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- 2. Outlines to becovered in this module Blood flow Peripheral circulation Arterial system o Arterial blood pressure o Arterioles & its control mechanism Microcirculation o Capillaries Venous system Regulation of flow through blood vessels Hypertension Circulatory shock. Cardiovascular Physiology 2 CVS 4/25/2024
- 3. Biophysics of bloodflow (Hemodynamic) - Hemodynamic: Relationship between blood flow, pressure and resistance - Blood flow (Q) through a vessel depends on the pressure gradient and vascular resistance. - The flow rate of blood (Q) is directly proportional to the pressure gradient and inversely proportional to vascular resistance Q = P (Ohm’a law) R where Q = flow rate of blood through a vessel ΔP = pressure gradient R = resistance of blood vessel Cardiovascular Physiology 3 CVS 4/25/2024
- 4. Pressure Gradient- - Thepressure gradient is the difference in pressure between the beginning and the end of a vessel. - Blood flows from an area of higher pressure to an area of lower pressure down a pressure gradient. - Contraction of the heart imparts pressure to the blood, which is the main driving force for flow through a vessel. - Because of frictional losses (resistance), the pressure drops as blood flows throughout the vessel’s length. - Note that the difference in pressure between the two ends of a vessel, not the absolute pressures within the vessel, determines flow rate Cardiovascular Physiology 4 CVS 4/25/2024
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- 7. Resistance to flow(R) - Is a measure of the hindrance or opposition to blood flow through the vessel R= measure of friction between Blood vessel & moving fluid. Fluid molecules within themselves. - As resistance to flow increases, it is more difficult for blood to pass through the vessel, so flow rate decreases - Viscosity - This is friction of molecules in the moving stream of fluid Cardiovascular Physiology 7 CVS 4/25/2024
- 8. Vascular resistanceto BF is - directly proportional to viscosity of the blood(η) - directly proportional to vessel length (L) - inversely proportional to the 4th power of radius of the vessel(r4 ) R = 8.η. L π r4 - The lengths of the tubes/blood vessels/ are approximately the same, and the viscosity of the fluid is constant - Therefore, differences in resistance offered by the tubes are due solely to differences in their radii. - Obviously, the widest tubes have the greatest flows. Cardiovascular Physiology 8 CVS 4/25/2024
- 9. Cardiovascular Physiology 9 CVS As theradius of a tube decreases, the resistance to flow increases 4/25/2024
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- 11. Types of bloodflow 1.Laminar flow Normal and noiseless. All elements of the fluid move in a stream line, that are parallel to the axis of the tube. No fluid move in radial or circumferential direction. Layer of fluid in contact with the wall is motionless (thin layer, adherent to wall, hence motionless). Fluid that move along the axis of the tube has max.Velocity. Cardiovascular Physiology 11 CVS 4/25/2024
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- 13. 2.Turbulent blood flow Variouselements of fluid move irregularly in axial radial and circumferential direction More pressure required to drive blood than laminar (Energy wasted in propelling blood radially & axially) Often accompanied by noise (murmurs) because of more driving pressure. Occur at valves and aorta (normal) & at site of blood clot (pathological) Cardiovascular Physiology 13 CVS 4/25/2024
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- 16. Components of thevascular tree - The vascular tree consists of arteries, arterioles, capillaries, venules, and veins. - Arteries- carry blood from the heart to the organs - When a small artery reaches the organ it is supplying, it branches into numerous arterioles. - Arterioles branch further within the organs into capillaries - Capillaries rejoin to form small venules, which further merge to form small veins that leave the organs. - The small veins progressively unite to form larger veins that eventually empty into the heart. Cardiovascular Physiology 16 CVS 4/25/2024
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- 18. The Vessel Wall Thewalls of the arteries and veins have three layers called tunics: 1. Tunica interna (intima) - Inner lining in direct contact with blood - Endothelium continuous with endocardial lining of heart - Active role in vessel-related activities such as secretion of vasoconstrictors and vasodilators . 2. Tunica media - the middle layer, is usually the thickest. - the thickness varies among vessel types - It consists of smooth muscle, collagen, and sometimes elastic tissue. - The smooth muscle regulates diameter of the lumen 3. Tunica externa - is the outermost layer. - Helps anchor vessel to surrounding tissue Cardiovascular Physiology 18 CVS 4/25/2024
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- 20. The Vessel Wall CardiovascularPhysiology 20 CVS Endothelium Elastin fibers Smooth muscle Elastin fibers Connective Tissue coat Endothelium Smooth muscle; elastin fibers Large artery Arteriole Capillary Large vein Connective tissue coat 4/25/2024
