2.1 - Heart as a Pump Flashcards
Systemic + pulmonary circulation – low or high pressure?
- Systemic = high pressure (ie from left side)
- Pulmonary = low pressure (ie from right side)
Systole and diastole definitions
- systole = conctraction + ejection of blood from ventricles
- diastole = relaxation + filling of ventricles
How much blood does the heart pump
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
Heart muscle
- 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
Why is the cardiac action potential considered relatively abnormal
Cardiac action potential is relatively long, lasts for durations of a single contraction
Needs to pass through the whole of the cardiac myocardium
280ms
What is the volume of blood in the average adult
4.9L (same amount that the heart pumps a min)
Heart valves
Right = tricuspid + pulmonary
Left = mitral + aortic
General mechanisms of heart valves
- 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
Conduction system
- 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
What are the 7 phases of the cardiac cycle + which are diastole / systole (details on sep card)
- Atrial contraction (D)
- Isovolumetric contraction (S)
- Rapid ejection (S)
- Reduced ejection (S)
- Isovolumetric relaxation (D)
- Rapid filling (D)
- Reduced filling (D)
Total systole = 0.35 s
Total diastole = 0.55 s
Total = 0.9 s for one cycle
When increased HR, what remains the same – diastole or systole?
Systole remains the same, diastole filling time reduces
What is a wiggers diagram
- 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
Phase 1: atrial contraction
- 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
What is the end diastolic volume
- 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
Phase 2: isovolumetric contraction
- 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
Phase 3: rapid ejection
- 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
Phase 4: reduced ejection
- 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
Phase 5: isovolumetric relaxation
- 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
Phase 6: rapid filling
- 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
Phase 7: reduced filling
- 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
Abnormal valve function (stenosis + regurgitation)
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
Aortic valve stenosis
- 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)
Aortic valve regurgitation
- 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)
What is quinke’s sign
- Sign of aortic valve regurgitation
- Nailbeds flush red-pale with every beat of the heart
Mitral valve regurgitation
☞ 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
What are the main functions of the chordae tendineae + papillary muscle
- Maintain the tension + position of the atrioventricular valves
- Normally prevent prolapse of valves during systole
Mitral valve stenosis
- 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
mitral valve stenosis complications
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
