#The heart as a pump and function of the heart valves

Done By: Rami AL Mashni
Endontic Resident
R.M.S

Outline
 Physiology of Cardiac Muscle
 Cardiac Cycle
 Relationship of the Heart Sounds to Heart
Pumping
 Work Output of the Heart
 Chemical Energy Required for Cardiac
Contraction: Oxygen Utilization by the Heart
 Regulation of Heart Pumping

Physiology of Cardiac Muscle
 The heart is composed of three major types of cardiac muscle:
atrial muscle, ventricular muscle, and specialized excitatory
and conductive muscle fibers.
o The atrial and ventricular types of muscle contract in
much the same way as skeletal muscle, except that the
duration of contraction is much longer.
o The specialized excitatory and conductive fibers exhibit
either automatic rhythmical electrical discharge in the form of
action potentials or conduction of the action potentials
through the heart, providing an excitatory system that controls
the rhythmical beating of the heart.

Physiologic Anatomy of Cardiac
Muscle
 cardiac muscle fibers arranged in a latticework > with
the fibers dividing, recombining, and then spreading
again.
 striated in the same manner as in skeletal muscle.
 typical myofibrils that contain actin and myosin lie
side by side and slide along one another during
contrction (almost identical to those found in skeletal
muscle)
 But >>>> cardiac muscle is quite different From
skeletal muscle:

Cardiac Muscle as a Syncytium.
 Cardiac Muscle as a Syncytium:
o intercalated discs: are cell membranes that
separate individual cardiac muscle cells from one
another.
o That is, cardiac muscle fibers are made up of many
individual cells connected in series and in parallel with
one another.

Cardiac Muscle as a Syncytium
 intercalated discs :The dark areas crossing the cardiac
muscle fibers.

 cardiac cells are so interconnected (gap junctions)
(At each intercalated disc) that when one of these cells
becomes excited, the action potential spreads to all of
them, from cell to cell throughout the latticework
interconnections.

 Two syncytiums:
o The atrial syncytium, which constitutes the walls of
the two atria.
o The ventricular syncytium, which constitutes the
walls of the two ventricles.

 The atria are separated from the ventricles by fibrous
tissue that surrounds the atrioventricular (A-V)
valvular openings between the atria and ventricles.
o potentials are not conducted from the atrial
syncytium into the ventricular syncytium directly
through this fibrous tissue.
o Instead, they are conducted only by way of a
specialized conductive system called the A-V
bundle.

 Two syncytiums:
o The atrial syncytium.// The ventricular syncytium.
 Potentials conducted
only by A-V bundle

 So WHY Two syncytiums division ??
 To allow the atria to contract a short time ahead of
ventricular contraction, which is important for
effectiveness of heart pumping.

Action Potentials in Cardiac
Muscle

Action Potentials in Cardiac Muscle
 action potential in a ventricular muscle fiber:
o About 105 millivolts:
 means that the intracellular potential rises from a
very negative value, about −85 millivolts to +20
millivolts during each beat.
o After the initial spike, the membrane remains
depolarized for about (0.2-0.3) second, exhibiting a
plateau then abrupt repolarization.
 0.2 in atrial muscle and 0.3 in ventricular muscle

 What Causes the Long Action Potential and the
Plateau? >> First reason:
 Two types of channels in cardiac muscle:
o (1) fast sodium channels as those in skeletal muscle
o (2) slow calcium channels, also called calcium-sodium
channels. (nt in skeletal muscles) :differs from the fast sodium
channels in:
 Slower to open and, even more important ..
 Remain open for several tenths of a second > During this
time, a large quantity of both calcium and sodium ions
flows through these channels to the interior of the cardiac
muscle fiber, and this maintains a prolonged period of
depolarization, causing the plateau in the action potential.

 Second reason of the platue:
o Immediately after the onset of the action potential,
The Permeability of the cardiac muscle membrane
for potassium ions decreases about fivefold. >>>

 NOW After the platue:
 Slow calcium-sodium channels close at the end of
(0.2 to 0.3) second > then membrane permeability
for potassium ions also increases rapidly; this rapid
loss of potassium from the fiber > immediately
returns the membrane potential to its resting level >
ending the action potential.