- 21. Arterial system: 1. Arteries -Vessels that transport blood away from the heart - Structurally it consists of Larger arteries, Elastic (conducting) arteries Medium arteries, Muscular (distributing) arteries Arterioles, tiny arteries Metarteriole Cardiovascular Physiology 21 CVS 4/25/2024
- 22. 1. Conducting (elastic)arteries - Found in largest arteries, aorta, pulmonary arteries, and common carotid arteries. - Their tunica media consists of numerous sheets of elastic tissue, this makes the arteries to have elastic properties - Functions. - To conduct blood to medium-sized arteries - To act as a pressure reservoir to provide the driving force for blood when the heart is relaxing. Cardiovascular Physiology 22 CVS 4/25/2024
- 23. Wall of Conducting(elastic) arteries Cardiovascular Physiology 23 CVS Endothelium Elastin fibers Smooth muscle Elastin fibers Connective Tissue coat 4/25/2024
- 24. Function as pressurereservoir - As the heart pumps blood into the arteries during ventricular systole, a greater volume of blood enters the arteries - The highly elastic arteries expand to temporarily hold this excess volume of ejected blood - When the heart relaxes and temporarily stops pumping blood into the arteries, the stretched arterial walls passively recoil. - This recoil exerts pressure on the blood in the arteries during diastole. - The pressure pushes the excess blood contained in the arteries into the vessels downstream. - This ensuring continued blood flow to the organs when the heart is relaxing and not pumping blood into the system Cardiovascular Physiology 24 CVS 4/25/2024
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- 27. 2. Muscular arteries/distributing arteries - Tunica media contains more smooth muscle and fewer elastic fibers than elastic arteries - Walls relatively thick - Capable of great vasoconstriction/ vasodilatation to adjust rate of blood flow - The brachial, femoral, and splenic arteries are examples of distributing arteries. Cardiovascular Physiology 27 CVS 4/25/2024
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- 29. 3. Arterioles - Eachnutrient artery entering an organ branches six to eight times to be called arterioles. - The arterioles themselves branch two to five times to be capillaries. - Internal diameters of arterioles is only 10 to 15 micrometers. - Capillaries are originate from the terminal arterioles called metarterioles - The metarterioles do not have a continuous muscular coat, but smooth muscle fibers encircle the vessel at intermittent points. - The junction of metarterioles and capillaries is encircled by smooth muscle fiber called precapillary sphincter. - This sphincter can open and close the entrance to the capillary. Cardiovascular Physiology 29 CVS 4/25/2024
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- 31. Arterioles are majorresistance vessels and their diameters can change many fold. 1. Increased degree of resistance help to regulate arterial blood pressure - Arterioles converts the pulsatile systolic-to-diastolic pressure swings in the arteries into the non-fluctuating pressure present in the capillaries by - Dropping mean arterial pressure from 93 mm Hg to capillary pressure of 35 mm Hg. 2. To distribute cardiac output among systemic organs, depending on body’s momentary needs Cardiovascular Physiology 31 CVS 4/25/2024
- 32. Mechanisms involved inadjusting arteriolar resistance - The MAP is identical throughout the body - Differences in flows between organs depend entirely on the relative resistances offered by the arterioles of each organ. - Arterioles contain smooth muscle, which can contract and decrease the vessel radius (vasoconstriction) or relax and cause the vessel radius to increase (vasodilation) - Thus the pattern of blood-flow distribution depends upon the degree of arteriolar smooth-muscle contraction within each organ and tissue. Cardiovascular Physiology 32 CVS 4/25/2024
- 33. How can thearterioles resistance be changed? Arteriolar smooth muscle Possesses a large degree of spontaneous activity Can contract independent of any neural, hormonal, or paracrine input). This spontaneous contractile activity is called intrinsic tone. The intrinsic tone/ level of contraction can be increased or decreased by external signals, such as neurotransmitters. An increase in contractile force above the vessel’s intrinsic tone causes vasoconstriction, whereas a decrease in contractile force causes vasodilation. Cardiovascular Physiology 33 CVS 4/25/2024
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- 35. -The mechanisms controllingvasoconstriction and vasodilation in arterioles fall into two general categories: (1) local controls (2) extrinsic controls. Cardiovascular Physiology 35 CVS 4/25/2024
