Guyton Physiology Chapter 9 Outline 4i6j4s

R: Chapter 9 (8/15/2011) I.

Physiology of cardiac muscle A. 3 types of cardiac muscle: atrial, ventricular, and specialized excitatory and conductive fibers 1. Atrial and ventricular fibers contract in the same manner as skeletal muscle, but the duration of contraction is longer 2. Excitatory and conductive fibers contract very little, but instead act to either: a. Automatically discharge a. Conduct action potentials generated by automatically discharging fibers through the heart muscle B. Physiologic anatomy of cardiac muscle 1. Appear striated 2. Myofibrils contain actin and myosin that act in the same manner as in skeletal muscle 3. Differences with skeletal muscle a. The presence of the protein Titin i.

Definition = a protein that allows ive elastic elongation of the sarcomeres after contraction

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Importance = required as there is no antagonist muscle contracting to help elongate the heart muscle

a. Cardiac muscle as a syncytium i.

Intercalated discs = gap junctions that lie between the cardiac muscle fibers connected in series (such that cardiac muscle fibers are much shorter than skeletal muscle fibers) and parallel 1. Function = allow an action potential transmitted through one muscle fiber to be transmitted to an adjacent muscle fiber 2. Atrial vs. ventricular syncytia 1. Separated from each other by fibrous tissue that surrounds the AV openings 2. Action potentials between the atria and ventricles only through specialized conduction tissue called the AV bundle a. Importance = allows the atria to contract a short time ahead of the ventricles

C. Action potentials in cardiac muscle 1. Basics

a. Normal membrane potential of cardiac muscle = -85mV and the action potential of cardiac muscle = 105 mV (this means that the membrane potential increases to about +20mV) a. Plateau phase = period of time (0.2 sec) after the initial depolarization during which cardiac muscle remains depolarized before repolarization occurs i.

Note: this is 15x longer than skeletal muscle

2. What causes the long action potential and its plateau? a. Action potentials in cardiac muscle are generated by both fast sodium channels (as in skeletal muscle) as well as slow sodium/calcium channels. Slow channels have the unique characteristics of both opening more slowly and closing later after depolarization than do the fast channels. The opening of both of these channels allows a large quantity of sodium and calcium to flow into the muscle fiber. a. Potassium channels in cardiac muscle have decreased permeability (5x less permeable) when the membrane is depolarized. This effect seems to be due to the presence of excess calcium (from the slow channels) within the muscle fiber. This can be demonstrated by the fact that after the delayed closing (0.2-0.3 seconds) of the calcium channels, permeability of the membrane to potassium increases greatly and repolarization occurs. 3. Velocity of conduction in cardiac muscle a. Atrial and ventricular fibers = 0.3-0.5 m/sec (very slow) a. Purkinje fibers 4 m/sec (allows rapid conduction of the excitatory signal) 4. Refractory period of cardiac muscle a. Ventricular fibers = absolute refractory period of 0.25-0.3 sec (+ an additional relative refractory period of 0.05 sec) i.

Note the relative refractory period can be overcome with a very strong excitatory signal

a. Atrial fibers = absolute refractory period of 0.15 seconds (much shorter than the ventricles) D. Excitation-contraction coupling/function of calcium ions and the transverse tubules 1. Steps in common with skeletal muscle a. Action potential arrives on surface of muscle fiber >action potential propagated to the interior of the fiber by the T-tubules > arrival of AP at the SR causes the SR to release calcium into the sarcoplasm > contraction of myofibrils 2. Unique steps of cardiac muscle contraction a. During depolarization, calcium enters the fiber and diffuses through the T-tubules (whose volume is 25x as great as in skeletal muscle) into the sarcoplasm of the myofibrils > contraction

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Note: This is critical because the SR’s in cardiac muscle are underdeveloped (cannot store adequate amounts of calcium). Therefore without adequate influx of calcium from the extracellular environment, cardiac muscle fibers would be unable to contract.

