Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves Flashcards
The
heart is
actually two separate pumps:
- a right heart that pumps blood through the lungs, and
- a left heart that pumps blood through the peripheral organs
Each of these hearts is a pulsatile two-chamber
pump composed of an :
atrium and a ventricle
What is the funciton of atrium?
Each atrium
is a weak primer pump for the ventricle, helping to move
blood into the ventricle.
The ventricles then supply the main
pumping force that propels the blood either
(1) through the pulmonary circulation by the right ventricle or
(2) through the peripheral circulation
by the left ventricle
What is cardiac rhythmicity?
Special mechanisms in the heart cause a continuing
succession of heart contractions called cardiac rhythmicity, transmitting action potentials throughout the cardiac muscle to cause the heart’s rhythmical beat.
This rhythmical
control system is explained in Chapter 10.
In this chapter,
we explain how the heart operates as a pump, beginning with the special features of cardiac muscle itself.
The heart is composed of three major types of cardiac muscle:
- atrial muscle,
- ventricular muscle, and
- specialized excitatory and conductive muscle fibers.
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
The specialized excitatory and conductive fibers, however, contract only feebly because they contain few contractile fibrils; instead, they 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.
Describe the cardiac muscle as a muscle.
cardiac muscle is striated in the same manner as in skeletal muscle.
Further, cardiac muscle has typical myofibrils that contain actin and myosin filaments almost identical to those found in skeletal muscle; these filaments lie side by side and slide along one another during contraction in the same manner as occurs in skeletal muscle (see Chapter 6). But in other ways, cardiac muscle is quite different from skeletal muscle, as we shall see.
De scribeCardiac Muscle as a Syncytium.
The dark areas crossing the cardiac muscle fibers are called intercalated discs; they are actually cell membranes that separate individual cardiac muscle cells from one another. That is, cardiac muscle fibers are made up of many individual cells connected in series and in parallel with one another.
At each intercalated disc the cell membranes fuse with
one another in such a way that they form permeable “communicating”
junctions (gap junctions) that allow rapid
diffusion of ions. Therefore, from a functional point of
view, ions move with ease in the intracellular fluid along action potentials travel easily from one cardiac muscle cell to the next, past the intercalated discs.
Thus, cardiac
muscle is a syncytium of many heart musclecells in which the cardiac cells are so interconnected that when one of these cells becomes excited, the action potential spreads to all of them, from cell to cell throughout the latticework
interconnections.
the longitudinal axes of the cardiac muscle fibers so that action potentials travel easily from one cardiac muscle cell to the next, past the intercalated discs.
Thus, cardiac
muscle is a syncytium of many heart muscle cells in which the cardiac cells are so interconnected that when one of these cells becomes excited, the action potential spreads to all of them, from cell to cell throughout the latticework
interconnections.
The heart actually is composed of two syncytiums:
- the atrial syncytium, which constitutes the walls of the two atria, and the
- ventricular syncytium, which constitutes the walls of the two ventricles.
How are potentials conducted to the atria?
The atria are separated from the ventricles by fibrous tissue that surrounds the atrioventricular (A-V) valvular openings between the atria and ventricles.
Normally, potentials are not conducted from the atrial syncytium into the ventricular syncytium directly through this fibrous tissue.
Instead, they are conducted only by way of a specialized conductive system called the A-V bundle, a bundle of conductive fibers several millimeters in diameter that is discussed in detail in
What is the reason for the division of the muscle of the heart into two functional syncytium?
This division of the muscle of the heart into two functional
syncytiums allows the atria to contract a short time
ahead of ventricular contraction, which is important for
effectiveness of heart pumping.
Action Potentials in Cardiac Muscle
The action potential recorded in a ventricular muscle fiber averages about 105 millivolts, which means that the intracellular potential rises from a very negative value, about −85 millivolts, between beats to a slightly positive value, about +20 millivolts, during each beat.
After the initial spike, the membrane remains depolarized for about 0.2 second, exhibiting a plateau as shown in the figure, followed at the end of the plateau by abrupt repolarization.
The presence of this plateau in the action potential causes ventricular contraction to last as much as 15 times as long in cardiac muscle as in skeletal muscle.
What Causes the Long Action Potential and the
Platea?
Why
is the action potential of cardiac muscle so long and
why does it have a plateau, whereas that of skeletal muscle does not?
