1. Copyright © 2010 Pearson Education, Inc. Blood Tests

2. Copyright © 2010 Pearson Education, Inc. Diagnostic Blood Tests Hematocrit Blood glucose tests Microscopic examination reveals variations in size and shape of RBCs, indications of anemias Differential WBC count Prothrombin time and platelet counts assess hemostasis SMAC, a blood chemistry profile Complete blood count (CBC)

3. Copyright © 2010 Pearson Education, Inc. Regulation of Blood Pressure and Heart Rate Autoregulation (meaning that the tissue or organ regulates blood pressure and flow locally)

4. Copyright © 2010 Pearson Education, Inc. Autoregulation Automatic adjustment of blood flow to each tissue in proportion to its requirements at any given point in time Is controlled intrinsically by modifying the diameter of local arterioles feeding the capillaries Is independent of MAP, which is controlled as needed to maintain constant pressure Two types of autoregulation 1.Metabolic 2.Myogenic

5. Copyright © 2010 Pearson Education, Inc. Figure 19.15 Metabolic controls pH Sympathetic  Receptors  Receptors Epinephrine, norepinephrine Angiotensin II Antidiuretic hormone (ADH) Atrial natriuretic peptide (ANP) Dilates Constricts Prostaglandins Adenosine Nitric oxide Endothelins Stretch O2O2 CO 2 K+K+ Amounts of: Nerves Hormones Myogenic controls Intrinsic mechanisms (autoregulation) Distribute blood flow to individual organs and tissues as needed Extrinsic mechanisms Maintain mean arterial pressure (MAP) Redistribute blood during exercise and thermoregulation

6. Copyright © 2010 Pearson Education, Inc. Long-Term Autoregulation Angiogenesis Occurs when short-term autoregulation cannot meet tissue nutrient requirements The number of vessels to a region increases and existing vessels enlarge Common in the heart when a coronary vessel is occluded, or throughout the body in people in high-altitude areas

7. Copyright © 2010 Pearson Education, Inc.

8. Reminder: repeated from previous set of slide, purpose of blood is - Diffusion of O 2 and nutrients from the blood to tissues CO 2 and metabolic wastes from tissues to the blood Lipid-soluble molecules diffuse directly through endothelial membranes Water-soluble solutes pass through clefts and fenestrations Larger molecules, such as proteins, are actively transported in pinocytotic vesicles or caveolae

9. Copyright © 2010 Pearson Education, Inc. Fluid Movements: Bulk Flow Extremely important in determining relative fluid volumes in the blood and interstitial space Direction and amount of fluid flow depends on two opposing forces: hydrostatic and colloid osmotic pressures

10. Copyright © 2010 Pearson Education, Inc. Hydrostatic Pressures Capillary hydrostatic pressure (HP c ) (capillary blood pressure) Tends to force fluids through the capillary walls Is greater at the arterial end (35 mm Hg) of a bed than at the venule end (17 mm Hg) Interstitial fluid hydrostatic pressure (HP if ) Usually assumed to be zero because of lymphatic vessels

11. Copyright © 2010 Pearson Education, Inc. Colloid Osmotic Pressures Capillary colloid osmotic pressure (oncotic pressure) (OP c ) Created by nondiffusible plasma proteins, which draw water toward themselves ~26 mm Hg Interstitial fluid osmotic pressure (OP if ) Low (~1 mm Hg) due to low protein content

12. Copyright © 2010 Pearson Education, Inc. Net Filtration Pressure (NFP) NFP—comprises all the forces acting on a capillary bed NFP = (HP c —HP if )—(OP c —OP if ) At the arterial end of a bed, hydrostatic forces dominate At the venous end, osmotic forces dominate Excess fluid is returned to the blood via the lymphatic system

13. Copyright © 2010 Pearson Education, Inc. Figure 19.17 HP = hydrostatic pressure Due to fluid pressing against a wall “Pushes” In capillary (HP c ) Pushes fluid out of capillary 35 mm Hg at arterial end and 17 mm Hg at venous end of capillary in this example In interstitial fluid (HP if ) Pushes fluid into capillary 0 mm Hg in this example OP = osmotic pressure Due to presence of nondiffusible solutes (e.g., plasma proteins) “Sucks” In capillary (OP c ) Pulls fluid into capillary 26 mm Hg in this example In interstitial fluid (OP if ) Pulls fluid out of capillary 1 mm Hg in this example Arteriole Capillary Interstitial fluid Net HP—Net OP (35—0)—(26—1) Net HP—Net OP (17—0)—(26—1) Venule NFP (net filtration pressure) is 10 mm Hg; fluid moves out NFP is ~8 mm Hg; fluid moves in Net HP 35 mm Net OP 25 mm Net HP 17 mm Net OP 25 mm

14. Copyright © 2010 Pearson Education, Inc. Circulatory Shock Any condition in which Blood vessels are inadequately filled Blood cannot circulate normally Results in inadequate blood flow to meet tissue needs

