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CVS > 2.1 - Heart as a Pump > Flashcards

2.1 - Heart as a Pump Flashcards

1
Q

Systemic + pulmonary circulation – low or high pressure?

A
  • Systemic = high pressure (ie from left side)
  • Pulmonary = low pressure (ie from right side)
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2
Q

Systole and diastole definitions

A
  • systole = conctraction + ejection of blood from ventricles
  • diastole = relaxation + filling of ventricles
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3
Q

How much blood does the heart pump

A

Stroke volume = at rest each ventricle pumps 70ml blood per beat
At a heart rate of 70bpm = 4.9 L/min per min
This is the approx volume of blood in body

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4
Q

Heart muscle

A
  • Specialised form of muscle
  • Form of striated muscle
  • Discrete cells but interconnected electrically
  • Cells contract in response to action potential in membrane
  • Action potential → rise in intracellular calcium
  • Left side is working at higher pressure: therefore thicker heart muscle
  • Duration of single contraction of heart = 280 ms (action potential is relatively long)
  • Action potentials are triggered by spread of excitation from cell-cell via intercalated discs
  • autorhythmicity so no neurones involved throughout cardiac muscle, just AVN and SAN
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5
Q

Why is the cardiac action potential considered relatively abnormal

A

Cardiac action potential is relatively long, lasts for durations of a single contraction
Needs to pass through the whole of the cardiac myocardium
280ms

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6
Q

What is the volume of blood in the average adult

A

4.9L (same amount that the heart pumps a min)

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7
Q

Heart valves

A

Right = tricuspid + pulmonary
Left = mitral + aortic

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8
Q

General mechanisms of heart valves

A
  • Mitral + tricuspid valves have chordae tendineae that anchor cusps of valve + prevent valve prolapse
  • Open or close depending on differential BP on each side
  • Valve cusps are pushed open to allow blood flow
  • Close together to seal and prevent backflow
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9
Q

Conduction system

A
  • Pacemaker cells in sinoatrial node generate an action potential
  • Activity spreads over atria = atrial systole
  • Reaches AVN and delayed for 120ms (so atria can finish emptying)
  • From AVN, the excitation spreads down the septum between ventricles
  • Next spreads through ventricular myocardium from inner (endocardial) to outer (epicardial) surface
  • Ventricle contracts by Purkinje fibres from the apex up
  • This forces blood through outflow valves
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10
Q

What are the 7 phases of the cardiac cycle + which are diastole / systole (details on sep card)

A
  1. Atrial contraction (D)
  2. Isovolumetric contraction (S)
  3. Rapid ejection (S)
  4. Reduced ejection (S)
  5. Isovolumetric relaxation (D)
  6. Rapid filling (D)
  7. Reduced filling (D)

Total systole = 0.35 s
Total diastole = 0.55 s
Total = 0.9 s for one cycle

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11
Q

When increased HR, what remains the same – diastole or systole?

A

Systole remains the same, diastole filling time reduces

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12
Q

What is a wiggers diagram

A
  • Plots the pressure and volume in the different chambers of the heart
  • Correlates this to the time and the ECG trace
  • Typically a Wiggers diagram is plotted for the left side of the heart
  • The Wiggers diagram for the right would be similar but lower pressures
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13
Q

Phase 1: atrial contraction

A
  • Cells in SA node fire an impulse
  • Can be seen as P wave on ECG
  • This causes the atria to contract (atrial depolarisation)
  • Resulting increase in atrial pressure = A wave on Wiggers
  • This atrial contraction accounts for the final 10% of ventricular filling aka atrial kick
  • End diastolic volume (EDV) has been reached (the amount the ventricle contains before ejection)
    ☞ mitral/tricuspid: open
    ☞ aortic/pulmonary: closed
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14
Q

What is the end diastolic volume

A
  • This has been reached at the end of phase 1 (atrial contraction)
  • The amount of blood the ventricle contains before ejection
  • Aka maximal ventricular volume
  • The heart doesn’t pump all of this at one time
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15
Q

Phase 2: isovolumetric contraction

A
  • Ventricle contracts
  • The QRS complex = ventricular depolarisation
  • As ventricle contracts, ventricular pressure rises above atrial (shut mitral valve)
  • Shutting of mitral valve = S1 sound
  • As valves are closed, blood cannot exit ventricle and therefore blood in ventricle doesn’t change
  • Slight increase in atrial pressure (C wave) due to closing of mitral valve
    ☞ mitral/tricuspid: closed
    ☞ aortic/pulmonary: closed
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16
Q

