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Week 7 Lecture Notes

by: Maddie Butkus

Week 7 Lecture Notes phys 215

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Maddie Butkus
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These notes cover everything from the week of 2-22-16 They include the class material as well as extra information given during lecture.
Human Physiology
Dr. Kelly-Worden
Class Notes
PHYS 215, Worden, notes, class notes
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This 16 page Class Notes was uploaded by Maddie Butkus on Monday February 22, 2016. The Class Notes belongs to phys 215 at Ball State University taught by Dr. Kelly-Worden in Summer 2015. Since its upload, it has received 68 views.


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Date Created: 02/22/16
Week 7 Lecture Notes Cardiac Physiology: The circulatory system has three main components: • The heart establishes a pressure gradient to pump the blood • The blood vessels are passageways for the distribution of pumped blood throughout the body. • The blood is a transport medium, serving the needs of body cells. – The pulmonary circulation is a loop of blood vessels between the heart and the lungs. – The systemic circulation is the circuit of blood vessels between the heart and other body systems. • Two systems: pulmonary and systemic • The human heart is about the size of a fist. • It is located in the chest cavity posterior to the breastbone in between the lungs and superior to the diaphragm. • It is the organ responsible for supplying blood and oxygen to the body. The heart wall consists of three layers. – The endocardium is the inner layer of epithelium. – The myocardium is the middle layer of cardiac muscle tissue. – The epicardium is the external membrane. • Cardiac muscle fibers are interconnected by intercalated discs. They form a functional syncytia. Exam 3, 4,5 we will need to know structure and function  The heart is surrounded by a fluid filled sac (the pericardium).  While the heart is relaxed, venous blood flows from the right atrium into the right ventricle through the open tricuspid valve.  The right atrium then contracts and more blood flows into the right ventricle.  The right ventricle then contracts, the tricuspid valve closes and the pulmonary valve opens.  Valves block the openings and allows flow to occur when it should  When the muscular wall of the right ventricle contacts, the blood inside the heart chamber is put under more pressure, and the tricuspid valve closes.  Blood exits through the pulmonary semilunar valve into the pulmonary trunk, which divides to form the right and left pulmonary arteries.  Blood returns from the lungs through the pulmonary veins.  Semilunar Valve > Pulmonary > pulmonary arch > pulmonary arteries  Arteries: carry blood away from heart • After contraction of the left ventricle, the aortic valve closes and the mitral valve opens. Blood flows from the left atrium into the left ventricle. • The left atrium contracts, more blood flows into the left ventricle. • The left ventricle contracts again, the mitral valve closes and the aortic valve opens. Blood flows into the aorta. The action of heart valves ensure that blood flows in the proper direction. • The AV valves – tricuspid on the right and bicuspid on the left. – allow blood to flow from the atria into the ventricles • occurs when atria pressure is greater than ventricular pressure, during ventricular filling. – during ventricular emptying • when ventricular pressure exceeds atrial pressure – the AV valves close. – prevents the blood from flowing backwards – The semilunar valves – close when the pressure in the ventricles falls below the pressure in the pulmonary on the right and aortic on the left. – open when the ventricular pressures exceed the pressures in the pulmonary arteries and aorta. • Once blood goes into aorta or pulmonary arches > the blood then forces shut the semilunar • They open when there’s contraction in the ventricles • Two sounds are heard during each heart beat often called Lub- Dub noises. When the valves between the atria and ventricles close, a "lub" sound is heard (when AVs close) • When the valves in the pulmonary and aortic arteries leaving the heart close, a "dub" sound is heard followed by a longer pause- Lub-Dub (when we close semi-lunars) • Heart murmur: irregular sound that is caused by a problem with the valves • When we listen to the heart we can determine which valve has the problem • Stenotic: valve that has trouble opening • Lub-Whistle-Dub (Semi-Lunar having trouble opening) • Lub-Dub-Whistle (AV having trouble opening) • Insufficient implies the valves are not closing properly • Lub-Swish-Dub (Semi-Lunar are not closing properly) Cardiac Muscle • Remember – primarily involuntary – only in the heart – Mono-nucleated – has own inherent rhythm and can contract without an external stimulus – has faint striations and are branched – gap junctions are common. Pacemaker Potential and Cardiac Channels – Pacemaker cell is responsible for heart rate • Potassium channel – K+ permeability decreases between action potentials • Sodium channel – Not voltage gated – Slow inward leak between action potentials – Leak Channel – sodium is always coming in the cell • T-type