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Physiology Lecture Outline: Cardiovascular Physiology

The Cardiovascular System


In simplest terms, the cardiovascular system consists of a central pump (the heart) and a series of tubes (blood vessels) connected to this pump which pushes fluid (blood) through these tubes. It's primary function is the transportation of these materials between all parts of the body and the heart. These materials include nutrients, water, waste, signal molecules, immune cells and gases (O2 and O2). The Heart The heart is a muscular organ that lies in the center (left) of the thoracic cavity. It is composed mostly of myocardium (cardiac muscle) and is enclosed in the pericardial sac. The heart has four chambers, divided into left and right halves. !ach half contains an upper chamber, the atrium (for receiving blood) and a lower chamber, the ventricle (for pumping blood). One"way flow in the heart is ensured by # heart valves$ 1) the right (tricuspid) atrioventricular (%&) valve. 2) the left (bicuspid/mitral) atrioventricular (%&) valve. 3) the pulmonary semilunar valve in between the right ventricle and the pulmonary trun'. 4) the aortic semilunar valve in between the left ventricle and the aorta. The pulmonary trun' leaves the right ventricle and aorta leaves the left ventricle. (lood between the two sides do not mi). !ach of the sides contract together in a coordinated fashion, first both of the atria contract, this is then followed by both of the ventricles contracting. Arteries " are vessels that carry blood away from the heart. Veins " are vessels that carry blood toward the heart. % ring of fibrous connective tissue (called the fibroskeleton) surround the openings between the top and bottom chambers. The fibros'eleton has several functions$ 1. *rovides a site of attachment for %& valves and helps 'eep theses openings patent during contraction. 2. +aintains integrity of the shape of the heart when ventricles contract, while allowing the ape) and the base to be pulled together 3. It electrically separates (insulates) the atria from the ventricles, thus guarding against the spread of electrical signals that are not through the intrinsic electrical conduction system (discussed later). The Heart Functions as a Dual Pump: The Circuits of the Heart ,ithin the cardiovascular system there are two circuits or circulations " the pulmonary and systemic. Pulmonary Circulation " *umps blood to and from the -ungs. Often termed the .right side. of the heart. This circuit can also be thought of as starting at the / ventricle and ending at the - atrium. Systemic Circulation " *umps blood to and from the body. Often termed the .left side. of the heart. This circuit can also be thought of as starting at the - ventricle and ending at the / atrium. &olumes and *ressures of the 0ual *ump The cardiovascular system is a closed circulatory system, and for that to e)ist, the volume of blood in both sides of the pump must be equal. The pressures of the fluid in either side of the heart, however, are very different. The pro)imity of the lungs to the heart (about # inches) means that the right pump (/ ventricle)

