Haemorrhage

[Ref: WG21: p640-642; KB2:p57-58; BL8:p278-282]

Loss of blood volume

--> Decrease cardiac output and BP

Compensatory mechanisms

• Neural mediated
  * Mostly mediated by baroreceptors and chemoreceptor
• Hormone-mediated
  * Mostly by volume receptors and renal mechanisms

Sensors

1. Baroreceptors
   * Carotid sinus baroreceptor plays major role
   * Aortic baroreceptor not as significant
2. Chemoreceptors
3. Volume receptors (low pressure receptors)
   * In right atrium and great veins
4. Renal
   * Intrarenal baroreceptor mechanism
   * Macula densa

1. Baroreceptors responses

Acts on ??vasomotor area in brain

1.1. Reduced vagal tone

1.2. Enhanced sympathetic stimulation

• 1.2.1. Increased heart rate
• 1.2.2. Increased contractility
• 1.2.3. Generalised venoconstriction
  * Mobilisation of blood reservoir
• 1.2.4. Generalised vasoconstriction
  * Redistribution of cardiac output
  * Reabsorption of interstitial fluids
• 1.2.5. Increased adrenal gland response

 

1.2.3. Venoconstriction

Receptor responsible not settled

Mobilisation of blood reservoir from

• Splanchnic (including liver)
• Skin
• Lung
  * 7.5% of total blood volume
• Spleen (minor in human)

Has the effect of storing effective blood volume and filling pressure

1.2.4. Vasoconstriction

1.2.4.1. Redistribution of cardiac output

Most pronounced in

• Skin
• Skeletal muscle
• Splanchnic
• Kidney (late effect)

Slight or absent in

• Coronary circulation
• Cerebral circulation

Renal blood flow

In early stages of mild-to-moderate haemorrhage

• Renal blood flow autoregulated from 75-170mmHg
• Little changes in renal blood flow due to autoregulation

With more prolonged or severe haemorrhage

• Both afferent and efferent arterioles are constricted
• Efferent arteriole constricts more
• Outer cortex constricts more

Which resulted in:

• GFR decreased
• RPF decreased even more
• Increased retention sodium and nitrogen waste
• Decreased urine production

1.2.4.2. Reabsorption of ISF

Decreased blood pressure and increased vasoconstriction

--> Decreased capillary hydrostatic pressure

--> Promotes net absorption of ISF into intravascular compartment

Can reabsorb up to 15mL per kg per hour (about 1L/hr)

1.2.5. Increased adrenal gland response

1.2.5.1. Increased circulating catecholamine

Probably contribute relatively little to the generalised vasoconstriction

May stimulate reticular formation

--> Increased restlessness

--> Increased muscle pump mechanism

1.2.5.2. Increased cortisol secretion

[BL8:p281]

May mediate shift of fluid from intracellular to extracellular compartment

"Appears to be essential for a full restoration of plasma volume after haemorrhage"

2. Chemoreceptor responses

Stimulation of carotid and aortic bodies by

• Lactic acidosis
• Anaemia and stagnant hypoxia secondary to decreased local blood flow

Resulting in:

Stimulation of vasomotor area
--> Increased vasoconstriction

Stimulation of respiration
--> Increased thoracic pump

NB:

• No baroreceptor discharge when pressure is below 60-70mmHg
• Stimulation by chemoreceptors help increasing vasoconstriction beyond the maximum that can be produced by baroreceptor inhibition

3. Volume receptor responses

3 effects:

1. Decreased ANF release
2. Increased release of ADH (acting on hypothalamus)
3. Stimulate vasomotor centre

Effects of ADH (vasopressin)

• Vasoconstriction
  * Significant role in maintaining BP
• Retention of water

4. Renal response

Increased renin secretion due to:

• Reduced arteriolar BP at JG cells
  * Detected by intrarenal baroreceptors (i.e. JG cells)
• Decreased Na+ and Cl- in distal tubules
  * Detected by macula densa cells
• Sympathetic stimulation, via
  * postganglionic renal sympathetic nerves
  * circulating catecholamines (beta1 receptors)

Increased renin secretion

--> Increased angiotensin II

Effects of angiotensin II

[WG21: p460]

• Vasoconstriction
  * One of the most powerful vasoconstrictor
• Increased thirst
  * via subfornical organ (SFO) and organum vasculosum of the lamina terminalis (OVLT)
• Increase aldosterone secretion
• Increased ADH and ACTH
• Contraction of mesangial cells
  --> Decreased GFR
• Constriction of arterioles (efferent greater than afferent)
  * [WG21:p707]
• Increased Na+ resorption (direct effect on ??proximal tubules)

 

Summary of factors affecting renal output

Angiotensin II --> Increased Na+ resorption

Aldosterone --> Increased Na+ resorption

ADH --> Increased water resorption

Note on aldosterone

• Aldosterone take 30min to exert effect
• Initial decline in urine volume and Na+ excretion is mostly due to haemodynamic changes in kidney

 

Others: Ischaemic CNS response

Severe hypotension (<40mmHg) may result in ischaemic CNS response

--> Massive sympathetic stimulation to maintain cerebral perfusion at the expense of the rest of body

With more severe degree of cerebral ischaemia, vagal centers also become activated

 

End-result

• Plasma volume return to normal by 12 to 72 hours
• Incresased protein synthesis
• Increased erythropoiesis (increased erythropietin release)
  * Reticulocyte level peak at 10 days
  * RBC level restored by 4 to 8 weeks

Overall, protein is decreased and haematocrit is decreased further

NB:

Post-haemorrhage

--> Increase in 2,3-DPG (??mechanism)

--> Decreased oxygen affinity

--> Increased offloading of oxygen at tissue level

--> Increased tolerance for low haematocrit

Other notes

Mayer waves

Slow regular oscillations in MABP that occurs at a rate of one every 20-40 seconds during hypotension.

Hypoxia stimulate chemoreceptor

--> BP increases, perfusion improved

--> Hypoxic stimulus removed

--> Loss of chemoreceptor input

--> BP drops

--> Hypoxic stimulation of chemoreceptor