Physio Ch.9 - Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves

How do the aortic and pulmonary valves differ from the AV valves?

AV valves are thin and require almost no backflow to cause closure semilunar valves are heavier and require rather rapid backflow for a few ms to close -> the semilunar valves snap closed in contrast to the much softer closure of the AV valves Because of smaller openings, the velocity of blood ejection through the aortic and pulmonary valves is much greater than that of the 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 that the AV valves the AV valves are supported by chordae tendinae, which is not true for the semilunar valves therefore, they must be constructed with an especially strong, yet very pliable fibrous tissue to withstand the extra physical stresses

Syncytium:

"a single cell or cytoplasmic mass containing several nuclei, formed by fusion of cells or by division of nuclei." Cardiac muscle is a syncytium of many heart muscle cells in which the cardiac cells are so interconnected that when one cell becomes excited, the action potential rapidly spreads to all of them.

Basic 2 components for regulating heart pumping;

(1) intrinsic cardiac pumping regulation in response to changes in volume of blood flowing into the heart (2) control of heart rate and heart strength by the autonomic nervous system

Velocity of conduction in both atrial and ventricular muscle fibers:

0.3 to 0.5 m/sec(1/20thfarslowerthanskeletal)

Stroke volume output:

as the ventricles empty during systole, the volume decreases by about 70 mL

Period of isovolumetric (isometric) relaxation:

at the end of systole, ventricular relaxation begins suddenly, allowing both the R and L intraventricular pressures to decrease rapidly the elevated pressures in the distended large arteries that have just filled with blood from the contracted ventricles immediately push blood back toward the ventricles, which snaps the aortic and pulmonary valves closed, AV valves are also closed for .03 to .06 s, the ventricular muscle continues to relax, even though the ventricular volume does not change the intraventricular pressures rapidly decrease back to their diastole levels - then the AV valves open to begin a new cycle of ventricular pumping

3 major types of cardiac muscle and the difference in their contractions:

atrial muscle ventricular muscle ^ these 2 contract in much the same way as skeletal muscle, except duration of contraction is longer specialized excitatory and conductive muscle ^ contracts feebly because they contain few contractile fibrils; instead, they exhibit 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

Bainbridge reflex:

atrial reflex Stretching of the R atrial wall directly increases HR by 10-20% which also helps increase the amount of blood pumped each minute stretch of atrium activates stretch receptors and a nervous reflex that is transmitted by the vagus nerve and may increase HR an additional 40-60%

Action potential in ventricular muscle (values)

avgs about 105 mV means intracellular potential rises from -85 to +20 during each beat exhibits a plateau for about 0.2 s where it remains depolarized the presence of this plateau in the AP causes ventricular contraction to last longer

Duration of cardiac muscle contraction:

begins a few seconds after AP begins, ends a few seconds after AP ends Therefore, the duration of contraction of cardiac muscle is mainly a function of the duration of the action potential, including the plateau—about 0.2 second in atrial muscle and 0.3 second in ventricular muscle.

Periods considered "isovolumetric" are those when:

both valves are closed, so only changes in pressure are occurring

Cardiac muscle histology:

branching, striated, actin and myosin filaments

How can stroke volume output be increased?

by both increasing the end-diastolic volume and decreasing the end-systolic volume (can be increased to more than double that which is normal)

Deficiency of extracellular calcium:

cardiac weakness (similar to high potassium)

Excess extracellular potassium:

causes heart to become dilated and flaccid and slows HR block conduction of cardiac impulse causes severe weakness of the heart, abnormal rhythm, and death high K concentration in the extracellular fluids decreases resting membrane potential, partially depolarizing the cell membrane, causing the membrane potential to be less negative As membrane potential decreases, intensity of AP decreases, making contraction of the heart progressively weaker

How does ventricular stiffening w/ age or diseases affect diastole?

causes less blood to fill the ventricles in the early portion of diastole and requires more volume or more filling from the atrial contraction to maintain adequate cardiac output