3. Duration of contraction = begins a few ms after arrival of the AP and continues a few ms after cessation of the AP (this means that the contraction length is dependent upon the plateau phase of the action potential) a. Atrial contraction time = 0.2 sec a. Ventricular contraction time = 0.3 sec II. The cardiac cycle A. Basics 1. Cycle initiated by spontaneous generation of an action potential in the sinus node a. Location = superior lateral wall of the right atrium near the opening of the superior vena cava 2. The action potential then propagates through the atria, the AV bundle, and finally the ventricles a. Note: the delay between the arrival of the AP at the atria and the ventricles = .01 sec B. Diastole and systole 1. Diastole = period of relaxation when the heart fills with blood a. Times associated with diastole: total time = 0.53 sec i.

Ventricular events 1. Isovolumic relaxation = 0.53 2. Filling = 0.12 1. Rapid filling = 0.11 2. Reduced filling = 0.19

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Atrial events 1. Atrial systole = 0.11

a. Note: with higher heart rates, less time is spent in diastole relative to systole 2. Systole = period of contraction a. Times associated with systole: total time = 0.27 sec i.

Isovolumic contraction = 0.05

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Ejection = 0.22 1. Rapid ejection = 0.09 2. Reduced ejection = 0.13

C. Relationship of the electrocardiogram to the cardiac cycle 1. P wave: represents the spread of depolarization through the atria near the end of diastole a. This is followed by atrial contraction (represented by a slight increase in atrial pressure at the end of diastole) 2. QRS complex: represents the spread of depolarization through the ventricles at the very end of diastole a. This is followed by ventricular contraction (represented by a large increase in the ventricular pressure at the beginning of systole) a. Occurs about 0.16 sec after the ONSET of the P wave 3. T wave: represents the repolarization of the ventricles near the end of systole a. This is followed by ventricular relaxation at the very beginning of diastole D. Function of the atria as primer pumps 1. Basic idea = 80% of the blood that flows back into the heart es through the atria directly into the ventricles during diastole. The other 20% of the blood is pushed into the ventricles during atrial contraction. a. This means that the atria only function to increase the pumping capacity of the ventricles by 20% a. Note: Due to the small influence of the atria to the total amount of blood pumped out by the ventricles and the fact that the heart can normally pump 300-400% more blood than is required by the body at rest, failure of the atria to function is not noticeable, except during exercise (when tissue demands for oxygen are greater) 2. Pressure changes in the atria (the a, c, and v waves) a. A wave: represents pressure increases during atrial contraction i.

Right atrium = 4-6 mmHg

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Left atrium = 7-8 mm Hg

a. C wave: represents 2 events occurring during the beginning of ventricular contraction i.

Slight backflow of blood from the ventricles into the atria

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Bulging of the AV valves backward towards the atria due to increased ventricular pressure during contraction (this event is by far more significant)

a. V wave: represents the initial refilling of the atria at the end of systole while the AV valves are still closed and disappears at the end of ventricular contraction when the AV valves open and pressure is released E. Function of the ventricles as pumps 1. Filling of the ventricles a. First 3rd of diastole = rapid filling of the ventricles i.

Occurs because a significant amount of blood accumulated in the atria during systole (as the AV valves were closed) and the opening of the AV valves at the end of systole allows the blood to flow rapidly into the ventricles.

a. Middle 3rd of diastole = slow filling of the ventricles i.

Occurs because at this point the gradient for rapid flow into the ventricles has been diminished and the only force pushing blood through the atria is venous return.

a. Last 3rd of diastole = atrial contraction (pumping the remaining 20% of blood into the ventricles) 2. Emptying of the ventricles during systole a. Period of isovolumic (isometric) contraction = the brief period of time at the beginning of systole during which ventricular muscle fiber tension is increasing, but not yet great enough to open the semilunar valves (muscle fibers are not shortening). During this period pressure rises abruptly. i.

Delay between ventricular contraction and ejection = 0.02-0.03 sec

a. Period of ejection = occurs once ventricular pressure has risen high (left ventricle = above 80 mmHg/ right ventricle = above 8 mm Hg) enough to push the semilunar valves open i.

