Blood Vessels and Hemodynamics PDF

Title Blood Vessels and Hemodynamics
Course Anatomy II
Institution Purdue University
Pages 10
File Size 461.5 KB
File Type PDF
Total Downloads 22
Total Views 144

Summary

blood vessel notes...


Description

Blood Vessels and Hemodynamics  





Left side pumps 60000 miles of blood vessel. For every kilogram of weight you put on, you need 400 miles/kg more blood vessels. Overweight people are overstrained. Hemodynamics forces involved in circulating the blood throughout the body. Blood from aorta  arteries arterioles  capillaries (where blood exchange between capillaries and cells take place through interstitial fluid)  venules  veins Defibrillators – used when heart is not working properly. There is fibrillation in the heart so they try to give electric shock to the heart to get rid of it. This is done in order to reset the heart conduction system. From arterioles branches the metarteriole. The metarteriole branches the capillaries. The capillaries make up the capillary bed (can have 10- 100 capillaries) capillary bed supplies everything. o Capillaries have an arteriole end and a venule end. o Capillary beds have precapillary sphincters that close and prevent blood from going to capillaries o There is a thoroughfare channel. Blood is not always in all the capillaries. When you have eaten, blood needs to go to digestive system so capillaries need to be filled. Precapillary sphincters are relaxed and blood can flow through. When not eating, precapillary sphincters are closed/contracted so blood is not flowing to capillaries, only flowing through thoroughfare channel to venules.

Various Types of Capillaries: Exchange vessels; need a lot of surface area for there to be good exchange. They are thin because only have endothelial cells and basement membrane (no smooth muscle). 1. Continuous capillary- most abundant; located in skeletal, skin, brains, lungs. a. Have intercellular cleft that allows things like monocytes into particular regions. In the blood brain barrier, there are tight junctions between continuous capillary so stuff cannot flow through.

2. Fenestrated capillary – have fenestrations or pores that are covered by endothelial membrane and things can move through it more easily than continuous capillary. a. Located in kidneys, villi of small intestine, and ventricles in brain (where lots of filtration occurs). 3. Sinusoid – incomplete basement membrane; a. have winding and large fenestrations. Very large intercellular clefts. Allows proteins made by liver to go in and RBC from red bone marrow to go to circulatory system and spleen (degrade red blood cells) b. Allows RBC and proteins to go in and out. c. Sinusoid in liver has macrophages that gets rid of anything that comes in.

Blood distribution in veins and venules is in systemic veins blood reservoir. takes place in heart. 13% in arterioles. 7% in time. This is where place between interstitial fluid.

body: majority is in systemic (64%). Max amount of blood and venules and they act as Exchange of O2 and CO2 pulmonary vessels (9%). 7% in systemic arteries and systemic capillaries at one blood exchange is taking capillaries and cells via

Capillary Exchange:  





Most of the exchange occurs by diffusion. Substances moving in and out from high concentration to low concentration. Simple diffusion – O2 and CO2 moving in and out due to concentration differences. Can also be done with glucose, amino acids, or hormones. It moves through intercellular clefts or fenestrations or by diffusion through endothelial cells. o Albumin enters blood form liver, Red bone marrow makes RBC that enters blood Transcytosis – formation of pinocytosis vesicles. Substances brough into a cell by endocytosis and goes out of cell by exocytosis (in one end, out the other). o Active process and requires energy. o Ex. Insulin traveling in blood and pushed out into interstitial blood. Bulk flow – plays a major role in homeostasis. This occurs in capillary exchange. It is a passive process where large numbers of ions, particles or molecules in a fluid move together.