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- 37. Local Controls - Theterm local controls denotes mechanisms independent of nerves or hormones by which organs and tissues alter their own arteriolar resistances, thereby self-regulating their blood flows. - It does include changes caused by autocrine/paracrine agents. - This self-regulation includes the phenomena of - active hyperemia - reactive hyperemia - flow autoregulation, and - local response to injury. Cardiovascular Physiology 37 CVS 4/25/2024
- 38. Active Hyperemia - Mostorgans and tissues manifest an increased blood flow (hyperemia) when their metabolic activity is increased this is termed active hyperemia. - For example, the blood flow to exercising skeletal muscle increases in direct proportion to the increased activity of the muscle. - Active hyperemia is the direct result of arteriolar dilation in the more active organ or tissue. - Local chemical changes in the extracellular fluid surrounding the arterioles causes arteriolar smooth muscle dilation - Some of these local chemical changes that occur in the extracellular fluid are PO2, PCO2, H+ , bradykinine & other Cardiovascular Physiology 38 CVS 4/25/2024
- 39. Reactive Hyperemia - Whenblood flow to a tissue is blocked for few seconds and then is unblocked, the flow through tissue increases almost 4-7 times normal. - During the period of no blood flow, the arterioles in the affected organ or tissue dilate, owing to the local factors described above. - The excess blood flow lasts long enough to repay the tissue oxygen deficit that has occurred during occlusion. Cardiovascular Physiology 39 CVS 4/25/2024
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- 42. Flow Autoregulation - Autoregulation– maintenance of constant blood flow to an organ in spite of fluctuations in blood pressure. - For example, when arterial pressure in an organ is reduced, local controls cause - arteriolar vasodilation, which tends to maintain flow relatively constant. - The opposite events occur when, for various reasons, arterial pressure increases Cardiovascular Physiology 42 CVS 4/25/2024
- 43. 43 Arterial pressure in organ Blood flow to organ PO2 , metabolites, vessel-wall stretch in organ Arteriolar dilation in organ Restoration of blood flow toward normal in organ Flow Autoregulation 4/25/2024
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- 45. Two basic mechanismsthat explain local control of blood flow 1. Myogenic theory Increase in blood flow Stretches the vessel Contraction of vascular smooth muscle Decrease blood flow back to normal Cardiovascular Physiology 45 CVS 4/25/2024
- 46. 2. Metabolic theory Increasein rate of metabolism Accumulation of vasodilator substances in active tissues Blood vessels dilate Increase blood flow Vasodilator metabolites O2 tension, H, CO2 tension, Temperature, K+, lactate, Adenosine, Histamine. Cardiovascular Physiology 46 CVS 4/25/2024
- 47. Response to Injury -Tissue injury causes a variety of substances to be released locally from cells or generated from plasma precursors. - These substances make arteriolar smooth muscle relax and cause vasodilation in an injured area. - This phenomenon, a part of the general process known as inflammation Cardiovascular Physiology 47 CVS 4/25/2024
- 48. Extrinsic Controls Sympathetic Nerves -Most arterioles receive a rich supply of sympathetic postganglionic nerve fibers. - These neurons release mainly norepinephrine, which binds to alpha- adrenergic receptors on the vascular smooth muscle to cause vasoconstriction. - Increase sympathetic stimulation causes arteriolar vasoconstriction. - Decrease sympathetic stimulation causes arteriolar vasodilation. Parasympathetic Nerves - There is no parasympathetic innervations to arterioles. Cardiovascular Physiology 48 CVS 4/25/2024
- 49. Cardiovascular Physiology 49 CVS -No parasympatheticinnervations to arterioles. 4/25/2024
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- 51. Hormones Epinephrine - Bind toalphaadrenergic receptors on arteriolar smooth muscle and cause vasoconstriction. - The arterioles in skeletal muscle have a large number of beta adrenergic receptors, circulating epinephrine usually causes vasodilation. Angiotensin II- constricts most arterioles. Vasopressin - released from the posterior pituitary gland causes arteriolar constriction Atrial natriuretic factor-is the hormone secreted by the cardiac atria is a potent vasodilator. Cardiovascular Physiology 51 CVS 4/25/2024
- 52. Cardiovascular Physiology 52 CVS Angiotensin II-Vasoconstrictor Vasopressin –Vasoconstrictor Atrial natriuretic factor– Vasodilator 4/25/2024
- 53. 4. Microcirculatory unit The arterioles, capillaries, and venules are collectively referred to as the microcirculation, because they are only visible through a microscope. - The microcirculatory vessels are all located within the organs. The microcirculation refers to the smallest blood vessels in the body: - the smallest arterioles - the metarterioles - the precapillary sphincters - the capillaries - the small venules Cardiovascular Physiology 53 CVS 4/25/2024
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- 55. Capillary Beds - Amicrocirculation moving from arterioles to venules - Consist of two types of vessels: Vascular shunts – metarteriole–thoroughfare channel connecting an arteriole directly with a postcapillary venule True capillaries – the actual exchange vessels Cardiovascular Physiology 55 CVS 4/25/2024
