Shock Flashcards

1
Q

Define clinical shock

A

Acute circulatory failure with poorly distributed tissue perfusion leading to cellular hypoxia

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2
Q

What is normal MAP

A

100mmHg

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3
Q

What is MAP is a person with clinical shock

A

60mmHg

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4
Q

Describe how cellular hypoxia leads to cel death

A
  • Cells switch from aerobic to anaerobic
  • Lactic acid is produced
  • Cell function ceases, swells
  • Membrane becomes more permeable
  • Electrolytes and fluids move in and out
  • Na+/K+ pump damage
  • Mitochondria damage
  • Cell death
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5
Q

What 2 things control heart rate

A

Baroceptors in carotid sinus activate/ inhibit ANS

Concious threat perception

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6
Q

What 2 things control stroke volume

A

Preload

Myocardial contractability

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7
Q

Is it usually heart rate or stroke volume

A

Stroke volume

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8
Q

When is it heart rate impaired

A

Drugs/ CNS involved

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9
Q

Define preload

A

Amount of blood in heart before it contracts

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10
Q

The greater the preload…

A

Greater force of contraction

Greater the stroke volume

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11
Q

3 ways that increase myocardial contractility

A

Sympathic nervous system
Circulating catecholamines
Inotrope drug (b1 agonists)

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12
Q

3 ways that myocardial contractility can decrease

A

Cardiac disease
Hypoxia
pH/ electrolyte disturbance
Drugs (bb, ccb)

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13
Q

What mainly regulates systemic venous resistance

A

Arteriolar constriction at end organs

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14
Q

4 ways that arteriolar constriction is regulated

A
  • Sympathetic nervous system releasing noradrenaline
  • Circulating hormones like angiotensin 2
  • Endothelin released from lining enodthelium constricts arterioles and NO
  • Prostacyclin is vasodilator
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15
Q

Where is noradrenaline released from

A

Outside the nerve terminal

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16
Q

What receptors does noradrenaline act on and where are these located?

A

Catecholamine alpha receptors in the tunica media

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17
Q

What receptors does angiotensin act on

A

AT1 receptors lining the lumen

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18
Q

Another name for prostaglandin

A

PG12

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19
Q

Where is prostglandin produced and from what

A

Endothelial cells from arachiodonic acid

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20
Q

2 functions of prostaglandin

A

Prevents formation of platelet plug by inhibiting platelet activation
Local vasodilator that acts by reducing calcium entry

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21
Q

Name the 4 classifications of shock

A

Obstructive
Distributive
Hypovolaemic
Cardiogenic

22
Q

2 stages of shock

A
  • Stage 1= compensated shock

- Stage 2= decompensated shock

23
Q

Define obstructive shock

A

Physical obstruction to vessels leaving and entering the heart

24
Q

Causes of obstructive shock

A

Pulmonary embolism
Pneumothorax
Cardiac tamonade

25
Q

Signs and symptoms of obstructive shock if its tension pneumothorax

A
  • Tachycardia
  • Chest pain
  • Absent pulse
  • Breath signs
26
Q

Signs and symptoms of obstructive shock if its pulmonary embolism

A
  • Hypoxia
  • Sudden onset chest pain
  • Shortness of breath
27
Q

Define cardiogenic shock

A

Failure of the heart to pump efficiently

28
Q

Name some causes of cardiogenic shock

A
  • mi
  • heart failure
  • valvular disease
29
Q

What do people with cardiogenic shock always present with

A

Chest pain, shortness of breath, nausea and vomiting

30
Q

What do people with cardiogenic shock sometimes present with

A

Pulmonary oedema

Acute circulatory collapse

31
Q

Define distributive shock

A

Loss of vasoconstriction at one end organ leading to excess blood flow at this organ but lack of blood flow at other organs

32
Q

Define sepsis

A

Systemic response to presence of pathogens in blood or other organs

33
Q

Define septic shock

A

Sepsis with hypotension

34
Q

Temperature in somebody with sepsis

A

36 degrees

35
Q

Heart rate in somebody with sepsis

A

90bpm

36
Q

Resp rate in somebody with sepsis

A

> 20 breaths per min

37
Q

White blood cell count in somebody with sepsis

A

> 12x10^9/L

38
Q

Descibe process by which bacterial infection to shock

A
  • Excessive host response
  • Micro-vascular damage
  • Lower systemic vascular resistance
  • Low BP
  • Shock
39
Q

How do lipoproteins in bacterial wall lead to prevention of constriction

A
  • Stimulates neutrophils and monocytes to release cytokines
  • Affects endothelium preventing constriction
  • Lowers SVR
40
Q

Signs of hypovolaemic shock

A

Confusion, cold and clammy skin, high BP and HR, slow capillary refill time

41
Q

How much blood loss is acutely life threatening

A

> 40%

42
Q

What are the immediate compensatory responses of shock

A
  • BP fall detected by baroceptors and these increase sympathetic outflow
  • Increased HR
  • Large vein constriction to restore preload
  • Medullary vasomotor signals to hypothalamus to release ADH and reduces ANP release
  • Reduced urine flow
43
Q

What are the long term compensatory responses of shock

A
  • Increases renin and aldosterone
  • Thirst stimulated by angiotensin 2 receptors in brain
  • Peritubular cells sensitive to hypoxia and increase release of erythropoietin
44
Q

What is class 1 shock (blood loss, pulse, BP, compensated?)

A
  • 15% blood volume lost
  • Pulse <100
  • Normal BP and PP
  • Fully compensated by immediate compensatory effects
45
Q

What is class 2 shock (blood loss, heart rate and resp rate, pulse pressure? signs and symptoms?)

A
  • Loss of 15-30% blood volume
  • Tachycardia and tachypnoea
  • Low pulse pressure
  • Clammy skin, delayed capillary refill
46
Q

What is class 3 shock (how much blood lost, BP? Treatment required)

A
  • > 30% blood loss
  • Persistent BP drop
  • Patients require blood transfusion, plasma volume
  • May have end organ damage
47
Q

What is class 4 shock (how much blood lost, signs and symptoms

A
  • > 40% blood loss
  • Confused/ unconcious
  • No urine output
  • Severly decreased systolic pressure
  • immediate transfusion required
48
Q

What are the goals of shock treatment

A

Central venous pressure 8-12mmHg
MAP> 65mmHg
urine output 0.5ml/kg
SVC>70%

49
Q

How can circulating blood volume be restored

A
  • IV colloids or crystalloids to restore preload
50
Q

What drugs are used to treat shock

A
  • Noradrenaline
  • Phenylephrine
  • ADH