Week 6 - Control of Cardiac Output Flashcards
What are the effects on arterial and venous pressure if total peripheral resistance falls? (Cardiac output stays the same)
- Arterial pressure: falls
- Venous pressure: rises
What are the effects on arterial and venous pressure if total peripheral resistance rises? (Cardiac output stays the same)
- Arterial pressure: rises
- Venous pressure: falls
What are the effects on arterial and venous pressure if cardiac output rises? (total peripheral resistance stays the same)
- Arterial pressure: rises
- Venous pressure: falls
What are the effects on arterial and venous pressure if cardiac output falls? (total peripheral resistance stays the same)
- Arterial pressure: falls
- Venous pressure: rises
What controls cardiac output?
- Stroke volume x heart rate = cardiac output
- Arterial and venous pressures affect both, so hence control cardiac output
What is demand-led pumping?
If the body needs more blood, then the heart needs to pump more to meet the demand
- Demand is expressed as changes in arterial and venous pressure
- If the heart responds to falls in arterial pressure and rises in venous pressure by pumping more blood, then it will meet the demand
How does the total peripheral resistance relate to the body’s need for blood?
Total peripheral resistance is inversely proportional to the body’s need for blood
What is stroke volume?
The difference between end diastolic volume and end systolic volume
What determines the filling of the ventricles?
Venous pressure
- The ventricles fill until the walls stretch enough to produce an intraventricular pressure equal to venous pressure
- The relationship between venous pressure and ventricular volume is known as the ventricular compliance curve
What is the relationship between stroke volume and venous pressure?
Rises in venous pressure automatically leads to rises in stroke volume
- The more the heart fills the harder it contracts (up to a limit)
- The harder it contracts the bigger the stroke volume
What is contractility?
The nature of the relationship between stroke volume and venous pressure
- (Force of contraction)/(fibre length)
- Can be affected by neurotransmitters, hormones or drugs
What is the end systolic volume?
How much the ventricle empties
- Depends on: how hard it contracts, how hard it is to eject blood
What determines the force of contraction?
- End diastolic volume
- Contractility
What is pre-load?
The end-diastolic volume at the beginning of systole (end-diastolic stretch)
What is after-load?
The force necessary to expel blood into the arteries
- It determines the effect of a given force of contraction during systole
- If it is easy to eject blood, then the volume in the ventricle will fall a lot in systole, but the pressure will only rise a little
- So falls in total peripheral resistance increase stroke volume by decreasing after-load
How are changes in arterial blood pressure corrected?
- The carotid sinus walls and aortic walls contain stretch receptors which detect changes in arterial blood pressure
- This information is released to the medulla in the brain
- Collections of neurones can then modify the behaviour of the heart and circulation via the autonomic nervous system
- Baroreceptors ensure that if arterial pressure falls, both heart rate and stroke volume tend to rise
What are the effects of rises in venous pressure on heart rate?
- Leads to reduced parasympathetic activity
- So heart rate rises
- Not very important
How can baroreceptors increase the heart rate?
By reducing parasympathetic activity and increasing sympathetic activity
How can baroreceptors increase contractility?
By increasing sympathetic activity
How can changes to arterial pressure affect flow resistance?
Falls in arterial pressure increases the flow resistance to certain tissues
How can changes to arterial pressure affect venous capacitance?
Falls in arterial pressure reduces venous capacitance by venous constriction
How can eating a meal affect the whole CVS?
- Increased metabolic activity in the gut produces vasodilator mediators and metabolites
- These cause local vasodilatation
- Total peripheral resistance falls and hence venous pressure rises and arterial pressure falls
- Rises in venous pressure leads to increased stroke volume
- Falls in arterial pressure triggers rise in heart rate and stroke volume
- So cardiac output rises
- This brings venous pressure back down to normal and arterial pressure back up to normal
- Demand has been met
What effect does increasing the heart rate alone have on the cardiac output?
- Initially cardiac output will tend to rise, and total peripheral resistance remains the same
- This reduces venous pressure
- So stroke volume falls
- So as the heart rises, stroke volume will tend to fall, keeping cardiac output the same
How can exercising affect the whole CVS?
Following an enormous increase in metabolic demand:
- Venous pressure would rise greatly, causing total peripheral resistance to fall (due to massive metabolic decompensation)
- Arterial pressure would fall greatly
- These changes may be too big to cope with
- It tends to overfill the heart, limiting the capacity of the vesicles to control cardiac output
What is a risk associated with CVS and exercising?
Pulmonary oedema
- Because the outputs of the right and left ventricle cannot be matched
- Normally prevented due to a rise in heart rate at the onset of exercising
- – Triggered by activation of the sympathetic system
- – Occurs before large changes in arterial and venous pressure
How can standing up affect the whole CVS?
The effects of gravity increase transmural pressure of the superficial veins in the lower limb
- Blood tends to ‘pool’ in the legs
- This produces a transient fall in central venous pressure
- This causes cardiac outlet to fall
- So arterial pressure falls
- – Triggers: rises in heart rate, vasoconstriction in skin and gut to increase total peripheral resistance and veno-constriction
- Total peripheral resistance rises, tending to stabilise arterial pressure and maintain perfusion to the vital organs
How can a haemorrhage affect the whole CVS?
- Reduced blood volume, so less blood flow in the venous capacitance and hence venous pressure falls
- Cardiac output then falls
- Arterial pressure then falls
- – Detected by baroreceptors
- – Reflex rise in heart rate and rise in TPR
- The low venous pressure is exacerbated both by attempts to increase cardiac output and the rise in TPR
How can sustained increases in blood volume affect the whole CVS?
Occasionally because of changes in the kidney or diet, blood volume tends to increase
-This produces a sustained increase in venous pressure
- TPR has not changed
- This causes an increased cardiac cycle
- Leads to an increased arterial pressure
More blood is forced through tissues
- The tissues that ‘autoregulate’ increase arteriolar tone to return flow to normal
- This increases TPR
- So arterial pressure rises further and stay up
- Partial solution = reversal of the rise in blood volume will, particulary in the early stages, reduce blood pressure back towards normal
What is a problem with the sustained increase in arteriolar ligaments in resistance vessel walls?
May lead to long-term damage in the resistance vessel walls
- So the TPR rise is more or less permanent
- Arterial pressure is now persistently elevated
How can you resolve low venous pressure?
Increase it by veto-constriction and auto-transfusion
- Movement of fluid from extra-cellular space into the circulation
- Eventually replace blood volume lost (water, electrolytes and RBCs) eventually replaced by homeostatic mechanisms
