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CR 2 > Shock > Flashcards

Shock Flashcards

(50 cards)

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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

Study These Flashcards
A

Obstructive
Distributive
Hypovolaemic
Cardiogenic

22
Q

2 stages of shock

Study These Flashcards
A
  • Stage 1= compensated shock

- Stage 2= decompensated shock

23
Q

Define obstructive shock

Study These Flashcards
A

Physical obstruction to vessels leaving and entering the heart

24
Q

Causes of obstructive shock

Study These Flashcards
A

Pulmonary embolism
Pneumothorax
Cardiac tamonade

25
Signs and symptoms of obstructive shock if its tension pneumothorax
- Tachycardia - Chest pain - Absent pulse - Breath signs
26
Signs and symptoms of obstructive shock if its pulmonary embolism
- Hypoxia - Sudden onset chest pain - Shortness of breath
27
Define cardiogenic shock
Failure of the heart to pump efficiently
28
Name some causes of cardiogenic shock
- mi - heart failure - valvular disease
29
What do people with cardiogenic shock always present with
Chest pain, shortness of breath, nausea and vomiting
30
What do people with cardiogenic shock sometimes present with
Pulmonary oedema | Acute circulatory collapse
31
Define distributive shock
Loss of vasoconstriction at one end organ leading to excess blood flow at this organ but lack of blood flow at other organs
32
Define sepsis
Systemic response to presence of pathogens in blood or other organs
33
Define septic shock
Sepsis with hypotension
34
Temperature in somebody with sepsis
36 degrees
35
Heart rate in somebody with sepsis
90bpm
36
Resp rate in somebody with sepsis
>20 breaths per min
37
White blood cell count in somebody with sepsis
>12x10^9/L
38
Descibe process by which bacterial infection to shock
- Excessive host response - Micro-vascular damage - Lower systemic vascular resistance - Low BP - Shock
39
How do lipoproteins in bacterial wall lead to prevention of constriction
- Stimulates neutrophils and monocytes to release cytokines - Affects endothelium preventing constriction - Lowers SVR
40
Signs of hypovolaemic shock
Confusion, cold and clammy skin, high BP and HR, slow capillary refill time
41
How much blood loss is acutely life threatening
>40%
42
What are the immediate compensatory responses of shock
- 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
What are the long term compensatory responses of shock
- Increases renin and aldosterone - Thirst stimulated by angiotensin 2 receptors in brain - Peritubular cells sensitive to hypoxia and increase release of erythropoietin
44
What is class 1 shock (blood loss, pulse, BP, compensated?)
- 15% blood volume lost - Pulse <100 - Normal BP and PP - Fully compensated by immediate compensatory effects
45
What is class 2 shock (blood loss, heart rate and resp rate, pulse pressure? signs and symptoms?)
- Loss of 15-30% blood volume - Tachycardia and tachypnoea - Low pulse pressure - Clammy skin, delayed capillary refill
46
What is class 3 shock (how much blood lost, BP? Treatment required)
- >30% blood loss - Persistent BP drop - Patients require blood transfusion, plasma volume - May have end organ damage
47
What is class 4 shock (how much blood lost, signs and symptoms
- >40% blood loss - Confused/ unconcious - No urine output - Severly decreased systolic pressure - immediate transfusion required
48
What are the goals of shock treatment
Central venous pressure 8-12mmHg MAP> 65mmHg urine output 0.5ml/kg SVC>70%
49
How can circulating blood volume be restored
- IV colloids or crystalloids to restore preload
50
What drugs are used to treat shock
- Noradrenaline - Phenylephrine - ADH

CR 2 (33 decks)

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