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By the time blood reaches the capillaries, the pressure has gone down (BHP). BCOP stays the same because proteins don’t go out. BHP = blood hydrostatic pressure BCOP = blood colloid osmotic pressure / consider solute concentration and ability to draw fluid. More solute, more osmotic pressure. In capillaries, generally BCOP = 26 mmHg. BHP wants to push the fluid out (hitting wall of blood vessel with pressure). BCOP wants to bring fluid in. Interstitial fluid hydrostatic pressure (IFOP) is low because there are hardly any proteins in interstitial fluid. It is typically 1 mmHg and wants to draw fluid towards it. Interstitial fluid hydrostatic pressure IFHP (amount of water here is very small). It is not under any pressure so IFHP is 0 mmHg. If there is edema (swelling), hydrostatic pressure goes up. In normal conditions, IFHP and IFOP are negatable. Pressure is promoting filtration – IFOP and BHP are pushing blood out so subtract from pressures that want to push fluids in (BCOP and IFHP). Arterial End – Filtration ; 20 L go out.  Net filtration pressure = (BHP + IFOP) – (BCOP + IFHP)  = (35+1) –(26+0) = 10 mmHg. Promotes filtration.

Venous End – reabsorption; 17L reabsorption.

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Net filtration pressure = (BHP + IFOP) – (BCOP + IFHP) = (16 + 1) – (26 + 0) = -9 mmHg. Promotes reabsorption. Hydrostatic pressure is lowered. 20 L goes out at arterial end and 17 go in at venous end. 3 L is picked up by lymphatic fluid which returns it to blood.

Hemodynamics: Factors affecting blood flow    





Blood flow = amount of blood flowing through any tissue in a given period of time. ml/min. Cardiac out = total blood flow; CO= HR x SV How blood is distributed in the tissue depends on 2 main factors. Difference in pressure that causes the blood to move and resistance in blood flow. Blood pressure o Hydrostatic pressure exerted by the blood on the walls of the blood vessel. If the pressure between one and other is high, then the blood flow will be more. o BP = systole/diastole = 110/70 normal BP o Mean arterial pressure – pressure difference drives movement of blood and resistance.  MAP = diastolic BP and 1/3(systolic-diastolic) = 70 +1/3(110-70) = 83 mm.  Cardiac output (CO) = MAP/resistance  If resistance is constant and CO geos up, then MAP goes up. Anything that causes blood volume to go up is going to cause an increase in pressure. Vascular resistance o Directly proportional to viscosity and length of blood vessels and viscosity. Inversly proportional to the size of lumen. o Resistance is opposition to blood flow due to friction between blood and wall of blood vessel. o Increased rsistance, leads to increase BP. o R equivalent to 1/(d4) ; If you decrease diameter by ½, R will increase in 16 fold. 1. Size of lumen – decrease diameter, increase resistance because more blood touching the wall. Heart controls blood pressure by changing diameter of arterioles (controlled by sympathetic system). a. Arterioles have a tone (slightly constricted) depending on situation vasoconstriction or vasodilation can control flow to specific tissue. 2. Viscosity – depends on RBC/blood plasma and roteins in blood. Higher the viscosity, the higher the resistance. Can be caused by dehydration which lowers the volume of blood plasma. a. Anemia decreases RBC and decreases viscosity. Polycythemia increases the number of red blood cells in blood and increases viscosity. 3. Total length of blood vessel – longer length, higher resistance. For every kg gained, 400 miles added of blood vessels. Systemic vascular resistance o Total resistance offered by all the blood vessels. It is controlled by arterioles because it has greatest affect due to diameter. Takes all resistance factors into account. o MAP = CO x SVR o SVR – MAP = CO x SVR



Venous return o Control volume of blood returning to heart. Determines cardiac output. o It is based on pressure difference coming in through atria. There is no problem with superior vena cava because blood comes down due to gravity. o Two mechanisms controlling return  1. Skeletal muscle pump – when you move, your skeletal muscle are contracting and relaxing. Valves opening and closing and pushing the venous blood up. People that stand and work for a long period of time have problems because valves stop working properly. They develop varicose.  2. Respiratory – diaphragm flattens when you breathe in which puts pressure on blood vessels and venous blood pushed up.