does not have to wor' very hard to move the blood to the lung tissue. The minimum pressure re1uired from the pulmonary circuit is normally about 25 mmH . The systemic circuit, however, is much more involved and the left pump (- ventricle) needs to wor' very hard to move the blood to every part of the body. The minimum pressure re1uired from the systemic circuit is normally about !" mmH . Therefore, the pressure generated by the left side of the heart is over three times greater than that generated by the right side. %s a conse1uence, the muscular wall of the left ventricle is about three times thic'er than the right ventricle. CA#$%AC &'SC() A*$ +H) H)A#+ There are two types of cardiac muscle cells (myocardiocytes) in the heart$ 1) autorhythmic myocardiocytes and 2) contractile myocardiocytes. %bout 23 of myocardial cells are autor,yt,mic and they spontaneously generate action potentials (%*s) without nervous stimulation. In this way, control of heart rate is considered intrinsic myogenic control " that is, derived from within the heart muscle itself. In contrast, s'eletal muscle is neurogenic " that is, it re1uires stimulation by the nervous system to initiate contraction. In cardiac muscle, input from autonomic neurons and hormones can modify the contraction rate set by the pacema'er cells and modifies the force of contraction. 4owever, the heart will contract in the absence of all neural input. %utorhythmic cells are anatomically distinct from contractile myocardiocytes. They are smaller, have few contractile fibers, organelles and contain no organi5ed sarcomeres " so they don't contribute to force generation. %bout 663 of cardiac muscle cells are contractile myocar-iocytes. These cells are striated, have organi5ed sarcomeres and have high energy demands, 278 of cell volume is mitochondria. % characteristic of cardiac muscle are that they contain intercalate- -isks, which are interdigitated membranes 9oined by desmosomes and gap junctions. The desmosomes are a type of cell attachment, so that ad9acent cells are physically attached to each other to cope with the stressful mechanical activity of the heart. :ap 9unctions are simply protein channels connecting ad9acent myocardiocytes, they allow ions to pass though and thus waves of depolari5ation to spread throughout the muscle tissue " creating nearly simultaneous contraction. ).citation/Contraction Cou0lin in Car-iac &uscle is Similar to Skeletal &uscle ontraction occurs by the same sliding filament activity as in s'eletal muscle. 4owever, an important difference is that the %* opens membrane voltage"gated a 2; channels for e)tracellular a2; entry. This entry of a2; from the ! < is re1uired for cardiac muscle contraction. Ca21/ %n-uce- Ca21 #elease In cardiac muscle, about 6=3 of the a2; used in contraction is stored in the >/, and about 2=3 comes from the ! <. The influ) of a2; from the ! < triggers release of >/ a2; stores, without the ! < a2;, no a2; would be released from the >/. The a 2; diffuses through cytosol to contractile elements and bind troponin allowing crossbridge cycling and contraction. a 2; removal re1uires a2;"%T*ase (>/). a2; removal also achieved by ?a;" a2; indirect active transporter (! <). %n Car-iac &uscle2 Contraction can be 3ra-e% single muscle fiber can e)ecute graded contractions, so that the fiber varies the amount of force it generates. :raded contractions in s'eletal muscle occur through motor unit recruitment (spatial summation) or with increased firing fre1uency of the somatic motor neuron (temporal summation). 4owever, the force generated in cardiac muscle depends on the number of cross bridges formed. ,hen cytosolic @ a2;A is low, fewer crossbridges activated, giving a wea'er force of contraction. If cytosolic

@ a A is increased, more crossbridges formed giving additional force generated. Thus, the strength of myocardial contraction is directly related to the amount of a 2; present in the cytosol. The more a2; free inside the cell the, the stronger the contraction. The cytosolic concentration of a 2; can be increased two ways$ 1) by increasing the amount of a2; that enters the cell through voltage"gated calcium channels. 2) by storing more a2; in the sarcoplasmic reticulum. Catec,olamines an- )lectrical Activity ?orepinephrine (?!) and epinephrine (!) are atecholamines. These catecholamines regulate the amount of a2; available for cardiac muscle contraction. ! and ?! bind 2 (beta"l) receptors on cardiac muscle membrane to increase force of contraction. ?! and ! increase the open probability of a 2; channels in the myocardial contractile cell, but at the same time they also increase the B; permeability, enhancing outward B; flow and terminating the plateau. Thus, ! and ?! increase a2; entry and enhance intracellular sarcoplasmic reticulum stores of a 2; without increasing the duration of the contraction. <unctionally, this ma'es sense. >ince ! and ?! also increase heart rate, it would be counterproductive to lengthen the time of cardiac contraction. ?! and ! also activate second messenger systems in myocardiocytes and trigger signal transduction which causes phosphorylation of proteins inside the cell, including a 2; channels. *hosphorylated voltage"gated a2; channels increase the probability of them opening, this allows more a2; to enter cell. P,os0,olamban is a regulatory protein on the >/ and helps to concentrate a2; in the >/. >timulation of ?! receptors (2) triggers phosphorylation of phospholamban, which then enhances the a 2;"%T*ase activity on the >/. This means that more a 2; can be stored in the >/ and more 1uic'ly. The net result is a stronger contraction and a shorter duration of cardiac contraction (heart beats faster). %nother property of cardiac muscle is that when it is stretched, it contracts more forcefully. This is due to the length"tension relationship that we have already seen in s'eletal muscle. The degree of overlap between thic' and thin filaments will effect the tension generated by that muscle cell. >tretching myocardial cells also allows more a2; entry, this also leads to a stronger contraction. The degree of stretch of myocardiocytes at any one time depends on blood volume in the chambers when filling is occurring. Action Potentials in &yocar-ial Cells ontractile cells and autorhythmic cells show distinctive %* generation. contrast to s'eletal muscle and neurons. a2; is important in the %*, in

