What is the definition of shock?
acute circulatory failure with inadequate or inappropriately distributed tissue perfusion
What defines the mean arterial pressure?
the average pressure driving blood into tissues throughout the cardiac cycle - reflects tissue perfusion pressure, not just the “average” of systolic and diastolic values
How is the mean arterial pressure calculated?
What is the normal MAP value and what is the minimum required value for vital organ perfusion?
normal MAP: 70-100
minimum required: >60 mmHg
What are the 4 types of shock?
hypovolaemic
mechanical
cardiogenic
distributive
What are the different types of hypovolaemic shock?
How does loss of blood volume lead to hypovolaemic shock?
What is the compensatory mechanism for hypovolaemic shock?
What causes hypovolaemic shock?
a loss of blood or fluid volume e.g haemorrhages, burns, dehydration - leading to decreased mean arterial pressure and poor tissue perfusion
What initially happens when MAP decreases?
the body detects the drop in pressure via baroreceptors and chemoreceptors, triggering sympathetic nervous system activation
What are the main physiological responses to decreased MAP?
Following a detection in reduced MAP, what does increased sympathetic activity do?
causes vasoconstriction -> increases TPR
increases HR and contractility
stimulates renin release from the kidneys
What is the main role of renin in hypovolaemic shock?
What occurs after?
renin converts angiotensinogen -> angiotensin I which is later converted to angiotensin II by ACE
angiotensin II:
- causes systemic vasoconstriction which increases TPR
- stimulates aldosterone release from the adrenal cortex
aldosterone:
- promotes sodium and water reabsorption and potassium excretion in the kidneys -> increases blood volume and pre-load
What triggers ADH release in hypovolaemia? What does ADH then do?
baroreceptors in the carotid sinus and aortic arch sense low pressure -> stimulate ADH secretion from posterior pituitary
ADH then causes water retention in the kidneys and increases blood volume and preload
During compensation for hypovolaemic shock, what factors help with water retention - what does this do?
What helps with vasoconstriction - what does this do?
water retention: ADH released after low MAP is detected via carotid sinus and aortic sinus baroreceptors = INCREASES PRE-LOAD
vasoconstriction: ANGIOTENSIN II after renin was released due to low MAP detection via JGA baro/chemoreceptors = INCREASE TPR
sodium and water retention: ALDOSTERONE from RAAS = increase PRE-LOAD
How can hypovolaemic shock lead to multi-system organ failure?
via DECOMPENSATED SHOCK
What happens during the initial compensatory stage of hypovolaemic shock?
sympathetic nervous system and angiotensin II cause widespread vasoconstriction, maintaining blood pressure and perfusion to vital organs
What is the main effect of prolonged vasoconstriction?
peripheral organs receive less blood flow, leading to tissue hypoxia and metabolic acidosis due to anaerobic metabolism
Why does metabolic vasodilation occur in shock?
Hypoxic tissues release metabolic vasodilators (like adenosine, CO₂, lactic acid), causing vasodilation and a reduction in total peripheral resistance (TPR)
What happens to total peripheral resistance (TPR) during metabolic vasodilation?
TPR falls, which reduces mean arterial pressure (MAP) and compromises perfusion to vital organs
What is meant by circulatory collapse?
When TPR and MAP drop, blood flow to vital organs (like the brain and heart) becomes inadequate, leading to decompensated shock
What marks the transition from compensated to decompensated shock?
the loss of vasoconstrictor control and onset of metabolic vasodilation, causing falling MAP and organ hypoperfusion
What causes irreversible shock?
prolonged hypoxia and acidosis damage capillaries and endothelium, leading to fluid leakage, tissue injury, and organ failure that persist even if BP is restored
Can tissue damage in irreversible shock be reversed by restoring blood pressure?
No. By this stage, cell death and metabolic derangement are too severe to recover from, even with normalised BP
How can a prolonged reduced MAP lead to irreversible shock? Explain the steps.