Shock Flashcards

(52 cards)

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
what drugs increase inotropy
beta and dopaminergic agents beta- dobutamine, adrenaline dopamine- dopamine, dopexamine others- milrinone/ levosimendan
26
when might you give inotropic drugs
when someone has cardiogenic shock after MI but also have pulmonary oedema due to heart failure
27
what is an intra-aortic balloon pump
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
what is obstructive shock
involves a physical obstruction to either the heart of great vessels = reduced preload and cardiac output mainly affects cardiac filling rather than ejection
29
what is the treatment for obstructive shock
depends on cause: PE- anticoagulation +/- thrombosis cardiac tamponade- pericardial drainage tension pneumothorax- decompression and chest drainage
30
what are the causes of obstructive shock
PE- stops blood getting back from lungs | tamponade and tension pneumothorax- heart compressed and unable to fill
31
what does a PE look like on echo
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
what does a pericardial effusion/ tamponade look like on echo
fluid accumulation in pericardial sac compresses each of the chamber impairs cardiac filling and contraction in all four chambers
33
why does a tension pneumothorax cause obstructive shock
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
what is disruptive shock
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
what are the subtypes of distributive shock
septic- bacterial endotoxin mediated capillary dysfunction anaphylactic- mast cell release of histaminergic vasodilators neurogenic- loss of thoracic sympathetic outflow follow spinal injury
36
what is the role of sympathetics in blood vessels
tonically constricts them
37
how can you detect hypoperfusion in septic shock before hypotension occurs
shown in rising lactate levels
38
what is the management for septic shock
sepsis 6 + vasopressors after usually 2 bags of fluid with no response
39
what is anaphylactic shock
uncontrolled activation and degranulation of mast cells =release of histamine =uncontrolled widespread vasodilation =distributive shock
40
how does adrenaline help in anaphylatic shock
acts as a vasoconstrictor and a mast cell stabiliser
41
what test confirms analphylaxis
serum mast cell tryptase levels
42
what is neurogenic shock
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
what is the treatment for neurogenic shock
dopamine + vasopressors
44
what is spinal shock
NOT SAME AS NEUROGENIC SHOCK | loss of spinal reflexes following a cord transection (can be temporary)
45
cord transection above what level causes you to loose sympathetic function
T1/2
46
why does the vagus nerve still work in a cord transection
as is a cranial nerve
47
what are the reversible causes of cardiac arrest
4H's - hypovolaemia - hypoxia - hypokalaemia/ hyperkalaemia - hypothermia 4T's - tamponade - tension pneumothorax - thrombosis - toxins
48
why are recoils important in CPR
release of intrathoracic pressure allows blood to be sucked into the chest before it is pushed out again
49
what are the four rhythms you can get in cardiac arrest
shockable: VF (will not have a pulse), pulseless VT non shockable: pulseless electrical activity (could be normal rhythm but no pulse), asystole
50
what usually causes pulseless electrical activity
hypovolaemia- will have sinus tachycardia on ECG but no pulse
51
what usually causes asystole
(bad) severe hypoxia usually an end stage for other forms of arrest associated with significant brain damage if do resuscitate
52
what usually causes the shockable rhythms of arrest
acute MI toxins electrolyte abnormalities