Blood pressure in various blood vessels:    

Systolic blood pressure is when heart is pumping blood out into aorta. Diastolic blood pressure is when blood is pushed into arteries, the arteries expand then contract to give diastolic pressure. There is a large difference between systolic and diastolic blood pressure due to elastic recoil. If valves don’t close properly when ventricles contract, blood will go back to atria. Atria pressure is 0 mmHg so that blood fills the atria. Blood pressure highest is aorta  arteries (have large diameter so not all blood touches the walls so resistance is low)  arterioles (where pressure is dropping until it reaches 35 mmHg)  capillaries (thin blood vessels without smooth muscle so there is no recoil)  at venule end, pressure is 16 mmHg  veins and vena cavae (pressure keeps falling)  atrial blood pressure is 0 mmHg.

Control of blood pressure and blood flow: 

You can make adjustments to HR, SV, SVR, and total blood volume in order to control blood pressure and blood flow.  Vasomotor center is also in cardiovascular center. Cerebral cortex, limbic system, hypothalamus sending input to the cardiovascular center. Proprioceptors monitor





movement and send in info. Baroreceptors measure blood pressure. Chemoreceptors monitor blood acidity. Role of cardiovascular center o Receives input and depending on the input, it sends output via the following: o Vagus nerve (parasympathetic to decrease HR o Cardiac accelerator (sympathetic) sends signal to increase HR and contractility in the heart. o Vasomotor nerves (sympathetic to cause vasoconstriction of the blood vessels; usually for skin and abdominal viscera. Neural regulation o Baroreceptors reflex – baroreceptors monitor the blood pressure in the carotid sinus. When the left and right carotid artery branch out, there is a widening where the baroreceptors are located that monitor the blood supply to the brain. Baroreceptors in carotid sinus monitor blood supply to the brain. o Baroreceptors located in carotid sinus, arch of aorta, and large arteries. They pick up info about blood pressures and carries it to the cardiovascular center by glossopharyngeal nerve. Then cardiovascular center sends signal.  If want to decrease HR, send signal via the vagus nerve  vagus nerve interacts with the SA node and the AV node to release Ach and reduce HR.  If want to increase HR, send signal via preganglionic nerve to post ganglionic. Cardiac accelerator nerve releases NE to increase HR and contractility.

o

Carotid body (by glossopharyngeal nerve) and aortic body (vagus nerve) have chemoreceptors that carry info about O2, CO2, H+, levels in the blood.



Can have hypoxia (not enough oxygen being delivered to tissue) or hypercapnia (level of CO2 high in blood)

Glossopharyngeal nerve takes info from carotid sinus and carotid body, baroreceptors and aortic sinus and body to cardiovascular system. o Vagus nerve can receive info from baroreceptors in aorta and send out Ach to reduce HR. o Cardiac accelerator nerve releases NE and E to increase HR. Hormonal regulation o If blood volume or blood flow to kidney goes down, then kidney releases enzyme called renin. Renin breaks down angiotensin in blood to angiotensin I (hormone). In lungs, ACE enzyme converts angiotensin I to angiotensin II. Angiotensin II is a potent vasoconstrictor.  Kidneys do it because filtration of plasma occurs here so blood pressure happens here. It stimulates release of aldosterone which causes absorption of H2O and NaCl which increase blood volume.  RAA system o E and NE increase CO and HR and contractility. It causes vasoconstriction of arterioles and veins in skin and abdominal viscera. o ADH is a vasoconstrictor released by body due to dehydration or blood volume decrease. It is made by hypothalamus and released to pituitary. Increase retention of water and increase blood pressure. o ANP released by atria to reduce blood volume. Causes more fluid and sodium to be loss by urinary system. o



Baroreceptor Reflex: Brings pressure back to normal. The controlled condition is blood pressure. When blood pressure decreases, homeostasis is disrupted.  



