Cardiovascular mechanics 2 Flashcards
What are the 2 main phases in a heart beat?
Diastole (lasts 2/3 of each beat)= ventricular relaxation (fills ventricles with blood) and is split into 4 distinct phases
Systole (lasts 1/3 of each beat)= ventricular contraction- ventricle generates pressure then eject blood into the arteries. It is split into 3 distinct phases
What is the end diastolic volume?
The volume of blood in the ventricle just before the ventricles are about to contract
What is the end-systolic volume?
The volume left in the ventricles after contraction
How do you calculate stroke volume
Stroke volume is the volume of blood that is pushed out of the ventricle per beat of the heart.
End-diastolic volume- end-systolic volume = stroke volume
What is the ejection fraction?
It is the proportion of blood pushed out compared to the amount of blood that enters- it is a clinical sign of vitality.
(100 x stroke volume ) / End-diastolic volume = ejection fraction (%)
Describe atrial systole
This is the contraction of atria. It is stimulates by the pacemaker potential from SAN in the RA. Those cells can be modulates in how fast they fire AP.
The depolarisation/ stimulation of atrial cells is the P wave on the ECG.
The atria are full of blood (due to passive filling driven by pressure gradient from vena cava into atrium) already and the contraction pushes blood into the ventricle to get rid of most of its blood.
Describe isovolumetric contraction
The QRS complex on the ECG marks the start of ventricular depolarisation. Contraction against closed valves- this is the bit between the AV valves shutting and the SL valves opening. The muscle fibres can’t shorten and pressure is generated (it increases). The volume stays the same. There is no shortening of the ventricles. The first heart sound (‘lub’) can be heard here- this is the AV valves shutting.
(3) Describe Rapid ejection
Ventricular pressure overcomes backpressure (pressure in the aorta or pulmonary artery).
Opening of the SL valves mark the start of this phase.
As the ventricles contract pressyre within them exceeds the pressure in the major arteries. SL valves are pushed open. The blood is pushed up and out so there is a decreased volume (due to the isotonic contraction). There are no heart sounds for this phase
(4) Reduced ejection
This phase marks the end of the systolic period. Ventricle begin to repolarise (the AP going from + potential back to RMP).
There is a reduced pressure gradient means aortic & pulmonary valves begin to close.
This phase is denoted by the T wave on an ECG.
The pressure fall in the ventricles mean that in arteries, blood begins to flow back causing SL valves to close.
(5) Isovolumetric relaxation
Shutting of the SL valves- second heart sound (Dub)
Ventricular pressure falls and there is no change in the volume. The atrial pressure will begin to rise slowly due to rebound backpressure against aortic valve as the aortic wall relaxes.
AV valves will only open when the pressure in the atria is greater than in the ventricle.
(6) Rapid passive filling
Occurs during the isoelectric (flat) of the ECG, between cardiac cycles.
Once the AV valves open, blood in the atria flow rapidly into the ventricles.
You could hear a third sound if the valves have some sort of incompetency- more turbulent than normal- known as ventricular gallop.
(7) Reduced passive filling
This phase is also known as diastasis.
Gradual filling up of the ventricle more and more. No electrical events. Aortic pressure decreasing.
Ventricles fills- this defines the preload which defines the stretch and defines the force of the contraction.
Volume and pressure CHANGES are the same but generally the pressure is greater on the LHS vs RHS.
Pulmonary circuit pressures
The patterns of pressure changes in the RHS of the heart are essentially identical to those on the LHS.
Quatitatively, the pressures on the RHS are much lower than on the LHS.
Even though the lower side has lower pressure, the right ventricle still ejects the same volume as the left (it is just pumping the same quantity of blood into a lower pressure circuit.
Describe the following image
Red- systemic circuit pressure. Systolic and dialstoli that decays away in the arterioles and capillaries
Blue- RHS of the heart- similar decaying away of the pressures but at a much lower pressure to begin with compared to the LHS of the heart.
How can you measure pulmonary pressure?
Measure it by putting a cathter into the vena cava. They can enter the RA and RV. Have a ballon at the end of the catheter that acts like a transducer.
Pressure changes through the chambers of the heart. Increase from Ra to RV.
Balloon can pump up to assess the backpressure of the lungs. Clinical advantage to assess the function of the left artiral side of the heart- this is known as the pulmonary capillary wedge pressure
Pressure loop volumes
Wrt ventricular pressure (y axis) and volume (x axis)
A= end diastolic volume. Quite low ventricles not activated
A-B= ventricles activated so increase the pressure without changing the volume. Isovolumetric contraction
B= Aortic pressure encountered. Ventricular pressure over comes the back pressure and the aortic valves opens.
C= End systolic volume- after the ventricles have contracted, a lot of the blood is pushed out and so the volume decreases
C-D= isovolumic relaxtion. No change in volume but decline in ventricular pressure
D- after isovolumetric relaxation.
D-A- ventricles begin to fill up with blood again.
What are the preload and afterload factors for the heart?
Preload (point A)- is the blood filling the muscle fibres and stretching it.
B- afterload- what the ventricle is encountering in terms of diastolic blood pressure (i.e. the blood pressures in the great vessels)
How does the PV loop fit in with the force stretch graph that we have seen previously?
The PV loop sits inbetween the active force and passive force lines.
The point that touches the active force is the end systolic volume- the tangent is the end-systolic PV line.
Change the axis.
How does changing the preload and afterload affect the PV loop?
Increasing the amount of blood that returns to the heart, you cnrease the preload and the stretch of the End diastolic ventricular volume. The stroke volume would increase and the PV loop gets fatter. You move up the active force line (gradient/ tangent above the loop)- frank starling relationship
If you increase the back pressure the ventricle has to overcome inorder to eject blood, you are increasing the afterload. The stroke volume will be smaller since there has to be a greater pressure in the ventricle to overcome the back pressure. You need more force to overcome this pressure so there is less shortening. If there is less shortening there is less stroke volume. The PV loop will be thinner and taller.
How are PV loops affected by:
1) hardening and narrowing of the aortic valve
2) acute blood loss
3) Exercise
