Chapter 12 - Human Physiology
Chapter 12 - Human Physiology BIOL 2213
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Chapter 12 – Cardiovascular Physiology Part I System Overview – The 3 main components that make up the circulatory system are the heart, blood vessels, and blood. Blood is composed of formed elements suspended in plasma. The plasma carries dissolved particles like proteins, nutrients, and metabolic wastes. Cells in the blood include erythrocytes (RBC), leukocytes (WBC) and platelets. Hematocrit is defined as the percentage of blood volume that is erythrocytes. Overall Layout of Circulation – There are 2 components of circulation: systemic and pulmonary circulation. In systemic circulation, the vena cava carry deoxygenated blood to the heart and the aorta carries oxygenated blood away from the heart. In pulmonary circulation, the pulmonary arteries carry deoxygenated blood to the lungs and the pulmonary veins carry oxygenated blood to the heart from the lungs. Blood Vessel Definitions: 1. Pulmonary circulation – blood pumped from the right ventricle through the lungs and then to the left atrium 2. Systemic circulation – blood pumped from the left ventricle through all the organs and tissues of the body and then back to the right atrium 3. Arteries – vessels carrying blood away from the heart 4. Veins – vessels carrying blood to the heart 5. Arterioles – the smallest arteries which branch into capillaries 6. Venules – the smallest veins that arise from capillaries 7. Inferior Vena Cava – collects blood from below the heart 8. Superior Vena Cava – collects blood from above the heart 9. Pulmonary Trunk – the area in which blood leaves the heart via the right ventricle 10. Pulmonary Arteries – arise from the pulmonary trunk with each artery supplying blood to one of the lungs 11. Pulmonary Veins – the vessels in which blood ultimately leaves the lungs which empty into the left atrium Pressure, Flow, and Resistance – There are 3 things that are in direct relationship to each other. These things are blood flow, blood pressure, and resistance to blood flow. These 3 factors are collectively referred to as hemodynamics. Blood flow is always from a region of high pressure to a region of low pressure. The pressure exerted by any fluid is called hydrostatic pressure. This pressure is generated by the contraction of the heart. Resistance to flow is described as how difficult it is for blood to flow between two points at any given pressure difference. This equation is outlined below: (P 1P 2) Flow Rate= R Resistance – One determinant of resistance is the fluid property known as viscosity, which is a function of the friction between molecules of a flowing fluid. Other factors of resistance include: 1. Length of Tube 2. Radius of Tube – The larger the radius (relaxed vessel) the lower the resistance Anatomy of the Heart – Know the entire anatomy of the heart as shown in the picture below: Specific Anatomy of the Heart – The heart is a muscular organ enclosed in a fibrous sac called the pericardium. The inner layer of the pericardium is closely affixed to the heart and is called the epicardium. Between this space is a watery fluid that lubricates the heart as it moves. The following terms are necessary in the understanding of the anatomy of the heart: 1. Myocardium – this is the wall of the heart that is composed primarily of cardiac muscle cells. The inner surface of the cardiac chambers is lined by a thin layer of cells called endothelial cells. The layer of endothelial cells is called the endothelium. The endothelium lines the interior of all blood vessels as well. In the heart, the endothelium is called the endocardium. So, endocardium → myocardium → epicardium 2. Interventricular Septum – a muscular wall separating the right and left ventricles. 3. Papillary Muscle – these are muscular projections that attach to the AV valves that prevent the AV valves from being pushed up into the atria while the ventricles are contracting blood into pulmonary and system circulation. 4. Chordae Tendineae – these are fibrous strands that connect the AV valves to the papillary muscles. Cardiac Muscle – The heart is comprised of tightly bound layers of cardiac muscle cells. Cardiac muscle cells completely surround the chambers of the heart. When the walls of the chamber contract, cardiac muscle cells come together like a squeezing fist and exert pressure on the blood they enclose. Every cardiac muscle cell contracts with every beat, unlike skeletal cells. 