Shock natural history, complications and prognosis: Difference between revisions
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==Natural History | |||
= | ==Natural History== | ||
[[Image:Shock-cell2.PNG|500px|thumb|left|Effects of inadequate perfusion on cell function.]] | |||
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| [[Image:Shock-cell2.PNG|500px|thumb|left|Effects of inadequate perfusion on cell function.]] | |||
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There are four stages of shock, although shock is a complex and continuous condition and there is no sudden transition from one stage to the next.<ref name="Armstrong">{{cite book|last=Armstrong|first=D.J.|date=2004|title=Shock|location=In: Alexander, M.F., Fawcett, J.N., Runciman, P.J. ''Nursing Practice. Hospital and Home. The Adult.''(2nd edition)|publisher=Edinburgh: Churchill Livingstone}}</ref> | There are four stages of shock, although shock is a complex and continuous condition and there is no sudden transition from one stage to the next.<ref name="Armstrong">{{cite book|last=Armstrong|first=D.J.|date=2004|title=Shock|location=In: Alexander, M.F., Fawcett, J.N., Runciman, P.J. ''Nursing Practice. Hospital and Home. The Adult.''(2nd edition)|publisher=Edinburgh: Churchill Livingstone}}</ref> | ||
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; Initial : During this stage, the hypoperfusional state causes [[Hypoxia (medical)|hypoxia]], leading to the [[mitochondria]] being unable to produce [[adenosine triphosphate]] (ATP). Due to this lack of oxygen, the [[cell membranes]] become damaged, they become leaky to extra-cellular fluid, and the cells perform [[anaerobic respiration]]. This causes a build-up of [[lactic acid|lactic]] and [[pyruvic acid]] which results in systemic [[metabolic acidosis]]. The process of removing these compounds from the cells by the [[liver]] requires oxygen, which is absent. | ; Initial : During this stage, the hypoperfusional state causes [[Hypoxia (medical)|hypoxia]], leading to the [[mitochondria]] being unable to produce [[adenosine triphosphate]] (ATP). Due to this lack of oxygen, the [[cell membranes]] become damaged, they become leaky to extra-cellular fluid, and the cells perform [[anaerobic respiration]]. This causes a build-up of [[lactic acid|lactic]] and [[pyruvic acid]] which results in systemic [[metabolic acidosis]]. The process of removing these compounds from the cells by the [[liver]] requires oxygen, which is absent. | ||
; Compensatory (Compensating) : This stage is | ; Compensatory (Compensating) : This stage is characterized by the body employing physiological mechanisms, including neural, hormonal and bio-chemical mechanisms in an attempt to reverse the condition. As a result of the [[acidosis]], the person will begin to [[hyperventilate]] in order to rid the body of carbon dioxide (CO<sub>2</sub>). CO<sub>2</sub> indirectly acts to acidify the blood and by removing it the body is attempting to raise the pH of the blood. The [[baroreceptors]] in the [[artery|arteries]] detect the resulting [[hypotension]], and cause the release of [[adrenaline]] and [[noradrenaline]]. Noradrenaline causes predominately [[vasoconstriction]] with a mild increase in [[heart rate]], whereas [[adrenaline]] predominately causes an increase in [[heart rate]] with a small effect on the [[Blood vessel|vascular]] tone; the combined effect results in an increase in [[blood pressure]]. [[Renin]]-[[angiotensin]] axis is activated and [[arginine vasopressin]] is released to conserve fluid via the kidneys. Also, these hormones cause the vasoconstriction of the [[kidneys]], [[gastrointestinal tract]], and other organs to divert blood to the heart, [[lungs]] and [[brain]]. The lack of blood to the [[renal]] system causes the characteristic low [[urine]] production. However the effects of the [[Renin]]-[[angiotensin]] axis take time and are of little importance to the immediate [[homeostatic]] mediation of shock. | ||
; Progressive (Decompensating) : Should the cause of the crisis not be successfully treated, the shock will proceed to the progressive stage and the compensatory mechanisms begin to fail. Due to the decreased perfusion of the cells, [[sodium]] ions build up within while [[potassium]] ions leak out. As anaerobic metabolism continues, increasing the body's metabolic acidosis, the arteriolar and precapillary [[sphincters]] constrict such that blood remains in the [[capillaries]]. Due to this, the hydrostatic pressure will increase and, combined with [[histamine]] release, this will lead to leakage of fluid and [[protein]] into the surrounding tissues. As this fluid is lost, the blood concentration and [[viscosity]] increase, causing sludging of the micro-circulation. The prolonged vasoconstriction will also cause the vital organs to be compromised due to reduced perfusion. | ; Progressive (Decompensating) : Should the cause of the crisis not be successfully treated, the shock will proceed to the progressive stage and the compensatory mechanisms begin to fail. Due to the decreased perfusion of the cells, [[sodium]] ions build up within while [[potassium]] ions leak out. As anaerobic metabolism continues, increasing the body's metabolic acidosis, the arteriolar and precapillary [[sphincters]] constrict such that blood remains in the [[capillaries]]. Due to this, the hydrostatic pressure will increase and, combined with [[histamine]] release, this will lead to leakage of fluid and [[protein]] into the surrounding tissues. As this fluid is lost, the blood concentration and [[viscosity]] increase, causing sludging of the micro-circulation. The prolonged vasoconstriction will also cause the vital organs to be compromised due to reduced perfusion. | ||
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; Refractory : At this stage, the vital organs have failed and the shock can no longer be reversed. [[Brain damage]] and cell death have occurred. Death will occur imminently. | ; Refractory : At this stage, the vital organs have failed and the shock can no longer be reversed. [[Brain damage]] and cell death have occurred. Death will occur imminently. | ||
==Prognosis== | |||
