Download Cardiac Muscle and Mechanics I

Cardiopulmonary I
Tues., 01/28/03, 2 pm
Dr. Downey
Eric Lawrence for Michelle Law
Page 1 of 6
Cardiac Muscle and Mechanics I
Dr. Downey started the lecture by making a point about the bundle branch
blocks:
Bundle branch blocks cause:
1. longer QRS complex
2. Change in QRS conformation
3. shift in axis of depolarization
eg/ damage to branch to left ventricle:
-right ventricle depolarizes normally
-left ventricle depolarizes later, THUS
shift in axis of depolarization to the left
Left Axis Deviation is due to:
1. left ventricular hypertrophy
2. left ventricular bundle block
He didn’t go over them, but he said to be familiar with the structures from the first
slide in this lecture, also found in Berne and Levy, Fig 23-2
Excitation-Contraction Coupling

Contractile Cell Action Potential
-long plateau due to opening of Ca++ channels and entry of Ca++ into cell
-Ca++ in cell triggers opening of sarcoplasmic reticulum and release of
more Ca++
- Ca++ binds tropomyosin, which removes obstructions from crossbridges
in thick and thin filaments,
-thus removing tension in crossbridges and shortes sarcomeres
Cardiopulmonary I
Tues., 01/28/03, 2 pm
Dr. Downey
Eric Lawrence for Michelle Law
Page 2 of 6

Ca++ removal from cytosol
o Ca++ ATPase in sarcolemma – pumps Ca++ out of cell against
electrochemical gradient
o Na/K exchanger – maintains normal Na and K across the cell
o Na/Ca exchanger – expense of bringing Na into cell, but remove
Ca from cell

Altering Ca++ Levels in Cell
(the more Ca++, the more contractile force produced)
o alter Ca++ channel function – open more channels
o alter efflux mechanisms – Na/K exchanger modulates Ca++ levels in
cell indirectly
eg/ Catecholamines –contraction and relaxation both elevated
--phosphorylate Ca++ channels (stimulate beta receptors) and
increase probability of channel opening
--also, phosphorylate phospholambin to increase sarcoplasmic
reticulum uptake of Ca++
--also, phosphorylate troponin to inhibit binding of Ca++
-contraction and relaxation are both elevated
eg/ Digitalis
-used to treat cardiac failure (decreased contractility)
-depresses Na/K pump
-some increase in Na inside of cell
- Na/Ca exchanger is driven by the Na electrochemical
gradient on the membrane,
-when gradient is compromised, less drive is available for
extruding Ca++ , thus
-Ca++ efflux is reduced and intracellular Ca++ increases
-thus, improvement in myocardial contractility
Cardiac Function
Equations:
CO = HR x SV
SV = EDV -- ESV
Ejection fraction = SV / EDV
CO = cardiac output
HR = heart rate
SV = stroke volume (volume ejected by ventricle)
EDV = end-diastolic volume
ESV = end-systolic volume
Cardiopulmonary I
Tues., 01/28/03, 2 pm
Dr. Downey
Eric Lawrence for Michelle Law
Page 3 of 6
-CO refers to a single ventricle
Ejection volume:
normal = 50 – 60%
decreased with impaired heart

Normal Values for Left Ventricle (70 kg resting man)
EDV – ESV = SV
125 mL -- 50 mL = 70 mL
SV x HR
= CO
70 mL x 70 /min = 4900 mL/min

Cardiac Output
-CO is what the body demands
-SV and HR can be altered to change CO
-SV can be altered by EDV or ESV
-distensibility (compliance) of ventricle = capability of ventricle to be stretched
o altered by cardiac hypertrophy – wall becomes stiffer, and has higher
filling pressures (end-diastolic pressures)
o stiffer in older people and infarcted hearts
-Factors of systolic ejection:
1. afterload = pressure the ventricle ejects against (aortic or pulmonary
trunk pressure)
2. contractility = strength of contraction
normal heart: cardiac output = venous return
venous return = rate that blood returns to heart
-circulatory events determine the venous return
-venous return controls cardiac output
Cardiopulmonary I
Tues., 01/28/03, 2 pm
Dr. Downey
Eric Lawrence for Michelle Law
Page 4 of 6
Mechanical Function of Heart
Contractility and preload are 2 ways that force and contractility of the
heart can be directly altered.
1. Preload = tension on muscle cell prior to activation
o amount of preload determines the diastolic sarcomere length
o preload is determined by amount of end-diastolic filling
o preload does not equal venous return
o change in preload does not cause change in contractility
-the greater a muscle is stretched, then a faster and more forceful
contraction
-until sarcomeres are stretched beyond optimal length
tension
Lmax
-skeletal muscles operate close to Lmax on
tension/length diagram
-cardiac muscle operates on the up slope of
the tension/length diagram
length
-tension refers to contractile function
-thus, small changes in cardiac sarcomere length produces large
changes in force of systole
Demonstration of preload
-small weight of preload stretches the muscle (diastole)
-a greater preload would stretch muscle more
Cardiopulmonary I
Tues., 01/28/03, 2 pm
Dr. Downey
Eric Lawrence for Michelle Law
Page 5 of 6
2. Contractility
= change in cardiac mechanical performance which is not due to a
change in preload (change in sarcomere length)
o referred to as ionotropic state
o alteration of intracellular Ca++ can alter contractility
Lmax
tension
B
A
L
length
o greater degree of tension on B curve at length L (same sarcomere length),
than on the A curve = change in contractility
o at length L there is change in contractility and no change in preload

Muscle force versus Muscle Length
passive force = resistance to
stretch (nonlinear distensibility)
passive force
+ active force
total force
Cardiopulmonary I
Tues., 01/28/03, 2 pm
Dr. Downey
Eric Lawrence for Michelle Law
Page 6 of 6

Increase sarcomere length increases contractility due to:
1. more favorable overlap between actin and myosin
-more crossbridges to be formed thus produce more tension
2. improve excitation-contraction coupling with stretching of the muscle
-more uniform distribution of Ca++ thru T-tubules when stretched
-inc. up to Lmax, but not beyond

Factors that affect ventricular preload
1. venous return
-greater end-diastolic filling
2. heart rate
-CO and venous return can stay the same, but preload changes
with increase in heart rate
3. end-diastolic volume increase due to less contractility (ischemia)
a. less ejection from left ventricle
b. more blood in ventricle after ejection,
c. chamber gets larger, thus increase preload, with no change in
venous return.
4. chamber stiffness
-filling and preload less if diastolic filling pressure doesn’t increase

Cardiac Function Graph
o graph of cardiac function (CO, SV, or stroke work) plotted against a
variable of sarcomere length
o sarcomere length measured by changes in end-diastolic volume
o illustrate effects of changes and preload on cardiac performance
o illustrate changes in contractility at a particular preload
Starling Curve
o values for one ventricle
o stroke volume plotted against
sarcomere length (end diastolic
ventricular pressure)
o same degree of contractility at
any point on each line
change in contractility occurs at different lines:
failure < normal < norepinephrine