1% of cardiac muscle cells do not function in contraction and have specialized features. These cells constitute a network known as the conducting system. The conducting system is in contact with all cardiac muscle cells via gap junctions. The conducting system initiates the heartbeat. Innervation – The heart contains both sympathetic and parasympathetic nerve fibers. Parasympathetic fibers are contained in the vagus nerves. The sympathetic fibers innervate the entire heart and release primarily norepinephrine. Parasympathetic fibers terminate on cells found in the atria and release Ach. Blood Supply – The arteries that supply the myocardium are called the coronary arteries. The coronary arteries exit from behind the aortic valve cusps in the first part of the aorta. The blood flowing through the coronary arteries is called the coronary blood flow. All of the cardiac veins (coronary veins) drain into a single large vein called the coronary sinus, which empties into the right atrium. Heartbeat Coordination – Contraction of cardiac muscle is triggered by a depolarization of the plasma membrane. Gap junctions connect myocardial cells are allow action potentials to spread from one cell to another. The initial depolarization arises in a small group of conductingsystem cells called the sinoatrial (SA) node. The SA node is located in the right atrium near the entrance of the superior vena cava. Sequence of Excitation: SANode→ Atrial Myocardium(Internodal Pathway)→ AV Node→bundleof His→¿∧¿Branches→PurkinjeFibers→Ventricles→PapillaryMuscles Cardiac Action Potential – Different types of heart cells express unique combinations of ion channels that produce different action potential shapes. There are two basic types of action potential graphs. One is the action potential of a ventricular muscle cell and the other is the action potential of a cardiac nodal cell. The 3 basic steps are outlined as followed: 1. Sodium enters 2. Calcium enters 3. Potassium exits Node Cells – Node cells are found in the SA node, AV node, atrioventricular bundle (bundle of His), bundle branches, and Purkinje fibers. These cells demonstrate automaticity. The SA is considered the pacemaker of the heart. Electrocardiogram – an EKG is primarily a tool for evaluating the electrical events within the heart. A typical EKG is shown below: P is the atrial depolarization (contraction) QRS is the ventricular depolarization T is ventricular repolarization Effects of Damage on an EKG – Sometimes, the AV node can be damaged. This results in a heart block. The AV node is the only form of electrical communication between the atrium and ventricles. A total block causes the ventricles to beat at their intrinsic rate due to the action of Purkinje fibers. Any type of blockage due to damage to the AV node will cause a slow electrical impulse and an external pacemaker will need to be used. ExcitationContraction Coupling in Cardiac Muscle – The following outlines the mechanism for excitationcontraction coupling in cardiac muscle: 1. The plasma membrane of the cardiac cell is depolarized. 2+ 2+ 2. Voltagegated Ca channels open in the Ttubules. These channels are called Ltype Ca channels and cause a small rise in cytosolic Ca concentration. 2+ 3. There is an influx of Ca from the sarcoplasmic reticulum. In skeletal muscle, the release of Ca from the sarcoplasmic reticulum via ryanodine is a voltagegated system. In the sarcoplasmic reticulum of cardiac muscles, ryanodine operates on a ligandgated ion channel system, where the ligand is the cytosolic Ca from the Ltype Ca channels. 4. Contraction occurs in the exact same way as in skeletal muscle. Refractory Period of the Heart – Ventricular muscle is incapable of tetanus (summation of contractions). The inability of the heart to generate tetanic contractions is the result of the long absolute refractory period of cardiac muscle. In ventricular muscle, there is a prolonged depolarized plateau in the cardiac muscle action potential. Mechanical Events of the Cardiac Cycle – Several terms need to be described before any detailed mechanical analysis can occur. The cardiac cycle is divided into 2 major phase: systole and diastole. 1. Systole – the period of ventricular contraction and blood ejection 2. Diastole – the alternating period of ventricular relaxation and blood filling. In this book, the dividing line between systole and diastole occurs when ventricular contraction stops and the semilunar valves close. 3. Isovolumetric Ventricular Contraction (Part of Systole) – the ventricles are contracting but all valves in the heart are closed. The ventricular muscles develop tension, but do not shorten. 4. Ventricular Ejection (Part of Systole) – this occurs once the rising pressure in the ventricles exceeds that in the aorta and pulmonary trunk. The volume of blood ejected from each ventricle during systole is called stroke volume. 5. Isovolumetric Ventricular Relaxation (Part of Diastole) – This is a very short period in which ventricular volume is not changing. This period, along with IVC, are the only periods in which all valves of the heart of are closed. They are very short periods of time. 6. Ventricular Filling – The AV valves open and blood flows from the atria into the ventricles. Atrial contraction occurs at the end of diastole, once most ventricular filling has already taken place. Other Terms Necessary to Describe the Cardiac Cycle: 1. End Diastolic Volume – the amount of blood in the ventricles after diastole (filling) has completed. 2. End Systolic Volume – the amount of blood remaining after ejection 3. Atrial fibrillation – this is a condition in which the cells of the atria contract in a completely uncoordinated manner and so fail to serve as effective pumps. This does not affect a healthy individual much since most ventricular filling occurs in early diastole. Pulmonary Circulation Pressures – Typical pulmonary artery systolic and diastolic pressures are 25 and 10, respectively, compared to systemic arterial pressures of 120 and 80. Pulmonary circulation is a lowpressure system. Despite these major pressure differences, the stroke volume of each ventricle is the same. Heart Sounds – Two heart sounds result from cardiac contractions. The first sound is soft low pitched lub is associated with the closure of the AV valves. The second sound is a louder dub which is associated with closer of the pulmonary and aortic valves. 