At least two major differences between the membrane
properties of cardiac and skeletal muscle account for the
prolonged action potential and the plateau in cardiac muscle.
- First, the action potential of skeletal muscle is caused almost entirely by sudden opening of large numbers of socalled fast sodium channels that allow tremendous numbers of sodium ions to enter the skeletal muscle fiber from the extracellular fluid.
These channels are called “fast” channels because they remain open for only a few thousandths of a second and then abruptly close.
At the end of
this closure, repolarization occurs, and the action potential is over within another thousandth of a second or so.
- The second major functional difference between cardiac muscle and skeletal muscle that helps account for both the prolonged action potential and its plateau is this:
Immediately after the onset of the action potential, the permeability
of the cardiac muscle membrane for potassium
ions decreases about fivefold, an effect that does not occur in skeletal muscle This decreased potassium permeability may result from the excess calcium
influx through the calcium channels just noted.
Regardless of the cause,
the decreased potassium permeability greatly decreases the outflux of positively charged potassium ions during the action potential plateau and thereby prevents early return of the action potential voltage to its resting level.
When the
slow calcium-sodium channels do close at the end of 0.2 to 0.3 second and the influx of calcium and sodium ions ceases, the membrane permeability for potassium ions also increases rapidly; this rapid loss of potassium from the fiberimmediately returns the membrane potential to its resting level, thus ending the action potential.
In cardiac muscle, the action potential is caused by opening of two types of channels:
- (1) the same fast sodium channels as those in skeletal muscle and
- (2) another entirely different population of slow calcium channels, which are also called calcium-sodium channels.
Explain the
different population of slow calcium channels, which are
also called calcium-sodium channels in the cardiac muscle.
This second population
of channels differs from the fast sodium channels in
that they are 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.
Further, the calcium ions that enter during this plateau phase activate the muscle contractile process, while the calcium ions that cause skeletal muscle contraction are
derived from the intracellular sarcoplasmic
reticulum.
The second major functional difference between cardiac
muscle and skeletal muscle that helps account for
both the prolonged action potential and its plateau is this:
Immediately after the onset of the action potential, the permeability of the cardiac muscle membrane for potassium ions decreases about fivefold, an effect that does not occur in skeletal muscle.
The second major functional difference between cardiac
muscle and skeletal muscle that helps account for
both the prolonged action potential and its plateau is this:
Explain the reason for decreased potassium permeability
This decreased potassium permeability
may result from the excess calcium
influx through the calcium channels just noted.
Regardless of the cause,
the decreased potassium permeability greatly decreases the outflux of positively charged potassium ions during the action potential plateau and thereby prevents early return
of the action potential voltage to its resting level.
When the slow calcium-sodium channels do close at the end of 0.2 to 0.3 second and the influx of calcium and sodium ions ceases, the 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, thus ending the action potential.
Velocity of Signal Conduction in Cardiac Muscle
The velocity of conduction of the excitatory action potential signal along both atrial and ventricular muscle fibers is about 0.3 to 0.5 m/sec, or about 1⁄250 the velocity in very large nerve fibers and about 1⁄10 the velocity in skeletal muscle fibers.
The velocity of conduction in the specialized heart conductive system—in the Purkinje fibers—is as great as 4 m/sec in most parts of the system, which allows reasonably rapid conduction of the excitatory signal to the different parts of the heart, as explained in Chapter 10.
Explain the Refractory Period of Cardiac Muscle.
Cardiac muscle, like all excitable tissue, is refractory to restimulation during the action potential.
Therefore, the refractory period of the
heart is the interval of time, during which anormal cardiac impulse cannot reexcite
an already excited area of cardiac muscle
What is the normal refractory pd of the ventricle?
The normal
refractory period of the ventricle is 0.25 to 0.30 second,
which is about the duration of the prolonged plateau action potential.
Describe the early “ premature” contraction.
There is an additional relative refractory period of about 0.05 second during which the muscle is more difficult than normal to excite but nevertheless can be excited by a very strong excitatory signal, as demonstrated by the early “premature” contraction in the second example of Figure 9-4.
What is the refactory period of the atrial muscle?
The refractory period of atrial muscle is much shorter than that for the ventricles (about 0.15 second for the atria compared with 0.25 to 0.30 second for the ventricles).
