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Cardiorespiratory CC > Shock > Flashcards

Shock Flashcards

1
Q

Clinical Shock

A

Acute circulatory failure with inadequate or inappropriately distributed perfusion resulting in cellular hypoxia

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2
Q

Cellular hypoxia effect

A 
Cells switch from aerobic to anaerobic
Lactic acid production
Cell function ceases + swells
Membrane more permeable
Electrolytes + fluids seep in + out of cell
Na+/K+ pump impaired
Cells swell
Mitochondrial damage
Cell death
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3
Q

Normal CO

A

5l/min

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4
Q

Normal Systolic BP

A

120mmHg

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5
Q

Mean Arterial Pressure

A

100mmHg

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6
Q

Shock diagnosis

A

Likely if MAP<60mmHg

Clinical signs of hypo-perfusion of vital organs (tachycardia, tachypnoea, mental confusion, pallor)

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7
Q

BP equation

A

BP = Co x systemic vascular resistance

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8
Q

Low CO

A

Either HR low or Stroke Vol low

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9
Q

HR controlling factors

A

Feedback signals from baroreceptors in carotid sinus –> activate or inhibit medullary vasomotor centres –> activate or inhibit autonomic NS
Conscious perception of arousing stimuli activates or inhibits ANS

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10
Q

Stroke Volume controlling factors

A

Amount of blood in heart before start to contract- “preload”

Myocardial contractility

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11
Q

Stroke volume

A

Volume of blood pumped from left ventricle per beat

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12
Q

Preload on SV

A

Greater the preload –> greater the force of contraction –> greater the stroke volume

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13
Q

Starling’s Law

A

The force of contraction increases as the end diastolic volume increases

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14
Q

Decrease in Myocardial Contractility

A 
Cardiac disease
Hypoxia/hypercapnia
pH or electrolyte distribution
Drugs
Shock
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15
Q

Systemic vascular resistance

A

Maintained by balance between vasoconstrictors and vasodilators

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16
Q

Vasoconstrictors place of action

A

Mainly arterioles in end organs

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17
Q

Vasoconstrictor mechanism

A

1) Sympathetic NS- Release noradrenaline locally on alpha receptors on outside of arterioles
2) Angiotensin II in plasma acts on angiotensin AT1 receptor on endothelium lining arterioles –> contraction of underlying smooth muscle

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18
Q

Local vasoconstrictors

A

Released locally from endothelium

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19
Q

Endothelin

A

Local Vasoconstrictor

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20
Q

Prostacyclin

A

Vasodilator
Produced in endothelial cells from arachidonic acid
PGI2

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21
Q

Prostacyclin MOA

A

Reduces Ca entry into smooth muscle cells surrounding the endothelium
–> Reduces contractility of smooth muscle

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22
Q

Nitric Acid

A

Vasodilator
Gas
Produces in endothelial cells from arginine
Continually produced in healthy arterioles by action of moving blood on glycoproteins on the endothelial membrane

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23
Q

Nitric Acid MOA

A

Diffuses into underlying smooth muscle where it stimulates cyclic AMP formation –> decreases Ca entry and relaxes muscle

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24
Q

Adenosine

A

Released from endothelial cells + smooth muscle during activity

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25
Q

Vasoconstrictors

A

Noradrenaline
Angiotensin 2
Endothelin
5HT

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26
Q

Vasodilator

A

Prostacyclin
Nitric Oxide
Adenosine

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27
Q

Tissue Perfusion

A

Requires good CO and appropriate BP

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28
Q

Cardiac Output regulation

A

Preload

Heart Rate

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29
Q

BP regulation

A

CO

Systemic vascular resistance

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30
Q

Shock

A

Systemic vascular resistance not maintained OR

Preload decreases

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31
Q

Obstructive shock

A

Physical obstruction to vessels entering or leaving heart

e.g. pulmonary embolism

32
Q

Distributive shock

A

Loss of vasoconstriction in one or more end organs

Produce excess blood flow in system + poor perfusion of organs

33
Q

Hypovolaemic shock (Haemorrhagic shock)

A

Normally due to haemorrhage

34
Q

Cardiogenic shock

A

Due to failure of heart to pump efficiently and supply blood to the body

35
Q

Cardiopulmonary obstructive shock

A

Cardiogenic and obstructive shock grouped together

36
Q

Septic shock

A

In US

Distributive shock due to sepsis

37
Q

Obstructive shock example

A

Pulmonary embolism
Pneumothorax
Cardiac tamponade

38
Q

Distributive shock example

A

Sepsis
Anaphylaxis
Neurogenic

39
Q

Hypovolaemic shock example

A

Haemorrhage
Burns
Surgery or trauma
Loss of fluid + electrolytes from gut

40
Q

Cardiogenic shock examples

A

MI
Heart failure
Arrhythmias
Ventricular septal rupture

41
Q

Hypovolaemic shock signs explanation

A

Indicate that SNS attempting to maintain O2 supply to heart + brain despite decreased preload

  • -> if succeeding, compensating shock
  • -> if failing, decompensating shock
42
Q

Hypovolaemic shock signs

A 
Confusion/anxiety
Cold
Clammy skin
Low BP
High HR
Slow capillary refill
Greyish pallor
Oliguria- low output of urine
43
Q

Suspected GI bleeding

A 
Hematemesis
Melena
Alcohol drinking history
Excessive NSAID use
Coagulopathies
44
Q

