CIRCULATORY SHOCK   AND SEPTICEMIA              

SEPTIC SHOCK

  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 cause

i)                     Local and general vasodilatation causing fall in BP.

ii)                   Damage to vascular endothelium of all the organs allowing fluid to leak out from the capillaries to the interstitial spaces causing hypovolumia.

iii)                  Similarly increased permeability of alveolar capillaries cause pulmonary oedema (ARDS)

iv)                  Myocardial depression and decrease in cardiac output .

v)                    Disseminated  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.

HAEMORRHAGE

 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.

HYPOVOLUMIA

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 Nor adrenaline)

B)      Mediators are released which maintain vascular tone and perfusion.

DECOMPENSATED SHOCK

In de-compensated shock, mortality is more than 90% even with best management.