Download isovolumetric ventricular contraction

Circulatory physiology
• The circulatory system contributes to
homeostasis by transporting O2,CO2,
wastes,electrolytes and hormones from
one part of the body to another.
Introduction
Circulatory system (transport system) consists
of 3 basic components
• Heart : pump, imparting pressure to the blood
• Blood vessels: passageways
• Blood : transport medium, dissolved or
suspended ;flow down a pressure gradient
• Pulmonary circulation :carry
blood between the heart and lungs
• systemic circulation:
carry
blood between the heart and organ
systems
Pulmonary and systemic circulation in
relation to the heart
The function of the heart
• Pumping
• Endocrine
-- atrial natriuretic peptide (ANP)
-- brain natriuretic peptide (BNP)
The heart is a dual pump
• The right and left side of the heart function
as two separate pumps:
the right half of the heat is receiving and pumping O2-poor
blood
the left half of the heat receives and pumps O2-rich blood
The right and left side of the heart simultaneously pump
equal amounts of blood, but the left side performs more
work
Dual pump action of the heart
Comparison of the thickness of the
right and left ventricular walls
The role of heart valves
Heart valves ensure that the blood flows in the proper
direction through the heart
• Atrioventricular(AV) valves: between the atrium and the
ventricle, these valves is the right and left Atrioventricular (AV)
valves
• Semilunar valves : aortic and pulmonary valves; at the juncture
where the major arteries leave the ventricles
chordae tendin
Heart valves
Aortic or pulmonary valve
Right AV valve
Left AV valve
Mechanism of valve action
Valve opened
When pressure is greater behind the valve , it opens
Mechanism of valve action
Valve closed; does not open in opposite direction
When pressure is greater in front of the valve, it closed. It is a one-way valve
Overview of heart physiology
• Three major types of cardiac muscle:
--atrial muscle (contraction, excitability, conductivity )
--ventricular muscle (contraction, excitability,
conductivity )
--specialized excitatory and conductive muscle
(excitability, conductivity, autorhythmicity)
Anatomy of the heart
Intercalated discs:
•
desmosomes adhering
junction that mechanically
holds cells
• gap junction: low electrical
resistance—single functional
syncytium
Two types of cardiac muscle cells
• Contractile cells:
99%. These cells do the
mechanical work of pumping and these working cells
normally do not initiate their own action potential
• Autorhythmic cells:
the remainder cell ,
these cells do not contract but specialized for
initiating and conducting the action potentials
responsible for contraction of the working cells
Electrical activity of the heart
• Autorhythmicity : the heart contracts , or
beats, rhythmically as a result of action
potentials that it generated by itself
Pacemaker activity
• The sinoatrial node (SA node) is the normal pacemaker of
the heart
• Pacemaker activity: their membrane potential slowly depolarizes by
themselves until the threshold is reached , the membrane has an action
potential (without any nervous stimulation)
•
Through the repeated cycles of drift and fire, these autorhythmic cell initiate
action potentials, which then spread throughout the heart to trigger rhythmic
beating
Pacemaker potential
• The mechanism of pacemaker potential
(auto-depolarization)
It depend on the interactions of several different ionic
mechanisms.
e.g. Ca2+, K+, and Na+
The Rp of these cell does not remain constant , following an Ap the
membrane slow depolarized to threshold
Pacemaker potential
1. A decreased passive
outward K+ current (K+
channels slowly close at
negative potentials)
2. a constant inward Na+
current (the inside becomes
less negative- depolarization)
3. As the slow depolarization
proceeds , An increased
inward Ca2+ current
through T-Ca2+ channels
before the membrane
reaches threshold, and then
the influx of Ca2+ further
depolarized the membrane
Pacemaker activity of cardiac autorhythmic cells
to threshold
Pacemaker potential
4. Once the membrane reaches
threshold, longer-lasting
Ca2+ channels (L-Ca2+ )
open. The resultant rapid
influx of Ca2+ produce the
rising phase of the selfinduced Ap
5. The falling phase is brought
about by a rapid K+ efflux .
