Cardiac Pump
OBJECTIVES
• Describe
how the heart enable it to pump blood through
the systemic and pulmonary circulations.
• Discuss the pressure changes in the heart chambers and
great vessels during a complete cardiac cycle.
• List the factors that determine cardiac contractile force.
• Explain how electrical excitation of the heart is coupled
to its contractions.
The Structures of the Heart is Designed for Optimal
Function
Several important morphological and functional differences
exist between myocardial and skeletal muscle cells
• A striking difference is that
cardiac muscle appears to be a
syncytium (a functional
syncytium, not a true anatomical
syncytium )
• with branching and
interconnecting fibers,
whereas skeletal muscle cells
do not interconnect.
Cardiac muscle functions as a syncytium because a wave
of depolarization, followed by contractions of the atria and
ventricles (an all-or-none response), occurs when a
uprathreshold stimulus is applied.
As the wave of excitation
approaches the end of a cardiac
cell, the spread of excitation to
the next cell depends on the
electrical conductance of the
boundary between the two cells.
Gap junctions (nexuses) with
high conductance are present
in the intercalated disks
between adjacent cells.
cardiac impulse from one
cell to the next, are made up
of connexons,
• cardiac muscle is richly
endowed with mitochondria
(sarcosomes) which contain the
respiratory enzymes necessary
for oxidative phosphorylation.
• To provide adequate O2 and substrate for its metabolic
machinery, the myocardium is also endowed with a rich
capillary supply, about one capillary per fiber.
The cardiac chambers consist of two atria, two
ventricles, and four valves
The cardiac valves consist of
thin flaps of tough, flexible,
endothelium-covered fibrous
tissue firmly attached at the
base to the fibrous valve rings.
Movements of the valve
leaflets are essentially passive,
and the orientation of the
cardiac valves is responsible
for the unidirectional flow of
blood through the heart.
Cardiac valves are interposed between atria and ventricle
• Atrioventricular
valves .
The tricuspid valve lies
between the right atrium
and right ventricle and is
made up of three cusps,
The mitral valve lies
between the left atrium
and left ventricular and
has two cusps.
• Semilunar valves
The valves between the right
ventricle and pulmonary artery
and between the left ventricle
and aorta consist of three cuplike
cusps attached to the valve rings.
At the end of the reduced
ejection phase of ventricular
systole, blood flow reverses
briefly toward the ventricles.
This flow reversal snaps the
cusps together and prevents
regurgitation of blood into the
ventricles.
The pericardium is an epithelialized fibrous sac
that invests the heart
The pericardium consists of a visceral
layer that is adherent to the
epicardium and a parietal layer
separated from the visceral layer by a
thin layer of fluid. The fluid layer
provides lubrication for the continuous
movement of the enclosed heart. The
pericardium is nor very distensible and
thus strongly resists a large, rapid
increase in cardiac size. Therefore the
pericardium helps prevent sudden over
distention of the heart chambers.
The Cardiac Cycle is the Sequential Contraction and
Relaxation of Atria and Ventricles
Ventricular systole is initiated by
Ventricular excitation
(1) lsovolumic contraction
• The interval between the start of
ventricular systole and the opening of the
semilunar valves is called isovolumic
contraction because ventricular volume is
constant during this brief period.
• Ventricular pressure rises abruptly
(2) Ejection
rapid ejection: The rapid-ejection
phase is characterized by the sharp rise
in ventricular and aortic pressures that
terminates at the peak ventricular and
aortic pressures, an abrupt decrease in
ventricular volume, and a large aortic
blood flow.
reduced ejection: During the reduced
ejection period, runoff of blood from
the aorta to the periphery exceeds
ventricular output, so aortic and
ventricular pressures decline.
Throughout ventricular systole the
blood returning to the atria
progressively increases atrial pressure.
At the end of ejection a volume of
blood approximately equal to that
ejected during systole remains in the
ventricular cavities. This residual
volume is fairly constant in normal
hearts.
However, it is smaller ?
when heart rate increases or when
outflow resistance is reduced,
Ventricular filling occurs during diastole
(1) Isovolumic relaxation
The period between closure of the
semilunar valves and opening of the AV
valves is called isovolumic relaxation.
It is characterized by a precipitous
fall in ventricular pressure without a
change in ventricular volume.
(2) Rapid filling phase
Ventricular filling occurs immediately
after the AV valves open. The blood that
had returned to the atria during the
previous ventricular systole is abruptly
released into the relaxing ventricles. The
atrial and ventricular pressures decrease
despite the increase in ventricular volume
(3) Diastasis (slow filling)
During diastasis, blood returning from the
periphery flows into the right ventricle,
and blood from the puhnunary circulation
flows into the left ventricle.
This small, slow addition to ventricular
filling is indicated by gradual increases
in atrial, ventricular, and venous
pressures and in ventricular volume.
(4) Atrial systole
The onset of atrial systole occurs soon
after the beginning of the P wave of the
electrocardiogram. The transfer of
blood from atrium to ventricle.
A Graph of the Cardiac Pressure-Volume Relationship
Reveals the Sequence of Dynamic Changers During
Single Cardiac Cycle
The two major heart sounds are produced mainly by
closure of the cardiac valves
Four sounds are usually produced by the heart, but only two are
ordinarily audible through a stethoscope.