First 3rd of period of ejection = period of rapid ejection (70% of blood empties)

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Last 2/3rds of period of ejection = period of slow ejection (remaining 30% empties)

a. Period of isovolumic (isometric) relaxation = occurs as a result of large vessel contraction after being filled with blood from the ventricles. This contraction forces blood back into the direction of the ventricles snapping shut the aortic and pulmonary valves. Therefore, even though the ventricular muscle fibers are relaxing, there is no change in blood volume (until atrial pressure increases enough to open the AV valves and allow the ventricles to begin filling again). a. End-diastolic volume, end-systolic volume, stroke volume output, and cardiac output i.

End-diastolic volume = volume of blood in a ventricle at the end of diastole 1. Normal = 110-120 ml

2. With large diastolic volumes (in a healthy heart) = 150-180 ml i.

End-systolic volume = blood volume remaining in a ventricle after systole 1. Normal = 40-50 ml 2. With strong heart contractions = 10-20 ml

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Stroke volume output = amount of blood from the end-diastolic volume that is emptied during systole 1. Normal = 70 ml 2. With a simultaneous increase in end-diastolic volume and decrease in endsystolic volume = may be doubled 3. Note: as heart rate increases, SV decreases as there is less time for filling to occur. This effect is minimized in highly trained athletes due to athletic hypertrophy which allows the heart to contract higher volumes of blood out at a given venous return.

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Ejection fraction = fraction of the end-diastolic volume that is ejected during systole 1. Normal = 60% (Barsotti says normal > 55%) 2. Clinical relevance = valuable index of the severity of heart disease in patients

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Cardiac output = the amount of blood pumped by the heart in one minute (L/min) 1. Equation: CO = SV x HR = (EDV-ESV) x HR 2. Determinants: 1. Load-dependent regulation (preload and afterload) 2. Load-independent regulation (contractility and heart rate) a. Contractility = contractile strength at a given amount of ventricular filling i.

Indices of contractility = 1) increased contractility effects on the pressure-volume curve = ejection curve shifts up and to the left. It shifts up because the ventricle is pushing with greater force. It shifts left because the greater pumping power allows the ventricle to increase its stroke volume. 2) peak ventricular systolic pressure 3) dP/dtmax = the derivative or rate of the maximal rate of ventricular pressure rise during the isovolumic contraction period. This is represented as an increase in the slope of the line corresponding to the rate of ventricular force development on a left ventricular pressure vs. time graph. This increase occurs with respect to a given amount of ventricular filling.

ii. Main cellular determinants of increased contractility = calcium kinetics (size of the transient rise in intracellular calcium that occurs during depolarization), myosin ATPase activity, ATP levels, number of cross bridges formed 3. Function of the valves a. Atrioventricular valves i.

Basics 1. Tricuspid = right AV valve 2. Mitral = left AV valve)

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Function = to prevent backflow of blood into the atria during systole

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Notes: 1. Open and close ively 2. Require almost no backflow to close (this is different from the semilunar valves, which require significant backflow to close)

a. Function of the papillary muscles = to provide a pull on the valve cusps in the direction of the ventricle so that during systole, the cusps aren’t pulled too far into the atria such that significant backflow occurs i.

Anatomy = papillary muscles are attached at one end to the walls of the ventricles and at the other end to chordate tendineae (which are in turn attached directly to the valve cusps). These contract as the ventricles contract. This allows them to exert their pulling force at the same time the ventricular pressure is pushing the valve cusps back towards the atria.

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Note: damage to one of these muscles may result in increased backflow and potentially a cardiac insufficiency

a. Aortic and pulmonary artery valves i.

Basics 1. Aortic valve = left semilunar valve 2. Pulmonary valve = right semilunar valve

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Function = to prevent backflow of blood into the ventricles during systole

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Critical differences with AV valves 1. High pressures generated by arterial contraction (upon receiving blood from the ventricles) result in the snapping shut of the semilunar valves 2. Have smaller openings that do AV valves, thus generate greater velocities of blood ejection

3. Due to the faster closure and more rapid ejection velocities, the semilunar valves are subject to much more mechanical stress. 4. No chordate tendineae present, so much more durably constructed 4. Aortic pressure curve (systole = 120 mm Hg/diastole = 80 mm Hg) a. Steps i.

