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CR2 > 32 - Haemorrhage and Shock > Flashcards

32 - Haemorrhage and Shock Flashcards

1
Q

What is clinical shock

A

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

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2
Q

How is tissue perfusion usually maintained

A

CO - 5l/min
BP - 120mmHg
MAP - 100mmHg

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3
Q

What are the signs of shock

A

MAP <60mmHg and hypo perfusion of vital organs (tachycardia, tachypnea, mental confusion , pallor)

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4
Q

What causes low BP

A

Low cardiac output

Low vascular resistance

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5
Q

What are the effects of cellular hypoxia

A 
Cells switch to anaerobic metabolism
Lactic acid produced
Cell function ceases and swells
Membrane becomes more permeable
Electrolytes and fluids seep in and out
Na+/K+ pump impaired
Cells swell 
Mitochondria damagge
Cell death
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6
Q

What are the factors controlling heart rate

A

Baroreceptors in carotid sinus

Arousing stimuli - ANS

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7
Q

What are factors controlling stroke volume

A

Blood in heart before it contracts

Myocardial contractility

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8
Q

What is starling’s law of the heart

A

Greater the preload, the greater the force of contraction
Greater the stroke volume
(If preload decreases then SV decreases)

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9
Q

What increases myocardial contractility

A

Sympathetic NS
Circulating catecholamines
Ionotrope drugs - B1 agonists

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10
Q

What decreases myocardial activity

A

Cardiac disease
Hypoxia/hypercapnia
Ph or electrolyte disturbance
Drugs - BB, CCB

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11
Q

What is prostacyclin

(PG12) produced from

A

Produced in endothelial cells from arachidonic acid

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12
Q

What is the action of prostacyclin

A 
= Prevents formation of platelet plug –inhibits platelet activation
= Local vasodilator – reduces Ca entry into smooth muscle to reduce contractility
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13
Q

What is the action of thromboxane

A

local vasoconstriction and platelet aggregation

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14
Q

What causes shock

A

SVR not maintained - arterioles no longer constrict

Preload decreases - loss of blood volume or obstruction

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15
Q

What is compensation

A

The initial stage where homeostatic mechanisms are activated

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16
Q

What is decompensation

A

When • Arterioles cannot maintain constriction/preload too great, end organs start to fail

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17
Q

What is distributive shock

A

Loss of vasoconstriction
Excess blood flow
poor perfusion of other organs

18
Q

What are causes of distributive shock

A

Sepsis
Anaphylaxis
Neurogenic

19
Q

What are signs of distributive shock

A

Low BP
Tachycardia
Fatigue

20
Q

What is septic shock

A

Type of distributive shock

Sepsis is when the host response leads to micro vascular damage in one or more end organs

21
Q

What causes lack in vasoconstriction in sepsis

A

Neutrophils and monocytes release cytokines that prevent normal vasoconstricion
may be severe enough to reduce BP to shock level

22
Q

What is hypovolemic shock

A

Due to haemorrhage (often called haemorrhagic shock)

23
Q

What are some causes of hypovolemic shock

A

Haemorrhage
Burns
Surgery or trauma
Loss of fluid and electrolytes

24
Q

Signs of hypovolemic shock

A 
Confusion/anxiety
Cold
Low BP
High HR
Slow capillary refill 
(Make sure you check the history as internal bleeding is not as obvious)
25
Q

What is life threatening blood loss values

A

Total body water is 45 litres (IC 27 and EC 18)

So if Blood volume is 4.5-5 litres – loss >40% (>2 litres ) is life threatening

26
Q

What is the

immediate compensatory response to haemorrhage

A

Immediate = baroreceptors increase sympathetic outflow, increase HR and contractlity, vasomotor centre in medulla signals to hypothalamus to release vasopressin to reduce preload and release ANP so urine flow and excretion decrease

27
Q

What is the long term compensatory response to haemorrhage

A 
Increased renin release 
Aldosterone released from adrenal cortex by angiotensin II
Thirst is stimulated
Increase in water intake
Na+ and H20 retention is increased
Albumin is stimulated
28
Q

What is class I of hypovolemic shock

A

– Loss of <15% blood volume (blood donation, minor injury, fully compensated, fatigue/slightly normal)

29
Q

What is class II of hypovolemic shock

A
  • Loss of 15-30% of blood (tachycardia, tachypnea, dc in PP, slight anxiety, delayed cap refill, rest and water/food, will compensate)
30
Q

What is class III of hypovolemic shock

A
  • Loss of >30% of blood (persistent drop in BP, anxious patient, confused, require plasma volume expanders or blood transfusion, may have end-organ damage)
31
Q

What is class IV of hypovolemic shock?

A

Loss of >40% of blood volume (confused/unconscious, tachycardia, no urine output, severely decreased systolic pressure, life threatening hemorrhage, need blood transfusion)

32
Q

What is cardiogenic shock

A

Failure of the heart to pump efficiently and supply blood to the body

33
Q

Causes of cardiogenic shock

A

 myocardial infarction, heart failure, arrhythmia, ventricular septal rupture, Ischaemic Cardiomyopathy, Valvular Disease

34
Q

What are signs of cardiogenic shock

A

AMI = Chest pain, SOB, Nausea

Pulmonary oedema, acute circulatory collapse

35
Q

What pathways are disrupted in neurogenic shock

A

Automatic pathways in SC

36
Q

How do you manage shock if the cause is hypovolemia

A

Restore circulating BV with IV colloids (gelatins, dextrans, hydroxyethyl starches, or 4% or 20% albumin) or crystalloids (isotonic or hypertonic saline, or Ringer lactate solution)

37
Q

What drugs restore BP

A

Vasopressor drugs - Dopamine, noradrenaline, phenylephrine, ADH

38
Q

What do you give to a patient if the cause of shock is sepsis

A

Antimicrobials

39
Q

central venous pressure

A

8 – 12 mmHg

40
Q

Mean arterial pressure

A

≥ 65 mmHg

41
Q

Urine output

A

0.5 mL/kg/h

42
Q

Mixed venous oxygen saturation

A

≥ 70%

CR2 (34 decks)

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