 Summary >>>
 AP > open fast Na Chan. And Slow Ca+ chan. > k+
chan. (decreased permeability) {K+ dosent efflux}
PLUS large quantity of Na+ and Ca+ influx >>
PLATUE >> 0.2-0.3 sec. > close Slow Ca+ chan. > stop
Ca+ and Na+ influx > increase K+ chan permeability
rapid K+ efflux >>>End of the AP > rest mem.
Potintial …

Refractory Period of Cardiac
Muscle
 Absolute refractory period:
o it is the interval of time during which a normal
cardiac impulse cannot re excite an already excited
area of cardiac muscle.
 Relative refractory period
o It’s the period during which an AP can be elected but
more than usual current is required
o Immediately after Absolute refractory period

Force of ventricular heart muscle contraction, showing also duration of the refractory
period and relative refractory period, plus the effect of premature contraction. Note that
premature contractions do not cause wave summation, as occurs in skeletal muscle.

Excitation-Contraction Coupling
Function of Calcium Ions and the Transverse Tubules
 Part similar to skeletal muscle:
o action potential >interior of the cardiac muscle fiber
along the membranes of the transverse (T) tubules >
membranes Of The longitudinal sarcoplasmic tubules
> release of calcium ions into the muscle sarcoplasm
from the sarcoplasmic reticulum > calcium ions diffuse
into the myofibrils > promote sliding of the actin and
myosin filaments along one another > muscle
contraction.

Excitation-Contraction Coupling
Function of Calcium Ions and the Transverse Tubules
 Part that is different from skeletal muscle:
o action potential Cause the opening of voltage-
dependent calcium channels in the membrane of the T
tubule it self > extra calcium ions also diffuse into
the sarcoplasm > activates calcium release channels
(ryanodine receptor channels) in the sarcoplasmic
reticulum membrane > triggering the release of
calcium into the sarcoplasm > Calcium ions in the
sarcoplasm then interact with troponin to initiate
cross-bridge formation and contraction.

2 sources of Ca+: extracellular fluids + sarcoplasmic reticulum

Excitation-Contraction Coupling Function
of Calcium Ions and the Transverse Tubules
 Why this mechanism:
o The sarcoplasmic reticulum of cardiac muscle is less
well developed than that of skeletal muscle > less
calcium stored.

 Important note:
o The strength of contraction of cardiac muscle
depends to a great extent on the concentration of
calcium ions in the extracellular fluids.
 T tubules act as a direct passage between the
cardiac muscle cell membrane and the extracellular
spaces surrounding the cells. While …
o skeletal muscle contraction is caused almost
entirely by calcium ions released from the
sarcoplasmic reticulum inside the Skeletal Muscle
fiber.

 At the end of the plateau of the cardiac action
potential:
 calcium ions in the sarcoplasm are rapidly pumped
back out of the muscle fibers into both the
sarcoplasmic reticulum and the T tubule extracellular
fluid space. >>>>>

 From sarcoplasm > S.R
(calcium-ATPase pump)
 From sarcoplasm > ECF.
(sodium-calcium exchanger)
o The extra Na+ is returned by
(sodium-potassium ATPase pump)

Duration of Contraction
 Cardiac muscle begins to contract a few milliseconds
after the action potential begins and continue to
contract until a few milliseconds after the action
potential ends. Therefore, the duration of contraction
of cardiac muscle is mainly a function of the duration
of the action potential.
 Including the plateau— its about 0.2 second in atrial
muscle and 0.3 second in ventricular muscle.

Cardiac Cycle
 The cardiac cycle: the cardiac events that occur from
the beginning of one heartbeat to the beginning of the
next.
 cycle is initiated by spontaneous action potential in
the sinus node. >>AP > rapidly through both atria and
then through the A-V bundle into the ventricles.

Cardiac Cycle
 The atria contract before ventricular thereby pumping
blood in to the ventricles before the strong ventricular
contraction begins. So….
 the atria act as primer pumps for the ventricles
 ventricles in turn provide the major source of
power for moving blood through the body.

Diastole and Systole
 Diastole : period of the relaxation during which the
heart fills with blood. Followed by..
 Systole: period of contraction.
 The total duration of the cardiac cycle (including
systole and diastole) is the reciprocal of the heart
rate. >> if heart rate is 72 beats/min, the duration of
the cardiac cycle is 1/72 beats/min—about 0.0139
minutes per beat, or 0.833 second per beat.

events during the cardiac
cycle for the left side of the heart

events during the cardiac
cycle for the left side of the heart
 The first three curves show the pressure changes in
the aorta, left ventricle and left atrium, respectively.
 The fourth curve >> the changes in left ventricular
volume.
 The fifth >> electrocardiogram.
 The sixth >> a phonocardiogram, which is a
recording of the sounds produced by the heart—
mainly by the heart valves.

