SHOCK INTERNAL EVENTS

7. PATH PHYSIOLOGY OF SHOCK

Hypo-perfusion, and O2 lack, are common to all types of shock
syndromes.
Shock syndromes, may vary in severity, from silent tissue hypoxia,
to multiple organ failure.
In cases of septic shock, hyper-dynamic circulatory state, is
accompanied by a high O2 debt, due to excessive O2 demand in the presence of infection resulting in hypoxia.

Any Impaired tissue perfusion, leads to low delivery of oxygen in
relation to tissue needs,this is the basic cause of shock state.
The precise role of hypoxia, in pathogenesis of shock, is not clear as yet.
With improved techniques, it is hoped this role will be better
understood. However the events that follow shock states are;

7.1 Acidosis

As the oxygen delivery is deficient to meet O2 demand of tissues,
anaerobic glycolysis (breakdown) starts.
In the absence of O2 pyruvate is converted to lactate, and two molecules of adenosine troposphere (ATP) are made available.
In cases of adequate O2 3 molecules of ATP are released per one molecule of glucose utilized.

As the O2 diminishes, lactate increases and pyruvate diminishes.
This high Lactate level has been correlated with survival in
studies where lactate concentration increase beyond O-2m mol per
liter.

The effects of metabolic acidosis are;
-bradycardia,
-vasodilatation,
-decreased cardiac output and
-ventricular fibrillation.

7.2 Circulatory Redistribution

As a result of hypoxia, the homeostatic response is to preserve
oxygen delivery, to heart and the brain.
This is achieved by diverting blood flow, from other organs (skin, GI tract).
This is achieved through vasoconstriction of skin and visceral
circulation.
The agents responsible for this vasoconstriction
are :

* Catecholamine
* Angiotensin-II
* Vasopressin
* Endothelin
* Thromboxane A2

The changes in microcirculation in redistribution of blood flow
leads to slowing of flow, high viscosity of blood and sludging,
leading to intravascular coagulation and occlusion of capillary
channels.

As a consequence, intestinal mucosal injury occurs, gut
permeabilty may increase, and enteric bacteria and toxins move
across the gut wall, and invade the circulation via lymphatics and
portal venous system.
This is known as bacterial translocation.
Thus, the end effect of vasoconstriction in gut circulation can
lead to ischaemia and irreveresable shock, SIRS and MODS.
Any questions be sent to drmmkapur@gmail.com
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