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circulation and breathing > cardiodynamics > Flashcards

cardiodynamics Flashcards

1
Q

what is another word for cardiodynamics and what is it the study of

A
  • haemodynamics
  • study of blood flow i.e cardiac output
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2
Q

what is the equation for flow in terms of pressure

A

flow= change in pressure/ resistance

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3
Q

what is the change in pressure

A

mean arterial pressure- right atrial pressure

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4
Q

what determines resistance

A
  • diameter and length of vessel
  • viscosity of blood
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5
Q

what is equation for flow in terms of heart rate

A

flow= stroke volume x heart rate

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6
Q

what is the equation for mean arterial pressure

A

MAP= DP+ 1/3(SP-DP)

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7
Q

where is the biggest drop in pressure

A
  • aterioles
  • arterioles are the greatest resistors so many drugs target arterioles
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8
Q

what is the mechanism behind sepsis

A
  • causes vasodilation due to inflammatory cytokines released
  • vasodilation would reduce after load to an extent but will also reduce effective circulation volume and venous return therefore decreasing pre load
  • furthermore sepsis causes vessels to become more permeable resulting in relative hypovolemia
  • can also cause myocardial depression and therefore affect contractility
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9
Q

what factors affect cardiac output (flow)

A
  • stroke volume
  • heart rate
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10
Q

what are the two types of control

A
  • intrinsic control (determined by degree of stretch in myocardial fibres)
  • extrinsic control (activity of autonomic nervous system and circulating hormones)
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11
Q

what are the factors that impact stroke volume

A
  • pre load (increases CO)
  • Contractility (increases CO)
  • after load (decreases CO)
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12
Q

how does heart rate affect cardiac output

A
  • increasing HR increases CO until a certain point after that point CO decreases due to the fact that the heart is in less time in diastole so less filing of the ventricle and thus preload decreases and therefore stroke volume decreases. moreover at high HR myocardial muscles are overworking and therefore oxygen demand increases but this demand is not so ejection of blood doesn’t happen properly
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13
Q

what happens to heart rate and SV during exercise

A
  • heart rate increases significantly due to sympathetic activation
  • sv increases slightly and levels off (the amount of increase in sv can vary from person to person, athletes have a greater increases)
  • even though heart rate increases significantly sv doesn’t decrease it just levels off and this is due to the compensatory mechanisms such as epinephrine and norepinephrine, these increase contractility of the myocardial muscles and furthermore increase venous return thus increasing pre load
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14
Q

what can we do if heart rate is too fast- tachycardia (>100 bpm)

A
  • drugs which cause activation of parasympathetic nervous system
  • vagal manoeuvres (lifting legs up, carotid sinus massage)
  • cardioversion
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15
Q

what can we do If heart rate is too slow- bradycardia (<60 bpm)

A
  • adrenaline drugs- activation of sympathetic nervous system)
    -pacing
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16
Q

what is the stroke volume

A
  • volume at end of diastole minus volume at end of systole
17
Q

what is a pressure volume loop

A

a graph to show the changes in volume and pressure during different stages of the cardiac cycle- makes a loop structure/diagram

18
Q

how does the pressure volume loop differ between right and left ventricle

A
  • left ventricle has a much bigger loop compared to right ventricle
  • the increase in pressure is also much greater in pressure volume loop in left
  • changes in volume roughly the same between the two
19
Q

what is the ejection fraction

A
  • proportion of blood that is ejected out of the left ventricle compared to the amount of blood that is in it
  • normal humans 55-65%
  • (EDV-ESV)/ EDV
  • OR SV/EDV
20
Q

what does it mean if ejection fraction is low

A
  • contractility is impaired/low
21
Q

what does it mean if ejection fraction is high

A
  • low preload
22
Q

what is wall tension

A
  • increased pre load= end diastolic tension in myocardial fibres= wall stress
  • pre load proportional to end diastolic pressure/tension
23
Q

what is the Stalin curve and preload

A
  • increase pre load increase stretch in myocardial fibres= increased length of myocardial fibres and therefore tension= increases sv until a certain point
  • graph shows an increase in sv until a certain point where it levels off
24
Q

what is ESPVR on pressure volume loops

A
  • end systolic pressure volume relationship
  • gives an indication of the contractility of heart
  • greater/steeper the end systolic pressure volume relationship greater the contractility
  • weaker slope- decreased contractility can suggest heart failure
25
Q

what is EDPVR on pressure volume loops

A
  • end diastolic pressure volume relationship
  • greater/steeper the EDPVR the lower the compliance ( more stiff- so changes in volume causes large changes in pressure)
  • can be less compliant due to left ventricle hypertrophy
26
Q

what does an increased pre load have on an pressure volume loop

A
  • graph becomes wider (due to increased volume)
27
Q

factors affecting pre load

A
  • venous return ( blood volume, skeletal muscle activity)
  • filling time (heart rate)
28
Q

what Is the surrogate for pre load

A

right atrial pressure (increased pre load increases right atrial pressure)

29
Q

what is the relationship between right atrial pressure and venous return

A
  • increased right atrial pressure causes a decreases in venous return as the pressure gradient between the venous and right atria becomes smaller so less blood drawn in
30
Q

what is the pressure is called when there is no flow

A

mean systemic filling pressure

31
Q

what is hypovolemia and causes, signs

A
  • loss of volume of fluid/blood in blood vessels
  • due to vomiting, diarrhoea, haemorrhage
  • loss of blood volume causes a decrease In venous return and therefore decreased pre load and thus decreased CO
  • signs include cold and dry looking
32
Q

what is relative hypovolemia and causes, signs

A
  • abnormal distribution of fluid in vessels which is due to vasodilation and permeable vessel walls which lead to decreased venous return
  • no actual loss of blood from body
  • causes include sepsis, anaphylaxis, neurogenic
  • signs- warm and flushed due to vasodilation
33
Q

what affect does contractility have on Stalin curve

A
  • at an given pre load the sv would be greater at increased contractility
  • curve would be higher for increased contractility and lower for decreased
34
Q

what are the effects of contractility on pressure volume loops

A
  • end systolic pressure volume relationship would be steeper at higher contractility
  • end systolic pressure is higher
  • end systolic volume lower
  • end systolic pressure higher
35
Q

what is after load and its impacts on SV

A
  • after load is the pressure in systemic circulation
  • higher afterload= higher systemic pressure= greater the resistance
  • heart needs to work harder against that greater resistance
  • decreases sv and therefore cardiac output
36
Q

what is the impacts of afterload on pressure volume relationships

A
  • increased after load shifts curve to the right
  • curve higher in terms of pressure
  • also volume is smaller (stroke volume)

circulation and breathing (11 decks)

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