Heart Muscle: The Heart as a Pump and Function of the Heart Valves

• 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. In turn, each of these hearts is a pulsatile two-chamber pump composed of an atrium and a
ventricle.
• Special mechanisms in the heart cause a continuing succession of heart contractions called cardiac thythmicity, transmitting
action potentials throughout the heart muscle to cause the heart’s rhythmical beat.
Physiology of Cardiac Muscle
• The heart is composed of atrial muscle, ventricular muscle and excitatory and conductive muscle fibers.
• Physiologic anatomy of Cardiac Muscle
o Cardiac muscles are arranged in a latticework, with the fibers dividing, recombining, and then spreading again.
Cardiac muscle is striated in the same manner as in typical skeletal muscle (actin and myosin filaments)
o Cardiac muscle as a syncytium
 Intercalated discs: cell membranes that separate individual cardiac muscle cells from one another
(cardiac muscle fibers are made up of many individual cells connected in series and in parallel with one
another.)
 At each disc, the cell membranes fuse with one another  permeable, communicating gap junctions
(allow free diffusion of ions)
 Heart is composed of 2 syncytiums
• Atrial syncytium: walls of the two atria
• Ventricular syncytium: walls of the two ventricles
• The atria are separated from the ventricles by fibrous tissue that surrounds the AV valvular
openings between the atria and ventricles. Potentials are not conducted from the atrial
syncytium into the ventricular syncytium directly through this fibrous tissue  conduction by
way of a specialized conduction system: AV bundle
• The division 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 pumping.
• Action Potentials in Cardiac Muscle
o The presence of a plateau in the action potential causes ventricular contraction to last as much as 15 times as long
in cardiac muscle as in skeletal muscle
o What causes the long action potential and the plateau?
 In cardiac muscle, the action potential is caused by the opening of 2 types of channels:
• Fast sodium channels (same as in skeletal muscle)
• Slow calcium channels (slower to open and remain open for several tenths of a second) 
activate muscle contractile process
 A large quantity of both calcium and sodium ions flows through these channels and this maintains a
prolonged period of depolarization, causing the plateau in the action potential.
 Immediately after the onset of the action potential, the permeability of the cardiac muscle membrane for
potassium ions decreases about 5-fold (does NOT occur in skeletal muscle)  decreases the outflux of
+-charged potassium ions during the action potential plateau  prevents early return of the action
potential voltage to its resting level
 End of the action potential: permeability for potassium ions increases rapidly  returns membrane
potential to resting level
o Velocity of Signal Conduction in Cardiac Muscle
o Refractory Period of Cardiac Muscle
o Excitation-Contraction coupling – Function of Calcium Ions and the Transverse Tubules
 In addition to the Ca ions that are released into the sarcoplasm from the SR, a large quantity of extra
calcium also diffuses from the T tubules themselves at the time of an action potential.
 The strength of contraction of cardiac muscle depends to a great extent on the concentration of calcium
ions in the extracellular fluids.
The Cardiac Cycle
• Cardiac cycle: cardiac events that occur from the beginning of one heartbeat to the beginning of the next
• Each cycle is initiated by spontaneous generation of an action potential in the sinus node  travels through both atria and
then through the AV bundle into the ventricles
• Diastole and Systole
 o Diastole: period of relaxation; heart fills with blood
o Systole: period of contraction
• Relationship of the Electrocadriogram to the Cardiac Cycle
• Function of the Atria as Primer Pumps
• Function of the Ventricles as Pumps
o Filling of the ventricles
 Period of rapid filling of the ventricles: as soon as systole is over and the ventricular pressures fall again,
the moderately increased pressures that have developed in the atria during ventricular systole push the
AV valves open and allow blood to flow rapidly into the ventricles
o Emptying of the Ventricles during Systole
 Period of isovolumic contraction
• Ventricular pressure rises rapidly  AV vales close  pressure buildup  aortic/pulmonary
valves open
• Contraction is occurring in the ventricles but there is no emptying (tension is increasing in the
muscle but little/no shortening of the muscle fibers is occurring)
 Period of ejection
 Period of isovolumic relaxation
• End of systole: ventricular relaxation allows both R and L intraventricular pressures to decrease
 aortic/pulmonary valves close
 End-diastolic volume, end-systolic volume, and stroke volume output
• End-diastolic volume: during diastole; normal filling of the ventricles increases the volume
• End-systolic volume: remaining volume in each ventricle after systole
• Stroke volume output: volume decrease when the ventricles empty during systole
• Function of the Valves
o Atrioventricular valves
 The AV-valves (tricuspid/mitral) prevent backflow of blood from the ventricles to the atria during
systole.
 Semilunar valves (aortic/pulmonary) prevent backflow from the aorta and pulmonary arteries into the
ventricles during diastole.
 The valves close and open passively (they close when a backward gradient pushes blood backward, and
they open when a forward pressure gradient forces blood in the forward direction)
o Function of the papillary muscles
 They pull the vanes of the valves inward toward the ventricles to prevent their bulging too far backward
toward the atria during ventricular contraction.
o Aortic and pulmonary artery valves
 The high pressures in the arteries at the end of systole cause the semilunar valves to snap to the closed
position, in contrast to the much softer closing of the AV valves.