Beginning of systole: aortic valve opens > aortic pressure rises rapidly

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Middle of systole: aortic pressure starts to drop as there is little blood being ejected from the ventricles and the increased pressure in the aorta has caused some bulging backward of the aortic valve into the ventricle

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End of systole: the aortic valve closes > brief increase in aortic pressure as the snapping back of the valve cusps back in the direction of the aorta pushes blood back into the aorta

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Diastole: aortic pressure continues to decrease due to the elasticity of the arteries pushing the blood through the peripheral vessels back into the veins

a. Note: the pressure curves in the right ventricle and pulmonary artery are the same as those of the left ventricle and aorta, except that the pressures they generate are about 1/6th as large III. Relationship of the heart sounds to heart pumping A. Basic idea = sounds represent the vibrations given off by closure of the AV and semilunar valves 1. First heart sound: represents the closure of the AV valves at the end of diastole a. Sound = low pitch and long-lasting 2. 2nd heart sound: represents the closure of the semilunar valves at the end of systole a. Sound = rapid snap IV. Work output of the heart A. Basic definitions 1. Stroke work output = the amount of energy that the heart converts to work during each heartbeat 2. Minute work output = the total amount of energy that the heart converts to work in one minute (stroke work output x HR/min) 3. Forms of work output a. Volume/pressure (external) work = work done by the ventricles to move blood from the low pressure veins to the high pressure arteries i.

Most important type of work

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Right ventricle external work = 1/6th that of left ventricle external work due to the differences in pressure

a. Kinetic energy of blood flow = work done by the ventricles to accelerate the blood to its ejection velocity through the semilunar valves i.

Less important type of work, normally ignored in the calculation of the total work output of the heart (represents <1% of total work), except in conditions of aortic stenosis, in which great amounts of energy are required to accelerate the blood through the stenosed valve (up to 50% of total work output)

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KE = mass of blood x velocity of ejection2

B. Graphical analysis of ventricular pumping

1. a. Curve explanations i.

Diastolic pressure curve: represents the effect of increasing left ventricular volume on diastolic pressure 1. Note that until about 150 ml, there is very little change in diastolic pressure relative to increases in volume. After this point however, for every increase in volume, the pressure rises dramatically. This is due to nearing the elastic stretch capacity of the fibrous tissue of the ventricle as well as the volume increase the surrounding pericardium is able to tolerate.

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Systolic pressure curve: represents the pressure that is generated at each volume of ventricular filling. 1. Note that systolic pressure increases almost linearly with increases in ventricular blood volumes until around 150-170 ml. At this point, the actin and myosin filaments are pulled far apart such that the strength of their overlap is less than optimal. 2. Maxium systolic pressure values 1. Left ventricle = 250-300 mm Hg (average)

2. Right ventricle = 60-80 mm Hg a. Volume-pressure diagram during the cardiac cycle: cardiac work output (represented by red lines on the graph) i.

Phases 1. Phase I = period of filling 1. Begins at: a. Ventricular volume of 45 ml (this is the end-systolic volume) b. Diastolic pressure of 0 mmHg 2. Ends at: a. Ventricular volume of 115 ml (this is the end-diastolic volume) i.

Note that this is an increase of about 70 ml

b. Diastolic pressure of about 5 mmHg (, diastolic pressure doesn’t rise much until ventricular volume rises above about 150 ml) 2. Phase II = period of isovolumic contraction 1. Systolic pressure increases from 5 mmHg to about 80 mmHg (the pressure of the aorta) 3. Phase III = period of ejection 1. Ventricular volume decreases from 115 ml to about 45 ml 2. Systolic pressure continues to increase (as the ventricle is still contracting) to about 120 mmHg 4. Phase IV = period of isovolumic relaxation 1. Diastolic pressure decreases to its baseline to around 0 mmHg i.

