Coordinated cardiovascular responses Flashcards

1
Q

What 3 things drives the flow of blood through the body?

A

pressure
gravitational energy
kinetic energy.

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2
Q

How does the gravitational gradient change when lying down vs. standing?

A

Lying down: Small gravitational gradient due to small height difference.
Standing: Greater gravitational gradient between blood at head (high energy) and feet (low energy).

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3
Q

what is the siphon principle

A
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4
Q

How does the siphon principle explain blood flow in rigid tubes?

A

The flow depends only on the energy gradient between the inlet (LV) and outlet (RV), not the path blood takes. Gravity’s upward and downward effects cancel each other out.

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5
Q

Why does blood still flow when standing despite gravity?

A

Pressure energy drives blood flow. The arterial pressure remains higher than venous pressure, ensuring flow continues through the closed system.

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6
Q

What happens to blood flow when standing in real blood vessels?

A

Blood flow decreases because veins are not rigid. Gravity affects venous flow more significantly, reducing return to the heart.

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7
Q

How does the body minimize reduced blood flow when standing?

A

The cardiovascular system has a coordinated response to orthostasis (standing up) to compensate for gravitational effects on blood flow.

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8
Q

What does the siphon diagram demonstrate?

A

Blood flows from the high-pressure LV (95 mmHg) to the low-pressure RV (4 mmHg) regardless of the gravitational path due to the energy gradient.

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9
Q

Why does the siphon principle not fully apply to human vasculature?

A

Blood vessels, especially veins, are not rigid. This causes flow reductions when standing due to gravitational effects on venous return.

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10
Q

What is orthostasis?

A

Orthostasis refers to the effect of standing upright on blood pressure distribution in the body due to gravity.

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11
Q

What is the mean capillary pressure when supine (lying down)?

A

Approximately 25 mmHg.

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12
Q

How much do vascular pressures increase in the feet when standing upright?

A

Vascular pressures increase by about 90 mmHg.

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13
Q

What are the arterial and venous pressures in the feet when upright?

A

Artery: 185 mmHg
Vein: 105 mmHg

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14
Q

What are the arterial and venous pressures in the feet when lying down?

A

Artery: 90 mmHg
Vein: 10 mmHg

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15
Q

What is the pressure gradient across the foot capillary bed during standing?

A

80 mmHg (185 mmHg in artery - 105 mmHg in vein).

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16
Q

Why do feet swell when standing for long periods?

A

Foot capillary pressure rises, leading to increased filtration, causing fluid to leak into tissues, resulting in feet swelling.

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17
Q

Is blood flow directly affected by gravity?

A

No, the pressure gradient across the vascular bed is unchanged, so flow is not directly affected by gravity.
BUT it is indirectly affected (e.g., increased pressure in feet).

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18
Q

Why do veins play a significant role in blood redistribution when standing?

A

Veins are compliant (distensible), meaning they expand when pressure increases, causing blood to pool in the lower body when standing.

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19
Q

What happens to venous valves when you stand?

A

Increased pressure causes blood to accumulate below the heart, closing the one-way valves in the legs and briefly reducing venous return to the heart.

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20
Q

Where does blood redistribute when standing?

A

Upper legs: Most compliant, major blood pooling.
Abdomen: Increased venous blood volume.
Calves, ankles, feet: Less compliant, smaller pooling.
Arteries in the legs: Slight volume increase.

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21
Q

How much blood volume accumulates in the veins below the heart after standing?

A

Approximately 300-600 ml of blood accumulates in distended veins.

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22
Q

Why does central venous pressure (CVP) fall when standing?

A

Central venous pressure is reduced (by ~3 mmHg), and therefore, by the Frank-Starling mechanism, cardiac output falls.

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23
Q

How long does it take for veins below the heart to distend with blood after standing?

A

Approximately 45 seconds.

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24
Q

What are the key events when standing upright?

A

Blood pools in compliant veins (upper legs, abdomen).
Venous valves close, reducing venous return.
Veins fill, valves reopen, and flow stabilizes.
CVP and cardiac output fall due to Frank-Starling mechanism.

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25
Q

What happens to stroke volume (SV) and cardiac output (CO) during orthostasis?