Intercalcating discs:

cell membranes that separate individual cardiac muscle cells from one another at each intercalcated disc, the cell membranes fuse with one another to form permeable communication junctions (gap junctions) that allow diffusion of ions ions move with ease in the intracellular fluid along the longitudinal axes of the cardiac muscle fibers so that APs travel easily from one cardiac muscle cell to the next

What 2 changes occur during autonomic nervous system stimulation?

changes in HR changes in contractile strength of the heart

What causes the valves to open and close?

close when a backward pressure gradient pushes blood backward open when a forward pressure gradient forces blood in the forward direction

First heart sound (S1)

closure of the AV valves as the ventricles contract vibration pitch is low and relatively long lasting

Second heart sound (S2)

closure of the aortic and pulmonary valves at the end of systole heard as a snap - these valves close rapidly and the surroundings vibrate for a short period

End-diastole volume:

during diastole, normal filling of the ventricles increases the volume of each ventricle to 110-120 mL

How does extracellular fluid calcium concentration impact the strength of skeletal muscle contraction?

hardly affected by mod changes skeletal muscle contraction is caused almost entirely by calcium ions released from the SR inside the skeletal muscle fiber

Excess extracellular calcium

heart moves toward spastic contraction direct effect of calcium ions to initiate cardiac contractile process

The total duration of the cardiac cycle is the reciprocal of:

heart rate a heart rate of 72 beats per minute gives 0.0139 min/beat or 0.833 sec/beat

Refractory period of cardiac muscle - length, atria vs ventricles

like all excitable cells, cardiac muscle is refractory to restimulation during the AP Nl refractory period = .25-.3 sec, which is about the duration of the prolonged plateau AP there is an additional relative refractory period of about 0.05 s during which the muscle is more difficult to excite than normal but can be excited by a very strong excitatory signal (ex. early premature contraction) the refractory period for atrial muscle is much shorter than that for the ventricles

Max ventricular pressure during systole / what happens if volume increases further?

max at ventricular volume of 150-170 mL max pressure is 250-300 mmHg for L ventricle max rt ventricle - 60-80 mmHg as the volume increases further, the systolic pressure actually decreases under some conditions this occurs 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 optimal

What happens when the ventricle is abnormally dilated? (eccentric hypertrophy)

much more chemical energy is expended because T= Pxr happens during heart failure

At what point will L ventricular diastolic pressure increase rapidly?

once volume of noncontracting ventricle rises above 150 mL up to this point, 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

Why are heart sounds heard only for the closing of valves?

one does not hear the opening of the valves because this is a relatively slow process that normally makes no noise when the valves close, the vanes of the valves and the surrounding fluids vibrate under the influence of sudden pressure changes, giving off sound that travels in all directions through the chest

What is the function of the papillary muscles?

papillary muscles attach to the vanes fo the AV valves via chordae tendinae the papillary muscles contract when the ventricular walls contract, but they DO NOT help the valves close they pull the vanes of the valves inward toward the ventricles to prevent their bulging too far backward toward the atria during ventricular contraction if these structures are damaged or paralyzed due to MI, the valve bulges far backward, sometimes so far that it leaks severely and results in severe or even lethal cardiac incapacity

How is diastole split up in terms of ventricular filling/

rapid filling = first 1/3 of diastole middle third =. small amount of blood normally flows into the ventricles; this is blood that continues to empty into the atria from the veins and passes through the atria directly into the ventricles last third = atria contract (20% of filling)

How does the AP generated by the SA node travel?

rapidly from both atria and then through the AV bundle into the ventricles

Cardiac efficiency (normal value):

ratio of work output to total chemical energy used to perform the work Max efficiency of the nl heart = 20-25% in persons with heart failure, this efficiency can decrease to as low as 5%

