Week 4 Reading Notes
Week 4 Reading Notes Bio Sci E109
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Bio Sci E109
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This 19 page Class Notes was uploaded by Muni Notetaker on Saturday October 24, 2015. The Class Notes belongs to Bio Sci E109 at University of California - Irvine taught by LOUDON, C. in Summer 2015. Since its upload, it has received 29 views. For similar materials see HUMAN PHYSIOLOGY in Biology at University of California - Irvine.
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Date Created: 10/24/15
Lecture 10 Sunday Bomber 18 2 15 947 PM Chapter 4 Cardiovascular Physiology T he primary function is to deliver blood to the tissues providing essential nutrients t the cells for metabolism and removing waste products form the cell 0 M the pump which generates pressure to drive the blood through a series of blood vessels 0 Arteries vessels that carry blood from the heart to the tissues an contain a relatively small amount of blood and are under high pressure 0 Veins carry blood from the tissues back to the heart under low pressure have the largest amount of blood 0 Capillaries found within the walls of tissues are interposed between veins and arteries and the exchange nutrients wastes and fluids Has multiple homeostatic functions 0 Regulation of arterial blood pressure 0 Delivers regulatory hormones 0 Regulation of body temperature 0 Homeostatic adjustments to altered physiologic states Circuitry of the Cardiovascular System Left and Right Sides of the Heart 0 Each side of the heart has two chambers an atrium and a ventricle which are connected by oneway valves called atrioventricular AV valves which allow for blood to ow in one direction from atrium to ventricle 0 Systematic circulation the left heart and the systematic veins arteries and capillaries are in charge of pumping blood to all organs of the body except the lungs 0 Pulmonary circulation the right heart and the pulmonary arteries capillaries and veins are in charge of pumping blood to the lungs 0 Blood is pumped sequentially from the left heart to the systematic circulation to the right heart to the pulmonary circulation and back to the heart Cardiac output the rate at which blood is pumped from either ventricle O Venous return rate at which blood is returned to the atria from the veins 0 In steady state the right cardiac output and the venous return equal the left and the cardiac output form the heart is equal to the venous return to the heart Blood Vessels 0 Functions 39 Serve as a closed system of passive conduits delivering blood to and from the tissues where nutrients and wastes are exchanged 39 Regulation of blood ow to the organs Circuitry Reading Notes Page 1 mum HEAJFIT LEFT EHEQR T Pulmonary artery lemmw vein up Lu r 7 g E lL High er Ln i ti39iumi 19 Tr uamquot quot M rai39 39 value p I value v Flight ventricles Left m 1 Hana E u ma 1 i III39FEIME ARTEHIES l Oxygenated blood lls the left ventricle via the mitral valve 2 Blood is ejected from the left ventricle into the aorta via the aortic valve 3 Cardiac output is distributed among various organs i The percentage of distribution is not xed 4 Blood ow from the organs is collected in the veins the vena cava 5 Venous return to the right atrium 6 Mixed venous blood lls the right ventricle via the tricuspid valve 7 Blood is ejected from the right ventricle into the pulmonary artery 8 Blood ow from the lungs is returned to the heart via the pulmonary vein Hemodynamics Hemodynamics the principles that govern blood ow in the cardiovascular system Types of Characteristics of Blood Vessels O Conduits through Which blood is carried from the heart to the tissues and from the tissues back to the heart 39 Capillaries a type of blood vessel is so thin walled the substances can exchange across them 0 The direction of blood ow is from artery to arteriole to capillaries to venule to vein Reading Notes Page 2 T l quotH39E xl39l a39ul39i FI39EII39I39I 39t national 39H39E l39l HIE E ll l Win r n f Q NEE lEilEiEIEI Ia39IEIILIiTIEa EEECI an 53 g sir i5 E a 3 E m G was a W I r El v I u Jimm Mferlea Miarlnlns Eapllelaries WINEi vernal Balm HLirr Ibm 1 11133 mi in 1n 1 Arteries function is to deliver oxygenated blood to the organs 39 Thick walled structures with extensive development of elastic tissue smooth muscle connective tissue 39 Under the highest pressure 39 Stressed volume is the