Distributive shock

From WikiLectures

Distributive shock is characterized by a decreased peripheral vascular resistance, or generalized vasodilatation causing fluid to leak out of the vessels. The vasodilatation is not related to tissue hypoxia or an increased demand of nutrients, but it is caused by pathogenic shock-inducing stimulus e.g., bacterial toxin in septic shock or degranulation products of allergen-stimulated mast cells in anaphylactic shock.

Division[edit | edit source]

  1. Septic-toxic shock
  2. Anaphylactic shock
  3. Neurogenic shock
  4. Endocrine shock

Septic-toxic shock[edit | edit source]

Cause[edit | edit source]

  • Bacterial infection, usually preceded by bacteremia (septic shock is sepsis (i.e. SIRS due to infection) with persistent arterial hypotension)

Pathogenesis[edit | edit source]

The production of endotoxin (lipopolysacharide G–) or exotoxin G+ and pro-inflammatory cytokines (IL-1, TNF-α) as a result of infection, stimulate the endothelium and macrophages. The gene for inducible NO-synthase is expressed and NO is produced, which causes generalized vasodilation and is followed by a decreased arterial pressure and a decreased afterload. Thus, the ejection fraction and stroke volume of LV will increase. Hypotension causes sympathoadrenal activation, which further increases myocardial contractility and heart rate which causes cardiac output to increase (in contrast to hypovolemic and cardiogenic shock), hence the name hypercirculatory shock.

In septic shock despite the increased organ perfusion similar changes as in hypovolemic or cardiogenic shock occur. The cause may be the bypassing of the own nutritional microcirculation by arterio-venous junctions, which also open during generalized vasodilation or an increase in pH (resulting from respiratory alkalosis from hyperventilation, which is caused by hyperpyrexia from flushing out the endogenous pyrogen IL-1), during which it is more difficult to release oxygen from hemoglobin.

In the later stages of shock, the contractility of the myocardium decreases (the cause is not exactly clear, it is referred to as myocardial depression factor) and the permeability of the capillary wall increases, causing fluid to leak from the vascular bed into the interstitium. Both of these facts further worsen the arterial hypotension.

Further complications of septic shock are the development of DIC due to the generalized inflammation, as well as thrombi formation due to a decreased blood flow in the dilated parts of the vascular bed, which are especially dangerous in the pulmonary circulation where they impair the oxygenation of venous blood.

Clinical picture[edit | edit source]

In the early phase, so-called warm hypotension can be seen (the extremities are reddened, warm and dry).

The late phase is characterized by a decreased myocardial contractility which causes further worsening of hypotension. Furthermore, there is an increase in the permeability of capillaries, which leads to the leakage of fluids from the vascular bed into the interstitium, which leads to a decrease in the circulating blood volume and further exacerbation of the hypotension.

Prognosis[edit | edit source]

  • Poor, mortality 50%

Anaphylactic shock[edit | edit source]

Cause[edit | edit source]

  • Parenteral antigen penetration

Pathogenesis[edit | edit source]

Antigen binds to IgE which is bound on the surface of mast cells and causes their degranulation. The released mediators (histamine, serotonin, prostaglandins, etc.) cause vasodilation and increase the permeability of capillaries, thereby decreasing cardiac output and causing arterial hypotension. Complications can be other manifestations of allergy (Antigen action on other tissues), especially swelling of the airways and bronchospasm.

Prognosis[edit | edit source]

  • Good

Main differences between septic and anaphylactic shock:

Type of shock Progress Prognosis Cause
Septic Slow Bad Infectious agent
Anaphylactic Rapid Good Non-infectious agent

Neurogenic shock[edit | edit source]

Neurogenic shock occurs when the autonomic system is dysregulated due to spinal cord damage. The most common cause of spinal cord trauma is transverse spinal cord injury. Other less common causes are myelitis, toxins affecting CNS, spinal anesthesia or Guillain-Barré syndrome. In children, it can rarely occur with trisomy 21, skeletal dysplasia or tonsillopharyngitis. In the case of trauma, it is diagnosed per exclusionem, as the more frequent cause of shock is definitely hemorrhage.

Pathophysiologically, sympathetic activity is limited in case of damage above the vertebral level Th6 (more often in the thoracic spine area) or by a combination of primary damage (vertebral displacement/fracture) and secondary damage to sympathetic fibers (edema, devascularization, ...). Thus, the tone of the parasympathetic system does not have a natural opposition in its effect on the heart and blood vessels, and systemic circulation disorders occur.

As therapy, the basis is fluid support and possibly the use of vasopressors to maintain systemic pressure. This will also prevent secondary damage to the spinal cord. Another integral part is the immobilization of the cervical spine and subsequent consideration of neurosurgery. [1]

Links[edit | edit source]

Original text is from WikiSkripta https://www.wikiskripta.eu/index.php?curid=10422

Related articles[edit | edit source]

References[edit | edit source]

  1. SAGAR, Dave – CHO, Julia J. Neurogenic Shock [online]. StatPearls Publishing, ©2021. [cit. 2021-04-11]. <https://www.ncbi.nlm.nih.gov/books/NBK459361/>.

Source[edit | edit source]

Distributive shock

Table comparing different types of shock