1. Clinical Issues – abnormal heart sounds are called heart murmurs. Murmurs signal that blood flow is turbulent. Blood flow should be silent if it is flowing smoothly. If it hits anything that obstructs it, it will cause a heart murmur. Sometimes, turbulent flow can be caused by blood flowing rapidly in the usual direction through an abnormally narrowed valve. This condition is called stenosis. Cardiac Output – Cardiac output is the volume of blood that each ventricle pumps per minute. It is usually expressed in liters per minute and can be found by multiplying heart rate by stroke volume. The total blood volume in a human body is approximately 5L, so the heart pumps the entire circulation in one minute (5L/min). Regulation of Heart Rate – This is the first variable that affects cardiac output. The heart will beat at approximately 100 beats/min in the absence of any nervous or hormonal influence on the SA node. A large number of postganglionic fibers end on the SA node from both the sympathetic and parasympathetic nervous system. Parasympathetic nerves cause the HR to decrease while the sympathetic nerves cause HR to increase. Epinephrine and norepinephrine increase heart rate. Epinephrine comes from the adrenal medulla and norepinephrine comes from the nervous system. Regulation of Stroke Volume – This is the second variable that affects cardiac output. The ventricles do not completely empty themselves upon contraction. Therefore, a more forceful contraction will eject more blood causing a greater stroke volume. Again, stroke volume is the amount of blood that the ventricles eject during systole. Mathematically, it can be described as the difference between EDV and ESV. Changes in stroke volume can be produced by three main factors: 1. Preload – changes in end diastolic volume 2. Changes in magnitude of sympathetic nervous system input to the ventricles 3. Afterload – the arterial pressures against which the ventricles pump FrankStarling Mechanism – This describes the relationship between ventricular enddiastolic volume and stroke volume. In other words, the FrankStarling mechanism describes the relationship between preload and stroke volume. The critical factor affecting stroke volume is preload, or changes in enddiastolic volume (EDV). As EDV increases, stroke volume increases because the ventricle has to contract more forcefully. The FrankStarling mechanism is due to the following physical phenomena: 1. The greater the EDV/preload, the more the sarcomeres are stretched, and the greater the force of the contraction. However, there are several key differences between this length tension relationship for skeletal and cardiac muscle. In skeletal muscle, the normal sarcomere stretch for a resting individual is at optimal length for contraction. In cardiac muscle, the normal sarcomere stretch is well below its “optimal” point. This means that if the cardiac sarcomere is stretched, it will get closer to its optimal length, and generate greater tension when preload is increased. 2. Now we need to describe how EDV/preload increases. The amount of blood in the ventricles is controlled by venous return. Any increase in venous return at any heart rate will increase stroke volume and ultimately cardiac output. For example, if the right side of the heart begins to pump more blood than the left, then the left side would automatically produce an increase in left ventricular output. This ensures that no blood accumulates in pulmonary circulation. A slow heart rate or exercise will increase venous return and increase stroke volume, making the heart more efficient. Sympathetic Regulation of Stroke Volume – Sympathetic nerves are distributed across the myocardium. The sympathetic neurotransmitter norepinephrine can act on betaadrenergic receptors and increase ventricular contractility. Contractility is defined as the strength of contraction at any given EDV/preload. So, this describes “2” in the three major things that affect stroke volume. Plasma epinephrine also increases myocardial contractility. These things are independent of EDV/preload. So, even though ventricular contraction increases due to the Frank Starling mechanism, this is not considered contractility. Contractility means that, at the same EDV, the force of contraction can be different. So, this 2 phenomena work together in generating stroke volume. Finally, not only does the sympathetic nervous system increase contractility, it also causes contraction and relaxation to occur more quickly. Since increased sympathetic activity also increases heart rate, there needs to be a way for diastolic filling to be maintained, so the quicker return to relaxation helps account for this problem. One way to quantify contractility is through the ejection fraction (EF). EF is defined as the ratio of stroke volume to