A

Both stroke volume and cardiac output decrease because of reduced venous return.

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26
Q

How does orthostasis affect blood flow to the brain and mean arterial blood pressure (MABP)?

A

Blood flow to the brain and MABP in the upper body decrease due to reduced cardiac output.

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27
Q

What receptors are activated in response to decreased blood pressure during orthostasis?

A

Baroreceptors and volume receptors are activated to detect reduced blood pressure.

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28
Q

What mechanisms are triggered to compensate for orthostasis?

A

Increased heart rate (HR)
Vasoconstriction in arteries and veins
Increased total peripheral resistance (TPR)

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29
Q

How does blood pressure change during orthostasis?

A

Systolic blood pressure slightly decreases or stabilizes, while diastolic blood pressure increases due to vasoconstriction.

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30
Q

What are the two mechanisms that reduce blood flow to the lower extremities on standing?

A

Reflex sympathetic vasoconstriction via baroreceptors.

A local sympathetic axon reflex (veno-arteriolar reflex).

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31
Q

How does the baroreceptor reflex reduce capillary pressure?

A

Baroreceptor reflex constricts arteries and arterioles in the lower extremities, reducing blood flow and hydrostatic pressure in the capillaries.

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32
Q

Why is arteriolar constriction important during orthostasis?

A

It minimizes filtration in the capillaries of the lower extremities, helping to prevent excessive fluid leakage into tissues.

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33
Q

What triggers the local veno-arteriolar reflex?

A

Increased blood volume and pressure in veins stretch their walls, activating sympathetic sensory fibers

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34
Q

How does the veno-arteriolar reflex work?

A

Stretch in vein walls triggers action potentials in sympathetic fibers, which stimulate nearby arterioles to constrict, reducing blood flow further.

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35
Q

What is the combined effect of the baroreceptor reflex and veno-arteriolar reflex?

A

Both mechanisms act to:

Reduce capillary pressure.
Minimize fluid filtration in the lower extremities during standing

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36
Q

What happens to arteriolar pressures in the lower extremities due to vasoconstriction?

A

Arteriolar pressures decrease, helping to reduce capillary hydrostatic pressure and prevent swelling.

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37
Q

How do sympathetic sensory fibers connect veins and arterioles?

A

Stretch-activated fibers in vein walls innervate arterioles, triggering vasoconstriction through the local veno-arteriolar reflex.

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38
Q

What is the mean ABP and CVP when lying down?

A

CVP = 4 mmHg
mean ABP = 95mmHg

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39
Q
A
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40
Q

What is the mean ABP and CVP when standing up?

A

CVP = 1 mmHg

Mean ABP = 95mmHg

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41
Q

What is the role of the skeletal muscle pump in orthostasis?

A

The skeletal muscle pump helps the cardiovascular system cope with orthostasis by pumping blood in veins towards the heart, preventing blood pooling in the lower extremities.

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42
Q

What happens during muscle contraction in the skeletal muscle pump?

A

Contraction increases pressure in the vein segment.

Blood is pushed forward through the upper valve.

The lower valve closes, preventing backflow.

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43
Q

What happens when the muscle relaxes in the skeletal muscle pump?

A

Pressure in the vein segment decreases.

The lower valve opens, allowing blood to fill the segment from below.

Blood flows forward towards the heart.

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44
Q

What is the “milking” action of veins?

A

Repeated muscle contractions exert a pumping action, pushing blood through the veins in a forward direction.

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45
Q

How does the skeletal muscle pump affect venous pressure in the feet?

A

During walking, it can lower venous pressure in the feet to 20-30 mmHg.

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46
Q

What is the role of the skeletal muscle pump during exercise?

A

It acts like an ancillary heart, contributing up to half of the energy needed to increase blood flow in the cardiovascular system.

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47
Q

What is the venous pressure in the foot when standing still?

A

Approximately 120 cm H₂O (88 mmHg) due to the effect of gravity.

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48
Q

What happens when valves in superficial veins fail?

A

Valve failure exposes superficial veins to chronic high pressures, leading to varicose veins.

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49
Q

What are varicose veins, and how do they appear?