Effect of Heart Rate on Duration of
Cardiac Cycle.
 If heart rate increases > duration of each cardiac cycle
decreases > contraction and relaxation phases
decrease. BUT …
 relaxation phase (diastole) decrease more than
The duration of the action potential and the period of
contraction (systole) decrease. Meaning that …
 the heart beating at a very fast rate does not remain
relaxed long enough to allow complete filling of the
cardiac chambers before the next contraction.

Relationship of the Electrocardiogram
to the Cardiac Cycle
 Recording the electrical activity of the heart over a period
of time.
 The ECG shows 5 waves >> P, Q, R, S, and T waves:
 P wave: spread of depolarization through the atria, and
this is followed by atrial contraction, which causes a
slight rise in the atrial pressure curve immediately
after the electrocardiographic P wave.
 QRS waves: depolarization of the ventricles, which
initiates contraction of the ventricles and causes the
ventricular pressure to begin rising. (note: QRS complex
begins slightly before the onset of ventricular systole).

Relationship of the Electrocardiogram
to the Cardiac Cycle
 T wave: repolarization of the ventricles when the
ventricular muscle fibers begin to relax. (note: the T
wave occurs slightly before the end of ventricular
contraction).

Function of the Atria as Primer
Pumps
 The atria simply function as primer pumps that
increase the ventricular pumping effectiveness 20%
only. How? ….
o Blood flows from the great veins to >> the atria
[80% flows directly into the ventricles before the atria
contract] >> atrial contract >> [additional 20% filling
of the ventricles]. Still ….

Function of the Atria as Primer
Pumps
 the heart can continue to operate under most
conditions even without this extra 20% effectiveness
[coz heart has the capability of pumping 300 to 400%
more blood than is required by the resting body]. SO
when atria fail to function, the difference is unlikely
to be noticed. Unless ..
 Do exercises >> acute signs of heart failure >>
shortness of breath.

Pressure Changes in the Atria—a,
c, and v Waves

c, and v Waves
 They are three minor pressure elevations in atria.
 a wave: is caused by atrial contraction.
 c wave: occurs when the ventricles begin to contract.
o 2 reasons:
 by slight backflow of blood into the atria at the
onset of ventricular contraction (minor).
 bulging of the A-V valves backward toward the
atria because of increasing pressure in the ventricles
(Main reason)

c, and v Waves
 v wave: occurs toward the end of ventricular
contraction; caused by > slow flow of blood into the
atria from the veins while the A-V valves are closed
during ventricular contraction. >>
 then ventricular contraction is over > A-V valves open
> stored atrial blood to flow rapidly into the ventricles
> v wave disappear.

Function of the Ventricles as
Pumps.. Filling of the Ventricles During Diastole

Function of the Ventricles as Pumps
 Filling of the Ventricles During Diastole. (3 phases):
 Phase One: (1st third)
o During Ventricular systole(contracting) > A-V valves
closed > large amounts of blood accumulate in the right
and left atria. NOW >>>
o systole is over > ventricular pressures fall > the
moderately pressures in the atria immediately push the A-
V valves open and allow blood to flow rapidly into the
ventricles > rise of the left ventricular volume
o This is called the period of rapid filling of the
ventricles

Function of the Ventricles as Pumps
 Phase 2 : (2nd third): middle phase
o small amount of blood normally flows into the
ventricles; this is blood that continues to empty into
the atria from the veins and passes through the atria
directly into the ventricles. (Remember: this
happened before the atria contract)
 Phase 3:
o the atria contract and give an additional thrust (the
20% only) to the inflow of blood into the Ventricles.

Emptying of the Ventricles During
Systole

Systole
 Period of Isovolumic (Isometric) Contraction.
 Now ..ventricular contraction begins > ventricular pressure
rises >and A-V valves still close > vent. Pressure keep
rising to build up sufficient pressure to push the semilunar
(aortic and pulmonary) valves to open against the pressures
in the aorta and pulmonary artery. Therefore …
 This is called the period of isovolumic or Isometric
contraction. Why? ..
o Contraction is occurring in the ventricles, but there is
no emptying >> tension is increasing in the muscle but
little or no shortening of the muscle fibers.

Systole
 Period of Ejection:
 First 1/3 of the period (70% of blood emptying):
 left ventricular pressure rises > push the semilunar
valves open > blood begins to pour out of the
ventricles (70% at this stage). and the remaining 30%
emptying during the next two thirds So ..
 The first third is called the period of rapid ejection,
and the last two thirds, the period of slow ejection.

