Shock

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.

Types:

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

Septic shock

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

cause:

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

STAGES

[1]COMPENSATORY STAGE:

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.

[2]PROGRESSIVE STAGE:

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.

[3]IRREVERSIBLE STAGE:

Lysosomal enzyme leakage from widespread cell injury further aggravating shock with

myocardium dysfunction

Ischemic injury of bowel mucosa causes bacterial transmigration

ATN may lead to complete renal shutdown

ARDS

MODS: multiorgan dysfunction syndrome

with almost inevitable death.

MORPHOLOGY

BRAIN: Changes of ischemic encephalopathy

Heart: sub-endocardial ischaemia, Coagulation necrosis, contraction band necrosis

Kidney: ATN

Lungs: ARDS aka shock lung or non cardiogenic pulmonary edema

GI: mucosal necrosis, hemorrhagic enteropathy

Liver: fatty change, hemorrhagic necrosis.