22-09-22 – Control of Blood Volume Flashcards
Learning outcomes
- To describe the hormonal mechanisms involved in long-term regulation of blood pressure (i.e. vasopressin, the renin-angiotensin-aldosterone system and atrial-natriuretic peptide) and how their involvement is regulated.
- To predict the short-term, intermediate and long-term physiological changes in the cardiovascular system in response to increased/decreased plasma volume, or changes in plasma osmolarity.
- To identify other systems that integrate with the cardiovascular system and can influence blood pressure.
How is the body fluid volume controlled by the kidneys?
How does arterial pressure affect urine output in this system?
- Body fluid is controlled by the kidneys through the renal-body fluid feedback system
- When arterial pressure increases, urine production increases
- When arterial pressure decreases, urine production decreases
What are the 2 primary determinants of MABP in the long-term?
How can MAPB be calculated through a graph of these determinants?
How is urine production regulated?
How are these things regulated?
- 2 primary determinants of MABP in the long-term:
1) The renal output curve for salt and water – depicts relationship of mean arterial pressure to sodium output
2) The level of salt and water intake - It is impossible to change long term MABP without changing one or both of these determinants
- When the renal output curve for salt and water and the water and salt intake are graphed, the point at which they intersect is the equilibrium, and can be taken as the MABP
- By changing sodium and water intake and pressures, we have 2 key ways of regulating urine production
- Renal baroreceptors regulate and control kidney function so we can stay at a set point
What is anti-diuretic hormone (aka ADH / vasopressin)?
What effect does it have on the kidneys and urine production?
What is it released by?
What 4 things is it released in response to?
- Anti-diuretic hormone (aka ADH/vasopressin) is a chemical produced in the brain that causes kidneys to release less water, decreasing the amount of urine production
- ADH is released by the pituitary gland in the brain in response to:
1) Increased osmotic pressure
* Sensed by hypothalamic osmoreceptors which respond to changes of extracellular fluid (ECF) osmolality
* These osmoreceptors have a set concentration of solutes and nutrients (e.g Na+/K+ ions), if there is a concentration gradient outside of the receptor, this can cause fluid to go into receptors, causing swelling
* Water moves from low osmotic pressure to high osmotic pressure
* This will stimulate the osmoreceptors, leading to ADH release from the pituitary gland
2) Hypovolaemia (decrease in blood volume – 10% or more)
* Atrial baroreceptors normally inhibit ADH releases
* Atria, baroreceptors are cardiopulmonary baroreceptors that sense changes in volume
* Decrease blood volume leads to decreased firing rate of atrial baroreceptors, which increases ADH release
3) Hypotension (may not be volume related, but is treated that way)
* Decrease in arterial baroreceptor firing
* Increases sympathetic activity and increase in ADH release
4) Angiotensin 2 (II)
* Can trigger ADH release
How does ADH increase blood volume?
How does ADH change in severe hypovolaemic shock?
How are blood volume and blood osmotic pressure sensed?
- ADH increases blood volume by increasing water permeability in the renal collecting ducts, which decreases urine production
- In severe hypovolaemic shock, ADH release is high
- High concentrations of ADH cause vasoconstriction, which increases total peripheral resistance, which increased blood pressure, which increases venous return
- A big decrease in blood volume and increased blood osmotic pressure are sensed the same way
What is renin?
Where is it released from?
What system is renin part of?
What 3 things is it released in response to?
- Renin is a proteolytic enzyme release from juxtaglomerular cells (aka granular cells) in the kidneys
- Renin is part of the Renin-angiotensin-aldosterone system (aka RAAS)
- Renin is released in response to:
1) Sympathetic nerve activation
* Mediated by baroreceptor feedback
2) Renal artery hypotension
* Independent of baroreceptor feedback
* Allows an increase in blood volume if the renal artery falls in pressure
3) Decreased sodium in kidney tubules (more in 3002)
The RAAS system.
Describe the pathway in which decreased arterial pressure produces angiotensin 2.
What are 3 roles of angiotensin 2?
What do all of these roles lead to?
What is the purpose of the RAAS system?