Systole
 Period of Isovolumic (Isometric) Relaxation.
 At the end of systole > ventricular relaxation begins
suddenly > the intraventricular pressures to decrease
rapidly .. Why? > becoz the elevated pressures in the
distended large arteries that have just been filled with
blood from the contracted ventricles immediately push
blood back toward the ventricles, which snaps the aortic
and pulmonary valves closed.
 Its called period of isovolumic or isometric relaxation .
Why ?
o Coz For another 0.03 to 0.06 second, the ventricular
muscle continues to relax, even though the ventricular
volume does not change.

Systole
 Durning this period,(Period of Isovolumic Relaxation)
the intraventricular pressures decrease rapidly back to
their low diastolic levels. > open A-V valves >> begin a
new cycle of ventricular pumping.

End-Diastolic Volume, End-Systolic
Volume, and Stroke Volume Output.
 end-diastolic volume:
o the volume of the blood at the end of the diastol.
o normal filling of the ventricles increases the volume of each
ventricle to about 110 to 120 ml.
 stroke volume output:
o it’s the volum of the blood that ventricles empty during
systole. the volume decreases about 70 ml
 end-systolic volume:
o its the remaining volume in each ventricle, about 40 to 50 ml
 ejection fraction—usually 60% >> The fraction of the end-
diastolic volume that is ejected.

Function of the Valves
 Atrioventricular Valves: (tricuspid and mitral valves)
o The A-V valves prevent backflow of blood from the
ventricles to the atria during systole.
 Aortic and pulmonary artery valves: (semilunar
valves)
o prevent backflow from the aorta and pulmonary
arteries into the ventricles during diastole.

 For anatomical reasons, the thin, filmy A-V valves require
almost no backflow to cause closure, whereas the much
heavier semilunar valves (Aortic and pulmonary artery
valves) require rapid backflow for a few milliseconds.
 Simple note:
o tricuspid valve: bt. (RA) & (RV).
o mitral valve: bt. (LA) & (LV).
o Aortic valve: bt. the (LV) and the aorta.
o pulmonary valve: bt. (RV) and the pulmonary artery.

Function of the Papillary Muscles.
 papillary muscles that attach to the vanes of the A-V valves
by the chordae tendineae.
 The papillary muscles contract when the ventricular walls
contract, but they do not help the valves to close.
 Instead, they pull the vanes of the valves inward toward
the ventricles to prevent their bulging too far backward
toward the atria during ventricular contraction.
 If a chorda tendinea becomes ruptured or if one of the
papillary muscles becomes paralyzed, the valve bulges far
backward during ventricular contraction, sometimes so far
that it leaks severely and results in severe or even lethal
cardiac incapacity.

Function of the Papillary Muscles.

Aortic Pressure Curve
 left ventricle contracts > the ventricular pressure
increases rapidly until the aortic valve opens > the
pressure in the ventricle rises much less rapidly
(because blood immediately flows out of the ventricle
into the aorta) > blood enter into the arteries causes
the walls of these arteries to stretch and the pressure to
increase to about (120 mm Hg = Systolic p.). Now ….
 the left ventricle stops ejecting blood and the aortic
valve closes - (end of systole)- the elastic walls of the
arteries maintain a high pressure in the arteries,
even during diastole.

Aortic Pressure Curve
 [Incisura: immediately before closure of the valve, it is
caused by a short period of backward flow of blood
followed by sudden cessation of the backflow.]
 Now .. aortic valve has closed > the pressure in the
aorta decreases slowly throughout diastole (because
the blood stored in the distended elastic arteries flows
continually through the peripheral vessels back to the
veins) >the aortic pressure usually fall to about (80
mm Hg = diastolic p)
 diastolic p is two thirds the systolic p that occurs in
the aorta

Relationship of the Heart Sounds
to Heart Pumping
 Opening of the valves >> no sound
 Closure of the valves, >> Sound.
o The vanes of the valves and the surrounding
fluids vibrate under the influence of sudden pressure
changes, giving off sound that travels in all directions
through the chest.

to Heart Pumping
 The first heart sound:
o It’s the sound caused by closure of the A-V valves
(tricuspid and mitral valves) When the ventricles
contract.
o The vibration is low in pitch and relatively long-
lasting.

to Heart Pumping
 The second heart sound:
o Caused by aortic and pulmonary valves (semilunar
valves) closure at the end of systole.
o rapid snap sound because these valves close rapidly,
and the surroundings vibrate for a short period.

to Heart Pumping
 The third heart sound:
o Rapid flow of blood from atria into ventricles
o Its normal in children BUT associated with desease
in adults.

