Lecture 16: Responses of the Cardiovascular system Flashcards

Tuesday 18th February 2025

1
Q

Do reflexes induced by haemorrhage
become counterproductive?

A

Yes

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2
Q

Describe haemorrhage

A

rapid loss of blood

1. Respond to reduction in blood volume

2. Maintains blood pressure and cardiac output

3. Restore circulating fluid volume
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3
Q

Does blood pressure mainatin caridac output?

A

Yes

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4
Q

During haemorrhage, what does a loss of pressure
leads to?

A

During haemorrhage a loss of pressure leads to lowered cardiac output due to a fall in venous return.

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5
Q

the total peripheral resistance doesn’t immediately compensate enough, then what might happen?

A

If CO drops, and TPR doesn’t immediately compensate enough, BP falls.

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6
Q

Blood Pressure =

A

(Blood Pressure = Cardiac Output × Total Peripheral Resistance)

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7
Q

Haemorrhage = less blood → less pressure → weaker heart pumping → lower blood pressure → dangerous for survival if not fixed fast.

A

Haemorrhage = less blood → less pressure → weaker heart pumping → lower blood pressure → dangerous for survival if not fixed fast.

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8
Q

🩸 Bleeding happens →
🫥 Veins have less blood →
🫀 Heart has less to pump out →
💔 Arteries lose pressure →
🆘 Body goes into shock if not fixed.

A

🩸 Bleeding happens →
🫥 Veins have less blood →
🫀 Heart has less to pump out →
💔 Arteries lose pressure →
🆘 Body goes into shock if not fixed.

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9
Q

During haemorrhage, what do the intial corrections come from?

A

During haemorrhage inital corrections
come from baroreceptor reflexes

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10
Q

Baroreceptors -> Vasomotor centres -> Autonomic nervous system

A

Baroreceptors -> Vasomotor centres -> Autonomic nervous system

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11
Q

During a haemorrhage, the first thing your body tries to do to save itself is use baroreceptor reflexes to correct the falling blood pressure. Describe this process

A
  • Baroreceptors (pressure sensors) detect the drop in blood pressure (because of blood loss).
  • They send a signal to the vasomotor centres in the brainstem (medulla).
  • The vasomotor centres activate the autonomic nervous system (especially the sympathetic branch).
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12
Q

What does the autonomic nervous system do after being activated by the baroreceptors?

A
  • (A) Increase cardiac output (make the heart pump harder and faster):
  • Elevating heart rate — via sympathetic nerves (and less parasympathetic “braking”).
  • Enhancing contractility — so the heart squeezes stronger.
  • (B) Increase drive to blood vessels (mainly sympathetic):
  • Constriction of arterioles in areas like skin, gut (GI), and skeletal muscle — to raise TPR (Total Peripheral Resistance) and maintain blood pressure.
  • Constriction of veins (“raising venometer tone”) — pushing more blood back to the heart (increasing venous return).
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13
Q

How may increasing cardiac output increase the rates of haemorrhage?

A
  • raising blood pressure too much can sometimes worsen bleeding if the wound isn’t sealed (but the body prioritises perfusion of vital organs first).
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14
Q
A
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15
Q
A
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16
Q

When increasing the drive to the vasculature, more blood will be sent back to the brain and heart, but this limits blood and oxygen supply to other organs. So a person may recover from the haemorrhage with significant organ damage, even though it keeps them alive in the moment.

A

When increasing the drive to the vasculature, more blood will be sent back to the brain and heart, but this limits blood and oxygen supply to other organs. So a person may recover from the haemorrhage with significant organ damage, even though it keeps them alive in the moment.

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17
Q

During haemorrhage what happens when hydrostatic pressure decreases below oncotic pressure?

A
  • Extreme Reabsorption of fluid into the capillary bed at the expense of viscosity
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18
Q

Is angiotensin II one of the most powerful vasoconstrictors found in the body?

A

Yes

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19
Q

How does the secretion of renin correct for the loss of blood volume?

