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Review Slides for A&P II Lecture Exam 1 PowerPoint Presentation
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Review Slides for A&P II Lecture Exam 1

Review Slides for A&P II Lecture Exam 1

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Review Slides for A&P II Lecture Exam 1

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  1. Review Slides for A&P II Lecture Exam 1

  2. Please note: These slides highlight the MAJOR points you will need to know, but they do not contain everything you need to know for the exam! Your Study Guide for this exam is your reference for what you need to know for the exam. DO NOT RELY ONLY ON THESE SLIDES FOR YOUR EXAM PREPARATION - USE YOUR STUDY GUIDE!

  3. Blood Transport, Stability of interstitial fluid, distribute heat, hemostasis, prevent infection -cytosis = abnormal increase in cell number -penia = abnormal decrease in cell number • straw colored • liquid portion of blood • 55% of blood Volume ≈ 5L 45% of blood (hematocrit)  globulins globulins γglobulins

  4. Blood Cell Counts #RBCs - Average is about 5 x 106 RBCs / µl (1 mm3 = 1 microliter, µl) Number of RBCsreflects blood’s oxygen carrying capacity Anemia – deficiency of RBCs or Hb in RBCs; reduces O2-carrying capacity of blood #WBCs - 5,000 – 10,000 per mm3 (or μl) of blood • leukopenia(-penia = deficiency of cell number) • low WBC count • typhoid fever, flu, measles, mumps, chicken pox, AIDS • leukocytosis(-cytosis = increase in cell number) • high WBC count • acute infections, vigorous exercise, great loss of body fluids #Platelets - 150,000 – 500,000 per mm3of blood (average ≈ 350,000 per µl)

  5. Red Blood Cell Turnover The average life span of an RBC is about 120 days Iron is carried in the blood by transferrin to red bone marrow, liver Figure From: Martini, Anatomy & Physiology, Prentice Hall, 2001 Porphyrin from worn out RBCs is converted into biliverdin an bilirubin

  6. Blood Viscosity and Osmolarity • Viscosity (thickness) • Resistance to flow of blood • Whole blood is about 5x as viscous as water • Changes in viscosity can put strain on the heart • Erythrocytosis (polycythemia)  viscosity • Osmolarity • Due to NUMBER of particles dissolved, not the type • Na+, proteins, erythrocytes • Osmolarity determines fluid flow between blood and tissues

  7. Blood Clots • After forming, blood clot retracts (~60%) and pulls the edges of a broken vessel together • Platelet-derived growth factor stimulates smooth muscle cells and fibroblasts to repair damaged blood vessels • Thrombus – abnormal blood clot • Embolus – blood clot moving through blood Serum is the fluid expressed from a clot, i.e., the plasma minus clotting factors

  8. White Blood Cells Two major classes of leukocytes (WBC) WBCs leave the bloodstream and enter tissues by the process of diapedesis • granulocytes • neutrophils • eosinophils • basophils • agranulocytes • lymphocytes • monocytes

  9. Plasma Proteins • Albumins • most numerous plasma proteins (~55%) • ‘transport’ proteins • originate in liver • help maintain osmotic pressure of blood • Alpha and Beta Globulins • originate in liver • transport lipids and fat-soluble vitamins • Gamma Globulins • originate inlymphatic tissues (plasma cells) • constitute the antibodies of immunity • Fibrinogen • originates in liver • plays key role in blood coagulation

  10. Hemostasis • cessation of bleeding • Platelet Plug Formation • triggered by exposure of platelets to collagen • platelets adhere to rough surface to form a plug • Blood Vessel Spasm • triggered by pain receptors, platelet/endothelial cell release of various substances • smooth muscle in vessel contracts (vascular spasm) • Blood Coagulation • triggered by cellular damage and blood contact with foreign surfaces • blood clot forms 1. Vascular phase 2. Platelet phase 3. Coagulation phase

  11. Blood Coagulation • Three cascades: • Instrinsic • Extrinsic • Common Coagulation is an example of positive feedback ~ 15 sec. ~ 3-6 min. Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2001

  12. Prevention of Coagulation • The smooth lining (endothelium) of blood vessels discourages the accumulation of platelets • Prostacyclin released by endothelial cells(aspirin) • Some cells secrete heparin (an anticoagulant) • As a clot forms, fibrin absorbs thrombin and prevents the reaction from spreading • Antithrombin (in plasma) interferes with the action of excess thrombin • Plasmin digests blood clots (generated from plasminogen via the action of a plasma enzyme, kallikrein) *

