2) Control of Cardiac Output Flashcards
1
Q
What is cardiac output?
A
- The amount of blood ejected from the heart per minute
2
Q
What is heart rate?
A
- How often the heart beats per minute
3
Q
What is stroke volume?
A
- How much millilitres of blood is ejected per beat
4
Q
What factors does cardiac output affect?
A
- Blood pressure
- Blood flow
5
Q
What is the equation for blood pressure?
A
Blood pressure = Blood flow (Cardiac output) x Total peripheral resistance (TPR)
6
Q
What controls heart rate?
A
- Sympathetic innervation and parasympathetic innervation to the Sino atrial node (SAN) pacemaker
7
Q
What causes/affects the strength of contraction in the heart?
A
- Sympathetic innervation and circulating adrenaline causes a rise in intracellular calcium levels
- Increased calcium leads to increased contraction
8
Q
What is Preload?
A
- Stretching of the heart at rest which increases stroke volume
- Due to Starling’s law
9
Q
What is Starling’s law of the heart?
A
- ‘Energy of contraction of cardiac muscle is relative to the muscle fibre length at rest’
- A greater stretch of the ventricle during diastole (blood entering) causes a greater energy of contraction and so a greater volume in systole (blood leaving)
10
Q
Explain the effect of an increase in Central venous pressure (CVP) on Stroke volume (SV)?
A
- Initially as CVP increases there is an increase in SV
- This is because an increase in CVP means an increase in stretching of the cardiac muscles.
- This increased stretching causes an increased force of contraction resulting in more volume being pumped out (i.e. a higher stroke volume)
- However this curve begins to level out
- Eventually there comes a point where an increase in CVP causes a decrease in SV.
- This is because when CVP reaches these levels there is an excess filling leading to overstretched cardiac muscles
11
Q
What is actin linked to in cardiac muscles?
A
- Z-band
12
Q
Describe the structure of an un-stretched cardiac muscle fibre?
A
- Overlapping actin/myosin
- Mechanical interference so less cross-bridge formation available for contraction
13
Q
Describe the structure of a stretched cardiac muscle fibre?
A
- Less overlapping of actin/myosin
- Less mechanical interference so more cross-bridge formation can occur
- Increased sensitivity to Ca2+ ions
14
Q
What is the role of Starling’s Law?
A
- Balances the outputs of the left and right ventricles
- Responsible for fall in cardiac output during drop in blood volume or vasodilation (for eg: haemorrhage)
- Restores cardiac output in response to fluid transfusions
- Responsible for fall in cardiac output after standing for a long time leading to postural hypotension and dizziness as blood pools in legs
- Contributes to increased stroke volume and cardiac output during exercise
15
Q
Where does the preload enter the heart and where does it come from?
A
- Vena cavae (Preload from body)
- Pulmonary vein (Preload from lungs)
16
Q
Where does the output leave the heart from and where does it go?
A
- Aorta (Output to body)
- Pulmonary artery (Output to lungs)
17
Q
What is afterload?
A
- Opposes contraction which ejects blood from the heart.
- It is determined by wall stress directed through the heart wall
18
Q
What prevents cardiac muscle contraction?
A
- Stress through the wall of the heart (Afterload)
19
Q
How is ejection produced?
A
- More energy of contraction is put in to overcome wall stress (afterload)
- This produces cell shortening and ejection
20
Q
What is the relationship between wall tension (T), pressure (P) and radius of ventricle (r)?
A
- T α Pr
- Tension is increased by increasing Pressure or increasing radius
21
Q
What is the equation for wall stress?
A
- wall stress (S)= tension(T)/ wall thickness (w)
- since t=Pr we can also say that S= (Pr)/2w
- (It is divided by 2w as there are two directions of curvature)
- Afterload/ stress is increased by increasing pressure, increasing radius of ventricle and decreasing wall thickness
22
Q
Why does radius affect wall stress/ ejection?
A
- Small radius: Greater wall curvature so more wall stress directed towards centre of chamber. There is less afterload and better ejection
- Large radius: Less wall curvature so more wall stress directed through heart wall. There is more afterload and less ejection
- Huge theoretical radius: Negligible wall curvature so all stress is directed through wall.
23
Q
What is the importance of Laplace’s law?
A
- Opposes Starling’s law at rest. An increase in preload causes the chambers to stretch more. This increases the radius and decreases curvature which increases afterload. (In a healthy heart Starling’s law always overcomes Laplace’s law)
- Facilitates ejection during contraction: Contraction reduces chamber radius so less afterload when the chamber empties. This increases stroke volume and ensures all blood is expelled
- Contributes to a failing heart at rest and during contraction: In a failing heart the chambers are often dilated and the radius is large. This increases afterload and opposes ejection
24
Q
What does an acute rise in blood pressure cause?
A
- It affects Starling’s law as it increases stretch of the cardiac walls giving increased contraction and increased stroke volume
- This also happens with certain hormones such as noradrenaline
- Baroreflexes decreases sympathetic tone which decreases blood pressure
25
What does a chronic increase in blood pressure cause?
- When undergoing exercise the body attempts to maintain stroke volume however eventually it will decrease
- Decrease in blood pressure would increase efficiency of the heart
- An increase in blood pressure will reduce cardiac output
- Therefore blood pressure needs to be kept constant during exercise
26
How does heart failure cause increased wall stress?
- In some heart failures the heart does not contract properly and can lead to some blood being left in the ventricle
- This eventually leads to volume overload causing the increased radius
- In some heart failures there is an increase in the pressure/afterload in the chamber causing pressure overload.
- This leads to increased pressure
- An increase in radius or pressure increases wall stress and opposes ejection
27
How does the heart deal with increased wall stress?
- The heart uses ventricular hypertrophy (increased muscular size) to cope with increased wall stress.
- It uses greater myocyte size and more sarcomeres to increase wall thickness
- This decreases wall stress per sarcomere and hence afterload.
- This maintains SV and CO
28
What is a disadvantage of ventricular hypertrophy?
- It requires more energy as more sarcomeres are used.
- As the amount of energy required increases the contractility will decrease as the heart will struggle to supply adequate oxygen for respiration.
- Hence producing more heart failures
29
What is the energy of contraction?
- The amount of work required to generate stroke volume
| - It depends on Starling's law and contractility
30
What is the function of stroke work (the work performed by the left ventricle to eject a volume of blood)?
- Contract until chamber pressure is greater than aortic pressure
- This causes ejection from ventricle
31
How does an increased preload affect the ventricular pressure-volume loop.
- Increased exercise leads to increased preload and increased EDV.
- This is because increased exercise leads to an increased venous return. This fills the ventricle more and so we end diastole with a higher volume in the ventricle.
- This higher volume stretches the walls more leading to a higher force of contraction.
- After contraction the ventricle will eject the volume of blood to the same end systolic volume (ESV) we started with.
- Hence there is more blood pumped out leading to a higher SV
32
How does an increased afterload affect the pressure volume loop
- Hypertension leads to increased afterload.
- There is a longer time spent in the (isovolumetric) contraction phase to increase pressure in the chamber located above the aorta
- This opens the aortic valve
- This uses more energy and lowers the force of contraction reducing stroke volume and increases the end-systolic volume (ESV).