15. Copyright © 2010 Pearson Education, Inc. Circulatory Shock Hypovolemic shock: results from large-scale blood loss Vascular shock: results from extreme vasodilation and decreased peripheral resistance Cardiogenic shock results when an inefficient heart cannot sustain adequate circulation

16. Copyright © 2010 Pearson Education, Inc. Figure 19.18 Signs and symptoms Acute bleeding (or other events that cause blood volume loss) leads to: 1. Inadequate tissue perfusion resulting in O 2 and nutrients to cells 2. Anaerobic metabolism by cells, so lactic acid accumulates 3. Movement of interstitial fluid into blood, so tissues dehydrate Initial stimulus Result Physiological response Chemoreceptors activated (by in blood pH) Baroreceptor firing reduced (by blood volume and pressure) Hypothalamus activated (by pH and blood pressure) Major effectMinor effect Brain Activation of respiratory centers Cardioacceleratory and vasomotor centers activated Sympathetic nervous system activated ADH released Neurons depressed by pH Intense vasoconstriction (only heart and brain spared) Heart rate Central nervous system depressed Adrenal cortex Kidney Renin released Renal blood flow Aldosterone released Kidneys retain salt and water Angiotensin II produced in blood Water retention Urine output Rate and depth of breathing Tachycardia, weak, thready pulse Skin becomes cold, clammy, and cyanotic Thirst Restlessness (early sign) Coma (late sign) CO 2 blown off; blood pH rises Blood pressure maintained; if fluid volume continues to decrease, BP ultimately drops. BP is a late sign.

17. Copyright © 2010 Pearson Education, Inc. Maintaining Blood Pressure The main factors influencing blood pressure: Cardiac output (CO) Peripheral resistance (PR) Blood volume

18. Copyright © 2010 Pearson Education, Inc. Maintaining Blood Pressure F =  P/PR and CO =  P/PR Blood pressure = CO x PR (and CO depends on blood volume) Blood pressure varies directly with CO, PR, and blood volume Changes in one variable are quickly compensated for by changes in the other variables

19. Copyright © 2010 Pearson Education, Inc. Cardiac Output (CO) Determined by venous return and neural and hormonal controls Resting heart rate is maintained by the cardioinhibitory center via the parasympathetic vagus nerves Stroke volume is controlled by venous return (EDV)

20. Copyright © 2010 Pearson Education, Inc. Cardiac Output (CO) During stress, the cardioacceleratory center increases heart rate and stroke volume via sympathetic stimulation ESV decreases and MAP increases

21. Copyright © 2010 Pearson Education, Inc. Figure 19.8 Venous return Exercise Contractility of cardiac muscle Sympathetic activity Parasympathetic activity Epinephrine in blood EDVESV Stroke volume (SV) Heart rate (HR) Cardiac output (CO = SV x HR Activity of respiratory pump (ventral body cavity pressure) Activity of muscular pump (skeletal muscles) Sympathetic venoconstriction BP activates cardiac centers in medulla Initial stimulus Result Physiological response

22. Copyright © 2010 Pearson Education, Inc. Control of Blood Pressure Short-term neural and hormonal controls Counteract fluctuations in blood pressure by altering peripheral resistance Long-term renal regulation Counteracts fluctuations in blood pressure by altering blood volume

23. Copyright © 2010 Pearson Education, Inc. Short-Term Mechanisms: Neural Controls Neural controls of peripheral resistance Maintain MAP by altering blood vessel diameter Alter blood distribution in response to specific demands

24. Copyright © 2010 Pearson Education, Inc. Short-Term Mechanisms: Neural Controls Neural controls operate via reflex arcs that involve Baroreceptors Vasomotor centers and vasomotor fibers Vascular smooth muscle

25. Copyright © 2010 Pearson Education, Inc. The Vasomotor Center A cluster of sympathetic neurons in the medulla that oversee changes in blood vessel diameter Part of the cardiovascular center, along with the cardiac centers Maintains vasomotor tone (moderate constriction of arterioles) Receives inputs from baroreceptors, chemoreceptors, and higher brain centers

26. Copyright © 2010 Pearson Education, Inc. Short-Term Mechanisms: Baroreceptor- Initiated Reflexes Baroreceptors are located in Carotid sinuses Aortic arch Walls of large arteries of the neck and thorax

27. Copyright © 2010 Pearson Education, Inc. Short-Term Mechanisms: Baroreceptor- Initiated Reflexes Increased blood pressure stimulates baroreceptors to increase input to the vasomotor center Inhibits the vasomotor center, causing arteriole dilation and venodilation Stimulates the cardioinhibitory center

28. Copyright © 2010 Pearson Education, Inc. Figure 19.9 Baroreceptors in carotid sinuses and aortic arch are stimulated. Baroreceptors in carotid sinuses and aortic arch are inhibited. Impulses from baroreceptors stimulate cardioinhibitory center (and inhibit cardioacceleratory center) and inhibit vasomotor center. Impulses from baroreceptors stimulate cardioacceleratory center (and inhibit cardioinhibitory center) and stimulate vasomotor center. CO and R return blood pressure to homeostatic range. CO and R return blood pressure to homeostatic range. Rate of vasomotor impulses allows vasodilation, causing R Vasomotor fibers stimulate vasoconstriction, causing R Sympathetic impulses to heart cause HR, contractility, and CO. Sympathetic impulses to heart cause HR, contractility, and CO. Stimulus: Blood pressure (arterial blood pressure falls below normal range). Stimulus: Blood pressure (arterial blood pressure rises above normal range). 3 2 1 5 4a 4b Homeostasis: Blood pressure in normal range 4b 3 2 1 5 4a