- This full system is the RAAS system
- The pathway in which decreased arterial pressure produces angiotensin 2
1) Decreased arterial blood pressure
2) Leads to renin (enzyme) release from the juxtaglomerular cells of the kidneys
3) Renin substrate angiotensinogen is released from the liver
4) Venous blood from the liver and kidneys are mixes together
5) Renin breaks down angiotensinogen into angiotensin 1
6) This venous blood then circulates to the heart and then the lungs
7) Converting enzyme in the lungs converts angiotensin 1 to angiotensin 2 (active for short period of time)
8) Angiotensin 2 rich blood then comes around the systemic circulation - Angiotensin 2 acts on resistance vessels
- Angiotensin 2 acts as an AT1 and AT2 receptor agonist
- Role of angiotensin 2:
1) Vasoconstriction
* Angiotensin causes vasoconstriction of renal arteries, which increases total peripheral resistance and constricts blood flow via the kidneys
2) Release of aldosterone
* Angiotensin 2 causes the release of aldosterone from the zona glomerulosa (outermost region) of the adrenal glands, which decreases the volume of water excreted from the kidney by increasing Na+ and water reabsorption
3) Stimulation of release of ADH (vasopressin) from the pituitary
* ADH increases blood volume by increasing water permeability in the renal collecting ducts, which decreases urine production
- All of these roles of angiotensin 2 lead to an increase in blood pressure
- The role of the RAAS system is to increase MABP
What is atrial-natriuretic hormone (aka atrial-natriuretic peptide)?
Where is it synthesised and stored?
What is it released?
What does it help oppose?
- Atrial-natriuretic hormone (aka atrial-natriuretic peptide) is a 28-amino acid peptide
- It is synthesised and stored in muscle cells of the atria
- Atrial-natriuretic hormone is released in response to stretch of the atria
- It helps oppose the effects of the RAAS system
- This may help counteract volume overload by causing vasodilation and telling the kidney to lose fluid
What is hypovolaemia?
What different substances can be lost with hypovolaemia?
What are the 4 classifications of shock?
- Hypovolaemia is the loss of blood volume
- Different substances that can be lost with hypovolaemia:
1) Loss of whole blood e.g haemorrhage
2) Loss of Plasma e.g burns
3) Loss of sodium e.g vomiting - Depending on what substances are lost, this can trigger different corrective mechanisms
- Classifications of shock:
1) Class 1- 10-15% blood loss
2) Class 2 – 15-30% blood loss
3) Class 3 – 30-40% blood loss
4) Class 4 – more than 40% blood loss - The further down we go in classes, the more likely it is we have to intervene, and replace with whole blood instead of just fluids
What are the immediate (reflex) response to hypovolaemia? What are the changes seen in:
* Stroke volume (SV)
* Heart rate (HR)
* Cardiac output (CO)
* Total peripheral resistance (TPR)
* Mean arterial blood pressure (MABP)
- immediate (reflex) response to hypovolaemia is the baroreceptor reflex, with the degree of volume loss affecting how successful the reflex is
What are 3 changes in later responses to hypovolaemia
- 3 changes in the later responses to hypovolaemia:
1) Arteriolar constriction
* Decreases hydrostatic pressure in the capillaries
* Favours fluid reabsorption
* Temporary redistribution – changes Starlings forces across tissues to encourage more fluid measurement into the CV space to temporarily increase blood volume, but this can’t be done long term, as it will come at the cost of maintaining tissue viability and homeostasis being disrupted
2) Decrease renal blood flow
3) Baroreceptor thirst response
What happens if volume of fluid lost can be compensated for?
What 3 things can be transfused?
What is a fluid challenge?
What is it a test of?
When can this test be done?
- If volume of fluid lost cant be compensated for, this can lead to damage to tissues and organs and heart failure
- Resuscitation fluids:
1) Colloids (gel/starch/albumin)
2) Hartmann’s solution – clear solution of electrolytes, proteins, and water
3) Blood - A fluid challenge is a method of identifying patients likely to benefit from an increase in intravenous volume in order to guide further volume resuscitation.
- It is a dynamic test of the circulation.
- The principle of the fluid challenge technique is to administer a bolus of intravenous fluid under tightly controlled conditions and to evaluate the patient’s hemodynamic response
- This test can be done whilst monitoring ventral venous pressure
Integrated control of blood pressure flow chart
Integrated control of blood pressure flow chart
What are 3 factors that affect blood pressure control?
- 3 factors that affect blood pressure control:
1) Cortex
* Conscious effects of emotions
* Nerves from cortex to medullary CVC centre
2) Time of day
* Diurnal variations due to hormones (e.g cortisol) and cortical input
* Blood pressure drops in late afternoon/evening
3) Respiration
* Via mechanical movements
* Via chemoreceptors – regulated respiratory activity
* Chemoreceptors in Aortic and carotid bodies detect changes in pO2
* If there is a decrease in pO2 then an increase in rate of firing of chemoreceptors