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- 58. True Capillaries - Thecapillary wall is thin & consists of a single layer of endothelial cells surrounded by a very thin basement membrane. - The total thickness of the capillary wall is only about 0.5 micrometer. - The internal diameter of the capillary is 4 to 9 micrometers. - Lumen narrow, thus RBC change shape to pass through - The peripheral circulation of the whole body has about 10 billion capillaries with a total surface area estimated to be 500 to 700 square meters - Velocity of blood flow=1mm/s - Therefore ideal for exchange (nutritional flow) Cardiovascular Physiology 58 CVS 4/25/2024
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- 60. Types of Capillaries Accordingto the size of the pores capillaries are classified into three: - Continuous capillaries - Fenestrated capillaries - Sinusoids capillaries Cardiovascular Physiology 60 CVS 4/25/2024
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- 62. Continuous Capillaries - Continuouscapillaries are abundant in the skin and muscles - Endothelial cells provide an uninterrupted lining - Adjacent cells are connected with tight junctions - Intercellular clefts about 4 nm wide between them ,allow the passage of fluids & small solutes, such as glucose. - But plasma proteins, other large molecules, and formed elements are held back. - Brain capillaries do not have clefts (blood-brain barrier). Cardiovascular Physiology 62 CVS 4/25/2024
- 63. Fenestrated Capillaries - Foundwherever active capillary absorption or filtrate formation occurs (e.g., glomerular capillaries of kidney, pancreas and salivary glands and small intestines) Characterized by: - Fenestrations are about 20 to 100 nm in diameter - They allow for the rapid passage of small molecules - Fenestrate keep plasma proteins back - Greater permeability than continuous capillaries Cardiovascular Physiology 63 CVS 4/25/2024
- 64. Sinusoids Capillaries - Theclefts between the capillary endothelial cells are wide open - Found in the liver, bone marrow and spleen - Allow large molecules (proteins and blood cells) to pass between the blood and surrounding tissues Cardiovascular Physiology 64 CVS 4/25/2024
- 65. Capillary Exchange - Capillaryexchange refers to the two-way movement of fluid between the blood and surrounding tissues. - Substances pass between the blood and tissue fluid by diffusion, transcytosis, filtration, and reabsorption Movement across capillary influenced by: - Nature of substance (size, shape, lipid solubility) - Balance between hydrostatic and colloid osmotic pressure force across membrane (Starling’s law) - Capillary surface area available for exchange - Physical characteristics of capillary membrane (continuous, fenestrated, discontinuous) Cardiovascular Physiology 65 CVS 4/25/2024
- 66. Diffusion - The mostimportant mechanism of exchange is diffusion. - Glucose and oxygen, being more concentrated in the systemic blood than in the tissue fluid, diffuse out of the blood. - Carbon dioxide and other wastes, being more concentrated in the tissue fluid, diffuse into the blood. - Lipid-soluble substances as steroid hormones, O2, CO2 diffuse easily through the plasma membranes. - Substances insoluble in lipids, such as glucose and electrolytes, must pass through membrane channels. Cardiovascular Physiology 66 CVS 4/25/2024
- 67. Transcytosis - Transcytosis isa process in which endothelial cells pick up droplets of fluid on one side of the plasma membrane by pinocytosis, transport the vesicles across the cell, and discharge the fluid on the other side by exocytosis. - Fatty acids, albumin, and some hormones such as insulin move across the endothelium by this mechanism. Cardiovascular Physiology 67 CVS 4/25/2024
- 68. Permeability of Capillaries CardiovascularPhysiology 68 CVS 4/25/2024
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- 71. Filtration and Reabsorption -Fluid filters out of the arterial end of a capillary and osmotically reenters it at the venous end. - The rate of filtration and reabsorption at any point along the capillary depends on a balance of forces. - The rate of filtration and reabsorption at any point along the capillary depends on a balance of forces – STARLINGS FORCES. - These forces are hydrostatic and osmotic pressure on each side of membrane Cardiovascular Physiology 71 CVS 4/25/2024
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- 73. 1. Capillary bloodpressure (PC) - Is the hydrostatic pressure exerted on the inside of the capillary walls by blood. - This pressure tends to force fluid out of the capillaries into the interstitial fluid. - On average, the hydrostatic pressure is 35 mm Hg at the arteriolar end and 16 mm Hg at the capillary’s venular end. Cardiovascular Physiology 73 CVS 4/25/2024
