Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Haematology > Shock > Flashcards

Shock Flashcards

1
Q

normal tissue perfusion relies on what 3 factors?

A

cardiac function
capacity of vascular bed
circulating blood volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how can normal perfusion be measured?

A

no perfect method

can use BP and MAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how is MAP measured?

A

CO X SVR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

classifications of shock?

A

hypovolaemic (blood loss)
cardiogenic (blood not working)
distributive (includes septic, anaphylactic, neurogenic etc)
obstructive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what can cause hypovolaemic shock?

A

acute haemorrhage
severe dehydration
burns
volume depletion > reduced SVR > vasoconstriction > reduced pre-load > reduced CO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what causes cardiogenic shock?

A 
pump failure (reduced CO)
usually ischaemia induced dysfunction of heart
can be cardiomyopathy, valvular problem, dysrhythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what causes obstructive shock?

A

mechanical obstruction to normal cardiac output in an otherwise normal heart
direct obstruction of CO eg PE, air embolism
restriction of cardiac filling eg tamponade, tension pneumothorax etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what causes distributive shock?

A

“hot shock”
septic, anaphylactic, acute liver failure, spinal cord injury
causes disruption of normal vascular autoregulation and profound vasodilation
results in poor perfusion despite cardiac output causing regional perfusion differences and alteration of oxygen extraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

endocrine shock?

A

severe uncorrected hypothyroidism, Addisonian crisis can cause reduced CO and vasodilation
paradoxically thyrotoxicosis can also cause it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

most common shock?

A

distributive (septic, anaphylactic etc)

realistically more mixed in most cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the sympatho-adrenal response?

A

pathways to preserve normal cardiac output and hence BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

organs have a degree of autoregulation between what MAP?

A

50-60 <> 150

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the neuroendocrine response?

A

release of pituitary hormones (ACTH, ADH and endogenous opiods) to maintain BP
cortisol = fluid retention, antagonises insulin
glucagon released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

pathophysiology of shock?

A

lack of perfusion > cell ischaemia > cascade of inflammatory mediators > cycle of vasoconstriction and oedema causing worsening cell ischaemia and cytotoxic damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is reperfusion injury?

A

cellular hypoxia causes local vasoconstriction, thrombosis, regional variations in perfusion, release of free-radicals and direct cellular trauma
followed by activation of neutrophils, release of pro-inflammatory cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

inflammatory response in shock?

A

can be due to pathological process (sepsis) or consequence of persisting hypoperfusion of tissues
causes harm when disseminated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what follows inflammatory response in shock?

A

2ndary immune suppression leaving predisposition to 2ndary infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

components of inflammatory response in shock?

A

complement cascade = attraction and activation of leucocytes
cytokine release = interleukins, TNF alpha
platelet activating factor = increased vascular permeability, platelet aggregation
lysosomal enzymes = myocardial depression, coronary vasoconstriction
adhesion molecules = damage to vessel walls, leucocyte attraction
endothelium derived mediators (NO)
imbalance between antioxidents and oxidents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what haemodynamic changes occur in shock?

A

vascular abnormalities (vasodilation/constriction)
maldistribution of blood flow
microcirculatory abnormalities (AV shunt, changed flow in capillary beds, failure of capillary recruitment, increased capillary permeability)
inappropriate activation of coagulation system
DIC
reperfusion injuries

20
Q

how does loss of vascular reactivity occur in shock?

A

inflammation pathways activate isoform of cNOS (iNOS) in vessel smooth muscle walls which produces lots of NO resulting in failure of vascular smooth muscle constriction (NO = vasodilator)

21
Q

what causes myocardial dysfunction?

A

(not due to reduced coronary blood flow)
circulating cytokines have direct myocardial effect
downregulation of beta receptors
decreased cardiomyofilament calcium sensitivity

22
Q

clinical features of cardiogenic shock?

A

hypotension + signs of myocardial failure

23
Q

signs of septic shock?

A

hypotension + pyrexia, vasodilation, rapid cap refill

24
Q

signs of hypovolaemic/obstructive? shock?

