Shock or Distributive Shock: Types, Pathophysiology, Prognosis and Complications

What is a Distributive Shock?

It is a hyperdynamic process that results from excessive vasodilation. The alteration of blood flow causes inadequate tissue perfusion, which can damage the final organ.

Although the most common etiology is septic shock, anaphylactic and other etiologies should be considered.

The distributive shock results from excessive vasodilatation and impaired blood flow distribution.

Septic shock is the most common distributive shock and is characterized by considerable mortality (treated, about 30%, untreated, probably 80%).

In the United States, this is the leading cause of non-cardiac death in intensive care units (ICU).

Other causes of distributive shock include systemic inflammatory response syndrome (SIRS) due to noninfectious inflammatory conditions such as burns and pancreatitis and toxic shock syndrome (SST).


Similarly, anaphylaxis, reactions to drugs or toxins, including insect bites, transfusion reaction, and heavy metal poisoning; Addisonian crisis; liver failure; and neurogenic shock due to the brain or spinal cord injury.

Types of shock

Shock is a clinical syndrome characterized by inadequate tissue perfusion that results in a dysfunction of the final organ. It can be divided into the following four categories:

  • The distributive shock (vasodilation) is a hyperdynamic process.
  • Cardiogenic shock (failure in pumping).
  • Hypovolemic shock (loss of intravascular volume).
  • Obstructive shock (physical obstruction of the blood circulation and inadequate blood oxygenation).
  • Systemic inflammatory response syndrome.

The Committee of the Consensus Conference of the American College of Heart Physicians / Society of Critical Medicine defined it as the presence of at least 2 of the following four criteria:

  • Core temperature greater than 38 ° C (100.0 ° F) or below 36 ° C (96.8 ° F).
  • Heart rate of more than 90 beats per minute.
  • Respiratory rate of more than 20 breaths per minute or carbon dioxide blood pressure (PaCO 2) less than 32 mm Hg.
  • White blood cell (WBC) count of more than 12,000 / μL, less than 4,000 / μL, or more than 10% of immature forms (band).
  • The clinical suspicion of systemic inflammatory response syndrome by an experienced clinician is of paramount importance.


In distributive shock, inadequate tissue perfusion is caused by the loss of normal responses of the vascular smooth muscle to vasoconstrictive agents, together with a direct vasodilatory effect.

The net result in a patient resuscitated with fluid is a hyperdynamic hypotensive state associated with an increase in mixed venous saturation of O2; However, evidence of tissue ischemia is manifested by an increase in serum lactate.

Early septic shock (warm or hyperdynamic) causes a decrease in diastolic blood pressure, increased pulse pressure, flushing, and hot extremities.

But also the energetic capillary refill of peripheral vasodilatation, with a compensatory increase in cardiac output.

In late septic shock (cold or hyperdynamic), myocardial contractility is combined with peripheral vascular paralysis to induce a pressure-dependent reduction in organ perfusion.

The result is hypoperfusion of critical organs such as the heart, brain, and liver.

The hemodynamic disorders observed in septic and distributive shock are due to a complicated cascade of inflammatory mediators.

Inflammatory mediators are released in response to several factors, such as infection, inflammation, or tissue injury.

For example, bacterial products such as endotoxin activate the inflammatory response of the host, increasing pro-inflammatory cytokines, for example, tumor necrosis factor (TNF), interleukin (IL) -1, and IL-6.

They play a critical role in response to pathogens and the excessive inflammatory response that characterizes the distributive shock; these receptors are considered possible drug targets.

Cytokines and mediators derived from phospholipids act synergistically to produce complex alterations in the vasculature (e.g., increased microvascular permeability, impaired microvascular response to endogenous vasoconstrictors such as norepinephrine).

Also, myocardial function (direct inhibition of myocyte) leads to maldistribution of blood flow and hypoxia.

Hypoxia also induces the positive regulation of the enzymes that create nitric oxide, a potent vasodilator, which further exacerbates hypoperfusion.

Coagulation is also affected by septic shock. Activated monocytes and endothelial cells are sources of tissue factors that activate the coagulation cascade; Cytokines, such as IL-6, also play an essential role.

The coagulation response is significantly altered, including the deterioration of antithrombin and fibrinolysis. Thrombin generated as part of the inflammatory response can trigger disseminated intravascular coagulation.

It is found in 25-50% of patients with sepsis and is a significant risk factor for mortality.

During the distributive shock, patients risk various organ system dysfunctions that can progress to multiple organ failures.

Mortality from severe sepsis increases markedly with the duration of sepsis and the number of organs that fail.

In the distributive shock due to anaphylaxis, the decrease is mainly due to the massive release of histamine from mast cells after activation by immunoglobulin E (IgE) bound to the antigen, as well as increased synthesis and release of prostaglandins.

Neurogenic shock is due to the loss of sympathetic vascular tone from a severe injury to the nervous system.


The mortality rate after the development of septic shock is 20-80%. The data suggest that mortality due to septic shock has decreased slightly due to new therapeutic interventions.

Early recognition and appropriate therapy are essential to maximizing good results.

We are identifying patients with septic shock in the emergency department instead of identifying them outside results in a significant improvement in mortality.

In one study, the mortality rate of patients identified by the emergency department was 27.7%, compared to 41.1% of patients identified outside the emergency department.

The highest mortality rates have also been associated with the following:

  • Advanced age.
  • The finding of positive blood cultures.
  • Infection with organisms resistant to antibiotics such as Pseudomonas aeruginosa.
  • Elevated levels of serum lactate.
  • I have impaired immune function.
  • Consumption of alcohol.
  • Poor functional status before the onset of sepsis.

Mortality rates associated with other forms of distributive shock are not well documented.


The duration of delirium is an independent predictor of long-term cognitive decline. At three months and 12 months of follow-up, as many as 79% and 71% of patients have cognitive impairment. Approximately one-third remain seriously affected.