amount of blood in the arteries Arterioles smallest branches of the arteries that have an extensive development of smooth muscle and they are the site of the highest resistance to blood ow 39 Where resistance can be changed by altercations in sympathetic nerve activity by circulating catecholamines and other vasoactive substances Capillaries thin walled structures that are lined with a single layer of endothelial cells which is surrounded by basal lamina 39 Site where nutrients gases water and solutes are exchanged between the blood the tissues and in the lungs between the blood and the alveolar gas 39 Not all capillaries are perfused with blood at all times Venules and Veins venules are thinwalled structures 39 The wall if the vein are composed of endothelial cell layer elastic tissue smooth muscle and connective tissue 39 Veins have the largest percentage of blood in the cardiovascular system Reading Notes Page 3 39 Unstressed volume the volume of blood contained in the veins Velocity of Blood Flow 0 The rate of displacement of blood per unit time it f where it Flunit Lil blimtl aw muf ed El Flow ij39IE EHE Er area Em 39 Velocity of blood ow v linear velocity and refers to the rate of displacement of blood per unit time cm sec 39 Flow Q volume ow per unit time mL sec 39 Area A crosssectional area of a blood vessel or a group of blood vessels Iul 1m 1m mum I quot Ema t 1 cm 1E3 C1112 rm torn Flow 1 1E mLfser 1D mussec 1121 mLiser Willem v 1 1 n1 39 As vessel diameter increases the velocity of ow through the vessel decreases Relationships between Blood Flow Pressure and Resistance 0 Pressure difference and resistance determine the blood ow through a blood vessel or a series of blood vessels 39 Pressure difference the driving force for blood ow the inlet and the outlet 39 Resistance impediment to ow 1 135 Iiquot where J l iuw Eml min 53F Pregame differeme rim Hg Iiiquot Jrlio iamnnn mm liigfmlhfmirt 39 Blood ow Q is directly proportional to the size of the pressure difference P 39 Resistance R is inversely proportional to blood ow III By changing the resistance of blood vessels arterioles the blood ow in the cardiovascular system can be changed III Total peripheral resistance resistance of the entire systematic vasculature which can be measure with the ow pressure and Reading Notes Page 4 resistance relationship by substituting cardiac output for ow and the difference in pressure III Resistance in a single organ Resistance to Blood Flow 0 Poiseuille Equation describes the relationship between resistance blood vessel diameter and the blood viscosity 0 The total resistance is dependent on whether the vessels are arranged in series or in parallel Poiseuille Equation R 8 Kr where R Resistance 1 Viscosity of lll Length of blood vessel Radius of blood vessel raised to the fourth power r 39 Viscosity is directly proportional to resistance ow 39 Length is directly proportional to resistance ow 39 Fourth power of the radius is inversely proportional to the resistance ow Series and Parallel Resistances 39 Series resistance each organ is supplied with blood by a major artery and drained by a major vein III Total resistance of the system arranged in series is equal to the sum of the individual resistances III The total ow through each level of the system is the same III Although total ow is constant at each level in the series the pressure decreases progressively as the blood ows through each sequential component The greatest decrease occurs in the arterioles 39 Parallel resistance the distribution of blood ow among the various major arteries branching off the aorta Simultaneous blood ow through each of the circulations III The total resistance in a parallel arrangement is less than any of the individual resistances III When blood ow is distributed through a set of parallel resistances the ow through each organ is a fraction of the total blood ow III No loss of pressure in the major arteries Adding resistance to the circuit causes total resistance to decrease If the resistance of one of the individual vessels in a parallel arrangement increase then total resistance increases Pressures in the Cardiovascular System 0 Blood would not ow if the blood pressure were equal through the cardiovascular Reading Notes Page 5 system because the pressure is the driving force of blood ow Pressure Pro le in the Vasculature Decrease in pressure occurs as blood ows through the vasculature