Heart Muscle
Heart Muscle
Heart Muscle
Special mechanisms in the heart cause a continuing succession of heart contractions called cardiac rhythmicity
Muscle as a Syncytium
The dark areas - intercalated discs; cell membranes that separate individual cells
series and in parallel with one another
permeable “communicating” junctions (gap junctions) - almost free diffusion of ions
ions move with ease in intracellular fluid along longitudinal axes of cardiac muscle fibers
past the intercalated discs
AP ventricular muscle fiber- 105 mv(-85 +20) spike-> depol 0.2 s plateau -> repol
ventricular contraction 15 times as long in cardiac muscle as in skeletal muscle
action potential of skeletal muscle - sudden opening of fast sodium channels -remain open for few
thousandths of a second
At the end of this closure, repolarization occurs, and the action potential is over within another
thousandth of a second or so.
In cardiac muscle- two types of channels:
fast sodium channels as those in skeletal muscle
slow calcium channels or calcium-sodium channels
slower to open and, remain open for several tenths of a second
large quantity of both calcium and sodium ions flows
maintains a prolonged period of depolarization- plateau in the AP
calcium ions that enter - activate the muscle contractile process
Immediately after the onset of the action potential, the permeability of the cardiac muscle membrane
for potassium ions decreases fivefold, an effect that does not occur in skeletal muscle.
may result from the excess calcium influx
decreases the outflux of positively charged potassium ions
prevents early return of the action potential voltage to its resting level
When the slow calcium-sodium channels close at the end of 0.2 to 0.3 sec-influx of Ca++, Na+ ceases,
the membrane permeability for potassium ions also increases rapidly
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.
mechanism by which the action potential causes the myofibrils of muscle to contract
AP spreads to the interior of the cardiac muscle fiber along the membranes of the (T) tubules
T tubule AP act on membranes of the longitudinal sarcoplasm tubules - release of Ca from SR
1/1000s -calcium diffuse into the myofibrils - muscle contraction.
large quantity of extra calcium ions also diffuses into the sarcoplasm from the T tubules
T tubules of cardiac muscle have a diameter 5 times as great as that of the skeletal
inside the T tubules - large quantity of mucopolysaccharides - electronegatively charged –Ca++
keeping these always available
At the end of the plateau -influx of calcium ions - cut off
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.
0.2 second in atrial muscle and 0.3 second in ventricular muscle
Each cycle is initiated in the sinus node
superior lateral wall of the right atrium near the opening of the superior vena cava
AP travels
o through both atria and then
o through the A-V bundle into the ventricles.
o delay 0.1 s during passage of the cardiac impulse from the atria into the ventricles
o atria to contract ahead of ventricular contraction
o the atria act as primer pumps for the ventricles
o ventricles provide the major source of power
Diastole and Systole
different events during the cardiac cycle for the left side of the heart
top three curves - pressure changes in the aorta, left ventricle, and left atrium
fourth curve the changes in left ventricular volume,
the fifth the electrocardiogram
sixth a phonocardiogram
The P wave -spread of depolarization through atria-> atrial contraction-> rise in atrial pressure curve
immediately after the electrocardiographic P wave.
0.16 second after the onset of the P wave,
the QRS (depolarization of the ventricles) -> contraction of the ventricles ->ventricular pressure+
QRS complex begins slightly before the onset of ventricular systole
ventricular T -repolarization of the ventricles - ventricular muscle fibers relax- slightly before the end
of ventricular contraction
Atria as Primer Pumps Blood normally flows continually from the great veins into the atria;
80% blood flows directly through the atria into the ventricles before atria contract
atrial contraction + 20 % filling of the ventricles. Therefore, the atria simply function as
primer pumps that increase the ventricular pumping effectiveness as much as 20 per cent
heart can continue to operate under most conditions even without this extra 20 per cent
normally has capability of pumping 300-400 % more blood than required by resting body
atria fail to function-difference is unlikely to be noticed unless a person exercises
acute signs of heart failure occasionally develop, especially shortness of breath
In the atrial pressure curve - three minor pressure elevations, called the a, c, and v atrial pressure
waves
a wave - caused by atrial contraction
o right atrial pressure increases 4 to 6 mm Hg during atrial contraction
o left atrial pressure increases about 7 to 8 mm Hg
c wave occurs when the ventricles begin to contract caused by
o slight backflow of blood into the atria at onset of ventricular contraction
o bulging A-V valves backward toward atria because of increasing pressure in ventricles
v wave occurs toward the end of ventricular contraction
o blood flow in atria from veins while A-V valves closed during ventricular contraction
o when ventricular contraction is over, A-V valves open, allowing stored atrial blood to flow
rapidly into ventricles and causing v wave to disappear
Period of Ejection
A-V (tricuspid and mitral) prevent backflow of blood from ventricles to atria during systole
semilunar(aortic, pulmonary artery) from aorta, pulmonary arteries to ventricles in diastole
valves close and open passively
close when a backward pressure gradient pushes blood backward
open when a forward pressure gradient forces blood in the forward direction
the thin, filmy A-V valves require almost no backflow to cause closure
the much heavier semilunar valves require rather rapid backflow for a few milliseconds
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.
