Control of BV

Question 1

How does long-term regulation of blood pressure occur ? Describe the mechanism involved.

Answer 1

Overall, through the control of body fluid volume by the kidneys (when arterial pressure increases, urine production increases and vice versa).

Increase Extracellular fluid V → Increased BV → Increased mean circulatory filling P → Increased venous return of blood to heart → Increased CO → (→ autoregulation → increased total peripheral resistance →) Increased Arterial P → Increased urine output → Deceased extracellular fluid V (etc., up until decreased arterial P)

Question 2

What are the main determinants of the long term regulation of blood pressure ? Why are these said to be determinants of the long term regulation of blood pressure ?

Answer 2

1) The renal output curve for salt and water
2) The level of salt and water intake

Because it is impossible to change long-term mean arterial blood pressure without changing one or both of these!

Question 3

What is the effect of increase intake of water and salt on BP in the long term ?

Answer 3

Increases BP

Question 4

Show, in graphical form, the effect of an increase of arterial pressure on urinary output. What is the name of this curve ? How may we change its shape ?

Answer 4

Refer to slide 5 in lecture on ‘“Control of Blood Volume”
Renal function curve
By modifying the permeability of kidneys to water and sodium, changing blood flow going to the kidneys (through ADH, and renin?).

Question 5

Show, in graphical form, the effect of an increase in water and salt intake on arterial pressure. Then, in graphical form, show how the body deals with this.

Answer 5

Refer to slide 6 in lecture on “Control on Blood Volume”

Question 6

Explain the process through which the body deals with increased water and salt intake. Why is this necessary ?

Answer 6

By modifying the kidney’s permeability to salt and sodium, thereby changing the blood flow going to the kidneys.
Because otherwise, would get a large increase in blood pressure (this allows to maintain blood pressure even with increased salt and water intake)

Question 7

Why is it problematic if kidney function becomes compromised (wrt to blood volume etc.).

Answer 7

Because then we cannot change the permeability of it to salt and water (i.e. changing the shape of the curve). This means that we cannot adjust blood pressure if there is increased salt and water intake, possibly resulting in hypertension.

Question 8

What are other names for Antidiuretic hormone ?

Answer 8

Vasopressin, Arginine vasopressin

Question 9

Where and in response to what, is ADH released ?

Answer 9

Released by the pituitary gland in response to:
1) ↑ Osmo tic Pressure
• Sensed by hypothalmic osmoreceptors (i.e. higher ion concentration → receptors dehydrated → receptors shrink → signals high osmolarity, needs to be diluted
VICE VERSA)

2) Hypovolemia (10% loss or greater)
• Atrial baroreceptors normally inhibit ADH release
• ↓ volume leads to ↓ firing rate, so ↑ ADH release

3) Hypotension
• ↓ arterial baroreceptor firing
• ↑ sympathe tic ac tivity and ↑ ADH release

Question 10

What is ADH’s function ? How does it fulfill this function ?

Answer 10

1) “Regulates the amount of water in your blood (if increased ADH, increases blood volume, cardiac output and arterial pressure)”
2) Can also cause vasoconstriction (and hence increase total peripheral resistance) in response to severe hypovolemic shock (because high ADH release)

Increases blood volume by
– ↑ water permeability in renal collecting ducts (leads to ↓ urine production because water pushed out by filtration can come back in)

Question 11

Make a diagram, explaining all the elements which contribute to the regulation of blood osmolarity.

Answer 11

↓ Blood volume → ↓ Atrial baroreceptor firing rate → Hypothalamus
↑ Blood osomatic Pressure (via osmoreceptors) → Hypothalamus

Hypothalamus → Hypothalamic thirst center → ↑ Fluid intake (increases intake of fluid)
Hypothalamus → Posterior pituitary → ↑ ADH output → ↓ Kidney Fluid Loss (decreases loss of fluid)

All these us to get BV back to normal

Question 12

What does RAAS stand for ?

Answer 12

Renin-angiotensin- aldosterone system

Question 13

What kind of enzyme is renin ?

Answer 13

Proteolytic enzyme

Question 14

Where, and in response to what is renin released ?

Answer 14

Renin is released from the juxtaglomerular cells in the kidneys in response to:

1) Sympathetic nerve activation
• Mediated by baroreceptor feedback (when BV or BP dropping)

2) Renal artery hypotension (low flow to kidneys)
• Independent of baroreceptor feedback

3) Decreased sodium in kidney distal tubules

Question 15

What is the main difference between ADH and renin, with respect to osmotic balance ?

Answer 15

Renin is more blind to osmotic balance (more associated with if correct volume in the system or not)

Question 16

Draw a diagram to illustrate the role of RAAS in the regulation of blood volume.

Answer 16

Refer to slide 11 in lecture on “Control of Blood Volume”

Question 17

Describe the main elements of the RAAS.