Slow closure of these K+
channels after the Ap is
over initiates the next slow
depolarization to threshold
(PNa+ is unchanged )
Pacemaker activity of cardiac autorhythmic cells
Types of Ca2+ channels in cardiac cell
• T-type (transient, during slow depolarization)
(Nowycky,1985)
• L-type (long lasting, during rising phase) (Nowycky,1985)
The comparison of the pacemaker potential (Ap)
and action potential on a nerve cell
Pacemaker activity of cardiac
autorhythmic cells
The action potential on a nerve cell
Specialized noncontractile cardiac cells
capable of autorhythmicity
• The sinoatrial
node (SA node):
a small specialized region
in the right atrial wall
near the opening of the
superior vena cava
• The atrioventricular
node (AV node):
a small bundle of
specialized cardiac
muscle cells located
above the junction of the
atria and ventricles
Specialized noncontractile cardiac cells
capable of autorhythmicity
• The bundle of His
(atrioventricular
bundle): a tract of
specialized cells that
originates at the AV node and
enters the interventricular
septum, where it divides to
form the right and left bundle
• Purkinje fibers: small
terminal fibers that extend
from the bundle of His and
spread throughout the
ventricular myocardium
The rate of slow depolarization for the
various autorhythmic cells
• The rate of slow depolarization for the various
autorhythmic cells is different so the rates at which
they are normally capable of generating Ap also differ
tissue
Action potentials
per minute*
SA node (normal pace maker)
70-80
AV node
40-60
Bundle of His and Purkinje fibers
20-40
*In the presence pf parasympathetic tone
Different autorhythmic rates and
pacemaker
• The different autorhythmic cell has different autorhythmic
rates
• A cell has a faster rate of depolarization , it reaches
threshold more quickly . e.g. the SA node
• Pacemaker : the SA node which normally exhibits the fastest rate
of autorhymicity at 70-80 action potentials per minute , drives the rest
of the heart at this rate and is known as the Pacemaker
• Latent pacemakers: the non-SA nodal autorhythmic tissues
Different autorhythmic rates
Because cell A has a faster
rate of depolarization , it
reaches threshold more quickly
than cell B and therefore
generates action potentials
more frequently
Different autorhythmic rates
Because of the different
autorhythmic rates , the entire
heart is triggered and the
heart to beat at the pace or
rate set by SA node . The
other autorhythmic tissues are
unable to assume their own
naturally slower rates, because
they are activated by the Ap
initiated in the SA node
Analogy of pacemaker activity
Normal pacemaker activity by the SA node
Takeover of pacemaker activity by the AV node when the SA node is nonfunctional
lantent pacemakers—non-SA nodal autorhythmic tissues
Analogy of pacemaker activity
Takeover of ventricular rate by the slower ventricular autorhythmic tissue in the
condition of heart block even though the SA node is still functioning
Takeover of pacemaker activity by an ectopic focus
(often response to lack of sleep , anxiety, excess caffeine)
•
What factors are able to influence
autorhythmicity?
The spread of cardiac excitation
three criteria:
• Atrial excitation and contraction should
be complete before the onset of
ventricular contraction.
three criteria:
• Excitation of cardiac muscle fibers
should be coordinated to ensure that
each heart chamber contracts as a unit
to accomplish efficient pumping.
Such random,uncoordinated excitation and contraction
of the cardiac cells is known as fibrillation.
three criteria:
• The pair of atria and pair of ventricles
should be functionally coordinated so
that both members of the pair contract
simultaneously.
• This permits synchronized pumping of blood into the
pulmonary and systemic circulation.
The spread of cardiac excitation
First spreading throughout both atria through the interatrial pathway and
internodal pathway,
AV node is the only point where an action potential can spread from the atria
to the ventricles
Then Ap spread through the ventricles by the bundle of His and Purkinje
fibers
Atrial excitation
• The interatrial pathway:
extends from the SA node .