A
  • It secretes Angiotensinogen
  • This eventually allows for the secretion of angiotensin II , which in the short term will result in: Constriction of arterioles, Increase TPR, Constriction of veins, Restore filling pressure.
  • In the long term: Secretion of aldosterone, Fluid retention, Thirst, Restoring ECF
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20
Q

What does the secretion of erythropoietin do?

A

Secretion of erythropoietin corrects
for loss of red blood cells

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21
Q

Secretion of erythropoietin corrects
for loss of red blood cells

A
  • Reabsorption of interstitial fluid partially restores blood volume
  • Expense of haematocrit and plasma proteins (colloid osmotic pressure will fall)
  • Other longer term physiological mechanisms will restore extracellular fluid volume :
  • Secretion of aldosterone, anti-diuretic hormone,
  • Atrial natriuretic peptide.
  • Secretion of erythropoietin will restore red cell count
22
Q

How many classes of heamorrhage are there?

23
Q

Describe Class I Hemorrhage

A
  • Loss of 15% of blood volume
  • No change in vital signs (i.e. blood donation)
24
Q

Describe Class II Hemorrhage

A
  • Loss of 15-30% of total blood volume.
  • Tachycardia, narrowing of the difference between the systolic and diastolic blood pressures, peripheral vasoconstriction.
  • Skin looks pale and is cool to the touch.
  • The patient may exhibit changes in behavior.
25
Describe Class III Hemorrhage
- The loss of 30-40% of blood volume - Heart rate increases, blood pressure drops, the peripheral hypoperfusion (shock), mental status worsens. - Fluid resuscitation with crystalloid and blood transfusion are necessary.
26
Describe Class IV Hemorrhage
- loss of >40% of circulating blood volume. - The limit of the body's compensation is reached and aggressive resuscitation is required to prevent death.
27
What clinical interventions are required when someone is undergoing haemorrhage?
1. Treat the cause of blood loss - prevent further bleeding 2. Give fluids – preferably blood, but otherwise saline with colloid to maintain oncotic pressure 3. Monitor oxygen saturation (oximetry) 4. In severe situations, monitor the filling pressure of the heart (left atrial pressure) with catheter.
28
What is needed for exercise?
Provide skeletal muscle with radically increased blood supply Raise cardiac output and balance changes in peripheral resistance Increase coronary blood flow
29
Is it true that exercise requires the redistribution of blood supply to the skeletal muscles?
Yes
30
How is the blood supply redistributed to the skeletal muscles during exercise?
Vasoconstriction in peripheral tissues Vasodilatation in muscle blood vessels
31
Athletes do a lot of training that increases their sympatheic output and descreases parasympathetic output.
Athletes do a lot of training that increases their sympatheic output and descreases parasympathetic output.
32
Sympathetic drive increases adrenaline. Vasoconstriction occurs through adrenaline acting at α-receptors But the muscle has β2 receptors. And adrenaline causes vasodilation via β2 receptors. So blood flow will be constricted to all other organs and places in the body, except for the skeletal muscle.
Sympathetic drive increases adrenaline. Vasoconstriction occurs through adrenaline acting at α-receptors But the muscle has β2 receptors. And adrenaline causes vasodilation via β2 receptors. So blood flow will be constricted to all other organs and places in the body, except for the skeletal muscle.
33
Local vasodilator metabiolites..
- Potassium concentration will increase. This potassium relaxes vascular smooth muscle. - ATP will be converted to adenosine, which is an important paracrine vasodilator. -Anaerobic respiration will cause lactate to be produced. The acidification from lactate will lead to vasodilation
34
Is it true that the local effects that cause vasodilation will override any sympathetic vasoconstriction?
Yes (Vasoconstriction= - Sympathetic tone - Angiotensin II - ADH )
35
Staling's law
Normally, Starling’s law states that if you increase venous return (blood returning to the heart), the heart stretches more, and it pumps out more blood (higher stroke volume → higher cardiac output). But during exercise, the body does not just rely on that Starling mechanism.
36
During exercise, blood flow to muscles needs to increase massively. This increase can't just depend on Starling’s law (venous return stretching the heart). Instead, cardiac output must be actively increased — not just passively by more filling.