enddiastolic volume (EDV/preload). EF=SV/EDV. 1. Ejection Fraction – This normally ranges between 50% and 75% in resting individuals. As sympathetic activity increases, stroke volume increases, causing an increase in ejection fraction. Basically, increased contractility yields an increased ejection fraction. Afterload – Increased arterial pressure tends to decrease stroke volume. Arterial pressure acts as a load that the contracting ventricle must overcome. Anything that increases systemic or pulmonary arterial pressure can increase afterload, and decrease stroke volume. Chapter 12 – Cardiovascular Physiology Part II Overview of Blood Vessels – There is only one structural unit in common for the entire vascular system and that is smooth, singlecelled layer of endothelial cells. The endothelium lines the inner bloodcontacting surface of vessels. Overview of Terms and Relationships: The maximum arterial pressure reached during peak ventricular ejection is called systolic pressure. The minimum arterial pressure occurring just before ventricular ejection is called diastolic pressure. Pulse pressure is the difference between systolic and diastolic pressure. The 3 main factors in determining the magnitude of pulse pressure are stroke volume, speed of ejection of the stroke volume, and arterial compliance. Arteriosclerosis is a condition in which arteries are less compliant, in which the arteries stiffen that progresses with age and increases pulse pressure. Another term, mean arterial pressure, is the average pressure in the arteries at any given time, which is expressed by diastolic pressure plus 1/3 pulse pressure. Measurement of Systemic Arterial Pressure – A sphygmomanometer is a device used to measure systolic and diastolic pressure. An inflatable cuff is attached around the upper arm. The cuff is inflated to a pressure greater than systolic pressure, completely compressing the artery and preventing blood flow. The air in the cuff is released, and the pressure at which blood begins to flow again is the systolic pressure. This initial high velocity blood flow is turbulent and produces vibrations called Korotkoff’s sounds. When the cuff pressure decreases below diastolic pressure, all sounds stop because blood flow is now continuous and nonturbulent. Arteries – There are 4 types of arteries in the human body; elastic, muscular, arterioles, and capillaries. 1. Elastic Arteries are conduit vessels near the heart which carry blood for circulation. These are large lumen vessels that have low resistance. This is because they contain more elastin that muscular arteries. To quantify the ability of elastic arteries to stretch, we use a term called compliance. Compliance is defined as the change in volume over the change in pressure. The greater the compliance, the more easily the artery stretches. During systole, a volume of blood equal to only onethird the stroke volume leaves the arteries. During diastole, when ventricular contraction ends, the stretched arterial walls recoil, driving blood into the arterioles. Because of this recoil, they are called “pressure reservoirs.” As blood leaves the arteries, the arterial volume and pressure decrease until the next ventricular contraction. Therefore, arterial pressure never returns to zero. 2. Muscular Arteries – These arteries deliver blood to specific organs. They have the thickest layer of smooth muscle out of all the artery types and are very active in vasoconstriction, which is the decrease in vessel radius. These arteries play a big role in the regulation of blood pressure. 3. Arterioles – The arterioles play 2 major roles. First, the arterioles in individual organs are responsible for determining the relative blood flow to those organs at any given mean arterial pressure. Second, the arterioles as a whole are a major factor in determining mean arterial pressure itself. a. Blood Flow – blood flow equals the change in pressure over resistance. The driving pressure in each tube will always be the same. So, differences in flow are determined by differences in the resistance to flow in each individual arteriole. Resistance is solely determined by vessel radii. Arterioles contain smooth muscle so increasing the radii is called vasodilation and will decrease resistance while decreasing the radii is called vasoconstriction and will increase resistance. Arteriole restriction is determined by neural, hormonal, and paracrine output. However, arterioles can have spontaneous contractile activity called intrinsic tone. Regulation of Arterioles – Arterioles can be regulated in 3 ways: local controls, nerves, and hormones. 