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3 Haematology > Shock > Flashcards

Shock Flashcards

1
Q

what does the normal perfusion of tissue rely on

A

Cardiac function
Capacity of vascular bed
Circulating blood volume

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2
Q

how is perfusion measured

A

no easy way to measure

blood pressure is a surrogate

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3
Q

how do you calculated mean arterial pressure (MAP)

A

cardiac output x systemic vascular resistance

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4
Q

what are the causes of shock

A

Hypovolaemia - not enough blood in the system

Cardiogenic - pump not working

Distributive - circuit gets bigger (eg mass vasodilation)

Obstructive (somethings blocking normal CO)

Endocrine

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5
Q

what is hypovolaemic shock (and causes)

A

Tissue under perfusion due to loss of blood/plasma from the circuit

caused by :

  • acute haemorrhage
  • severe dehydration
  • burns
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6
Q

what is the physiology behind hypovolaemic shock

A

volume depletion

causes reduced systemic vascular resistance

causes reduced preload leading to reduced cardiac output

overall causing a major drop in MAP

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7
Q

what is cardiogenic shock

A

‘pump failure’ - heart can no longer pump blood around the body causing big drop in CO therefore big drop in MAP

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8
Q

Causes of cariogenic shock

A

Ischaemia due to myocardial dysfunction

Cardiomyopathies

Vascular problems

Dysrhthmias

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9
Q

if an MI causes cardiogenic shock what does it suggest

A

> 40% of the left ventricle is involved

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10
Q

what is obstructive shock

A

mechanical obstruction to cardiac output in a normal heart

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11
Q

causes of obstructive shock

A

direct obstruction to cardiac output

  • PE
  • Air-embolism

Restriction of cardiac filling:

  • tamponade
  • tension pneumothorax
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12
Q

what is distributive shock

A

‘hot’ shick

due to disruption of normal vascular auto-regulation causing profound vasodilation

poor perfusion despite increased cardiac output

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13
Q

causes of distributive shock

A

sepsis
anaphylaxis
acute liver failure
spinal cord injuries

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14
Q

causes of endocrine shock

A

severe uncorrected hypothyroidism

addisonian crisis

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15
Q

what is endocrine shock

A

reduced CO and vasodilation with endocrine cause

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16
Q

what is the most common type of shock

A

Distributive (septic)

17
Q

what is the sympatho-adrenal response

A

pathways to preserve normal cardiac output and hence blood pressure

increased sympathetic response
increased noradrenaline
increased adrenaline

causes and increase in HR, contractility, and decreased veno-dilation

this maintains cardiac output

(RAAS maintains BP)

18
Q

what is the neuroendocrine response

A

release of pituitary hormones (adrenocorticotrophic hormone, anti-diuretic hormone, endogenous options)

release of cortisol leads to fluid retention

release of glucagon

some shock states blunt the ACTH response

19
Q

what is the pathophysiology behind shock

A

poor perfusion

cascade of inflammatory mediators as a consequence of ischaemia

causes a vicious cycle of vasoconstriction and oedema which worsens cellular ischaemia and causes direct cytotoxic damage

20
Q

what causes the inflammatory response in shock

A

Part of the pathological process (sepsis)

a consequence of persisting hypo perfusion

can lead to secondary immunosuppression leading to infection

21
Q

what is the inflammatory response

A

activation of complement cascade and leukocytes

cytokine release (interleukins, TNF alpha)

lysosomal enzymes released (myocardial depression, coronary vasoconstriction)

adhesion molecules (damage to vessel walls, further leukocyte attraction)

endothelium mediators (nitric oxide)

imbalance between antioxidants and oxidants

22
Q

haemodynamic changes in shock

A

vascular abnormalities (vasodilation or vasoconstriction)

maldistribution of blood flow

circulatory abnormalities (AV shunting, increased permeability etc)

inappropriate activation of coagulation

reperforation injuries

23
Q

what does nitric oxide do

A

regulates blood flow, coagulation, neural activity and immune function

activated by inflammatory pathway to prevent vasoconstriction

24
Q

what is myocardial dysfunction

A

reversible biventricular systolic and diastolic dysfunction

NOT because of reduced coronary blood flow but because of:

  • circulating cytokines with myocardial effect
  • beta-receptor down regulation
  • decreased cardiomyofilament calcium sensitivity
25
Q

what are they types of hypovolaemia

A 
Class I - <15% blood loss
Class II (mild) - 15-30% blood loss 
Class III (moderate) - 31-40% blood loss 
Class IV (severe) - >40% blood loss
26
Q

Clinical signs of hypovolaemic shock

A

Examination
-pale, cold skin, prolonged cap refill

Urine output
-indicator of renal perfusion

Neuro exam
-disturbed consciousness means decreased cerebral perfusion

biochemical markers

  • acidosis
  • lactate levels
27
Q

how do you monitor cardiac output

A

thermodilution with a PA catheter (gold standard)

pulse contour analysis

doppler ultrasound

28
Q

management of shock

A

Prompt diagnosis and treatment critical

ABC approach

establish wide bore IV access and resuscitate will investigating

identify and treat underlying cause

29
Q

what are the goals of shock management

A

re-establish sufficient perfusion to allow adequate tissue oxygen delivery

MAP target 65-70 but depends on patient

30
Q

what are the biggest components to oxygen delivery

A

Hb
SpO2
CO

correct anaemic and insure SpO2 is normal

31
Q

how do manage fluids in shock treatment

A

Increase pre-load

Rapid fluid replacement (minutes)

balance between rapid volume replacement and fluid overload

shock patients are more susceptible to pulmonary oedema

32
Q

what is a fluid challenge

A

rapid administration of fluid and assessment of response

not so fast to provoke stress response

usually 300-500ml over 10-20 mins

33
Q

what types of fluids can be used

A

Crystalloids

  • convenient, safe, cheap
  • rapidly lost to extravascular space so need to give a lot

colloids

  • cheapish, reduced volume required
  • can also cause anaphylaxis and no benefit over crystalloids

blood

  • oxygen carrying and will stay in circulation
  • scarce resource, multiple risks
34
Q

If fluids stop working, what can be used instead to bring up blood pressure

A

Pharmacological treatments

Adrenaline (alpha/beta adrenergic agonist)

Noradrenaline (alpha agonist)

Vasopressin (ADH)

Dopamine (precursor to the above)

Dobutamine/dopexamine

35
Q

what to do if fluids and pharmacological management fail to increase MAP

A

mechanical support

cariogenic shock - balloon pumps, ventricular assist devices

VA-ECMO (mechanical circulatory support)

36
Q

what are the side effects of resuscitation

A

Extravascular fluid overload

sub-cutaneous oedema obvious

bowel oedema, acute respiratory distress, lung oedema

37
Q

four stages of shock management

A

salvage (get a minimal acceptable BP)

optimise (provide adequate oxygen deliver)

Stabilisation (provide organ support)

de-escalation (wean from vasoactive agents, get a -ve fluid balance)

38
Q

what does de-escalation (de-resuscitation) involve

A

removing extra fluid once shock has resolved

diuretics, dialysis, spontaneous

3 Haematology (25 decks)

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