Cardiac Haemodynamics Flashcards

1
Q

what is the most likely diagnosis of an elderly woman which becomes breathless and cannot lie flat with lower O2 sat and respiration is fats and shallow

A

pulmonary oedema - fluid in the lungs - seen as white areas - usually at the bottom of the lungs

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2
Q

what is the basic structure of skeletal muscle in the heart

A

each muscle fibre is made up of individual myofibrils which contain rows of adjacent sarcomeres
actin and myosin filament overlap and this shortens the row of sarcomeres

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3
Q

what initiates heart contraction

A

calcium binds to troponin which induces conformational change in troponin-tropomyosin complex
exposes binding sites of actin

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4
Q

describe the power stroke in the heart

A

myosin beds can bind once Ca influx has occurred - then ATP is required for binding - initiates power stroke and pulling

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5
Q

how much ATP do myocardial cells use up

A

6kg per day

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6
Q

what does the use of ATP do in myocardial cells

A

force generation
myofilamant shortening
transforms basic mechanical energy into useful hydraulic function

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7
Q

which directions does the heart contract

A

longitudinal, horizontal, twisting - torson

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8
Q

what did william harvey discover

A

circulation

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9
Q

what causes higher demand on the heart

A

exercise
incurrent illness
fluid overload
pregnancy - almost doubles

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10
Q

what is cardiac functional reserve

A

the capacity to augment performance on demand

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11
Q

how do you calculate cardiac reserve

A

maximal cardiac output - cardiac output at rest

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12
Q

what is the difference n CO at rest compared to during exercise

A

5 l/min

20 l/min

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13
Q

what is cardiac reserve innervated by to affect HR

A

sympathetic innervation
speeds up SAN depolarisation = more AP - increases conduction through AVN and bundle
also by adrenaline - B1 agonism

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14
Q

how can we augment stoke volume

A

sympathetic stimulation
prolonged ca channel opening enhances muscle contraction
also depends on preload

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15
Q

what happens if there is too much stretch in sarcomere

A

then there is less tension and less contraction - in the graph you always want to be on the left side down slope

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16
Q

how does sarcomere length affect tension

A

small changes in sarcomere length cause large changes in tension - normally stretching the LV will aid contraction

17
Q

what determines stretch of the LV

A

EDV - greater the preload the greater the cardiac performance

18
Q

what is the starling law of the heart

A

the energy of contraction is a function of the length of the muscle fibre

19
Q

what happens to contraction if preload is decreased

A

reduced muscle contraction

20
Q

what causes shifts in the frank starling graph

A

left shift - exercise, pharmacological stimulation

right shift - pharmacological depression and myocardial loss

21
Q

what does a decrease or increase in after load look like in a frank starling graph

A

decreased after load shift up and left

increased after load in down and right

22
Q

what happens to the frank starling curve with sympathetic stimulation and why

A

shift to the left and NA and A stimulate cAMP so more Ca enter and greater cross bridge linking in sarcomeres

23
Q

how do you calculate ejection fraction

A

stroke volume / EDV

24
Q

what is physiological Ef and what is it during exercise

A

55-75%

90% in exercise

25
Q

what does high BP do to after load

A

increases it

26
Q

what happens to CO in heart failure

A

ischeamia - scarred myocardium - less movement of walls
wall thinning due to infection
increased after-load - chronic high output

27
Q

if there is too much preload and too much stretch to sarcomeres

A

move to the right downward line on the sarcomere graph and shift to the right in frank starling graph

28
Q

if there was failing LV and fluid entering then lungs how would you resolve this

A

give o2
morphine to relax pulmonary vessels - reduce preload and take strain of LV - also reduce pain
furosemide - take fluid out of lungs, reduce preload