The prognosis of shock depends on the underlying cause and the nature and extent of concurrent problems. Hypovolemic, anaphylactic and neurogenic shock are readily treatable and respond well to medical therapy. Septic shock however, is a grave condition and with a mortality rate between 30% and 50%. The prognosis of cardiogenic shock is even worse. | The prognosis of shock depends on the underlying cause and the nature and extent of concurrent problems. Hypovolemic, anaphylactic and neurogenic shock are readily treatable and respond well to medical therapy. Septic shock however, is a grave condition and with a mortality rate between 30% and 50%. The prognosis of cardiogenic shock is even worse. | ||
Shock is said to evolve from reversible to irreversible in experimental hemorrhagic shock involving certain animal species (dogs, rats, mice) that develop intense vasoconstriction of the gut. Death is due to hemorrhagic necrosis of the intestinal lining when shed blood in | Shock is said to evolve from reversible to irreversible in experimental hemorrhagic shock involving certain animal species (dogs, rats, mice) that develop intense vasoconstriction of the gut. Death is due to hemorrhagic necrosis of the intestinal lining when shed blood in re-infused. In pigs and humans 1) this is not seen and cessation of bleeding and restoration of blood volume is usually very effective; however 2) prolonged hypovolemia and hypotension does carry a risk of respiratory and then cardiac arrest. Perfusion of the brain may be the greatest danger during shock. Therefore urgent treatment (cessation of bleeding, rapid restoration of circulating blood volume and ready respiratory support) is essential for a good prognosis in [[hypovolemic shock]]. | ||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
[[Category:Medical emergencies]] | [[Category:Medical emergencies]] | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Natural History
 |
There are four stages of shock, although shock is a complex and continuous condition and there is no sudden transition from one stage to the next.[1]
- Initial
- During this stage, the hypoperfusional state causes hypoxia, leading to the mitochondria being unable to produce adenosine triphosphate (ATP). Due to this lack of oxygen, the cell membranes become damaged, they become leaky to extra-cellular fluid, and the cells perform anaerobic respiration. This causes a build-up of lactic and pyruvic acid which results in systemic metabolic acidosis. The process of removing these compounds from the cells by the liver requires oxygen, which is absent.
- Compensatory (Compensating)
- This stage is characterized by the body employing physiological mechanisms, including neural, hormonal and bio-chemical mechanisms in an attempt to reverse the condition. As a result of the acidosis, the person will begin to hyperventilate in order to rid the body of carbon dioxide (CO2). CO2 indirectly acts to acidify the blood and by removing it the body is attempting to raise the pH of the blood. The baroreceptors in the arteries detect the resulting hypotension, and cause the release of adrenaline and noradrenaline. Noradrenaline causes predominately vasoconstriction with a mild increase in heart rate, whereas adrenaline predominately causes an increase in heart rate with a small effect on the vascular tone; the combined effect results in an increase in blood pressure. Renin-angiotensin axis is activated and arginine vasopressin is released to conserve fluid via the kidneys. Also, these hormones cause the vasoconstriction of the kidneys, gastrointestinal tract, and other organs to divert blood to the heart, lungs and brain. The lack of blood to the renal system causes the characteristic low urine production. However the effects of the Renin-angiotensin axis take time and are of little importance to the immediate homeostatic mediation of shock.
- Progressive (Decompensating)
- Should the cause of the crisis not be successfully treated, the shock will proceed to the progressive stage and the compensatory mechanisms begin to fail. Due to the decreased perfusion of the cells, sodium ions build up within while potassium ions leak out. As anaerobic metabolism continues, increasing the body's metabolic acidosis, the arteriolar and precapillary sphincters constrict such that blood remains in the capillaries. Due to this, the hydrostatic pressure will increase and, combined with histamine release, this will lead to leakage of fluid and protein into the surrounding tissues. As this fluid is lost, the blood concentration and viscosity increase, causing sludging of the micro-circulation. The prolonged vasoconstriction will also cause the vital organs to be compromised due to reduced perfusion.
- Refractory
- At this stage, the vital organs have failed and the shock can no longer be reversed. Brain damage and cell death have occurred. Death will occur imminently.
Prognosis
The prognosis of shock depends on the underlying cause and the nature and extent of concurrent problems. Hypovolemic, anaphylactic and neurogenic shock are readily treatable and respond well to medical therapy. Septic shock however, is a grave condition and with a mortality rate between 30% and 50%. The prognosis of cardiogenic shock is even worse.
Shock is said to evolve from reversible to irreversible in experimental hemorrhagic shock involving certain animal species (dogs, rats, mice) that develop intense vasoconstriction of the gut. Death is due to hemorrhagic necrosis of the intestinal lining when shed blood in re-infused. In pigs and humans 1) this is not seen and cessation of bleeding and restoration of blood volume is usually very effective; however 2) prolonged hypovolemia and hypotension does carry a risk of respiratory and then cardiac arrest. Perfusion of the brain may be the greatest danger during shock. Therefore urgent treatment (cessation of bleeding, rapid restoration of circulating blood volume and ready respiratory support) is essential for a good prognosis in hypovolemic shock.
References
- ↑ Armstrong, D.J. (2004). Shock. In: Alexander, M.F., Fawcett, J.N., Runciman, P.J. Nursing Practice. Hospital and Home. The Adult.(2nd edition): Edinburgh: Churchill Livingstone.