Effects of increased blood volume pumped by the heart to the volume-pressure diagram = diagram becomes much larger 1. Extends further to the right because of greater filling during diastole 2. Extends further upwards because the ventricle contracts with greater pressure at high end-diastolic volumes. 3. Extends further to the left because the ventricle will contract to a smaller end-systolic volume (only if the heart is stimulated by the SNS such that its contractility increases)

2. Concepts of preload and afterload a. Preload = the degree of tension on a muscle when it begins to contract/enddiastolic pressure

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Barsotti definition = ive stretch (tension) on the cardiac walls by the amount of chamber filling

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Regulation = Frank Starling mechanism (so is an intrinsic property)

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Determinants 1. Central venous pressure (CVP) = atrial pressure = most important 1. Determined by: a. Venous smooth muscle tone b. Blood volume c. Body position d. Intrathoracic pressure e. Skeletal muscle pump activity on the veins f. Resistance to blood in the circulation 2. This effect of this mechanism on ventricular filling is increased proportionately greater at high heart rates 2. Pericardial sac pressure = usually not a key determinant 1. However, increases in pericardial pressure will result in limited diastolic filling 3. Ventricular compliance = usually not a key determinant 1. However, in hypertrophic cardiomyopathies, decreased ventricular compliance results in decreased filling

a. Afterload = the load against which a muscle exerts its contractile force/the pressure in the artery into which the ventricle is pumping i.

Changes to the PV loop as a result of changes in afterload 1. Increased afterload 1. Isovolumic line extends further upwards as higher aortic pressures require the generation of higher ventricular pressures to open the aortic valve a. This is a result of the relationship that exists between velocity of shortening and the load against which the muscle is contracting. Higher loads result in decreased velocity of shortening. In the heart, this means that as aortic pressure increases, ventricular contraction slows and therefore blood is able to be ejected. 2. Ejection line shortens as higher aortic pressures result in the early closure of the aortic valve and thus decreased stroke volumes

3. Filling line is shifted to the right as less blood is able to be pumped out of the ventricle with the higher afterload. i.

Determinants of ventricular afterload 1. Aortic diastolic pressure or MAP 1. Note: aortic pressure doesn’t begin to significantly affect the cardiac output until it reaches pressures above 160 mmHg 2. Aortic compliance 3. Aortic valve resistance

V. Chemical energy required for cardiac contraction: oxygen utilization by the heart A. Energy source for cardiac muscle = oxidation of fatty acids, lactate, and glucose B. Efficiency of cardiac contraction = the ratio of work output to total chemical energy expenditure 1. Normal heart = 20-25% maximum 2. Heart failure = 5-10% VI. Regulation of heart pumping A. Definition of cardiac index = cardiac output /body surface area 1. Important because the purpose of cardiac output is to meet the demands of the tissues. This means that with increases in surface area, the cardiac output should increase in the same propotion. B. Normal volume of blood pumped at rest= 4-6 L/min (may be increased 4-7x this during severe exercise) C. Intrinsic regulation of heart pumping: the Frank Starling Mechanism 1. Definition = the greater the volume of blood returning to the heart (within physiologic limits), the greater the force of contraction generated by the ventricles and the greater the quantity of blood pumped into the aorta. 2. What is the explanation of the Frank Starling mechanism? a. The greater the incoming volume of blood, the greater the stretch on the cardiac muscle fibers, and the more optimal the overlap of the actin and myosin filaments. This allows a contraction of much greater force. i.

Notes: 1. Increased stretch of the right atrial wall also contributes to greater cardiac output (but to nowhere near the extent as Frank-Starling). This is because increased right atrial wall stretch results in HR increases of 10-20%. 2. Sarcomere length and tension curve

1. Ascending limb = sarcomere lengths at which at which lengthening results in greater tension a. Shorter sarcomere lengths require about twice as much calcium to reach the same levels of tension as longer sarcomere lengths 2. Peak = occurs at about 2.0-2.25 the normal resting sarcomeric length 3. Descending limb = sarcomere lengths at which further lengthening results loss of tension a. Other mechanisms contributing to Frank Starling effectiveness i.

