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
Q

how does a small luminal radius affect ejection

A

greater wall curvature
more wall tension directed to centre of chamber
more pressure developed
more ejection

26
Q

how does larger luminal radius affect ejection

A

less wall curvature
less wall tension directed towards centre of chamber
less pressure developed
less ejection

27
Q

how does laplace’s oppose starling law at rest

A

increased pre load > increased stretch of chamber > increased chamber radius > decreased curvature

28
Q

Which law is dominant in a healthy heart

A

Starling’s overcomes laplace’s for good ejection

29
Q

how does laplace’s facilitate ejection

A

in ventricular contraction, radius decreases and curvature is increased

30
Q

how does laplace’s contribute to a failing heart

A

in heart failure, chambers are often dilated i.e. increased radius - not enough wall tension converted to pressure.

31
Q

what contributes to wall tension (T)

A

wall stress S * wall thickiness w, so P = 2Sw/r

32
Q

rearrange the eqn for wall tension to find the eqn for wall stress S (or afterload)

A

S = (P*r)/2w

33
Q

why does afterload oppose contraction

A

it’s directed within chamber wall NOT directed towards the chamber centre

34
Q

what effect does increased wall thickness have on wall stress

A

increased wall thickness reduces wall stress