A

Varicose veins are swollen, twisted veins that bulge out from the skin, often blue or dark purple in color, caused by valve failure in superficial veins.

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50
Q

What are tributary veins?

A

Veins under the surface of the skin.

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51
Q

What happens to venous pressures above the heart when standing?

A

Gravity causes venous pressures above the heart to fall, and veins outside the cranium partially collapse a few centimeters above the heart.

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52
Q

Why do veins outside the cranium collapse when standing?

A

Collapsing prevents internal pressures from falling below zero while still allowing blood to flow through the margins of the veins.

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53
Q

Do veins within the cranium collapse?

A

No, cranial veins do not collapse, their pressure falls to about -10 mmHg, maintaining the arterial-to-venous pressure gradient for brain blood flow.

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54
Q

How is blood flow to the brain affected by standing?

A

Blood flow to the brain decreases by ~20% due to the fall in cardiac output.

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55
Q

Why can prolonged standing cause fainting?

A

Blood pooling in the lower extremities reduces brain perfusion, potentially leading to fainting. Falling or lying down restores blood flow to the brain.

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56
Q

What is the significance of cranial vein pressures falling below zero?

A

The negative pressure (-10 mmHg) helps maintain the pressure gradient driving blood flow through the brain.

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57
Q

How does fainting restore brain blood flow?

A

Falling or lying down reduces gravitational effects, improving venous return and perfusion to the brain.

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58
Q

Why don’t veins within the cranium collapse when standing?

A
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59
Q

How does venous pooling affect central blood volume when moving from supine to upright?

A

decreases by ~400 mL

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60
Q

What happens to central venous pressure (CVP) when standing up?

A

decreases by ~3 mmHg.

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61
Q

How does stroke volume change when transitioning from supine to upright?

A

decreases by 40%.

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62
Q

What reflex responses occur when standing to compensate for venous pooling?

A

Heart rate increases by 25%.
Contractility increases, helping to maintain cardiac output.

63
Q

What is the net effect on cardiac output when moving upright?

A

decreases by ~25%

64
Q

How does limb and splanchnic blood flow change when standing?

A

decrease by 25%

65
Q

How does total peripheral resistance (TPR) change upon standing?

A

TPR increases by 25%

66
Q

What happens to cerebral blood flow when standing?

A

decreases by ~20%

67
Q

What are the 4 progressive changes during prolonged quiet standing?

A
  1. Venous pooling increases.
  2. Pulse pressure decreases.
  3. Heart rate and total peripheral resistance (TPR) rise as compensatory mechanisms.
  4. Eventually, mean blood pressure (BP) starts to fall.
68
Q

what is a vasovagal syncope?

A

fancy way of saying fainting due to standing, from fall in blood pressure

69
Q

What causes sudden syncope (fainting) during prolonged standing

A
70
Q

What symptoms precede vasovagal syncope?

A

Pallor, sweating, nausea, blurred vision, and a gradual sensation of faintness.

71
Q

another term for vasovagal

A

Bezold-Jarisch reflex

72
Q

whats another condition that can lead to syncope (fainting) upon standing?

A

chronic autonomic failure

73
Q

What is chronic autonomic failure, and how does it cause syncope?

A

It is a degeneration of sympathetic nerves that prevents the normal reflex response to orthostasis, leading to rapid BP drops and fainting.

^ happens in eldery a lot

74
Q

How is tilt table testing used to diagnose orthostatic syncope?

A

One way of diagnosing different forms of orthostatic syncope is to strap a patient to a tilt table and then tilt them from a supine to a more upright position while monitoring their cardiovascular functions.

HOWEVER - because their feet are not on the ground, the skeletal muscle pump is not active, and so its compensatory effects don’t occur.

75
Q

What is the vasovagal (Bezold-Jarisch) reflex?

A

A sudden reflex causing bradycardia and vasodilation, leading to syncope.

76
Q

What should be done if someone faints from postural hypotension?

A

Do not sit or stand them up. Keep them lying flat to restore cerebral blood flow.

77
Q

What triggers the sudden change in the reflex response from tachycardia and vasoconstriction to bradycardia and vasodilatation?

