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Heart as a Pump

Outline
‡ Overview of heart anatomy and function ‡ Cardiac cycle ‡ Volume--‐Pressure Diagram ‡ Cardiac Output and Venous Return ‡ Regulation of Cardiac Output

Learning Ob ectives
•Describe the cardiac cycle by e!plaining "ig# $% in &uyton and Hall •'naly(e ventricular pumping with a volume ‐ pressure diagram •)nderstand cardiac output and venous return - *uantitatively +now cardiac output •,now how cardiac output is regulated - "ran+-tarling mechanism and autonomic regulation

Cardiovascular -ystem
Note, right side is the right side of the person or animal. Two pumps in the heart: Right side pumps blood through the lungs Left side through the peripheral organs Each side has an atrium and a entricle !trium is a primer pump for the entricle "entricle supplies the main pumping force

Heart 'natomy

!trio entricular al es: tricuspid #right$ and mitral #left$ %emilunar al es: pulmonar& #right$ and aortic #left$

period of contraction .period of rela!ation when the heart fills with blood ' -ystole .Cardiac Cycle •.he cardiac cycle includes the events that occur from the beginning of one heartbeat to the beginning of the ne!t •.he cardiac cycle consists of two periods/ ' Diastole .

The AV valves open and blood flows into the relaxed ventricles. .Beginning just after a ventricular contraction Semilunar valves closed AV valves opened Diastole: Passive ventricular filling. accounting for most of the ventricular filling.

Semilunar valves closed AV valves opened Diastole: Passive ventricular filling.Semilunar valves closed AV valves opened Diastole: Active ventricular filling. .

. The atria contract and complete ventricular filling.Semilunar valves closed AV valves opened Diastole: Active ventricular filling.

Diastole: Active ventricular filling. .Semilunar valves closed AV valves closed Semilunar valves closed AV valves opened Systole: Period of isovolumic contraction.

Semilunar valves closed AV valves closed Systole: Period of isovolumic contraction. Ventricular contraction causes the AV valves to close. which is the beginning of ventricular systole. . The semilunar valves were closed in the previous diastole and remain closed during this period.

. Systole: Period of ejection.Semilunar valves closed AV valves closed Semilunar valves opened AV valves closed Systole: Period of isovolumic contraction.

ontinued ventricular contraction pushes blood out of the ventricles. causing the semilunar valves to open. .Semilunar valves opened AV valves closed Systole: Period of ejection.

. Semilunar valves closed AV valves closed Diastole: Period of isovolumic relaxation.Semilunar valves opened AV valves closed Systole: Period of ejection.

"ote that the AV valves closed. also. which is the beginning of ventricular diastole. .Semilunar valves closed AV valves closed Diastole: Period of isovolumic relaxation. Blood flowing bac! toward the relaxed ventricles causes the semilunar valves to close.

. Diastole: Passive ventricular filling.Semilunar valves closed AV valves closed Semilunar valves closed AV valves opened Diastole: Period of isovolumic relaxation.

Cardiac Cycle in Left -ide .

#echanical $vents% The ardiac ycle .

.he Cardiac Cycle • Cardiac cycle refers to all events associated with blood flow through the heart from the start of one heartbeat to the beginning of the ne!t • During a cardiac cycle ( 0ach heart chamber goes through systole and diastole ( Correct pressure relationships are dependent on careful timing of contractions .

Phases of the Cardiac Cycle • 'trial diastole and systole ( 1lood flows into and passively out of atria 2345 of total6 • 'V valves open ( 'trial systole pumps only about 745 of blood into ventricles • Ventricular filling/ mid-to-late diastole ( Heart blood pressure is low as blood enters atria and flows into ventricles ( 345 of blood enters ventricles passively ( 'V valves are open8 then atrial systole occurs ( 'trial systole pumps remaining 745 of blood into ventricles .

Phases of the Cardiac Cycle • Ventricular systole ( 'tria rela! ( Rising ventricular pressure results in closing of 'V valves 29st heart sound : .lubb<6 ( =sovolumetric contraction phase • Ventricles are contracting but no blood is leaving • Ventricular pressure not great enough to open semilunar valves ( Ventricular ejection phase opens semilunar valves • Ventricular pressure now greater than pressure in arteries 2aorta and pulmonary trun+6 .

