By
Dr.M.Anand, MD, DNB
Def
 Shock : a state of circulatory failure that impairs tissue
perfusion & leads to tissue hypoxia
3rd International Consensus Definitions
for Sepsis & Septic Shock (2016)
 Sepsis : Life threatening organ dysfunction due to
dysregulated host response to infection
 Septic shock : A subset of sepsis – circulatory, cellular
& metabolic abnormalities are a/w a greater risk of
abnormality than sepsis alone
 Systemic Inflammatory Response Syndrome (SIRS):
sepsis like condition a/w systemic inflammation,
which may be triggered by a variety of non microbial
insults e.g Burns, trauma &/or pancreatitis
 Pathogenic feature common to Septic shock & SIRS :
Massive outpouring of inflamm mediators
 Result in arterial vasodilation, vascular leakage &
venous blood pooling
 Chimeric Antigen Receptor T cell therapy (CART): a
similar iatrogenic syndrome observed in cancer
patients--- Cytokine Release Syndrome
 Neurogenic shock : Loss of vascular tone – may occur
following spinal cord injury
 Anaphylactic shock : IgE mediated Hypersensitivity
reactions triggers vascular dilation & vascular
permeability
Pathogenesis
 Progressive disorder leading to death if underlying cause is
not corrected
 3 stages of shock, which are best seen in hypovolumeic
shock
1. Initial Non progressive stage : Reflex compensatory
mechanisms are activated & vital organ perfusion is
maintained
2. Progressive stage : tissue hypoperfusion occurs with
worsening circulatory & metabolic derangements
3. Irreversible stage : Severe tissue & cellular injury which
cannot be reversed by hemodynamic correction & lead to
fatality
 Non progressive phase : Neural & hormonal loops maintain
cardiac output & BP
 By increasing heart rate, constricting arterioles & reducing urine
output
 Coronary & cerebral vessels : less sensitive to sympathetic signals
 Maintain relatively normal calibre, blood flow & oxygen delivery
 Blood from peripheral circulation shunted to vital organs
 Progressive phase : widespread tissue hypoxia
 Persistent O2 deficit : Anaerobic resp instead of
aerobic – Lactic acidosis
 Lowered tissue pH – lowered vasomotor response –
Arterioles dilate & blood pools in microcirculation
 Lower BP & make endothelial cells @ risk for anoxic
injury
 Endothelial injury – tissue edema & DIC
 Progress to myocardial dysfn due to NO synthesis
 Progress to renal failure due to renal ischemia
Severe cellular and
tissue injury
Leakage of lysosomal
enzymes,
Myocardial contractile
function worsens-(Nitric
oxide synthesis)
Superimposed
bacteraemia shock.
Ischemic intestine allows
microbes-
Acute tubular necrosis.
DEATH
Morphology
 Fibrin thrombi all over the body, esp kidney
 Lungs resistant to hypoxic injury – but trauma & sepsis
leads to diffuse alveolar damage & ARDS
Pathophysiology of Cardiogenic
Shock
Pathophysiology of Hypovolemic
Shock
Copyright © 2010, 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
Pathophysiology of
Neurogenic Shock