2;

&yocar-ial Contractile Cells >table resting membrane potential ("6= m&). %ction potentials similar to those of s'eletal muscles and neurons. /apid depolari5ation is due to ?a; entry and repolari5ation due to B; efflu). % uni1ue feature of %*s in myocardial contractile cells is the absence of a hyperpolari5ation phase at the end. The myocardial cell returns directly to its stable resting membrane potential of "6= m& (the e1uilibrium potential for potassium). (ecause efflu) and influ) are e)actly balanced at "6= m&, there is no driving force to cause B ; to leave the cell and hyperpolari5e it. The myocardiocyte %* is lengthened compared to s'eletal muscle %*, due to a2; entry creating the elongated plateau phase before repolar5ation. Typical s'eletal muscle %* duration is 2"C msec but for contractile myocardial cells %* duration is about 2C= msec. +ost of this %* is in the absolute refractory period and this helps to prevent tetanus and allows chambers to fill.

41 C,annels in Contractile &yocar-ioicytes There are multiple forms of B; channel in myocardial cells, each with different properties. There are 8 channels involved in the contractile cell action potential. 1) iBl channel (inward rectifier)$ This channel is open during the resting phase. They are voltage"sensitive and begin to close when the cell depolari5es, but they are slow and do not actually close until the beginning of the plateau phase. 2) ito channel (transient outward rectifier)$ This channel opens at the end of depolari5ation and closes very rapidly. B ; efflu) through this channel is the reason for the 1uic' drop in membrane potential 9ust before the plateau. 3) iB channel (delayed outward rectifier)$ This channel open at the end of the plateau and is responsible for the repolari5ation phase. They are activated by the depolari5ation but are slow to react. Autor,yt,mic &yocar-iocytes *acema'er ability results from unstable membrane potential. It starts at "D= m& and drifts upward, this can be called a pacemaker potential. ,hen it reaches threshold ("#=m&), the cell fires an %*. The membrane potential instability is caused by .funny. (I f ) cation channels that allow ?a; and B; permeability at "D= m&, this channel allows more ?a; in than B; out and induces current flow and the drifting membrane. Open If channels creates net influ) of positive charge, depolari5ing autorhythmic cells. 0epolari5ation then closes If channels and opens a2; channels. %t threshold, many a2; channels open, thus creating a2; influ) and rapid depolari5ation. /epolari5ation is due to B; efflu) through open B; channels. The timing of %*s in these cells can be influenced by norepinephrine and epinephrine. These stimulate 2 receptors and increase ion flow in If and a2; channels. This then increases the rate of depolari5ation, which increases heart rate. % h acts on muscarinic receptors (as part of the parasympathetic division of %?>) to slow heart rate by altering B; and a2; permeability. )lectrical Con-uction System The electrical conduction system in the heart coordinates contraction. The %*s originates in one part of the strategically located autorhythmic cells and then spreads this signal between cells via gap 9unctions in intercalated dis's. The depolari5ation of muscle cells is followed by a wave of muscle contraction that passes across the atria then moves into the ventricles. The electrical conduction system consists of five ma9or sites$ 1) sinoatrial (>%) node nodeE 2) atrioventricular (%&) nodeE 3) %& (undle (of 4is)E 4) right and left bundle branchesE and 5) *ur'in9e fibers. The sinoatrial (>%) node, in the superior, posterior portion of the right atrium, initiates contraction of the heart because it fires %*s at the highest rate (see table below). <or this reason, it is called the pacemaker of heart. The internodal pathway connects >% node to atrioventricular (%&) node, located in the floor of right atrium. This connects to the %& (undle (of 4is) located in the I& septum. This then splits into right and left bundle branches running down the I& septum and finally into *ur'in9e fibers at the ape) of the heart. 0ue to the electrical insulation of the fibros'eleton, the direction of the %* is controlled and results in ape)"to"base contraction of ventricles. Thus, blood is s1uee5ed out of the ventricles from the bottom to the top of the chambers. (lood e9ection is also aided by the spiral arrangement of muscles in the walls.