  13. Pathway of Blood Through Heart veins Figure from: Saladin, Anatomy & Physiology, McGraw Hill, 2007 Know This!

  14. Heart Valves Heart valves ensure one-way flow of blood through the heart Atrioventricular (AV) valves • Tricuspid Valve • right A-V valve • between right atrium and right ventricle • Attached to chordae tendineae • Bicuspid (Mitral) Valve • left A-V valve • between left atrium and left ventricle • Attached to chordae tendineae • Pulmonary Valve • semilunar valve • between right ventricle and pulmonary trunk • Aortic Valve • semilunar valve • between left ventricle and aorta

  15. Wall of Heart • Three layers • endocardium • forms protective inner lining • membrane of epithelial and connective tissues • myocardium • cardiac muscle • contracts to pump blood • epicardium • serous membrane (visceral pericardium) • protective covering • contains capillaries and nerve fibers Know all the layers depicted in the diagram, and know their correct order.

  16. Cardiac Conduction System Specialized myocardial cells. Instead of contracting, they initiate and distribute impulses throughout the heart. S-A node = Pacemaker Pacemaker firing rates: SA Node – 80-100 bpm AV Node – 40-60 bpm Purkinje – 30-40 bpm

  17. Electrocardiogram • recording of electrical changes that occur in the myocardium during the cardiac cycle • used to assess heart’s ability to conduct impulses, heart enlargement, and myocardial damage Important points to remember: - Depolarization precedes contraction - Repolarization precedes relaxation P wave – atrial depolarization QRS wave – ventricular depolarization T wave – ventricular repolarization Three waves per heartbeat

  18. Regulation of Cardiac Rate Tachycardia > 100 bpmBradycardia < 60 bpm Parasympathetic impulses reduce CO (rate); sympathetic impulses increase CO (rate/strength) **ANS activity does not ‘make’ the heart beat, it only regulates its beat Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2004

  19. Summary of Factors Influencing CO – Table Form

  20. Coronary Circulation Coronary vessels fill mainly during diastole

  21. Systole and Diastole Systole = contraction; Diastole = relaxation Atrial Diastole/Ventricular Systole Atrial Systole/Ventricular Diastole

  22. Review of Events of the Cardiac Cycle Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2004 • Atrial contraction begins • Atria eject blood into ventricles • Atrial systole ends; AV valves close (S1) • Isovolumetric ventricular contraction • Ventricular ejection occurs • Semilunar valves close (S2) • Isovolumetric relaxation occurs • AV valves open; passive atrial filling S2 S1

  23. Factors Affecting Cardiac Output Figure adapted from: Aaronson & Ward, The Cardiovascular System at a Glance, Blackwell Publishing, 2007 ANSParasympathetic Sympathetic HR Contractility CO = HR x SV ESV Afterload = EDV - ESV SV EDV CVP CO – Cardiac Output (~5L/min). Dependent upon Stroke Volume (SV; ~70 ml) and Heart Rate (HR) CVP – Central Venous Pressure; Pressure in vena cava near the right atrium (affects preload; Starling mechanism) Contractility – Increase in force of muscle contraction without a change in starting length of sarcomeres Afterload – Load against which the heart must pump, i.e., pressure in pulmonary artery or aorta ESV – End Systolic Volume; Volume of blood left in heart after it has ejected blood (~50 ml) EDV – End Diastolic Volume; Volume of blood in the ventricle before contraction (~120-140 ml)

  24. Regulation of Cardiac Output Recall: SV = EDV - ESV Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2001 CO = heart rate (HR) x stroke volume (SV) Be sure to review, and be able to use, this summary chart

  25. The Frank-Starling Mechanism • Amount of blood pumped by the heart each minute (CO) is almost entirely determined by the venous return • Frank-Starling mechanism • Intrinsic ability of the heart to adapt to increasing volumes of inflowing blood • Cardiac muscle reacts to increased stretching (venous filling) by contracting more forcefully • Increased stretch of cardiac muscle causes optimum overlap of cardiac muscle (length-tension relationship)

  26. Comparison of Skeletal and Cardiac Muscle • Ca2+ ions enter from • Extracellular fluid (20%) • Sarcoplasmic reticulum (80%) • So, Cardiac muscle is very sensitive to Ca2+ changes in extracellular fluid • Cardiac and skeletal muscle differ in: • Nature of action potential • Source of Ca2+ • Duration of contraction Recall that tetanic contractions usually cannot occur in a normal cardiac muscle cell Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2001

  27. Overview of the Cardiovascular System (CVS) CVS = Heart + Blood Vessels

  28. Overview of Blood Vessels Large/med sized arteries regulate blood flow to organ systems; high press. Arterioles regulate blood flow to capillary beds Capillaries are site of fluid exchange Arteries and veins are constructed of three layers: 1) tunica intima 2) tunica media 3) tunical externa Veins return blood to heart, hold most of body’s blood and have valves; low press. 3 types: - continuous (muscle) - fenestrated (endocrine glands, kidney, small intestine) - sinusoids (liver, spleen, bone marrow) Figure from: Saladin, Anatomy & Physiology, McGraw Hill, 2007

