Difference between revisions of "Shock"
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** Histologically, the tubular epithelial cells die and fall into the lumen, the basement membranes rupture and irritant material escapes into the interstitium. | ** Histologically, the tubular epithelial cells die and fall into the lumen, the basement membranes rupture and irritant material escapes into the interstitium. | ||
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Revision as of 10:56, 20 August 2010
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What is Shock?
- "Shock" is a clinical term to describe a condition in which:
- The body temperature is subnormal.
- Reflexes are subnormal.
- Respiration is shallow.
- There is a rapid thready pulse.
Cause of Shock
- The cause of shock is circulatory failure.
- This leads to impaired perfusion of tissues, resulting in inadequate cellular oxygenation.
Types of Shock
Hypovolaemic shock
- This is caused by massive reduction in circulating blood volume.
- For example, due to loss in
- Severe haemorrhage.
- Extensive body burns.
- There is excessive loss of tissue fluid from the injured areas.
- For example, due to loss in
Trauma, pain and major surgery
- Trauma, pain and minor surgery affect the vasomotor control of the peripheral circulation.
- The capillaries become dilated and blood pools in the peripheral circulation.
- A secondary hypovolaemia occurs.
Endotoxic shock
- Endotoxic shock occurs in severe infections by Gram negative bacteria.
- The toxins produced by the bacteria are thought to induce clotting of the blood in very small vessels.
- The flow is blocked and blood pools in the peripheral tissues.
thereby blocking the flow and causing pooling of blood in the peripheral
- The condition is known as Disseminated Intravascular Coagulation.
Cardiogenic shock
- Cardiogenic shock occurs when a suddenly developing cardiac failure causes circulatory collapse, e.g.
- Myocardial infarction
- Severe arrhythmia
- Sudden failure of the valves.
Pathophysiology of Shock
- In haemorrhagic and burn shock, there is reflex vasoconstriction of the peripheral and splanchnic blood vessels.
- The body becomes starved of oxygen.
- There is no constriction of the cerebral or coronary blood vessels - this protects the brain and the heart.
- The fall in blood pressure stimulates the release of renin from the kidney.
- Angiotensin from the liver is activated.
- Causes an increase in blood pressure.
- Stimulates the adrenal cortex to secrete aldosterone, which causes the kidney to retain sodium and water.
- The flow of urine may cease.
- Angiotensin from the liver is activated.
- The kidney is particularly vulnerable to shock.
- If the condition is prolonged, acute tubular necrosis will develop.
- After a sustained period of oxygen deficit, the vasomotor control over the blood vessels is lost.
- Blood becomes pooled in the capillary beds.
- This state is termed "irreversible shock" and is quickly followed by death.
Post-Mortem Findings
- Post-mortem findings are non-specific.
- The lungs are wet and heavy, showing congestion and oedema.
- The alveolar capillaries are distended with blood.
- The alveoli are filled with haemorrhage and oedema fluid.
- A degree of atelectasis (collapse) also develops.
- In the intestine, the blood vessels are congested and there is patchy haemorrhage of the mucosa due to localised anoxia.
- There is also a considerable amount of blood stained fluid within the lumen.
- May be mistaken for inflammation.
- There is also a considerable amount of blood stained fluid within the lumen.
- The kidneys cortex appears pale due to tubular necrosis, while the medulla is darkened by congestion.
- Histologically, the tubular epithelial cells die and fall into the lumen, the basement membranes rupture and irritant material escapes into the interstitium.