Control of BP and Shock

Mean arterial blood pressure (MABP) is the driving force for tissue perfusion. Without adequate perfusion, cells cannot receive oxygen and nutrients, nor can they remove carbon dioxide and hydrogen ions. MABP is calculated as cardiac output multiplied by total peripheral resistance (MABP = CO x TPR). Cardiac output is itself the product of heart rate and stroke volume (CO = HR x SV). At rest, normal cardiac output is approximately 5-6 L/min, heart rate 55-95 beats/min, and stroke volume is the volume of blood ejected per beat.

The body continuously monitors MABP via baroreceptors — mechanoreceptors located in the carotid sinus and aortic arch. These receptors are stimulated by stretch in the vessel wall and send constant signals to the cardiovascular centres in the brainstem. When MABP changes, the brainstem responds via the autonomic nervous system: sympathetic (fight-or-flight) output increases heart rate and contractility, while parasympathetic (vagal) output decreases them. TPR is also adjusted through arteriolar vasomotor tone.

Shock occurs when homeostatic reflexes can no longer maintain adequate MABP, leading to hypotension and impaired tissue perfusion. There are three broad categories. Hypovolaemic shock results from insufficient cardiac filling — haemorrhage reduces venous return, decreasing stroke volume, cardiac output, and MABP. Distributive shock involves widespread vasodilation that lowers TPR: anaphylactic shock triggers increased vascular permeability and vasodilation; septic shock produces a similar inflammatory-driven response; neurogenic shock results from loss of sympathetic vasomotor tone. Cardiogenic shock arises from pump failure — the heart itself cannot generate adequate output.

In haemorrhage, the body mounts a tiered compensatory response. Immediately, the baroreceptor reflex activates: decreased stretch reduces baroreceptor firing, the brainstem detects this and increases sympathetic output, raising HR and TPR. Within minutes to hours, autotransfusion occurs — reduced capillary hydrostatic pressure (from fluid loss) shifts the Starling equilibrium, drawing interstitial fluid into the capillaries and expanding plasma volume. Over hours to days, longer-term hormonal responses sustain compensation: ADH is released to retain water and reduce urine output; activation of the RAAS retains sodium and water; EPO is released from the kidneys, stimulating red blood cell production from bone marrow (full RBC restoration takes approximately six months); thirst is increased.

Critically, compensatory reflexes do not restore MABP fully to normal. If they did, the reflexes would cease and the patient would decompensate again. Instead, MABP, SV, HR, and TPR are held below normal resting levels so the reflexes remain active. This is a physiological equilibrium that keeps the patient alive.

In clinical practice, the perfusion pressure to vital organs — brain, heart, kidneys — must be maintained. If a haemorrhaging patient is not stabilised within approximately one hour, irreversible ischaemic damage begins. The term "hypovolaemia" breaks down etymologically: hypo (low) + vol (volume) + aemic (blood).