Page 126 - Textbook of Pathology, 6th Edition

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SECTION I

Figure 5.15 Pathogenesis of circulatory shock.

General Pathology and Basic Techniques
After these general comments on mechanisms in shock, PATHOGENESIS OF SEPTIC SHOCK. Septic shock results
features specific to pathogenesis of three main forms of shock most often from Gram-negative bacteria entering the body
are given below: from genitourinary tract, alimentary tract, respiratory tract
or skin, and less often from Gram-positive bacteria. In septic
PATHOGENESIS OF HYPOVOLAEMIC SHOCK. Hypo- shock, there is immune system activation and severe systemic
volaemic shock occurs from inadequate circulating blood inflammatory response to infection as follows:
volume due to various causes. The major effects of
hypovolaemic shock are due to decreased cardiac output and i) Activation of macrophage-monocytes. Lysis of Gram-
low intracardiac pressure. The severity of clinical features negative bacteria releases endotoxin, a lipopolysaccharide,
depends upon degree of blood volume lost, haemorrhagic into circulation where it binds to lipopolysaccharide-binding
shock is divided into 4 types: protein (LBP). The complex of LPS-LBP binds to CD14
molecule on the surface of the monocyte/macrophages which
< 1000 ml: Compensated are stimulated to elaborate cytokines, the most important
1000-1500 ml: Mild ones being TNF-α and IL-1. The effects of these cytokines
1500-2000 ml: Moderate are as under:
>2000 ml: Severe a) By altering endothelial cell adhesiveness: This results in
Accordingly, clinical features are increased heart rate recruitment of more neutrophils which liberate free radicals
(tachycardia), low blood pressure (hypotension), low urinary that cause vascular injury.
output (oliguria to anuria) and alteration in mental state b) Promoting nitric oxide synthase: This stimulates increased
(agitated to confused to lethargic). synthesis of nitric oxide which is responsible for
vasodilatation and hypotension.
PATHOGENESIS OF CARDIOGENIC SHOCK. Cardio- ii) Activation of other inflammatory responses. Microbial
genic shock results from a severe left ventricular dysfunction infection activates other inflammatory cascades which have
from various causes. The resultant decreased cardiac output profound effects in triggering septic shock. These are as
has its effects in the form of decreased tissue perfusion and under:
movement of fluid from pulmonary vascular bed into a) Activation of complement pathway: End-products C5a and
pulmonary interstitial space initially (interstitial pulmonary C3a induce microemboli and endothelial damage.
oedema) and later into alveolar spaces (alveolar pulmonary b) Activation of mast cells: Histamine is released which
oedema). increases capillary permeability.