Patel, 34 yrs Mangalore, had a car accident. He lost two pints of blood. He walked to the hospital aided by passerbys. There
he was transfused with 2 bottles of blood & his superficial injuries treated. He subsequently developed Hepatitis C due
to transfusion and developed Liver Failure. He now lives Life hopelessly considering Liver Transplant.
CIRCULATORY SHOCK AND SEPTICEMIA
5% of patients admitted to Acute Care Unit develop Hospital
acquired infection including Urinary Tract Infection , Pneumonia , Bacteriaemia and wound infection.
A) Bacteria may enter blood during dental procedures or even during brushing. Unless there is a focus where they can multiply
like an abnormal valve, they are rapidly destroyed and circulatory failure does not always occur.
B) Septic state is not always caused by microorganisms. Since only 10% have positive blood cultures. Sepsis may be associated
with shock along hypovolumia, trauma , tissue necrosis causing a systemic inflammatory response syndrome.
C) If Septic shock occurs, infection causes systemic activation of leucocytes
and vascular endothelial cells and releases cytokines, complement and other mediators which cause beneficial inflammation
against the locally infected tissue. But only if there is dissemination of response it can produce widespread tissue damage.
Nitric oxide is synthesized and released from endothelial cells. It regulates perfusion, maintains vascular tone, kills bacteria
and inhibits platelet aggregation and cerebrial perfusion.
SYSTEMIC IMMUNE RESPONSE SYNDROME IN CIRCULATORY SHOCK ( ANY TYPE )
In the SIR's ,
progression to multiple organ failure only occurs in severe cases. Once it occurs , death is the usual outcome. The mediators
Local and general vasodilatation causing
fall in BP.
Damage to vascular endothelium of all the
organs allowing fluid to leak out from the capillaries to the interstitial spaces causing hypovolumia.
Similarly increased permeability of alveolar
capillaries cause pulmonary oedema (ARDS)
Myocardial depression and decrease in cardiac
Intravascular Coagulation due to haemoconcentration and hypovolumia, widespread clotting occors; all coltting factors
are used up and haemorrhage occurs.
COMPENSATORY MECHANISM IN SHOCK
The low periferal
resistance reflexly increases cardiacoutput and the hypoxia causes constriction of the pre capillary arterioles and less constriction
of the post capillary venules thus reducing capillary b pressure and encouraging
interstitial fluid to move into the intravascular compartment thus increasing blood volume and thus venous return and thus
cardiac output. 80% of Hypovolumic shock recover , whereas 75% of cardiogenic and septic shock die even with treatment.
Blood Volume is 6 litres. A
sudden loss of 1 litre can be managed by the body. A gradual loss of 3 litres over 24 hours can also be managed by the body.
After 2 litres of gradual blood loss, the BP remains unchanged. 3 litres of blood loss, the BP falls but the body is in a
state of compensated shock. A 4 litres gradual loss or a 2 litre sudden loss
is usually fatal even with treatment.. Arterial clotting is many (3-5) times more faster than venous clotting mechanisms.Severe
trauma to vessel wall clot forms in 15 secs, if minor trauma it takes2 minutes.
A) In dehydration , and hypovolumia, the body compensates by increasing the systolic
BP, heart rate, increased force of contraction ( increased PR ) and periferal vasoconstriction and by lowering urine
output and decreased venous capacitance ( decreased Venous Pooling i.e. increased venous return due to venoconstiction by
B) Mediators are released which maintain vascular tone and perfusion.
shock, mortality is more than 90% even with best management.
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