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CR2 > Shock > Flashcards

Shock Flashcards

1
Q

What is clinical shock?

A

an acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in cellular hypoxia

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2
Q

How can cellular hypoxia lead to cell death?

A

switch to anaerobic metabolism from aerobic -> lactate production -> cells stop functioning and swell -> membrane increased permeability -> electrolytes and fluids seep in & out -> Na+/K+ pump impaired, cells swell so mitochondria damage, cell death

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3
Q

For adequate tissue perfusion what must CO and blood pressure be?

A

CO 5l/min
systolic bp 120mmHg
mean arterial pressure 100mmHg

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4
Q

What are the signs of shock?

A

Mean arterial pressure <60mmHg

clinical signs: hypo-perfusion of vital organs (tachycardia, tachypnea, mental confusion, pallor)

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5
Q

What does bp=

A

CO X systemic vascular resistance

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6
Q

What factors could cause shock?

A

A low bp, therefore according to equation -> low CO or low vascular resistance

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7
Q

What factors would produce a low CO?

A

CO = HR x SV so either low heart rate or stroke volume

However normally SV as heart rate is often compensatory for change, unless change is from drugs/CNS

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8
Q

What factors control heart rate?

A
  • baroreceptors in carotid sinus produce feedback signals to either activate or inhibit vasomotor centres in the medulla to then activate or inhibit the ANS
  • arousing stimuli can activate or inhibit ANS
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9
Q

What factors affect stroke volume?

A
  • preload/EDV: amount of blood in heart before it begins to contract
  • myocardial contractility
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10
Q

What is Starling’s law of the heart?

A

The greater the preload(EDV), the greater the force of contraction and so the greater the SV

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11
Q

What is myocardial contractility normally increased by?

A

Sympathetic NS
Circulating catcholamines
Iontrope drugs - beta 1 agonists

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12
Q

What is myocardial contractility decreased by?

A

cardiac disease
hypoxia/hypercapnia
pH or electrolyte disturbance
drugs - beta blockers, calcium channel blockers

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13
Q

What maintains SVR?

A

systemic vascular resistance maintained by arteriole constriction - vasoconstriction and vasodilation balance

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14
Q

What is arteriole constriction mediated by?

A
  • SNS releases noradrenaline locally on alpha receptors on arterioles
  • angiotensin 2 is a circulating hormone which produces arteriolar vasoconstriction
  • local factor endothelin released from lining constricts and dilates by acting on receptors, some receptors release NO which is a vasodilator
  • prostacyclin is a vasodilator produced in endothelial cells from prostaglandin (regulation unclear)
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15
Q

How does noradrenaline affect arterioles?

A

Released from nerve terminals on outside of arteriole, penetrate tunica adventitia and act on catecholamine alpha receptors (G protein coupled receptors on SM of tunica media)

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16
Q

How does adrenaline affect arterioles?

A

relatively ineffective as must pass through endothelium to access alpha receptors

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17
Q

How does angiotensin II affect arterioles?

A

carried in plasma acting on angiotensin AT1 receptors on endothelium lining of arterioles and SM, produces vasoconstriction

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18
Q

What and where are the receptors for noradrenaline and angiotensin II?

A

noradrenaline - catecholamine alpha adrenoreceptor, on SM of tunica media
angiotensin II - angiotensin ATI receptor on endothelial lining of SM and arterioles

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19
Q

Where is prostacyclin produced and from what?

A

Produced in endothelial cells from arachidonic acid

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20
Q

What are the main functions of prostacyclin?

A

prevents formation of the platelet plug in primary haemostasis by inhibiting platelet activation
- local vasodilator reducing calcium entry into SM cells surrounding endothelium so reduces contractility

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21
Q

What is an antagonist to prostacyclin?

A

Thromboxane - produces local vasoconstriction and platelet aggregation whereas prostacyclin produces local vasodilation and stops platelet aggregation

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22
Q

What is the initial stage of shock?

A

COMPENSATION

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23
Q

What is decompensation?

A

A later stage of shock where arterioles cannot maintain constriction or blood preload reduction is too great, end organs not perfused with oxygen so begin to fail, fatal

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24
Q

What is the link between compensation and decompensation?