because energy is consumed in overcoming the frictional resistances Mean pressure is high in the aorta which is due to two things III The large volume of blood pumped from the left ventricle into the aorta III The low compliance of the arterial wall The large arteries have high pressure because of the elastic recoil of the arterial walls thus energy is lost as blood ows from the aorta through the arterial tree Arterial pressure decreases in the small arteries with the highest amount of decrease located in the arterioles Capillaries the pressure decreases further due to two reasons III Frictional resistance to ow III The ltration of uid out of the capillaries Pressure decreases even further when it reaches the venules and veins Pressures in the Pulmonary Circulation The entire pulmonary vasculature is at much lower pressure than the systemic vasculature Pressure is highest in the pulmonary artery and decreases as the blood ows through Pulmonary vascular resistance is much lower than systemic vascular resistance Reading Notes Page 6 Lecture 11 39Menday ct ber 19 Z 15 1224 PM IChapter 4 Cardiovascular Physiology Cardiac Electrophysiology Includes all of the processes involved in the electrical activation of the heart The function of the heart is to pump blood through the vasculature and for the heart to serve as a pump the ventricle must be electrically activated and then contract Electrical activation is cardiac action potential which originates in the sinoatrial node Contraction then follows in a sequence that is critical because the atria must be activated and contract before the ventricles which must occur before the apeX Cardiac Action Potentials Origin and Spread of Excitation within the Heart 39 There are two kinds of muscle cells in the heart III Contractile cells the majority of the atrial and ventricular tissues and are the working cells of the heart Action potentials lead to contraction and generation of force or pressure D Conducting cells constitute the tissues of the SA node the atria internodal tracts the AV node the bundle of His and the Purkinje system They are specialized cells that do not contribute significantly to generation of force they instead function to rapidly spread action potentials over the entire myocardium 9 Capacity to generate action potentials spontaneously li ll mi quot1ng THJHFE39nll39EIHJLEI39J E39I E rd uJquot LEI WEE mranm Ei 39l mr j a 39n W it warm 11 t n a u 39 Purl3111a INDEE Reading Notes Page 1 1 2 3 4 SA Node the action potential of the heart is initiated in the specialized tissue of the SA Node which serves as the pacemaker There is a speci c sequence and timing for the conduction of action potentials to rest of the heart Atrial internodal tracts and atria action potential spreads from the SA node to the right and left atria via the atrial internodal tracts Simultaneously the action potential is conducted to the AV node AV Node conduction of velocity is slower here than in the other cardiac tissues Slow conduction through the AV node ensures that the ventricles have sufficient time to fill with blood before they are activated and contract Increase in conduction velocity here results in decreased ventricular filling and decreased stroke volume and cardiac output Bundle of His Purkinje system and ventricles action potential enters the conducting system of the ventricles however first conducted in bundle of His It then invades the Purkinj e system which occurs fast to rapidly distribute the action potential to the ventricles Normal sinus rhythm the pattern and timing of the electrical activation of the heart are normal because the follow three criteria are met III The action potential originates in the SA node III The SA nodal impulses occur regularly at a rate of 60 to 100 impulses per minute III The activation of myocardium occurs in the correct sequence and in the correct timing and delays Concepts Associated with Cardiac Action Potentials 1 2 3 4 5 6 The membrane potential of the cardiac cells is determined by the relative conductance to ions and the concentration gradients for the permeant ions Equilibrium potential will occur when the cell membrane is permeable to an ion that ows down its electrochemical gradient Membrane potential is expressed in mV The resting membrane potential of cardiac cells is determined primarily by K ions At the rest the conductance of K is high and the resting membrane potential is close