  29. Capillaries • smallest diameter blood vessels (fit 1 RBC at a time) • extensions of inner lining of arterioles • walls consist of endothelium and basement membrane only – NO smooth muscle • semipermeable (plasma fluid can escape, but not proteins) 3 types: - continuous (muscle) - fenestrated (endocrine glands, kidney, small intestine) - sinusoids (liver, spleen, bone marrow)

  30. Exchange in the Capillaries • major mechanism involved in exchange of solutes is diffusion • substances move in and out along the length of the capillaries according to their respective concentration gradients • Fluid movement in systemic capillaries is determined by two major factors • 1. hydrostatic pressure;varies along portions of capillary • 2. osmotic pressure; remains about the same along the length of the capillary Excess tissue fluid is drained via lymphatics

  31. Arterial Blood Pressure Blood Pressure – force the blood exerts against the inner walls of the blood vessels • Arterial Blood Pressure • rises when ventricles contract • falls when ventricles relax • systolic pressure – maximum pressure • diastolic pressure – minimum pressure Pulse pressure – difference between systolic and diastolic pressures (systolic : diastolic : pulse pressure ~ 3:2:1) - Pulse pressures usually rise with age because of an increase in blood vessel resistance (arteriosclerosis) Recall: Blood Flow (CO)  Pressure / Resistance

  32. Mean Arterial Pressure Mean Arterial Pressure (MAP) – Average effective pressure driving blood flow through the systemic organs MAP = CO x Total Peripheral Resistance (TPR) **Thus ALL changes in MAP result from changes in either cardiac output or peripheral resistance If CO increases, MAP ? If TPR decreases, MAP ? If TPR decreases, what must be done to keep MAP the same? If blood volume decreases, what must be done to keep MAP the same? MAP can be estimated by the equation: diastolic bp + (pulse pressure / 3)(Roughly 1/3 of the way between systolic and diastolic pressures)

  33. Factors Affecting Blood Pressure (MAP) 1/radius4; Vessel length; Viscosity; Turbulence MAP (BP) TPR ANSParasympathetic Sympathetic HR Contractility CO ESV Afterload SV EDV CVP Figure adapted from: Aaronson & Ward, The Cardiovascular System at a Glance, Blackwell Publishing, 2007 MAP – Mean Arterial Pressure = Average effective pressure driving blood flow through the systemic organs **The MAP is dependent upon CO and TPR, i.e., MAP = CO x TPR TPR – Total Peripheral Resistance; depends upon *blood vessel radius, vessel length, blood viscosity, and turbulence

  34. Factors Affecting Blood Pressure (MAP) MAP = X TPR 1 / radius4 Vessel length Viscosity Turbulence

  35. Autoregulation of Blood Flow/Pressure • Local vasodilators increase blood flow • Decreased O2 (except pulmonary circulation) or increased CO2 • Increase in lactic acid production • Release of nitric oxide (NO) • Increased K+ or H+ • Mediators of inflammation (histamine, NO) • Elevated local temperature • Local vasoconstrictors decrease blood flow • Prostaglandins, thromboxanes (released by activated platelets and WBCs) • Endothelins released by damaged endothelial cells

  36. Central Venous Pressure • Central Venous Pressure= pressure in the vena cava near the right atrium (~ 2-4 mm Hg) • determines the filling pressure of the right ventricle • determines the EDV of the right ventricle which • **determines ventricular stroke volume (Frank-Starling) • affects pressure within the peripheral veins • weakly beating heart causes an increase in central venous pressure (backup of blood) • increase in central venous pressure causes blood to back up into peripheral veins

  37. Hepatic Portal Vein Hepatic portal vein drains one set of capillaries and leads to another set of capillaries before it becomes a vein Note that veins in the abdominal cavity drain into the hepatic portal vein

  38. Aorta and Its Principal Branches **Need to know this table; if I give you an artery, you need to know which branch of the aorta it arises from

  39. Major Veins - Upper Limb and Shoulder * * Median cubital vein is often used to draw blood (venipuncture) * (deep) * (superficial) * (superficial) * * * * *

  40. Arteries to Neck, Head, and Brain * * * * * *

  41. Major Veins of the Brain, Head, and Neck External jugular v. drains blood from face, scalp, and superficial neck regions * * * * *

  42. Arteries to Shoulder and Upper Limb * * * = pulse points * * *

  43. Cerebral Arterial Circle • Also called the Circle of Willis • Formed by anterior and posterior cerebral arteries, which join the internal carotid and basilar arteries Know the names of the vessels that make up the cerebral arterial circle