The slow conduction of the electrical signal through %& node cells lengthens their refractory period, this helps to create the AV nodal delay and allows the atria to complete their contraction before ventricular contraction begins. If the >% pacema'ers malfunction and fire at a very rapid rate, %& nodal delay prevents every action potential from passing into the ventricles, in this way permitting the ventricles to function at a slower pace so that they have time to fill with blood. The >% node sets the heart rate because it fires %*s at the fastest rate and the other regions follow the lead of the >% node. If the >% node is damaged, then another pacema'er sets the heart rate. +able 1. The rate of action potentials7min for the autorhythmic myocardiocytes. These are average values for a intact heart inside a healthy individual at rest. )lectrical Con-uction S0ontaneous #ate of #e ion Action Potentials5minutes >% ?ode F="G= %& ?ode """"" %& (undle #="D= / and - (undle (ranches """"" *ur'in9e <ibers 2="#= +,e )lectrocar-io ram #eflects t,e )lectrical Activity of t,e Heart The !lectrocardiogram (! : or !B:) is a recording of the electrical activity of the heart, detected by recording electrodes placed on the s'in. (ecause the ventricles have more muscle than the atria, they create a larger electrical signal so the waves associated with the ventricles are usually larger than the waves associated with the atria. %n ! : is not a single action potential, but shows the sum of all the electrical potentials generated by all heart cells at any moment. >ome basic definitions for an !B: trace$ >egment H a straight line. ,ave H a deflection from the straight line (= milivolts). Interval H a segment and a wave. omple) H a series of waves. +,e &ain Com0onents of an )C3 P 6ave7 0epolari5ation in the atria. 8#S com0le.7 0epolari5ation of ventricles (and atrial repolari5ation, typically mas'ed on the ! :). + 6ave7 /epolari5ation of the ventricles. P8 or P# interval7 /epresents %& nodal delay. +/P se ment7 &entricular diastole (filling). In -ab we perform !B:s on fellow students using the &ernier -ab pro computer program. ?o two !B:s will be identical or e)actly li'e a InormalJ e)ample but there are fundamental properties that are shared amongst all InormalJ !B: traces. In the lab manual, there is a normal trace, indicating the typical orientation (up or down), amplitude (height) and duration (time interval) of the segments, interval, wave and comple)es. +echanical events lag slightly behind their electrical signals. %trial contraction begins really as the * wave ends and continues during *"/ segment. &entricular contraction begins 9ust after K wave and continues through >"T segment. ommon terms include$ tac,ycar-ia " fast heart rate (above 2==)E bra-ycar-ia " slow heart rate (below D=). %t very rapid heart rates, there may be less blood pumped per beat because the muscle has not had time to rela) completely, but remember, the longer refractory period of myocardial cells