to the K equilibrium potential The Na conductance is low at rest therefore contributes little to the resting membrane potential Na K ATPase maintains the Na and K concentration gradients across the cell membrane however makes a small direct electrogenic contribution to the membrane potential Changes in membrane potential are caused by ow of ions into or out of the cell Depolarization means the membrane potential has become less negative and occurs when there is net movement of positive charge into the cell called inward current Hyperpolarization is when the Reading Notes Page 2 membrane potential has become more negative and occurs when there is net movement of positive charge out of the cell called outward current 7 There are two ways to produce a change in membrane potential Change in the electrochemical gradient for a permeant ion and the change in conductance to an ion 8 Threshold potential is the potential difference at which there is a net inward current which gives rise to the upstroke of the action potential Action Potentials of Ventricles Atria and the Purkinje System 39 The action potential in these tissues share the following characteristics III Long duration the duration of the action potential determines the duration of the refractory period therefore they have longer refractory periods Stable resting membrane potential III Plateau a sustained period of depolarization which accounts for the long duration of the action potential and consequently the long refractory period 39 Phases of the action potential Membrane mmmial my C i FUTEHTEA LE Hem EIa A Irium 321 1 1 39rl 13 2 4m u 395quot mar i a mum I l 1 l El Pu 1cm mam l mu minus D Phase 0 upstroke action potential begins with a phase of rapid depolarization called upstroke Q Q O This is caused by a transient increase in Na conductance which leads to an inward Na current which drives the membrane potential toward the Na equilibrium potential however not reaching due to the closing of the inactivation gates The rate of rise of the upstroke is called dVdT which is the rate of change of the membrane potential as a function of time and its units are Vsec Variation occurs depending on the resting membrane potential called the responsiveness relationship dVdT is greatest when the resting membrane potential is most negative dVdT also correlates with the size of the inward current Reading Notes Page 3 III Phase 1 initial repolarization brief period of repolarization which is followed after the upstroke The inactivation gates of the Na channels close causing a decrease in Na current and there is an outward current of K which is caused by the large driving force of K ions III Phase 2 plateau there is a long period of relatively stable depolarized membrane potential which no net current ow across the membrane 9 There is an inward Ca2 current that occurs because of the opening of the Ltype channels which are inhibited by the Ca2 channel blockers This is balanced by outward K current driven but he electrochemical driving force on K ions The release of Ca2 stores for the excitationcontraction coupling called Ca2 induced Ca2 release III Phase 3 repolarization repolarization results from a decrease in Ca2 and an increase in the outward K current with K moving down a steep electrochemical gradient At the end the outward K current is reduced because repolarization brings the membrane potential closer to the K equilibrium potential decreasing the driving force D Phase 4 resting membrane potential or electrical diastole The membrane potential is once again stable and the inward and outward currents are equal Action Potentials in the Sinoatrial Node 39 What features of the action potential of the SA node are different from those in atria ventricles and Purkinj e bers III The SA node exhibits automaticity spontaneously generate action potentials without neural input III Unstable resting membrane potential III No sustained plateau 39 Phases of the SA node action potential SlumFm Ii39i atl i m rm l in Er 7 a 4 inter is aniufnu any I I C mu mam Reading Notes Page 4 Phase 0 upstroke result of the increase of Ca2 and inward Ca2 current Phase 1 and 2 are absent Phase 3 repolarization due to an increase in K because of the electrochemical driving forces on K there is an outward K current which repolarizes the membrane Phase 4 spontaneous depolarization or pacemaker potential the longest portion of the SA node action potential