Lecture 9 - Integration Flashcards
What is the resting MABP?
Usually close to 90mmHg
This blood pressure is regulated to avoid flucuations
What are the reflex mechanisms which maintain normal arterial pressure?
- Arterial baroreceptors “high pressure receptors”
- Carotid and aortic chemoreceptors
- Cardiopulmonary baroreceptors (Located in atria, ventricles and pulmonary vessels - “low pressure receptors”)
- Central chemoreceptors (in medulla)
These operate all the time as negative feedback mechanisms to maintain arterial pressure at or near normal
What mechanism does the short term control for MABP?
- The arterial baroreceptor reflex performs short term control of MABP.
- The baroreceptor sensors are in the aortic arch and carotid sinus.
- Their afferent fibres travel in vagus and glossopharyngeal nerves (CN. X and IX) to CVS centres in brainstem
How does the baroreceptor flex mechanism respond to an arterial pressure rise?
A pressure rise will increase the rate of baroreceptor firing and hence will increase activity in afferent fibres, and this travels back to the CVS centre in the brainstem via the vagus and glossopharyngeal nerves. This decreases symathetic activity, and increases parasympathetic activity - this lowers the blood pressure back to the set point by decreasing: HR, CO, TPR. (decreases cardiac contractiliy, heart rate and causes venodilation and vasodilation)
How does the baroreceptor reflex respond to a decrease in arterial pressure?
There will be a decrease in baroreceptor firing, which decreases efferent activity. This causes an increase in symapthetic output and a decrease in parasympathetic output in ordre to increase arterial blood pressure back towards the set point. It achieves by the increase sympathetic output increasing cardiac contractility, heart rate, and increase in vaso and venoconstriction
What do baroreceptors act as in relation to the body?
Act as a bufer system for the blood pressure
What happens to SV when someone stands up?
There is a decrease in venous return due to gravity, and it gets stored in venous pooling which decreases central venous pressure. This decreases venous return, causing a decrease in SV which reducings CO.
Describe the sequence of events of how standing up can cauase orthostatic hypotension?
- There is a decrease in central venous pressure
- Decrease venous pressure decreases venous return (results in decrease in left ventricular filling pressure)
- Decrease left ventricular filling pressure reduces stroke volume
- Reduced SV reduces arterial pressure
- This decreaes cerebral perfusion (so reduced O2 supply), causing cerebral underperfusion causing dizziness and visual fade
Describe how the baroreceptor reflex maintains arterial pressure when standing up
- A decrease in arterial pressure causes a decrease in afferent input from the baroreceptors (high pressure receptors) and cardiopulmonary receptors (low pressure receptors) back to the medulla (Nucleus tractus solitarius - NTS)
- There is then an increase in sympathetic output to the heart and blood vessels
- Increase in cardiac contractility, HR (rate of SA node firing, CO
- And an increase in vaso and venoconstriction (causing an increase in TPR)
- There is also a decrease in parasympathetic activity
How do skeletal muscles help to return venous blood?
They act as mechanical pumps to help return venous blood to the heart
How does the CVS have to do when in exercise, and how are these demands met?
Increase lung O2 uptake: Increase RV output
Increase O2 transport around body: Increase left ventricle output
Direct the increased O2 supply specifically to the exercising muscle: Increase O2 extraction from muscle blood and decrease vascular resistance in exercising muscle (metabolic vasodilation)
Stabilisation of BP: Vasoconstrition in non-exercing tissues, and by resetting the baroreflex
What is pulmonary blood flow proportional (equal) to?
Pulmonary flow = Cardiac output.
So if there’s an increase in pulmonary blood flow, there will be an increase in cardiac output.
What causes the HR to increase during exercise?
- There will be withdrawl of vagal inhibiton on SA node (causing HR to increase - since its usually 100)
- There is stimulation of muscle group III mechanoreceptors
- And there is sympathetic drive to pacemaker cells
What causes SV to increase during exercise?
There is an increase in venous return due to 3 factors
- Skeletal muscle pump
- Venoconstriction
- Splanchnic vasoconstriction (organs not active in exercise vasoconstrict)
What factors cause an increased venous return during exercise?