Increased intracellular calcium release into the myoplasm with increased stretch, so more contraction possible

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Increased sensitivity of the contractile fibers to calcium at greater lengths, so more ability of the fibers to actually use the increased amount of calcium to contract more strongly

3. Ventricular function curves a. Ventricular stroke work output

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Just shows that ventricular output will increase as more blood flows into the atria (up to a physiologic limit)

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Just shows that ventricular output will increase as more blood flows into the atria (up to a physiologic limit)

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D. Control of the heart by the sympathetic and parasympathetic nervous systems 1. Basics a. Possible effect of sympathetic stimulation (at a given level of atrial pressure) = > 100% increase in cardiac output (amount of blood pumped per minute) a. Possible effect of parasympathetic stimulation (at a given level of atrial pressure) = decrease in cardiac output to zero 2. Mechanism of excitation of the heart by the sympathetic nerves a. 2 mechanisms i.

Increased HR (up to 250 bpm)

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Increased force of heart contraction > increased volume of blood pumped and increased ejection pressure

a. Net effect = increase in CO 2-3x Frank Starling alone a. Notes: i.

SNS fibers almost exclusively distributed to the ventricles

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SNS tonicity maintains the pumping at 30% above normal, so inhibition of the SNS will depress the CO about 30%

a. Note: HR decreases with age mostly due to decreased adrenergic receptors on the heart muscle 3. Parasympathetic (vagal) stimulation of the heart a. 2 mechanisms i.

Decreased HR (strong vagal stimulation may actually stop the heart, but the heart usually escapes to a rate of 20-40 bpm as vagal stimulation persists) 1. This is the more significant effect as vagal fibers are mainly distributed to the atria

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Decreased strength of cardiac muscle contraction (maximal decrease of 20-30%)

a. Net effect = decreased ventricular pumping of 50% or more 4. Effect of sympathetic or parasympathetic stimulation on the cardiac function curve E. Effect of potassium and calcium ions on heart function 1. Effects of excess potassium ions in extracellular fluids = more extracellular potassium results in decreased membrane potential > higher threshold for depolarization a. Note: if cardiac potassium concentration increases to 8-12 mEq/L (2-3x the normal value), complete conduction blocks can occur 2. Effect of calcium ions

a. Excess calcium ions > spastic contraction (due to abundance of calcium entering the sarcoplasm from the T-tubules a. Deficiency of calcium > effect similar to excess potassium F. Effect of temperature on heart function 1. Effect on HR a. Increased BT > increased HR (decreased BT > decreased HR) a. Effect due to the increased permeability of the cardiac membrane for the ions that control its action potentials at higher temperatures 2. Effect on the contractile strength of the heart a. Increased BT > i.

Moderate increase in contractile strength initially

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Contractile weakness later as the metabolic system of the heart fatigues

G. Increasing the arterial pressure load (up to a limit) does not decrease the cardiac output 1. Pressures up to around 160 mmHg in the aorta do not decrease the cardiac output, thus CO is still determined completely by tissue need and venous return VII.Differences between the cardiac cycles of the right and left hearts A. Examples 1. Systolic ejection longer for the right side of the heart as the pulmonic valve opens prior to aortic valve and closes after the aortic valve 2. Diastolic filling longer for the right side of the heart as the tricuspid valve opens prior to the mitral valve and closes after the mitral valve B. Cause = because the right side of the heart generates much smaller pressures than the left side, less pressure is required to open and close the valves on the right side of the heart

Description of the cardiac cycle curves

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Late diastole (reduced filling) A. Aortic pressure curve = decreasing as no new blood is being pumped into the aorta by the left ventricle B. Atrial pressure curve = slightly higher than ventricular pressure with the a wave occurring just before systole begins. This represents the contraction of the atria to pump the remaining 20% of blood volume into the ventricles C. Ventricular pressure curve = near 0 mmHg as the walls of the ventricles are very wide compared to the amount of blood within them. There is a small increase in pressure lagging behind and corresponding with the atrial a wave. D. Ventricular volume curve = increases slowly near the end of diastole as most of the blood has already ed into the ventricles from the atria in early diastole E. ECG curve = the initiation of the QRS complex just precedes ventricular contraction F. Phonocardiogram curve = 4th heart sound occurs during atrial contraction and results from vibrations generated by the turbulence set up by the collision of the new incoming blood into the ventricle with the blood already present

II. Early systole (isovolumic contraction) A. Aortic pressure curve = continues to decline until it reaches about 80 mmHg. This is because this is as far as it can decline before ventricular pressure has risen to match it. B. Atrial pressure curve = rises slightly due to mitral valve prolapse with the initiation of ventricular contraction. This rise is referred to as the c wave.

C. Ventricular pressure curve = rises rapidly from 0 mmHg to 80 mmHg resulting in opening of the aortic valve 1. Note: isovolumic periods (contraction and relaxation) correspond with the largest changes in ventricular pressure during the cardiac cycle D. Ventricular volume curve = no change because at this point both of the valves bounding the ventricular blood are closed E. ECG curve = the completion of the QRS complex occurs as the ventricle begins to contract F. Phonocardiogram curve = 1st heart sound occurs due to the vibrations caused by the closure of the mitral valve III. Later systole (rapid and reduced ejection) A. Aortic pressure curve = rises from 80 mmHg to 120 mmHg. It curves initially slightly underneath the ventricular pressure curve as the force generated by the ventricular contraction is greater than the force of smooth muscle contraction of the aorta. Later during ejection however, the increased blood volume in the aorta results in increases in aortic pressure such that the smooth muscle contraction force becomes greater than the ventricular force (begins at around 120 mmHg). This results in the peak aortic pressure occurring just after peak ventricular pressure. Eventually the left ventricle empties enough that the differences between the aortic pressure and the ventricular pressure become so great that the aortic valve closes (at around 100 mmHg). B. Atrial pressure curve = returns to zero from its slight increase as the elastic nature of the mitral valve propels the blood back into the ventricle and then gradually increases throughout systole as it is being filled. The initial return to zero is referred to as the x curve and represents the lowest atrial pressure. It also occurs at the same time as peak ventricular pressure. C. Ventricular pressure curve = rises to a maximum of 120 mmHg at peak ventricular contracion before decreasing back down to 80 mmHg as the aortic valve closes and the ventricle empties D. Ventricular volume curve = decreases rapidly initially and more slowly later as the pressure gradient between the ventricle and the aorta is dissipated E. ECG curve = S-T interval followed by the T wave during the period of reduced ejection. The T wave slightly precedes ventricular repolarization F. Phonocardiogram curve = 1st heart sound continues briefly into the beginning of ejection. This is followed by and absence of sounds during the rest of ejection. IV. Early diastole (isovolumic relaxation) A. Aortic pressure curve = rises slightly due to the elastic recoil of the aortic valve in the direction of the aorta after its initial prolapse in the direction of the ventricle during closing B. Atrial pressure curve = continues to increase with atrial filling and is referred to as the v curve

C. Ventricular pressure curve = drops rapidly from 80 mmHg to near 0 mmHg D. Ventricular volume curve = completely flat as both of the valves bounding the ventricle are closed during isovolumic relaxation E. ECG curve = descending portion of the T wave occurring F. Phonocardiogram curve = 2nd heart sound corresponds to the vibrations within the aorta generated by the elastic recoil of the aortic valve V. Later in diastole (rapid filling) A. Aortic pressure curve = decreases linearly as blood flows away from the aorta and into the systemic circulation B. Atrial pressure curve = decreases back to zero as the mitral valve opens. This portion of the curve is referred to as the y curve. C. Ventricular pressure curve = continues to decrease very slightly as the muscle continues to relax D. Ventricular volume curve = rapid increase in ventricular volume E. ECG curve = the end of the rapid filling period corresponds with the P wave. This wave just precedes atrial contraction. F. Phonocardiogram curve = 3rd heart sound occurs at the end of the first 3 rd of diastole and is caused by vibrations within the ventricle resulting from turbulence generated by the collision of new blood coming into ventricle with old blood already present.