Cardiac haemodynamics Flashcards

1
Q

How do cardiac cells join?

A

Cardiac cells joined together by desmosomes

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2
Q

What does calcium do for muscles to contract?

A

Calcium outside of cell, calcium channels open and come into cell. Calcium used to start a cardiac contraction. Calcium passes into cells and binds to troponin. Induces conformational change in troponin-tropomyosin complex. Exposes binding sites of actin.

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3
Q

What happens when the the actin-myosin biding site is exposed?

A
  • Myosin heads can then bind to actin
  • This process requires ATP
  • Myosin exerts, “pulling” action on actin
  • Initiates muscle contraction
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4
Q

What do troponin and tropomyosin do?

A

Pre-contraction, troponin and tropomyosin form a complex that blocks the myosin binding site on actin.

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5
Q

Then in systole what happens with the calcium ions?

A

Then, in systole, calcium ions arrive inside the sarcoplasm and bind to troponin, moving the Tn-Tm complex and exposing the myosin binding.

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6
Q

What does the myosin head do when it binds to the binding site?

A

Myosin heads dock in and exert a “pulling” action on the actin, resulting in contraction. The energy needed for this is derived from ATP turnover.

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7
Q

Cardiac energetics- what does ATP do wand what does it result in?

A

• Chemical energy is stored within ATP: Phosphate group released from ATP to ADP
• In this way, the chemical energy stored within ATP is converted into mechanical energy
• This results in:
– Force generation
– Myofilament shortening
– Transforms basic mechanical energy into useful hydraulic function for the whole organ

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8
Q

What is hydraulic function and what does it do?

A
  • Force generation-some ejection
  • Longitudinal filament shortening- horizontal and circumferential thickening
  • Reduces LV chamber diameter and causes further ejection
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9
Q

How can you maximise ejection fraction?

A

The increased wall stress raises fluid pressure in the chamber, causing LV pressure to exceed Ao pressure and force the aortic valve open. Furthermore, the myocardial fibres thicken in several directions, leading to a complex geometric reconfiguration that causes further blood to be displaced from the ventricle into the circulation. This sophisticated pump action maximises ejection fraction.

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10
Q

How are cardiac cells organised?

A

Cardiac cells organised longitudinally (top to bottom), circumferential muscle (around the heart).

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11
Q

How does myocardium contract?

A

Myocardium contracts horizontally, longitudinally and twisting which gives maximum amount of blood ejected from heart.

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12
Q

What does the cardiac system have resistance?

A

The system into which blood is propelled has inherent resistance as it branches out into increasingly small and dense vessel networks.

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13
Q

How is the friction of the cardiac system overcome?

A

To overcome this “friction”, cardiac output needs to be maximised by effective power generation in the pump.

Therefore a diastolic period is essential – thus, the electrics repolarise, the myocardium relaxes and allows LV filling. Meanwhile the aortic valve shuts, the coronary sinuses fill so the coronaries are perfused, and the myocardium receives oxygen and glucose to allow more ATP to be generated.

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14
Q

What is cardiac functional reserve?

A

Cardiac reserve is the capacity to augment performance on demand.

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15
Q

What does the body need the cardiac functional reserve?

A

– Exercise
– Intercurrent illness
– Fluid overload
– Pregnancy

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16
Q

What is the equation for CO?

A

CO= HR x SV

17
Q

What is the equation for cardiac reserve?

A

Cardiac reserve = Maximal CO – Cardiac output at rest

18
Q

What does sympathetic innervation do?

A

– Speeds up SA node depolarisation
– More frequent action potentials
– Increases conduction through AV node/Bundle

19
Q

What does the body release for cardiac reserve?

A

Adrenaline- ẞ1 agonism

20
Q

How many litres of blood can come out the heart per minute when exercising?

A

20L

21
Q

How else can we increase CO?

A

– Prolonged opening of Ca2+ channels
– Enhances calcium action in excitation/contraction coupling mechanisms described earlier

More calcium binds to troponin, more myosin binds to actin myosin binding site.

22
Q

What is preload?

A

Preload- what is in the V before systole- end diastolic volume- amount of blood in ventricle before contraction starts

23
Q

What is the sarcomere function?

A
  • At physiological stretch, ventricular sarcomere length is on the ascending limb
  • So stretching the LV will aid contraction
  • LV end-diastolic volume (or pressure) determines how stretched the LV wall is
  • ↑ preload, ↑cardiac performance
24
Q

How does when the sarcomere stretch more contraction can occur?

A
  • As muscle stretches, the diameter of the myofibrils is reduced
  • Thick and thin filaments are closer together
  • More myosin heads can interact with actin
  • More contraction can occur
25
Q

How does venous return correlate with CO?

A

• Venous return always correlates with CO
– Equilibrates right and left heart output
– (LV CO = RV preload, and vice versa)
– Exercise and other demands
– Increased venous return
– Allows augmentation of stroke volume

If you exercise- skeletal muscle pump- squeezing leg muscles- squeezes veins- more venous return, more blood in RV, increased pre-load so LV needs to pump harder.

26
Q

What is the Frank- Starling curve?

How is it affected?

A

Curve represents the relationship between stroke volume and end diastolic volume. The law states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction (the end diastolic volume), when all other factors remain constant.

Sympathetic stimulation move left.
Heart failure- moves right.

  • Left shift -Exercise, pharmacological stimulation
  • Right shift- Pharmacological depression, myocardial loss
27
Q

What is sympathetic stimulation?

A

• Noradrenaline and adrenaline stimulate cAMP
• More calcium can enter the cell
– Greater cross-bridge linking in sarcomeres
• The Frank-Starling curve shifts to the LEFT
• Cardiac output is augmented at all levels of ventricular preload

28
Q

What is the equation for ejection fraction?

A

Ejection fraction = SV/ End diastolic volume

29
Q

What is ejection fraction?

A

EF is the proportion of blood that is ejected out of heart related how much was in it in the first place.

  • Physiological EF is 55-75%
  • In exercise, EF can reach 90%
  • And a failing heart shows reduced EF
30
Q

If the myocardium is diseased how does it affect the heart?

A

– Ischaemia- scarred myocardium
– Viral infection/alcohol -wall thinning
– Increased afterload- chronic high-output
– We try and compensate for a failing ventricle
– SNS overactivates
– Renin-angiotensin-aldosterone system kicks in

31
Q

How does heart failure affect preload?

A
  • These measures raise the preload
  • This works for a while, but the heart stretches
  • Eventually, LV stretch exceeds physiological levels
  • We move to the descending limb of the sarcomere tension curve
32
Q

What does morphine affect in the body?

A

• Morphine- relaxes the pulmonary vessels- reduces preload and afterload on RV reducing the strain