A

Exact trigger unknown, but thought to be due to the Bezold-Jarisch reflex (which can also be provoked by thrombolytic agents)

78
Q

what is an advantage of fainting?

A

One advantage of fainting is that it usually leads to a horizontal posture which instantly restores venous return and therefore cardiac output.

But note: if for some reason the person remains upright (e.g., ‘helpful’ passenger holding them up as she faints on the tube) then BP will remain low and brain damage is possible.

79
Q

What is haemorrhage?

A

Haemorrhage is the loss of blood from the circulatory system.

80
Q

What is revealed haemorrhage?

A

Bleeding that is obvious, although the exact quantity can be hard to measure accurately.

81
Q

What is concealed haemorrhage?

A

Bleeding that is not visible and occurs within the body, often due to trauma or internal conditions.

82
Q

What do the effects of haemorrhage depend on?

A

The volume and speed of blood loss.

83
Q

What are the effects of chronic, slow but persistent blood loss?

A

Leads to iron deficiency anemia over time.

84
Q

What are the effects of acute, large blood loss?

A

Causes a reduced circulating volume, which can lead to circulatory shock.

85
Q

What is the most important consequence of significant blood loss?

A

Circulatory shock - Generalised inadequacy of blood flow throughout the body - If prolonged, this is sufficient to cause tissue damage because of inadequate delivery of oxygen and other nutrients

86
Q

haemorrhage can cause circulatory shock alongside 4 other things like

A

Other hypovolumic (burns, severe vomiting/diarrhoea)
Cardiogenic (e.g. acute MI)
Anaphylaxis
Sepsis

87
Q

What are the signs, symptoms and consequences of shock?

A
88
Q

What are the average blood volumes for men and women?

A
89
Q

How does the WHO classify haemorrhage severity?

A

Based on percentage of blood loss:

90
Q

How does the rate of blood loss affect severity?

A
91
Q

What is the primary goal of rapid compensatory responses to haemorrhage?

A

To minimise a fall in blood pressure and maintain perfusion of vital organs.

92
Q

What are the four key reflexes involved in compensatory responses to haemorrhage?

A

High-pressure baroreceptors
Low-pressure baroreceptors
Peripheral chemoreceptors
Central chemoreceptors

93
Q

What do high-pressure baroreceptors monitor?

A

Blood pressure in the carotid sinuses and aortic arch.

94
Q

What do low-pressure baroreceptors monitor?

A

Blood volume in the heart and large pulmonary vessels.

95
Q

Where are peripheral chemoreceptors located, and what do they sense?

A

Located in the carotid and aortic bodies, they sense:

Decreased pO₂
Increased pCO₂
Decreased pH

96
Q

What do central chemoreceptors sense?

A

Decreased pH associated with reduced blood flow in the brainstem.

97
Q

How do these reflexes act on medullary cardiovascular control centres?

A

They stimulate an autonomic response (mainly due to ↑ sympathetic drive but ↓ parasympathetic drive makes a contribution by increasing the HR).

98
Q

What are the 3 key reflex responses to haemorrhage?

A
99
Q

How do reflex responses affect blood pressure?

A

They help ameliorate the fall in mean BP, though pulse pressure decreases.

100
Q

What are the accompanying effects of reflex responses?

A
101
Q

Why is the sympathetic system important in the immediate period after haemorrhage?

A
102
Q

What are cardiopulmonary stretch receptors, and what do they respond to?

A

These mechanoreceptors in the heart and large pulmonary vessels respond to changes in blood volume. They activate reflexes which act to reverse the change in volume and support BP and CO.

103
Q
  • The cardio-pulmonary stretch receptors are turned on by what
A

increased blood volume.

104
Q

what are the main effects of cardio-pulmonary stretch receptors when turned on:

A

is to cause:
- decreased vasoconstriction
- and decreased thirst and water reabsorption.

105
Q

increased ADH in Cardio-pulmonary stretch receptors cause what

A
106
Q

increased adrenaline in Cardio-pulmonary stretch receptors cause what

A
107
Q

What do peripheral chemoreceptors respond to?

A
108
Q

How do peripheral chemoreceptors respond to blood gas changes?

A

Afferents project to the nucleus tractus solitarius.