1. Local Controls – Organs and tissues alter their own arteriole resistances, thereby self regulating their blood flows. Local controls include active hyperemia, flow auto regulation, reactive hyperemia, and local response to injury. a. Active Hyperemia – An increase in blood flow/decrease in resistance to an organ or tissue is called hyperemia. An increase in blood flow due to metabolic activity is called active hyperemia. The factors that cause smooth muscle to relax during active hyperemia are local chemical changes in the extracellular fluid surrounding the arterioles. These changes are caused by increased metabolic activity from nearby cells. For example, oxygen decreases (needed for ATP production) and + + CO 2ncreases. H increases from lactic acid, K increases from repeated action potential repolarizations, and nitric oxide increases from endothelial cells. Overall, it increases blood flow. b. Flow Autoregulation – This is the change in resistance to maintain a constant blood flow when there is a pressure change. For example, when arterial pressure in an organ is reduced, local controls cause arterial vasodilation, maintaining a constant flow of blood. Overall, it alters resistance. c. Reactive Hyperemia – This is an extreme form of flow autoregulation. When an organ or tissue has had its blood supply completely occluded, a major increase in blood flow occurs after the occlusion is gone. 2. Neural Control – Sympathetic nerves release norepinephrine, which bind to alpha adrenergic receptors causing vasoconstriction. This method can also induce vasodilation if no norepinephrine is released. This means there is always a baseline discharge of norepinephrine on arterials. Increased epinephrine has the effect of increasing blood pressure. Compare this to the effect of increased norepinephrine on the heart which has the effect of increasing heart rate. Parasympathetic nerves have no effect on arterioles. 3. Hormonal Control – The following hormones are important in the arterioles: a. Epinephrine – this is released by the adrenal medulla and binds to alpha adrenergic receptors to cause vasoconstriction, increasing blood pressure. b. Angiotensin II – This is a peptide hormone that causes vasoconstriction. c. Vasopressin – This is released by the posterior pituitary gland to produce vasoconstriction. d. Atrial Natriuretic Peptide – This is a peptide hormone released by the cardiac atria that aids in vasodilation. Endothelial Cells and Vascular Smooth Muscle – Endothelial cells excrete several paracrine agents that diffuse to adjacent vascular smooth muscle and induce either relaxation or dilation. The most important paracrine substance is nitric oxide. NO is crucial to vasodilation and is readily produced during inflammation. Capillaries – The capillaries permeate almost every tissue in the body. An adult has an estimated 25,000 miles of capillaries. Basically, capillaries are the sites of gas exchange. Capillaries are a thin walled tube of endothelial cells resting on a basement membrane. The cells of the endothelium are not tightly attached to each other and are separated by a narrow, waterfilled space called the intercellular cleft. Sometimes, the endothelium contains large numbers of endocytotic and exocytotic vesicles that fuse to form fusedvesicle channels. Arterioles or metarterioles connect to capillaries at a ring of smooth muscle called the precapillary sphincter. Types of Capillaries – There are 3 types of capillaries as outlined below: 1. Continuous Capillary – These have tight junctions and are found in the skin and muscle 2. Fenestrated Capillary – These are more permeable and found in the intestines, hormone producing tissues, and kidneys 3. Sinusoidal Capillary – This has an incomplete basement membrane and is found in the liver, bonemarrow, and lymphoid tissues. Velocity of Capillary Blood Flow – When a continuous stream moves through consecutive sets of tubes arranged in parallel, the velocity of flow decreases as the sum of the crosssectional area of the tubes increase. This means that the blood flows rapidly through the overall small cross sectional area of the aorta and major arteries and then slows considerably as it travels through the overall large crosssectional area of all the capillaries combined. This increased time maximizes the time available for substances to exchange between the blood and interstitial fluid. So, even though capillaries provide a lot of resistance (which decreases blood flow), there are so many capillaries that the total resistance of all capillaries is much lower than that of the arterioles. Diffusion Across Capillary Wall – Three basic mechanisms allow substances to move between the interstitial fluid and the plasma: diffusion, vesicle transport, and bulk flow. 1. Diffusion – in all capillaries, excluding those in the brain, diffusion is the only important means by which net movement of nutrients, oxygen, and metabolic end products occurs across the capillary walls. Ions and polar molecules travel through the intercellular clefts and lipidsoluble substances travel through the cell membrane. 