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Good day, Today we are discussing about shock.

Table of content :

  • Definition of the term shock
  • The main physiological changes that occur during shock
  • The underlying pathophysiology of the main causes of shock.

Shock (circulatory failure) occurs when the metabolic needs of cells are not being met because of inadequate blood flow. In effect, there is a reduction in circulating blood volume, in blood pressure and in cardiac output. This causes tissue hypoxia, an inadequate supply of nutrients and the accumulation of waste products. A number of different types of shocks are described.

A diagram of shock
A diagram describing shock

Hypovolaemic shock

This occurs when the blood volume is reduced by 15-25%. Cardiac output may fall because of low blood volume and hence low venous return, as a result of different situations:

  • severe haemorrhage – whole blood is lost
  • extensive burns – serum is lost
  • severe vomiting and diarrhoea – water and electrolytes are lost.

Cardiogenic shock

This occurs in acute heart disease when damaged heart muscle cannot maintain an adequate cardiac output, e.g. in myocardial infarction.

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Septic shocks (bacteraemic, endotoxic)

This is caused by severe infections in which bacterial toxins are released into the circulation. These toxins trigger a massive inflammatory and immune response, and many powerful mediators are released. Because the response is not controlled, it can cause multiple organ damage, depression of myocardial contractility, poor tissue perfusion and tissue death (necrosis). Profound hypotension occurs because the inflammatory mediators cause profound vasodilation.

Neurogenic shock

The causes include sudden acute pain, severe emotional experience, spinal anaesthesia and spinal cord damage. These interfere with normal nervous control of blood vessel diameter, leading to hypertension.

Anaphylactic shock

Anaphylactic is a severe allergic response that may be triggered in sensitive individuals by substances like penicillin, peanuts or latex rubber. Vasodilation, provoked by systemic release of inflammatory mediators, e.g. histamine and bradykinin, causes venous pooling and hypotension. Severe bronchoconstriction leads to respiratory difficulty and hypoxia. Onset is usually sudden, and in severe cases can cause death in a matter of minutes if untreated.

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physiological changes during shock

In the short term, changes are associated with physiological attempts to restore an adequate blood circulation compensated shocks . If the state of it persists, the longer-term changes may be irreversible.

Compensated shock

  • As the blood pressure falls, a number of reflexes are stimulated and hormones secretions increased in an attempt to restore it. These raise blood pressure by increasing peripheral resistance, blood volume and cardiac output.
  • Increased sympathetic Stimulation increases heart rate and cardiac output, and also causes vasoconstriction, all of which increase blood pressure. Low blood volume and increased osmolarity of the blood cause secretion of ADH and activation of the renin-angiotensin- aldosterone system. consequent release of aldosterone reduces water and sodium excretion and promotes vasoconstriction. The veins also constrict, helping to reduce venous pooling and support venous return.
  • If these compensatory mechanisms, plus any medical interventions available, are sufficient then perfusion of the heart and brain can be maintained and the patient’s condition may be stabilized.

Uncompensated shock

If the insult is more severe, shocks becomes a more self-perpetuating sequence of deteriorating cardiovascular function-uncompensated shock. Hypoxia causes cellular metabolism to switch to anaerobic pathways ,resulting in accumulation of lactic acid and progressive acidosis, which damages capillaries. The capillaries then become more permeable, leaking fluid from the vascular system into the tissues, further lowering blood pressure and tissue perfusion. Also, the accumulation of wast product causes vasodilation, making it harder for control mechanisms to support blood pressure. Organs, including the heart, are deprived of oxygen and may start to fail.

Eventually, the cardiovascular system reaches the stage when, although its compensatory mechanisms are running at maximum, it is unable to supply the brain’s requirements. As the brain, including the cardiovascular and respiratory centres in the brain stem, becomes starved of oxygen and nutrients, it begins to fail and there is loss of central control of the body’s compensatory mechanisms. Circulatory collapse follows. Finally, degenerating cardiovascular function leads to irreversible and progressive brain-stem damage, and death follows.

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