Trigger sympathetic vasoconstriction.
Increase ventilation, reducing pCO₂ and inhibiting the vagal control center, leading to tachycardia.

109
Q

Where are central chemoreceptors located, and what do they sense?

A

Located in the medulla, they sense ↓ pH caused by increased CO₂ levels in the brain.

110
Q

When does the CNS ischaemic response activate?

A

When mean blood pressure < 50 mmHg, indicating severe hypotension.

111
Q

What effects does the CNS ischaemic response have?

A

Powerful sympathetic vasoconstriction of peripheral arteries and veins.
Severe reduction in gut and renal perfusion to prioritize blood flow to vital organs.

112
Q

Why is the CNS ischaemic response dangerous if sustained?

A

Prolonged reduction in gut and renal perfusion can lead to organ damage and worsen the systemic condition.

113
Q

How does lung stretch from increased ventilation affect heart rate?

A

It reduces pCO₂ and inhibits the vagal control center, causing tachycardia.

114
Q

What happens to cardiac output in moderate haemorrhage?

A

Cardiac output is reduced due to decreased blood volume and venous return

115
Q

How does sympathetic vasoconstriction affect blood flow during moderate haemorrhage?

A

In moderate haemorrhage the vasoconstriction is directed to the gut, kidney, the muscle and the skin as they are not crucial to keep you alive.

116
Q

where does vascular resistance increase/ decrease during moderate haemorrhage?

A
117
Q

which regions maintain normal blood flow during moderate haemorrhage?

A

Cerebral and coronary circulations maintain normal blood flow to protect the brain and heart.

118
Q

In which regions is blood flow reduced during moderate haemorrhage?

A

Splanchnic (gut).
Renal (kidneys).
Skeletal muscle.
Skin.

119
Q

How is arterial blood pressure maintained during moderate haemorrhage?

A

Maintained as normal due to increased total peripheral resistance (TPR) compensating for low cardiac output.

Pulse pressure is low.

120
Q

How do cardiac output (CO) and blood pressure (BP) change with increasing blood loss?

A

CO decreases more rapidly than BP.

BP is better preserved initially to protect tissue perfusion.

121
Q

When does the CNS ischaemic response occur?

A

When blood pressure drops to ≤50 mmHg, triggering profound vasoconstriction via the sympathetic nervous system.

122
Q

How long does it take to restore the blood volume in a moderate haemorrhage?

A

It takes around a day, generally with a haemorrhage of around 25%, to restore the blood volume.

123
Q

What is the initial mechanism to restore blood volume?

A

Internal transfusion which occurs within hours

^ This is the movement of fluid of water from the tissues in the cells into the vascular system - so there is a shift of volume into the vascular system.

124
Q

What is associated with the internal transfusion during blood volume restoration?

A

Haemodilution, where plasma volume increases, diluting blood cells - Haemodilution is maximal after a day.

125
Q

what are the 3 slower mechanisms to help restore blood volume (takes days):

A
126
Q

What does the internal transfusion mechanism depend on?

A

It depends on the balance between hydrostatic pressure and oncotic pressure.

127
Q

What happens to capillary hydrostatic pressure during haemorrhage?

A

It is reduced due to vasoconstriction and a fall in venous pressure, promoting fluid reabsorption.

128
Q

From where is fluid reabsorbed into the plasma?

A

Fluid is reabsorbed from the interstitium into the plasma, increasing blood volume by approximately 0.5 liters, depending on plasma protein levels.

129
Q

How does fluid move from intracellular to interstitial compartments?

A

Driven by increased hepatic glucose production and release

130
Q

What are the renal mechanisms to restore blood volume?

A
  • There’s a fall in blood pressure and a fall in blood volume.
  • This acts on the baroreceptors and the cardiopulmonary receptors.
  • These report to the brainstem.
  • This leads to thirst.
  • The decrease in atrial stretch leads to the decreased release of atrial natriuretic peptide (ANP) - this promotes Na+ and water reabsorption.
  • Along with thin the input into the hypothalamus and brain stem increases the release of antidiuretic hormone, which conserves water and decreases diuresis.
  • The input also increases the sympathetic renal nerve activity which increases renin, angiotensin 2 and aldosterone which all helps to promote Na+ and water reabsorption.
  • This helps to restore the blood volume.
  • At the same time, the fall in blood pressure and the fall in blood volume are direct stimuli for the RAAS which again increases the reabsorption of Na+ and water.
131
Q

The haemoglobin concentration is a measure of

A

haemodilution

132
Q

Describe how the quality of blood is restored using a graph.

