MYOCARDIAL PERFORMANCE
General Effects of Autonomic Control on Heart:
- SYMPATHETICS:
- Positive chronotropic effect
-- faster heart rate.
- Positive inotropic effect --
greater contractility for the same fiber length.
- PARASYMPATHETICS: Negative chronotropic effect, but
no inotropic effect.
PRELOAD: The diastolic filling pressure, or
end-diastolic volume.
AFTERLOAD: Ventricular systolic pressure, which is equal
to arterial systolic pressure under normal circumstances.
LAPLACE'S LAW: The stress on the
ventricular wall is proportional to the Ventricular Pressure
x Ventricular Radius, where the size of the ventricle is
determined by stretching, i.e. by ventricular volume.
STARLING'S LAW OF THE HEART: Within
limits, increases in end-diastolic volume result in a corresponding increase in
stroke volume. Most simplified, within limits, the volume that comes into the
heart goes back out.
- MECHANISM: Increased Filling Volume ------> Stretch
Ventricular Muscle ------> Augmented ventricular fiber length ------>
greater inotropic state ------> faster velocity of ejection
------> Greater Cardiac Output.
- Increased fiber length results in more forceful
contraction, within limits.
- Optimal muscle fiber length = 2.2
micron. Heart normally works slightly below this level to give
room for optimal filling.
PRESSURE-VOLUME LOOP: P/V graph, with
both diastolic and systolic lines plotted on it. You use this graph to plot
the pressure and volume at all points in the cardiac cycle.
- END-SYSTOLIC CURVE: The upper limit to the loop.
- END-DIASTOLIC CURVE: The lower limit to the loop.
- CARDIAC CYCLE in LOOP:
- DIASTOLE:
- ISOVOLUMIC RELAXATION: Volume is constant
while pressure goes straight down.
- VENTRICULAR FILLING: Pressure remains
constant while volume increases.
- SYSTOLE:
- ISOVOLUMIC CONTRACTION: Volume constant
while pressure goes straight up.
- EJECTION: Pressure continues to
increase as blood is ejected from the ventricle. The
end-pressure at this point is systolic arterial pressure.
- The pressure continues to rise during
systole because pressure is rising in the arterial network. You are
putting more blood into the arterial tree then is being put out on
the other side. Ventricle must match that rise in pressure to force
blood out.
- AORTIC VALVE CLOSES: At the end of systole,
the ventricular pressure (i.e. fiber length) decreases to the point
that the aortic valve can't stay open, so it closes.
- STROKE WORK: The area of the
Pressure-Volume Loop. Mathematically, that means: Stroke Work =
(Stroke Volume) x (Mean Arterial Pressure)
- STROKE WORK is equivalent to stroke volume, but
it is normalized for differences in blood pressure. Thus it is a good
indicator of heart performance.
- Because we have normalized for blood pressure,
a shift in the curve for stroke work means that there must be an
increase in the inotropic state.
VENTRICULAR FUNCTION CURVE: A
comparison of End-Diastolic Volume (or Pressure or Fiber Length) and Stroke
Volume (or Stroke Work). The curve is essentially a line that levels off at high
values. It is a way of expressing Starling's Law.
- If you plot Stroke Work -vs- LVEDV, you will get
the same curve for the same inotropic state, regardless
of blood pressure. So using Stroke Work normalizes for blood pressure,
and it makes the curve represent the inotropic state.
EFFECT OF PRELOAD ON STROKE-WORK:
- Standing at Rest: The least stroke work is
performed.
- SUPINE ------> Preload (venous return) increases
------> Fiber-length increases ------>------> Higher Stroke Work.
- PRONE, with LEGS RISEN: Even more pronounced effect
as above ------> higher stroke work.
EFFECT OF AFTERLOAD ON STROKE VOLUME: A higher afterload
------> Higher systolic pressure must be developed ------> Higher end-systolic
volume to achieve that pressure, but the end-diastolic volume remains the same
------> lower stroke volume.
AUTOREGULATION OF AFTERLOAD: Due to heterometric
autoregulation, within limits, stroke volume will be maintained even in
face of a higher blood pressure, but it takes a few beats for the mechanism to
kick in.
- High afterload ------> Lower
stroke volume ------> Since pulmonary arterial pressure hasn't changed,
the right heart continues to pump the same stroke volume as before
------> Pulmonary blood volume increases ------> Higher venous return back
to left atrium ------> Higher preload ------> Higher fiber length + velocity
of ejection ------> ------> Stroke volume returns to normal
- But a new pressure-volume curve is carved
out on the P/V-Loop. Stroke-work overall has increased.
- In compensating for the higher blood pressure, we
must use some of our Starling Reserve -- the extra capacity
in the heart to do stroke work, strictly because of the Starling mechanism.
TOTAL RESERVE: The total stored
capacity the heart has to do extra stroke work. It is equal to Starling
Reserve + Inotropic Reserve + Heart-Rate Reserve.
- STARLING RESERVE: The extent to
which we can increase Cardiac Output simple by increasing filling, at the
same inotropic state.
- INOTROPIC RESERVE
- HEART-RATE RESERVE
INOTROPIC STATE: It's the contractile
force in the muscle, at any particular fiber-length. That is the same
as the Ca+2 concentration in the sarcomeres.
- It increases stroke volume, DUH??
HEART-RATE AND STROKE VOLUME: Heart rate extremes lead
to lower stroke volume.
- Bradycardia: Heart-rate slower than 40. Cardiac
Output goes way down because the stroke volume can't increase enough to
compensate for the lower heart-rate. You've reached the maximum of the
heart's inotropic state.
- Tachycardia: Heart-rate faster than 180. Cardiac
Output goes way down because there is no longer enough time between
beats for sufficient ventricular filling, i.e. the short diastolic time
cuts into the "Fast-Filling Phase" of diastole.
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