2. Vesicle Trasnport – Vesicle transport is useful for proteins like hormones. The vesicles release their hormones through endocytosis at the luminal site and exocytosis at the interstitial side. 3. Bulk Flow – Aside from nutrient and hormone exchange, bulk flow refers to the bulk flow of plasma. Bulk flow is the distribution and shifting of extracellular fluid volume. This occurs because most capillary walls are highly permeable to water. Therefore, in the presence of hydrostatic pressure differences, the capillary wall behaves like a porous filter that allows all plasma solutes to pass through except proteins (which require vesicle transport). So, filtration refers to the bulk flow from the plasma to the interstitial fluid while absorption refers to the bulk flow from the interstitial fluid to the plasma. The net filtration pressure (NFP) depends on 4 variables. Positive numbers favor filtration and negative numbers favor absorption. a. Capillary hydrostatic pressure b. Interstitial hydrostatic pressure c. Osmotic Force due to plasma protein concentration – osmotic pressure is the force that opposes hydrostatic pressure. It does not vary from one end of the capillary to the other, like hydrostatic pressure does. d. Osmotic force due to interstitial protein concentration The equation for net filtration pressure is as follows: NFP= (HP – HP ) – (OP – OP ). c if c if So, because hydrostatic pressure is the variable that changes the most from one end of the capillary to the other, filtration rate is faster at the arteriole end of the capillary compared to the venule end. Venous System – Veins vary in structure as they progress away from the capillaries. Veins have 3 distinct layers called tunics. The walls are also thinner than in the arteries. Veins are the last set of tubes that take blood back to the heart. The driving force behind venous return is the pressure difference between the peripheral veins and the right atrium, which is at a much lower pressure. Peripheral veins include all veins not contained within the chest cavity. Veins are considered a low resistance conduit, which means that flow is maintained even with a low pressure difference ∆ P (F= R ) . Varicose Veins – Veins have valves that permit blood flow in only one direction. Varicose veins occur when the valves become leaky and the entire vein becomes dilated and does not transfer blood back to the heart as well. Determinants of Venous Pressure – Blood pressure in veins is approximately 15mmHg. This is not sufficient to move blood back to the heart, so there are certain pumps that do this. Blood pressure in any elastic tube is determined by the volume of fluid and compliance of the blood vessels. Veins carry most of the total volume of blood in the body and also have walls that are more compliant, so the veins can accumulate large amounts of blood. There is smooth muscle in veins that is controlled by the sympathetic nervous system which releases norepinephrine. This causes smooth muscle to contract and force blood to the right atrium. An important thing to note is that when arteries constrict, it decreases forward flow. When veins constrict, it increases forward flow. Two other mechanisms can increase venous pressure and facilitate venous return. 1. Skeletal Muscle Pump – skeletal muscles contract and squeeze veins. 2. Respiratory Pump – pressure changes in the central cavity due to the pressure changes occurring during breathing. This propels blood back to the heart. Relationship between Venous Pressure and Cardiac Output – As venous pressure increases, end diastolic volume increases, increases stroke volume, and ultimately increasing cardiac output. Basically, the more efficient the veins are, the more efficient the entire circulatory system. The Lymphatic System – The lymphatic system is a network of small organs and tubes through which lymph (a fluid derived from interstitial fluid) flows. Within the interstitium of all organs and tissues are lymphatic capillaries that are distinct from blood capillaries. Lymphatic capillaries are permeable to all interstitial constituents, including proteins. Small amounts of interstitial fluid continuously enter the lymphatic capillaries by bulk flow. Eventually, these tubes drain into the veins near the jugular. Thus, the lymphatic vessels carry interstitial fluid back to the cardiovascular system. The lymphatic system also houses phagocytes and lymphocytes for the immune system. Heart→Arteries→Capillaries→Interstitial Fluid→LymphaticSystem→Veins→Heart Mechanism of Lymph Flow – Fluid is moved by smooth muscle pumps in the walls of the lymph vessels that act using inherent rhythmic contractions. This produces a oneway flow of flood towards the circulatory system. Clinical Issues with the Lymphatic System – If the lymphatic system becomes overwhelmed, the lymph nodes can swell, producing buboes. Also, metastasizing cancers live and spread in the lymph system so this is why lymph nodes for breast cancer. Regulation of Arterial Pressure – The major cardiovascular variable being regulated is mean arterial pressure, which is defined as the product of cardiac output and total peripheral resistance. All changes in mean arterial output must be the result of changes in cardiac output and/or total peripheral resistance. Also, cardiac output is the product of heart rate and stroke volume. Baroreceptor Reflexes – Baroreceptors are pressure receptors. Afferent neurons from the baroreceptors to the brainstem provide input to the neurons of the cardiovascular control centers. The higher the arterial pressure, the action potential frequency of the baroreceptors increases. Therefore, the rate of baroreceptor action potentials is directly proportional to MAP. Specific baroreceptors include the carotid sinus baroreceptor and the The Medullary Cardiovascular Center – The medullary cardiovascular center is the primary integrating center for baroreceptor reflexes. This is located in the medulla oblongata. When arterial baroreceptors increase