Cardiovascular+system+DF+lectures+19-21++w2011+FINAL

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Unformatted text preview: Cardiovascular system: I. The Blood Vessels and Control of Blood Flow Lectures 19-21 Recommended (not required) reading in Sherwood 7th edition : Main topics: Chapter 10: 343-376 (6th ed. pp 337-369) Plus, a brief mention of cardiac blood supply in Chapter 9: 332-333 (6th ed. pp 326-328) And, recall smooth muscle properties Chapter 8: pp 289-294 (6th ed. ) •  Topics to be covered in these lectures: Control of Cardiac Output Recap autonomic control of the heart Effect of venous return volume on heart contraction strength Frank-Starling law of the heart Sympathetic control of heart contraction strength & venous return •  General structure of the cardiovascular system Blood flow to organs at rest and during exercise A special note about the coronary circulation •  How blood flow is regulated (general concepts) •  Structure and function of different components of the vascular tree =>Definition of mean arterial pressure (will return to this as well) –  Arteries –  Arterioles: major resistance vessels Vasodilation versus vasoconstriction Extrinsic versus intrinsic control Important side note: General properties of smooth muscle Nitric oxide as a vasodilating signal –  Capillaries Determinants of bulk flow –  Veins and venous return 1 What determines & adjusts cardiac output? 1)  2)  3)  4)  Autonomic control of heart rate @ SA node Autonomic control of conduc<on velocity @ AV node Effect of venous return volume on heart contrac<on strength Sympathe<c control of heart contrac<on strength & venous return these schema)cally show where different controls are exerted in a 4 ­chambered heart para 1 symp Symp can ↑ & Parasymp can ↓ heart rate volume para 2 Parasymp can ↓ conduc<on @ AV node 3 volume Larger venous return can ↑ ventricular contrac<on 4 symp Symp can ↑ ventricular contrac<on (& also increase venous return) 1 are these entirely separate controls? and are they simply on or off ? answer to both questions: no autonomic control is usually a combination of sympathetic & parasympathetic inputs increase in sympathetic input and decrease in parasympathetic input combine to increase heart rate; opposite for decrease in heart rate this implies parasympathetic input at rest: in fact, this input is relatively strong also, see tonic (continuous) sympathetic control of blood pressure if stop all autonomic input to heart, heart rate rises from 70 beats/min to approx 100 beats/min creates vasomotor tone also, see mutual pre-synaptic inhibition (not shown in this figure) vagus nerve (ACh) can inhibit norE release; sympathetic fiber can inhibit ACh release without this, blood pressure can fall to 40-60 mm Hg. this can occur when spinal anesthesia induces spinal shock by blocking efferent sympathetic fibers 2 What determines & adjusts cardiac output? 1)  2)  3)  4)  Autonomic control of heart rate @ SA node Autonomic control of conduc<on velocity @ AV node Effect of venous return volume on heart contrac<on strength Sympathe<c control of heart contrac<on strength & venous return these schema)cally show where different controls are exerted in a 4 ­chambered heart para 1 3 symp Symp can ↑ & Parasymp can ↓ heart rate para 2 Parasymp can ↓ conduc<on @ AV node volume 3 volume Larger venous return can ↑ ventricular contrac<on 4 symp Symp can ↑ ventricular contrac<on (& also increase venous return) Larger venous return can ↑ ventricular contrac<on.. Frank ­Starling law of the heart 1)  During systole (contrac)on & emptying), the heart normally pumps out what arrived during diastole (relaxa)on & filling) 2)  Increased venous return produces larger end ­diastolic volume ( EDV  ­ ­ amount of blood returning to the heart aBer relaxa)on & filling of ventricles) 3)  This leads to increased stroke volume (volume of blood ejected by a ventricle during each heartbeat) Fig. 9-21, p. 329 3 4 Sympathe<c output can ↑ ventricular contrac<on (& also increase venous return).. Sympathe<c input leS ­shiSs the Frank ­Starling curve Fig. 9-23, p. 330 4 Sympathe<c output can ↑ ventricular contrac<on (& also increase venous return).. Sympathe<c input to veins increases blood flow (in veins) & thus increases end ­diastolic volume that way as well Note : sympathe<c effects on blood vessels will be explained in more detail later Fig. 9-20, p. 328 4 4 Sympathe<c output can ↑ ventricular contrac<on (& also increase venous return).. (c) Sympathe<c s<m: heart and veins (b) Sympathe<c s<m: heart (a) Normal Fig. 9-22, p. 329 To summarize: autonomic effects on cardiac output (CO)… CO=HR x SV (HR) (CO) (SV) Fig. 9-24, p. 330 5 The Cardiovascular System Heart •  Serves as pump that establishes the pressure gradient needed for blood to flow to tissues Blood vessels •  Passageways