Primer pumps:

the atra act as primer pumps fro the ventricles; the ventricles provide the major souce of power for moving blood about 80% of blood flows directly through the atria into the ventricles, even before the atria contract. Then atrial contraction usually causes an additional 20% filling of the ventricles therefore, the atria function as primer pumps that increase the ventricular pumping effectiveness as much as 20%. However, the heart can continue to operate under most conditions even without this extra 20% effectiveness; if atria begin to fail, sx of heart failure may develop when a person exercises

The 2 syncytia of the heart:

the atrial syncytium - consitutes the walls of the atria ventricular syncytium - constitutes the walls of the 2 ventricles The atria are separated from the ventricles by fibrous tissue that surrounds the atrioventricular 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 only conducted by way of a specialized conductive system called the A-V bundle Allows the atria to contract a short time ahead of ventricular contraction, which is important for the effectiveness of heart pumping

Cardiac cycle:

the cardiac events that occur from the beginning of one heartbeat to the beginning of the next

The strength of contraction of cardiac muscle depends to a great extent on

the concentration of calcium ions in the extracellular fluids (a heart placed in a calcium calcium-free solution will quickly stop beating)

Preload:

the degree of tension on the muscle when it begins to contract For cardiac contraction, the preload is usually considered to be the end-diastolic pressure when the ventricle has become filled

During normal heart function, cardiac output is determined almost entirely by:

the ease of blood flow through the body's tissues, which in turn controls venous return of blood to the heart

Ejection fraction:

the fraction of the end-diastolic volume that is ejected -> normal = ~60% The ejection fraction percentage is often used clinically to assess cardiac systolic (pumping ) capability

How are extracellular fluid calcium concentrations reestablished following cardiac action potential?

the influx of calcium ions to the interior of the muscle fiber is suddenly cut off, and calcium ions is in the sarcoplasm are rapidly pumped back out of the the muscle fibers into the SR and T-tubule extracellular fluid space via calcium-ATPase pump as well as sodium-calcium cotransport (the sodium that enters the cell during this exchange is then transported out of the cell by sodium-potassium ATPase pump)

Frank-Sterling Mechanism

the intrinsic ability of the heart to adapt to increasing volumes of inflowing blood the amount of blood pumped by the heart each minute is normally determined almost entirely by the rate of blood flow into the heart from the veins (venous return) within physiological limits, the heart pumps all the blood that returns to it by way of the veins the more the heart is stretched during filling, the greater the force of contraction (the actin and myosin filaments are brought to a more nearly optimal degree of overlap for force generation), and the greater the quantity of blood pumped into the aorta This ability of stretched muscle, up to an optimal length, to contract w/ increased work output is characteristic of all striated muscle

Afterload:

the load against which the muscle exerts its contractile force / the arterial pressure against which the ventricle must contract the pressure in the aorta leading from the ventricle

What is the graphical significance of the pressure-volume diagram? What does the area under the curve represent?

the net external work output of the ventricle during its contraction cycle When the heart pumps large quantities of blood, the area of the work diagram becomes much larger - it extends farther to the right because the ventricles fill with more blood during diastole and it rises much higher because the ventricles contract with greater pressure. It extends to the left because the ventricles contract to a smaller volume - especially if the ventricle is stimulated to increase activity by the sympathetic nervous system

Where does calcium in the T tubules come from

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. 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.

End systole volume:

the remaining volume in each ventricle (40-50 mL) after ventricular contraction ceases

Oxygen consumption has also been shown to be nearly proportional to

the tension that occurs in the heart muscle during contraction multiplied by the duration of time that the contraction persists (the tension-time index) Because tension is high when systolic pressure is high, correspondingly more oxygen is used

Periods of rapid and slow ejection:

the ventricular pressures push the semilunar valves open immediately, blood is ejected out of the ventricles into the aorta and pulmonary artery ~60% of the blood in the ventricles at the end of diastole is ejected during systole; about 70% of this portion flows out during the first third of the ejection period, with the remaining 30% emptying during the next 2/3 First 1/3 = rapid ejection Second 2/3 = slow ejection