- Exercise increases activity of skeletal muscle pump
- Increased depth and frequency of inspiration (increased intrathroacic pressure squeezes the thoracic veins)
- Sympathetic activation of venous tone
- Greater ease of blood flow from arteries to veins through dilated skeletal muscle arterioles
what are the concequences if venous return doesn’t increase during exercise?
During exercise there is a faster heart rate. This means there is a shortened filling time, and without an increase in venous return there will be a decrease in venous return, and thus a reduction in stroke volume
Exercise effects summary
What can CO increase to during exericse? and where does the extra blood used for?
5L/min to 35L/min
Most of the increase in cardiac output goes to exercising muscles.
The blood can fit the blood because of the extensive vasodilation. Due to metabolic hyperemia (O2 and CO2 levels), and by the release of vasodilators by skeletal muscles.
Describe how exercise leads to an increase in cardiac output, vasoconstriction in abdominal organs and kidneys.
Skeletal muscle contractions stimulate mechanoreceptors, which send afferent input to the NTP in the medulla. And local chemical changes both dilate arterioles in the muscle due to local chemical changes, and stimulate chemoreceptors in muscles, which increases afferent actvity to the NTP in the medulla.
Both of these responses act to increase SNS input to the heart, veins, arterioles in abdominal organs, kidneys and decrease parasympathetic output.
What can muscle do to increase O2 uptake to meet O2 demands during exercise?
- Recruitment of capillaries occurs.
- This increases total surface area for diffusion
- And this shortens the diffusion distance.
In strenuous exercise, what happens to the blood vessels in the skin?
There is a decrease in symapthetic vasoconstrictor acitivty, causing them to vasodilate to facilitate heat loss
Skin temperature increases in response to ________
Core & ambient temperature
How does vasodilation of skin blood vessels occur during strenuous activity?
Caused by an increase in sympathetic cholinergic fibre activty to skin resistance vessels, and a decrease in sympathetic constrictor drive to AVAs in extermities
How much blood is there in the body?
And at what point does blood loss become significant?
It’s tightly regulated at 5-6L (70ml/kg) for optimal CVS function.
- 10% blood loss: No significant threat (blood donation)
- 20-30% loss: Clinical shock, CO falls followed by arterial pressure.
- >40% blood loss: Can cause severe irreversible shock - reduced cerebral and coronary perfusion
How does haemorrhage result in a decreased arterial pressure?
- Haemorrhage decreases blood volume
- This decreases venous pressure
- Decreases venous return
- Decreases atrial pressure
- decreases ventricular EDV
- Decreases SV
- Decreases CO
- Decreases Arterial blood pressure
Which mechaisms are deemed as the rapid, intermediate, and longterm responses to blood loss (in a haemorrhage)
- Rapid, within seconds = baroreceptors
- Intermediate, within minutes = fluid reabsorption
- Long term, days = kidney
Flow chart of of the rapid response to blood loss (baroreceptors) DRAW THIS
The last two bits join up to say increased arterial pressure
How is blood volume from haemorrhage replaced?
- We can transfer fluid from the interstitial space into the circulation to restore circulating volume due to decreased capillary hydrostatic pressure
- Or by slower replacement of lost volume (salt and water) via endocrine and renal methods (Aldosterone, ADH, renin)
How can we increase blood volume using starlings equillibrium?
Haemorrhage decresaes blood volume, and this decreases capillary hydrostatic pressure, which increases fluid reabsorptioin from the interstitial fluid at the venous end of a capillary.
Describe the long term response, and how it replaces volume
Reduced renal perfusion due to haemorrhage (blood loss) triggers renin release to increase angiotensin II.
Angiotensin II is a:
- Vasoconstrictor
- Reduces renal perfusion to reduce urine (works with aldosterone)
- Reduces renal Na loss
- Stimulates aldosterone
- Stimulates thirst
So it pretty much increases fluid intake and reduces fluid loss
Okay, we’ve replaced fluid volume using 3 types of responses, but how are RBCs and albumin replaced?
RBCs come from bone marrow
And albumin is synthesised by the liver
this takes around 6 weeks.
