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CLASP - Sudden Death > Shock > Flashcards

Shock Flashcards

1
Q

what is shock?

A

condition of inadequate perfusion to sustain normal organ function

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2
Q

what are the 5 main classes of shock?

A 
hypovolaemic 
cardiogenic (MI dysfunction)
obstructive
distributive
cytotoxic
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3
Q

what is hypovolaemic shock?

A

insufficient circulating volume to fill the circuit

can be from loss of blood, interstitial fluid or pure water (rare)

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4
Q

clinical features of hypovolaemic shock?

A

depend on the degree of hypovolaemia

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5
Q

why is hypovolaemic shock so dangerous in young people?

A

as they compensate very well for a longer time and then suddenly deteriorate

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6
Q

4 main compensatory mechanisms in maintaining circulating volume?

A

baroreceptor reflex
sympathetic chronotropy/inotropy
capillary absorption of interstitial fluid
hypothalamo-pituitary-adrenal response

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7
Q

describe the baroreceptor reflex?

A

Stretch sensitive receptors in the carotid sinus (CNIX) and aortic arch (CNX)

Decreased stretch > decreased afferent input to medullary CV centres

Inhibition of parasympathetic (CNX) and enhanced sympathetic output > results in constriction of blood vessels to maintain BP

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8
Q

describe the sympathetic chronotropy/inotropy compensatory mechanism?

A

Release of circulating vasoconstrictors (adrenaline, angiotensin, noradrenaline, vasopressin)
Redirects fluid from peripheral and secondary organs

Resulting lactic acidosis drives chemoreceptors to enhance response

Circulating vasodilators also increased (involved decompensatory stages)

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9
Q

describe capillary absorption of intetstitial fluid?

A

reduced capillary hydrostatic pressure = inward net filtration

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10
Q

how can Cardiac output (CO) be increased?

A

increase HR
increase SV (inotropy)
increase both

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11
Q

why cant young children increase SV?

A

immature muscle

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12
Q

how does giving fluids change stroke volume?

A

should increase SV
greater volume loading during diastole increases SV
inotropy increases contractility

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13
Q

how is the frank starling curve affected in heart failure?

A

decreased contractility = curve shifted downwards

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14
Q

what is cardiogenic shock?

A

where heart doesnt work effectively as a pump to meet circulatory demands

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15
Q

most common cause of cardiogenic shock?

A
  • Most commonly a complication of MI but may also follow acute valve dysfunction
    ○ E.g acute mitral prolapse, myocarditis, cardiomyopathy etc
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16
Q

clinical signs of cardiogenic shock?

A

Poor forward flow, heart cant pump blood forward (hypotension/shock, fatigue, syncope)
Backpressure (pulmonary oedema, elevated JVP, hepatic congestion)

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17
Q

how is cardiogenic shock managed?

A

focused on increasing CO
give drugs which stimulate sympathetic NS and shift curve upwards
- dobutamine, adrenaline
- dopamine, dopexamine
- others (milrinone, levosimendan)
if heart is so impaired that drugs cant sort CO then use an intra-aortic balloon pump

18
Q

how does an intra-aortic balloon pump work?

A

Provides counterpropulsion
® Inflation during ventricular diastole (increased diastole = increased perfusion of coronary arteries)
® Deflation during ventricular systole (reduces afterload and systolic pressure = decreased force that heart has to pump against)

19
Q

why arent fluids given in cardiogenic shock?

A

there is often already oedema so fluids would make it worse

20
Q

what is obstructive shock?

A

where there is a physical obstruction to either the heart or the great vessels
(mainly affects filling of the heart rather than cardiac ejection)

21
Q

what can cause obstructive shock?

A

PE
pericardial effusion/tamponade
tension pneumothorax
basically anything blocking filling of the heart

22
Q

how is obstructive shock managed?

A

treat underlying cause

  • PE = anticoagulation +/- thrombolysis
  • tamponade = pericardial drainage
  • tension pneumothorax = decompression and chest drainage
23
Q

how is obstructive shock diagnosed?

A

ECHO (point of care testing)

  • PE = dilated and non-mobile right ventricle, bowing of IV septum due to pressure difference between ventricles
  • pericardial effusion/tamponade = fluid in pericardial sac compressing each chamber, impaired filling and contraction
24
Q

what is distributive shock?

A

circuit is dilated (too big) so blood volume si normal but bc the circuit is increased its not not enough to perfuse and BP drops
AKA vasodilatory/warm shock

25
Q

3 subtypes of ditributive shock?

A

Septic (bacterial endotoxin mediated capillary dysfunction)
Anaphylactic (inappropriate release of histamine from mast cells)
Neurogenic (loss of thoracic sympathetic outflow following spinal injury)

26
Q

describe septic shock management

A

Raising lactate levels can indicate hypoperfusion before hypotension occurs
Every hour delay of antibiotics increases mortality by 7.5%
Early use of vasopressors (vasoconstrictors) improves perfusion and minimises excessive fluid volumes

27
Q

what causes anaphylactic shock?

A

Uncontrolled activation of mast cells and degranulation

Release of histamine = vasodilation

28
Q

what is given in anaphylactic shock?

A

Adrenaline acts as a mast cell stabliser (stops degranulation) and also is a vasoconstrictor
Serum mast cell tryptase levels confirm the diagnose

29
Q

neurogenic shock vs spinal shock?

A

neurogenic = caused by spinal cord damage, spinal cord not attached, due to loss of sympathetic tone
spinal shock = also die to spinal injury but spinal cord still attached, loss of spinal reflexes, will recover?

30
Q

what causes neurogenic shock?

A

hypotension due to loss of descending sympathetic tone

inappropriate bradycardia occurs due to unopposed vagal tone (can be exacerbated by suction etc)

31
Q

mainstays of treatment for neurogenic shock?

A

dopamine alongside vasopressors

32
Q

4 Hs and 4 Ts causing cardiac arrest?

A
  • hypoxia
  • hypotension
  • hypothermia
  • hypo/hyperkalaemia
  • toxins
  • tamponade
  • thrombosis
  • tension pneumothorax
33
Q

how does CPR work?

A
  • Cyclical changes in intrathoracic pressure alternately pushes blood out of and sucks blood back into the chest
    ○ Hence importance of allowing recoil between compressions
34
Q

what rhythms are shockable?

A

VF

pulseless VT

35
Q

describe VF?

A

chaotic and unrecognisable ECG with no recognisable QRS complexes
can occur after MI, toxins, electrolyte abnormality etc

36
Q

describe pulseless VT?

A

can be monomorphic (rapid, broad QRS with constant QRS morphology) or polymorphic (torsades de pointes)

37
Q

what rhythms arent shockable?

A

pulseless electrical activity

asystole

38
Q

what usually causes pulseless electrical activity?

A

usually hypovolaemia

usually almost normal rhythm but just not enough blood

39
Q

how is pulseless electrical activity managed?

A

adrenaline 1mg IV every 3-5 mins

40
Q

how us asystole managed?

A

same as pulseless electrical activity

CLASP - Sudden Death (5 decks)

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