calcium channel – Transient, opens before membrane threshold is reached – Opens in the second half of the pacemaker potential – L-type calcium channel – Opens when threshold is reached – Responsible for the rising phase • Transient (t-type): doesn’t stay open long • We see no hyperpolarization because sodium is constantly leaking in Autorhythmic Cells; Nodes, Bundles and Fibers • SA node- responsible for normal heart rate – right atrial wall near the superior vena cava – 70-80 bpm – AV node- – Base of the right atrium near the septum – 40-60 bpm (if it’s in charge which is unusual) • Bundle of His – Tract of cells running from the AV node to the interventricular septum and dividing into right and left branches – 20-40 bpm • Purkinje fibers – Run from the bundle of His and spread through the ventricular myocardium – 20-40 bpm SA is always supposed to be in charge SA- in charge of purkinje fibers Atria – in charge of ventricles SA- AV- Bundle of His-Purkinjes (this is in charge of setting the rate which the heart contracts) – pacemaker cells Contractile cells are muscles cells Phases of the Cardiac Action Potential • Phase 0 (Rapid depolarization) – Opening of voltage gated sodium channels – Potassium channels close • Phase 1 (Initial repolarization) – Opening of transient potassium channels – Sodium channels start to close • Phase 2 (Plateau phase) – Calcium enters through L-type calcium channels – Opening of delayed and ir potassium channels • Phase 3 (Repolarization) – Kir potassium conductance increases • Phase 4 (Resting membrane potential) – Rest – Diastole – NO hyperpolarization • When calcium channel opens (voltage-gated) calcium and potassium are budding heads because calcium is trying to enter cytosol and potassium is trying to leave • Inward rectifier- Kir Cardiac Waves • P wave – Not firing of SA node – Atrial depolarization – PR segment – Current flows through the AV node – QRS complex – Depolarization of the ventricles – Atrial repolarization – ST segment – Ventricles contract and empty • T wave – Ventricular repolarization – TP interval – Ventricles relaxing and filling Arrhythmia (irregular heartbeat) • Variation from normal rhythm and sequence of excitation • Tachycardia (abnormal rapid heart beat) • Bradicardia (abnormal slow heart beat) • Extrastoles (premature beats) – Common deviation – Atrial Flutter – Rapid, regular atrial depolarization (200-380 bpm) • Atrial Fibrillation – Rapid, irregular atrial depolarization – No P waves – Irregular ventricular rhythm – Pulse deficit (not getting blood leaving the heart) • Ventricular Fibrillation (the worst) – Ventricles are out of sync – Serious rhythmic abnormality – 4 minutes before brain damage or death • Heart Block – Normal atrial – Lower than normal ventricular rate The Blood Vessels and Blood Pressure – Ch. 10 Organs that receive excessive blood flow: digestive organs, kidneys, and skin. • Blood is maintained at a relatively constant composition. • Accomplished by the digestive organs, kidneys and skin • They can withstand temporary reduction in blood flow. • The blood flow distributed to other organs is less, – supplying their metabolic needs – and adjusted to their level of activity – They do not tolerate significant reductions in blood • Resting and digesting you have more blood that flows to GI • Flow rate of blood flow through a vessel • F = delta P R • delta P – the pressure difference between the beginning and end of a vessel. – F (blood flow) – is from an area of higher pressure to an area of lower pressure (pressure gradient). – R (resistance) – opposition to blood flow through a vessel. – depends on three factors: • blood viscosity (thickness of blood), • vessel length, • vessel radius. (major determinant) – A slight change in radius produces a significant change in blood flow. • Blood flow: goes from area of higher pressure to lower pressure • More think the slower blood moves The vascular tree: consists of arteries, arterioles, capillaries, venules, and veins • The systemic and pulmonary circulations each consist of a closed system of vessels. • Arteries carry blood away from the heart to the tissues. • Arteries branch into arterioles near an organ. • Regulation of the diameter of arterioles supplying an organ adjusts the volume of blood sent to that organ. • Arterioles branch into capillaries, the smallest vessels. • They are the microscopic exchange vessels with all cells, offering blood that supplies the metabolic needs of the cells. • Capillaries merge into venules that send blood into small veins. • Venules and veins return blood to the heart. Arteries • large radius (less resistance) • little resistance to blood flow. • elastic recoil in the walls – drives the flow of blood during cardiac relaxation (ventricular diastole) – due to a thick middle layer of smooth muscle with elastic fibers – expand from a large volume of blood sent into them when the heart pumps blood (ventricular systole) Arterial blood pressure • Arteries are compliant (distensible). • During ventricular systole, – stroke volume enters the arteries – About one-third as much blood leaves the arteries at this time. • No blood enters the arteries during diastole. (at rest) – The blood continues to leave the arteries by elastic recoil. – Systolic pressure – the maximum