3. Physiology
        3.2. Cardiovascular
            3.2.6. Special circumstances
3.2.6.3. Haemorrhage

Haemorrhage

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

Loss of blood volume

--> Decrease cardiac output and BP

Compensatory 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

 

1.2.3. Venoconstriction

Receptor responsible not settled

Mobilisation of blood reservoir from

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

Slight or absent in

Renal blood flow

In early stages of mild-to-moderate haemorrhage

With more prolonged or severe haemorrhage

Which resulted in:

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

Resulting in:

Stimulation of vasomotor area
--> Increased vasoconstriction

Stimulation of respiration
--> Increased thoracic pump

NB:

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)

4. Renal response

Increased renin secretion due to:

Increased renin secretion

--> Increased angiotensin II

Effects of angiotensin II

[WG21: p460]

 

Summary of factors affecting renal output

Angiotensin II --> Increased Na+ resorption

Aldosterone --> Increased Na+ resorption

ADH --> Increased water resorption

Note on aldosterone

 

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

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

 

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Created20050608
Reviewed20050816


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