3. Mechanical Properties of the Heart 2 Flashcards
What is diastole and systole?
- Diastole: ventricular relaxation - ventricles fill with blood (4 sub-phases)
- Systole: ventricular contraction - blood pumped into the arteries (2 sub-phases)
What happens during the diastole before excitation?
- Late, slow filling
- Atrial contraction
- Allows the topping up of ventricular volume
- End diastolic volume (EDV) - volume in ventricles just before contraction starts (maximum blood for cardiac cycle and determines how stretched the muscle fibres are before contraction)
What happens during systole?
- Period of contraction but no change in volume - isovolumetric contraction
- Pressure builds up in the ventricles but blood isn’t expelled until pressure gets to the point where it overcomes afterload
- Period of ventricular ejection
What happens during diastole after excitation?
- Isovolumetric ventricular relaxation - aortic valve closes and mitral valve opens
- Ventricular muscle decreases its tension, without lengthening so volume remains unaltered
- Rapid filling
What is the stroke volume and ejection fraction?
- SV = EDV - ESV (blood expelled from the ventricle)
- EF = SV/EDV (proportion of the end diastolic volume pumped out of the heart, normally about 65%, exercise 80%, heart failure 35%)
What 7 events can the cardiac cycle be split into?
- Atrial systole
- Isovolumetric contraction
- Rapid ejection
- Reduced ejection
- Isovolumetric relaxation
- Rapid ventricular filling
- Reduced ventricular filling
What happens during atrial systole (physically and ECG)?
- Just before, blood flows passively through open AV valves into ventricles
- SA node => atria contract
- Atrial systole pushes more blood into ventricles
- Left side at higher pressure than right
- Jugular pulse - small pulse in jugular vein due to atrial contraction pushing some blood back up the jugular vein
- P wave - atrial depolarisation
- S4 - abnormal heart sound caused by valve incompetency (leading to turbulent flow) happens at this time
- S4 occurs with pulmonary embolism, congestive heart failure and tricuspid incompetence
What happens during isovolumetric contraction (physically and ECG)?
- Between AV valves closing and semi-lunar valves opening
- Ventricles sealed off
- Ventricles start to contract against closed valves - no volume change = isovolumetirc
- Rapid increase in pressure
- First heart sound (S1) occurs - closing AV valves (lub)
- Ventricular pressure > aortic pressure = afterload
- Aortic valve opens - blood ejected from ventricles - end of isovolumetric contraction
• QRS complex - ventricular depolarisation
What happens during rapid ejection (physically and ECG)?
- Aortic and pulmonary valves open
- End of isolvolumetric contraction (afterload) marks the start of rapid ejection
- Semi-lunar valves open - ventricular volume decreases
- ‘c wave’ seen in atrial pressure = right ventricular contraction pushing the tricuspid valve into atrium - small wave into jugular vein
- Aortic pressure increases in line with ventricular pressure
- No closing valves - no sounds
• No wave on ECG
What happens during reduced ejection (physically and ECG)?
- End of systole
- Ventricular pressure falls as blood leaves
- Aortic and pulmonary pressure > ventricular pressure
- Valves will begin to close
• T wave - ventricular repolarisation
What happens during isovolumetric relaxation (physically and ECG)?
- Beginning of diastole
- Aortic and pulmonary valves shut
- AV valve remains shut
- No change in ventricular volume - pressure decreases - isovolumetric relaxation
- ‘v wave’ in the atrial pressure caused by blood pushing the tricuspid valve and giving a second jugular pulse
- Dichrotic notch - small, sharp increase in aortic pressure - rebound pressure against aortic valve as the distended aortic wall relaxes after being stretched while ventricles contracted
- Second heart sound (S2) - aortic and pulmonary valves close - (dub)
What happens during rapid ventricular filling (physically and ECG)?
- AV valve opens and blood flows rapidly from atria to ventricles
- Ventricular volume increases
- Atrial pressure decreases
- Passive
• S3 - abnormal third heart sound
- can signify turbulent ventricular filling
- can be due to severe hypertension (leaking valve) or mitral incompetence (calcification of valve)
- ventricular gallop
What is diastasis?
- Slow filling of the ventricles
- No changes in ECG and no heart sound
- Information can be shown on Wiggers diagram
What is the difference in the volume of blood that the right and left ventricles eject?
- Same volume
* Lower pressure on right
What are the normal systemic and pulmonary blood pressure values?
- Systemic - 120/80mmHg
* Pulmonary - 25/5mmHg
What is pulmonary artery wedge pressure (PAWP) and how can you measure it?
• Preload on the left side of the heart
- Insert catheter with pressure tip into a large vein => right atrium => right ventricle
- Diastolic pressure rises in pulmonary artery as you have the valve closing
- Balloon at the end prevents blood from passing
- Pressure changes further up the pulmonary system => left atrium, measured distal to the balloon
What might an elevated pulmonary artery wedge pressure (PAWP) indicate?
- Problems with left side of heart
- Particularly left atrium
- Problems with mitral valve
What does a pressure-volume loop show?
- Ventricular (LV) pressure (y-axis) agasint ventricular volume (x-axis)
- Point 1 (bottom right) - EDV, large ventricular volume, no pressure yet, preload
- Point 2 - Isovolumetric contraction - increased pressure, no change in volume, afterload just after P2 when LV encounters aortic pressure
- Point 2 to 3 (stroke volume) - ventricles expel blood, volume decreases, ventricular pressure rises then falls (curves back)
- Point 3 - ESV
- Point 4 - low pressure due to isovolumetric relaxation, same volume
- Heart refills back to point 1
How does the pressure-volume loop fit into the Frank-Starling relationship when increasing the amount of blood flowing back to the heart?
- Point 1 and 2 move further right
- Preload increases (Point 1, related to passive force, elastic recoil) - so EDV increases
- Point 2 further from point 3 so stroke volume increases
- End systolic PV line - active force curve of FSr up to point 3 (ESV)
How does the pressure-volume loop fit into the Frank-Starling relationship when increasing the afterload?
- Decreased shortening as working against increased afterload
- Decreased stroke volume (P3 and 4 move right) so ESV (P3) is higher
- Ventricular muscle has to work harder to eject blood against the higher pressure
- When afterload is increased, more pressure is needed to open the aortic valve - Point 2 moves up (y direction)
- Point 1 remains the same as EDV is the same
- End systolic PV line from active curve is longer
How can you change the stroke volume?
- Changing the amount of blood returning to the heart
- Changing the arterial pressure
- i.e. preload and afterload
- Altering contractility (force of contraction) e.g. adrenaline
What is contractility, how can it be measured and increased?
- Contractile capability of heart
- Measured using ejection fraction
- Increased by sympathetic stimulation
How does a change in contractility change the ESV PV lines?
- Increased - more blood pumped out, stroke volume increases, P3 moves left, ESV PV line is steeper
- Decreased - less blood pumped out, stroke volume decreases, P3 moves right, ESV PV line is shallower
- P1 and 2 don’t change
What happens to contractility and the PV relationship during exercise?
- Increased sympathetic activity => contractility
- Changes in peripheral circulation (e.g. venoconstriction and muscle pump) - more blood returned to the heart - End diastolic volume increases (P1 and 2 are pushed right)
- Increased contractility - P3 and 4 are pushed left
- Therefore, increased stroke volume