This ensures that both atria
become depolarized to
contract more or less
simultaneously
• The inter-nodal pathway :
extend from the SA node to
the AV node . This ensure
sequential contraction of
the ventricles following
atrial contraction
Transmission between the atria and the ventricles
• AV nodal delay : 0.1sec .the Ap is conducted relatively slow through the
AV node ( unique way )
• Significance : it prevent the atria and the ventricle contract
simultaneously
Ventricular excitation
• The ventricles excited by the impulse traveling down the bundle
of His and Purkinje fibers
• The speed of the action potential conduction
the slowest place: transmission between the atria and the
ventricles (the AV nodal delay , 0.02m/s)
the fastest place: in the ventricles (the Purkinje fibers, 4m/s)
The Ap of contractile cardiac muscle cells
• Unlike autorhythmic cells, the membrane of contractile cells
remains at rest at about -90mV. And the Ap shows a
characteristic plateau
The Ap in the cardiac contractile cells differs from the autorhythmic cells
(a constant Rp: -90mV)
The rising phase is caused by a fast Na+ influx and the falling phase results from a
slow influx of Ca2+ coupled with a marked decrease in K+ permeability
1
0
2
Phase 0: a fast Na+ influx
3
4
Phase 1:
1
0
PNa+ decrease, PK+ increase ,
K+ efflux
2
3
4
1
0
Phase 2: (plateau) PK+
decrease , K+ efflux
decrease, PCa2+ increase,
Ca2+ influx
2
3
4
Phase 3 : PK+ increase , K+ efflux
increase
1
0
2
Phase 4: Na+-K+ pump(3Na+ outside ,
2K+ inside ) , Na+-Ca2+ antiport(3Na+
inside , 1 Ca2+ outside) and Ca2+ pump
functioning
3
4
The excitation-contraction coupling in cardiac contractile cells
clinical point:
• If K+o↑
tend to develop ectopic foci as well as
cardiac arrhythmias
• If Ca2+o ↑→plateau phase↑→[Ca2+] in
cytosol→strength of cardiac
contraction↑
verapamil
Refractory period
Relationship of an Ap and the
refractory period to the duration of
the contractile response in cardiac
muscle
The period of contraction (300msec)
and the duration of the action
potential’s refractory period
(250msec) is almost same
Between the Ap and contractile
response , there is a slightly
delay
Valuable protective mechanism: the long refractory period means that
cardiac muscle cannot be restimulated until contraction is almost over and
this makes summation and tetanus of cardiac muscle impossible
Cardiac muscle Ap and contraction curve
skeletal muscle Ap and contraction curve
Why is the summation of contractions and tetanus of
cardiac muscle is impossible and for the skeletal muscle it
is possible
•
In skeletal muscle , the refractory period of Ap is very short compared with the
duration of the resultant contraction (after the Ap), so the fiber can be
restimulated again before the first contraction is complete to produce
summation of contractions, rapidly repetitive stimulation results in a sustained ,
maximal contraction known as tetanus
•
In contrast, cardiac muscle has a long Ap refractory period that lasts about
250msec . This is almost as long as the period of contraction—300 msec
(between the Ap and contractile response , there is a slightly delay),so the
cardiac muscle cannot be restimulated until contraction is almost over,
summation of contractions and tetanus of cardiac muscle is impossible .
•
Significance : the pumping of blood requires alternate periods of contraction
(emptying) and relaxation (filling) . A prolonged tetanic contraction is fatal
Premature excitation , premature systole
(extrasystole) and compensatory pause
2nd part
physiological properties of cardiac cells
excitability
ARP:
0 phase~3 phase (-55mv)
LRP(local response period):
-55mv~-60mv
RRP:
-60~-80mv
supernormal period:
-80~-90mv
｝
ERP
Factors affecting excitability
• Resting potencial or maximal
repolarization potencial
• threshold potential
• ion channel state in 0 phase
autorhythmicity
conductivity
conductivity
Electrocardiogram (ECG)
• The ECG is a record of the overall spread of electrical
activity through the heart (the current spread into the tissues
surrounding the heart and conduct through the body fluids )
• EKG: based on the ancient Greek word
(electrokardiogram)
it is the same as ECG
Three important points should be remembered when considering
what an ECG actually represents:
•
An ECG is a recording of that portion of the electrical activity reaches the
surface of the body, not a direct recording of the actual electrical activity of
the heart
•
The ECG is a complex recording representing the overall spread of electrical
activity throughout the heart during depolarization and repolarization. It is not
a recording of a single Ap in a single cell at a single point in time
•
The recording represents comparisons in voltage detected by electrodes at two
different points on the body surface, not the actual potential
The significance of ECG
P wave = atrial depolarization
PR segment = AV node delay
QRS complex = ventricular depolarization (atrial repolarizing simultaneously)
The significance of ECG
ST segment = time during which ventricles are contracting and emptying
T wave = ventricular repolarization
TP interval = time during which ventricles are relaxing and filling
Tachycardia—abnormalities in rate
Atrial fibrillation
ventricular fibrillationabnormalities in rhythm
Mechanically change : Cardiac cycle
• The cardiac events that occur from the beginning
of one heart beat to the beginning of next one
• Systole (contraction)
• Diastole (relaxation)
Mechanical events of the cardiac cycles
• The cardiac cycles consists of alternate periods of systole
(contraction and emptying ) and diastole (relaxation and filling)
0.0
0.1
0.2
0.3
0.4
0.5
0.6
Time (s)
Atrium
systole
ventricle
diastole
systole
diastole
AV valve
open
close
open
semilunar
valve
close
open
close
diastole
cardiac cycles
0.7
0.8
What happens in the heart during each cardiac
cycle
• Pressure
• Volume
• Valves
• Blood flow
cardiac cycles (A)
• 1 During early ventricular
diastole,the atrium is still
also in diastole---TP
interval
• 2 the ventricular volume
slowly continues to rise
even before atrial
contraction takes place.
