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DEPARTMENT OF PATHOPHYSIOLOGY
PREPARED BY
SARPONG KWADWO
ROLL NO. 913905004
PARTNERS
EVANS YAW PEPRAH
ERIC KOBBY ANKOMAH
MIRRIAM NAKAMBA NAWALE
ARIANE MAELLE FEUKENG
INSTRUCTOR
PROF. SHIMIN CHEN
CLASS
2014 INTERNATIONAL CLASS
DATE OF EXPERIMENT
2016/06/8
ABSTRACT
The main focus of this experiment is to observe the major changes and
compensatory mechanisms that occur during hemorrhagic shock. With
rabbit used as experimental model, blood was drawn from the rabbit and
the major changes during shock were seen. From increasing in the blood
pressure as a compensatory mechanism, cold temperature in the
periphery to blood pressure starting to decrease as more blood was drawn
from the circulatory system.
INTRODUCTION
Shock refers to a dangerous systemic pathologic process under the effect
of various drastic etiological factors characterized by acute circulatory
blood volume, inadequate tissue perfusion, cell damage and dysfunction of
multiple organs. Shock can occur with normal blood pressure and
hypotension can occur without shock. Shock can be classified into
hypovolemic, anaphylactic, neurogenic and obstructive shock. In this
experiment, using rabbit as a model, hypovolemic shock i.e. hemorrhagic,
was performed to observe the major changes that occur during shock.
MATERIALS AND METHODS
Animals
One rabbits
Trachea cannula
Stethoscope
Silk thread
Cotton thread
Cotton ball
Filter paper
100ml syringe
6 needles
50 ml beaker
Balance
Thermometer
1% procaine
3% pentobarbital sodium
PROCEDURES
Anterior neck skin was cut longitudinally to isolate the trachea and
right vena jugularis externa.
BEFORE
DRAWING
BLOOD
AFTER
DRAWING
BLOOD
(10MINS)
AFTER
RESETTING
BLOOD
PRESSURE
BLOOD PRESSURE
42.89mmHg
43.08mmHg
72.61mmHg
CVP
-2.5
-4
-0.5
HEART RATE
72 bpm
60 bpm
92 bpm
TEMPERATURE
38.4C
38C
37.6C
BREATHING RATE
76/min
57/mins
74/mins
DISCUSSION
From the table able above, stages of shock can be clearly seen. Just
before the blood was drawn, the blood pressure and other parameters
were normal. 10 minutes after the blood was drawn from the aorta, the
blood pressure increased, due to the activation of the sympathetic
nervous system, this increase the heart rate and constricts peripheral
arterioles to redistribute blood to the vital organs. Constriction of the
peripheral arterioles caused the fall in temperature in periphery. There
is also activation of renin angiotensin aldosterone system. This leads to
conversion of angiotensin I to angiotensin II, which is a strong
vasoconstrictor. This also helps in maintaining the blood pressure.
20 minutes later, there was further increase in the blood pressure but
the intravascular volume was decreased. The breathing rate was
increase compared to just after the blood was drawn from the aorta.
Decrease in perfusion leads to hypoxia, the endothelia cells produce NO
with dilates the vessels. Also less oxygen delivery cause decrease in
aerobic glycolysis, hence producing more lactic acid. The NO and the
lactic acid are strong vasodilators, causing stagnant hypoxia. As a result
of this blood is pulled to the periphery, decreasing venous return.
Pulling of blood can lead hypercoagulability.
After 35% of blood volume is drawn, the condition may progress to
refractory stage. This stage is mostly resistant to treatment, but can be
reversed. Blood begins to coagulate in the microcirculation, which can
cause DIC. Lactic acid accumulates around the cells, this destroys the
cell membrane. Decrease in aerobic glycolysis reduces the production
of ATPs, which is used to provide energy for Na-K, ATPases, hence
accumulation of Na in the cells. Na being highly osmotic draws water
into the cells causing the cells to burst.
At this stage, if there is not proper treatment, the shock can lead to
Multiple Organs Dysfunction, then death.
CONCLUSION
From the discussion it can be concluded that progressive decrease in
intravascular volume with immediate and effective treatment can cause
severe damage from cellular level to the organ level and can be fatal too
REFERENCE