Phases of the Cardiac Cycle • Ventricular diastole ( Ventricles rela! ( 1ac+flow of blood in aorta and pulmonary trun+ closes semilunar valves 27nd hear sound .dubb<6 • Dicrotic notch : brief rise in aortic pressure caused by bac+flow of blood rebounding off semilunar valves ( 1lood once again flowing into rela!ed atria and passively into ventricles .

>ormal Volume of 1lood in Ventricles •'fter atrial contraction8 994-974 ml in each ventricle 2end-diastolic volume6 •Contraction e ects ?@4 ml 2stro+e volume output6 •.he fraction e ected is then ?%45 2e ection fraction6 .hus8 A4-B4 ml remain in each ventricle 20nd ‐ systolic volume6 •.

Left Ventricle Volume--‐Pressure Curve )e able to use these pressure and olume alues !ortic al e closes !ortic al e opens *itral al e opens *itral al e closes End's&stolic olume End'diastolic olume .

tension on muscle when it begins to contract 2end-diastolic pressure6 •'fterload .Preload and 'fterload •Preload .load against which the muscle e!erts its contractile force8 which is the pressure in the artery leading from the ventricle# Phase === on volume-pressure diagram .

Cardiac Output and Venous Return •Cardiac output is the *uantity of blood pumped into the aorta each minute# Cardiac output C stro+e volume ! heart rate •Venous return is the *uantity of blood flowing from the veins to the right atrium# •0!cept for temporary moments8 the cardiac output should e*ual the venous return .

>ormal Cardiac Output •>ormal resting cardiac output/ ' -tro+e volume of @4 ml ' Heart rate of @7 beatsDminute ' Cardiac output ? B litresDminute •During e!ercise8 cardiac output may increase to E 74 litersDminutes •Fou should be able to get stro+e volume and heart rate from volume--‐pressure curves and 0C& recordings8 respectively .

Cardiac Output • -tro+e Volume C the vol of blood pumped by either the right or left ventricle during 9 ventricular contraction# -V C 0DV : 0-V @4 C 97B : BB CO C -V ! HR B87B4 C @4 mlDbeat ! @B beatsDmin CO C B#7B LDmin .

Cardiac Output • Regulation of -tro+e volume • Preload/ Degree of stretch of heart muscle 2"ran+--tarling6 : greatest factor influencing stretch is venous return 2see 1elow6 • Contractility : -trength of contraction =ncreased Ca7G is the result of sympathetic nervous system .

' -imple Hodel of -tro+e Volume .

g.G8 Ca7G channel bloc+ers# 'fterload/ 1ac+ pressure e!erted by arterial blood# Regulation of Heart Rate • 'utonomic nervous system • Chemical Regulation/ Hormones 2e.Cardiac Output • Other chemicals can affect contractility/ .Positive inotropic agents/ glucagon8 epinephrine8 thyro!ine8 digitalis# .8 epinephrine8 thyro!ine6 and ions# .>egative inotropic agents/ acidoses8 rising .

Regulation of Cardiac Output • "ran+--tarling Hechanism --‐ Cardiac output changes in response to changes in venous return# • 'utonomic control --‐ Control of heart rate and strength of heart pumping by the autonomic nervous system# .

he hormones epinephrine and thyro!ine increase heart rate • =ntra.and e!tracellular ion concentrations must be maintained for normal heart function .Chemical Regulation of the Heart • .

0-V • 0DV C end diastolic volume ( amount of blood in a ventricle at end of diastole • 0-V C end systolic volume ( amount of blood remaining in a ventricle after contraction • 0 ection "raction .5 of 0DV that is pumped by the ventricleI important clinical parameter ( 0 ection fraction should be about BB-%45 or higher .Regulation of -tro+e Volume • -V/ volume of blood pumped by a ventricle per beat -VC end diastolic volume 20DV6 minus end systolic volume 20-V6I -V C 0DV .

vol# of blood returning to heart ( Preload : amount ventricles are stretched by blood 2C0DV6 • 0-V ."actors 'ffecting -tro+e Volume • 0DV .affected by ( Venous return .affected by ( Contractility : myocardial contractile force due to factors other than 0DV ( 'fterload : bac+ pressure e!erted by blood in the large arteries leaving the heart .