their rate of discharge, the result is a decrease in sympathetic outflow to the heart, arterioles, and veins, and an increase in parasympathetic outflow to the heart. This helps restore normal blood pressure and reduce MAP (by decreasing cardiac output and total peripheral resistance). So, if blood pressure is too high, the reflex causes blood pressure to decrease. If blood pressure is too low, the reflex causes blood pressure to increase. Other Baroreceptors – Baroreceptors also exist in veins, the pulmonary vessels, and the walls of the heart. These all function in a manner analogous to the arterial receptors. LongTerm Regulation of Arterial Pressure – Increases blood volume increases arterial pressure. Increasing arterial volume then decreases blood volume by moving blood through the kidney, inducing plasma excretion. Thus, 2 things can occur through negative feedback: 1. Higher blood volume leads to higher arterial pressure. 2. Higher arterial pressure leads to decreased blood volume Hypotension – Hypotension refers to low blood pressure. One cause of hypotension is loss of blood volume, which decreases arterial pressure. Orthostatic hypotension is the drop in blood pressure resulting from standing up from a reclined position. Whenever blood pressure decreases, reflexes restore some blood pressure to normal as described in the figure on the previous page. Other forms of hypotension are hemorrhages, and chronic hypotension resulting from poor nutrition, low viscosity of blood, or Addison’s disease. Finally, shock is characterized as any situation in which a decrease in blood flow to the organs or tissues damages them. This is often diagnosed by acute hypotension. The below diagram is a useful diagram in examining how reflexes compensate for sudden hypotension (such as hemorrhaging): Hypertension – Hypertension is defined as a chronically increased systemic arterial pressure. Most people do not know they have it until it has caused serious damage. Interventions to lower blood pressure should be instituted at systolic pressures of 130139 and diastolic pressure of 85 89. Prolonged hypertension is the major cause of heart failure, renal failure, stroke, and vascular disease. Primary hypertension is apparent in over 90% of cases and the causes are not identifiable. Secondary hypertension is apparent in about 10% of cases and the causes are identifiable. Secondary hypertension is usually the result of tumor in the adrenal medulla, Cushing’s disease, obstruction of the renal arteries, kidney disease, arteriosclerosis, or hyperthyroidism. Factors involved in Hypertension – Environmental factors involved in hypertension are a high cholesterol diet, obesity, age (normally occurs before the age of 40), gender (males get it more), diabetes, genetics, stress, and smoking. Plasma – Plasma consists of a large number of organic and inorganic substances dissolved in water. Plasma proteins constitute most of the plasma solutes by weight. Their role in exerting osmotic pressure favors absorption of extracellular fluid. Plasma proteins can be divided into 3 groups: albumins, globulins, and fibrinogen. Serum is any plasma that lack fibrinogen. Most plasma proteins perform their functions in the plasma itself and do not travel to other cells in the body. The plasma’s overall function is to carry electrolytes, nutrients, waste, gases, and hormones throughout the body. Erythrocytes – The major function is to carry oxygen taken in by the lungs and carbon dioxide produced by the cells. They contain large amounts of hemoglobin, in which oxygen can bind to iron atoms. They have a high surface area to volume ratio because of their biconcave shape, so diffusion can occur rapidly. Erythrocytes have no nucleus and no organelles, including ribosomes. Erythrocytes are produced in the bone marrow. Young erythrocytes in the bone marrow are called reticulocytes, because they have a network of ribosomes in which they will eventually lose. The average lifespan of an RBC is 120 days, because they lack a nucleus and mitochondria so they cannot reproduce or maintain function very long. Destruction of damaged or dying red blood cells occurs in the liver and spleen. When hemoglobin is broken down, bilirubin is produced which is returned to circulation and gives plasma its characteristic yellow color. Importance of Iron – Iron is the element in which oxygen binds in hemoglobin. The body has a considerable store of iron in the liver. This iron is bound up in a protein called ferritin. 