Accounts for automaticity and the most negative value of the membrane potential is approximately 65mV called maximum diastolic potential 9 There is depolarization by the opening of Na channels and inward Na current 9 The rate of phase 4 depolarization sets the heart rate Latent Pacemakers 39 Include cells of the AV node bundle of His and Purkinj e bers which have automaticity 39 Overdrive suppression when the SA node drives the heart rate and the latent pacemakers are suppressed 39 Ectopic pacemaker ectopic focus when latent pacemaker takes over and becomes the pacemaker of the heart III III I SA node ring rate decreases or stops The intrinsic rate of ring of one of the latent pacemakers should become faster than that of the SA node The conduction of action potentials from the SA node to the rest of the heart is blocked because of disease in the conducting pathways Autonomic Effects on the Heart and Blood Vessels 0 Effects the heart rate conduction velocity myocardial contractility and vascular smooth muscle Sympathetic RammedHie Hemmer Witmtt39 tt Wartime Heart rate T T Ir 1 M J I T m Be an t t nnttiue tett veiledin 39T it T IEd 1 Ma 4 in Ii H212 Eu39iti eetllit39gt T t 1quot I 1 atria lli y Ml i ZF39hnepherylatien 11f T i J phneplmlmmlmn iiieuiihtr emmth nueele timetthninn mi littletten ttelteasee Mg m 39EltitIL rental i ll ti lili i splattelmie vesicular emmth muscle Dilatim if Dilatimt t elleagee Mk eh010ml mtttelle REEF Fitne39trietimt t1 Electrocardiogram O ECG or EKG is a measurement of tiny potential differences on the surface of the body that re ect the electrical activity of the heart Reading Notes Page 5 39 These are measurable due to the timing and sequence of depolarization and repolarization of the heart R l N 4 A v v Interval 39 P Wave represents depolarization of the atria and correlates With conduction time through the atria 39 PR interval the time from initial depolarization of the atria to initial depolarization of the ventricles This includes the P wave and PR segment isoelectric at portion of the ECG that corresponds to AV node conduction 39 QRS Complex consists of three waves Q R and S Represent the depolarization of the ventricles 39 T Wave repolarization of the ventricles 39 QT interval includes the QRS complex the ST segment and the T wave Represents the rst ventricular depolarization to the last ventricular repolarization III ST segment is an isoelectric portion of the QT interval that correlates With the plateau Heart rate measured by counting the number of QRS complexes per minute Cycle length RR interval Arrhythmia abnormal heart rate Which can be caused by increased heart rate Which leads to refractory periods that are shortened Reading Notes Page 6 Lecture 12 Memc ayp ct ber 19 2 15 1229 PM Chapter 4 Cardiovascular Physiology Cardiac Muscle Contraction Myocardial Cell Structure 0 The cardiac muscle is composed of sarcomeres which are composed of thick and thin laments 39 Thick laments are composed of myosin which have the actinbinding sites and ATPase activity 39 Thin laments are composed of three proteins actin tropomyosin and troponin III Actin globular protein with a myosin binding site III Tropomyosin is located on actin and functions to block the myosin binding site III Troponin globular protein composed of a complex of three subunit 0 Sliding lament model when cross bridges form between myosin and actin and then break the thick and thin laments move past each other which allows for contraction 0 Transverse T tubules invaginate cardiac muscle cells at the Z lines are continuous with the cell membranes and function to carry action potentials to the cell interior 0 Sarcoplasmic reticulum site of storage and release of Ca2 for excitationcontraction coupling ExcitationContraction Coupling Reading Notes Page 1 Eardliae action untiemial Zakinduced Gag releaee from SE3 239 reaccumulated in ER Fielaxatimi E 1 E U I I U E 1 ii Grnaerbridge walling 1 Cardiac action potential is initiated in the myocardial cell membrane and the depolarization spreads to the interior of the cell via the T tubules 2 Entry of Ca2 into the myocardial cell produces an increase in intracellular Ca2 concentration which is no suf cient alone to initiate contraction but it triggers the release of more Ca2 form the sarcoplasmic reticulum 3 Combined 3 and 4 Ca2 is released from the sarcoplasmic reticulum which causes the intracellular Ca2 concentration to