Work Output of the Heart
 Stroke work output:
o The amount of energy that the heart converts to
work during each heartbeat while pumping blood
into the arteries.
 Minute work output:
o The total amount of energy converted to work in 1
minute = (stroke work output * the heart rate)

 Two forms of work output:
 volume-pressure work or external work:
o used to move the blood from the low pressure veins
to the high-pressure arteries.(major)
 kinetic energy of blood flow:
o used to accelerate the blood to its velocity of
ejection through the aortic and pulmonary valves.
(minor)

 Right ventricular external work output is normally
about 1/6 the work output of the left ventricle
because of the sixfold difference in systolic pressures
that the two ventricles pump.

Graphical Analysis of Ventricular
Pumping
 two curves labeled “diastolic pressure” and “systolic
pressure.” curves - volume-pressure curves.
 The diastolic pressure curve:
o is determined by filling the heart with progressively
greater volumes of blood and then measuring the diastolic
pressure immediately before ventricular contraction
occurs, which is the end-diastolic pressure of the
ventricle.
 The systolic pressure curve:
o is determined by recording the systolic pressure achieved
during ventricular contraction at each volume of filling.

“Volume-Pressure Diagram” During the
Cardiac Cycle; Cardiac Work Output

 Phase I: Period of filling:
o Begins at end-systolic volume (The amount of blood
that remains in the ventricle after the previous heartbeat,
50 ml) and a diastolic pressure of 2 to 3 mm Hg.
o As venous blood flows into the ventricle from the left
atrium, the ventricular volume normally increases to about
120 ml, called the end-diastolic volume, an increase of 70
ml.
o During phase I the volume increasing to 120 ml and the
Diastolic pressure rising only to about 5 to 7 mm Hg

 Phase II: Period of isovolumetric contraction:
o the volume of the ventricle does not change
because all valves are closed…. However …
o the pressure inside the ventricle increases to
equal the pressure in the aorta, at a pressure value of
about 80 mm Hg, as depicted by point C.

 Phase III: Period of ejection:
o the systolic pressure rises even higher because of
still more contraction of the ventricle. >> now aortic
valve has opened >>
o the volume of the ventricle decreases because the
and blood flows out of the ventricle into the aorta.

 Phase IV: Period of isovolumetric relaxation:
o the aortic valve closes, and the ventricular
pressure falls back to the diastolic pressure level.
o No change in volume. So …
o ventricle returns to its starting point, with about 50
ml of blood left in the ventricle and at an atrial
pressure of 2 to 3 mm Hg

 The area labeled EW
represents the net
external work output
of the ventricle during
its contraction cycle.

Concepts of Preload and Afterload
 Preload:
o is the degree of tension on the muscle when it begins to
contract
o Its the end-diastolic pressure when the ventricle has become
filled.
 Afterload: (resistance in circulation)
o the load against which the muscle exerts its contractile force.
o It is the pressure in the aorta leading from the ventricle.
o The afterload of the ventricle corresponds to the systolic
pressure described by the phase III curve of the volume-
pressure diagram.

Chemical Energy Required for Cardiac
 oxygen consumption of the heart and the chemical
energy expended during contraction are directly
related to the external work (EW) and an additional
portion called the potential energy (PE).
o The potential energy represents additional work
that could be accomplished by contraction of the
ventricle if the ventricle should empty completely all
the blood in its chamber with each contraction.

 Oxygen consumption has also been shown to be nearly
proportional to what we called the tension-time
index
o the tension that occurs in the heart muscle during
contraction multiplied by the duration of time that
the contraction persists

 Efficiency of Cardiac Contraction:
o The expended chemical energy is converted into heat
and a much smaller portion into work output.
o efficiency of cardiac contraction (efficiency of the heart):
 The ratio of work output to total chemical energy
expended the
 In normal heart Maximum efficiency of is between (20-
25%)
 In heart failure, this can decrease to as low as (5 – 10%)

Regulation of Heart Pumping
 at rest > the heart pumps only 4 to 6 liters of blood
each minute.
 During severe exercise > the heart may be required
to pump four to seven times this amount.
 The basic means by which the volume pumped is
regulated :
(1) intrinsic cardiac regulation of pumping in
response to changes in volume of blood flowing into
the heart.
(2) control of heart rate and strength of heart pumping
by the autonomic nervous system.