prevents tetanusL Tetanus would not allow the heart to rela) at all. In that state, no blood would be pumped to the brain and the rest of the body. Arr,yt,mias can result from benign e)tra beats or more serious conditions discussed in lab. +H) CA#$%AC C9C() The cardiac cycle is the period of time from the beginning of one heartbeat to the beginning of the ne)t. There are two main stages$ $iastole " the time during which cardiac muscle rela)es and Systole " the time during which cardiac muscle is contracting. %tria and ventricles do not contract at same time, but each side of the heart contracts at the same time. <or convenience, the cardiac cycle can be divided into C stages. Atrial an- Ventricular $iastole7 +,e Heart at #est The heart is at rest and the atria and ventricles are rela)ing. The atria are filling with venous blood. The %& valves open as ventricles rela) and blood flows by gravity from atria to ventricles. 0uring this phase, the ventricles are about G=3 of filled with blood, this is termed passive filling. Atrial Systole7 Com0letion of Ventricular :illin ,hen the atria contract (systole), the remaining 2=3 of blood fills the ventricles, this is li'e a .topping off. of the ventricles. %trial systole begins following depolari5ation of the >% node, as a wave of depolari5ation (electrical signal) across the atria is followed by a wave of contraction that pushes blood into the ventricles to complete ventricular filling. >ome blood is forced bac' into veins, creating a small retrograde blood movement, measured as a pulse in the 9ugular vein. %t this time, 9ust prior to ventricular systole (the ne)t stage), the ventricles are full of blood, this is termed !nd 0iastolic &olume ()$V) and represents the ma.imum ventricular volume. %t rest in a F= Bg male, this value is typically 28Cml in each ventricle. Clinical Note: Because most of ventricular filling occurs passively pathologies in !hich atrial contraction is disturbed may have very little effect on overall cardiovascular function" #t is not uncommon for people !ith atrial fibrillation to have fe! symptoms" )arly Ventricular Systole ;0art one) an- t,e :irst Heart Soun&entricular systole begins at the ape) of the heart as spiral bands of muscle s1uee5e blood upward toward the base. The increasing pressure of the blood in the ventricles forces the %& valves closed " creating the first heart sound, the .lub. of .lub dub.. (oth ventricles are now 'sealed' compartments in that the %& and semilunar valves are closed. The ventricles are continuing to contract, but if all valves are closed, the blood goes nowhere. The heart is in %sovolumic Ventricular Contraction. This occurs when the blood volume inside the ventricles remains the same (prefi) iso" means 'same'), but pressure is increasing. 0uring this phase, the atria repolari5e and rela) as the ventricles continue to contract. Ventricular Systole ;0art t6o)7 Ventricular )<ection ,hen ventricular contraction generates enough pressure it opens the semilunar valves, and blood enters arteries (/& MN pulmonary trun'7artery, -& MN aorta). The high"pressure blood is forced into the arteries (e9ection of blood from ventricles), which displaces lower"pressure blood, creating blood movement. /emember that each ventricle has e1uivalent blood volumes but different pressures. The /& re1uires a min of 2C mm4g and the -& re1uires a min of G= mm4g to open the semilunar valves. %t these respective pressures, the pressure gradient which drives blood flow is established. %t this time, 9ust after ventricular systole, the ventricles have 9ust e9ected blood but the ventricles do not empty. In fact, at rest they only e9ect about half of the blood volume in the ventricle. The blood volume

