The heart

two separate pumps:

 right pumps blood through the lungs

 left pumps blood through the peripheral organs
 Each atrium is a weak primer pump for the ventricle

Special mechanisms in the heart cause a continuing succession of heart contractions called cardiac rhythmicity

Physiology of Cardiac Muscle

 cardiac muscle: atrial, ventricular muscle, specialized excitatory;conductive muscle fibers

 The atrial and ventricular - same way as skeletal muscle, much longer.
 the specialized excitatory and conductive fibers contract feebly contain few contractile fibrils;
 either automatic rhythmical electrical discharge (AP) or conduction of AP excitatory
 striated in the same manner as in typical skeletal muscle
 typical myofibrils that contain actin and myosin filaments

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

actually is composed of two syncytiums:

 the atrial syncytium -the walls of the two atria

 ventricular syncytium that constitutes the walls of the two ventricles
 atria separated from ventricles by fibrous tissue that surrounds the (A-V) valvular openings
 potentials not conducted from atrial into ventricular syncytium directly
 conducted by specialized conductive system called the A-V bundle-millimeters in
 allows atria contract short time ahead ventricular contraction- effective heart pumping

Action Potentials in Cardiac Muscle

 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

What Causes the Long Action Potential and the Plateau

 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

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.

in the specialized heart conductive system—in the Purkinje fibers—4 m/sec

Refractory Period of Cardiac Muscle.

 Cardiac muscle- refractory to restimulation during the action potential.

 0.25 to 0.30 s-about the duration of the prolonged plateau action potential
 additional relative refractory period 0.05-hard to excite - early “premature” contr
 The refractory period of atrial muscle 0.15 second ; 0.25 to 0.30 ventricles

Excitation-Contraction Coupling—Function of Calcium Ions and the Transverse Tubules

 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

The cardiac cycle

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

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

 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

Function of the Ventricles as Pumps

Filling of the Ventricles

 rapid filling of the ventricles

o During ventricular systole, blood gather in right, left atria because closed A-V valves.
o systole is over, ventricular pressures fall to low diastolic values
o the moderately increased pressures that developed in atria during ventricular systole push
the A-V valves open and allow blood to flow rapidly into ventricles
o The period of rapid filling lasts for about the first third of diastole.
 middle third of diastole- small amount flows into ventricles; this is blood that continues to empty into
atria from the veins and passes through the atria directly into the ventricles
 last third of diastole, atria contract and give an additional thrust to the inflow of blood into the
ventricles; this accounts for about 20 per cent of the filling of the ventricles during each heart cycle

Emptying of the Ventricles During Systole

Period of Isovolumic (Isometric) Contraction.

 Immediately after ventricular contraction begins

 the ventricular pressure rises abruptly
 the A-V valves close
 0.02 to 0.03 s required for ventricle to build up sufficient pressure to push semilunar (aortic and
pulmonary) valves open against pressures in aorta and pulmonary artery
 during this period, 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 is occurring

Period of Ejection

 left ventricular pressure rises above 80 mm Hg (right above 8 mm Hg)

 ventricular pressures push the semilunar valves open
 blood begins to pour out of the ventricles
 70 per cent of blood emptying occurring during 1/3 of the period of ejection
 30 per cent emptying during the next 2/3
 first third, period of rapid ejection, and last two thirds, period of slow ejection

Period of Isovolumic (Isometric) Relaxation

 At the end of systole, ventricular relaxation begins suddenly

 both the right and left intraventricular pressures to decrease rapidly
 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
 another 0.03 -0.06 s ventricular muscle relaxes even though ventricular volume dont change
 intraventricular pressures decrease rapidly back to their low diastolic levels
  A-V valves open to begin a new cycle of ventricular pumping

End-Diastolic Volume, End-Systolic Volume, and Stroke Volume Output.

 During diastole, normal filling of ventricles increases volume to 110-120 milliliters

 This volume is called the end-diastolic volume.
 ventricles empty during systole, volume decreases to 70 milliliters - stroke volume output.
 remaining volume in each ventricle, 40 to 50 milliliters, is called the end-systolic volume.
 The fraction of end-diastolic volume that is ejected is called ejection fraction— usually 60 %
 When heart contracts strongly, end-systolic volume is decreased to 10 - 20 milliliters
 when large amounts of blood flow into the ventricles during diastole, the ventricular end-diastolic
volumes can become as great as 150 to 180 milliliters in the healthy heart.
 increasing the end-diastolic volume+decreasing the end-systolic, the stroke volume output x2

Function of the Valves Atrioventricular Valves

 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

Function of the Papillary Muscles.

 The papillary muscles contract when the ventricular walls contract

 they do not help the valves to close.
 they pull the vanes of the valves inward toward the ventricles
 prevent their bulging too far backward toward 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.