Answer 17

Decreased arterial Pressure → Renin released from kidney juxtoglomerular cells → → Renin (from kidneys) binds to angitensinogen (in liver, since veinous blood from both kidneys and liver will mix) and converts it to angiotensin 1 → Blood will be going to pulmonary circulation and coming into contact with ACE enzyme which converts Angiotensin 1 into Angiotensin 2 → Angiotensin 2 stimulates retention of water and salt (through release of aldosterone from the adrenal glands), stimulates vasoconstriction of renal arteries (increased total peripheral resistance, leads to decreased blood flow via kidneys, preventing loss of fluid via urine) and stimulates release of ADH from pituitary (decreased urine production), all of which result in increased arterial pressure → Angiotensin 2 can be inactivated by Angiotensinase

Question 18

How may angiotensin 2 be inactivated ?

Answer 18

Through Angiotensinase

Question 19

Describe any systems in place to oppose effects of the RAAS system (help counteract volume overload).

Answer 19

Atrial-natriuretic hormone (a.k.a. Atrial-natriuretic peptide), a 28-amino acid peptide synthesized and stored in muscle cells of the atria.
Released in response to stretch of the atria

Question 20

Define hypovolemia. What are the main types of hypovolemia ?

Answer 20

Loss of blood volume (resulting in drop of blood pressure)
• ↓ whole blood, e.g. hemorrhage
• ↓ plasma, e.g. burns
• ↓ sodium, e.g. vomiting

Question 21

What are the different classes of shock ?

Answer 21

– Class 1, 10-15% blood loss
– Class 2, 15-30% blood loss
– Class 3, 30-40% blood loss
– Class 4, >40% blood loss

Question 22

Describe the effect of a hemorrhage on cardiac output.

Answer 22

Hemorrhage → ↓ Blood Volume → ↓ Venous Pressure → ↓ Venous Venous Return → ↓ Atrial Pressure → ↓ EDV → ↓ Stroke Volume → ↓ CO

Question 23

Describe the immediate (reflex) response to hypovolemia. What is the problem with this response in the long term ?

Answer 23

Baroreceptor Reflex (Degree of volume loss affects how successful)

1) Increase Stroke Volume (to increase CO): 1) increase veinous return leading to increased EDV through vasoconstriction 2) if EDV stays the same, can influence force of contraction by calcium channels (sympathetic NS stimulation)
2) Increase Heart Rate (to increase CO): Through sympathetic innervation (Using just stroke volume and heart rate, CO back to 2/3 of what it was prior to hemorrhage)
3) Increase force of contraction (to increase MABP): via sympathetic innervation (vasoconstriction)

Problem: This does not solve the problem with the BV, only with the BP (that’s where angiotensin and everything kicks in)

Question 24

How much blood loss can immediately reflex response to hypovolemia fully compensate for ?

Answer 24

10%

Question 25

Draw a graph, showing the evolution SV, HR, CO, TPR, and MABP following the hemorrhage and then following the immediate reflex response.

Answer 25

Refer to slide 16 in lecture on “Control of BV” (refer to panopto for filled in graph)

Question 26

Describe the intermediate response to hypovolemia.

What is the problem with this response in the long term ?

Answer 26

1) Arteriolar constriction (to reduce flow to non-essential tissues)
–↓ hydrosta tic pressure in the capillaries
– Favors fluid reabsorption
– Temporary redistribution
2) Decreased renal blood flow
3) Baroreceptors plus thirst

Problem: What’s left inside capillaries is blood that is high in oncotic P which will draw fluid from tissue space into capillaries which can drain into veins and can contribute to Blood volume (and hence arterial pressure). However, this comes at a cost to fluid in tissues (will make tissues dehydrated + hypoxic) so it cannot be a long term answer but it will help get BP back to normal when reflex mechanisms don’t quite do the full job .

Question 27

What is the long term response to hypovolemia (in short) ?

Answer 27

RASS, ADH

Through control of blood volume

Question 28

Why is severe hypovolemia (to the extent where volume of fluid cannot be compensated for) problematic for the body ?

Answer 28

– Damage to tissues and organs can occur

– Heart fails

Question 29

What are the treatment options in severe hypovolemia ?

Answer 29

FLUID REPLACEMENT:

– Resuscitation fluids (depending on what was lost)
• Colloid (gel/starch/albumin) or Hartmann’s
• Blood

– Fluid challenge algorithm
• Whilst monitoring central venous pressure (To ensure neither over nor underfilling. The latter can occur if compensatory mechanisms work particularly well)

Question 30

What is the main disadvantage of fluid replacement (in severe hypovolemia) ?

Answer 30

Added fluid will go to veinous system, which will increase veinous return. This will trigger, reflex mechanisms to counter act sudden return of blood. Eventually, reflex hypertension followed by complete hypotension (not enough fluid in body).

Question 31

Draw a diagram representing the integrated control of blood pressure.

Answer 31

Refer to slide 19, lecture on “Control of Blood Volume”

Question 32

Identify factors (besides those already identified) which affect BP control.

Answer 32

Cortex, via conscious effects of emotions (nerves from cortex to medullary CVC centre)

Time of day (diurnal variations due to hormones and cortical input)

Respiration ( Via mechanical movements in terms of veinous return to the heart, and via chemoreceptors (Aortic and carotid bodies detect changes in pO2. If↓pO2 then rate of firing↑) )