A

Compensation is the first mechanism to try and perfuse organs if either systemic vascular resistance is reduced or preload is reduced. If this allows successful perfusion end organs are maintained and there is survival. However if this is not enough a state of decompensation occurs and end organ failure begins.

25
Q

What are the 4 types of shock? Explain them?

A

Obstructive shock - physical obstruction to vessels entering or leaving the heart (e.g. pulmonary embolism)
distributive - loss of vasoconstriction in one or more end organs so excess blood flow in the system and poor perfusion of other organs
hypovolaemic - haemorrhage
cardiogenic - heart fails to pump efficiently and supply blood to body

26
Q

What is neurogenic shock?

A

distributive shock producing hypotension, slowed heart rate, disruptions to autonomic pathways in spinal cord after damage to CNS for example

27
Q

What are some examples of the 4 types of shock?

A

Obstructive - pulmonary embolism, cardiac tamponade, pneumothorax
distributive - sepsis, anaphylaxis, neurogenic
hypovolaemic - haemorrhage, burns, surgery/trauma, loss of fluid and electrolytes from gut
cardiogenic - MI, heart failure, arrhythmias, ventricular septal failure, ischemic cardiomyopathy, valvular disease

28
Q

What are some signs of someone with hypovolaemic shock?

A

low BP, high heart rate, slow capillary refill, greyish pallor, oliguria, absent bowel sounds (all because of reduced blood flow to these areas)
history is vital - secondary to external blood loss, internal bleeding less obvious, GI bleeding ask about diet and drugs

29
Q

What are the signs of cardiogenic shock?

A

AMI - cardiac ischemia

pulmonary oedema, acute circulatory collapse

30
Q

What are the signs of septic shock? (distributive)

A

low BP, tachycardia, fever (adaptive response so pathogens don’t multiply in high heat), chills

31
Q

What are the signs of obstructive shock?

A

tension pneumothorax - tachycardia, chest pain, breath sounds absent on affected hemiothorax, deviated trachea

32
Q

What should normal body water volume be (intracellular and extracellular) and blood volume?

A

Total body water = 45L (IC 27L EC 18L)

blood volume = 4.5-5L

33
Q

How much blood loss is life threatening?

A

acute loss of >40% (>2L)

34
Q

What is the immediate response to a haemorrhage?

A

venous bleed = drop in venous return (preload) = reduced SV = reduced CO = BP fall -> baroreceptors detect and increase symp outflow so HR and contractility increased, large veins constricted to move blood out of venous reservoir and restore preload, also vasomotor signals hypothalamus to release ADH)

35
Q

How is the arterial bleed response in a haemorrhage different to a venous bleed?

A

Arterial - blood pressure drops immediately so detected by baroreceptors quicker

36
Q

What does the vasomotor centre do in a immediate haemorrhage response?

A

vasomotor centre in the medulla signlas to hypothalamus to release ADH (vasopressin) and reduced preload reduces release of ANP so urine flow and sodium excretion is reduced

37
Q

What is the long term response to haemorrhage?

A

Kidney releases renin which leads to aldosterone release from the adrenal cortex by angiotensin II to increase sodium retention. Thirst stimulated by angiotensin II receptors in the brain to increase water intake, sodium and water retention therefore increased restoring circulating blood volume.

38
Q

What stimulates thirst and where from?

A

Angiotensin II receptors in the brain in the subfornical organ above the hypothalamus

39
Q

Aside from renin what other long term responses are there to a haemorrhage?

A

Haematocrit is restored by EPO release when peritubular cells are sensitive to hypoxia, RBCs brought back to normal levels
Stimulation of albumin and other plasma proteins in liver to restore them too

40
Q

What is class I hypovolemic shock?

A

<15% loss of blood volume
after donation or minor injury
full compensated
normal or slightly fatigued patient

41
Q

What is class 2 hypovolemic shock?

A

loss of 15-30% of blood
tachycardia, tachynpnea, pulse pressure decrease, cool clammy skin, delayed capillary refill, anxiety
rest and normal access to water & food, will fully recover w/o intervention eventually

42
Q

What is class 3 hypovolemic shock?