through which blood is distributed from heart to all parts of body and back to heart •  Coronary circulation (heart), Pulmonary circulation (lungs), Systemic circulation (the rest) Blood •  Transport medium within which materials being transported are dissolved or suspended Airway RIGHT SIDE Lungs LEFT SIDE Air sac Pulmonary capillaries Arterioles Venules Pulmonary circulation Pulmonary artery Pulmonary veins Aorta (major systemic artery) Systemic veins Systemic circulation Systemic capillaries Venules Tissues Arterioles Smaller arteries branching off to supply various tissues Fig. 10-4, p. 347 6 A note on nourishing the heart muscle •  Muscle is supplied with oxygen and nutrients by blood delivered to it by coronary circulation (not from inside) •  Heart receives most of its own blood supply during diastole –  During systole, coronary vessels are compressed by contracting heart muscle •  Coronary blood flow normally varies to keep pace with cardiac oxygen needs So, where does the blood go?? Distribution of Cardiac Output at Rest: Blood Flow-general considerations •  Blood is constantly reconditioned so composition remains relatively constant •  Reconditioning organs receive more blood than needed for metabolic needs –  Digestive organs, kidneys, skin –  Adjust extra blood to achieve homeostasis •  Blood flow to other organs can be adjusted according to metabolic needs •  Brain can least tolerate disrupted supply Fig. 10-1, p. 344 7 Magnitude and Distribution of Cardiac Output at Rest versus During Moderate Exercise Fig. 10-12, p. 355 Blood Flow •  Flow rate through a vessel (volume of blood passing through per unit of time) F = ΔP R Recall: V V=IR (Ohm s law) I = R F = flow rate of blood through a vessel ΔP = pressure gradient R = resistance of blood vessels 8 Blood Flow (cont.) Resistance (R) is measure of opposition of blood flow through a vessel –  Depends on: blood viscosity (η), vessel length (L), vessel radius (r) From Poiseuille s Law R= (pwä-zwēz' ) 8 ηL πr4 F= πΔPr4 8 ηL –  So, a major determinant of resistance to flow is vessel’s radius R is proportional to 1 r4 Slight change in radius produces significant change in blood flow To understand this just imagine drinking liquid from a straw. Vary radius, viscosity (water vs. syrup), length… Relationship of Resistance and Flow to Vessel Radius Fig. 10-2, p. 345 9 Fig. 10-3, p. 345 Vascular Tree •  Closed system of vessels (in vertebrates like us) Aorta r=cm arteries mm arterioles 0.1mm capillaries 0.01mm venules 0.1mm veins mm Vena cava cm LUNGS 25 mm Hg 8-10 mm Hg Blood pressure 0-3 mm Hg 93 mm Hg Artery and Vein. A distributing artery (right) and a medium-sized vein (left) surrounded by connective tissue. SEM X305. 10 Mean Arterial Pressure (MAP) •  Average pressure driving blood forward into tissues throughout cardiac cycle MAP= Cardiac output (CO) X Total peripheral resistance (TPR) Recall factors that control CO (Heart rate and stroke volume) Where is site of highest resistance? Arteries? Arterioles? Capillaries? A clue: Where is biggest pressure drop? WHY? Huge excess of capillaries vs. arterioles Sum all capillaries together- largest cross-sectional area of all blood vessels Fig. 10-9, p. 352 Arterioles! Figure 10-11 pp.354 11 Since: F = ΔP R Important for gas, nutrient, waste exchange Fig. 10-16, p. 362 Arteries Specialized to –  Serve as rapid-transit passageways for blood from heart to organs (large radius, low resistance) –  Act as pressure reservoir to provide driving force for blood when heart is relaxing •  Arterial connective tissue contains –  Collagen fibers: Provide tensile strength –  Elastin fibers: Provide elasticity to arterial walls Fig. 10-6, p. 349 12 Arterioles -major controllers of Mean Arterial Pressure (MAP) •  Major resistance vessels •  Have tonic vascular tone but… •  Radius supplying individual organs can be adjusted independently to –  Distribute cardiac output among systemic organs, depending on body’s momentary needs –  Help regulate arterial blood pressure Red and white blood cells within an arteriole. SEM X6130. Mechanisms involved in adjusting arteriolar resistance Normal arteriolar tone 1.  