remaining in the ventricles after e9ection is termed !nd >ystolic &olume ()SV). % typical value for a F= Bg male at rest is about DCml per ventricle that remains in the heart after e9ection. ,e can calculate how much blood left the heart (called Stroke Volume) if we 'now the ma)imum volume, !0&, and subtract the volume remaining after contraction, !>&. This means that about F=ml of blood is e9ected per beat. >ee calculation below from this formula$ Stroke Volume ;SV) = )$V / )SV Ventricular $iastole an- t,e Secon- Heart Soun%s the ventricles rela), the pressure of the blood inside decreases. The blood in the large arteries leaving the ventricles falls bac' toward the heart as the driving force subsides. This reversal of blood toward the heart fills the cusps of the semilunar valves, slamming them closing them " creating the second heart sound, .dub. of .lub dub.. The %& valves remain closed because ventricular pressure is still greater than the atrial pressure. %s the ventricles rela), the pressure of the blood inside decreases and once the semilunar valves close, the compartment is again 'sealed'. ?ow the ventricles are undergoing %sovolumetric Ventricular #ela.ation. This is a state where pressure is decreasing but volume remains constant. ,hen ventricular pressure becomes less than atrial pressure, the weight of the blood in the atria opens the %& valves (li'e a trap door) and blood moves into ventricles. The cardiac cycle is now complete because it is at the filling stage again, where we started. $isor-ers of Heart Valves &alvular >tenosis refers to a narrowing of the opening of the valves, often associated with stiffness of the valve. In cases such as %& valve stenosis, atrial systole becomes significant. The atria must contract more forcefully to get the blood through a narrower opening into the ventricle. This causes turbulent blood flow which can be detected as sound, commonly referred to as a heart murmur. This reduces the heart's efficiency and thus increases its wor' load. &alvular *rolapse " occurs when there is incomplete closure of the %& valves, allowing retrograde flow of blood. These are often called incompetent or insufficient valves. It is an inherited wea'ness of the chordae tendineae (the 'cords' that attach to the 'flaps' of the %& valve) so that during ventricular sytole, there is sum bac' flow into the atria. Typically is ma'es a click followed by a s!ish sound when blood lea's bac' into atria. These murmurs can range from harmless to severe. +ost valvular disorders commonly occur on the left side of the heart because these valves are sub9ected to greater forces during contraction of the powerful left ventricle. <or instance, mitral valve prolapse is the most common valvular disorder. Heart #ate is &o-ifie- by Autonomic *eurons an- Catec,olamines The rhythm and rate of the heart is initiated by >% node, but modulated by neural and hormonal input. In a normal adult heart, the resting rate of the >% node is about F= action potentials (%*s) per minute, this translates to a heart rate of about F= bpm. The parasympathetic and sympathetic branches of the %?> e)ert antagonistic control over heart rate. *arasympathetic activity slows heart rate and >ympathetic activity increases heart rate and force of contraction. If the heart were separated from %?> innervation, the intrinsic rate of the >% node would actually be about 6="2== %*s per minute, but inside the body it is brought down to about F= by parasympathetic modulation via the vagus nerve. The parasympathetic division releases % h from the vagus nerve on to muscarinic receptors at autorhythmic cells of the >% and %& nodes to decrease heart rate, by increasing B; efflu). The sympathetic division releases ?! and ! on 2 receptors to increases heart rate (via %& node conduction). This can elevate heart rate up to 22= bpm and greater. Stroke Volume is t,e Volume of >loo- Pum0e- by ?ne Ventricle in ?ne Contraction >tro'e volume (ml7beat) M %mount of blood pumped by one ventricle during a single contraction. It is calculated as$ Stroke Volume ;SV) = )$V / )SV

<or e)ample, if we use the values given in the cardiac cycle describe above, we can calculate >&. If !0& M 28Cml and !>& M DCml, then >& M !0& " !>&E MN 28Cml " DCml M F=ml7beat (per beat). >tro'e volume isn't constant, it is homeostatically regulated. It can decrease when you are at rest and increase greatly during e)ercise. &ulti0le :actors %nfluence Stroke Volume >tro'e volume is directly related to the force generated by cardiac muscle during contraction. :reater force means greater stro'e volume. The force is affected by 2 parameters, 1) the length of muscle fiber at beginning of contraction and 2) the contractility of the heart. ontractility is the intrinsic ability of cardiac muscle fiber to contract at any given fiber length. (en t,/+ension #elations,i0s an- Starlin @s (a6 of t,e Heart %s the sarcomere length in cardiac muscle increases, the tension generated by the contracting muscle increases. This leads to increases in stro'e volume, as the more forceful the contraction, the greater amount of blood can be e9ected. %s additional blood flows into ventricles, this causes muscle fibers to stretch, lengthening the fibers and hence increasing the force of contraction. >tretch and force are related by the <ran'">tarling law of the heart$ >tretch (sarcomere length) is proportional to !0&. <orce is proportional to stro'e volume. Stroke Volume an- Venous #eturn The heart contracts more forcefully as additional blood enters the heart. The blood that returns to the heart from the venous circulation are termed 'venous return' and the greater the venous returnE the more forceful the heart will pump. &enous return determines !0& and this determines stro'e. The *re"load stretch is the degree of myocardial stretch created by venous return. >everal factors affecting venous return, such as the s'eletal muscle contractions (s'eletal muscle pump), this s1uee5es low pressure veins and push blood toward heart. The /espiratory pump is also a factor in venous return. It is created by the movement of thora) during respiration. Increases in pressure in abdominal veins, flow 'down' into the decreased pressure in thoracic veins. The result is that the lower thoracic pressure draws more blood in from the abdominal veins. %lso, the constriction of veins via sympathetic activity has an important impact on moving more blood into heart. >ympathetic innervation of veins allows also allows for redistribution of venous blood to the arterial side of the cardiovascular circulation. Car-iac ?ut0ut is a &easure of Car-iac Performance ardiac output ( O) is an indicator of total blood flow through the circulation. It doesn't describe blood distribution among tissues. O (-7min) M %mount of blood pumped per ventricle per unit time. It is calculated as$ C? = Heart #ate ;H#) . Stroke Volume ;SV) %t rest in a F= Bg man, O is about C -7min (average). ?ormally, both sides have e1ual O. If for some reason O's become une1ual, blood will pool behind the wea'er side of the heart. Blood Flow through the Cardiovascular System Pressure2 Volume2 :lo6 an- #esistance -i1uids and gases flow from areas of higher pressure to areas of lower pressure " that is to say, they flow do!n their pressure gradients. The high pressure generated when the ventricles contract forces blood to flow into vessels that e)ist at lower pressure. The pressure of the fluid (blood pressure) continues to fall as blood moves away from the heart. The vessels with the highest pressure are the aorta and other large systemic arteries. The vessels with lowest pressures are the veins the superior and inferior venae cavae.