A

> 30% loss of blood
persistent drop in bp
anxious, confusion
require plasms volume expanders or blood transfusion and may have end-organ damage, especially to kidneys

43
Q

What is class IV hypovolemic shock?

A

> 40% loss of blood volume
very confused, unconscious, tachycardia, no urine output, severely decreased systolic pressure, life threatening
blood transfusion initiated immediately

44
Q

What is sepsis and septic shock?

A

sepsis - systemic response to the presence of pathogens in blood or other organs
septic shock - type of distributive shock, sepsis with hypotension

45
Q

What is sepsis manifested by?

A 
2 or more of:
Temp > 38oC or < 36oC
HR > 90 bpm
RR > 20 bpm or PaCO2 < 32 mmHg
WBC > 12 x 109/L, or >10% band form
46
Q

How does septic shock occur?

A

bacterial infection-> excessive host response -> microvascular damage -> reduced systemic vascular resistance -> low blood pressure -> shock

47
Q

How do LPS cause septic shock?

A

(lipopolysaccharide) in gram-negative bacterial cell walls stimulates neutrophils and monocytes to release cytokines that affect endothelium and prevent normal vasoconstriction -> vascular resistance reduced in affected organs -> lowers bp to shock levels
OR microvascular occlusion due to thrombus

48
Q

How is shock managed?

A
  • if hypovolemic shock: restore circulating blood with IV colloids or crystalloids, restores preload and CO
  • use standard vasopressor drugs to restore bp
  • if sepsis: use antimicrobials
49
Q

What are the therapeutic goals after shock?

A

Central venous pressure: 8 – 12 mmHg
Mean arterial pressure: ≥ 65 mmHg
Urine output: 0.5 mL/kg/h
Central venous (SVC) or mixed venous oxygen saturation: ≥ 70%

50
Q

What vasodilators are there?

A
  • prostacyclin produced in endothelial cells from arachidonic acid reduces calcium entry into SM cells around endothelium so reduces SM contractility
  • NO produced in endothelial cells from arginine diffuses into SM stimulates cAMP formation which decrease calcium entry and relaxes muscle
  • adenosine released from endothelial cells and SM during activity
51
Q

What is oliguria?

A

Less urine loss as restricted blood flow through the kidney

52
Q

What is the hematologic system’s physiological response to hypovolemic shock?

A

activates coagulation cascade contracting bleeding vessels (TXA2) and platelet activation to form immature clot of bleeding source

53
Q

What is the cardiovascular’s system physiological response to hypovolemic shock?

A

activate SNS, increased HR, increased myocardial contractility, peripheral blood vessel constriction in skin/muscle/Gi tract to redistribute blood to brain, heart, kidneys

54
Q

What is the renal system’s physiological response to hypovolemic shock?

A

RAAS - angiotensin II allows vasoconstriction of arteriolar SM in skin, muscle, GI tract AND aldosterone secretion by adrenal cortex to increase sodium and therefore water reabsorption (oliguria)

55
Q

What is the neuroendocrine system’s physiological response to hypovolemic shock?

A

releases ADH from posterior pituitary gland in response to BP decrease detected by baroreceptors and plasma sodium conc decrease detected by osmoreceptors, ADH leads to increased water reabsorption and salt by DCT, collecting ducts and loop of Henle

56
Q

What are the main clinical presentations of hypovolemic shock? Why?

A 
tachycardia
pale/shut down
sweaty/clammy
oliguria
confusion
(SNS attempts to maintain oxygen supply to heart and brain despite reduced preload)
57
Q

What is the key difference between class 1 and 2 hypovolemic shock?

A 
class 1 - no significant tachycardia, normal bp and resp rate
class 2 - tachycardia!, increased resp rate
58
Q

What is the key difference between class 2 and 3 hypovolemic shock?

A 
class 2 - bp normal even though resp rate high and tachycardia
class 3 - extreme tachycardia, resp rate, urine output decrease, reduced bp to compensate

CR2 (35 decks)

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