Problems with  Peripheral Resistance (distributive shock)

Shock caused by low peripheral vascular resistance is caused by loss of tonic vasoconstriction (vasoplegia), due to sympathectomy, anaphylaxis or sepsis, leading to relative hypovolemia.

 Distributive shock is a problem with the peripheral vascular resistance. Blood vessels are normally kept in a state of tonic vasoconstriction, maintained by the interaction between the baroreceptors and sympathetic nervous system. Under certain circumstances, injuries may reverse this process, blood vessels dilate, and the patient becomes hypotensive. An example of this situation occurs with spinal shock, due to high transection of the spinal cord, or spinal anesthesia, which causes a sympathetic blockade. The patient develops a “relative hypovolemia” – the amount of fluid is the same, but the tubing is bigger. A similar picture occurs in anaphylactic shock: there is extensive mast cell degranulation in response to an allergen, and the histamine release causes vasodilatation.

In sepsis, there are three fundamental physiologic upsets: increased synthesis of nitric oxide, activation of ATP-sensitive potassium channels in vascular smooth muscle, and deficiency of vasopressin.

The plasma concentration of nitric oxide is markedly increased in septic shock. The production of this endogenous vasodilator appears to occur due to the expression of inducible nitric oxide synthetase by cytokines. This agent appears to be responsible for the end organ resistance to catecholamines and endothelin in sepsis.

Tissue hypoxemia, acidosis and nitric oxide cause the activation of ATP sensitive potassium channels, which facilitates entry of potassium into smooth muscle cells and causes hyperpolarization of the membrane: the cells become resistant to depolarization and contraction.

Vasopressin functions normally as part of the water conservation reflex system. However, this hormone is an effective vasoconstrictor in shock. In patients with vasodilated septic shock there appears to be an absolute deficiency of vasopressin, the reason for which is not clear. Administration of exogenous vasopressin appears to be very effective at reversing hypotension, even in very small doses. Vasopressin appears to enhance the effect of norepinephrine, and interfere with nitric oxide.

To learn more about distributive shock in sepsis click here.

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