50% of body iron is in hemoglobin, 25% is in other hemecontaining proteins, and 25% is in ferritin. When RBCs are destroyed by the spleen, iron is released into the plasma and bound to an iron transport protein called transferrin. Transferrin delivers the iron to the bone marrow to be incorporated into new erythrocytes. Folic Acid and Vitamin B – 12lic acid is essential for the formation of thymine, so it is necessary for the formation of DNA and essential for normal cell division. Thus, when there is a folic acid deficiency, fewer erythrocytes are produced in the bone marrow. Vitamin B is also 12 necessary for the action of folic acid and is found only in animal products. Therefore, vegetarian diets tend to be vitamin B 12eficient. Regulation of Erythrocyte Production – Erythropoiesis is RBC production. Although iron, folic acid, and vitamin B 12e all necessary for RBC production, they are not the signals the regulate production rate. RBC production rate is the job of a hormone called erythropoietin, which is secreted into the blood stream by a group of hormonesecreting connective tissue cells in the kidneys. Erythropoietin acts on the bone marrow to stimulate the proliferation of erythrocyte progenitor cells and their differentiation into mature erythrocytes. Life of Iron in the Body: Hemoglobin→Bilirubin→Transferrin→BoneMarrow→ Hemoglobin Leukocytes – Leukocytes (WBCs) function in the defense of the body. WBCs are divided into 2 groups: polymorphonuclear granulocytes and agranulocytes. The 3 types of granulocytes are neutrophils, eosinophils, and basophils. The 2 types of agranulocytes are monocytes and lymphocytes. All of these WBCs are produced in the bone marrow, just like RBCs. Platelets – Platelets are colorless, nonnucleated cell fragments that contain numerous granules are much smaller than erythrocytes. Platelets are produced when cytoplasmic portions of large bone marrow cells called megakaryocytes pinch off and enter circulation. Platelets function in blood clotting. Regulation of Blood Cell Production – All blood cells are descended from a single population of bone marrow cells called pluripotent hematopoietic stem cells. These are pluripotent stem cells can give rise to either lymphoid stem cells or myeloid stem cells. Proliferation and differentiation are dependent on hematopoietic growth factors (HGF). Erythropoietin, the hormone described earlier, is an HGF. Hemostasis: The Prevention of Blood Loss – The stoppage of bleeding is called hemostasis. Hemostasis is a 3step process that involves vascular spasm, formation of platelet plug, and blood coagulation. 1. Vascular Spasm – When a blood vessel is severed or injured, its immediate response is to constrict. This shortlived response slows the flow of blood in the affected area. This vascular spasm also causes the opposed endothelial surfaces of the vessels to press and stick together. 2. Formation of Platelet Plug – Platelets adhere to the collagen of the exposed connected tissue of the blood vessel. This binding causes the platelets to release the contents of their secretory vesicles, which contain a variety of chemical agents. These agents induce multiple changes in metabolism, shape, and surface proteins in a process called platelet activation. These changes cause new platelets to adhere to old ones in a positive feedback phenomenon called platelet aggregation, which creates a platelet plug inside the vessel. Adhesion also induces the platelets to synthesize thromboxane A . Thi12is released into the extracellular fluid and acts locally to further stimulate platelet aggregation and release more vesicle contents. 3. Blood Coagulation – Blood coagulation, or clotting, is the transformation of blood into a solid gel called a clot or thrombus. Thrombus consists mainly of a protein called fibrin. Clotting occurs around the platelet plug. A plasma protein called prothrombin is converted to the enzyme thrombin, which catalyzes a reaction in which several large polypeptides are split from molecules of the large, rodshaped plasma protein fibrinogen. The fibrinogen remnants bind to each other to form fibrin. Fibrin is a mesh of interlacing strands that is stabilized by enzymemediated crosslinking. Steps leading to the ProthrombinThrombin Reaction – The early reactions in the process consist of 2 seemingly parallel pathways that merge at the step just before the prothrombinthrombin reaction. 1. Intrinsic Pathway – everything necessary for this step is in the blood. 2. Extrinsic Pathway – everything necessary for this step is outside the blood. Clotting Factors – Clotting factors are produced in the liver and secreted into the blood in inactive forms which are activated during the clotting cascade. Hemophilia is a genetic disorder characterized by deficiencies in clotting factors, especially in factor VIII. The symptoms of hemophilia are excess bleeding. Also, people with liver problems have problems with excess bleeding, because the liver is the site that produces clotting factors. The liver also produces bile salts which are important for the normal intestinal absorption of vitamin K. Vitamin K is necessary for the liver to produce prothrombin and several other clotting factors. Tissue Factors – These are derived from the extrinsic pathway, while most of the clotting factors are involved in the intrinsic pathway. The extrinsic pathway begins with a protein called tissue factor, which is located on the outer plasma membrane of various tissue cells, including fibroblasts and other cells in the walls of blood vessel outside the endothelium. Tissue factor binds to factor VII. Dissolving Blood Clots – The primary mechanism for dissolving blood clots is the fibrinolytic system. A fibrin clot is not meant to last forever. First, a plasma proenzyme called plasminogen is activated to the active enzyme called plasmin by protein plasminogen activators. Plasmin digests fibrin, dissolving the clot.
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