29. Copyright © 2010 Pearson Education, Inc. Figure 19.9 step 5 Baroreceptors in carotid sinuses and aortic arch are inhibited. Impulses from baroreceptors stimulate cardioacceleratory center (and inhibit cardioinhibitory center) and stimulate vasomotor center. CO and R return blood pressure to homeostatic range. Vasomotor fibers stimulate vasoconstriction, causing R Sympathetic impulses to heart cause HR, contractility, and CO. Stimulus: Blood pressure (arterial blood pressure falls below normal range). 2 3 1 4b 4a 5 Homeostasis: Blood pressure in normal range

30. Copyright © 2010 Pearson Education, Inc. Short-Term Mechanisms: Baroreceptor-Initiated Reflexes Baroreceptors taking part in the carotid sinus reflex protect the blood supply to the brain Baroreceptors taking part in the aortic reflex help maintain adequate blood pressure in the systemic circuit

31. Copyright © 2010 Pearson Education, Inc. Short-Term Mechanisms: Chemoreceptor-Initiated Reflexes Chemoreceptors are located in the Carotid sinus Aortic arch Large arteries of the neck

32. Copyright © 2010 Pearson Education, Inc. Short-Term Mechanisms: Chemoreceptor-Initiated Reflexes Chemoreceptors respond to rise in CO 2, drop in pH or O 2 Increase blood pressure via the vasomotor center and the cardioacceleratory center Are more important in the regulation of respiratory rate (Chapter 22)

33. Copyright © 2010 Pearson Education, Inc. Influence of Higher Brain Centers Reflexes that regulate BP are integrated in the medulla Higher brain centers (cortex and hypothalamus) can modify BP via relays to medullary centers

34. Copyright © 2010 Pearson Education, Inc. Short-Term Mechanisms: Hormonal Controls Adrenal medulla hormones norepinephrine (NE) and epinephrine cause generalized vasoconstriction and increase cardiac output Angiotensin II, generated by kidney release of renin, causes vasoconstriction

35. Copyright © 2010 Pearson Education, Inc. Short-Term Mechanisms: Hormonal Controls Atrial natriuretic peptide causes blood volume and blood pressure to decline, causes generalized vasodilation Antidiuretic hormone (ADH)(vasopressin) causes intense vasoconstriction in cases of extremely low BP

36. Copyright © 2010 Pearson Education, Inc. Long-Term Mechanisms: Renal Regulation Baroreceptors quickly adapt to chronic high or low BP Long-term mechanisms step in to control BP by altering blood volume Kidneys act directly and indirectly to regulate arterial blood pressure 1.Direct renal mechanism 2.Indirect renal (renin-angiotensin) mechanism

37. Copyright © 2010 Pearson Education, Inc. Direct Renal Mechanism Alters blood volume independently of hormones Increased BP or blood volume causes the kidneys to eliminate more urine, thus reducing BP Decreased BP or blood volume causes the kidneys to conserve water, and BP rises

38. Copyright © 2010 Pearson Education, Inc. Indirect Mechanism The renin-angiotensin mechanism  Arterial blood pressure  release of renin Renin  production of angiotensin II Angiotensin II is a potent vasoconstrictor Angiotensin II  aldosterone secretion Aldosterone  renal reabsorption of Na + and  urine formation Angiotensin II stimulates ADH release

39. Copyright © 2010 Pearson Education, Inc. Figure 19.10 Arterial pressure Baroreceptors Indirect renal mechanism (hormonal) Direct renal mechanism Sympathetic stimulation promotes renin release Kidney Renin release catalyzes cascade, resulting in formation of ADH release by posterior pituitary Aldosterone secretion by adrenal cortex Water reabsorption by kidneys Blood volume Filtration Arterial pressure Angiotensin II Vasoconstriction ( diameter of blood vessels) Sodium reabsorption by kidneys Initial stimulus Physiological response Result

40. Copyright © 2010 Pearson Education, Inc. Figure 19.11 Activity of muscular pump and respiratory pump Release of ANP Fluid loss from hemorrhage, excessive sweating Crisis stressors: exercise, trauma, body temperature Bloodborne chemicals: epinephrine, NE, ADH, angiotensin II; ANP release Body size Conservation of Na + and water by kidney Blood volume Blood pressure Blood pH, O 2, CO 2 Dehydration, high hematocrit Blood volume BaroreceptorsChemoreceptors Venous return Activation of vasomotor and cardiac acceleration centers in brain stem Heart rate Stroke volume Diameter of blood vessels Cardiac output Initial stimulus Result Physiological response Mean systemic arterial blood pressure Blood viscosity Peripheral resistance Blood vessel length