 5L/minfor each circuit Up to 35 L/min in strenuous exercise

  6. S 6 What’s missing? Pulmonary circuit CO = 5 liters/min CO = 5 liters/min Arterial Blood Pressure Recall Portal Systems! Systemic Circuit Resistance Vessels Microcirculation Exchange Vessels Capacitance vessels

  7. S 7 Pulmonary circuit Pressuregradients makes fluids move. Moving fluids flow, but flow is limited by resistance. Resistance creates pressure. Systemic Circuit Arterioles establish Mean Arterial Pressure

  8. S 8 F=Q=ΔP/R Flow = Pressure gradient/Resistance from Ohm’s Law (V=IR) Radius of arterioles regulates Q to organs Double radius … 16x flow Half radius….1/16th flow R = 8Lη/πr4 Q=ΔP πr48LηPoiseulle’s equation Smooth muscles determine radius

  9. S 14 MAP = CO x TPR MAP = (HR x SV) x TPR Mean Arterial Pressure = Cardiac Output x Total Peripheral Resistance

  10. S 1 Cardiac Output = Heart Rate X Stroke VolumeWhat regulatesheart rate?CO = HR x SV5L/min = 72 beat/min x 70 ml/beat What regulatesStroke Volume? The Cardiac Cycle animation

  11. Problems with valves: ….Stenosis (narrowing) →Heart Murmurs (turbulent flow past a constriction) note: origin of neonatal heat murmurs (foramen ovale) ….Prolapse (eversion) allows backflow (also generates murmurs) Bicuspid=Mitral Tricuspid Heart murmurs ≠ heart sounds Figure 12.07 S 4 Heart sounds produced by valve closings SemilunarValves Animation

  12. S 3 Figure 12.13 Plateau phase Cardiac Myofiberaction potential Long refractory period prevents summation in cardiac myofibers CardiacMyofiber

  13. S 4 Figure 12.11 S 5 SA node cells do not have stable resting membrane potential, spontaneously produce AP, are Pacemaker cells

  14. S 5 Figure 12.14 Cardiac Pacemakeraction potential Ectopic Pacemaker Locations other than SA Node Pacemaker Cells in Conducting System: SA Node andBundle of His These cells set the rhythm & control Heart Rate.

  15. S 15 Figure 12.22 Intrinsic Rate = 100 beat/min 2 effects of Parasymp:hyperpolarization &slower depolarization

  16. S 6 Figure 12.23 NE EPI ACh mAChR Beta-adrenergic receptors Effect of atropine Effect of “Beta blockers”

  17. S 7 What prevents the AP from being conducted from ventricles back to atria? Fibrous connective tissue between atria and ventricles prevents the conduction of action potential. Only route is via AV node, bundle of His, bundle branches, Purkinje fibers, and to ventriclular myofibers.

  18. S 8 “Sis-toe-lee” 1st Heart Sound = Closure of Atrioventricular (AV) valves at beginning of Ventricular Systole “die-ass-toe-lee” 2nd Heart Sound = Closure of Semilunar valves at beginning of Ventricular Diastole

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

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

  21. S 1 CO = HR x SV5L/min = 72 beat/min x 70 ml/beat 35L/min = ? beat/min x ? ml/beat 3 So far, we’ve dealt with the factors that control Cardiac Output by changing heart rate. 2 + sympathetic 1 - parasympathetic

  22. S 2 Figure 12.20 Stroke Volume Animation

  23. S 3 Frank-Starling Law of the Heart Does not depend on hormones or nerves Assures that the heart adjusts its output based on VENOUS RETURN Ventricular Function Curve Ways to enhance Venous Return:1) muscle contractions2) “respiratory pump”3) venoconstriction FS LoH = SV is proportional to EDV ↑VR→ ↑EDV → ↑SV

  24. S 4 Fig. 09.21 Length-tension “curve” for Cardiac muscle High EDV Low EDV Overinflation of ventricles leads to less effective pumping

  25. S 5 Overinflation of ventricles results in reduction in stroke volume Treatments? …..diuretics

  26. S 6 NE from Symp postganglionics & EPI from Adrenal medulla acting via B-adrenergic receptors on cardiac myofibers. Contractility Increase Ejection Fraction Note: cardiac myofibers NOT innervated by parasympathetic division

  27. S 7 3 Effects of SympatheticStimulation 1: Increase rate of contraction 2: Increase peak tension 3: Decrease twitch duration Why should the contraction be shorter?

  28. Afterload is analogous to trying to pump more air into a tire that is already fully inflated (heart contracting to overcome diastolic pressure.) S 9 High blood pressure increases the workload of the heart….. Cardiac hypertrophy….increase chance of irregular conduction of AP through heart Hypertrophic cardiomyopathy

  29. S 8 Summary: 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

  30. S 11 CO = HR x SV5L/min = 72 beat/min x 70 ml/beat35L/min = ? beat/min x ? ml/beat Factors that control Cardiac Output by changing heart rate and stroke volume. Afterload (MAP) EDV (FSLoH) + sympathetic contractility - parasympathetic

  31. 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.

  32. 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

More Related