28. Shock

Question 1

What is clinical shock?

Answer 1

This is an acute circulatory failure - with inadequate or inappropriately distributed tissue perfusion resulting in cellular hypoxia

Question 2

How can tissue perfusion be adequately maintained?

Answer 2

Via maintenance of cardiac output and blood pressure
CO - 5l/min
Systolic BP - 120mmHg
MAP - 10mmHg

Question 3

What can cause a drop in blood pressure sufficient to cause shock?

Answer 3

BP = CO x systemic vascular resistance

SO a drop in blood pressure leading to shock can be caused by a low cardiac output or a low vascular resistance

Question 4

Why might there be a low CO?

Answer 4

CO = HR x SV

A low heart rate may be due to inhibition of autonomic system (perception of threat)

A low stroke volume (more common) due to reduced preload or due to reduced myocardial contractility

Question 5

What factors can lead to a reduced myocardial contractility?

Answer 5

Cardiac disease
Hypoxia/hypercapnia
pH or electrolyte disturbance
Drugs e.g. beta blockers, calcium channel blockers

Question 6

Why is it important to maintain systemic vascular resistance?

Explain this

Answer 6

Need to maintain adequate resistance to ensure an adequate distribution of the blood

If the resistance to just one organ falls then the blood will take this route i.e. the path of less resistance
SO the blood supply to all the other organs will fall
SO must maintain the level of resistance and pressure in all the systemic arteries i.e. the systemic vascular resistance

Question 7

Which hormones act to maintain systemic vascular resistance?

Answer 7

Angiotensin 2 - acts on receptors of the endothelium to mediate constriction of the vascular muscle
Noradrenaline released from the nerves that innervate the smooth muscle to cause their constriction

SO angiotensin works on the lumen and noradrenalin works on the outside

Question 8

What happens when the body goes into shock (moderate and severe)?

Answer 8

When in moderate shock, compensation will occur (compensated shock) and the circulation will return back to normal

BUT if the shock is too severe, the body cannot compensate and will move into decompensated shock
This means that no matter what you do, you cannot raise the blood pressure enough to maintain tissue and organ perfusion and the person will most likely die

Question 9

What are the four classifications of shock?

Give the most common examples of each

Answer 9

Obstructive shock - physical obstruction causing failure of cardiac output e.g. pulmonary embolism

Distributive shock - loss of vasoconstriction leading to a failure of vascular resistance maintenance e.g. sepsis

Hypovolemic shock - where you have bled and lost too much blood so there is not enough circulating blood so that even if you were to increase the heart rate, preload cannot increase e.g. haemorrhage

Cardiogenic shock - failure of the heart to pump efficiently and supply blood to the body e.g. myocardial infarction/heart failure

Question 10

How does hypovolemic shock present?

Answer 10

SO generally due to haemorrhage - major blood loss
Body tries to compensate for this by shutting down circulation to the skin - greyish pallor to the skin, cold and clammy skin, slow capillary refill
Low blood pressure
Tachycardia

Oliguria - there will be a massive release of ADH as don’t want to lose any more water through the urine (already lost so much from the bleed)

Question 11

How does cardiogenic shock present?

Answer 11

Most of these patients have an AMI so present with chest pain, shortness of breath, nausea, vomiting

Question 12

How does distributive shock present?

Answer 12

Low BP
Tachycardia
Fever
Chills
Rigors 
Fatigue
Nausea
Vomiting
Difficulty breathing
Anxiety
COnfusion

Question 13

How does obstructive shock present?

Answer 13

Generally due to tension pneumothorax
Tachycardia
Anxiety
Chest pain
Breath sounds are absent on affected hemiothorax
Trachea deviates away from affected side

Question 14

How much blood loss is life threatening?

Answer 14

Total body water is 45 litres
Total blood volume is 4.5-5 litres
Acute loss of greater than 40% of blood volume i.e. greater than 2 litres is immediately life threatening

Question 15

Describe and explain the immediate compensatory response to haemorrhage

Answer 15

Works within seconds to minutes
The loss of blood results in a drop in blood pressure which is detected by baroreceptors
These then compensate by increasing sympathetic output to increase heart rate and contractility

The vasomotor centre in the medulla also signals to the hypothalamus to release ADH to reduce urine flow and sodium excretion

Question 16

Does a loss of blood always immediately lead to a reduced blood pressure? Explain this

Answer 16

Loss in arterial blood leads to a reduced blood pressure

Loss in venous blood causes a reduced venous return i.e. a reduced preload - this then reduces stroke volume and so reduces cardiac output
THIS leads to a reduced blood pressure

Question 17

What is the longterm compensatory response to haemorrhage?

Answer 17

This works between hours to days
Increased release of renin from the kidney and release of aldosterone from the adrenal cortex by angiotensin II - causes increased sodium retention
Thirst is stimulated by angiotensin II receptors in the brain to increase water intake
Stimulation of albumin and plasma proteins in the liver

Question 18

What are the four classes of hypovolemic shock?

Answer 18

Class 1 - loss of <15% of blood volume - will always be full compensation - this is what happens when you donate blood - urine output decreased and thirst increased

Class 2 - loss of 15-30% - some clinical symptoms of tachycardia, tachypnoea, cool clammy skin, delayed capillary refill

Class 3 - greater than 30% loss of blood - leads to drop in blood pressure - moving close to stage of decompensation - requires blood transfusion but at this point, most important thing is maintenance of fluid in general so any fluid transfusion is sufficient

Class 4 - greater than 40% loss in blood - immediately life threatening and requires immediate blood transfusion

Question 19

What is outlined by Starling’s law of the heart?

Answer 19

The greater the preload, the greater the force of contraction and therefore, the greater the stroke volume

Question 20

Define preload

Answer 20

The end diastolic volume - the end volume of blood that will be pumped to the body by the left ventricle

Question 21

How is the SVR maintained throughout the body?

Answer 21

Via constriction of blood vessels

Question 22

Which hormones are responsible for the maintenance of the systemic constriction of blood vessels and what receptors do these act on?

Answer 22

Noradrenaline via the sympathetic NS - alpha receptors on the outside of the arterioles
Angiotensin 2 - angiotensin receptors (AT1) of the endothelium - within the lumen

Question 23

What local factors can alter the SVR/size of the lumen of blood vessels?

Answer 23

Endothelin - vasoconstrictor
NO - vasodilator
Prostacyclin - vasodilator

Question 24

When is endothelin normally released?

Answer 24

When damage has occurred to the blood vessel

Question 25

What is the function of prostacyclin?

Answer 25

Local vasodilator - reduce calcium entry into smooth muscle

Inhibits platelet activation in primary haemostasis

Question 26

What is prostacyclin produced from?

Answer 26

Arachidonic acid

Question 27

What is meant by ‘cardiac tamponade’?

Answer 27

Blood gets into the space between the heart and the pericardial sac - this prevents the heart from expanding during diastole

Can result in cardiogenic shock