AV valves:

tricuspid and mitral

Sympathetic nerve excitation of the heart/its inhibition:

Increased HR and Increased contractile strength of the heart the sympathetic nerve fibers to the heart discharge continuously at a slow rate that maintains pumping at about 30% above that with no sympathetic stimulation

Graphic Analysis of Ventricular pumping:

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 (end-diastolic pressure) Systolic pressure curve - determined by recording the systolic pressure acheived during ventricular contraction at each volume of filling;

Period of rapid filling of the ventricles:

During ventricular systole, large amounts of blood accumulate in the right and left atria because of the closed AV valves as soon as systole is over, and the ventricular pressure falls again to their low diastolic values, the moderately increased pressures that have developed in the atria during ventricular systole immediately push the AV valves open and allow blood to flow rapidly into the ventricles (seen as a rise of the left ventricular volume curve)

Ventricular function curves are a way to express:

Frank-Sterling Mechanism of the heart - 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

Cardiac output =

HR x Stroke Volume

What motion aids in ventricular ejection and relaxation?

The left ventricle is organized into complex muscle fiber layers that run in different directions and allow the heart to contract in a twisting motion during systole. The subepicardial (outer) layer spirals in a leftward direction, and the subendocardial (inner) layer spirals in the opposite direction (rightward), causing clockwise rotation of the apex of the heart and counterclockwise rotation of the base of the left ventricle This causes a wringing motion of the left ventricle, pulling the base downward toward the apex during systole (contraction)

How does the heart compensate when systolic pressure (and therefore tension) is chronically elevated?

When systolic pressure is chronically elevated, wall stress and cardiac workload are also increased, including thickening of the left ventricular walls, which can reduce the ventricular chamber radius (concentric hypertrophy) and at least partially relieve the increased wall tension

How does volume the heart pumps change when at rest vs when performing strenuous exercise?

4-6 L / min at rest during exercise, the heart may pump 4-7 x this amount

Chemical Energy / Oxygen Utilization required for cardiac contraction:

70-90% of this energy is derived from oxidative metabolism of fatty acids 10-30% from other nutrients (glucose and lactate) the rate of oxygen consumption by the heart is an excellent measure of the chemical energy liberated while the heart performs its work Directly related to the external work and potential energy Most of the expended chemical energy is converted into heat and a much smaller portion is converted into work output

Delay between the passage of a cardiac impulse from the atria into the ventricles:

>0.1 sec allows atria to contract ahead of ventricular contraction, thereby pumping blood into the ventricles before the strong ventricular contraction begins

P, QRS, T waves of an EKG - what does each represent?

P = spread of depolarization through the atria -> followed by atrial contraction, which causes a slight rise in the atrial pressure curve immediately after the P wave QRS wave: result of electrical depolarization of the ventricles, which initiates contraction of the ventricles and causes the ventricular pressure to begin rising -> QRS complex begins slightly before the onset of ventricular systole ventricular T wave = represents the stage of repolarization of the ventricles when the ventricular muscle fibers begin to relax -> T wave occurs slightly before the end of ventricular contraction

Phases of cardiac muscle action potential (0-4):

Phase 0: (Depolarization) Fast Sodium Channels Open -cardiac cell stimulated and depolarizes, membrane potential becomes more positive -Sodium channels open and permit sodium to rapidly flow into the cell -Membrane potential reaches about +20 mV before sodium channels close Phase 1 (Initial repolarization): fast sodium channels close. Potassium leaves cell through open channels Phase 2 (Plateau): Calcium channels open and fast potassium channels close -> brief initial repolarization occurs and AP then plateaus as a result of increased calcium ion permeability and decreased potassium ion permeability Phase 3 (Rapid repolarization): calcium channels close and slow potassium channels open: the closure of calcium ion channels and increased potassium ion permeability, K ions exit the cell rapidly, ends the plateau and returns cell membrane potential to its resting level Phase 4 (resting membrane potential): about -80 to -90 mV

Volume - Pressure Diagram during the cardiac cycle 4 phases:

Phase I: Period of Filling -> ventricular volume ~50 mL (end-systolic volume) -> diastolic pressure of 2-3 mmHg -> As venous blood flows into the ventricle from the left atrium, the ventricular volume normally increases to about 120 mL (end-diastolic volume) -> pressure rises to about 5-7 mmHg phase II: Period of Isovolumetric Contraction: -> the volume of the ventricle does not change because all valves are closed, pressure inside ventricle increases to equal pressure of aorta (80 mmHg) phase III: Period of Ejection: -> systolic pressure rises even further ; more contraction -> volume of ventricle decreases because the aortic valve is now open and blood flows out of the ventricle into the aorta phase IV: Period of Isovolumetric relaxation: -> ventricular pressure falls back to diastolic pressure level; ventricle returns to its starting point w/ about 50 mL of blood left in the ventricle at an atrial pressure of 2-3 mmHg

How is each cardiac cycle initiated?

a spontaneous generation of an AP in the sinus node located in the superior lateral wall of the R atrium near the opening of the SVC

Stroke work output- what is it? What are the 2 forms/

amount of energy that the heart converts to work during each heartbeat while pumping blood into the arteries (1) the major proportion is used to move the blood from the low-pressure veins to the high-pressure arteries (volume-pressure work or external work) -> R ventricle = 1/6 that of L ventricle due to sixfold diff in systolic pressures (2) 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) -> = 1/2(mass of blood ejected)(velocity of ejection) ^2 -> Normally only about 1%, except in abnormal conditions like aortic stonsis, where it can be more than 50%

Semilunar valves:

aortic and pulmonary

Period of isovolumetric contraction

immediately after ventricular contraction begins, the ventricular pressure rises abruptly, causing the AV valves to close an additional .02 to 0.03 second is required for the ventricle to build up suff pressure ot push the semilunar (aortic and pulmonary) valves open against the pressures in the aorta and pulmonary artery during this period, contraction is occuring in the ventricles but no emptying occurs cardiac muscle tension is increasing but little to no shortening of the muscle fibers is occurring

Changes in body temp and cardiac function:

increased body temp (fever): increased HR decreased temp: decreased HR heat increases permeability of the cardiac muscle membrane to ions that control HR, resulting in acceleration of the self-excitation process Contractile strength of the heart often is enhanced temporarily by a moderate increase in temp, such as that which occurs during body exercise prolonged temp elevation exhausts the metabolic systems of the heart and eventually causes weakness

Excitation-contraction coupling - what step in this process is unque to cardiac mucsle?

refers to the mechanism whereby the action potential causes the myofibrils of muscle to contract 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 then act on the membranes of the longitudinal sarcoplasmic tubules to cause release of calcium ions into the muscle sarcoplasm from the sarcoplasmic reticulum. QUALITY UNIQUE TO CARDIAC MUSCLE; calcium ions also diffuse into the sarcoplasm from the T tubules at the time of the action potential, which opens voltage-dependent calcium channels in the membrane of the T tubule Calcium entering the myofibril 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 that described for skeletal muscle

A, c, and v waves on the atrial pressure curve:

represent minor pressure elevations a = caused by atrial contraction (left atria more than right) c = occur when ventricles begin to contract; caused partly by slight backflow of blood into the atria, but mainly by bulging of the AV valves backward toward the atria because of increasing pressure in the ventricles v = occurs toward the end of ventricular contraction; results from slow flow of blood into the atria from the veins while the AV valves are closed during ventricular contraction; then when ventricular contraction is over, AV valves open, allowing stored atrial blood to flow rapidly into the ventricles, causing the v wave to disappear

Potential energy of cardiac output:

represents additional work that could be accomplished by contraction of the ventricle if the ventricle could completely empty all the blood in its chamber with each contraction

