Cardiovascular strand: Lecture 7 - cardiac haemodynamics Flashcards

1
Q

If an elderly lady comes into A&E claiming she is breathlessness, cannot lie flat, her oxygen saturations have dropped and her respiration is fast and shallow, what might be wrong with her?

A

Fluid in the lungs

Pulmonary oedema (shown on X-ray)

Fuzziness - fluid

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2
Q

What is pulmonary oedema?

A

fluid accumulation in the tissue and air spaces of the lungs

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3
Q

Draw a graph of the changes in LV, LA and Aortic pressure during respiration, and label each point

A
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4
Q

What does the graph of an action potential in non-pacemaker cells look like? Include labels

A
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5
Q

What are desmosomes?

A

desmosomes stick the cells together so they’re electrically linked

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6
Q

Draw a diagram of a muscle fibre (with labels) and a myofibril

A
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7
Q

What happens during phase 2 of the non-pacemaker action potential?

A

increased permeability to Ca2+

decreased permeability to K+

Lots of calcium outside the cell that all move in

this calcium is used to help start a new cardiac contraction

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8
Q

What is actin wrapped up in?

A

tropomyosin and troponin

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9
Q

Explain how a muscle contraction is carried out (6 steps)

A
  1. Ca2+ binds to troponin
  2. Induces conformational chnage in troponin-tropomyosin complex
  3. Exposes the binding site of actin
  4. Mysosin head can then bind to actin. This requires ATP
  5. Myosin exerts “pulling” action on actin
  6. Initiates muscle contraction - myofilament shortens
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10
Q

How much ATP do myocardial cells usilise a day?

A

6 kg

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11
Q

How is maximum ejection of blood from heart achieved?

A

longitudinal filament shortening - horizontal and circumferential thickening

reduces LV chamber diameter and causes further ejection

Cells are different shapes so they contract different ways

There is horizontal, longitudinal and twisting contraction

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12
Q

Who discovered about blood circulation in the heart?

A

William Harvey

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13
Q

In what situations does the heart need to cope with higher demands?

A
  • exercise
  • intercurrent illness
  • fluid overload
  • pregnancy
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14
Q

What is cardiac reserve?

A

The capacity to augment performance on demand

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15
Q

How do we calculate cardiac output?

A

Cardiac output = heart rate x stroke volume

cardiac output - volume pumped out per min

heart rate - number of beats per min

stroke volume - volume pumped out per beat

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16
Q

How do we calculate cardiac reserve?

A

Cardiac reserve = maximal cardiac output - cardiac output at rest

17
Q

How does sympathetic innervation increase heart rate?

A
  • Speeds up SA node depolarisation
  • More frequent action potentials
  • Increases conduction through AV node/ bundle
18
Q

How can we augment stroke volume?

A
  • sympathetic innervation
  • prolonged opening of Ca2+ channels
  • enhances calcium action in excitation/contraction coupling mechanisms
19
Q

What is stroke volume dependant on?

A

PRELOAD

20
Q

What is the difference between length-tension relations between cardiac and skeletal muscle?

A

Cardiac has a much narrower range

So you don’t have to stress it very much to get a big increase in tension

But its also sensitive to too much tension

In health, you should always be in the upwards part of the curve for cardiac muscle

21
Q

Explain how increasing preload increases cardiac performance?

A
  • small changes in cardiac sarcomere length results in large variations in tension
  • so stretching the LV will aid contraction
  • LV end-diastolic volume (or pressure) determines how stretched the LV wall is
22
Q

What is Starling’s law of the heart?

A

“the same as the law of muscular tissue in general, that the energy of contraction however measured, is a function of the length of the muscle fibre”

23
Q

What is end diastolic volume/ pre-load ?

A

Volume of blood in the right and/or left ventricle at end load or filling in (diastole) or the amount of blood in the ventricles just before systole

24
Q

What is the relationship between stroke volume and end-diastolic volume? (graph)

A

the more you put in, the more you get out (because actin-myosin are closer together as sarcomere stretched, more myosin can bind to actin, more contraction)

but this is up to a certain point

THE FRANK STERLING CURVE

25
Q

Explain how venous return is ALWAYS correlated with CO?

A
  • equilibriates right and left heart output e.g LV CO= RV preload and vise versa
  • exercise and other demains cause increase venous return
  • which allows augmentation of stroke volume
  • so equilibrium is maintained
26
Q

When can the Frank Sterling curve shift?

A

left shift - exercise, pharmalogical stimulation (stroke volume > preload)

right shift - myocardial loss, pharmacological depression (preload > stroke volume)

27
Q

How does sympathetic stimulation of the heart work? Which way does the Frank-Sterling curve shift when this occurs?

A
  • noradrenaline and adrenaline stimulate cAMP
  • more Ca2+ enters cell
  • greater cross bridge linking in sarcomeres

curve shifts to the left

28
Q

What is ejection fraction and how is it calculated?

A

The proportion of blood ejected out of the heart related to how much was there in the first place

ejection fraction = stroke volume / end diastolic volume

av at rest is 65-75%.

increases during exercise, decreases if heart failure

29
Q

What happens if myocardium becomes diseased?

A

It contracts less

30
Q

What does ischaemia do to myocardium?

A

causes it to scar/die

31
Q

What effect do viral infections/ alcohol have on the heart?

A

wall thinning

32
Q

What is heart afterload?

A

Afterload is the pressure the heart must work against to eject blood during systole (ventricular contraction).

33
Q

When might a patient have increased afterload/ chronic high -output

A

High blood pressure

34
Q

Which two systems are activated when a ventricle fails?

A
  • sympathetic nervous system overactivates
  • renin-angiotensin-aldosterone system

These measures raise the preload

35
Q

When do we move to the descending limb of the sarcomere tension curve?

A

when heart stretches

eventually, LV stretch exceeds physiological levels

36
Q

How do we treat excess fluid in the lungs?

A
  • give oxygen to maximise alveolar ventilation
  • morphine to relax her pulmonary vessels and reduces her preload and takes the strain of the LV
  • furosemide - take fluid off her lungs (loop diueretic)
37
Q
A