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Haematology > Shock > Flashcards

Shock Flashcards

1
Q

what is shock

A

A syndrome in which tissue perfusion is inadequate for the tissue’s metabolic requirement that results in a state of cellular and tissue hypoxia due to either reduced oxygen delivery, increased oxygen consumption, inadequate oxygen utilisation, or a combination of these processes

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2
Q

how do you calculate mean arterial pressure

A

cardiac output x systemic vascular resistance

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3
Q

how can you measure perfusion

A

BP

lactate, urine output

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4
Q

what are the causes of shock

A

hypovolaemic (haemorrhage, dehydration, burns= volume depletion= reduced SVR= vasoconstriction= reduced pre load and CO)

cardiogenic (MI, cardiomyopathy, valvular problems, dysrthmias = pump failure= reduced CO)

distributive (septic, anaphlylaxis, acute liver failure, spinal cord injuries = disruption of normal vascular autoregulation + profound vasodilation flushed, hot = poorly perfused despite increase CO)

obstructive (CO obstructed- PE, air embolism. Cardiac filling obstructed= tamponade, tension pneumothorax)

endocrine (severe hypo/hyperthyroidism, addisonian crisis = reduced CO and vasodilation)

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5
Q

what is the most common type of shock

A

distributive (septic)

- in reality usually a mixed picture

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6
Q

what is the most important pathway in BP autoregualtion

A

sympatho-adrenal response
(baroreceptors and chemoreceptors increased sympathetic nervous activity)
adrenal medulla increases aldosterone and renin to activate RAAS system)

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7
Q

what is the neuroendocrine response to shock

A

release of pituitary hormones: ACTH, ADH, endogenous opioids

release of cortisol: fluid retension, antagonises insulin to release glucose

release of glucagon

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8
Q

what is reperfusion injury

A

when local vasoconstriction, thrombosis, regional variations in perfusion, release of free radicals and direct cellular trauma cause activation on inflammatory mediators

this results in worsening cellular ischaemia, vasoconstriction and oedema which make shock worse

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9
Q

what are the components of the inflammatory response in shock

A

Activation of complement cascade – attraction and activation of leucocytes

Cytokine release – Interleukins, TNF-alpha

Platelet activating factor – Increased vascular permeability, platelet aggregation

Lysosomal enzymes – Mycardial depression, coronary vasoconstriction.

Adhesion molecules – damage to vessel walls, further leucocyte attraction

Endothelium derived mediators – Nitric oxide

Imbalance between antioxidents and oxidents

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10
Q

what haemodynamic changes happen in shock

A 
vasodilation/ constriction 
maldistribution of blood flow 
microcirculatory abnormalities- AV shunting, poor functioning capillary beds, increased capillary permeability 
inappropriate coagulation activation 
DIC
reperfusion injuries
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11
Q

what happens to vascular reactivity in shock

A

vascular smooth muscle fails to constrict (nitric oxide plays big role)

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12
Q

what causes myocardial dysfunction in shock

A

circulatory cytokines with direct myocardial effect
beta receptor down regulation
decreased cardiomyofilament calcium sensitivity

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13
Q

what are the different clinical features for the types of shock

A

ALL usually hypetensive

cardiogenic- signs of myocardial failure: pale, clammy, cold

obstructive: myocardial failure + raised JVP, pulsus paradoxus, signs of cause

Distributive:

  • septic shock (distributive): pyrexia, vasodilation, rapid cap refill
  • anaphylaxis: profound vasodilation, erythema, bronchospasm, oedema
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14
Q

what are the classes of hypovolaemia

A 
(on approx blood loss) 
class 1 <15%
class 2 (mild) 15-30%
class 3 (mod) 31-40%
class 4 (severe) >40%
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15
Q

what are the signs of class 1 hypovolaemia

A

normal obs
base deficit 0 to -2
monitor need to blood products

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16
Q

what are the signs of class 2 hypovolaemia

A

Hr normal or increased
pulse pressure decreased
base deficit -2 to -6
possible need for blood products

17
Q

what are the signs of class 3 hypovolaemia

A 
HR increased 
BP normal/ decreased 
PP decreased 
RR normal/ increased 
urine decreased 
GCS decreased 
base deficit -6 to -10
need blood products
18
Q

what are the signs of class 4 hypovolaemia

A 
HR increase/ v increasd 
BP decreased 
PP decreased 
RR increased 
urine output V decreased 
GCS decreased 
vase deficit -10 or less 
massive transfusion protocol needed
19
Q

what is pulse pressure

A

the difference between diastolic and systolic BP

20
Q

what is urine output a measure of

A

renal perfusion

21
Q

what is GCS an indicator of

A

cerebral perfusion

22
Q

how can you measure BP

A

cuff

invasive- arterial line

23
Q

what is central venous pressure used to measure

A

response to fluid

useful to follow trends not so much for one off valvue

24
Q

what pulmonary pressures can be meausred

A

pulmonary artery pressure
pulmonary capillary wedge pressure
(not done in practise usually)

25
Q

how is cardiac output monitored

A

gold standard- thermodilution with a PA catheter
pulse contour analysis
doppler ultrasonography

26
Q

when do you start fluid resus

A

ASAP- when investigating cause

27
Q

what are the steps of shock management (hypovolaemic)

A

obtain minimal acceptable BP (70-80)
oxygen (optimise CO, SVO2, lactate)
provide organ support
wean from vasoactive agents, achieve a negative fluid balance

28
Q

what is the goal MAP for most

A

65-70

29
Q

what are the biggesr influences on oxygen delivery

A

Hb- correct anaemia
SpO2- oxygen
CO- optimise

30
Q

why do you have to be careful wit rapid fluid replacement in shock

A

as shocked patients more at risk of pulmonary oedema due to microvascular dysfunction

31
Q

what is a fluid challenge

A

300-500mls in 15-20mins
MUST asses response
avoid other procedures that will stress the patient in this time
can be repeated but if patient unresponsive should stop

32
Q

what are the pros and cons of each type of fluid

A

crystalloids (saline, hartmanns) P- convenient, safe, cheap. C- rapidly lost from circulation into extravascular space, large volumes required

colloids - P-cheap, reduced volumes required. C- can cause anaphlyaxis

blood P- O2 carrying capacity, will stay in circulation. C- scarce resource, multiple risks

33
Q

what drugs can be given in hypovolaemic shock

A

(only when fluids not working, only by experienced specialist)

adrenaline (alpha/beta adrenergic, increases HR, contractility, vasodilation)

noradrenaline (alpha agonist, vasoconstriction)

vasopressin (ADH)

dopamine (precursor to the above)

dobutamine/ dopexamine

34
Q

what mechanical methods can be used to treat shock

A

in cardiogenic: balloon pumps, L-VADs, RVADs

if severe- VA-ECMO

35
Q

what is the management for hypovolaemic shock

A

Assessment of bleeding – estimation of volume loss, and speed of ongoing loss.

Establish source – may require imaging if stable

Temporisation – Direct pressure, tourniquet’s

Damage limitation resuscitation – until definitive control

Damage limitation surgery

36
Q

what are possible side effects of resus

A

extra vascular overload- sub cutaneous oedema, wet lungs/ ARDS, bowel oedema

37
Q

what is de-escalation

A

removing extra fluid from patient once shock resolved- spontaenous, diuretic, dialysis

Haematology (27 decks)

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