Phase 2 uncompensated shock

In uncompensated shock, the compensatory mechanisms start to fail and the circulatory system is no longer efficient. Areas that have poor perfusion can no longer metabolise aerobically, and anaerobic metabolism becomes their major source of energy production. Anaerobic metabolism is comparatively inefficient. Only 2 moles of adenosine triphosphate (ATP) are produced for each mole of glucose metabolised compared to 38 moles of ATP per mole of glucose metabolised aerobically.

Anaerobic pathways produce excess lactate leading to systemic acidosis. The acidosis is compounded by intracellular carbonic acid formed because of the inability of the circulation to remove CO2. Acidosis reduces myocardial contractility and impairs the response to catecholamines.

A further result of anaerobic metabolism is the failure of the energy dependent sodium-potassium pump, which maintains the normal homoeostatic environment in which the cell functions.

Lysosomal, mitochondrial, and membrane functions deteriorate without this homoeostasis. Sluggish flow of blood and chemical changes in small vessels lead to platelet adhesion, and may produce damaging chain reactions in the kinin and coagulation systems leading to a bleeding tendency.

Numerous chemical mediators have been identified in shocked patients, but the roles of each have not been clearly identified. They include histamine, serotonin, cytokines (especially tumour necrosis factor and interleukin 1), xanthine oxidase (which generates oxygen radicals), platelet-aggregating factor, and bacterial toxins. They are largely produced by cells of the immune system, especially monocytic macrophages. It has been suggested that these mediators, which developed as initial adaptive responses to severe injury and illness, may have deleterious consequences in the "unnatural" setting of the resuscitated patient.When the role of these chemical mediators is more fully understood, blocking agents may be produced which will improve the treatment in phase 2 shock.

The result of these cascading metabolic changes is to reduce tissue perfusion and oxidation further. Blood pools in some areas because arterioles can no longer control flow in the capillary system. Furthermore, abnormal capillary permeability allows further fluid loss from the circulation into the interstitium.

Clinically, the patient in phase 2 shock has a falling blood pressure, very slow capillary return, tachycardia, cold peripheries, acidotic breathing, depressed cerebral state, and absent urine output.

0 0

Post a comment