how CO is governed by filling pressure and inotropic state Flashcards

1
Q

def of CO

A

the amount of blood ejected from the heart per minute

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2
Q

eqn for CO

A

HR * SV

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3
Q

def of SV

A

how much blood is ejected per beat

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4
Q

CO at rest

A

4900ml /min (approx 5l)

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5
Q

CO in exercise

A

approx 22l/min

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6
Q

CO * TPR =

A

BP

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7
Q

BP / TPR =

A

blood flow

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8
Q

what determines blood pressure and blood flow

A

cardiac output

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9
Q

what is preload

A

stretch of myocytes at rest

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10
Q

what is afterload

A

wall stress produced due to ejection of blood - pressure OPPOSING ejection

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11
Q

how is preload measured

A

EDV/central venous pressure

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12
Q

why can’t preload be measured directly

A

because it’s related to sarcomere length at end of diastole, which can’t be measured

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13
Q

what relates pressure, wall stress, and radius

A

Laplace’s Law

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14
Q

what is contractility

A

strength of contraction at a given resting stretch

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15
Q

what modulates contractility

A

sympathetic nerves, circulating adrenaline increasing [Ca}i

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16
Q

what is energy of contraction

A

amount of work needed to generate SV

17
Q

what determines energy of contraction

A

starling’s law and contractility

18
Q

what does stroke work do

A

increases chamber pressure > aortic pressure; ejection

19
Q

what is starling’s law of the heart

A

energy of contraction of cardiac muscle is proportional to the muscle fibre length at rest

20
Q

describe the ventricular function curve

A

y = SV = 70ml: normal filling pressure at rest, 5mmHg CVP
plateau at about SV = 100, from 10-15mmHg CVP
muscle overstretched at >15mmHg CVP

21
Q

what is the molecular basis of Starling’s Law

A

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

22
Q

What are the 5 roles of Starling’s Law

A
  1. Balances RV and LV output
  2. Responsible for fall in CO during drop in blood vol eg sepsis/haemorrhage
  3. Restores CO in IV fluid transfusion
  4. Responsible for fall in CO in orthostasis (standing); or else postural hypotension, dizziness
  5. increased SV in upright exercise
23
Q

What does Laplace’s law describe

A

how effectively wall tension (T) is converted into pressure (P) within a chamber (ventricle)

24
Q

Equations for Laplace’s law

A

P = 2T/r

therefore:

T proportional to r AND P

25
how does a small luminal radius affect ejection
greater wall curvature more wall tension directed to centre of chamber more pressure developed more ejection
26
how does larger luminal radius affect ejection
less wall curvature less wall tension directed towards centre of chamber less pressure developed less ejection
27
how does laplace's oppose starling law at rest
increased pre load > increased stretch of chamber > increased chamber radius > decreased curvature
28
Which law is dominant in a healthy heart
Starling's overcomes laplace's for good ejection
29
how does laplace's facilitate ejection
in ventricular contraction, radius decreases and curvature is increased
30
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.
31
what contributes to wall tension (T)
wall stress S * wall thickiness w, so P = 2Sw/r
32
rearrange the eqn for wall tension to find the eqn for wall stress S (or afterload)
S = (P*r)/2w
33
why does afterload oppose contraction
it's directed within chamber wall NOT directed towards the chamber centre
34
what effect does increased wall thickness have on wall stress
increased wall thickness reduces wall stress