Vasoconstriction: narrowing of a vessel Endothelium Major extrinsic (control from outside of vessels) regulator- Vasoconstriction • Increased sympathetic activity (general) (increased contraction of circular smooth muscle in the arteriolar wall) Other extrinsic hormonal influences including: • Epinephrine/norepinephrine (acting via α1 adrenergic receptors (not in brain)) Smooth muscle Lumen Connective tissue • Vasopressin (from pituitary) Resistance • Angiotensin II (precursor from liver-processed in bloodstream) Flow rate Fig. 10-10, p. 353 13 Mechanisms involved in adjusting arteriolar resistance 2. Vasodilation: enlargement in circumference and radius of vessel Normal arteriolar tone Endothelium Major extrinsic regulator• Decreased sympathetic activity Vasodilation (general) (decreased contraction Note: arterioles do not have parasympathetic innervation (except for sex organs) Smooth muscle Lumen of circular smooth muscle in the arteriolar wall) Connective tissue Other extrinsic hormonal influences including: • Epinephrine via β2 adrenergic receptors (heart and skeletal muscle arterioles only) Resistance Flow rate • Atrial natriuretic peptide (secreted by the heart) Fig. 10-10, p. 353 There are also important local (intrinsic: controling signals near or in vessels) influences on arteriolar radius (might override sympathetic activity level) Vasoconstriction caused by Chemical Physical • Increased O2 • Decreased CO2 and other metabolites • Cold • Endothelin (local acting hormone) Autoregulation Vasodilation caused by Chemical Physical • Heat • Decreased O2 • Increased CO2 and other metabolites • Histamine (injury, allergic response) • Nitric oxide (more on this later) Some tissues are able to keep arteriolar pressure relatively constant in the face of wide deviations in MAP (using some of the above mechanisms) Brain and kidney arterioles are very good at this but skeletal muscle arterioles aren t Fig. 10-13, p. 357 14 To understand changes in blood vessel diameter, we need to know a bit more about smooth muscle in general (recall Dr. Ishida s comparison slides) Fig. 8-29, p. 293 (Compare to striated muscle!!) Fig. 8-30, p. 294 Among best studied local vasoactive mediators is nitric oxide (NO) A gas (!) as a signaling molecule Protein kinase G targets: Multiple regulators 1)Phosphatase (an enzyme) that removes phosphate from smooth muscle myosin (can t form cross-bridges) 2) Smooth muscle calcium channels- causes them to close, decreasing contraction 15 Capillaries (Microcirculation) -Thin-walled, small-radius, extensively branched, no smooth muscle -Sites of exchange between blood and interstitial fluid: No specialized transporters (except in brain) Two types of passive exchanges Fig. 10-15, p. 361 1. Diffusion: Passive movement of solute down a concentration gradient Rate determined by: a. Maximized surface area and minimized diffusion distance b. Concentration difference determined in part by metabolic activity of cells c. Permeability of endothelial cells is restricted (O2, CO2, Urea…) d. Velocity of blood flow through capillaries is relatively slow (Provides adequate exchange time) Diffusion is most important means of nutrient and gas exchange Capillaries 2. Bulk flow: Mass movement of solute and water together through pores Fig. 10-18, p. 363 In this case, concentration differences don t directly dictate flux- balance of hydrostatic and oncotic (osmotic) pressures do Bulk flow is most important in the regulation of distribution of extracellular fluid (ECF) between blood plasma and interstitial fluid! 16 What determines the direction of bulk flow? Capillary hydrostatic pressure (Pc) Plasma oncotic (osmotic) pressure (πp) outward inward Varies 25 mm Hg (fairly stable) Interstitial hydrostatic pressure: (PIF) inward ~1 mm Hg Interstitial oncotic pressue (πIF) outward 0 mm Hg (normally) Net filtration pressure= (Pc + πIF) – (πp + PIF) Pc=37 Pc=17 Arterial end +11 mm Hg Venous end { } -9 mm Hg Fig. 10-23, p. 368 Bulk flow forces normally slightly favor ultrafiltration over reabsorption, so could lose 3 liters of fluid per day this way…What happens to it???? ? Lymphatic System •  Functions –  Return of excess filtered fluid (lymph) to heart via thoracic duct –  Defense against disease •  Lymph nodes have phagocytes –  Transport of absorbed fat from intestine –  Return of filtered protein Fig. 10-25, p. 370 17 Edema •  Swelling of tissues- too much interstitial fluid accumulates •  Causes of edema π –  Reduced concentration of plasma proteins (decreased p ) kidney, liver disease –  Increased permeability of capillary wall (inflammation) –  Increased venous pressure (increased Pc)-heart failure –  Blockage of lymph vessels (elephantiasis) medicine.ucsd.edu/clinicalmed Veins •  transport blood back to heart •  capillaries drain into venules then on to veins – Large radius offers little resistance to blood flow – Also serve as blood reservoir ( capacitance system ) Fig. 10-27, p. 371 18 Veins Valves assist blood flow back to heart Remember: blood flow back to the heart- i.e. venous returndetermines filling of heart and thus End Diastolic Volume or EDV affects stroke volume affects cardiac output Fig. 10-32, p. 375 Factors that Influence Venous Return Fig. 10-28, p. 372 19 ...
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This note was uploaded on 07/09/2011 for the course NPB 101 taught by Professor Fuller,charles/goldberg,jack during the Winter '08 term at UC Davis.

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