A

Gradually over time the haemodilution is reversed and that requires the provision of new blood cells and that’s what takes the longest time.

Gradually over time the haemodilution is reversed and that requires the provision of new blood cells and that’s what takes the longest time.

And the kidneys increase their synthesis and release of erythropoietin because they’re hypoxic due to the haemorrhage and lack of blood flow.

This stimulates production of new RBCs and during this period there are a lot of immature RBCs in the blood, which is an indication that cells are being released at a higher rate than usual from the bone marrow.

133
Q

what are immature RBCs called

A

reticulocytes

134
Q

Why is blood haemoglobin ([Hb]) normal immediately after haemorrhage?

A

Both the number of RBCs and the plasma volume decrease proportionally, maintaining a normal [Hb].

135
Q

What happens to [Hb] 12–24 hours after haemorrhage?

A

[Hb] falls due to haemodilution, as blood volume is restored while the RBC population has not yet recovered.

136
Q

How long does it take for haemoglobin levels to recover fully?

A

[Hb] slowly recovers, taking up to 6 weeks as RBCs are replaced.

137
Q

How is oxygen-carrying capacity affected after haemorrhage?

A

It is reduced, especially in the first 24 hours, due to lower RBC levels.

in the first 24 hours; effect of this is somewhat ameliorated by reduced blood viscosity which favours tissue perfusion.

138
Q

How does ventilation respond to haemorrhage?

A

Ventilation increases due to reduced blood flow through carotid bodies and acidosis from tissue underperfusion.

139
Q

What happens to platelet count during haemorrhage?

A

Platelet count increases, as platelets stored in the spleen are released into circulation.

140
Q

What happens to fibrinogen levels during haemorrhage?

A

Fibrinogen levels increase within minutes to aid clot formation.

141
Q

How is coagulation time affected by haemorrhage?

A

Coagulation time decreases, but clotting factors are gradually consumed, reducing their availability.

142
Q

What happens to white blood cell (WBC) count during haemorrhage?

A

WBC count, particularly neutrophils, increases within 2–5 hours, priming for acute lung injury (ALI) or acute respiratory distress syndrome (ARDS).

143
Q

What is non-progressive shock?

A
  • If a haemorrhage isn’t very large or if they’re transfused quickly enough the patient will develop non-progressive shock.

its a form of shock that resolves without treatment/ transfusion; so a fit young person can lose < ~20% blood volume without progressive shock (e.g. when donating blood ≈ 10%, you don’t go into shock).

144
Q

How long does it take for blood volume and cardiac output to recover in non-progressive shock?

A

Recovery occurs over 16–24 hours as compensatory mechanisms restore blood volume and cardiac output.

145
Q

What is progressive shock?

A

A stage of shock where cardiac output (CO) initially improves but then progressively declines unless treated, typically seen with blood loss <30%.

146
Q

Why is the timing of transfusion critical in shock management?

A

Transfusion within the golden hour (<1 hour) prevents irreversible decline in CO by addressing hypovolemia and restoring perfusion.

147
Q

How can transfusion impact the reversibility of shock?

A

Reversible shock: CO improves if transfusion is given in time.
Irreversible shock: Delayed transfusion results in cardiac damage, causing a permanent decline in CO.

148
Q

what is progressive shock?

A

A state of sustained circulatory failure leading to a vicious cycle of tissue hypoxia and multi-organ failure.

149
Q

As the gut and renal circulations are specifically curtailed in shock, there is risk of what

A

acute renal failure and intestinal mucosal damage.

150
Q

Why are transfusions less effective in progressive shock?

A

Increased vascular permeability and fluid loss to tissues reduce the ability of transfusions to restore volume.

151
Q

describe the cycle of progressive shock

A
152
Q

Orthostasis summary

A
153
Q

Haemorrhage Summary

A