shock

Question 1

what is it?

Answer 1

No standard definition - A syndrome in which tissue perfusion is inadequate for the tissue’s metabolic requirement
A state of cellular and tissue hypoxia due to either reduced oxygen delivery, increased oxygen consumption, inadequate oxygen utilisation, or a combination of these processes

Question 2

what does normal tissue perfusion rely on?

Answer 2

o Cardiac Function
o Capacity of vascular bed
o Circulating blood volume

Question 3

what is the imperfect estimation that is clinically used for tissue perfusion?

Answer 3

BP

Question 4

what are the types of shock?

Answer 4

• Hypovolaemic
• Cardiogenic
• Distributive
• Obstructive
• (Endocrine)

Question 5

how does hypovolaemic shock happen?

Answer 5

• An acute haemorrhage or fluid deplete states – severe dehydration or burns
• Volume depletion – leading to reduced SVR
• Reduced volume returning to heart – reduced pre-load and hence reduced CO.

Question 6

how does cardiogenic shock happen?

Answer 6

Pump failure” – reduced CO
o Reduced contractility – “stroke volume”
o Reduced heart-rate
Primarily ischaemia induced myocardial dysfunction Also: cardiomyopathies, valvular problems, dysrhthmias
If due to MI – suggests that >40% of LV is involved.

Question 7

what is the prognosis of cardiogenic shock?

Answer 7

Unless correctable pathology (E.g. valvular), mortality >75%

Question 8

how does obstructive shock happen?

Answer 8

Mechanical obstruction to normal cardiac output in an otherwise normal heart
Direct obstruction to cardiac output 
o	PE
o	Air/Fat/Amniotic fluid-embolism
Restriction of cardiac filling 
o	Tamponade
o	Tension pneumothorax

Question 9

how does distributive (vasopleic) shock happen?

Answer 9

‘hot’ shock
septic, anaphylaxis, acute liver failure, spinal cord injuries
- happens because one of the above disrupt normal vascular autoregulation and cause profound vasodilatation
• Poor perfusion – despite increased CO
• Regional perfusion differences
• Alteration of oxygen extraction

Question 10

how does endocrine shock happen?

Answer 10

• Severe uncorrected hypothyroidism, Addisonian crisis – both reduced CO and vasodilatation
• Paradoxically – thyrotoxicosis

Question 11

What is the neuroendocrine response to shock?

Answer 11

• Release of pituitary hormones – adrenocorticotrophic hormone, anti-diuretic hormone, endogenous opioids
• Release of cortisol – fluid retention, antagonises insulin
• Release of glucagon
• Suggestion that some shock states (sepsis) blunts the response to ACTH

Question 12

how does shock present?

Answer 12

pale
cold skin
prolonged capillary refill

Question 13

what are different physiological processes which can indicate shock and poor tissue perfusion?

Answer 13

• Urine output – Sensitive indicator of renal perfusion
• Neurological – Disturbed consciousness a good indicator of cerebral hypoperfusion
• Biochemical – Acidosis, lactate levels
• Blood pressure – either cuff, or invasive with arterial line
• Central Venous Pressure – Value in itself rarely useful, can be useful to assess “fluid responsiveness”

Question 14

what are pulmonary artery pressures and how are they useful in shock monitoring?

Answer 14

o Pulmonary capillary wedge pressures (surrogate for LA pressure)
o Rarely used in mainstream practice – due to risks of devices, and lack of familiarty with equipment/interpreting results.

Question 15

how is cardiac output monitoring done in shock?

Answer 15

o Gold standard – Thermodilution with a PA catheter – Again rarely used outside specialist units
o Pulse contour analysis
o Doppler ultrasonography

Question 16

basic principles of shock management?

Answer 16

• Prompt diagnosis, and treatment critical
• ABC approach
• Establishment of reliable, wide bore IV access and resuscitate while investigating
• Identify – and treat – underlying cause
• Fluid management

Question 17

how is fluid managed in shock?

Answer 17

increase pre-load
rapid fluid replacement (minutes) - have to balance this with risk of fluid overload
shocked patients are more at risk of pulmonary oedema because of microvascular dysfunction
o Crystalloids – Convenient, cheap, safe But: Rapidly lost from circulation to extravascular spaces, need significantly larger volumes than loss.
o Colloids – Cheap(ish), reduce volumes required But: Can cause anaphylaxis, no evidence of benefit
o Blood – oxygen carrying capacity, will stay in circulation. But: a scarce resource, and multiple risks

Question 18

what drugs can be given if fluids alone aren’t working?

Answer 18

Need to be administered in a critical care environment (HDU +)

• Adrenaline (Epinephrine) – alpha/beta adrenergic agonist, but at low dose primarily beta (Inc. heartrate, contractility, vasodilatation)
• Noradrenaline (Norepinephrine) – predominantly alpha agonist (vasoconstriction)
• Vasopressin (ADH)
• Dopamine – Natural precursor to the above. Complex dose-dependent effects
• Dobutamine/Dopexamine

Question 19

how is hypovolaemic shock managed?

Answer 19

o Assessment of bleeding – estimation of volume loss, and speed of ongoing loss.
o Establish source – may require imaging if stable
o Temporisation – Direct pressure, tourniquet’s
o Damage limitation resuscitation – until definitive control
o Damage limitation surgery

Question 20

how should de-escalation/de-resuscitation take place once the patients shock has resolved?

Answer 20

o Importance of removing extra fluid from a patient once their shock has resolved.
o Growing body of evidence associating gross positive balances in the recovery phase with increased morbidity/mortality
o Mortality benefit in getting patients “dry” as early in their hospital stay as possible.
o Various means: Spontaneous, Diuretic, Dialysis