Session 2.1 Flashcards

1
Q

What kind of junctions are between cardiac myocytes?

A

Gap junctions so contract in synchrony

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2
Q

Why are cardiac action potentials relatively long?

A

1 contraction = 1 heartbeat and you want it to be smooooooth

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3
Q

What is the purpose of chord tendons??

A

Anchor valve to stop it inverting

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4
Q

Briefly describe the conduction.

A

1) pacemaker cells in SAN generate an action potential in RA
2) activity spreads over the atria = atrial systole
3) reaches the atrioventricular node and delayed for 120ms
4) from a-v node excitation passes though septum between ventricles
5) then spreads through ventricular myocardium from inner endocardial to outer epicardial surface.
6) ventricles contract from atria upwards

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5
Q

What are the 7 phases of the cardiac cycle and which bits are systole And which are Diastole?

A

1) atrial contraction
2) isovolumetric contraction
3) rapid ejection
4) reduced ejection
5) isovolumetric relaxation
6) rapid filling
7) reduced filing

Stages 2-4 are systole, rest are diastole.

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6
Q

What happens to Systole and diastole when heart rate gets faster respectively ?

A

Systole stays the same, diastole gets shorter.

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7
Q

What side of the heart are wiggers diagrams plotted for?

A

The left side

The right side would be the same sort of diagram but at lower pressure

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8
Q

What is the name given to the maximum ventricular volume?

A

The end diastolic volume (EDV). Get at the end of phase 1 (atrial contraction) of the cardiac cycle

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9
Q

How would you work out stroke volume?

A

End diastolic volume - end systolic volume = stroke volume

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10
Q

How can you get stenosis?

A

Valve doesn’t open enough = get obstruction to blood flow = stenosis

This could be

  • degenerative.
  • congenital
  • a result of infection
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11
Q

How can you get regurgitation?

A

Valve doesn’t close all the way = back leakage when valve should be closed.

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12
Q

Where are defect valves most commonly found?

A

The left side - mitral and aortic valve.

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13
Q

What are the consequences of aortic valve stenosis?

A
  • increased LV pressure = less ventricular hypertrophy

- left sided heart failure = syncope (faint as lack of blood to brain), angina (less o2 supplied to heart)

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14
Q

What are the causes of aortic valve regurgitation?

A
  • aortic root dilation (leaflets pulled apart)
  • vlavular damage (endocarditis rheumatic fever)
  • blood flows back into LV during diastole
  • increase stroke volume
  • systolic pressure increases
  • diastolic pressure decreases
  • LV hypertrophy
  • bounding pulse (quinkes sign = beds of nails flush with colour in synchrony with heart)
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15
Q

What causes mitral valve regurgitation?

A
  • damage to papillary muscles after heart attack
  • left sided heart failure leads to LV dilation which can stretch valve
  • rheumatic fever can lea to leaflet fibrosis which disrupts seal formation
  • as some blood leaks back into LA, this increases preload as more blood enters LV in subsequent cycles = can LV hypertrophy.
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16
Q

What is rheumatic fever?

A

Fusion of the leaflets

17
Q

What causes mitral valve stenosis and what are the consequences?

A

Rheumatic fever
Causes increased LA pressure
= pulmonary oedema, dypnea and pulmonary hypertension = RV hypertrophy

Also LA dilation = atrial fibrillation (and thrombus formation) as well as oesophagus compression so get dysphagia

18
Q

What is the definition of afterload and preload?

A

Afterload - the load the heart must eject blood supply against
Preload - amount the ventricles are stretched during diastole

19
Q

What is the total peripheral resistance?

A

Resistance to blood flow offered by all systematicc vasculature