**5.1 Compensated shock**

When oxygen supply is inadequate, the body undergoes several physiological changes to maintain the oxygen delivery requirements and perfusion pressure. This stage is referred to as compensated shock and early signs of shock may be appreciated during this stage. Findings consistent with compensated shock are briefly mentioned in **Table 2**. At this point, it is important to identify the underlying cause and correct it to prevent any lasting complications. Homeostatic changes that occur are listen in **Table 1** and is stimulated by activation of two pathways. The first is **baroreceptor activation**. Decreased arterial pressure leads to decreased stretch of the baroreceptors located on the carotid sinus. There is a consequent decrease in afferent baroreceptor firing which increases efferent sympathetic firing and decreases efferent parasympathetic firing. Sympathetic activation results in an **increase in CO** via an increase in heart rate and stroke volume (increase in contractility). **Arteriolar vasoconstriction** allows for the redistribution of blood flow to more vital organs such as the brain, heart and kidneys. Additionally, increased sympathetic tone results in **constriction of venous circulation** thereby increasing venous return. As circulation is a closed system, an increase in venous return or preload brings about an increase in stroke volume and thereby cardiac output. Additionally, the sympathetic nervous system (SNS) directly stimulates the adrenal glands resulting in secretion of epinephrine, norepinephrine and cortisol which also aid in augmenting arteriolar and venous tone. The second pathway is activation of the **renin-angiotensin-aldosterone-system (RAAS).** A decrease in renal perfusion secondary to systemic hypotension triggers this activation. Aldosterone acts on the


#### **Table 1.**

*Compensatory mechanisms in response to systemic hypotension.*

principal cells in the collecting tubules of the kidney to increase sodium reabsorption. This results in fluid retention that ultimately improves cardiac output. The angiotensin II acts on AT1 receptors on vascular endothelial cells causing vasoconstriction. Angiotensin II also preferentially constricts the efferent arteriole maintaining the glomerular filteration rate (GFR) and preventing pre-renal acute kidney injury in the setting of shock. These mechanisms briefly mentioned here all aim to maintain perfusion pressure, direct blood to vital organs (e.g. brain, heart, and kidney) and increase oxygen delivery in the setting of systemic hypoxia. A comprehensive table listing the various compensatory mechanisms in response to hypoxia is given (**Table 1**).