 The velocity of blood ejection through the aortic and pulmonary valves is far greater than that through
the much larger AV 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 AV valves.
• Aortic Pressure Curve
o L ventricle contracts  ventricular pressure increases rapidly until the aortic valve opens  pressure in the
ventricle rises much less rapidly (blood immediately flows out of the ventricle into the aorta and then into the
systemic distribution arteries)  walls stretch and pressure increases
o At the end of systole, the elastic walls of the arteries maintain a high pressure
o Incisura: occurs when the aortic valve closes; caused by a short period of backward flow of blood immediately
before closure of the valve, followed by sudden cessation of the backflow
o Aortic valve closes  pressure in the aorta decreases slowly
Relationship of the Heart Sounds to Heart Pumping
• First heart sound: when the ventricles contract; sound caused by closure of the AV valves
• Second heart sound: aortic and pulmonary valves close at the end of systole
Work Output of the Heart
• Stroke work output: amount of energy that the heart converts to work during each heartbeat while pumping blood into the
arteries
 o By far the major proportion is used to move the blood from the low pressure veins to the high pressure arteries
(volume-pressure work)
o A minor proportion of the energy is used to accelerate the blood to its velocity of ejection through the aortic and
pulmonary valves (kinetic energy of blood flow)
o R ventricle external work output = 1/6 work output of L ventricle
o Graphical Analysis of Ventricular Pumping
 Diastolic pressure curve: fill the heart with progressively greater volumes of blood  measure the
diastolic pressure immediately before ventricular contraction
 Systolic pressure curve: systolic pressure achieved during ventricular contraction at each volume of
filling
o Volume-pressure Diagram During the Cardiac Cycle: Cardiac Work Output
 Phase I: Period of filling
 Phase II: Period of isovolumic contraction
 Phase III: Period of ejection
 Phase IV: Period of isovolumic relaxation
 When the heart pumps large quantities of blood, the area of the work diagram becomes much larger
• Extends far to the R because the ventricle fills with more blood during diastole
• Rises higher because the ventricle contracts with greater pressure
• Extends farther to the L because the ventricle contracts to a smaller volume (esp if the ventricle
is stimulated to increased activity by the sympathetic nervous system)
o Concepts of Pre-load and After-load
 Preload: degree of tension on the muscle when it begins to contract (end-diastolic pressure when the
ventricle has become filled)
 Afterload: the load against which the muscle exerts its contractile force (the pressure in the artery
leading from the ventricle; systolic pressure described by the phase II curve of the volume-pressure
diagram)
Chemical Energy Required for Cardiac Contraction: Oxygen Utilization by the Heart
• Efficiency of Cardiac Contraction
Regulation of Heart Pumping
• Intrinsic regulation of heart pumping—the Frank-Starling Mechanism
o Under most conditions, the amount of blood pumped by the heart each minute is determined almost entirely by
the rate of blood flow into the heart from the veins (venous return)
o Frank-Starling mechanism of the heart: the intrinsic ability of the heart to adapt to increasing volumes of
inflowing blood
o The greater the heart muscle is stretched during filling, the greater the force of contraction and the greater the
quantity of blood pumped into the aorta.
o What is the explanation of the Frank-Starling Mechanism?
 Extra amount of blood into ventricles  stretch cardiac muscle  muscle contracts with increased force
 extra blood pumped into arteries
 Stretch of R atrial wall  increases the hart rate by 10-20%  increases the amount of blood pumped
each minute
o Ventricular Function Curves
 As the atrial pressure for each side of the heart increases, the stroke work output for that side increases
until it reaches the limit of the ventricle’s pumping ability.
 As the R/L atrial pressures increase, the respective ventricular volume outputs per minute also increases.
 As the ventricles fill in response to higher atrial pressures, each ventricular volume and strength of
cardiac muscle contraction increase, causing the heart to pump increased quantities of blood into the
arteries.
o Control of the Heart by the Sympathetic and Parasympathetic Nerves
o Mechanisms of Excitation of the Heart by the Sympathetic Nerves
o Parasympathetic (Vagal) Stimulation of the Heart
• Effect of Sympathetic or Parasympathetic Stimulation on the Cardiac Function Curve
o Effect of Potassium Ions
 A high [K+] in the extracellular fluids decreases the resting membrane potential in cardiac muscles 
intensity of the action potential also decreases  contraction of the heart gets progressively weaker
 o Effect of Calcium Ions
 Excess of [Ca+] causes heart to go toward spastic contraction
 Deficiency of [Ca+] causes cardiac flaccidity
• Effect of Temperature on Heart Function
o Increased body temperature  increased heart rate
o Decreased temperature  decreased heart rate
o Heat increases the permeability of the cardiac muscle membrane to ions that control heart rate  acceleration of
the self-excitation process
• Increasing the Arterial Pressure Load (up to a limit) Does Not Decrease the Cardiac Output