What is “excitation-contraction coupling?
The term “excitation-contraction coupling” refers to the
mechanism by which the action potential causes the
myofibrils of muscle to contract. T
his was discussed for
skeletal muscle in Chapter 7. Once again, there are differences in this mechanism in cardiac muscle that have
important effects on the characteristics of heart muscle
contraction
As is true for skeletal muscle, when an action potential passes over the cardiac muscle membrane, the action potential spreads to the interior of the cardiac muscle fiber along the membranes of the transverse (T) tubules.
The T tubule action potentials in turn act on the membranes of the longitudinal sarcoplasmic tubules to cause release of calcium ions into the muscle sarcoplasm from the sarcoplasmic reticulum.
In another few thousandths of a second, these calcium ions diffuse into the myofibrils and catalyze the chemical reactions that promote sliding of the actin and myosin filaments along one another; this produces the muscle contraction.
Thus far, this mechanism of excitation-contraction coupling is the same as that for skeletal muscle, but there is a second effect that is quite different which is:
In addition to the calcium ions that are released into the sarcoplasm from the cisternae of the sarcoplasmic reticulum, calcium ions also diffuse into the sarcoplasm from the T tubules themselves at the time of the action potential, which opens voltage-dependent calcium channels in the membrane of the T tubule (Figure 9-5).
Calcium entering the cell then activates calcium release channels, also called 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 by the same basic mechanism as described for skeletal muscle in Chapter 6.
Without the calcium from the T tubules, the strength of cardiac muscle contraction would be reduced considerably why?
because the sarcoplasmic reticulum of cardiac muscle is less well developed than that of skeletal muscle and does not store enough calcium to provide full contraction.
The T tubules of cardiac muscle, however, have a diameter 5 times as great as that of the skeletal muscle tubules, which means a volume 25 times as great.
Also, inside the T tubules is a large quantity of mucopolysaccharides that are electronegatively charged and bind an abundant store of calcium ions, keeping these always available for diffusion to the interior of the cardiac muscle fiber when a T tubule action potential appears
The strength of contraction of cardiac muscle depends to a great extent on the______________.
concentration of calcium ions in the extracellular fluids.
In fact, a heart placed in a calcium- free solution will quickly stop beating.
The reason for this is that the openings of the T tubules pass directly through the cardiac muscle cell membrane into the extracellular spaces surrounding the cells, allowing the same extracellular
fluid that is in the cardiac muscle interstitium
to percolate through the T tubules as well.
Consequently,
the quantity of calcium ions in the T tubule system (i.e., the availability of calcium ions to cause cardiac muscle contraction) depends to a great extent on the extracellular fluid calcium ion concentration.
In comparison to skeletal muscle, is it affected by moderate changes in the extracellular fluid calcium concentration?
In contrast, the strength of skeletal muscle contraction
is hardly affected by moderate changes in extracellular
fluid calcium concentration because 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, what happens?
the influx of calcium ions to the interior of the muscle fiber is suddenly cut off, and the 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.
Transport of calcium back into
the sarcoplasmic reticulum is achieved with the help of a calcium-ATPase pump (see Figure 9-5).
Calcium ions are also removed from the cell by a sodium-calcium exchanger.
The sodium that enters the cell during this exchange is
then transported out of the cell by the sodium-potassium
ATPase pump. As a result, the contraction ceases until
a new action potential comes along.
Duration of Contraction.
Cardiac muscle begins to contract
a few milliseconds after the action potential begins
and continues 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— about0.2 second in atrial muscle and 0.3 second in ventricular
muscle
What is a cardiac cycle?
The cardiac events that occur from the beginning of one heartbeat to the beginning of the next are called the cardiac cycle.
How is the cardiac cycle initiated?
Each cycle is initiated by spontaneous generation of an action potential in the sinus node, as explained in Chapter 10.
This node is located in the superior lateral wall of the right atrium near the opening of the superior vena cava, and the action potential travels from here rapidly through both atria and then through the A-V bundle into the ventricles.
Because of this special arrangement of the conducting system from the atria into the ventricles, there is a delay of more than 0.1 second during passage of the cardiac impulse from the atria into the ventricles.
This allows the atria to contract ahead of ventricular contraction, thereby pumping blood into the ventricles before the strong ventricular contraction begins.