• 6. The corresponding rise in
ventricular pressure that
occurs simultaneous to the
rise in atrial pressure is due
to the additional volume of
blood added to the
ventricle by atrial
contraction.
cardiac cycles (B)
• 4.SA node fires , atrial
contraction, artria
pressure rise and
exceed ventricle, AV
valve remain open then
squeezes more blood
into the ventricle
• 7 the volume of blood
in the ventricle at the
end of diastole is
known as the enddiastolic volume (EDV),
which averages about
135 ml--maximum
amout of blood
cardiac cycles(C)
• 8.The QRS represents this
ventricular excitation,which
induces ventricular
contraction.
• the ventricular pressure
curve sharply increases
shortly after the QRS
complex.
• 9 After atrial contraction is
complete, the ventricular
contraction start ,and atrial
relaxation begin ,the
ventricular pressure
increases and exceed the
atrial pressure, AV valves
closed
cardiac cycles
AV valves closed .The aortic valves
is not open. The ventricles remains a
closed chamber– isovolumetric
ventricular contraction (no blood
enter or leave the ventricls). The
ventricular pressure sharply
increases (10). The volume remain
constant (11).
Ventricular pressure exceeds aortic
pressure, the aortic valve is forced
open and fast ejection of blood
begin (12) the ventricular volume
decrease(14) .
Ventricular systole:
Isovolumetric ventricular contraction
Ejection phase
cardiac cycles
only about half of the blood is
pumped out during the subsequent
systole.
the mount of blood remaining in the
ventricle at the end of systole when
ejection is complete is known as the
end-systolic volume(ESV) .
average about 65ml
the amount of blood pumped out of
each ventricle with each contraction
is known as the stoke volume(SV).
cardiac cycles（D）
• At the end of
ventricular systole, it
start to relax ,
ventricular pressure
falls below aortic
pressure and the aortic
valve closes (17).
• closure of the aortic
valve produces a
disturbance or notch
on the aortic pressure
curve known as the
dicrotic notch. (18)
cardiac cycles (E)
• The aortic valve closes.
ventricular pressure still
exceeds atrial pressure, the
AV valve is closed . The
ventricles remains a closed
chamber– isovolumetric
ventricular relaxation (no
blood enter or leave the
ventricls). The ventricular
pressure steadily falls (19).
The volume remain constant
(20).
cardiac cycles（A）
The ventricular pressure fall
below the atrial pressure, the
AV valve is open, ventricular
filling occurs. Ventricular filling
occurs rapidly at first. (23) The
speed of filling decrease(24).
The atrium also relax
simultaneously
During the late ventricular
diastole , the SA node fires
again.
Ventricular diastole:
isovolumetric ventricular
relaxtion
filling phase:
rapid-filling phase
reduced filling phase
Role of atria and ventricles during each
cardiac cycle
• Atria: primary pump
• Ventricle : major source of pumping
power
• when HR increases from 75 to 180
beats per minute………
Mechanical events of the cardiac cycles
0.0
0.1
0.2
0.3
0.4
0.5
0.6
0.7
0.8
Time (s)
Atrium
systole
ventricle
diastole
diastole
systole
diastole
During times of rapid heart rate , the length of diastole is reduced to a much greater
extent than is the length of systole
• HR is greater than 200beats per
minute……
Ventricular filling profiles
during normal and rapid heart
rates
Much of ventricular filling occurs early in diastole during the rapid-filling phase.
