Shock Flashcards

1
Q

Define shock

A

Term to describe acute circulatory failure with inadequate or inappropriately distributed tissue perfusion, resulting in generalised hypoxia and/or an inability of the cells to utilise oxygen

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2
Q

What is meant by ‘inadequate or inappropriately distributed tissue perfusion’

A

Inadequate substrate (glucose and oxygen) for aerobic cellular respiration

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3
Q

How would you recognise shock

A

Skin is pale, cold, sweaty and vaso-constricted
Pulse is weak and rapid
Pulse pressure is reduced (not arterial as this is maintained until large blood loss)
Reduced urine output
Confusion, weakness, collapse, coma

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4
Q

Is venous or mean arterial pressure (MAP) a better indicator of shock

A

Venous

Pulse pressure reduced from shock but MAP may be maintained (only decreases if v large amount of blood loss)

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5
Q

Effects of shock

A

Prolonged hypotension which can lead to life threatening organ failure after recovery from the acute event (possibly linked with inflammatory response)
Long capillary refill time (CRT)

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6
Q

Describe Capillary Refill Time as a measure of Shock

A

If takes >3 seconds to turn pink after 5 seconds of compression = early/accurate sign of shock

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7
Q

Types of shock

A

Hypovolaemic shock
Cardiogenic shock
Distributive shock (3 types)

Haemorrhagic shock
Heat exposure (heat exhaustion)

Unsure:
Anaemic shock
Cytotoxic shock

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8
Q

What are 3 types of distributive shock

A

Septic shock
Anaphylactic shock
Neurogenic shock

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9
Q

Cause of hypovolaemic shock

A

Low blood volume, as a result of loss of blood or loss of fluid
Can be secondary to haemorrhagic shock

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10
Q

Hypovolaemic shock: What can cause loss of blood?

A

Acute GI bleeding
Trauma
Peri-post-operative
Splenic rupture

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11
Q

Hypovolaemic shock: What can cause loss of fluid?

A

Dehydration - diarrhoea and vomitting
Burns - heat damage increase capillary permeability so plasma leaks
Pancreatitis

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12
Q

Causes of cardiogenic shock

A

Heart doesn’t pump due to:

  • Cardiac tamponade - blood in pericardial sack placing pressure on heart thereby limiting cardiac output
  • Pulmonary embolism - flow of blood to lungs is blocked
  • Acute MI
  • Fluid overload
  • Myocarditis - inflammation of the muscle itself
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13
Q

Why does cardiac tamponade prevent heart from pumping

A

Blood in pericardial sack places pressure on heart thereby limiting cardiac output

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14
Q

When do you get sepsis

A

When a systemic inflammatory response is associated with an infection

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15
Q

When do you get septic shock

A

When sepsis is complicated by persistent hypotension that is unresponsive to fluid resuscitation

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16
Q

What causes anaphylactic shock

A
  • Release of IgE due to allergic response
  • Massive release of histamine and other vasoactive mediators causing haemodynamic collapse
  • Accompanied by breathlessness and wheeze (due to bronchospasm)
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17
Q

What are the different groups of Haemorrhagic Shock classification

A

(Tennis score)

Class I, II and III

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18
Q

Haemorrhagic Shock classification: Describe class I

A
15% blood loss
Pulse <100bpm
BP normal
Resp rate 14-20
Urine output greater than 30ml/hr
Slightly anxious
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19
Q

Haemorrhagic Shock classification: Describe class II

A
15-30% blood loss
Pulse >100bpm
BP normal (due to ANS/ increased sympathetic activity)
Pulse pressure decreased
Resp rate 20-30
Urine output 20-30ml/hr
Mental status: mildly anxious
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20
Q

Haemorrhagic Shock classification: What is earliest sign of class II

A

Tachycardia

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21
Q

Haemorrhagic Shock classification: Describe class III

A
30-40% blood loss
Pulse >120bpm
BP decreased
Pulse pressure decreased
Resp rate 30-40
Urine output 5-15ml/hr
Mental status: confused
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22
Q

What haemorrhagic shock class would someone be is had a resp rate of 21, decreased pulse pressure but normal BP

A

Class II

therefore blood loss around 15-30%

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23
Q

What haemorrhagic shock class would someone be is had a urine output of 15ml/hr and pulse of 125bpm

A

Class III

therefore blood loss around 30-40%

24
Q

What signs would show someone to have 15% blood loss

A
Class I Haemorrhagic shock
Pulse <100bpm
BP normal
Resp rate 14-20
Urine output greater than 30ml/hr
Slightly anxious
25
Q

How does blood loss lead to release of adrenaline

A
  • Reduction in ventricular filling
  • Fall in BP and SV
  • Results in hypotension
  • Reduced stimulation of baroreceptors in aortic arch and carotid sinuses
  • Increased sympathetic activity with release of noradrenaline and adrenaline
26
Q

What is effect of adrenaline and nor-adrenaline on vascular system

A

Vasoconstriction

Increased myocardial contractility and heart rate, helps restore BP and CO

27
Q

What is autotransfusion

A

Reduced capillary BP leads to greater level of net movement of fluid into the vascular compartment from the tissues

