BIOL 460 1st Edition Lecture 23 Outline of Last Lecture I. Blood Clottinga. Platelets b. Hemostasis c. Platelet release reactiond. Formation of clotOutline of Current Lecture I. Dissolution of ClotsII. Anticoagulants III. Cardiac output IV. Stroke Volume Effectsa. Frank-Starling LawV. Venous Return Current LectureBlood Clotting Continued…1. Dissolution of Clotsa. Prekallikrein  [XII]  kallikreinb. Plasminogen  [kallikrein, thrombin, or tissue plasminogen activator]  Plasmin(enzyme that digests fibrin)c. Same steps that form clot also aid in dissolution of clot (thrombin, XII)d. TPA  used to dissolve clots in stroke and myocardial infarctions, produced by endothelial cellse. Also use streptokinase (produced by streptococcus) to dissolve fibrin2. Anticoagulantsa. Aspirin  inhibits COX-1, inhibits platelet release reactionb. Coumarin (warfarin)  inhibits activation of vitamin K, no Ca2+ binding to clotting factorsc. Heparin  inhibits thrombin (what blood-storing glassware is coated with )d. Citrate  binds Ca2+, making it unavailablee. EDTA  binds Ca2+, making it unavailableCardiac Output1. CO = SV * HR2. Average CO = 75ml/beat * 70 beats/min = 5500 ml/minThese 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.3. Anything that affects HR – chronotropic effecta. Can be + or –b. Determined by cardiac center in medullai. Influenced by higher brain centers and baroreceptors (measure BP)ii. Baroreceptors are located in carotid sinus and aortic archiii. Drop in BP causes a reflex increase in HRc. HR affected by balance of sympathetic and parasympathetic innervationd. Sympathetic Effecti. B1 receptorsii. Adenylate cyclase/cAMP 2nd messenger systemiii. Steepens slope of pacemaker potential by directly opening more HCN channels (cAMP)iv. Epinephrine  cAMP  HCN channels opene. Parasympathetic Effecti. Decreases slope of pacemaker potentialii. Muscarinic receptors open K+ channels in cells of SA nodeiii. Depolarizes more slowly4. What affects stroke volume?a. End diastolic volumei. Amount of blood in ventricleii. “Preload” – workload imposed on heart before it contractsiii. SV proportional to EDVb. Total Peripheral resistancei. Fluid moves through tube and experiences friction with walls of tubeii. Greater diameter decreases resistanceiii. Higher peripheral resistance increases arterial pressure, which means the heart must produce a higher pressure to reach ejection phaseiv. PR is actually frictionv. Sometimes called “afterload” – workload after contractionvi. Peripheral resistance increases, stroke volume decreasesvii. SV ≈ EDV/PRc. Contractility of Myocardiumi. How forcefully ventricles contract at any given momentii. Affected by norepinephrine and epinephrineiii. Said to be positive inotropic (ino=sinew) effectiv. Heart contracts more forcefully via sympathetic post-ganglionic neurons increasing Ca2+ in sarcoplasmd. Frank-Starling Law of the Heart (Otto Frank and Ernest Starling)i. The more the heart is stretched, the more forcefully it contractsii. Length-tension relationship like skeletal muscleiii. Increases distance that the thin filaments slide past thick filamentsiv. Can’t stretch so far that heart can’t contract1. Pericardial sac prevents2. Bands of tissue in ventricles (moderator bands) between walls of tissue and interventricular septume. Heart can adapt to changes in peripheral resistance (increase in PR counteracted)f. Can adapt to changing end diastolic volumesg. Intrinsic feature results in R ventricle and L ventricle always pumping same amount of bloodi. Heart attack affects thisii. RV  lungs  LV (stopped b/c of damage)iii. Blood backs up in pulmonary circuitiv. Increases pulmonary resistancev. Increases pressure in pulmonary arteryvi. R ventricle contracts more forcefully, causing an increase in blood pressure, which causes pulmonary hypertensionvii. This forces fluids out into lungs, causing pulmonary congestion (can drown in own fluids)Venous Return1. Essentially systemic circuit2. Affects end diastolic volume, which effects stroke volume3. 2 things affect venous return (VR)a. Venous pressure (increase in pressure increases return)b. Total blood volume (controlled by kidneys)4. Veins are thinner with less muscular walls5. Stretch in response to an increase in venous pressure – have high compliance6. Capacitance Vessels – store blood (2/3 of blood is in systemic veins at any given time)7. Arteries have much less compliance (resistance vessels)8. Average venous pressure is 2mmHg9. Average artery pressure is 90-100mmHg10. Big drop in BP due to friction (mostly in arterioles, which have a small lumen)11. What affects venous return?a. Change in pressure in veinsi. Venules – 10mmHgii. Superior and inferior vena cavae – 0mmHgiii.