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Cardiology > Lecture 9 - Cardiac muscle and pump function > Flashcards

Lecture 9 - Cardiac muscle and pump function Flashcards

1
Q

what does fluid around the heart in an alveolar bats wing like shape indicate?

A

pulmonary oedema

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2
Q

what happens during systole

A

Phase 1 . sodium entry into the cell - depolarises the cell
Phase 2 then entry of calcium into cell - causes contraction
Phase 3 - potassium exit - repolarisation and back to normal

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3
Q

When does the aortic pressure wave peak

A

during ventricular ejection of systole. reaches 120 mm/hg from 80 mmhg. returns to normal after

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4
Q

When does the left pressure wave peak

A

During isolvolumetric contraction - when the ventricles contract
drops during isovolumetric relaxation

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5
Q

What happens to the atrial pressure wave

A

it remains quite low and peaks a little during atrial contraction when the mitral valve opens (2 cusps)

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6
Q

what is a skeletal muscle composed of?

A

Each muscle fibre is composed of myofibrils, which contain adjacent rows of sarcomeres

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7
Q

What causes contraction of a myofibril

A

The overlap of the thin actin and thick myosin filaments shorten the row of sarcomeres resulting in contraction of the muscle.

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8
Q

What are the cardiac muscles like?

A

are branched and are connected by gap junctions which allow electrical activity and allow action potentials to travel through the heart.

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9
Q

Why is calcium important for contraction?

A

at rest there’s blocking of the myosin binding sights by troponin as they form a complex which block the binding sites on the actin thin filament.
when calcium comes it binds to the troponin and complex and moves it which allow it expose myosin binding sites - contraction starts

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10
Q

Why is troponin important

A

blocks binding sites

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11
Q

Cardiac energetics - what do they use?

A

myocardial cells use AT6 - 6kg per day.

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12
Q

what does ATP store?

A

Chemical energy which is converted to mechanical energy

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13
Q

what does the energy transfer result in

A

force generation

myofilament shortening

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14
Q

what transformations occur

A

basic mechanical energy to hydraulic function for the whole organ

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15
Q

what occurs in hydraulic function?

A

forced generation causes some ejection.
shortening of longitudinal filaments and horizontal thickening
reduces LV chamber diameter and causes further ejection

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16
Q

What is the wall of the left ventricle like

A

thick and muscular

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17
Q

what is cardiac adaptability??

A

The heart needs to pump at rest
Coping with higher demands
Exercise, intercurrent illness,fluid overload and pregnancy

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18
Q

What is cardiac reserve

A

is the capacity of the heart to increase its performance on demand (maximum capacity)

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19
Q

Equation for cardiac output

A

heart rate x stroke volume

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20
Q

Cardiac reserve equation

A

Maximum cardiac output - cardiac output at rest

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21
Q

What is cardiac reserve critically dependent on?

A

Sympathetic system

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22
Q

What does sympathetic innervation do?

A

speeds up heart rate through speeding up sa node depolarisation, more frequent action potentials which increase conduction through AV node

23
Q

How does adrenaline increase sympathetic activity?

A

Through b1 agonism

24
Q

how else can we augment cardiac output

A

increasing stroke volume
prolongued opening of calcium channels - enhances calcium action in excitation/contraction coupling mechanisms
ionitropic - force of contraction

25
Q

What does stroke volume also depend on

A

preload is the end diastolic volume (stretchin of cardiac muscle prior to contraction)

26
Q

what happens to sarcomeres with change in length

A

as they increase the tension increases to a certain point and then declines as the stretch becomes more extreme

27
Q

What factors affect cardiac output

A

cardiac rate and stroke volume

28
Q

what is franklin-starling law

A

the length of the muscle fibers is proportionate to the end diastolic volume.

29
Q

what does small changes in cardiac sarcomere length result in

A

large variations in tension

30
Q

what will stretching the LV do?

A

it will aid contraction.

31
Q

What does end LV diastolic volume determine

A

how stretched the LV wall is

32
Q

what will increasing preload do

A

increase cardiac output upto certain point.

33
Q

how does this contraction happen when muscle stretches?

A

as muscle stretches, the diameter of the myofibrils is reduced, acting and myosin filaments are closer together, leading to more contraction.

34
Q

what is starlings law?

A

energy of contraction is a function of the length of the muscle fibre. like elastic band

35
Q

What does the franklin-starling curve indicate?

A

relationship between end diastolic volume and stroke volume

36
Q

What does cardiac output correlate with?

A

venous return,

left cardiac output =rv preload

37
Q

What does exercise and other demands do?

A

increases venous return

allows augmentation of stroke volume

38
Q

What would cause a left shift in the frank-starling curve

A

exercise, pharmacological stimulation

39
Q

What would cause a right shift in the frank-starling curve

A

pharmacological depression, myocardial loss

40
Q

Describe effects of a left shift

A

during pharmacological stimulation there will be a decrease in the end diastolic volume as heart rate increases and the diastolic period will be shorter, this will increase the stroke volume as there is an increase in pressure. this will be followed by parasympathetic stimulation which will cause a decrease in the afterload.

41
Q

Describe effects of a right shift

A

an increase in the end diastolic volume caused by pharmacological depression will allow ventricles to fill for longer and hence decrease stroke volume due to a decrease in contractility. This will be followed by an increase in the afterload due to sympathetic stimulation.

42
Q

what happens to the curve on sympathetic stimulation

A

noradrenaline and adrenaline stimulate cAMP. more calcium enters the cell, cross-linking in sarcomeres
curve shifts to the left as edv decreases and stroke volume increases.

43
Q

When is cardiac output augmented

A

at all levels of ventricular preload

44
Q

ejection fraction

A

stroke volume/end diastolic volume

physiological ef - 50 to 75%

45
Q

what happens to EF in a failing heart

A

reduces

46
Q

what happens to EF on exercise

A

can reach 90%

47
Q

What happens during heart failure

A 
myocardium is diseased - contracts less
ischaemia - scarred myocardium
viral infection/alcohol - wall thinning
there is a right shift
increase in afterload - due to sympathetic overactivation due to a decreased stroke volume
RAA system kicks in
48
Q

during physiological ventricular stretch

A

ventricular sarcomere length is on the ascending limb

49
Q

during heart failure where does the sarcomere tension fall on the curve

A

on the descending limb

50
Q

during heart failure, what happens to the preload

A

preload rises
this works for a while but the heart stretches
but lv stretches exceeds physiological levels eventually

51
Q

what does a failing left ventricle cause

A

pulmonary oedema

52
Q

what can you do to help with pulmonary oedema

A

alveolar ventilation
high-flow oxygen
relaxing pulmonary vessels would reduce preload and take strain off left V
morphine - help breathing and pain
furosemide - takesome fluid off lungs (treats oedema)

53
Q

what does furosemide do

A

treats oedema - fluid retention

Cardiology (12 decks)

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