28
Q

What hormones counter hypotension

A
ADH/Vasopressin
Angiotensin II
Aldosterone
Cortisol
Glucagon
29
Q

How does ADH/Vasopressin counter hypotension

A

Vasopressin is released in response to decreased Blood Volume which which binds to V2 receptor resulting in insertion of Aquaporin 2 into the lumen of the collecting duct, resulting in increased water reabsorption

30
Q

How does RAAS counter hypotension

A

Reduction in the perfusion of renal cortex stimulates Juxtaglomerular appartus to release RENIN.
Renin converts Angiotensinogen (from liver) to Angiotensin I.
Angiotensin I is converted to Angiotensin II by ACE (in lungs).
Angiotensin II causes thirst, is a potent vasoconstrictor and stimulates secretion of Aldosterone by the adrenal cortex. Both cause Na+ and therefore water retention - to help restore circulating volume and blood pressure.

31
Q

How does Cortisol counter hypotension

A

Increases fluid retention

32
Q

How does Glucagon counter hypotension

A

Raises blood sugar levels

Fluid also moves into blood then due to osmotic effect

33
Q

Clinical presentation of hypovolaemic shock

A

Inadequate tissue perfusion
Increased sympathetic tone
Tachycardia - narrow pulse pressure and weak pulse
Sweating
BP may be maintained initially but later hypotension
Bradycardia

34
Q

Describe how you would differentially diagnose inadequate tissue perfusion (for someone with hypovolaemic shock) - Not capillary test

A
Skin = cold, pale, clammy, slate-grey
Brain = drowsiness and confusion
35
Q

Clinical presentation of cardiogenic shock

A

Signs of myocardial failure
Raised jugular venous pressure (JVP)
Gallop rhythm
Basal crackles and pulmonary oedema

36
Q

Clinical presentation of septic shock

A

Pyrexia and rigors
Nausea and vomiting
Vasodilation with warm peripheries
Bounding pulse

37
Q

Clinical presentation of anaphylactic shock

A
Signs of profound vasodilation 
Warm peripheries
Low BP
Tachycardia
Bronchospasm
Pulmonary oedema
38
Q

What organs are most at risk of shock

A

Kidneys
Lungs
Heart
Brain

39
Q

What could result from shock affecting kidneys

A

Acute tubular necrosis

40
Q

What could result from shock affecting the lungs

A

Acute Respiratory Distress Syndrome (ARDS)

41
Q

What could result from shock affecting the heart

A

Myocardial ischaemia and infarction

42
Q

What could result from shock affecting the brain

A

confusion
irritability
coma

43
Q

Treatment of shock

A

ABC

Airway Breathing Circulation

44
Q

Treatment of shock - B (of ABC)

A
Breathing
Give 100% O2
Correct any immediately life threatening problems such as:
Congestive HF
Bronchospasm
Tension pneumothorax
45
Q

Treatment of shock - C (of ABC)

A

Circulation
Establish secure IV access
Give fluid quickly and blood if acute blood loss
Ensure haemostasis i.e. stop bleeding

46
Q

What is acute respiratory distress syndrome

A

Type of resp failure characterised by rapid onset of widespread inflammation in the lungs

47
Q

Which of these is true in ARDS:
High Pulmonary Arterial pressure (PAOP)
No cardiac failure

A

No cardiac failure is true

Pulmonary Arterial Pressure is NORMAL

48
Q

Extrapulmonary causes of ARDS

A

Shock of any cause
Head injury
Drug reaction
Sepsis

49
Q

Pulmonary causes of ARDS

A

Pneumonia
Chemical pneumonitis
Smoke inhalation
Near drowning

50
Q

Pathophysiology of ARDS

A

Injury to alveolar capillary membrane results in leakage of fluid into alveolar spaces
There is resulting neutrophil invasion which attracts more neutrophils (exudative phase)
Eventually fibroblasts come in and initiate healing (proliferative phase)
Forms Scar tissue (fibrotic phase)
Results in severely stuff lungs and thus Severe difficultly in ventilation and thus O2 blood perfusion

51
Q

*Clinical presentation of ARDS

A

Cyanosis
Tachypnoea (quick breathing)
Tachycardia
Peripheral vasodilation

52
Q

Investigations and management of sepsis

A
BUFALO
Blood cultures
Urine output (measure)
iv Fluid (administer)
Administer broad spectrum Antibiotics
serum Lactate (measure)
administer high flow Oxygen
53
Q

What is septic shock

A

Life-threatening condition that is characterised by low blood pressure despite adequate fluid replacement, and organ dysfunction or failure

54
Q

Symptoms of septic shock

A
feeling dizzy or faint
a change in mental state – such as confusion or disorientation
diarrhoea 
nausea and vomiting
slurred speech
severe muscle pain
severe breathlessness
less urine production than normal – for example, not urinating for a day
cold, clammy and pale or mottled skin
loss of consciousness
55
Q

Define neurogenic shock

A

Distributive type of shock resulting in low blood pressure, occasionally with a slowed heart rate, that is attributed to the disruption of the autonomic pathways within the spinal cord.
It can occur after damage to the central nervous system, such as spinal cord injury and traumatic brain injury.

56
Q

Management of Hypovolaemic shock

A

pg.790 (also do management of other shocks)