State of inadequate perfusion to the vital organs of the body
Initially Hypoxic & Metabolic effects of Hypoperfusion cause Reversible cellular injury, persistence of shock eventually causes Irreversible cellular injury and can result in death of pt.
Hypovolemic shock: hemmorhage, fluid loss from fistula, burn, diarrhea
Cardiogenic shock: arrythmia, heart failure, infarction, cardiomyopathy, valvular stenosis and regurgitation, cardiac temponade; Failure of myocardial pump owing to intrinsic myocardial damage, extrinsic pressure, or obstruction to outflow
Distributive shock due to decreased peripheral vascular resistance and peripheral pooling:
Septic shock: Systemic Microbial Infection. Mostly Gram -ve Infection/Sepsis (Endotoxic Shock).
But, can occur with Gram +ve and Fungal infections; endothelial activation/injury; leukocyteinduced damage; disseminated intravascular coagulation; activation of cytokine cascades
Anaphylactic shock - Initiated by generalized IgE-mediated hypersensitivity response
Neurogenic shock: eg anesthetic, spinal cord transection, trauma, emotional stress
Endotoxins are bacterial wall lipopolysaccharides (LPS). All the hemodynamic effects of septic shock can be produced by injection of LPS alone.
LPS - LPS binding protein – CD14 receptor – TLR-4 - activates Monocytes, Macrophages, neutrophils which by production of TNF & IL-1, induce production of other Cytokines from endothelial cells (cytokine cascade) , which
Systemic vasodilation (Hypotension), Diminished Myocardial contractility, Widespread endothelial injury, Activation of coagulation system culminating in DIC.
SIRS( systemic inflammatory response syndrome)
Pulse greater than 90 beats per minute
Body temperature less than 36 or greater than 38°C
RR greater than 20 breaths per minute or, PaCO2 less than 4.3 kPa (32 mm Hg)
WBC count less than 4000 cells/mm³ or greater than 12000 cells/mm³ or the presence of greater than 10% immature neutrophils( left shift)
SIRS+ infection = sepsis
Sepsis + DBP less than 60 mmHG= septic shock
Neurohumoral mechanisms help maintain CO & BP. These are: Baroreceptor reflexes, Catecholamines, RAAS/ADH.
This results in Tachycardia, Peripheral vasoconstriction, Renal conservation of fluid. Skin vasoconstriction causes coolness and pallor of skin.
(In Septic shock the due to vasodilation skin may feel warm and flushed).
Coronary & Cerebral vessels are less responsive to above mechanisms and hence maintain their blood flow.
In this stage there is widespread HYPOXIA leading to Anaerobic glycolysis with excessive production of lactic acid.. Lactic Acidosis lowers pH and blunts the above Vasomotor Response.—so, the arterioles dilate and blood begins to pool in microcirculation. This reduces CO. Also, exposes endothelial cells to injury and subsequent development of DIC.
Hypoxia to Brain makes pt. Confused, and to kidney causes decline in UO
Failure of Multiple Organs eg. Brain, heart, kidneys, lungs, adrenals, GIT, liver.
Lysosomal enzyme leakage from widespread cell injury further aggravating shock with
Ischemic injury of bowel mucosa causes bacterial transmigration
ATN may lead to complete renal shutdown
MODS: multiorgan dysfunction syndrome
with almost inevitable death.
BRAIN: Changes of ischemic encephalopathy
Heart: sub-endocardial ischaemia, Coagulation necrosis, contraction band necrosis
Lungs: ARDS aka shock lung or non cardiogenic pulmonary edema
GI: mucosal necrosis, hemorrhagic enteropathy
Liver: fatty change, hemorrhagic necrosis.