A

hypotension + raised JVP
pulsus paradoxus
signs of cause

25
Q

signs of anaphylactic (distributive) shock?

A

hypotension + profound vasodilation, erythema, bronchospasm, oedema

26
Q

classes of hypovolaemia in terms of blood loss?

A 
class 1 = <15%
class 2 = 15-30%
class 3 = 31-40%
class 4 = >40%
27
Q

changes in class 2?

A

HR may increase
pulse pressure decreased
-2 to -6 mEg/L base deficit
possible need for blood products

28
Q

changes in class 3?

A 
increased HR
normal/decreased BP
decreased PP
normal/increased RR
reduced urine output
reduced GCS
-6 to -10 base deficit
needs blood products
29
Q

changes in class 4?

A 
increased/very increased HR
decreased BP
decreased PP
increased RR
very reduced urine output
reduced GCS
-10+ base deficit
needs massive transfusion protocol
30
Q

clinical monitoring in shock?

A

examination (colour, temp, cap refill)
urine output (indicator of renal perfusion)
neurological (GCS indicates cerebral perfusion)
biochemical (acidosis and lactate levels are measure of general perfusion)

31
Q

how can BP be measured?

A

cuff or invasive via arterial line

can be normal pressure due to vasoconstriction but still hypoperfusing tissues

32
Q

how can central venous pressure be measured?

A

put a line in and measure via fluid?

33
Q

what other pressures should be measured?

A

pulmonary artery pressure
pulmonary capillary wedge pressures (surrogate for LA pressure)
- rarely used in practice due to risk

34
Q

how is CO monitored in shock?

A

gold standard = thermodilation with a PA catheter (rarely used outside specialist units)
can use pulse contour analysis or doppler US

35
Q

how is shock managed?

A

ABCDE
establish reliable wide bore IV access and resuscitate while investigating
identify and treat cause

36
Q

4 stages of management of shock?

A 
salvage
- obtain minimal BP (70-80), perform lifesaving measures
optimization
- provide oxygen availability
- optimize CO, SvO2 and lactate
stabilization
- organ support, minimise complications
de-escalation
- wean from vasoactive agents, achieve negative fluid balance
37
Q

MAP goal in shock?

A

65-70
however needs to be assed with clinical picture (e.g if patient is oliguric at 65 then aim for higher, if still haemorrhaging aim for lower)

38
Q

how is oxygen delivery measured?

A 
CO X (1.39 x Hb x SpO2) + (PaO2 x 0.003)
SvO2 can help estimate balance between supply and demand
39
Q

biggest components of oxygen delivery?

A

Hb
SpO2
CO

40
Q

fluid management of shock?

A

increase pre-load
rapid fluid replacement (mins)
- fluid challenge (300-500ml over 10-20 mins) with a target in mind (stop if non responsive)
- use either crystalloids, colloids or blood

41
Q

risks of rapid fluid replacement in shock?

A

balance rapid volume replacement and risk of fluid overload as shock increases risk of pulmonary oedema due to microvascular dysfunction

42
Q

how to decide which fluids to use?

A

crystalloids cheap and safe but lost from circulation quickly
colloids cheap but blood volumes required and can cause anaphylaxis
blood has good O2 and stays in circulation but scarce resource with multiple risk

43
Q

what is used as pharmacological treatment in shock when fluids don’t work?

A 
adrenaline (apha/beta agonist)
noradrenaline (most commonly used, alpha agonist)
vasopressin (ADH)
dopamine (ADH precursor)
dobutamine/dopexamine
44
Q

what is used in shocj when drugs don’t work?

A

mechanical support
cardiogenic = balloon pumps, L-VADs, R-VADs
severe cases = VA- ECMO

45
Q

side effects of resuscitation?

A

positive fluid balance (volume delivered never remains intra-vascular)
extra-vascular overload in an intra-vascularly dry patient causes sub-cutaneous oedema, wet lungs/ARDS, bowel oedema etc

46
Q

how can excess fluid be removed after shock has resolved (de-escalation)?

A

spontaneously
diuretic
dialysis

Haematology (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions