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Module 14 > Management of Shock > Flashcards

Management of Shock Flashcards

1
Q

what are the fluid compartments

A
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2
Q

what are the cations and anions of the ECF

A

cations: sodium
anions: chloride, bicarbonate

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3
Q

what are the cations and anions of the ICF

A

cations: potassium
anions: phosphate, protein

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4
Q

what is responsible for the osmolarity of the fluid in the body

A

electrolytes

~300 mOsm/l in dogs

~310 mOsm/l in cats

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5
Q

what are the reasons to give fluids (6)

A

1. dehydration

2. shock

  1. provide maintenance requirements
  2. treat electrolyte imbalances
  3. maintain oncotic pressure (colloids)
  4. diuresis
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6
Q

what fluid deficit is dehydration

A

deficit in total body water

loss of water but often used clinically to refer to isotonic and hypotonic losses as well

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7
Q

what is the maintenance requirement in cats a dog

A

50 ml/kg/day

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8
Q

what is dehydration due to

A
  1. low consumption
  2. pathological fluid losses
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9
Q

what are clinical signs of dehydration

A
  1. skin tenting
  2. dry mucous membranes
  3. sunken eyes
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10
Q

what is circulatory shock

A

global energy deficit at cellular level

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11
Q

what is the most common shock

A

hypovolemic

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12
Q

what are the types of shock

A
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13
Q

what fluid loss is hypovolemic shock

A

loss of intravascular volume

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14
Q

what are the causes of hypovolemic shock

A
  1. dehydration
  2. blood loss
  3. 3rd spacing of fluids (pleura, peritoneum)
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15
Q

what is cardiogenic shock caused by (3)

A
  1. heart disease
  2. cardiac tamponade
  3. arrhythmias
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16
Q

why must cardiogenic shock be differentiated from other types of shock

A

large fluid volume is contraindicated

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17
Q

how do you differentiate cardiogenic shock from other types (3)

A
  1. signalment & history
  2. thoracic auscultation (heart murmurs, pulmonary edema heard as crackles)
  3. ascites/jugular distention
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18
Q

what is distributive shock

A

cardiac function and blood volume are not affected but there is a failure of the vascular tree to allow appropriate delivery

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19
Q

what does distributive shock cause

A
  1. loss of vascular tone: sepsis/endotoxemia, anaphylaxis
  2. venous blockage of blood (obstructive shock): GDV, pulmonary thromboembolism
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20
Q

can you treat distributive shock where there is loss of vascular tone due to sepsis/endotoxemia with fluid

A

yes –> vasodilation –> BP will drop

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21
Q

what are the classic clinical signs of hypovolemic shock (7)

A
  1. tachycardia (sympathetic response)
  2. poor pulse quality due to vasoconstriction and lack of blood volume
  3. decreased extremity temperature
  4. pale mucous membranes
  5. prolonged CRT
  6. decreased mentation due to inadequate brain perfusion
  7. tachypnea to increase oxygen uptake (not always evident)
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22
Q

list areas you can feel a pulse

A
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23
Q

in mild/compensated hypovolemia what would you expect the HR, MM colour, CRT, pulse amplitude, pulse duration, metatarsal pulse palpable to be

A

HR: 130-150

MM colour: normal/pinker

CRT: <1 sec

pulse amplitude: increased

pulse duration: mildly decreased

metatarsal pulse palpable: easily

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24
Q

in moderate hypovolemia what would you expect the HR, MM colour, CRT, pulse amplitude, pulse duration, metatarsal pulse palpable to be

A

HR: 150-170

MM colour: pink

CRT: ~2 seconds

pulse amplitude: decreased

pulse duration: decreased

metatarsal pulse palpable: just

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25
Q

in severe/decompensated hypovolemia what would you expect the HR, MM colour, CRT, pulse amplitude, pulse duration, metatarsal pulse palpable to be

A

HR: 170-200, may become bradycardic

MM colour: white/grey

CRT: > 2 seconds

pulse amplitude: severe decreased

pulse duration: severe decrease

metatarsal pulse palpable: absent

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26
Q

fill out this chart

A
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27
Q

what are exemptions to the rule of clinical signs (2)

A
  1. septic (distributive) shock: due to vasodilation animals may have brick red mucous membranes and bounding pulses (of decreased duration)
  2. cats: may have increased heart rates in early shock but frequently present with bradycardia in more severe shock
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28
Q

what are pathological consequences of hypovolemic shock (3)

