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
- Baroreceptors
* Carotid sinus baroreceptor plays major role
* Aortic baroreceptor not as significant
- Chemoreceptors
- Volume receptors (low pressure receptors)
* In right atrium and great veins
- 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:
- Decreased ANF release
- Increased release of ADH (acting on hypothalamus)
- 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