"ran+--tarling Law of the Heart • Preload8 or degree of stretch8 of cardiac muscle cells before they contract is the critical factor controlling stro+e volumeI 0DV leads to stretch of myocardium# ( preload -V stretch of muscle force of contraction ( )nli+e s+eletal fibers8 cardiac fibers contract HOR0 "ORC0")LLF when stretched thus e ecting HOR0 1LOOD 2 -V6 ( =f -V is increased8 then 0-V is decreasedJJ • -low heartbeat and e!ercise increase venous return 2VR6 to the heart8 increasing -V# ( VR changes in response to blood volume8 s+eletal muscle activity8 alterations in cardiac output ( VR 0DV and in VR in 0DV ( 'ny in 0DV in -V .

"ran+--tarling Law of the Heart • • Relationship between 0DV8 contraction strength8 and -V# =ntrinsic mechanism/ ( 's 0DV increases/ • Hyocardium is increasingly stretched# • Contracts more forcefully# • 's ventricles fill8 the myocardium stretches/ ( =ncreases the number of interactions between actin and myosin# • • 'llows more force to develop# 0!plains how the heart can ad ust to rise in .) .PR# &igure '(.

* .0!trinsic Control of Contractility • Contractility/ ( -trength of contraction at any given fiber length# • -ympathoadrenal system/ ( >0 and 0pi produce an increase in contractile strength# • G inotropic effect/ ( Hore Ca7G available to sarcomeres# • Parasympathetic stimulation/ ( Does not directly influence contraction strength# &igure '(.

+ue to more optimal o erlap of actin and m&osin filaments during stretch ' same in s.e olume increases.er #increasing heart rate$. with increase enous return and increased stretching. . *oreo er. the force of contraction increases and the stro."ran+--tarling Hechanism The force of cardiac muscle contraction increases as the muscle stretches.eletal muscle %o. within limits. stretching of the %! node increasing the firing rate of the pacema.

"ran+--‐-tarling -ummary/ within physiological limits8 the heart pumps all the blood that returns to it from the veins# Venous return increases when there is an increase in the blood flow through peripheral organs# -o8 peripheral blood flow is a ma or determinant of cardiac output .

"actors 'ffecting -tro+e Volume .

0!trinsic "actors =nfluencing -tro+e Volume • • • Contractility is the increase in contractile strength8 independent of stretch and 0DV Referred to as e!trinsic since the influencing factor is from some external source =ncrease in contractility comes from/ ( =ncreased sympathetic stimuli ( Certain hormones ( Ca7G and some drugs 'gentsDfactors that decrease contractility include/ ( 'cidosis ( =ncreased e!tracellular .G ( Calcium channel bloc+ers • .

0ffects of 'utonomic 'ctivity on Contractility • -ympathetic stimulation ( ( ( ( Release norepinephrine from symp# postganglionic fiber 'lso8 0P and >0 from adrenal medulla Have positive ionotropic effect Ventricles contract more forcefully8 increasing -V8 increasing e ection fraction and decreasing 0-V • Parasympathetic stimulation via Vagus >erve -C>K ( Releases 'Ch ( Has a negative inotropic effect • Hyperpolari(ation and inhibition ( "orce of contractions is reduced8 e ection fraction decreased .

Contractility and >orepinephrine • -ympathetic stimulation releases norepinephrine and initiates a cyclic 'HP 7ndmessenger system Figure 18.22 .

21 .Preload and 'fterload Figure 18.

timolol6 bloc+ beta-receptors and prevent sympathetic stimulation of heart 2neg# chronotropic effect6 .0ffects of Hormones on Contractility • 0pi8 >08 and .hyro!ine all have positive ionotropic effects and thus contractility • Digitalis elevates intracellular CaGG concentrations by interfering with its removal from sarcoplasm of cardiac cells • 1eta-bloc+ers 2propanolol.

/ to 01/'2// )3* ‡-an double force of contraction %&mpathetic ner es release norepinephrine ‡)elie ed to increase permeabilit& of -a24 and Na4. 3aras&mpathetic # agal$ decreases cardiac output ‡-an decrease heart rate to 2/'5/ )3* ‡-an decrease force of contraction b& 2/'6/7 3aras&mpathetic ner es release acet&lcholine ‡8ncreases permeabilit& to 9 4 .'utonomic Control of Cardiac Output %&mpathetic increases cardiac output ‡-an increase heart rate .

cardiac output : arterial pressure total peripheral resistance .Cardiac Output and Peripheral Resistance 8ncreasing the peripheral resistance decreases cardiac output.

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Other "actors 'ffecting Cardiac Output • 'ge • &ender • 0!erciseDbody temperature .