A
  1. low blood pressure causes activation of the sympathetic nervous system –> tachycardia & vasoconstriction
  2. the renin-angiotensin system is activated –> vasoconstriction & fluid retention
  3. hydrostatic pressure promotes movement of water by Starling’s forces from the interstitium
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29
Q

what % of blood volume can healthy animals tolerate

A

30-40%

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30
Q

how can shock kill animals

A
  1. lack of perfusion
  2. cellular hypoxia –> free radical generation –> inflammatory mediators
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31
Q

what occurs to the GI tract during hypovolemic shock

A

sympathetic activation tends to shunt blood away from GIT –> disproportionate hypoperfusion and inflammation

may amplify SIRS

may allow bacterial translocation causing sepsis

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32
Q

what is SIRS

A

a complex immune response follows involving activation of multiple inflammatory mediators throughout the body –> may lead to systemic inflammatory response syndrome

may lead to multiple organ dysfunction (MODS)

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33
Q

what are the aims of shock treatment

A
  1. rapid yet judicious use of fluid therapy to restore vascular volume, normalize tissue perfusion and reduce secondary injuries
  2. identification and control of any hemorrage is an important component of treatment in hypovolemic shock
34
Q

what are the routes of administration of fluid therapy

A

expanding vascular space so –> IV or intraosseous access is mandatory

35
Q

what is intra-osseous cannulation suitable for

A

small puppies, kittens

36
Q

what fluid is used for shock

A

isotonic crystalloids

equilibrate quickly with interstitial fluids –> therefore high volumes are needed “shock dose”

37
Q

what is the shock dose for cats and dogs and what is normally done

A

dogs: 80-90 ml/kg/hr
cats: 40-60 ml/lg/hr

but giving entire shock dose is outdated concept –> divide into 4 over 15 mins and check perfusion parameters (improvement of mentation, decrease in HR, pulse quality improved)

38
Q

what are examples of isotonic replacement crystalloids and what are their components

A
39
Q

which fluid has more Na (normal saline, ringer’s, hartmann’s)

A

normal saline > ringer’s > hartmann’s

40
Q

which fluid has more K (normal saline, ringer’s, hartmann’s)

A

ringers and hartmann’s have the same amount

normal saline doesnt have any

41
Q

which fluid has more Cl (normal saline, ringer’s, hartmann’s)

A

ringer’s > normal saline > hartmann’s

42
Q

which fluid has more Ca (normal saline, ringer’s, hartmann’s)

A

hartmann’s > ringer’s

normal saline doesn’t have any

43
Q

which fluid has lactate? (normal saline, ringer’s, hartmann’s)

A

hartmann’s

44
Q

which fluid has the highest osmolarity (normal saline, ringer’s, hartmann’s)

A

ringer’s > normal saline > hartmann’s

45
Q

which fluid would be of choice for a patient with metabolic acidosis

A

hartmann’s because it is alkalinizing

46
Q

when is hartmann’s contraindicated (5)

A
  1. cerebral edema (hyperosmotic so will cause additional fluid to enter cerebral cavity)
  2. severe liver failure: lactate cannot be metabolized
  3. severe abnormalities of sodium concentration
  4. hyperkalemia (renal/post-renal failure) because it has K
  5. contains Ca: cannot be mixed with blood products, sodium bicarbonate, or hypercalcemic animals
47
Q

even though Hartmann’s is contraindicated in hyperkalemia, explain why it is still okay to use in cats with uretheral blockage

A

it contains K but only 4mmol/l –> still dilutional

bicarbonate buffer normalizes acid bases status more rapidly than saline in cats with experiental urtheral blockage

48
Q

what are the advantages of crytalloids (4)

A
  1. cheap
  2. physiological
  3. few side effects
  4. widely available
49
Q

what are the disadvantages of crystalloids

A
  1. only transiently expand the vascular compartment
  2. don’t provide a replacement for albumin (oncotic support) –> important in hypoalbuminemic patients especially those with peripheral edema
50
Q

what are colloid fluids and how to they expand intravascular volume

A

large molecules which don’t cross the vascular endothelium

high oncotic pressure act to expand and maintain intravascular volume

51
Q

what is the colloid shock dose

A

dogs: 20ml/kg/hr
cats: 10ml/kg/hr

1/4 doses over 15 mins

52
Q

what is the colloid maintanence of oncotic pressure dose

A

20ml/kg/day

53
Q

what are common colloids

A

haemacel

pentastarch/tetrastarch 6%

54
Q

which colloid has larger molecule size (Haemacel or pentastarch/tetrastarch 6%)

A

haemacel: small molecular size (~25 kDa)

pentastarch/tetrastarch 6%: larger molecule size (~200 kDa)

55
Q

which colloid has a rapid volume expansion (Haemacel or pentastarch/tetrastarch 6%)

A

Haemacel

56
Q

which colloid has a longer duration of action (Haemacel or pentastarch/tetrastarch 6%)

A

pentastarch/tetrastarch 6%

~60% lost after 24hrs

haemacel: ~80% lost after 24hrs

57
Q

which colloid has a higher risk of coagulopathy (Haemacel or pentastarch/tetrastarch 6%)

A

pentastarch/tetrastarch 6%

at high doses (>20ml/kg/day or up to 50ml/kg/day with certain tetrastarches)

58
Q

which colloid has a higher risk of anaphylaxis (Haemacel or pentastarch/tetrastarch 6%)

A

haemacel

59
Q

what are the differences of crystalloids and colloids

A

no definitive evidence exists showing superiority of one over the other

cyrstalloids seem effect despite physiological inferiority

recent controversy with withdrawal of colloids in human med (renal complications)

60
Q

when are colloids particularly useful

A
  1. hypoalbuminemia
  2. large patients
  3. poor response to crystalloids
61
Q

what is hypertonic saline

A

7.2% NaCl

62
Q

how does hypertonic saline improve hypovolemia

A

high osmotic gradient draws interstitial fluid into the vascular space

63
Q

what volume of hypertonic saline is needed

A

small volumes required 4ml/kg over 10 minutes

64
Q

what does hypertonic saline cause

A

+ ionotropy and reduce inflammation

65
Q

what is hypertonic saline useful for

A

hypovolemic patients with head trauma

66
Q

when is hypertonic saline not to be administered

A

in already dehydrated patients

67
Q

what must you follow up with once you give hypertonic saline

A

crystalloids to repay the debt

can be mixed with colloids for shock resuscitation in severe cases

68
Q

when are blood products not indicated

A

as first line treatment for shock as it cannot be administered fast enough while avoiding potential transfusion reactions

animals in shock don’t die of anemia –> lack of vascular volume

once initial resuscitation has been carried out, transfusion may be required to maintain a PCV of greater than 20-25%

69
Q

what is hypotensive rescusitation

A

may be indicated in ongoing internal hemorrhage

restores blood pressure to acceptable limits (60 mmHg) without “popping the clot”

definitive volume restoration delayed until bleeding is surgically managed

70
Q

what are additional shock therapies (5)

A
  1. broad spectrum bacteriocidal antibiotics
  2. GI protectants
  3. vasopressors/iontropes (used is severe sepsis)
  4. bicarbonate
  5. glucocorticoids (but can cause immunosuppression + GI irritation, can be useful in septic shock)
71
Q

what additional monitoring is needed

A
  1. physical findings essential (mucous membranes, capillary refill time, pulse rate and quality, heart rate, respiratory rate)
  2. urine output (<1 ml/kg/hr could indicate hypovolemia and inadequate renal perfusion or renal failure)
  3. arterial blood pressure: monitor trends
  4. blood lactate: < 2mmol/L normal
72
Q

what are mild increases of lactate

A

2-5 mmol/L

73
Q

what are moderate increases in lactate

A

5-8 mmol/L

74
Q

what are severe increases in lactate

A

>8 mmol/L

75
Q

what are causes of increased plasma lactate concentrations (5)

A

type A

  1. inadequate oxygen delivery
  2. increased oxygen demand

type B

  1. inadequate oxygen utilization
  2. drugs/toxin (list not exhaustive)
  3. congenital errors of metabolism
76
Q

how does inadequate oxygen delivery lead to increased lactate concnetrations (3)

A
  1. inadequate tissue perfusion
  2. low arterial oxygen saturation
  3. low hemoglobin concentration
77
Q

how does increased oxygen demand lead to increased lactate concnetrations (3)

A
  1. exercise
  2. shivering
  3. seizures
78
Q

how does inadequate oxygen utilization lead to increased lactate concnetrations (5)

A
  1. sepsis
  2. SIRS
  3. neoplasia
  4. renal failure
  5. diabetes mellitus
79
Q

what drugs/toxins lead to increased lactate concentrations (5)

A
  1. ethylene glycol
  2. cyanide
  3. carbon monoxide
  4. strychnine
  5. acetaminophen
80
Q

what are complications of fluid therapy (4)

A
  1. iatrogenic electrolyte disturbances
  2. overzealous use of fluids may lead to volume overload
  3. catheter related tissues
  4. complications associated with individual products (coagulopathy with colloids)
81
Q

what are the signs of volume overload (7)

A
  1. chemosis
  2. serous nasal discharge
  3. increased respiratory rate
  4. effort and noise
  5. restlessness
  6. peripheral edema
  7. polyuria
  8. pulmonary and interstitial edema
82
Q

what patients are more susceptible to volume overload

A
  1. renal disease
  2. cardiac disease
  3. hypoalbuminemia
  4. pulmonary contusions

Module 14 (29 decks)

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