During exercise, blood flow to muscles needs to increase massively. This increase can't just depend on Starling’s law (venous return stretching the heart). Instead, cardiac output must be actively increased — not just passively by more filling.
37
How is cardiac output actively increased during exercise?
- Skeletal muscle movements (like when you run or lift weights) push blood back to the heart, increasing venous pressure. - Higher venous pressure → helps increase cardiac output (the amount of blood pumped by the heart). - Cardiac output and total peripheral resistance (TPR) together determine blood pressure (BP = CO × TPR).
38
"Starling’s Law: Increasing venous return, increases stroke volume, increases cardiac output" is crossed out because that's the classic rule — but exercise needs more than that.
"Starling’s Law: Increasing venous return, increases stroke volume, increases cardiac output" is crossed out because that's the classic rule — but exercise needs more than that.
39
Why does diastole reduce during exercise?
To stop the heart from overfilling
40
During exercise, heart rate and contractility increase through signals from the cerebral motor cortex and central command. These signals activate vasomotor centers, leading to inhibition of the parasympathetic system (which normally slows the heart) and recruitment of the sympathetic system (which speeds it up and strengthens contractions). As a result, both heart rate and contractility rise to meet the body's demands. These cardiovascular changes can even anticipate exercise before it starts, preparing the body in advance. Vasodilation in skeletal muscle is also partly anticipatory.
During exercise, heart rate and contractility increase through signals from the cerebral motor cortex and central command. These signals activate vasomotor centers, leading to inhibition of the parasympathetic system (which normally slows the heart) and recruitment of the sympathetic system (which speeds it up and strengthens contractions). As a result, both heart rate and contractility rise to meet the body's demands. These cardiovascular changes can even anticipate exercise before it starts, preparing the body in advance. Vasodilation in skeletal muscle is also partly anticipatory.
41
What are the 4 phases of exercise?
- Phase 1, phase 2, phase 3, recovery
42
What counters the increased blood pressure during exercise?
Reduced total peripheral resistance counters the increased blood pressure
43
IS it true that those whose ability to increase heart rate is compromised have limited ability to exercise?
yes
44
What contributes to thermoregulation during exercise?
Cutaneous vasodilation (widening of the blood vessels in the skin)
45
Cutaneous vasodilation: sympathetic vasodilation system
Cutaneous vasodilation: sympathetic vasodilation system
46
What is the problem with cutaneous vasodilation ?
Cutaneous vasodilation reduces peripheral resistance and will divert blood from muscles - Initially thermoregulation wins out - If central venous pressure falls sufficiently than thermoregulation is abandoned. - In hot climates, this may cause heat stroke
47
Coronary circulation ceases during systole because the contracting heart muscle compresses the coronary arteries, reducing blood flow to the heart, and blood flow resumes during diastole when the heart relaxes.
Coronary circulation ceases during systole because the contracting heart muscle compresses the coronary arteries, reducing blood flow to the heart, and blood flow resumes during diastole when the heart relaxes.
48
Coronary circulation flows during diastole
- Blood flow to myocardium occurs in diastole. - Heart needs more blood flow, due to increased workload - Heart very good at extracting oxygen (70% efficient) Can not increase O2 extraction - Vasodilator metabolites : - principally adenosine - Ensure that blood flow matches O2 consumption. - Coronary artery disease first expresses itself as angina during exercise, when compromised blood supply becomes insufficient
49
Cardiovascular changes during Exercise
- Baroreceptor reflexes keep blood pressure from rising substantially - Blood pressure = cardiac output x TPR - Arterial pressure- rises slightly - Heart rate- rises substantially - Stroke volume- rises 10- 20% - Cardiac output- rises substantially - Total peripheral resistance- falls (Increased blood flow to skeletal muscle and heart ) - Oxygen consumption- rises
50
To summarise this lecture has covered:
The responses to haemorrhage, particularly in terms of immediate and medium term responses The responses of the heart and circulation to exercise in terms of changes of CO and TPR The changes of the circulation to skeletal muscle and heart in exercise The pulmonary circulation and its low perfusions pressures and its regulation by oxygen levels.
51