Difference between revisions of "Shock"

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==What is Shock?==
 
==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.
 
−
* Tissue perfusion is decreased.
 
  
−
==Causes of 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.
  
−
The cause of the clinical signs of shock is circulatory failure, which results in impaired perfusion of tissues and inadequate cellular oxygenation. There are several different circumstances that might lead to the development of shock, such as:
+
==Cause of Shock==
  
−
===Hypovolaemia===
+
* The cause of shock is circulatory failure.
−
This is caused by massive reduction in circulating blood volume; for example due to loss in  
+
** This leads to impaired perfusion of tissues, resulting in inadequate cellular oxygenation.
−
severe haemorrhage or extensive body burns where there is excessive loss of tissue fluid from the injured area.
 
  
−
===Trauma, pain and major surgery===
+
==Types of Shock==  
−
These factors can affect the vasomotor control of the peripheral circulation; the capillaries become dilated and blood pools in the peripheral circulation. A secondary hypovolaemia then occurs.
 
  
−
===Endotoxaemia===
+
===Hypovolaemic shock===
−
Endotoxaemia can occur in severe infections by Gram negative bacteria. The toxins produced by the bacteria are thought to induce blood clotting in very small vessels, occluding blood flow and resulting in blood pools in the peripheral tissues. Endotoxaemia is a risk factor for the development of [[Disseminated Intravascular Coagulation|disseminated intravascular coagulation (DIC)]].
 
  
−
===Cardiac disruption===
+
* This is caused by massive reduction in circulating blood volume.
−
Acute cardiac malfunction such as myocardial infarction, severe arrhythmias or sudden failure of the valves can cause circulatory collapse.
+
** For example, due to loss in
 +
*** Severe haemorrhage.
 +
*** Extensive body burns.
 +
**** There is excessive loss of tissue fluid from the injured areas.
  
−
==Pathophysiology of Shock==
+
===Trauma, pain and major surgery===
−
In shock caused by haemorrhage or burns, there is reflex vasoconstriction of the peripheral and splanchnic blood vessels. The body becomes starved of oxygen but 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; consequently angiotensin from the liver is activated which causes an increase in blood pressure. This in turn stimulates the adrenal cortex to secrete aldosterone, which causes the kidney to retain sodium and water.
 
  
−
The kidney is particularly vulnerable to shock; the flow of urine may cease and if the condition is prolonged, acute tubular necrosis can develop.
+
* 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.
  
−
* After a sustained period of oxygen deficit, the vasomotor control over the blood vessels is lost. Blood becomes pooled in the capillary beds and this state is termed "irreversible shock" which is rapidly fatal.
+
===Endotoxic shock===
  
−
==Treatment of Shock==
+
* Endotoxic shock occurs in severe infections by Gram negative bacteria.
−
The aim of treatment is to recover full circulatory function and thus increase tissue perfusion to normal levels. The mainstay of treatment is [[Principles of Fluid Therapy|fluid therapy]] to increase circulatory volume and drug therapy as required to counteract the predisposing cause of the condition. Oxygen therapy will be required if signs of hypoxia are present.
+
* The toxins produced by the bacteria are thought to induce clotting of the blood in very small vessels.
−
Drug therapies may include antiprostaglandins, [[Antibiotics|antibiotics]], sympathomimetics, antiarrhythmics, vasodilators, bicarbonate and glucose, as indicated by the underlying cause and the diagnostic lab work. [[Steroids|Glucocorticosteriods]] are contra-indicated unless a specific deficiency is noted i.e [[Hypoadrenocorticism|hypoadrenocorticism]].
+
** 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|Disseminated Intravascular Coagulation]].
  
−
==Post-Mortem Findings==
+
===Cardiogenic shock===
−
Post-mortem findings are non-specific for shock, and include:
 
−
* The lungs are wet and heavy, showing congestion and oedema. A degree of atelectasis (collapse) also develops. The alveolar capillaries are distended with blood and the alveoli are filled with haemorrhage and oedematous fluid.
 
−
* 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 which can be mistaken for inflammation.
 
−
* 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.
 
  
−
{{Learning
+
* Cardiogenic shock occurs when a suddenly developing cardiac failure causes circulatory collapse, e.g.
−
|full text = [http://www.cabi.org/cabdirect/FullTextPDF/2009/20093135269.pdf ''' Nursing management of the hypovolemic shock patient.''' Davis, H.; The North American Veterinary Conference, Gainesville, USA, Veterinary technicians. Proceedings of the North American Veterinary Conference, Orlando, Florida, USA, 17-21 January, 2009, 2009, pp 19-22]
+
** Myocardial infarction
−
}}
+
** Severe arrhythmia
 +
** Sudden failure of the valves.
  
−
{{Chapter}}
+
==Pathophysiology of Shock==
−
{{Mansonchapter
 
−
|chapterlink = http://www.mansonpublishing.co.uk/book-images/9781840760811_sample.pdf
 
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|chaptername = Recognizing shock and its laboratory signs
 
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|book = Equine Pediatric Medicine
 
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|author = William Bernard, Bonnie S. Barr
 
−
|isbn =9781840760811
 
−
}}
 
  
 +
* 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.
 +
* 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.
 +
* 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.
  
 
[[Category:WikiBlood]]
 
[[Category:WikiBlood]]
−
[[Category:Cardiovascular System - Pathology]]
 
−
[[Category:Cardiology Section]]
 

Revision as of 12:37, 10 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.

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

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.
  • 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.
  • 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.
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