2 pumps of the heart:

right heart: pulmonary and left heart: systemic each of these is a pulsatile, 2 chamber pump composed of an atrium and a ventricle Each atrium is a weak primer pump for the ventrcle, helping to move blood into the ventricle The ventricles then supply the main pumping force that propels the blood

What causes the plateau in cardiac muscle action potential?

short answer: increased calcium ion permeability and decreased potassium ion permeability In cardiac muscle, the action potential is caused by opening of two types of channels: (1) the same voltage-activated fast sodium channels as those in skeletal muscle; and (2) another entirely different population of L-type calcium channels (slow calcium channels), which are also called calcium-sodium channels. This second population of channels differs from the fast sodium channels in that they are slower to open and, even more importantly, 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 activity maintains a prolonged period of depolarization, causing the plateau in the action potential. the calcium ions that enter during this plateau phase activate the muscle contractile process, whereas the calcium ions that cause skeletal muscle contraction are derived from the intracellular sarcoplasmic reticulum. 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 - decreases the efflux of positively charged potassium ions during the action potential plateau and thereby prevents early return of the action potential voltage to its resting level.

How do the pressure curves of the right ventricle and pulmonary artery compare to that of the aorta?

similar, but pressures are only about 1/6 as great

Ventricular function curves:

stroke work output curve (top) as atrial pressure for each side of the heart increases, stroke work output for that side increases until it reaches the limit of the ventricle's pumping ability ventricular volume output curve (bottom) As R and L atrial pressure increases, the respective ventricular volume outputs per minute also increase

How does increasing arterial pressure load affect cardiac output?

up to a limit, increasing pressure in the aorta does not decrease cardiac output until the mean arterial pressure rises above 160

Parasympathetic stimulation of the heart:

vagus nerve reduces HR and strength of contraction strong stimulation can stop the heartbeat for a few seconds, but then the HR usually "escapes" the beats at a rate of 20-40 bpm as long as parasympathetic stimulation continues can decrease HR contraction by 20-30% the vagal fibers are distributed mainly to the atria and not much of the ventricles, where the power contraction of the heart occurs explains why effect of vagal stimulation is decrease of HR mainly rather than decreased strength of contraction

Law of Laplace:

ventricular wall tension (T) = left ventricular pressure (P) x radius of the ventricle (r)

Why does cardiac muscle rely on calcium from the T tubules?

w/o the calcium from the T tubules, the strength of cardiac muscle contraction would be reduced considerably because the sarcoplasmic reticulum of cardiac muscle is less well developed that that of skeletal muscle and does not store enough calcium to provide full contraction In contrast, the T tubules of cardiac muscles are wide and well developed, and hold a lot of monosaccharides which bind to calcium and keep them available for diffusion

What is the relationship between heart rate and duration of cardiac cycle?

when the heart rate increases, the duration of each cardiac cycle decreases The duration of the action potential and systole also decrease, but not by as great a percentage as diastole. the heart beating very rapidly does not remain relaxed long enough to allow complete filling of the cardiac chambers before the next contraction.

Aortic pressure curve:

when the left ventricle contracts, the ventricular pressure increases rapidly until the aortic valve opens Then, after the valve opens, the pressure in the ventricle rises much less rapidly because blood immediately flows out of the ventricle into the aorta and then into the systemic distribution entry of blood into the arteries during systole causes the walls of the arteries to stretch and the pressure to increase to about 120 mmHg. Next, 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 An incisura (deep indentation) occurs in the aortic pressure curve when the aortic valve closes - this is caused by a short period of backward flow of blood immediately before closure of the valve, followed by sudden cessation of backflow After the aortic valve closes, pressure in the aorta decreases slowly throughout diastole because the blood stored in the distended elastic arteries flows continually through the peripheral vessels back to the veins Before the ventricle contracts again, the aortic pressure usually has fallen to about 80 mmHg (diastolic pressure), which is 2/3 the maximal pressure (120 mmHg - systolic pressure) that occurs during ventricular contraction