increase even further Ca2 then binds to troponin C and tropomyosin is moved out of the way which allows crossbridges to form and the break 5 The magnitude of the tension developed by the myocardial cells is proportional to the intracellular Ca2 concentration 0 Relaxation occurs when Ca2 is reaccumulated in the sarcoplasmic reticulum by the action of the Ca2 ATPase LengthTension Relationship in Cardiac Muscle O The maximal tension that can be developed by a myocardial cell depends on its resting length 0 In addition to the degree of overlap of thick and thin laments there are two additional methods 39 Increasing muscle length increases the Ca2 sensitivity of troponin C 39 Increasing muscle length increase Ca2 release from the sarcoplasmic reticulum O The lengthtension relationship for single myocardial cells can be extended to a lengthtension relationship for the ventricles Reading Notes Page 2 Va maria ular pmaau r5 V il i r arr r astnliie Upper curve the relationship between ventricular pressure developed during systole and enddiastolic volume This is an active mechanism Shows greater degrees of overlap of thick and thin laments greater crossbridge formation and cycling and greater tension When overlap is maximal the curve level39s off Cardiac muscle only operates on the ascending of the curve because the cardiac muscle is stiffer than the skeletal muscle therefore having a higher tension FrankStarling relationship systolic pressurevolume relationship for the ventricle Lower curve the relationship between ventricular pressure and ventricular volume during diastole when the heart is not contracting III Preload for the left ventricle is left ventricular enddiastolic volume which is the resting length from which the muscle contracts III Afterload for the left ventricle is aortic pressure Velocity of shortening of cardiac muscle is maximal when afterload Is zero and the velocity of shortening decreases as afterload increases Stroke Volume Ejection Fraction and Cardiac Output 0 Function of the ventricles is described by the following three parameters stroke volume ejection fraction and cardiac output Stroke volume volume of blood ejected by the ventricle on each beat Ejection fraction fraction of the enddiastolic volume ejected in each stoke volume which is a measure of ventricular efficiency Cardiac output the total volume ejected by the ventricle per unit time Ejection Fraction The effectiveness of the ventricle in ejecting blood The fraction of the enddiastolic volume that is ejected in one stroke volume Normally 55 an indicator of contractility with increases in ejection fraction re ecting an increase in contractility and decreases in ejection fraction re ecting a decrease in contractility Reading Notes Page 3 Emeline ealume Ejeeiien i raeiin m a E emdLel laetlle elume Cardiac Output 39 Total volume of blood ejected per unit time 39 Depends on the volume ejected on a single beat and the number of beats per minute 39Eareliae e uipui Strel ee V lumex Heart rate WhE fE ardiae enamelquot 1IiquotII1nm1e ejeeleei per minute mLJmim litrake eefllmue Eahrme ejeeleui in ne hear mm Heart rate Beale er minute treai39eg39rnim Ventricular PressureVolume Loops Normal Ventricular PressureVolume Loop 39 Function of the left ventricle can be observed over an entire cardiac cycle by combining two pressurevolume relationships called a ventricular pressurevolume loop e E 115a a El E is TE a 2 U E i E ll a e l 39 I 39 Ia ea 1e 1e Leii e39enilriieealr lu39 lum m ILjI 39 The dashed line shows the maximum possible pressure that can be developed for a given ventricular volume during systole 39 The ventricular pressurevolume loop describes one complete cycle of ventricular contraction ejection relaxation and refilling D Isovolumetric contraction 1gt 2 1 marks the end of diastole the left ventricle has lled with blood from the left atrium and the volume it is the enddiastolic volume Ventricle is activated because pressure is low and contraction occurs resulting in an increase in pressure however the volume remains constant III Ventricular Ejection 2gt3 At 2 left ventricular pressure becomes higher than aortic pressure causing the aortic valve to open Once ventricular pressure reaches the value of aortic pressure the aortic valve opens and the rest of the contraction is used for ejection Left ventricular pressure remains high because the ventricle is still contracting and ventricular volume