Receptor = baroreceptors; in carotid sinus and arch of aorta stretch less which decrease rate of nerve impulses to control centers. The control centers are CV center and adrenal medulla which activated sympathetic system. CV increases sympathetic stimulation and decrease parasympathetic. Leads to increase HR and contractility in heart. Adrenal medulla release E and NE to cause vasoconstriction in blood vessels. Effectors (heart and blood vessel) heart increase CO and blood vessels increase SVR. Returns to homeostasis when MAP and Blood pressure is back to normal.

Autoregulation : local regulation of blood flow. For example if a particular tissue is undergoing high metabolism.  

Autoregulation is proportional to metabolism. It is the ability to automatically adjust blood flow based on metabolic rate. Two ways it is regulated 1. Physical change – using smooth muscle of blood vessels, arteriole wall exhibits myogenic response to regulate blood flow. Ex. Lots of blood flow stretch walls of vessel so it contracts more to reduce blood flow. When there is less blood flow, vessel relaxes so more blood flows. 2. Chemicals – when metabolism is high in tissue, it is going to cause formation of various metabolites. Vasodilating chemicals are released by metabolically active tissues: K+, H+,

lactic acid, O2, NO potent (potent vasodilator). They act on precapillary sphincter and cause them to open so more blood comes in. Shock and homeostasis: Shock – failure of cardiovascular system to deliver enough oxygen and nutrients to meet cellular demands. 1. Hypo volumetric shock – when blood volume goes down a substantial amount (10%). a. Decrease blood volume can be caused by hemorrhage or due to trauma or aortic aneurysm or loss by vomiting/diarrhea. b. Also cause baroreceptors in carotid sinus and arch of aorta to send signals to hypothalamus. Hypothalamus causes posterior pituitary to release Adh and increase blood volume and SVR. c. Information also goes to CV center to increase sympathetic stimulation and increase blood vessel constriction and HR and contractility. d. Hypo volumetric shock disrupts homeostasis by moderately decreasing blood volume and BP due to hemorrhage or aneurysm(thinning blood vessel wall and blood rushes out)  body can compensate if 1-% of blood is gone  baroreceptor in kidneys pick up hampered filtration  cause secretion of renin  renin convert ANG to ANG I in liver  ANG I converted to ANG II in lung  ANG II increase SVR; released into blood and stimulate aldosterone  aldosterone is a potent vasoconstrictor and causes kidney to reserve Na and H2O to increase blood volume 2. Vascular shock – vasodilation leads to decrease in BP 3. Anaphylactic shock – tremendous release of histamine and causes vasodilation that results in death 4. Septicemia/septic shock – severe systemic bacterial infection that releases toxins and causes vasodilation. ADH is used to treat this. Hypertension and treatments:    





Chronically elevated BP; 30% of people over 50 are hypertensive. Generally appears at age 40 due to stress. Chronically elevated BP can damage heart and arteries which can cause heart failure and kidney failure, vascular disease, and stroke. Higher BP leads to higher risk. Essential hypertension (reason is unknown) Other factors involved in hypertension is hereditary, diet high in NaCl, saturated fat, and cholesterol, and deficiencies in potassium, calcium, and magnesium. In obesity, adipocytes where fat is stored release a hormone which causes increase in sympathetic tone. There is an increase in blood volume and BP, cortisol is responsible for BP. Smoking causes intense vasoconstriction of blood vessels that leads to high blood pressure by causing release of E and NE. Treatments – lose weight  Limit alcohol  Reduce intake of salt  Proper intake of K, Ca2+, Mg  Don’t smoke

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Manage stress to decrease E and NE by medulla Diuretics – cause more fluid loss from the body by increasing urin output so blood volume decrease; decreases BP. ACE inhibitor – decrease ANG II (vasoconstrictor) and aldosterone. Causes vasodilation and decrease secretion. Ex. Captophil Beta blockers – reduce renin production and reduce ANG II, decreasing HR. Metroprolol is a selective beta-1. In heart cardiac muscle, blocking it would decrease HR and contractility. Vasodilators – Ca2+ channel blockers. Reduce Ca2_ entry and decrease HR and force of contraction by causing vasodilation. Ex Cardiem and Plendil....


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