During the exercise the filling is not seriously impaired, so cardiac output is not
deficient
When heart beat is greater than 200 beats per minute ,the inadequate filling cause
cardiac output deficient
The heart sound
• The heart sounds associated with valve closures can be heard
during the cardiac cycle
• The first heart sound is low pitched, soft and relatively long.
(“lub”). It cause by the closure of the AV valves. The first
heart sound signal the onset of ventricular systole
• The second heart sound is higher pitched, sharper and relatively
short. (“dup”). It cause by the closure of the semilunar valves.
The second heart sound signal the onset of ventricular diastole
• Opening of the valves does not produce any sound.
•The first heart sound signal the
onset of ventricular systole
•The second heart sound signal
the onset of ventricular diastole
1st
2nd
Evaluation of heart pumping
SV = EDV - ESV
• 5. work of the heart
-- stroke work
-- minute work
-- cardiac efficiency
6. Cardiac reserve
• Cardiac reserve: the difference between the CO at rest and the
maximum volume of blood the heart is capable of pumping per
minute
CO is about 5 liters / min (at rest)
CO is about 20-25 liters / min (during exercise)
Achieved by an increase of stroke volume or heart rate or both of
them
• How can cardiac output vary so
tremendously,depending on the demands
of the body?
Cardiac output and its control
• Cardiac output (CO): the volume of blood pumped by each
ventricle per minute (not the total amount of blood pumped by
the heart)
• Stroke volume: the amount of blood pumped out of each
ventricle with each contraction. It is equal to the end-diastolic
volume (EDV 135ml) minus the end-systolic volume (ESV, 65ml) .
The Stroke volume is about 70 ml (60-80ml).
Cardiac output (CO)
• Cardiac output = heart rate x stroke volume
•
CO= 70 beats/min x 70 ml/beat
•
= 4900 ml/min ≈5 liters/min
• The body’s total blood volume averages 5 to 5.5 liters, each half of the
heart pumps the equivalent of the entire blood volume per minute (at
rest)
• During exercise the CO can increase to 20 to 25 liter per minute , even
as high as 40 liters.
• Cardiac output depends on the heart
rate and the stroke volume
The control of HR
• Heart rate is determined primarily by autonomic influence on
the SA node. (spontaneous rate of depolarization: 70 times per
minute)
• The heart is innervated by both divisions of the autonomic
nervous system (parasympathetic and sympathetic nerve). they
can modify the rate of contraction. (nervous stimulation is not
required to initiate contraction)
• Effect of parasympathetic stimulation on the heart
• Effect of sympathetic stimulation on the heart
• Atrium
• Parasympathetic
• nerve
• SA node
• AV node
ventricles
Sympathetic
nerve
Autonomic control of SA node activity
and heart rate
Increased the parasympathetic activity decreases the heart rate
Increased the sympathetic activity increases the heart rate
Effects of the autonomic nervous system on the
heart and structures that influence the heart
Area
affected
effect of parasympathetic stimulation
effect of sympathetic stimulation
decreases the rate of depolarization to
threshold ; decreases the heart rate
Increases the rate of depolarization to
threshold ; increases the heart rate
AV node
decreases excitability; increases the
AV delay
Increases excitability; decreases the
AV delay
Ventricular
conduction
pathway
little effect
Increases excitability; hasten
conduction through the bundle of His
and Purkinje cells
Atrial muscle
decreases the contractility;
weakens contraction
Increases the contractility; strengthens
contraction
Ventricular
muscle
No effect
Increases the contractility; strengthens
contraction
veins
No effect
Increase venous return, which increase
the strength of cardiac contraction
Adrenal
medulla
No effect
Promote secretion of epinephrine, a
hormone that augment the sympathetic
nervous
SA node
Autonomic control of SA node activity and heart rate
Parasympathetic stimulation
decreases the rate of SA node
depolarization, so has fewer Ap
and decrease the heart rate
sympathetic stimulation increases
the rate of SA node depolarization,
so has more Ap
Mechanism of the parasympathetic and sympathetic
function (nerve regulation)
Area affected
Heart rate
conductivity
Contraction
Parasympathetic nerve
(Ach)
decrease, increase the
PK+ of SA node
sympathetic nerve
(Norepinephrine)
increase, decrease the
PK+ of SA node
increase the PK+,
increase the AV nodal
delay
decrease the PK+,
decrease the AV nodal
delay
Decrease the slow inward
Ca2+ current, plateau phase
is reduced . The Atrial
contraction is weakened
increase the slow inward
Ca2+ current, plateau phase
is longer . The Atrial and
ventricular contraction is
strengthened
Little effect on ventricular
contraction
Parasympathetic and sympathetic effects on heart rate are antagonistic. At any
given moment , the effect is balanced. At rest , parasympathetic discharge is
dominant
• If all autonomic nerves to the heart
were blocked……
HR?
