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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 types of shock

A 
hypovolaemic 
cardiogenic
obstructive 
distributive 
cytotoxic
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3
Q

what is cytotoxic shock

A

uncoupling of tissue oxygen delivery and mitochondrial uptake

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4
Q

what can cause cytotoxic shock

A 
CO poisoning 
CN poisoning (cyanide)
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5
Q

what is hypovolaemic shock

A

insufficient circulating volume to fill the circuit

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6
Q

what can cause hypvolaemic shock

A

blood loss
interstitial fluid
pure water deficit (severe dehydration -rare)
third space losses (interstitial/ extravascular/ extracellular)

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7
Q

what are the clinical features of hypovolaemic shock

A

depends on degree of hypovolaemia

  • tachycardia
  • hypotension
  • tachypnoeic
  • reduced urine output
  • anxious -> confused and lethargic
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8
Q

who is most at risk in hypovolaemic shock

A

young people- as compensate very well and then crash

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9
Q

what are the compensatory mechanisms for hypovolaemic shock

A

baroreceptor reflexes
sympathetic mediated neurohormonal response
capillary absorption of interstitial fluid
hypothalamo-pituitary response

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10
Q

explain the baroreceptor compensatory mechanism for hypovolaemic shock

A

stretch sensitive receptors in the carotid sinus (CNIX) and aortic arch (CNX) sense decrease stretch
=decreased afferent input to medullary CV centres
=inhibition of parasympathetic (CNX) and enhanced sympathetic output

=increase HR and inotropy

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11
Q

explain the sympathetic mediated neurohormonal response compensatory mechanism for hypovolaemic shock

A

sympathetic chronotropy and inotropy from baroreceptor reflex
=release of circulating vasoconstrictors (adrenaline, angiotensin, norad, vasopressin)
=redirects fluid from peripheral and secondary organs
=lactic acidosis
=drives chemoreceptors to enhance response

in decompensatory stage circulating vasodilators also increased

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12
Q

explain capillary absorption as a compensatory mechanism for hypovolaemic shock

A

reduced capillary hydrostatic pressure causes inward net filtration of interstitial fluid

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13
Q

explain the hypothalamo-pituitary-adrenal response as a compensatory mechanism for hypovolaemic shock

A

internal baroreceptors mediate renin release from juxtaglomerular apparatus
resulting Ang II enhances vasoconstriction and ADH secretion
=enhances renal reabsorption of sodium and water

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14
Q

what is a increase in inotropy

A

increase in heart contractility

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15
Q

how does the heart increase its cardiac output

A

increase rate (nerves, hormones)
increase stroke volume (blood volume, vascular resistance)
or increase both

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16
Q

how does inotropy affect the frank starling curve

A

shifts it upwards- increases contractility

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17
Q

what happens to the frank starling curve in heart failure

A

failing heart has decreased contractility - curves shifts down

EDV increases to maintain SV but this results in pulmonary congestion

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18
Q

what does it mean when a patient is sensitive to fluids

A

given fluid when someone is hypovolaemic will have a much bigger effect - a small change in preload will result in a significant increase in contraction
this response lessens as the patient becomes more hypervolaemic

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19
Q

what do you need to consider before giving fluids

A

know what they are and the dose needed
consider constitution of patient
consider fluid and electrolyte balance
consider difference in fluid for resus and maintenance

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20
Q

what is cardiogenic shock

A

inability of the heart to pump to meet circulatory demands

myocardial dysfunction causing reduction in systolic function and cardiac output

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21
Q

what can cause cardiogenic shock

A 
mostly complication of MIs
acute valve lesion e.g acute mitral prolapse, MI affecting papillary muscle- valve prolapse 
myocarditis 
cardiomyopathy 
myocardial contusion (trauma)
22
Q

what are the clinical signs of cardiogenic shock

A

(caused by poor forward flow): hypotension/ shock, fatigue, syncope

(backpressure): pulmonary oedema, elevated JVP, hepatic congestion

23
Q

what is positive inotropy

A

increase in force of cardiac contraction regardless of preload

24
Q

what increases inotropy physiologically

A

sympathetic nervous stimulation

25
Q

what drugs increase inotropy

A

beta and dopaminergic agents

beta- dobutamine, adrenaline
dopamine- dopamine, dopexamine

others- milrinone/ levosimendan

26
Q

when might you give inotropic drugs

A

when someone has cardiogenic shock after MI but also have pulmonary oedema due to heart failure