Phase 3: rapid ejection

A
  • Ventricular pressure rises above aortic due to ventricular contraction
  • This opens aortic valve and blood is forced out
  • This causes a fall in ventricular volume
  • Corresponding fall in atrial pressure = X descent (wiggers) → this is because blood leaving ventricle pulls on mitral valve
    ☞ mitral/tricuspid: closed
    ☞ aortic/pulmonary: open
17
Q

Phase 4: reduced ejection

A
  • Ventricle repolarises (T wave on ECG)
  • Ventricle begins to relax → rate of ejection falls
  • Pressure in ventricle is still higher than the aorta (so blood continues to leave)
  • At same time, venous blood is returning to the atrium (V wave on wiggers)
    ☞ mitral/tricuspid: closed
    ☞ aortic/pulmonary: open
18
Q

Phase 5: isovolumetric relaxation

A
  • This occurs when ventricular pressure falls below the aortic pressure, the aortic valve closes
  • This marks the start of diastole
  • Closure of aortic valve = S2 sound and dicrotic notch in aortic pressure
  • Rapid decline in ventricular pressure as ventricle relaxes
  • The volume of blood inn the ventricle doesn’t change (no valves open)
  • End systolic volume is achieved
    ☞ mitral/tricuspid: closed
    ☞ aortic/pulmonary: closed
19
Q

Phase 6: rapid filling

A
  • Occurs as atrial pressure > ventricular pressure
  • This causes the mitral valve to open
  • Blood then flows passively into the ventricle
  • Y descent (wiggers) = blood exiting the atrium
  • Ventricular filling is normally silent, but sometimes produces a S3 sound (normal in children, sign of pathology in adults)
    ☞ mitral/tricuspid: open
    ☞ aortic/pulmonary: closed
20
Q

Phase 7: reduced filling

A
  • Rate of filling slows down = diastasis
  • Ventricle fills to 90% capacity
  • Further filling driven by venous pressure
  • The cycle then starts at phase 1 again
    ☞ mitral/tricuspid: open
    ☞ aortic/pulmonary: closed
21
Q

Abnormal valve function (stenosis + regurgitation)

A

stenosis = valve doesn’t open enough → obstruction to blood flow when valve normally open
regurgitation aka incompetence / insufficiency = valve doesn’t close all the way → back leakage when valve should be closed

22
Q

Aortic valve stenosis

A
  • Produces a crescendo-decrescendo murmur
  • Degenerative (senile calcification/fibrosis)
  • Congenital (bicuspid aortic valve, meant to be tricuspid)
  • Chronic rheumatic fever → inflammation → commissural fusion

Problems it can cause
- microangiopathic haemolytic anaemia (as less blood can get through valve at high pressure → shear stress)
- angina + syncope due to left sided heart failure
- LV hypertrophy due to increased LV pressure (as heart having to do more work, as less blood can get through valve)

23
Q

Aortic valve regurgitation

A
  • Produces an early decrescendo diastolic murmur
  • Caused by aortic root dilation (where leaflets pulled apart) and valvular damage (endocarditis rheumatic fever)
  • Blood flows back into LV during diastole
  • Increases stroke volume
  • Systolic pressure increases
  • Diastolic pressure decreases
  • Bounding pulse → bobbing head + quinke’s sign
  • LV hypertrophy (as having to work harder)
24
Q

What is quinke’s sign

A
  • Sign of aortic valve regurgitation
  • Nailbeds flush red-pale with every beat of the heart
25
Q

Mitral valve regurgitation

A

☞ Can produce holosystolic murmur
☞ causes:
- myxomatous degeneration (changes in collagen due to age) can weaken tissue, leading to prolapse of valve
- Damage to papillary muscle after heart attack
- Left sided heart failure → LV dilation → stretching of valve
- Rheumatic fever → leaflet fibrosis → disrupts seal formation
☞ as some blood leaks back into LA, this increases preload as more blood enters LC in subsequent cycles → causes LV hypertrophy

26
Q

What are the main functions of the chordae tendineae + papillary muscle

A
  • Maintain the tension + position of the atrioventricular valves
  • Normally prevent prolapse of valves during systole
27
Q

Mitral valve stenosis

A
  • Can cause a ‘snap’ as valve opens / diastolic rumble
  • Main cause = rheumatic fever
  • Commissural fusion of valve leaflets
  • Therefore harder for blood to flow LA → LV
28
Q

mitral valve stenosis complications

A

Complications:
- thrombus formation as increased LA pressure → LA dilation → atrial fibrillation increases risk of thombrus formation
- dysphagia (swallowing problems) as increased LA pressure → LA dilation → compression on oesophagus (as this passes through the same area)
- RV hypertrophy as increased LA pressure → pulmonary oedema, dyspnoea + pulmonary hypertension

CVS (4 decks)

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