how CO is governed by filling pressure and inotropic state Flashcards
def of CO
the amount of blood ejected from the heart per minute
eqn for CO
HR * SV
def of SV
how much blood is ejected per beat
CO at rest
4900ml /min (approx 5l)
CO in exercise
approx 22l/min
CO * TPR =
BP
BP / TPR =
blood flow
what determines blood pressure and blood flow
cardiac output
what is preload
stretch of myocytes at rest
what is afterload
wall stress produced due to ejection of blood - pressure OPPOSING ejection
how is preload measured
EDV/central venous pressure
why can’t preload be measured directly
because it’s related to sarcomere length at end of diastole, which can’t be measured
what relates pressure, wall stress, and radius
Laplace’s Law
what is contractility
strength of contraction at a given resting stretch
what modulates contractility
sympathetic nerves, circulating adrenaline increasing [Ca}i
what is energy of contraction
amount of work needed to generate SV
what determines energy of contraction
starling’s law and contractility
what does stroke work do
increases chamber pressure > aortic pressure; ejection
what is starling’s law of the heart
energy of contraction of cardiac muscle is proportional to the muscle fibre length at rest
describe the ventricular function curve
y = SV = 70ml: normal filling pressure at rest, 5mmHg CVP
plateau at about SV = 100, from 10-15mmHg CVP
muscle overstretched at >15mmHg CVP
what is the molecular basis of Starling’s Law
in a stretched fibre, c.f. an un-stretched one:
less overlapping actin & myosin means there’s less MECHANICAL inference, so there is greater potential for cross bridge formation and therefore increased Ca2+ sensitivity
What are the 5 roles of Starling’s Law
- Balances RV and LV output
- Responsible for fall in CO during drop in blood vol eg sepsis/haemorrhage
- Restores CO in IV fluid transfusion
- Responsible for fall in CO in orthostasis (standing); or else postural hypotension, dizziness
- increased SV in upright exercise
What does Laplace’s law describe
how effectively wall tension (T) is converted into pressure (P) within a chamber (ventricle)
Equations for Laplace’s law
P = 2T/r
therefore:
T proportional to r AND P
how does a small luminal radius affect ejection
greater wall curvature
more wall tension directed to centre of chamber
more pressure developed
more ejection
how does larger luminal radius affect ejection
less wall curvature
less wall tension directed towards centre of chamber
less pressure developed
less ejection
how does laplace’s oppose starling law at rest
increased pre load > increased stretch of chamber > increased chamber radius > decreased curvature
Which law is dominant in a healthy heart
Starling’s overcomes laplace’s for good ejection
how does laplace’s facilitate ejection
in ventricular contraction, radius decreases and curvature is increased
how does laplace’s contribute to a failing heart
in heart failure, chambers are often dilated i.e. increased radius - not enough wall tension converted to pressure.
what contributes to wall tension (T)
wall stress S * wall thickiness w, so P = 2Sw/r
rearrange the eqn for wall tension to find the eqn for wall stress S (or afterload)
S = (P*r)/2w
why does afterload oppose contraction
it’s directed within chamber wall NOT directed towards the chamber centre
what effect does increased wall thickness have on wall stress
increased wall thickness reduces wall stress