With electronic amplification the heart sounds, even the less
intense sounds, can be detected and recorded graphically as a
phonocardiogram.
The first heart sound is initiated at
the onset of ventricular systole and
consists of a series of vibrations of
mixed, unrelated low frequencies (a
noise). It is the loudest and longest
of the heart sounds.
The second heart sound, which occurs with closure of the
semilunar valves , is composed of higher-frequency vibrations
(higher pitch), is of shorter duration and lower intensity, and has a
more snapping quality than the first heart sound.
The third heart sound is usually not audible, but it is sometimes
heard in children with thin chest walls or in patients with left
ventricular failure.
A fourth, or atrial sound, consisting
of a few Iow-frequency oscillations, is
occasionally heard in healthy
individuals.
The length-force relationship of myocardial fibers
determines myocardial contraction
Skeletal muscle and cardiac
muscle show similar length-force
relationships. The developed
force is maximal when cardiac
muscle begins contracting at
resting sarcomere lengths of 2.0
to 2.4 m.
0.35
1.5µm
0.65
Z
0.35
M 0.65
0.20
sarcomere
At such lengths, overlap of the thick and thin filaments is
optimal, and the number of cross bridge attachments is
maximal
Z
Developed force (the force
attained during contraction) may
be expressed as ventricular
relationship of force-length or
systolic pressure,
pressure- initial volume.
Myocardial resting fiber length
This is known as the Frankmay be expressed as endStarling relationship, named after
diastolic ventricular volume.
the scientists who first described it.
The pressure-volume curve in
diastole is flat at low volumes.
Thus, large increases in volume
can be accommodated with only
small increases in pressure; that
is, the ventricle is compliant.
Nevertheless, the systolic
pressure is considerable at the
lower filling pressures. The
ventricle becomes much less
The normal heart operates
compliant with greater filling,
only on the ascending portion
however, as evidenced by the
sharp rise of the diastolic curve at of the Frank-Starling curve
(upper curve).
large intraventricular volumes.
Excitation-contraction coupling is mediated by Ca 2+
• The heart requires optimum concentrations of Na+, K+ and
Ca++ to function normally. ?
• Ca++ is also essential for cardiac contraction. Removal of
Ca++ from the extracellular fluid decreases contractile
force and eventually causes arrest in diastole.
• Conversely, an increase in the extracellular Ca++
concentration enhances contractile force, but very high Ca++
concentrations induce cardiac arrest in systole (rigor).
Preload and afterload are determinants
of cardiac performance
Preload and
afteload in a
papillary
muscle
A, Resting stage in the intact heart just before opening of the AV
valves. B, Preload in the intact heart at the end of ventricular
filling. C, Supported preload plus afterload in the intact heart just
before opening of the aortic valve. D, Lifting preload plus
afterload in the intact heart: ventricuiar ejection with decreased
ventricular volume. AL, Afterload; PL, preload; PL and AL, total
load.
The preload can be increased by greater
filling of the left ventricle during diastole.
At lower end-diastolic volumes,
increments in filling pressure
during diastole elicit a greater
systolic pressure during the
subsequent contraction. Systolic
pressure increases until a maximum
systolic pressure is reached at the
optimum preload.
If diastolic filling continues beyond
this point, no further increase in
developed pressure occurs. At very
high filling pressures, peak pressure
development in systole is reduced.
optimum preload
At a constant preload, a higher systolic pressure can be reached
during ventricular contractions by raising the afterload
(increasing aortic pressure). Increments in afterload produce
progressively higher peak systolic pressures.
If the afterload continues to
increase, it becomes so great that
the ventricle can no longer
generate enough force to open the
aortic valve At this point,
ventricular systole is totally
isometric there is no ejection of
blood and thus no change in the
volume of the ventricle during
systole.
Force and velocity are functions of the intracellular
concentration of free Ca++. When velocity is constant, force
equals the afterload during contraction of the muscle. Force
and velocity are inversely related.
Preloads and afterloads depend
on certain characteristics of the
vascular system and the behavior
of the heart.
In heart failure the preload can
be substantially increased ;
In essential hypertension the
high peripheral resistance
augments the afterload
Contractility
Contractility represents the performance of the heart at
a given preload and afterload at constant heart rate.
Contractility can be augmented by certain medications,
such as norepinephrine or digitalis, and by an increase in
contraction frequency (tachycardia). The increase in
contractility (positive inotropic effect) produced by any of
these interventions is reflected by increments in developed
force and velocity of contraction.
•
A hypodynamic heart is characterized by an elevated enddiastolic pressure, a slowly rising ventricular pressure, and a
somewhat reduced ejection phase (curve C).
A hyperdynamic heart (such as a heart
stimulated by norepinephrine) shows a
reduced end-diastolic pressure, a fastrising ventricular pressure, and a brief
ejection phase (curve B). The slope of the
ascending limb of the ventricular pressure
curve indicates the maximum rate of force
development by the ventricle (maximum
rate of change in pressure with time,
maximum dP/dt, the slope provides an
index of the initial contraction velocity and
hence contractility.