high pressures in arteries at the end of systole cause semilunar valves to snap closed, in contrast to
the much softer closure of the A-V valves
because of smaller openings, the velocity of blood ejection through the aortic and pulmonary valves is
greater than that through the much larger A-V valves
because of the rapid closure and rapid ejection, the edges of the aortic and pulmonary valves are
subjected to much greater mechanical abrasion than are the A-V valves
the A-V valves are supported by the chordae tendineae (not true for the semilunar)
constructed with strong yet very pliable fibrous tissue, to withstand extra physical stresses
left ventricle contracts, the ventricular pressure increases until the aortic valve opens
valve open, pressure in ventricle rise slower, cause blood fastly flows out ventricle into aorta
blood enters arteries -> walls of these arteries stretch and pressure increases to 120 mm Hg
at the end of systole, after the left ventricle stops ejecting blood and the aortic valve closes, the elastic
walls of the arteries maintain a high pressure in the arteries, even during diastole
incisura occurs in aortic pressure curve when aortic valve closes -short period of backward flow of
blood immediately before closure of valve, followed by sudden cessation of backflow
aortic valve has closed, pressure in aorta decreases slowly throughout diastole
Before ventricle contracts again, aortic pressure fallen to 80 mmHg (diastolic), which is 2/3 of maximal
pressure of 120 mm Hg (systolic) in aorta during ventricular contraction
pressure curves in right ventricle, pulmonary artery similar to aorta, but pressure 1/6 great
The stroke work output of the heart = amount of energy that the heart converts to work during each
heartbeat while pumping blood into the arteries.
Minute work output = total amount of energy converted to work in 1 minute; stroke work output x the
heart rate per minute.
Work output of the heart is in two forms.
First:
o major proportion, used to move blood: low-pressure veins to high-pressure arteries
o called volume-pressure work or external work
Second:
o minor proportion of the energy, used to accelerate blood to its velocity of ejection through
the aortic and pulmonary valves.
o kinetic energy of blood flow component of the work output
Right ventricular external work output is normally 1/6 L of left ventricle
o because of sixfold difference in systolic pressures that two ventricles pump
The additional work output of each ventricle required to create kinetic energy of blood flow is
proportional to the mass of blood ejected times the square of velocity of ejection.
Ordinarily, the work output of the left ventricle required to create kinetic energy of blood flow is only
about 1 per cent of the total work output of the ventricle and therefore is ignored in the calculation of
the total stroke work output.
But in certain abnormal conditions, such as aortic stenosis, in which blood flows with great velocity
through the stenosed valve, more than 50 per cent of the total work output may be required to create
kinetic energy of blood flow.
diastolic pressure curve - filling heart with bigger blood volumes, measure diastolic pressure before
ventricular contraction= end-diastolic pressure of the ventricle
systolic pressure curve - systolic pressure in ventricular contraction at each volume of filling
volume of noncontracting ventricle< 150 milliliters, the “diastolic” pressure does not increase
up to this volume, blood can flow easily into the ventricle from the atrium
Above 150 milliliters, ventricular diastolic pressure increases, fibrous tissue in the heart will stretch no
more, because the pericardium, becomes filled nearly to its limit.
During ventricular contraction, “systolic” pressure increases even at low ventricular volumes and
reaches a maximum at a ventricular volume of 150 to 170 milliliters.
volume increases further, systolic pressure decreases, actin and myosin filaments are pulled apart,
strength of each cardiac fiber contraction becomes less than optimal.
max systolic pressure for normal left ventricle=250-300, varies with heart strength, nerves
For the normal right ventricle, the maximum systolic pressure is between 60 and 80 mm Hg.
Readers well trained in the basic principles of physics should recognize that the area subtended by this
functional volume-pressure diagram (the tan shaded area, labeled EW) represents the net external work
output of the ventricle during its contraction cycle. In experimental studies of cardiac contraction, this diagram
is used for calculating cardiac work output.
When the heart pumps large quantities of blood, the area of the work diagram becomes much larger.
This energy derived from oxidative metabolism of fatty acids, lactate and glucose.
rate of oxygen consumption =measure chemical energy liberated while heart performs work
amount of blood pumped - determined almost entirely by the rate of blood flow into the heart from
the veins, which is called venous return
each peripheral tissue of the body controls its own local blood flow
all the local tissue flows combine and return by way of the veins to the right atrium.
This intrinsic ability of the heart to adapt to increasing volumes of inflowing blood is called the
FrankStarling mechanism of the heart, in honor of Frank and Starling, two great physiologists of a
century ago.
greater the heart muscle is stretched during filling, the greater is force of contraction and the greater
the quantity of blood pumped into the aorta.
the heart pumps all the blood that returns to it by the way of the veins
atrial pressure ++, stroke work output side++ -> reach limit of ventricle’s pumping ability
Strong sympathetic stimulation 70 -> 180 to 200 and, rarely, even 250
force of heart contraction to as much x2 -> +volume of blood pumped ; the ejection pressure
increase the maximum cardiac output x2-x3
Under normal conditions, sympathetic nerve fibers to heart discharge continuously slow rate
maintains pumping at about 30 per cent above that with no sympathetic stimulation
sympathetic nervous system is depressed below normal,
decreases both heart rate and strength of ventricular muscle contraction
K in extracellular fluids causes - heart become dilated and flaccid; slows the heart rate
Large quantities block conduction of impulse from atria to ventricles through A-V bundle
Elevation of potassium concentration 8-12 mEq/L(x2)— abnormal rhythm can cause death
high potassium concentration in extracellular fluids decreases resting membrane potential
intensity of the action potential also decreases, makes contraction progressively weaker
spastic contraction
calcium ions initiate the cardiac contractile process
deficiency – flaccidity
cardiac effects of abnormal calcium concentrations are seldom of clinical concern