Page 127 - Textbook of Pathology, 6th Edition

hyperdynamic circulation in septic shock, in contrast to 111
hypovolaemic and cardiogenic shock. Increased vascular
permeability causes development of inflammatory oedema.
Disseminated intravascular coagulation (DIC) is prone to
develop in septic shock due to endothelial cell injury by
toxins. Reduced blood flow produces hypotension,
inadequate perfusion of cells and tissues, finally leading to CHAPTER 5
organ dysfunction.

Pathophysiology (Stages of Shock)
Although deterioration of the circulation in shock is a
progressive and continuous phenomenon and compensatory
mechanisms become progressively less effective, historically
shock has been divided arbitrarily into 3 stages (Fig. 5.17):
1. Compensated (non-progressive, initial, reversible) shock.
2. Progressive decompensated shock.
3. Irreversible decompensated shock.

COMPENSATED (NON-PROGRESSIVE, INITIAL,
REVERSIBLE) SHOCK. In the early stage of shock, an
attempt is made to maintain adequate cerebral and coro-
nary blood supply by redistribution of blood so that the
vital organs (brain and heart) are adequately perfused and Derangements of Homeostasis and Haemodynamics
oxygenated. This is achieved by activation of various neuro-
hormonal mechanisms causing widespread vasoconstriction
and by fluid conservation by the kidney. If the condition that
caused the shock is adequately treated, the compensatory
mechanism may be able to bring about recovery and re-
establish the normal circulation; this is called compensated
Figure 5.16 Response of inflammatory mediators in shock.
or reversible shock. These compensatory mechanisms are
as under:
c) Activation of coagulation system: Enhances development of i) Widespread vasoconstriction. In response to reduced
thrombi. blood flow (hypotension) and tissue anoxia, the neural and
d) Activation of kinin system: Released bradykinin cause humoral factors (e.g. baroreceptors, chemoreceptors,
vasodilatation and increased capillary permeability. catecholamines, renin, and angiotensin-II) are activated. All
The net result of above mechanisms is vasodilatation and these bring about vasoconstriction, particularly in the vessels
increased vascular permeability in septic shock. Profound of the skin and abdominal viscera. Widespread vasoconstric-
peripheral vasodilatation and pooling of blood causes tion is a protective mechanism as it causes increased

Figure 5.17 Mechanisms and effects of three stages of shock.