Shock And Haemorrhage

Question 1

What is shock

Answer 1

State of inadequate perfusion to the vital organs

Question 2

What are the 2 states shock can be divided into

Answer 2

High output state- anaphylaxis and sepsis - there is a systemic vasodilation that lowers TPR the heart compensates by raising cardiac output to try to maintain ABP
Low output state- carcinogenic and hypovolaemic shock
Carcinogenic is a failure of the pumping heart
Hypovolaemic - lack of blood

Question 3

What does the drop in ABP activate via what and what does this lead to

Answer 3

Sympathetic NS by the baroreceptor reflex

This leads to widespread vasoconstriction everywhere but the brain

Question 4

What else does the strong synthetic drive activate

Answer 4

Kidneys - renin angiotensin system

Question 5

What receptors are in the kidney that respond to the increased sympathetic activation

Answer 5

Beta1 cells on the granular cells

Question 6

How else is the RAS activated in shock

Answer 6

The sympathetic constriction of vessels leads to decreased renal perfusion which activates the JGA

Question 7

What is hypovolaemia caused by

Answer 7

Loss of blood volume

• dehydration, diarrhoea and vomiting
• haemorrhage
• burns

Question 8

How is hypovolaemia and cardiogenic shock different

Answer 8

Hypovolaemia causes a drop in CVP
Cardiogenic shock inc the CVP this leads to an increase in hydrostatic pressure of the vasa recta, reducing the rate of fluid reabsorption

Question 9

What is losing less than 20% of blood volume

Answer 9

Not shock but hypovolaemia- cause tiredness, thirst

Question 10

What are the severities of shock

Answer 10

20% loss mild
30% loss moderate - blood pressure will fall below 90mmHg and HR will rise above 90 to compensate
40% loss severe
50% loss rapidly fatal

Question 11

Drop in cardiac output causes

Answer 11

A lack of adequate perfusion causes hypoxia of the tissues, enforcing a switch to anaerobic respiration
This leads to a lactic acidosis from the resulting H+ increase which must be cleared by the kidney

Question 12

What does tissue damage from hypoxia cause the release of from cells

Answer 12

Inc k+ release

Puts additional strain on the kidneys

Question 13

What can the prolonged hypotension and renal hypoxia lead to

Answer 13

Acute renal failure which is acute kidney injury

This is due to the death of renal tissue but also due to a fall in GFR causing blockage of the tubules

Question 14

Which part of the kidney does AKI have the most affect

Answer 14

Medulla
Already perfused you a secondary capillary bed so is already slightly hypoxia
And there is high metabolic activity in the medulla

Question 15

What happens in acute renal failure AKI

Answer 15

Fall in GFR even when bP and perfusion return to normal and the kidneys remain anuric

Question 16

What does fall in venous pressure act on the posterior pituitary gland

Answer 16

Release ADH
Lead to water retention via AQP
Also resultant transient hyponatraemia
Hyponatraemia is a trigger for aldosterone release - rare usual triggers are hyperkalaemia and AT2
RAS then helps to retain both Na+ and water
This tends the body towards metabolic acidosis

Question 17

What is the treatment of hypovolaemia

Answer 17

Administer fluids

Question 18

Which fluid isn’t given and why

Answer 18

Blood
It is a commodity - don’t want to use it when there is not a lack of Hb
And it reduces the risk of donor recipient infection

Question 19

What are the most commonly applied fluids and what are they

Answer 19

Crystalloids
Simple isotonic salt solution
That distribute through the extracellular fluid

Question 20

What is argued to be the most effective treatment in haemorrhage and why

Answer 20

Fluid that will remain entirely intravascular called colloids
As the reduction in circulating volume not extracellularly
So colloids maintain intravascular volume at the expense of interstitial volume
E.g. Collagen derived gelatins, polysaccharide dextrins, hydroxyethyl starches and albumin these substances have a high enough molecular mass to prevent passage through the endothelium