TRC: Theory of shock

Theory of shock

Tissue perfusion is dependent on delivery of adequately oxygenated blood to the tissues. Shock results from a lack of adequate tissue oxygen delivery. Blood delivery is estimated by the patient's cardiac output (CO). The priority is therefore to increase cardiac output and blood pressure (BP). Cardiac output is quantified as the product of heart rate (HR) and stroke volume (SV).

CO = HR x SV

Stroke volume is determined by the haemodynamic parameters of preload, afterload, and contractility. If one of these becomes compromised, cardiac output drops and tissue perfusion will suffer.

It is important to remember that hypovolaemic shock can be caused not only by loss of fluid volume (e.g. acute bleeding), but also by loss of plasma caused by burns or by sequestration into body cavities (also called third spacing).

BP = CO x SVR

SVR: systemic vascular resistance

Which kind of receptors do NOT play a role in antihypotensive treatment?

Extra info: Nicotinergic receptors are mainly localized in muscle and CNS. Adrenergic α-receptors are present in blood vessels, β-receptors in blood vessels (β2 only) and in the heart; and dopaminergic receptors in the blood vessel wall.

Option explanation:

α-adrenergic receptors

β-adrenergic receptors

dopaminergic receptors

nicotinergic receptors

Loss of blood pressure can be due to all of the following EXCEPT

Extra info: Fever in itself does not cause hypotension; however, the causes of fever (e.g. septic shock) can.

Option explanation:

Blood loss

Redistribution

Fever

Burns