- 74. 2. Plasma-colloid osmoticpressure (𝛑P) - Is a force caused by colloidal dispersion of plasma proteins. - Plasma has a higher protein concentration and a lower water concentration than interstitial fluid does. - It encourages fluid movement into the capillaries - Plasma-colloid osmotic pressure averages 26 mm Hg. 3. Interstitial fluid hydrostatic pressure (PIF) - Is the fluid pressure exerted on the outside of the capillary wall by interstitial fluid. - This pressure tends to force fluid into the capillaries. - The value of this pressure varies among tissues, (1 mm Hg ) Cardiovascular Physiology 74 CVS 4/25/2024
- 75. 4. Interstitial fluid–colloidosmotic pressure (𝛑IF) - It is a pressure exerted by the small fraction of plasma proteins that leak across the capillary walls into the interstitial spaces - The leaked proteins exert an osmotic effect that tends to promote movement of fluid out of the capillaries into the interstitial fluid. - The interstitial fluid–colloid osmotic pressure is essentially zero mm Hg Cardiovascular Physiology 75 CVS 4/25/2024
- 76. Net filtration pressurein Arterial end (NFP) Ultrafiltration pressure= Outward pressure - Inward pressure NFP = (Pc + π IF ) – (πp + IF) =(35 mm Hg +1) – (26 mm Hg + 0 mm Hg ) = 10 mm Hg - This 10 mm Hg cause filtration to occur. Cardiovascular Physiology 76 CVS 4/25/2024
- 77. Net reabsorption pressurein Venous end Ultrafiltration pressure= Outward pressure - Inward pressure NFP = (Pc + π IF ) – (πp + PIF) = (16 mm Hg +1) – (26 mm Hg + 0 mm Hg ) = - 9 mm Hg Net inward pressure of 9 mm Hg = Reabsorption pressure - Reabsorption of fluid takes place as this inward pressure gradient forces fluid back into the capillary at its venular end. Cardiovascular Physiology 77 CVS 4/25/2024
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- 79. Cardiovascular Physiology 79 CVS 4. Venouspart of the systemic circulation 4/25/2024
- 80. Venous part ofthe systemic circulation Structure of veins : Thin walled Small amount of elastic tissues and smooth muscle Veins of dependent parts of body have valves Valves prevent backflow of venous blood Function of veins: Store large quantity(>60%) of blood (making blood available when required) Propel blood forward by means of “venous pump” Regulate cardiac output Cardiovascular Physiology 80 CVS 4/25/2024
- 81. Venous Return. Def:- Volumeof blood returning from systemic circulation to heart. Any factor/condition increases venous return increases End diastolic volume. Cardiovascular Physiology 81 CVS 4/25/2024
- 82. Factors regulating venousreturn 1. Pressure gradient - Pressure generated by the heart is the most important force in venous flow. - Pressure in the venules ranges from 12 to 18 mmHg, and pressure at the point where the venae cavae enter the heart, called central venous pressure, averages 4.6 mmHg. - Thus, there is a venous pressure gradient (P) of about 7 to 13 mmHg favoring the flow of blood toward the heart - Increased pressure gradient causes increased venous return Cardiovascular Physiology 82 CVS 4/25/2024
- 83. 2. Effect ofgravity on Venous Return Veins When a person is in upright position - 500-700ml blood rapidly dislocated from thorax to lower extremities - hydrostatic pressure superimposed on pressure generated by heart -This adds hydrostatic pressure of 90mmHg This increased hydrostatic pressure below the heart causes 1. Increase the distensiblity of veins, so that their capacity is increased which in turn decreases venous return. 2. Marked increase in capillary blood pressure causes excessive fluid to filter out of capillary beds in the lower extremities, producing localized edema decreases venous return NB:- Vessels above heart has negative hydrostatic pressure Cardiovascular Physiology 83 CVS 4/25/2024
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- 85. Countering the Effectsof Gravity on the Venous System The gravitational effects can be counteract by A. Sympathetically induced venous vasoconstriction - the resultant fall in mean arterial pressure that occurs when a person moves from a lying-down to an upright position triggers sympathetically induced venous vasoconstriction, and promotes the return of blood to the heart B. The skeletal muscle pump Cardiovascular Physiology 85 CVS 4/25/2024
- 86. 3. Effect ofSkeletal Muscle Activity on Venous Return - Many large veins in the extremities lie between skeletal muscles. - Muscle contraction compresses the veins. - This external venous compression decreases venous capacity and increases venous pressure. - Increased muscular activity pushes more blood out of the veins and into the heart. - This pumping action, known as the skeletal muscle pump Cardiovascular Physiology 86 CVS 4/25/2024
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- 88. 4. Effect ofRespiratory Activity on Venous Return The respiratory pump. - The respiratory pump moves blood up toward the heart as pressure changes in the ventral body cavity during breathing. - As we inhale, abdominal pressure increases, squeezing local veins and forcing blood toward the heart. - At the same time, the pressure in the chest decreases, allowing thoracic veins to expand and speeding blood entry into the right atrium. - A decreased in intr-thoracic pressure lower right atrial pressure and thus facilitating venous return. Cardiovascular Physiology 88 CVS 4/25/2024