Cardiogenic shock Signs

A

Most have AMI- chest pain, shortness of breath, diaphoresis, nausea, vomiting
Pulmonary oedema
Acute circulatory collapse
Presyncopal or syncopal symptoms

45
Q

Septic (distributive) Shock signs

A

Low BP
Tachycardia
Non-specific symptoms- fever, chill, rigor, fatigue, malaise
Fever common in sepsis

46
Q

Septic shock fatality

A

Up to 50% patients will die/have permanent organ damage despite treatment

47
Q

Obstructive shock main cause

A

Tension pneumothorax

48
Q

Obstructive shock signs

A 
Tachycardia
Anxiety
Chest pain
Affected breath sounds
Tracheal deviation if pneumothorax
49
Q

Pulmonary embolism presentation

A

Abrupt onset of pleuritic chest pain
Shortness of breath
Hypoxia

50
Q

Hypovolaemic shock- haematological system

A

Activation of coagulation cascade
Contraction of bleeding vessels- local thromboxane A2 release
Activation of platelets- thromboxane A2
Immature clot formation

51
Q

Hypovolaemic shock- CV system

A

Sympathetic NS activation
Help redistribute blood to brain, heart and kidneys
Increased HR
Increased myocardial contractility
Constriction of peripheral blood vessels in skin, muscle + GI tract

52
Q

Hypovolaemic shock- Renal system

A

Increases renin secretion- Angiotensin II increase as a result

53
Q

Angiotensin II effect

A

Vasoconstriction of arteriolar smooth muscle in skin, muscle + GI tract
Stimulation of aldosterone secretion –> increases sodium reabsorption + water reabsorption

54
Q

Hypovolaemic shock- neuroendocrine system

A

Releases ADH from posterior pituitary in response to decreased BP + decreased Na plasma conc.

55
Q

ADH effect

A

Increased reabsorption of water + salt by distal tubule, collecting ducts + loop of Henle

56
Q

Total body water

57
Q

Intracellular water

58
Q

Extracellular water

59
Q

Blood volume

A

4.5-5 litres

60
Q

Life threatening blood loss

A

Acute loss >40% (>2 litres)

61
Q

Venous Bleed compensatory response- haemorrhage

Immediate- seconds to mins

A

Drop in venous return reduces SV + CO –> decreased BP
Baroreceptors increase sympathetic outflow –> increase in HR + contractility
Sympathetic NS constricts large veins to move blood out from venous reservoir + restore preload

62
Q

Arterial bleed compensatory response- haemorrhage

Immediate- seconds to mins

A

BP drops
Baroreceptors detect –> increase sympathetic outflow
Vasomotor centre in medulla signals to hypothalamus to release vasopressin (ADH)
Reduced preload –> reduced ANP –> urine flow + Na excretion decreased

63
Q

Haemorrhage Long term compensation

A

Increased renin release –> angiotensin II release
Aldosterone release by Angiotensin II- long lasting effect in increased Na retention
Thirst stimulated by Angiotensin II receptors in brain (subfornical organ above hypothalamus) –> increased water intake

64
Q

Haemorrhage long term compensation pt 2

A

Albumin + other protein synthesis in liver

Fibroblasts sensitive to hypoxia- release EPO to stimulate RBC production –> haematocrit back to normal

65
Q

Hypovolaemic shock CLASS 1

A 
Loss <15% BV
Blood donation/minor injury
Fully compensated normally
Normal/slightly fatigued
Don't drive for a few hours
66
Q

Hypovolaemic shock CLASS 2

A 
Loss 15-30% BV
Tachycardia
Tachypnoea
Decrease pulse pressure
Cool clammy skin
Delayed capillary refill
Slight anxiety
--> rest + food + water patients will recover
67
Q

Hypovolaemic shock CLASS 3

A 
Loss >30% BV
Persistent BP drop
Anxious/Confused
Most require plasma vol. expanders/blood transfusion
End-organ damage, especially kidneys
68
Q

Hypovolaemic shock CLASS 4

A 
>40% loss BV
V confused/unconscious
Tachycardia
No urine
Severely decreased systolic BP
Life threatening
Blood transfusion
69
Q

Sepsis

A

Systemic response to presence of pathogens in blood or other organs
Bacterial toxins and/or host response leads to microvascular damage in one or more organs

70
Q

Sepsis Manifestations

A 
equal or more than 2 of:
Temp >38 or <36
HR > 90bpm
RR > 20bpm
WBC > 12x109/L
71
Q

Septic shock

A

Sepsis without hypotension

72
Q

Sepsis damage

A

Lipolysaccharide (LPS) in Gram -ve bacterial cell walls stimulate neutrophils + monocytes to release cytokines

  • -> damage endothelium + prevent normal vasoconstriction
  • -> decreased vascular resistance in organs
73
Q

Management hypovolaemic shock

A 
Restore BV with IV colloids (gelatins, dextrans, 4% or 20% albumin) or crystalloids (isotonic or hypertonic saline, ringer lactate)
Vasopressor drugs (dopamine, noradrenaline etc.) to restore BP
74
Q

Sepsis shock management

A

Appropriate antimicrobials

75
Q

Therapeutic Goals shock

A

Central venous pressure 8-12mmHg
MAP >65mmHg
Urine output 0.5ml/kg/h
Central venous oxygenation saturation >70%

Cardiorespiratory CC (34 decks)

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