pressure in arteries when blood is ejected into them during ventricular systole – Diastolic pressure – the minimum pressure in arteries when the blood is draining off into the remainder of the vessels during ventricular diastole Blood pressure • It is measured by a sphygmomanometer – the cuff they wrap around your arm – When the pressure in the cuff is greater than the brachial artery – blood flow is blocked through the vessel – no sound is heard through a stethoscope placed over the brachial artery at the inside of the elbow – When the pressure in the cuff is slowly released, – vibrations and sound occur when it falls just below systolic pressure – the first heart sound indicates systolic pressure (e.g., 120 mm Hg). – When the falling cuff pressure drops below diastolic pressure, – vibrations and sound disappears – This indicates diastolic pressure (80 mm Hg). – The pulse pressure is the difference between the systolic and diastolic pressures (120 - 80). Mean arterial pressure • The equation is: – mean arterial pressure = diastole pressure + 1/3 the pulse pressure – As one example, from the previous data : 80 + 1/3 (40) equals 93 • This average is weighted, as about two-thirds of the cardiac cycle is spent in diastole. Arterioles Arteriolar radii can be regulated by vasoconstriction, chemicals or parasympathetic nervous system • offer high resistance to blood flow • Mean arterial blood pressure in systemic arterioles drops significantly (e.g., 93 to 37). This pressure drop drives the flow of blood. • Their pressure is not pulsatile. • Arteriolar radii can be changed to alter the distribution of blood flow to organs and to regulate arterial blood pressure. – vasoconstriction (narrowing) and vasodilation (enlargement) – middle layer of smooth muscle is subject to neural, hormonal, and local chemical control. – The vascular tone of this smooth muscle establishes a baseline of vascular resistance. This ongoing tone makes changes in radius size possible. Local control of arteriolar resistance • determines the distribution of the cardiac output • The driving force for blood flow is identical to all organs. • Differences in arteriolar resistance varies between organs. – determines the distribution of blood they receive • During exercise – more blood flow is shifted to the skeletal muscles – less flows to the digestive tract – arterioles to the skeletal muscles dilate, offering less resistance – arterioles serving the digestive tract constrict – Local chemical influences on the resistance of arterioles – local metabolic changes – histamine release – Local physical influences – heat and cold – myogenic responses to stretch Local chemical changes • Increased metabolic activity – e.g. exercise • local concentration of oxygen decreases • This and other local chemical changes relax the smooth muscle wall in arterioles • They dilate by this response, called active hyperemia. • Less metabolic activity causes the opposite condition and response of the arterioles. • Histamine release – synthesized and stored in special connective tissue cells – promotes vasodilation Other Local Chemical Changes • Other local chemical changes that relax the smooth muscle in arterioles, causing vasodilation, are: – increased carbon dioxide – increased acidity (product of breaking down ATP) – increased K+ ion concentration – increased osmolarity – adenosine release – prostaglandin release • Local vasoactive mediators also have an effect Local physical changes that influence arteriolar radius. – heat produces vasodilation – cold produces vasoconstriction. – Arteriolar smooth muscle that is passively stretched increases its tone. – By reactive hyperemia, arterioles in a region dilate when other local blood vessels are blocked. – By pressure autoregulation local mechanisms in the arterioles keep blood flow constant when there are wide variations in the mean arterial blood pressure driving the blood. Extrinsic sympathetic signaling • controls arteriolar radii – This regulates blood pressure – Sympathetic neurons supply the smooth muscle in the walls of most arterioles. • Increased sympathetic signaling produces generalized arteriolar vasoconstriction. – increases the total peripheral resistance (TPR) • Many arterioles constrict to produce this effect • Organs supplied by these constricting vessels receive less blood flow • However, some arterioles serving organs (e.g., skeletal muscles during exercise) dilate during this increase in TPR MAP II • Mean arterial pressure (MAP) equals: – cardiac output x TPR – As the TPR increases, • the mean arterial pressure increases by direct proportion • arterioles serving organs (e.g., skeletal muscles during exercise) that dilate during TPR increase receive more blood as the MAP increases. alpha-1 receptors • Binding produces vasoconstriction • Cerebral vessels lack these kind of receptors. • subject to local controls • Skeletal and cardiac muscle tissue have local control mechanisms that override generalized sympathetic control mechanisms • Parasympathetic innervation is absent at arterioles. • Low sympathetic tone: vasodilation • Lots of sympathetic tone: vasoconstriction cardiovascular control center • The medulla – the integrating center for sending signals through sympathetic motor pathways to the arterioles – medulla regulates blood pressure along with several hormones • Epinephrine and norepinephrine – reinforce sympathetic activity – secreted by the adrenal medulla • Vasopressin and angiotensin – Vasoconstrictors – Vasopressin controls water balance. – Angiotensin controls salt balance. • Where salt goes, water goes in the body. Capillaries • exchange accomplished mainly by diffusion – enhanced by thin walls and narrow openings of capillaries, plus their branching – Capillary walls – single, flat layer of epithelial cells – called the endothelium – Have pores – can allow water & ions to pass – Capillaries are very abundant – large surface area to serve cells • The blood through capillaries is slow – due to the tremendous cross-sectional area of all capillaries in an area – enhances the opportunity for diffusion – Compared to arterioles, – resistance offered by capillaries is low due to the large cross-sectional areas of these microscopic vessels. – Capillaries have smaller radius so less resistance Capillary pores • allow the passage of small, water-soluble substances – E.g. ions and glucose. – Lipid-soluble substances dissolve through the lipid bilayer. • Tight junctions connect the walls of capillary cells in the brain and form the blood-brain-barrier. • Histamine increases capillary permeability. Capillary blood flow control • Precapillary sphincters surround capillaries – A sphincter is a ring of smooth muscle around the entrance to a capillary – contraction of these sphincters reduces the blood flowing into the capillaries in an organ • The relaxation of these sphincters (e.g., an exercising skeletal muscle) has the opposite effect. • A metarteriole is a thoroughfare channel from an arteriole to a capillary – Some capillaries are served by them. Blood pressure is regulated. • mean arterial pressure = cardiac output x total peripheral resistance • Cardiac output – heart rate x stroke volume – Heart rate depends on autonomic control plus some hormone signaling. – Stroke volume depends on sympathetic stimulation. – Stroke volume also increases by venous return. – Venous return depends • several factors – such as venous vasoconstriction and the skeletal muscle pump. Total peripheral resistance • depends on the radius of arterioles plus blood viscosity • radius size depends on – sympathetic stimulation to the arterioles – local metabolic/chemical – hormonal controls. • Effective circulating blood volume influences the blood volume returning to the heart. – This blood volume depends on capillary exchange which in the long term means controlling salt and water balance. – Mean arterial pressure is controlled by long-term and short- term measures. The baroreceptor reflex • Is a short-term mechanism for regulating blood pressure. • Baroreceptors are found in the carotid sinus and aortic arch. – sensitive to fluctuations in pulse pressure – Baroreceptors generate action potentials through afferent pathways to a cardiovascular (integrating center) in the medulla. – autonomic nervous system – center in the medulla alters the ratio of sympathetic and parasympathetic activity to the heart and blood vessels. • Systolic – diastolic = pulse pressure • If you have a greater pulse pressure this reflex will notice The baroreceptor reflex. • Arterial blood pressure becomes elevated (opposite for drop) • Baroreceptors detect this change – increase the rate of action potentials firing along afferent pathways from the receptors to the medulla. – The cardiovascular center interprets this input. – Sympathetic output decreases. – Parasympathetic output increases. – decrease in – heart rate, – stroke volume, – arteriolar resistance – venous resistance (veins dilate) – Cardiac output and total peripheral resistance decrease. • The elevated blood pressure returns to normal. Other reflexes and responses influence blood pressure. • Left atrial receptors and hypothalamic osmoreceptors regulate salt and water balance. – control plasma volume for long-term blood pressure regulation. – Chemoreceptors in the carotid and aortic arteries – sensitive to low oxygen and high acid levels in the blood – increase respiratory activity to reverse these trends. – Behaviors and emotions from the cerebral cortex/hypothalamus influence cardiovascular responses. • Exercise modifies cardiovascular responses. • The hypothalamus controls skin arterioles for temperature regulation. • Vasoactive substances have an effect. Hypertension (too high of a blood pressure) • cause largely unknown • Secondary hypertension – secondary to other primary problems – categories are • renal (from the renin-angiotensin mechanism), • cardiovascular, • endocrine, • and neurogenic. • 90 percent of hypertension cases are primary – Potential causes include: • defects in salt management by the kidneys • excessive salt intake • diets low in fruits, vegetables, and dairy products • plasma protein abnormalities • variation in the gene that encodes for angiotensinogen • endogenous digitalis-like substances Hypertension (continued) • Baroreceptors adapt to hypertension. – regulate blood pressure, maintaining it at a higher level. – excess vasopressin – Can cause hypertension – Regulates water channels in kidneys Complications of hypertension – congestive heart failure – stroke – heart attack – Without complications, hypertension is without symptoms. – It can be treated with therapy. • Orthostatic hypotension results from transient inadequate sympathetic activity. – This is a fall in blood pressure. Circulatory shock • when blood pressure drops to a point where blood flow becomes inadequate. • There are four main types: – hypovolemic - caused by a fall in blood volume – cardiogenic - due to a weakened heart – vasogenic - from widespread vasodilation due to a release of vasodilator substances – neurogenic - from widespread vasodilation, but not from the release of vasodilator substances – Compensatory measure for circulatory shock include: – baroreceptor reflex with increased sympathetic activity and decreased parasympathetic activity to the heart ( heart rate) – fluid shifts in the capillaries and interstitial fluid (autotransfusion) – responses by the liver, urinary system, and thirst sensation Veins return blood to the heart. • large radii • low resistance • velocity of blood flow increases in the veins, – smaller total cross-sectional area. – veins are thinner-walled and less elastic. – Veins are capacitance vessels, serving as a large blood reservoir. • highly distensible, able to accommodate large volumes of blood. – hold 60% of the blood volume of the body at rest. – Extrinsic factors can drive this blood to the heart for pumping. Venous return – the volume of blood entering each atrium per minute. • Venous return is enhanced by: – increased sympathetic stimulation of the veins; • vasoconstriction – increased skeletal muscle activity; • compresses veins and increases venous pressure • Various mechanisms counteract the effect of gravity on venous return. – The closure of valves inside veins ensures that blood does not flow backward. – The respiratory pump creates a pressure gradient in the chest cavity, drawing fluid toward the heart. • See Figures 10-30 and 31 The interstitial fluid • 20 percent of the ECF is blood plasma. • 80 percent of the ECF is interstitial fluid located between the cells. • Exchange between the interstitial fluid and plasma membranes of tissue cells can be active (e.g., active carrier-mediated transport) or passive (e.g., diffusion). • Exchange across the capillary wall, between the plasma and interstitial fluid, is largely passive. • Diffusion across the capillary walls is important in solute exchange (e.g., gases). – Only the passage of plasma proteins is limited. – Some substances cross the capillary wall by bulk flow (from higher fluid pressure to lower fluid pressure) Starling’s Hypothesis • implies that, – through a semi-permeable capillary wall, – hydrostatic pressure shifts fluids outwards, – while the oncotic pressure of the plasma albumin (protein) holds fluid within the capillary. – (Starling Forces) The capillary wall acts as a sieve • Plasma proteins remain in the capillary – unable to pass through the pores in the capillary wall. – reabsorption – net inward movement of fluid from the interstitial fluid into the capillary. – Hydrostatic pressure is greater than oncotic pressure at the beginning of the capillary – After we’ve lost fluid at the end of the capillary, the oncotic pressure is greater than the hydrostatic pressure which causes reabsorption – occurs when inward-driving pressure exceeds an outward opposing pressure Bulk Flow • Capillary blood pressure: The hydrostatic pressure exerted on the inside of capillary walls by the blood. – This forces fluid out of the capillaries (the outward pressure). – The plasma-colloid pressure: Encourages fluid movement into the capillaries (the inward pressure). – The plasma has a higher protein concentration compared to the interstitial fluid. – produces a water concentration difference • Water enters the plasma from the interstitial fluid by osmosis. • Bulk Flow (cont.) • The interstitial fluid hydrostatic pressure – pressure exerted on the outside of the capillary wall by the interstitial fluid. It has a small value. • The interstitial fluid-colloid osmotic pressure is also insignificant in most cases, as plasma proteins normally remain in the blood plasma (not as much protein in fluid). • arteriolar end of the capillary – outward pressure is greater than the inward pressure. – Fluid leaves the capillary by this difference. – Ultrafiltration occurs. – venule end of the capillary – inward pressure is greater than the outward pressure – outward pressure has dropped due to a drop of blood pressure at this end compared to the arteriolar end. – Reabsorption occurs. • Bulk flow regulates the distribution of fluid between the blood plasma and interstitial fluid. Edema • An accumulation (build-up) of fluid in the interstitial fluid. • Can be caused by – A reduced concentration of plasma proteins allows a drop in the main inward pressure. More fluid enters the interstitial fluid. – An increased permeability of the capillary wall allows more plasma proteins to pass from the blood fluid into the interstitial fluid. – An increased venous blood pressure increases the capillary blood pressure. This elevates the outward pressure along the capillary wall. – Blockage of lymph vessels retains fluid in the interstitial fluid rather than returning the fluid to the capillaries


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