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- 91. Blood pressure (BP) Def/n:~ Pressure exerted by circulating blood upon the walls of blood vessels. During each beat: BP varies between maximum (systole) & minimum (diastole)….120/80mmHg Average blood pressure (mmHg) increases with age. 95/65 → for 1 year 100/65 → for 6-9 years 110/65-140/90 → for Adults BP is measured in millimeters of mercury (mmHg). Cardiovascular Physiology 91 CVS 4/25/2024
- 92. Average blood pressure(mmHg) increases with age. Cardiovascular Physiology 92 CVS 4/25/2024
- 93. Arterial pressure indices ■Systolic blood pressure (SBP) - is the highest arterial pressure during a cardiac cycle. - is measured after the heart contracts (systole) and blood is ejected into the arterial system. - averages 120 mm Hg ■ Diastolic blood pressure (DBP) - is the lowest arterial pressure during a cardiac cycle. - is measured when the heart is relaxed (diastole) - averages 80 mm Hg. ■ Pulse pressure (PP) - Is the difference between systolic and diastolic blood pressure. - Pulse pressure is palpated in the peripheral arteries. - It is detected during systole not in diastole. - When blood pressure is 120/80, pulse pressure is 40 mm Hg (120 minus 80 mm Hg) PP=SBP-DBP Cardiovascular Physiology 93 CVS 4/25/2024
- 94. ■ Mean arterialpressure (MAP) - Is the average pressure driving blood forward into the tissues throughout the cardiac cycle. - The value of arterial pressure remains closer to diastolic than to systolic pressure for a longer portion of each cardiac cycle. - At resting heart rate, about two thirds of the cardiac cycle is spent in diastole and only one third in systole. MAP= DBP +1/3 PP MAP = 80 + (1/3) 40 = 93 mm Hg MAP = Mean arterial blood pressure DBP = Diastolic blood pressure PP = Pulse pressure Cardiovascular Physiology 94 CVS 4/25/2024
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- 97. Blood Pressure Measurement -Bloodpressure can be measured 1. Directly by connecting a pressure-measuring device to a needle inserted in an artery. 2. Indirectly by means of a sphygmomanometer, an externally applied inflatable cuff attached to a pressure gauge. - During the determination of blood pressure, a stethoscope is placed over the brachial artery at the inside bend of the elbow just below the cuff. - No sound can be detected either when blood is not flowing through the vessel or when blood is flowing in the normal, smooth laminar flow - Turbulent blood flow, in contrast, creates vibrations that can be heard. Cardiovascular Physiology 97 CVS 4/25/2024
- 98. Cardiovascular Physiology 98 CVS Measurement ofarterial blood pressure 4/25/2024
- 99. Cardiovascular Physiology 99 CVS When cuffpressure is greater than 120 mm Hg - The brachial artery is occluded - No blood flows through the vessel. - No sound is heard because no blood is flowing. When cuff pressure is between 120 and 80 mm Hg: - Blood flow through the vessel is turbulent -The first sound (Korotkoff sounds) is heard at peak systolic pressure. -Intermittent sounds are produced by turbulent spurts of flow as blood pressure cyclically exceeds cuff pressure. When cuff pressure is less than 80 mm Hg - No sound is heard throughout the cardiac cycle: - Blood flows through the vessel in smooth, laminar fashion. - The last sound is heard at minimum diastolic pressure. - Thereafter because of uninterrupted, smooth, laminar flow. 4/25/2024
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- 104. Mean arterial pressure(MAP) REGULATION - Mean arterial pressure is the main driving force for propelling blood to the tissues. - Cardiovascular system is designed to monitor the MAP closely and held at approximately 93 mm Hg. - Blood pressure is regulated by controlling cardiac output and total peripheral resistance. - Determined by CO and Total Peripheral vascular resistance (TPVR) Cardiovascular Physiology 104 CVS MAP= CO .TPVR 4/25/2024
- 105. Classification of regulatoryprocess of MAP Regulatory processes classified into 3 groups according to time of action 1. Short term control mechanisms 2. Intermediate-term control mechanisms 3. Long-term control mechanisms Cardiovascular Physiology 105 CVS 4/25/2024
- 106. Regulation of BP CardiovascularPhysiology 106 CVS 4/25/2024
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- 108. A. Short-term controlmechanisms Predominantly vasomotor adjustment and neuronal control Include: Baroreceptor (Stretch) reflexes: Chemoreceptor reflexes Ischemic reflexes of CNS Common characteristics: Rapid onset of action (within few sec.) Response vigorous, but if activated continuously, within a few days, it either dies out completely- (baroreceptors) or attenuated -(chemoreceptors, CNS Ischemic response) Cardiovascular Physiology 108 CVS 4/25/2024