decreases Reading Notes Page 4 Width of the pressurevolume loop the volume of blood ejected or the stroke volume III Isovolumetric Relaxation 3gt4 point 3 the systole ends and the ventricle relaxes and the pressure decreases below the aortic pressure and the valve closes Ventricular volume remains constant at the endsystolic value because all the valves are closed again III Ventricular Filling 4gt1 Point 4 ventricular pressure has fallen to a level that now is less than left atrial pressure causing the mitral AV valve to open The left ventricle T1118 with blood and the left ventricular volume increase back to the end diastolic volume The ventricular muscle is relaxed and pressure increases Changes in Ventricular PressureVolume Loops WEEDEl 39 LIE HE File ul f f EEIJr i Pg LEI I EEFIiI IEIiLIJEF39lr lum B LiaTE mntnzcutar 393 M11 Emma 39IIEEUFITE 39 Ventricular pressurevolume loops can be used to visualize the effects of changes in preload afterload or contractility 39 Solid lines depict a a single normal ventricular cycle and are identical to the pressure volume loop 39 The dashed line shows the effects of various changes on a single ventricular cycle III A increased preload because venous return is increased which increase the end diastolic volume point 1 Afterload and contractility remain constant III B increased afterload or increased aortic pressure on the ventricular cycle The left ventricle must eject blood against a greater pressure This results in less blood being ejected from the ventricle during systole III C increased contractility on the ventricular cycle When contractility increases the ventricle develops a greater tension and pressure during systole and eject in larger volume of blood than normal Cardiac Cycle 0 There are 7 phases in the cardiac cycle Reading Notes Page 5 F fiuu ri i r39l39l l Hill I Atrial Systole A 0 An atrial contraction which is preceded by the P waver Which marks the depolarization od the atria O Contraction of the left atrium cause an increase in left atrial pressure Which is re ected back in the veins and appears as a wave The left ventricle remains relaxed because the mitral valve is opened and the ventricle is lling With blood from the atrium 0 Fourth heart sound is produced Isovolumetric Ventricular Contraction B O Begins during QRS complex Which represents the electrical activation of the ventricles When the left ventricle contracts the pressure begins to increases and once it exceeds the left atrial pressure the mitral valve closes 0 First heart sound is produced Rapid Ventricular Ejection C O Ventricle continues to contract and the ventricular pressure reaches its highest value and higher Reading Notes Page 6 0 than aortic pressure causing the aortic valve to open Blood rapidly ejects from the left ventricle into the aorta through the valve which results in the aortic pressure increase Atrial lling begins and the left atrial pressure slowly increases as blood is returned to the left heart from pulmonary circulation Reduced Ventricular Ejection O The ventricles begin to repolarize which is marked by the beginning to of the T wave Ventricular pressure falls since the ventricles are no longer contracting and blood continues to be ejected since the aortic valve is still open Ventricular volume begins to decrease and the left atrial pressure increases as the blood returns to the left heart from the lungs Isovolumetric Ventricular Relaxation O O Begins after the ventricles are fully repolarized marked by the end of the T wave When the left ventricular pressure decreases below the aortic pressure the aortic valve closes before the pulmonic valve Second heart sound is produced Rapid Ventricular Filling 0 0 When the ventricular pressure falls to its lowest level the mitral valve opens and the ventricle begins to fill with blood and the volume increases rapidly Ventricular pressure however remains low because the ventricle is relaxed The aortic pressure begins to decrease as blood runs off from the aorta into the atrial tree Third heart sound is produced Reduced Ventricular Filling Diastasis O Longest phase in the cardiac cycle and includes the final portion of the ventricular filling which occurs at a slower rate than the previous phase Changes in heart rate alter the time available for diastasis because it is the longest phase of the cardiac cycle Reading Notes Page 7
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