Aortic and Pulmonary Artery Valves

 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

Aortic Pressure Curve

 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

Relationship of the Heart Sounds to Heart Pumping

 valve opening - slow process, normally soundless

 close-vane of valve and surrounding fluid vibrate under influence of sudden pressure change
 ventricles contract- sound caused by closure of A-V valves
 vibration low in pitch, relatively long-lasting, known as the first heart sound
 aortic and pulmonary valves close at the end of systole, rapid snap because
 valves close rapid, and surroundings vibrate for short period, second heart sound

Work Output of the Heart

 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.

Graphical Analysis of Ventricular Pumping

These curves are volume-pressure curves.

 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.

volume-pressure diagram of the cardiac cycle

It is divided into four phases.

 Phase I: Period of filling.

o ventricular volume 45 milliliters (end-systolic vol) and diastolic pressure 0 mm Hg
o venous blood flows into ventricle - volume 115 ml, diastolic pressure to 5 mm Hg.
 Phase II: Period of isovolumic contraction.
o pressure inside the ventricle increases to equal the pressure in the aorta 80 mm Hg
 Phase III: Period of ejection.
o systolic pressure rises even higher because of still more contraction of the ventricle
o volume of the ventricle decreases because the aortic valve has now opened and blood flows
out of the ventricle into the aorta
 Phase IV: Period of isovolumic relaxation
o aortic valve closes, ventricular pressure falls back to the diastolic pressure level
o ventricle returns 45 milliliters blood left in the ventricle and atrial pressure 0 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.

Concepts of Preload and Afterload.

 Preload= degree of tension on the muscle when it begins to contract

 Afterload=load against which the muscle exerts its contractile force
 For cardiac contraction, preload = end-diastolic pressure when ventricle has become filled
 The afterload of the ventricle is the pressure in the artery leading from the ventricle.
 this corresponds to the systolic pressure described by the phase III
 Sometimes afterload is considered to be resistance in circulation rather than pressure
 The importance of the concepts
 In many abnormal functional states of the heart or circulation, are severely altered:
o the pressure during filling of the ventricle (the preload),
o the arterial pressure against which the ventricle must contract (the afterload)

Chemical Energy Required for Cardiac Contraction:

 This energy derived from oxidative metabolism of fatty acids, lactate and glucose.
 rate of oxygen consumption =measure chemical energy liberated while heart performs work

Efficiency of Cardiac Contraction.

 most chemical energy -> heat and work output

 Lu/Lt=efficiency of cardiac contraction/ heart efficiency max=20-25% heart failure 5-10%

Regulation of Heart Pumping

 person at rest 4-6 l/min; severe exercise x4/x7

 The basic means of regulation
o intrinsic cardiac pumping regulation-response to changes in vol of bloodflow to heart
o autonomic nervous system

Intrinsic Regulation of Heart Pumping—The Frank-Starling Mechanism

 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.

Basically, the Frank-Starling mechanism

 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

What Is the Explanation of the Frank-Starling Mechanism?

  extra amount of blood to ventricles, the cardiac muscle stretched to greater length
 muscle contract with increased force
 actin and myosin filaments brought to a more optimal degree of overlap for force generation
 ventricle pumps the extra blood into the arteries
 Stretch of right atrial wall directly increases heart rate by 10-20%;

Ventricular Function Curves

stroke work output curve

atrial pressure ++, stroke work output side++ -> reach limit of ventricle’s pumping ability

Control of the Heart by the Sympathetic and Parasympathetic Nerves

 cardiac output can be increased more than 100 % by sympathetic stimulation

 decreased to as low as zero or almost zero by vagal (parasympathetic) stimulation

Mechanisms of Excitation of the Heart by the Sympathetic Nerves.

 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

Parasympathetic (Vagal) Stimulation of the Heart.

 can stop the heartbeat for a few seconds

 then heart “escapes” and beats at a rate of 20 -40 bpm during stimulation
 decrease strength of heart muscle contraction by 20 to 30 %
 distributed mainly to the atria
 mainly decrease heart rate rather than decrease the strength of heart contraction
 decrease ventricular pumping 50 per cent or more.

Effect of Sympathetic or Parasympathetic Stimulation on the Cardiac Function Curve.

Effect of Potassium and Calcium Ions on Heart Function

Effect of Potassium Ions.

 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

Effect of Calcium Ions.

 spastic contraction
 calcium ions initiate the cardiac contractile process
 deficiency – flaccidity
 cardiac effects of abnormal calcium concentrations are seldom of clinical concern

Effect of Temperature on Heart Function

 Fever 2x heart rate

 Decreased temperature - few beats per minute
 heat increases permeability of cardiac muscle membrane to ions that control heart rate
 acceleration of the self-excitation process
 Contractile strength enhanced by a moderate increase in temperature( body exercise)
 prolonged elevation - exhausts the metabolic -> weakness
 Increasing the Arterial Pressure Load (up to a Limit) Does Not Decrease the Cardiac Output Note in
Figure 9–12 that increasing the arterial pressure in the aorta does not decrease the cardiac output
until the mean arterial pressure rises above about 160 mm Hg.