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$

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 - period of rela!ation when the heart fills with blood ' -ystole - period of contraction

Beginning just after a ventricular contraction

Semilunar valves closed

AV valves opened

Diastole: Passive ventricular filling. The AV valves open and

blood flows into the relaxed ventricles, accounting for most of the ventricular filling.

Semilunar valves closed AV valves opened

Diastole: Active 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 closed

Semilunar valves closed AV valves opened

Systole: Period of isovolumic contraction.

Diastole: Active ventricular filling.

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.

Semilunar valves closed AV valves closed

Semilunar valves opened AV valves closed

Systole: Period of isovolumic contraction.

Systole: Period of ejection.

Semilunar valves opened

AV valves closed

Systole: Period of ejection. 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 closed

AV valves closed

Diastole: Period of isovolumic relaxation. Blood flowing bac!

toward the relaxed ventricles causes the semilunar valves to close, which is the beginning of ventricular diastole. "ote that the AV valves closed, also.

Semilunar valves closed AV valves closed

Semilunar valves closed AV valves opened

Diastole: Period of isovolumic relaxation.

Diastole: Passive ventricular filling.

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 .hus8 A4-B4 ml remain in each ventricle 20nd systolic volume6 .he fraction e ected is then ?%45 2e ection fraction6

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

Preload and 'fterload

Preload - tension on muscle when it begins to contract 2end-diastolic pressure6 'fterload - 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

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

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#

Chemical Regulation of the Heart

.he hormones epinephrine and thyro!ine increase heart rate =ntra- and e!tracellular ion concentrations must be maintained for normal heart function

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 - 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

"actors 'ffecting -tro+e Volume

0DV - affected by
( Venous return - vol# of blood returning to heart ( Preload : amount ventricles are stretched by blood 2C0DV6

0-V - 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 '(.*

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

"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

Preload and 'fterload

Figure 18.21

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, timolol6 bloc+ beta-receptors and prevent sympathetic stimulation of heart 2neg# chronotropic effect6

'utonomic Control of Cardiac Output

%&mpathetic increases cardiac output -an increase heart rate ./ 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

Cardiac Output and Peripheral Resistance

8ncreasing the peripheral resistance decreases cardiac output.

cardiac output :

arterial pressure total peripheral resistance

Other "actors 'ffecting Cardiac Output

'ge &ender 0!erciseDbody temperature