Intrinsic Regulation of Heart Pumping—
The Frank-Starling Mechanism
 The amount of blood pumped by the heart each
minute is normally determined almost entirely by
venous return.
 This intrinsic ability of the heart to adapt to increasing
volumes of inflowing blood is called the Frank-
Starling mechanism of the heart.

Intrinsic Regulation of Heart Pumping—
The Frank-Starling Mechanism
 Explanation of the Frank-Starling Mechanism?
o extra amount of blood flows > into the ventricles >
stretched cardiac muscle itself > the muscle to
contract with increased force > the ventricle
automatically pumps the extra blood into the arteries.
 This ability of stretched muscle, up to an optimal
length, to contract with increased work output is
characteristic of all striated muscle, not only a
characteristic of cardiac muscle.

Regulation of Heart Pumping
 another factor increases heart pumping when its
volume is increased.
 Stretch of the right atrial wall > directly increases the
heart rate by (10-20%) … (minor effect)

Control of the Heart by the Sympathetic
and Parasympathetic Nerves
 Sympathetic nerves:
can increase the cardiac output
more than 100%
 parasympathetic (vagus) nerves:
can deccrease the cardiac output
as low as zero or almost zero.

sympathetic stimulation
 increase the heart rate in young adult humans from
the normal rate of 70 beats/min up to 180 to 200 and,
rarely, even 250 beats/min.
 increases the force of heart contraction to as much as
double normal
 increasing the volume of blood pumped
 increasing the ejection pressure.
 So … increase the maximum cardiac output as much
as twofold to threefold, in addition to the increased
output caused by the Frank-Starling mechanism

inhibition of the sympathetic
nerves
 But …. inhibition of the sympathetic nerves:
 Will decrease the cardiac pumping to a moderate
extent only … Why? …
o Under normal conditions, the sympathetic nerve
fibers to the heart maintains pumping at about 30%
above that with no sympathetic stimulation. So ..
o when the activity symp. depressed below normal,
this decreases the level of cardiac pumping as much as
30% below normal.

stimulation of the parasympathetic
nerve fibers (vagus)
 stop the heartbeat for a few seconds, but then the
heart usually “escapes” and beats at a rate of 20 to 40
beats/min as long as the parasympathetic stimulation
continues. In addition ..
 decrease the strength of heart Muscle contraction by
20 to 30 %

stimulation of the parasympathetic
nerve fibers (vagus)
 the effect of vagal stimulation mainly to decrease
heart rate rather than to decrease greatly the strength
of heart contraction …. Why?
o vagal fibers are distributed mainly to the atria
and not much to the ventricles.

Control of the Heart by the Sympathetic
and Parasympathetic Nerves

Effect of Potassium and Calcium
Ions on Heart Function
 Effect of Potassium Ions:
 Excess potassium in the extracellular fluids causes the
heart to become dilated and flaccid and also slows
the heart rate.
 Large quantities also can block conduction of the
cardiac impulse from the atria to the ventricles
through the A-V bundle.
 Elevation of potassium concentration to only 8 to 12
mEq/L— 2-3 times the normal value —can cause
such weakness of the heart and abnormal rhythm
that death occurs.

 Explanation of of Potassium effect:
 high potassium concentration in the extracellular
fluids will lead to >>
o decreases the resting membrane potential in the
cardiac muscle fibers > partially depolarizes the cell
membrane > the membrane potential less negative >
intensity of the action potential also decreases >
contraction of the heart weaker.

 Effect of Calcium Ions: (exactly opposite to those of
potassium)
 excess of calcium ions cause the heart to go toward
spastic contraction.
 deficiency of calcium ions causes cardiac flaccidity,
similar to the effect of high potassium.
 Fortunately, calcium ion levels in the blood normally
are regulated within a very narrow range. Therefore,
cardiac effects of abnormal calcium concentrations are
seldom of clinical concern.

Effect of Temperature on Heart
Function
 Effect of Temperature on Heart Function
 Increased body temperature (fever) > greatly
increased heart rate.
 Decreased temperature > a greatly decreased heart
rate, falling to as low as a few beats per minute (person
is near death from hypothermia)
This is due to:
 heat increases the permeability of the cardiac muscle
membrane to ions that control heart rate, resulting in
acceleration of the self-excitation process.

Effect of Temperature on Heart
Function
 moderate increase in temperature enhance
temporarily Contractile strength of the heart (during
body exercise) … But
 prolonged elevation of temperature exhausts the
metabolic systems of the heart and eventually causes
weakness.

#The heart as a pump and function of the heart valves

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#The heart as a pump and function of the heart valves