- 109. 1. Baroreceptor reflexes Baroreceptorsconvey information about: mean arterial pressure (MAP) Amplitude of pressure fluctuation Steepness of pressure rise rate of pressure change More sensitive to than pressure (P/t) More sensitive to sudden change More sensitive to decrease than increase pressure Stimulation of baroreceptors: stretch Cardiovascular Physiology 109 CVS 4/25/2024
- 110. The baroreceptor reflexincludes:- 1. A receptor - found in carotid sinus and aortic arch baroreceptors - sensitive to changes in mean arterial pressure. - When MAP , the baroreceptors increases the rate of firing in the corresponding afferent neurons. - Conversely, a in MAP slows the rate of firing generated in the afferent neurons by the baroreceptors. 2. The afferent neurons - contains vagus & glossopharyngial nerves - convoy signal to the medula oblongata 3. The integrating center - receives the afferent impulses about the state of MAP - is located at the cardiovascular control center, in the medulla 4. The efferent pathway - is the autonomic nervous system. 5. The effectors- Heart and blood vessels Cardiovascular Physiology 110 CVS 4/25/2024
- 111. N.B. - The carotidbaroreceptors provide the vasomotor center with information regarding arterial pressure within the range of 50–200 mm Hg, - whereas the aortic baroreceptors can only provide pressure information within the range of 100–200 mm Hg. Cardiovascular Physiology 111 CVS 4/25/2024
- 112. Baroreceptor reflexes forincreased blood pressure If an arterial blood pressure increase for any reason:- - Baroreceptors increase their firing rate to the medulla and this induces (1) Decreased sympathetic activity, which resulted in - decreased heart rate - decreased ventricular contractility - decreased stroke volume - decreased arteriolar constriction - decreased venous constriction (2) Increased parasympathetic activities, which resulted in - decreased heart rate The net result is - decreased cardiac output - decreased total peripheral resistance (arteriolar constriction), and - return of blood pressure toward normal. Cardiovascular Physiology 112 CVS 4/25/2024
- 113. Baroreceptor reflexes fordecreased blood pressure If arterial pressure decreases as during a hemorrhage, - Baroreceptors decrease their firing rate to the medulla and this induces (1) increased sympathetic activity, which resulted in - increased heart rate - increased ventricular contractility - Increased stroke volume - increased arteriolar constriction - increased venous constriction (2) decreased parasympathetic activities, which resulted in - increased heart rate The net result is - an increased cardiac output - increased total peripheral resistance (arteriolar constriction), and - return of blood pressure toward normal. Cardiovascular Physiology 113 CVS 4/25/2024
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- 116. Baroreceptor Reflex Control CardiovascularPhysiology 116 CVS 4/25/2024
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- 122. 2. Arterial chemoreceptors -A chemoreflex is an autonomic response to changes in blood chemistry such as decreased PO2, increased PCO2, & increased H+ - It is initiated by chemoreceptors called carotid and aortic bodies (located near aortic & carotid sinus). - The primary role of chemoreflexes is to adjust respiration to changes in blood chemistry by doing hyperventilation (increased minute volume). - Stimulation of chemoreceptors in the medulla oblongata act through the vasomotor center to cause widespread vasoconstriction. This increases overall Blood Pressure. Cardiovascular Physiology 122 CVS 4/25/2024
- 123. Chemoreceptor Reflex Control CardiovascularPhysiology 123 CVS Stimulus - decreased PO2, increased PCO2, & increased H+ Response - Hyperventilation - Widespread Vasoconstriction - Increase Blood pressure 4/25/2024
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- 126. 3. CNS ischemicresponse - Raises arterial pressure in response to diminished blood flow in vasomotor center of the brain. - CNS ischemic response is stimulated by BP (<60 mm Hg) brain ischemia Local hypoxia, hypercapnia & acidosis in medulla - The cardiac and vasomotor centers of the medulla oblongata send sympathetic signals to the heart and blood vessels that induce (1) an increase in heart rate and contraction force and (2) widespread vasoconstriction. - These actions raise the blood pressure and, ideally, restore normal perfusion of the brain. This control system is “last ditch” mechanism for blood pressure control. Cardiovascular Physiology 126 CVS 4/25/2024
- 127. B. Intermediate termcontrol 1. Stress-relaxation or reverse stress relaxation: Pressure stress on veins veins relax &pressure (stress relaxation) intravascular volume opposite effect. Severe bleeding → reverse stress-relaxation mechanism, i.e blood vessels tighten up around the blood that is left→ re-establish normal circulation. This mechanism cannot correct changes that are about 30% above normal or 15% below normal. Cardiovascular Physiology 127 CVS 4/25/2024
- 128. 2. Capillary fluidshifts:- in response to changes in capillary pressure Fluid moves into interstitial fluid space when BP rises→ normal BP. 3. Beginning of arteriolar vasoconstriction by Ang. II Cardiovascular Physiology 128 CVS 4/25/2024
