Transcript Haemorrhage

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‫االسراء اية ‪58‬‬
‫‪Dr abdelaziz Hussein, Mansoura‬‬
‫‪Faculty of Medicine‬‬
By
Dr. Abdel Aziz M. Hussein
Lecturer of Medical Physiology
Member of American Society of Physiology
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine
◊ Def,
• It means loss of blood from the CVS.
◊ Types:
• i) According to Site of bleeding:
 External (revealed) e.g. bleeding from open
wound.
 Internal (concealed) e.g. intra-abdominal,
intrathoracic, intracranial....etc.
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Faculty of Medicine
◊ Types:
ii) According to the amount of blood loss:
Mild →loss of few cc.
Moderate → loss up to 20-30%.
Severe → loss more than 30%
Loos of less than 20% is compensated by physiological
mechanisms, while loss of more than 20% is aided by blood
transfusion
iii) According to the rate of blood loss:
Acute → sudden loss of blood.
Chronic → repeated bleeding over a long period of time e.g. from
piles, parasitic infestation.
•Acute blood loss of large amount of blood is more dangerous than
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chronic bleeding.
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◊ Types:
iv) According to Source:
• The rate of blood loss depends on the injured vessels, it
may be:
a. Arterial→ bleeding from injured artery.
b. Venous→ bleeding from injured vein.
c. Capillaries→ bleeding from eroded or burned skin
surface.
d. Sinusoidal→ As in uterine bleeding.
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Faculty of Medicine
◊ Manifestations of haemorrhage:
1.↓ed ABP.
2.The pulse is rapid, weak and feeble
3.Respiration is rapid, but the depth of
respiration is at first deep then shallow.
4.The cutaneous veins are collapsed and fill
slowly when compressed centrally.
5.The skin is pale, cold, moist, and slightly
cyanotic.
6.Oliguria.
7.Fainting may occur.
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine
• Haemorrhage has 2 effects;
Delayed
Immediate
CVS system
Plasma volume
Respiratory
Plasma proteins
Kidney
RBCs
Endocrine
Tissue repair
Skin
Blood
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Recanalization of
blood vessel
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1. Cardiac
acceleratio
n or ↑Heart
Rate
2. ↑ed
vasoconstri
ctor
discharge
Vasoconstri
ction
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3.
Contraction
of blood
reservoir
a. Cardiac acceleration:
◊ Causes: ↑ed heart rate may be due to;
1. ↓ed ABP, ↑es heart rate by Mary's law.
2. ↑ed adrenaline secretion stimulates SAN directly.
3. Hypoxia in haemorrhage stimulates CAC directly.
◊ Significance:
• It ↑es the diastolic BP and the mean systemic BP→
maintains the blood flow through the cerebral and
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coronary blood vessels.
• b. ↑ed vasoconstrictor discharges:
◊ Site of VC
• It causes generalized VC except in the cerebral and
coronary vessels.
o VC of the skin → cold & pale skin.
o VC of the kidney vessels→ oliguria or even anuria.
o Cerebral arterioles are not constricted because their
VC innervation is functionally insignificant.
o Coronary arteries Drare
dilated due to accumulated
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• b. ↑ed vasoconstrictor discharges:
◊ Causes of VC:
1. ↑ed secretion of epinephrine and norepinephrine.
2. ↓ed depressor impulses from the arterial baroreceptors.
3. ↓ed VR leads to reflex VC of the arterioles and venules
(Mc Dowal َs reflex).
4. ↑ed secretion of vasopressin.
5. Release of serotonin from platelets.
6. Renal ischemia leads finally to VC by angiotensin II.
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b. ↑ed vasoconstrictor discharges:
◊ Importance of VC:
• helps the VR and maintains the cardiac filling, COP and ABP.
c) Contraction of blood reservoirs:
◊ Importance:
• Blood reservoirs mainly spleen are contracted driving its
content of blood into the general circulation.
◊ Causes: it is due to:
1. ↑ed sympathetic activity.
2. ↑ed adrenalin secretion.
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1.
Pulmonary
V.C.
2. ↑ed Rate
of
Respiration
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3. Depth of
Respiration
a. Pulmonary VC:
• It helps in reduction of the circulatory
capacity and maintenance of blood volume.
b. ↑ed Respiratory rate: helps;
1. More oxygenation of blood.
2. ↑ing the VR.
◊ Causes of ↑ed rate of respiration:
1.Local accumulation of metabolites in the
central chemoreceptors and in the respiratory
center neurons → due to ↓ of blood flow
through them.
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Faculty of Medicine
◊ Causes of ↑ed rate of respiration:
2. ↓ed inhibitory impulses from the arterial baroreceptors
due to ↓ ABP.
3. Cerebral ischemia ++ the VMC center that activates
the resp. center.
c. Depth of respiration;
• It is variable; at first it becomes deep and later
shallow.
abdelaziz Hussein,
Mansoura its failure.
• Periodic respiration Droccurs
before
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1.
Coagulation of
blood
2. VC of the
injured
vessels
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3. Formation
of
erythropoietin,
Adrenaline,
and serotonin
• a. Coagulation of blood:
• It is an important protective mechanism in stopping
hemorrhage.
• The thromboplastin released by the injured tissues
start the clotting mechanism.
• b. VC of the injured vessels and the drop of
blood pressure→ help the blood clot to seal the vessels.
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• c. Formation of erythropoietin;
• It stimulates the production of RBCs by the bone marrow.
• d. Release of serotonin:
• It is released from disintegrated platelets causing VC of
the blood vessels.
• e. Adrenaline release:
• It helps formation of fibrinogen, prothrombin and factor V
in the liver, for blood coagulation
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Faculty of Medicine
1. ↓ed Urine
volume
2. Renal
Ischemia
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• a) ↓ed Urine volume:
• -It occurs 1st due to:
a. ↓ed ABP.
b. ↓ed blood volume and COP.
c. ↑ed ADH.
d. VC of the renal blood vessels.
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Faculty of Medicine
• b) Renal ischaemia:
• It develops later on, it leads to:
• i) Release of renin that finally leads to production of
angiotensin-II, which leads to;
• Powerful VC.
• Release of aldosterone→ causes retention of Na and H2O and
excretion of excess K which is toxic.
• ii)↓ed formation of urine, so reduces the amount of water loss.
• iii) Release of erythropoietin → stimulates the bone marrow to
produce RBCs.
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• ↑ed sympathetic discharge leads to:
1. VC of the capillaries → pale skin.
2. VC of the arterioles → cold skin.
3. Excessive sweating → cold sweat.
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1.
Catecholami
nes
2.
Angiotensin
II and
Aldosterone
3. ACTH and
Glucocorticoi
ds
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4.
Erythropoieti
n
5. ADH
a- Catecholamines (adrenaline and noradrenaline)
• Cause
1. VC of both arterioles and veins.
2. ↑ heart rate and stroke volume.
3. ++ of secretion of ACTH and glucocorticoids.
4. Help blood clotting by releasing fibrinogen and prothrombin from
liver and activating factor V.
5. Stimulate CNS, so patient becomes restlessness.
6.
VR is ↑ed due to ↑ed ms pumps.
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7. Contraction of the spleenFaculty of Medicine
a- Catecholamines (adrenaline and noradrenaline):
•Their secretion is ↑ed from adrenal medulla due to ↑ed
sympathetic discharge.
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b- Angiotensin II and Aldosterone
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• c. ADH:
• It is secreted from posterior pituitary gland by;
o Hypothalamic impulses.
o Reflexly from baroreceptors.
• It causes VC and ↑es water reabsorption from the renal tub
ABP is ↑ed to normal.
• d- Erythropoietin: mentioned before
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Faculty of Medicine
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine
• This is done by:
• a. Withdrawal of fluid from interstitial and
intracellular compartments into the blood.
• b. ↑ed water reabsorption from the distal
renal tubules by the aldosterone and ADH.
• c. Intake of external fluid caused by thirst
sensation as a result of tissue dehydration.
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Faculty of Medicine
• a. Rapid replacement from labile proteins in
the liver and other tissues (completed within one
hour).
• b. Slow mechanism by new synthesis;
• The normal concentration of plasma proteins is
reached within one week.
• A diet containing proteins of high biological
value accelerates the synthesis.
• Plasma proteins are important to maintain the
effective osmotic pressure.
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a- Rapid restoration of RBCs by splenic
contraction due to adrenaline release and
sympathetic stimulation.
b- Slow restoration of RBCs by the bone marrow.
• This takes 3-5 weeks and is stimulated by:
1. Hypoxia.
2. Erythropoietin hormone
3. Growth hormone
4. Thyroxin hormone
5. Good nutrition with proteins, vitamins (B, C, B12,
folic acid) and minerals (iron, cooper, cobalt).
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Faculty of Medicine
• To restore the integrity of the damaged
tissues.
• By removal of the clots inside the vessels by
plasminolysis.
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine
THANKS
Dr abdelaziz Hussein, Mansoura
Faculty of Medicine