• The parasympathetic system controls
heart action in quiet,relaxed situations
when the body is not demanding an
enhanced cardiac output--negtive
effect
• Sympathetic stimulation”revs up” the
heart—positive effect
Humoral regulation of heart
• Epinephrine : a hormone secreted by adrenal medulla upon
sympathetic stimulation.
• Role : similar to norepinephrine (released by sympathetic nerve
terminal). Reinforcing the direct effect that the sympathetic
nervous system has on the heart
Regulation of stroke volume
• stroke volume is determined by the extent of venous return and by
sympathetic activity .
• Two types of controls influence stroke volume :
(1) intrinsic control: the extent of venous return (end-diastolic
volume)
(2) extrinsic control : the extent of sympathetic stimulation of the
heart
The both factors increase stroke volume by increasing the strength
of contraction of the heart
The relationship of end-diastolic volume
and stroke volume -intrinsic control
• Increased end-diastolic volume (EDV) result in increased stoke
volume
• This intrinsic control depends on the length-tension relationship
of cardiac muscle—Frank-Starling law of the heart
for skeletal muscle: the resting-muscle length is approximately
the optimal length at which maximal contractile tension can be
developed
for cardiac muscle: the resting muscle length (determined by the
venous filling) is less than optimal length
• The degree of diastolic filling determined
the cardiac muscle fiber length
• The greater the extent of diastolic filling, the larger the enddiastolic volume and the more the heart is stretched, the more the
heart is stretched , the longer the initial cardiac fiber length
before contraction, then the greater force on the cardiac
contraction , the greater the stoke volume
Frank–Starling curve
Increase the EDV, increase the length of cardiac muscle before contraction ,
increases the contractile tension of the fiber, then increases the stroke
volume
for cardiac muscle: the resting muscle
length (determined by the venous filling)
is less than optimal length
• the length-tension curve of cardiac
muscle normally does not have a
descending limb. That is , within
physiological limits, cardiac muscle does not
get stretched beyond its optimal length
Frank-Starling law of the heart
• The heart normally pumps all the blood
returned to it ; increased venous return
results in increased stroke volume .
• Preload : the extent of filling (It is the
workload imposed on the heart before
contraction begin)
venous return and stroke volume
• The built-in relationship matching venous return and
stroke volume has two important advantages:
-- 1st is: equalization of output between the right and
left sides of the heart to the pulmonary and systemic
circulation
-- 2nd is: when a larger cardiac output is needed, such
as during exercise , venous return is increased
through action of sympathetic nerve and then stroke
volume increased correspondently
extrinsic control of stroke volume
• Sympathetic stimulation and the role of epinephrine
(released by Adrenal medulla)
1. increase the contractility
contractility: the strength of contraction at any given enddiastolic volume;
Mechanism: increased ca 2+ influx triggered by norepinephrine and
epinephrine. the extra cytosolic Ca2+ allows the myocardial fibers to
generate more force through greater cross-bridge cycle
2. increase venous return (triggered
by sympathetic stimulation)
Mechanism: constrict the vein, which
squeezes more blood to the heart,
increase the EDV and then increase the
stroke volume
Effect of sympathetic stimulation on stroke volume
(a). normal SV
(b). SV during sympathetic stimulation (contractility increased)
(c). SV with combination of sympathetic stimulation and increased
EDV
Shift of the Frank-Starling curve to the left by sympathetic stimulation
For the same EDV , there is a larger stroke volume
Sympathetic stimulation increases
the cardiac output by increasing
both heart rate and stroke
volume
Summary of control of
cardiac output (control of
SV and HR )
High blood pressure increase the
workload of the heart
• Afterload : the workload imposed on the heart after
the contraction has begun (blood pressure)
• When the blood pressure is high or the valve is
stenotic the workload of the heart will be increase
(generate more pressure to eject blood)
The summary of factors influence
the cardiac output