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Types of circulatory shocks

Four different types of shocks:

Cardiogenic shock resulting from heart


abnormalities.

Circulatory Shock Hypovolumic shock.

Neurogenic shock resulting from sudden loss of


vasomotor tone.

Septic shock due to systemic bacterial infection

Physiology 2008 Anaphylactic shock due to powerful allergic


reaction.

Physiological causes of shock Cardiac output and blood pressure changes


during shock
1. Decrease cardiac output due to:
In most type of shock, the arterial blood pressure
Cardiac abnormalities that decrease the ability of
decreases at the same time the cardiac output
the heart to pump blood; myocardial infarction;
toxic state of the heart; severe heart valve decreases, but not as much.
dysfunction; arrhythmias.
Factors that decrease venous return; decreased
blood volume; decreased vascular tone;
obstruction of blood flow.
2. Abnormal tissue perfusion patterns.
3. Excessive metabolism of the body

Stages of shock 1. Hypovolumic shock


1. Non progressive stage or compensated stage. At
Hemorrhage leads to hypovolemia. Thus,
this stage, normal compensatory mechanisms
cause full recovery. the filling pressure of the circulation
2. Progressive stage. The shock becomes steadily
decreases, venous return decreases and
worth until death. Inadequate blood flow causes cardiac output falls below normal. Shock
the circulatory system to deteriorate which leads ensues.
to more decrease in cardiac output. It is a vicious
circle leading to death.
The amount of blood loss dictates the
3. Irreversible stage. The shock has progress to
degree of fall in cardiac output.
such an extent that therapy is ineffective.

positive feedback to decrease CO > tissue necrosis

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Compensatory mechanisms
Compensatory mechanisms
Sympathetic reflex activation initiated by the
baroreceptors and the low pressure vascular
When blood volume decreases,
stretch receptors. peripheral chemoreceptors
compensatory mechanisms are activated
to restore adequate circulation: CNS ischemic response.
Reverse stress-relaxation of the circulatory
system.
In compensated shock these mechanisms
are efficient to restore circulation back to Formation of vasopresin. ADH
normal Compensatory mechanisms to return blood
volume to normal (increase water
reabsorbtion for example).

Progressive / irreversible shock Positive feedbacks


Once shock has become severe enough,
Cardiac depression: BP decrease enough to decrease
various positive feedback develop causing coronary blood flow below required values for myocardium
a vicious circle of progressively decreasing metabolism. This depresses the heart further.
cardiac output. Vasomotor failure: Reduced blood flow to the vasomotor
center. Further loss in blood flow.
All these result in tissue necrosis Blockade of minute vessels due to clotting. Further loss in
decreased nutritional supply to tissue blood flow to key organs.
Increased capillary permeability. Loss of blood volume
Release of toxin by ischemic tissues.
Endotoxin. From dead bacteria in the intestine.
Acidosis. Due to metabolic derangements resulting from
inadequate blood supply to tissue cells.
General cellular deterioration.

2. Neurogenic shock

There is no blood loss, but the vascular


capacity increases so much due to loss of
vasomotor tone, that the normal amount of
blood can not fill the circulatory system.
The major causes are:
Deep general anesthesia
Spinal anesthesia
Brain damage

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3. Septic shock Septic shock:
A significant healthcare challenge

Septic shock is sepsis with hypotension


More than 750,000 sepsis cases/year in
despite fluid resuscitation.
the USA.
20 to 50% develop into septic shock.
Perfusion abnormalities main cause of organ failure
Mortality rate is 40 to 60%.

Multiple organ failure death.


Septic shock is the most common form
of shock in hospital setting

Septic shock: A complex disease Cardiovascular failure in hypo-dynamic phase


of septic shock
Irritability Hypotension Secondary mediators
Confusion Vascular hyporeactivity
Coma Myocardial depression Myocardial
Depression
Tachypnea Primary mediators
Hypoxaemia
Oliguria Vasodilatation
Acute renal failure (TNF-, IL-1, IL-6,
ARDS
IL-8, IFN- )
Coagulation Cardiovascular Failure
Jaundice
Anti-coagulation
Enzymes Fibrinolysis Endothelial cell
DIC Macrophage
Gram-negative
ARDS: adult respiratory distress syndrome Neutrophil Endotoxin bacteria
DIC: disseminated intravascular coagulation

large production of inflammatory receptors

4. Anaphylactic shock
Anaphylaxis is an allergic condition in which the cardiac
output and arterial pressure fall drastically.
Antigen-antibody reaction causes basophils and mast cells
to release histamine.
Histamine causes increase in vascular capacity because
of vasodilation. histamine increases the permeability of the capillaries
Dilation of arterioles and thus decrease in arterial
pressure.
Increase capillary permeability with rapid loss of fluid and
protein into the tissue space (edema).

The net effect is a large reduction in venous return and


often the shock is so severe that the person dies
within minutes.

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