In this article we will discuss about:- 1. Definition and Effects of Haemorrhage 2. Role of Atrial and Ventricular Receptors and the Sino-Aortic Baroreceptors in Haemorrhage 3. Compensatory Changes.
Definition and Effects of Haemorrhage:
Escape of blood, from ruptured blood vessels is called haemorrhage.
The effects of haemorrhage depend on the amount and rapidity of blood loss, and the efficiency of the compensatory power of the subject. If the haemorrhage be severe it may lead to circulatory collapse and death.
If it is moderate (5-15 ml per kg body weight) and the subject is healthy, compensatory, changes take place and normal condition is restored. From a professional healthy donor about, 500-1,000 ml of blood may be taken at a time, at three to four months’ intervals.
Haemorrhage produces the following disturbances:
(a) Blood volume is diminished
(b) Blood pressure— Due to decreased blood volume cardiac output is diminished and there is reflex vasoconstriction.
Vasoconstriction leads to increased peripheral resistance. There is also venous constriction and more blood is propelled towards the heart. Less blood goes to the skin, splanchnic area, muscle, etc. due to constriction of arterioles. There is fall of pressure in the arterioles. The pressure in the capillaries also falls and less amount of fluid is transuded from the blood to the tissue spaces.
Although the capillary pressure falls, but there is no change in the osmotic pressure and so fluid from the tissue spaces enters the blood and keeps the blood volume almost constant. If the haemorrhage occurs slowly the blood pressure level may be maintained for a considerable time.
In case of severe haemorrhage, there is fall of cardiac output and diminution of peripheral resistance, dilatation of the vessels of the skeletal muscles. All these lead to profound fall of blood pressure. The heart rate is markedly diminished. There is diminution of cerebral blood flow which results in sudden loss of consciousness or fainting,
(c) Heart rate is increased to maintain cardiac output,
(d) Respiration increases both in rate and depth. Anoxia develops due to less haemoglobin,
(e) Pallor of the skin occurs due to diminution of blood flow in the skin,
(f) Cold sweat the skin is cold and there is less evaporation of sweat,
(g) Excitement is caused by anoxia, and
(h) Diminution in urine flow occurs due to impaired renal circulation.
Role of Atrial and Ventricular Receptors and the Sino-Aortic Baroreceptors in Haemorrhage:
The discharge of impulses from the receptors in the atria and ventricles is not dependent upon the mean systemic pressure, but upon the venous return to the heart. In haemorrhage there is diminution of venous return, stroke volume and pulse pressure.
Due to the reduction of venous return the inhibitory effect of these afferents on arteriolar constriction is reduced. The resultant effect is the increase of peripheral resistance and consequently there is some improvement of the venous return.
Again, stimulation of the Sino-aortic baroreceptors is dependent on pulse pressure. In haemorrhage due to fall of pulse pressure the stimulation of the baroreceptors is diminished. So there are vasoconstriction and tachycardia due to reflex chemoreceptor’s influence following haemorrhage. Tachycardia further reduces the stroke volume and pulse pressure.
Compensatory Changes after Haemorrhage:
1. Changes in the Cardiovascular System:
The immediate need is to maintain the blood pressure.
To attain this need the following changes take place:
i. Heart rate rises to maintain cardiac output caused by low blood pressure, O2 lack, CO2 excess, etc., through central and Sino-aortic mechanism.
ii. General vasoconstriction caused by effects of
(a) O2 lack,
(b) CO2 excess, etc., directly on the vasomotor centre as well as reflexly through the chemoreceptors of the sino-aortic nerves,
(c) In the experimental animal it has been observed that after severe bleeding the blood pressure falls much below normal. The chemoreceptors of the Sino-aortic nerves bring about reflex vasoconstriction and exert their influence to maintain the mean systemic pressure in the bled animal. But after section of the vagi reflex vasoconstriction disappears and the blood pressure falls still further
iii. Adrenaline and Noradrenaline secretion—caused by reflex chemoreceptor’s activity and excitement leading to further vasoconstriction and increase of heart rate.
iv. Contraction of spleen and mesenteric blood vessels—expelling stored corpuscles into circulation.
v. Liver blood volume—the volume of liver blood is also decreased so as to compensate the blood loss following haemorrhage.
2. Changes in Respiration:
Respiration increases both in rate and depth and thus total pulmonary ventilation rises, caused by low blood pressure, anoxia, CO2 excess, etc., by central as well as sino-aortic process. Its purpose is to supply more oxygen.
3. Renal Changes:
Volume of urine decreases due to fall of blood pressure, renal vasoconstriction and consequent less renal circulation. But the filtration fraction is found to be more than normal, showing that the efferent glomerular vessels undergo a selective constriction. Besides these, angiotensin II that is formed due to interaction of plasma globulin substrate-(α2-fraction) and renin (secreted from the juxtaglomerular region of ischaemic kidney) has got the effect.
This renin-angiotensin system also stimulates the secretion of aldosterone and also glucocorticoids from the adrenal cortex. Aldosterone by maintaining electrolyte balance (Na+ retention and K+ excretion through the kidneys) restores blood volume. Under such state vasopressin (antidiuretic hormone) is also secreted from the posterior pituitary and this helps further in restoration of blood volume through excretion of less urine.
Due to less urine formation, nitrogen retention takes place in the blood and may lead to azotemia or uraemia. In case of prolonged hypotension there may occur severe renal tubular damage (lower nephron nephrosis).
4. Restoration of Blood:
The lost blood is regained. At first the fluid, then the plasma proteins and lastly the red cells and haemoglobin are restored.
The brief details are as follows:
The first change in the in drawing of water from the tissue spaces even before the haemorrhage is over. Due to low blood pressure, the capillary pressure falls much below the colloidal osmotic pressure of plasma. Hence, instead of normal filtration, water from the tissue spaces is drawn in and thus blood volume starts rising.
A definite increase of plasma volume takes place after one hour, as shown by dilution of plasma proteins and haemoglobin. In 24 hours plasma volume is fully restored and even may rise above normal to compensate for the low red cell count. During this period the subject feels thirsty and takes a lot of water. This is a great help for restoring blood volume.
Plasma proteins are replenished in two stages:
(a) The stored proteins (labile protein) are mobilised within a few hours from the tissues and organs, chiefly liver, and
(b) They are also actively manufactured by the liver. During this regeneration, a sequence is seen—at first the fibrinogen, then the globulin and lastly the albumin is regenerated. Provided the blood is adequate, the lost plasma proteins are fully restored in a few days.
iii. Red Cells:
Red cells are rapidly manufactured by the red marrow after a few days. Anoxia stimulates the marrow. Full restoration of the red cells and haemoglobin requires 3 to 5 weeks-time, if the diet is adequate.
iv. Clinical Aids:
The best remedy lies in whole blood transfusion, because it fully supplies all the materials lost. Plasma transfusion comes next. Dried plasma can be preserved and may be used after suitable dilution.
Summary of Compensatory Reactions in Haemorrhage:
(c) Increased secretion of epinephrine, norepinephrine, vasopressin, aldosterone arid glucocorticoids,
(d) Rapid rate of thoracic pumping and of skeletal muscular pumping (occasionally),
(e) Increased flow of interstitial fluid in the capillaries,
(f) Secretion of erythropoietin,
(g) Increased plasma protein synthesis, and