Thus, the atria act as primer pumps for the ventricles, and the ventricles in turn provide the major source of power for moving blood through the body’s vascular system.
What is a diastole?
The cardiac cycle consists of a period of relaxation called diastole, during which the heart fills with blood.
What is a systole?
a period of contraction that follows diastole
Describe the total duration of the cardiac cycle.
The total duration of the cardiac cycle, including systole
and diastole, is the reciprocal of the heart rate.
For example, 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
Figure 9-6 shows the different events during the cardiac cycle for the left side of the heart.
The top three
curves show the pressure changes in the aorta, left ventricle, and left atrium, respectively.
The fourth curve depicts
the changes in left ventricular volume, the fifth the electrocardiogram, and the sixth a phonocardiogram, which is a recording of the sounds produced by the heart—mainly by the heart valves—as it pumps.
It is especially important
that the reader study in detail this figure and understand
the causes of all the events shown.
Effect of Heart Rate on Duration of Cardiac
Cycle.
When heart rate increases, the duration of each
cardiac cycle decreases,including thecontraction and
relaxation phases.
The duration of the action potential
and the period of contraction (systole) also decrease, but not by as great a percentage as does the relaxation phase
(diastole).
At a normal heart rate of 72 beats/min, systole
comprises about 0.4 of the entire cardiac cycle.
At three
times the normal heart rate, systole is about 0.65 of the entire cardiac cycle.
This means 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
What is the P wave?
The P wave is caused by 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.
What is QRS wave?
About 0.16 second after the onset of the P wave, the
- *QRS waves appear as a result of electrical depolarizatio**n of the ventricles, which initiates contraction of the ventricles and causes the ventricular pressure to begin rising,as also shown in the figure. Therefore, the QRS complex
- *begins slightly before the onset of ventricular systole.**
What is the T wave?
Finally, one observes the ventricular T wave in the
electrocardiogram.
This represents the stage of repolarization
of the ventricles when the ventricular muscle
fibers begin to relax.
Therefore, the T wave occurs slightly
before the end of ventricular contraction.
Graphical Analysis of Ventricular Pumping
Figure 9-8 shows a diagram that is especially useful in explaining the pumping mechanics of the left ventricle.
The most
important components of the diagram are the two curves labeled “diastolic pressure” and “systolic pressure.”
These
curves are volume-pressure curves.
The diastolic pressure curve 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 is determined by recording
the systolic pressure achieved during ventricular contraction
at each volume of filling.
Until the volume of the noncontracting ventricle rises
above about 150 ml, the “diastolic” pressure does not increase
greatly. Therefore, up to this volume, blood can flow easily
into the ventricle from the atrium. Above 150 ml, the ventricular diastolic pressure increases rapidly, partly because of fibrous tissue in the heart that will stretch no more and partly because the pericardium that surrounds the heart becomes filled nearly to its limit.
During ventricular contraction, the “systolic” pressure
increases even at low ventricular volumes and reaches a maximum
at a ventricular volume of 150 to 170 ml. Then, as the
volume increases still further, the systolic pressure actually decreases under some conditions, as demonstrated by the falling systolic pressure curve in Figure 9-8, because at these
great volumes, the actin and myosin filaments of the cardiac muscle fibers are pulled apart far enough that the strength of each cardiac fiber contraction becomes less than optimal.
Note especially in the figure that the maximum systolic
pressure for the normal left ventricle is between 250 and 300 mm Hg, but this varies widely with each person’s heart strength and degree of heart stimulation by cardiac nerves.
For the normal right ventricle, the maximum systolic pressure is between 60 and 80 mm Hg
Effect of Sympathetic or Parasympathetic Stimulation
on the Cardiac Function Curve
Figure 9-13 shows four cardiac function curves.
They are similar to the ventricular function curves of Figure 9-11. However, they represent function of the entire heart rather than of a single ventricle; they show the relation between right atrial pressure at the input of the right heart and cardiac output from the left ventricle into the aorta.
The curves of Figure 9-13 demonstrate that at any given right atrial pressure, the cardiac output increases during increased sympathetic stimulation and decreases during increased parasympathetic stimulation.
These changes in
output caused by autonomic nervous system stimulation result both from changes in heart rate and from changes in contractile strength of the heart because both change in response to the nerve stimulation.