- 129. 4. Cardiac stretchreceptor reflex Atrial natriuretic peptide (ANP)= stretch receptors - Released from atria in response to increase atrial pressure - During increases in venous return ----- RA stretch Elicits 2 reflexes to increase CO 1.Stretch of SA node ---->increase HR, which helps to pump extra blood that is returning to the heart. Cardiovascular Physiology 129 CVS 4/25/2024
- 130. 2. Bain-bridge-reflex - Whenthe right sided filling pressure increased, the wall of the atrium is stretched. The stretch receptor present in the right atrial wall sends signal to Vasomotor center of medulla(VMC) via afferent vagal nerve. - The VMC in turn inhibit parasympathetic activity to increase heart rate and increase sympathetic NS to increase contractility. - This reflex causes an increase in HR, which also helps to pump out the excess venous return Cardiovascular Physiology 130 CVS 4/25/2024
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- 134. C. Long termcontrol -Renin-Angiotension-Aldosterone system (long-term control (RASS) -Long term control mechanism of control of ABP is shown below Cardiovascular Physiology 134 CVS 4/25/2024
- 135. Angiotensin II. - Thisis a potent vasoconstrictor that raises the blood pressure. Aldosterone. - This “salt-retaining hormone” primarily promotes Na retention by the kidneys. Since water follows sodium osmotically, Na retention promotes water retention, thus promoting a higher blood volume and pressure. Antidiuretic hormone. - ADH primarily promotes water retention, but at pathologically high concentrations it is also a vasoconstrictor—hence its alternate name, vasopressin. Both of these effects raise blood pressure. Cardiovascular Physiology 135 CVS 4/25/2024
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- 138. Circulatory shock Existswhen there is a generalized, severe reduction in blood supply and the metabolic needs of the tissues are not meet. Occurrence of low arterial pressure even with all cardiovascular compensatory mechanisms activated. Primary Disturbances Severely depressed myocardial functional ability or Inadequate cardiac filling due to low mean circulatory filling pressure. Cardiovascular Physiology 138 CVS 4/25/2024
- 139. Cardiogenic shock:occurs whenever cardiac pumping ability is compromised (e.g. severe arrhythmias, abrupt valve misfunction, coronary occlusions, and myocardial infarction). Decrease central venous volume and/or ventricular filling 1. Hypovolemic shock 2. Anaphylactic shock 3. Septic shock 4. Neurogenic shock Cardiovascular Physiology 139 CVS 4/25/2024
- 140. 1. Hypovolemic shock Accompanies significant hemorrhage (usually greater than 20% of blood volume), severe burns, chronic diarrhea, or prolonged vomiting. Induce shock by depleting body fluids and thus circulating blood volume. Pulmonary embolus:- evoke a shock that resembles hypovolemic shock in that left ventricular filling may be compromised. large emboli not only reduce cardiac output but interfere with gas exchange in the lungs. Cardiovascular Physiology 140 CVS 4/25/2024
- 141. 2. Anaphylactic shock Occurs as a result of a severe allergic reaction to an antigen . (e.g. insect bites, antibiotics, certain foods). It is also called an "immediate hypersensitivity reaction" which is mediated by several substances (such as histamine, prostaglandins, leukotrienes, bradykinin). It results in peripheral vasodilatation and increases microvascular permeability. Cardiovascular Physiology 141 CVS 4/25/2024
- 142. 3. Septic shock It is caused by vasodilator effects of substances released into the circulating blood by infective agents. One of the most common is endotoxin, a lipopolysaccharide released from bacteria. It induces the formation of a NO synthase (called inducible nitric oxide synthase to distinguish it from the normally present constitutive nitric oxide synthase) in endothelial cells, vascular smooth muscle, and macrophages. Cardiovascular Physiology 142 CVS 4/25/2024
- 143. 4. Neurogenic shock It is produced by loss of vascular tone due to inhibition of the normal tonic activity of the sympathetic vasoconstrictor nerves & often occurs with deep general anesthesia or in reflex response to deep pain associated with traumatic injuries. The transient vasovagal syncope evoked by strong emotions is a mild form of neurogenic shock. Cardiovascular Physiology 143 CVS 4/25/2024
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- 145. Stages of Shock Because the characteristics of circulatory shock change with different degrees of severity, shock is divided into the following three major stages: 1) A non progressive stage (Compensated stage): Normal circulatory compensatory mechanisms cause full recovery without help from outside therapy. 2) A progressive stage: - Without therapy, the shock becomes steadily worse until death. 3) An irreversible stage: - All forms of known therapy are inadequate to save the person’s life, even though, for the moment, the person is still alive. Cardiovascular Physiology 145 CVS 4/25/2024
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