Com0ressin a :lui- #aises its Pressure The 4ydrostatic *ressure (4*) of blood falls over distance as energy is lost to friction. &entricular contraction attempts to decrease volume of the ventricle as the pressure is increased. 0riving *ressure " is created within the ventricles to drive blood through the vessels. %s the heart chambers rela), pressure falls and allows blood to flow in (thus volume increases). (lood vessel volume can also change. In the body, when vasodilation (increase in blood vessel diameter) occurs this results in increased blood volume and decreased pressure. ,hen vasoconstriction (decrease in blood vessel diameter) occurs, this results in decreased blood volume and increased pressure. <or the heart, the term systole means contraction and also implies e9ection of blood. The term -iastole means rela)ation and indicates that filling of blood is occurring. >loo- :lo6s $o6n its Pressure 3ra-ient (lood flows from an area of higher pressure to one of lower pressure. 0ifferences in pressure between 2 ends of a tube creates a pressure gradient (*). <low * *2 *2

<luid flow depends on the change in pressureE *2 " *2 M *. The greater the pressure gradient, the greater the driving force for fluid flow. +,e Pressure 3ra-ient is t,e -rivin force for bloo- flo6. #esistance ?00oses :lo6 (lood flowing through blood vessels encounters friction from the vessel walls and the components of blood colliding with each other. The term #esistance (/) refers to the tendency of the cardiovascular system to oppose blood flow. Increased resistance leads to decreased flow. Thus, <low 27/ ( M proportional to). There are three parameters that contribute to resistance to flow of fluid through tube$ 1. +ube (en t, ;() " as the tube lengthens, resistance increases. In the body, length is determined by the anatomy of the vascular system and this remains fairly constant. 2 :lui- Viscosity ; ) " describes the 'thic'ness' of a fluid. The viscosity of blood is about C"D times greater than water (due to blood cells and plasma proteins). The more viscous the fluid the greater the resistance to flow. The viscosity of blood in the body is normally maintained to remain constant. 3. +ube #a-ius ;r) " the radius can be simplified to mean the diameter of the tube. %s the radius of the tube decreases, the resistance to flow increasesE conversely, as the radius of the tube increases, the resistance to flow decreases. This parameter does not remain constant in the body " the diameter of blood vessels change continuously " thus, the radius of blood vessels is the main determinant of resistance to blood flow in the body. The relationship between these parameters and flow of a fluid through a tube can be e)presses by$ Poiseuille@s la67 # = ! ( 5 r4

!"

4owever, in humans this can be simplified to$ / 27r as blood vessel radius becomes the main determinant. Vasoconstriction leads to increased resistance and decreased flow. Vaso-ilation leads to decreased resistance and increased flow. Therefore, blood flow is described by this formula$
#

Flo

P #

!"

P !$r4

If the driving force remains constant, flow varies inversely with resistance (determined by radius).

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