27
Q

what is an intra-aortic balloon pump

A

given to people in cardiogenic shock to due heart failure after an MI

  • inflates during ventricular diastole to increase diastolic pressure and increase coronary artery perfusion
  • deflates during systole to decrease systolic pressure (reduces the pressure the heart has to beat against lowering myocardial wall stress and O2 demands)
28
Q

what is obstructive shock

A

involves a physical obstruction to either the heart of great vessels = reduced preload and cardiac output
mainly affects cardiac filling rather than ejection

29
Q

what is the treatment for obstructive shock

A

depends on cause:
PE- anticoagulation +/- thrombosis
cardiac tamponade- pericardial drainage
tension pneumothorax- decompression and chest drainage

30
Q

what are the causes of obstructive shock

A

PE- stops blood getting back from lungs

tamponade and tension pneumothorax- heart compressed and unable to fill

31
Q

what does a PE look like on echo

A

dilated, hypokinetic RV (right side not contracting well due to high pressure)
bowing of interventricular septum to the left (less pressure on left side)
hyperkinetic RV apec (McConnels sign)

32
Q

what does a pericardial effusion/ tamponade look like on echo

A

fluid accumulation in pericardial sac
compresses each of the chamber
impairs cardiac filling and contraction in all four chambers

33
Q

why does a tension pneumothorax cause obstructive shock

A

air trapped in pleural cavity increases intrathoracic pressure- if this higher than venous pressure wont get cardiac filling

also displacement of mediastinal structures by air impairs cardiac filling and function

34
Q

what is disruptive shock

A

Significant reduction in SVR beyond the compensatory limits of increased cardiac output

(circuits too big)
aka vasodilatory/ warm shock
generally high cardiac output but insufficient to maintain forward perfusion

35
Q

what are the subtypes of distributive shock

A

septic- bacterial endotoxin mediated capillary dysfunction

anaphylactic- mast cell release of histaminergic vasodilators

neurogenic- loss of thoracic sympathetic outflow follow spinal injury

36
Q

what is the role of sympathetics in blood vessels

A

tonically constricts them

37
Q

how can you detect hypoperfusion in septic shock before hypotension occurs

A

shown in rising lactate levels

38
Q

what is the management for septic shock

A

sepsis 6 + vasopressors after usually 2 bags of fluid with no response

39
Q

what is anaphylactic shock

A

uncontrolled activation and degranulation of mast cells
=release of histamine
=uncontrolled widespread vasodilation
=distributive shock

40
Q

how does adrenaline help in anaphylatic shock

A

acts as a vasoconstrictor and a mast cell stabiliser

41
Q

what test confirms analphylaxis

A

serum mast cell tryptase levels

42
Q

what is neurogenic shock

A

form of distributive shock
commonly follows spinal cord/ central trauma
=loss of sympathetic tone
=hypotension
also = unopposed vagal tone= inappropriate bradycardia
(this can be exacerbated by suction, PR exams as these stimulate the vagal nerve)

43
Q

what is the treatment for neurogenic shock

A

dopamine + vasopressors

44
Q

what is spinal shock

A

NOT SAME AS NEUROGENIC SHOCK

loss of spinal reflexes following a cord transection (can be temporary)

45
Q

cord transection above what level causes you to loose sympathetic function

A

T1/2

46
Q

why does the vagus nerve still work in a cord transection

A

as is a cranial nerve

47
Q

what are the reversible causes of cardiac arrest

A

4H’s

  • hypovolaemia
  • hypoxia
  • hypokalaemia/ hyperkalaemia
  • hypothermia

4T’s

  • tamponade
  • tension pneumothorax
  • thrombosis
  • toxins
48
Q

why are recoils important in CPR

A

release of intrathoracic pressure allows blood to be sucked into the chest before it is pushed out again

49
Q

what are the four rhythms you can get in cardiac arrest

A

shockable: VF (will not have a pulse), pulseless VT

non shockable: pulseless electrical activity (could be normal rhythm but no pulse), asystole

50
Q

what usually causes pulseless electrical activity

A

hypovolaemia- will have sinus tachycardia on ECG but no pulse

51
Q

what usually causes asystole

A

(bad)
severe hypoxia
usually an end stage for other forms of arrest
associated with significant brain damage if do resuscitate

52
Q

what usually causes the shockable rhythms of arrest

A

acute MI
toxins
electrolyte abnormalities

CLASP Sudden Death (6 decks)

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