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Transcript
Cardio # 85
Wed /1/29/03 10am
Dr. Downey
S. Gartman
Proscribe Samera Kasim
Page 1 of 6
Cardiac Muscle and Mechanics III
This lecture began with the graph that addresses the effect of increasing end diastolic
volume….
I. Effect of increasing EDV (End diastolic volume) – (graph)
a. This is a Pressure v. Volume graph
b. EDV incr from line 1 to 2 to 3
c. Aortic pressure and contractility are constant
i. Termination at the same ESV indicates no change in contractility
ii. If there were an increase in contractility, there would be a decrease in
ESV
d. Notice the increased amount of blood ejection (incr stroke volume, SV) as we
move from 1 to 2 to 3.
e. Preload improves ventricular function
f. The mechanical function has improved by greater filling so that there is and
incr in SV
g. There is no change in contractility because the slope doesn’t change.
II. Increased Contractility –(graph)
a. ESV has changed
b. Preloads and aortic pressure for 1 and 2 are the same
c. 2 shows an increase in SV and mechanical function as a result of increased
contractility (notable by the increase in ejection)
d. note that the change in contractility can be seen as different ESV values
between 1 and 2
e. there is a constant EDV
f. shift of ESV up and to the left demonstrates an increase in contractility.
g. change in contractility:
i. + effects:
1. activation of the sympathetic nervous system,
2. drugs that increase contractility
3. Calcium administration
4. force frequency relationship
a. see below for more on this
ii. – effects
1. parasympathetic nerve stimulation (Ach)– very small effect
(physiological)
2. ischemia – as in myocardial diseases cause hypoxia and acidosis
from decrease ATP levels and buildup of by products in the cells
(pathological problem)
a. this is a major effector!!
Cardio # 85
Wed /1/29/03 10am
Dr. Downey
S. Gartman
Proscribe Samera Kasim
Page 2 of 6
III. Force frequency relationship
a. Intrinsic property of cardiac mm. contractility is related to HR
i. Increased HR results in incr contractility as a result of shorter relaxation
period so that Ca is not extruded from the cell.
b. An increased HR results in an increase in contraction
c. There is an increase in force (Tension) at the same preload
d. The increased frequency of activation increases the intracellular [Ca]
IV. Indices of Myocardial contractility
a. Ranges vary widely from person to person
b. Ejection fraction = (EDV – DSV)/ EDV
i. Can often be determined from EKG, thus is often used to determine the
fraction of EDV that was ejected
c. Velocity of ventricular ejection (contraction)
i. Incr velocity with incr contractility
d. Interventricular catheter injections measure the rate of ventricular contractility
i. Rate of rise of ventricular pressure can also be obtained
ii. Invasive, thus normally only used experimentally
V. Fig 23-9, Pressure v. Time graph
a. Note that this is pressure v. time, while the loops discussed above are
pressure-volume loop. Pay attention to this!!
b. Be able to draw these and superimpose aortic pressure wave forms.
c. A is normal
i. Note the rate of rise of contractility
d. B shows incr contractility
e. C shows decr contractility
f. Notice there is an increase in the slope with an incr in contractility
VI. Afterload
a. Afterload is determined by the pressure which must be exceeded for ejection to
take place and by the radius of the chamber.
b. Very important to remember that afterload is effect by pressure and
RADIUS!
c. Elevated pressure = elevated afterload
d. Afterload is the tension that the cell must overcome in able to shorten
e. This is LaPaces law
f. People with heart failure have greater afterload because their left ventricle is
larger (radius incr) and this is an important determinant of the force the cardiac
mm must overcome to contract.
g. The failing vent resorts to longer sarcomere length to overcome this problem
Cardio # 85
Wed /1/29/03 10am
Dr. Downey
S. Gartman
Proscribe Samera Kasim
Page 3 of 6
VII. Effect of increasing Aortic pressure of the PV loop – (graph)
a. Preload is constant, EDV unchanged, contractility, radius unchanged
b. 3 demonstrates the lowest SV
c. An incr in afterload (seen as aortic pressure incr) results in decr SV, or amount
of ejected blood
d. Incr in aortic pressure without compensation limits SV
e. ESV for 3 is larger than 1
f. The next diastole will have greater filling, or preload (w/o venous return
compensation) to compensate for the increased afterload
g. Thus there is an increase preload in able to distend the heart sufficiently to have
a normal SV.
i. Again, this is while assuming that venous return remains the same
h. Sometimes the output pressure could be so great that a normal SV cannot be
achieved
VIII. Chamber Radius affects afterload
a. Again, LaPlace’s law
b. The pressure is the same everywhere in the balloon, but the area with a larger
radius is taut and the area with the smaller radius is flaccid
c. This is because pressure is proportional to the radius
d. Volumes of heart change, which mean that an increase in force is required to
overcome this increase.
IX. Afterload and velocity of contraction: Fig 23-8 and next graph (A & B) in ppt.
a. An inverse relationship exists between afterload and velocity of contraction
i. True for both cardiac and skeletal mm
b. Increase afterload = decr velocity of contraction
c. Graph A: changes in length
i. Main idea: The long mm shows incr velocity with incr preload as long
as Lmax is not exceeded.
ii. Greater isometric force (no chg in length) is also created
1. this is the amt of force that is needed to equal the opposing force
just before shortening of the mm
iii. The contraction is more rapid and more forceful because the mm is
longer and more cross bridges can be activated to form
iv. If there is no preload, all muscles would shorten at about the same rate,
which is the rate that the cross bridges can cycle. (on the graph all the
lines would approach the short muscle line near 10 velocity)
1. EX: tug of war. People pulling in opposite directions of a rope
produce an opposing force. There are more people pulling on one
side of the rope. If the rope breaks, both sides will run away at
the same rate in the absence of force. It doesn’t matter that there
are more people on one side. They can only run so fast. So if
there’s no force, cross bridges can only cycle so fast.
Cardio # 85
Wed /1/29/03 10am
Dr. Downey
S. Gartman
Proscribe Samera Kasim
Page 4 of 6
d. Graph B: change in contractility
i. Demonstrates mm of the same length, but with different contractility
velocities.
ii. Greater isometric force is seen by the mm with higher velocities
(contractilities?)
1. EX: tug of war. On one side of the rope are young med school
students. The other side has older professors. If the rope breaks
and there is no opposing force, the med school students will be
able to run faster than the profs. The med students are
synonymous to mm with high contractility. So high contractility
results in higher velocity.
X. Responses to depressed contractility
a. ESV incr because of decreased ejection
b. EDV decr
c. Results in more favorable sarcomere lengths
d. Improved force and velocity of contraction despite decr contractility
e. The use of increase preload to increase the ejection results in consequences:
i. Radius, and thus afterload increases. If the improved contractile
function due to incr sarcomere length cannot overcome the increased
afterload, further increases in radius and afterload will result.
ii. In chronic heart failure, the beneficial effect of increased sarcomere
length is reduced because the effect of altered sarcomere length on
excitation-contraction coupling is attenuated.
1. This requires increased oxygen for the energy needed to to this
which was the problem in the first place. Thus the initial
problem is increased, resulting in further cardiac failure.
2. So incr sarcomere lengths are not as helpful as in a normal heart
3. Remember that contractility and preload are 2 different ways to
increase output; they may occur together or individually.
f. The following 3 graphs demonstrate the results of decr contractility
i. Graph A:
1. the “afterload” point on the graph is also the aortic diastolic
pressure wherein the aortic valves are open
2. there is no change in chamber radius on this graph
3. the fact that the ESPVR (end systolic pressure volume
relationship) has occurs at a higher volume means there has been
a decrease in contractility
4. preload is unchanged
ii. Graph B:
1. as a compensatory method, there is an increased preload, as seen
by an increase in pressure (bottom arrow) even in the presence of
a decr in contractility. Thus there is an incr in SV.
Cardio # 85
Wed /1/29/03 10am
Dr. Downey
S. Gartman
Proscribe Samera Kasim
Page 5 of 6
iii. Graph C:
1. demonstrates what occurs in the event that there is compensation
2. vasoconstriction occurs and a incr in arterial blood pressure
results
3. SV decr
4. preload and afterload decr (no, incr)
5. there is an incr in EDV, which will improve cardiac performance
iv. Graph D:
1. Fluid retention is seen in people who have cardiac Failure (which
is why dieterics are often administered
2. there is a compensatory incr in EDV (fluid retention) even in the
absence of incr aortic pressure
3.
4. contraction decr
5. SV incr
6. BUT preload and afterload also incr
7. NOTE to determine where all of these event occur on the graph,
look at Graph A and compare the initial values to those that are
on Graph B and/or C.
XI. Severe Ventricular Failure (cardiac failure)
a. Incr EDV because the heart is not relaxing as it should
b. Incr in EDV results in atrial Pressure incr and incr venous pressure going into
the atrium
c. If this problem is in the right ventricle, Pulmonary capillary and venous pressure
increases interfere with gas exchange (oxygen)
d. Pulmonary congestion/edema will lead to ruptured alveoli and subsequence
leakage of fluid into the extra-alveolar space
i. This is a penalty of the starling mechanism!!
XII. Autonomic control of heart function
a. This is Dr. Smith’s stuff. He’ll discuss more.
b. Parasympathetic (vagus n)
i. Reduces heart rate – primary effect
ii. Decr conduction velocity, particularly in AV node
iii. Depress contractile function – minor effect
c. Sympathetic
i. Incr HR
ii. Incr conduction velocity
iii. Incr contractility (incr force and velocity of contraction
XIII. The remaining slides
a. Most are a review or things that Dr. Smith will talk about. He actually further
discussed what we need to know in Thursday morning’s lecture.
Cardio # 85
Wed /1/29/03 10am
Dr. Downey
S. Gartman
Proscribe Samera Kasim
Page 6 of 6
b. Remember:
c. Normal arterial O2 content is 20mL/100mL of blood
d. Normal venous O2 content (mixed blood) is 15 mL/100mL of blood.
i. NOT zero!! (totally deoxygenated
e. Resting Cardiac Output: 5L/min
The following are additional notes that are not included in the ppt presentation. It
is recommended that you know the following….
On the Pressure-Volume loops,
 Pressure volume work (external work) - the area inside the “circle” is
the work done by the heart on the blood.
 A larger loop means the ventricles are working more
 P-V work is a major requirement for oxygen
 Internal work is the work the heart does on itself with each heart beat
such as muscle contractions and moving muscle components, such as ions
in/out (Ca, Na, K).
 Internal work is proportional to the area outside the loop
o Looking at fig 12-16 in the notes, this would be the lightly shaded
region outside the loop, but inside the dotted lines (which depict
EDV and ESV)
 Internal work is directly related to HR. Adequate coronary blood flow is
required.
 Because he same cardiac output (5L/min) can occur at different HR, it is
an advantage to have a lower HR
 A heart attack patient with an incr HR should be modified for this reason.
 Athletes have a low resting HR, while the elderly have higher HR and
must do more internal work
o The shaded region outside of the loop would be larger in and older
person vs an athlete.
 External work doesn’t change much with increases in HR; it changes
in response to increased SV and Afterload.