Hypovolaemia Flashcards
(25 cards)
What are the types of shock?
Cardiogenic.
Hypovolaemic.
Obstructive.
Distributive.
eg and clinical signs of cardiogenic shock.
MI. ECG, pulmonary and peripheral oedema.
eg and clinical signs of hypovolaemic shock
trauma. Dry, empty (weak pulse, cyanosed). Evidence of loss.
eg of obstructive shock
DVT, PE.
eg and clinical sign of distributive shock
Sepsis. known infection.
What is non-progressive stage shock?
normal circulatory responses will rectify without worsening or intervention. (May still need care though!)
What is progressive stage of shock?
Compensatory factors cause shock to get progressively worse in a vicious circle. Body tissue deteriorates, necrosis sets in, organ failure, death. Intervention is essential for survival.
What is irreversible stage shock?
Progressive shock is at such a stage that intervention will not save the patient. Giving fluids will be progressively ineffective, no matter how much is given.
What are the ‘Tennis Scores’ of shock?
Blood loss: 15% - thirsty, CO remains ok.
30% - tachycardia, CO about 50%, but compensatory mechanisms and intervention work.
40% - Irreversible.
What are the fast compensatory mechanisms for shock?
Baroreceptor reflex.
Chemoreceptor reflex.
CNS response.
What sensory nerve provide feedback for baroreceptor and chemoreceptor reflexes?
Vegus and glossopharyngeal.
What stimulates a sympathetic chemoreceptor response?
decreased O2, increased CO2, decreased pH.
Where are the baroreceptors?
Aortic arch and carotid.
What sympathetic response does the baroreceptor and chemoreceptor reflex trigger?
Vasoconstriction (to maintain return).
Arterial constriction to increase total peripheral resistance (increase BP)
increase HR.
What are the intermediate responses to shock?
ADH and renin release
Where is ADH release from and what are its main effects in shock compensation?
PPG. vasoconstriction, water retention.
What are the main effects of renin in shock compensation, and from where is it released?
JGA in kidney, it converts angiotensinogen into angiotensin, which is then converted into angiotensin II which caused vasoconstriction and inflammation. Angiotensin II also stimulates the release of aldosterone from the adrenal gland which stimulates reabsorption in the kidney DCT.
Give e.g. and explain isosmotic expansion
Too much saline.
increase in water and salts into ECF. ECF increases in volume, but osmol remains the same, so no movement of water from ICF to ECF.
Give e.g. and explain hyper osmotic expansion
Salt poisoning.
Increase in water and salts into ECF, but too much salt, so water drawn from ICF to ECF: osmol of ECF increases as does vol. ICF vol decreases, so osmol increases.
Give e.g. and explain Hyposmotic expansion
Syndrome of Inappropriate ADH.
ADH increases water retention. Too much will cause ECF water retention (increase in ECF volume) and therefore a decrease in ECF osmol. Water is then drawn into ICF so ICF vol also decreases.
Give e.g. and explain isosmotic contraction
Severe diarrhoea.
too much water and salt lost. ECF vol decreased, but relative osmol remains constant, therefore no movement of water from ICF to ECF.
Give e.g. and explain hyperosmotic contraction
dehydration - loss of water.
increased water loss, but not salt. ECF vol decreases, osmol increases. Water drawn from ICF to ECF so ICF vol also decreased and osmol raised.
give e.g. and explain hyposmotic contraction
Too little aldosterone.
Too much salt loss (form decreased reabsorption), normal water loss. ECF decreases osmol, water drawn from ECF to ICF - ICF osmol also decreased.
Initial signs of shock
decreased BP increased HR tachypnoea decreased sats cyanosed low urinary output
