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Patho > Q3 Shock/burns > Flashcards

Q3 Shock/burns Flashcards

1
Q

What is shock? 2 main reasons?

A

Imbalance between O2 supply and metabolic demand
Either through low perfusion or inadequate O2 reaching the tissue.

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2
Q

T/F: Shock can occur with a normal blood pressure.

A

True.

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3
Q

If there is low perfusion, then there will be _______ metabolic demand and _____ O2 extraction meaning the blood returning to the heart (SvO2) will _______

A

Increased (starved tissue), increased, decreased level of O2

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4
Q

If there is adequate perfusion, but O2 cannot be delivered to the cells, the blood returning to the heart (SvO2) will have -_______
Some causes?

A

Increased O2 levels because it couldn’t dump it off on the tissue.
Edema.

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5
Q

When the tissue fails to get adequate O2 what happens?

A

Lactate produced from anaerobic metabolism
Acidosis
Failure of NA/K pumps so Hydropic swelling with fluid accumulating in the cell
Free radical formation
Inflammatory cytokines
Activation of the autonomic response

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6
Q

When the tissues don’t get enough O2, the ANS is activated. How (2)?

A

SNS - NE, epi, dopamine and cortisol are released to cause vasoconstriction, increase HR and increase contractility (increase CO).
Renin-angiotensin axis - water and Na conservation = fluid retention + vasoconstriction. Increase blood volume and pressure.

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7
Q

The ANS response leading to increased HR, cardiac contractility and CO is caused by _________

A

SNS

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8
Q

The ANS response leading to increase in blood volume and blood pressure is _________. How?

A

Renin-angiotensin axis.
Retention of Na and water and vasoconstriction.

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9
Q

What is a reprerfusion injury? Likely to happen where?

A

When O2 is restored, ischemic cells produce a flood of free radicals which overwhelms the antioxidant system. This causes oxidative cell damage which causes the release of inflammatory cytokines and IL8 and adhesion molecules. Neutrophils attack the reperfused tissue. Lungs.

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10
Q

What are some possible interventions to reduce reperfusion injury?

A

Rapid reperfusion
Metabolite inhibitors

Metal chelations, free radical defense mechanisms

IL1 RAs and antibodies, TNF alpha antibodies.

Antibody and inhibitors to adhesion molecules

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11
Q

Homeostatic mechanisms are sufficient to maintain adequate tissue perfusion despite reduction in CO. This is ______ shock

A

Compensatory

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12
Q

How does the body maintain homeostasis in the compensatory shock stage?

A

Corticosteroid release from adrenal glands + renin from kidneys activates SNS to maintain blood pressure through vasoconstriction and shunting of blood to brain and heart. Glucose release from kidneys attempts to supply fuel for increased metabolic demand.

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13
Q

When the body’s compensatory mechanisms fail, you move on to ________ shock. This stage is marked by what S/s?

A

Progressive.
Hypotension, tissue hypoxia. Lactate production, cellular swelling, dysfunction and death.
Inflammatory cytokines are activated and the clotting cascade is activated.

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14
Q

How do cells respond to decreased O2 delivery?

A

Na/K and other ion pumps stop working. Hydropic swelling. Lactate production.

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15
Q

When the body is in shock, it shunts blood FROM ______ to ________

A

GI, MSK and kidneys

Heart and brain.

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16
Q

Presence of These two inflammatory markers are though to be important mediators of vascular failure and progressive organ damage

A

TNF alpha and IL1

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17
Q

Two pathologies that can arise from shock

A

DIC - due to inflammatory response activation of coagulation cascade and micro vascular clot formation
ARDS -

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18
Q

Examples of Cardiogenic shock

A

Pump failure.
MI
Arrhythmia
Cardiomyopathy
Myocardial contusion
Myocarditis

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19
Q

Sepsis is a form of ______ shock

A

Distributive.

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20
Q

Examples of Distributive shock

A

Sepsis, anaphylaxis, neurogenic shock, drug and toxin induced, endocrine.

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21
Q

Examples of hypovolemic shock

A

Hemorrhage
Non-hemorrhage
- burns
- pancreatitis
- dehydration

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22
Q

Examples of obstructive shock

A

PE,
Tension pneumothorax
Tamponade.

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23
Q

Name the type of shock:
Inadequate CO despite adequate vascular volume.

A

Cardiogenic.

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24
Q

In Cardiogenic shock, _____ is activated to ________ to maintain BP

A

SNS
Vasoconstrict

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25
Q

During Cardiogenic shock, you may see venous_______ due to __________. This causes ___________

A

High venous pressures due to increased after load (from vasoconstriction).
Fluid extravasation and edema.

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26
Q

In Cardiogenic shock, you would see ______ SvO2. Why?

A

Low.
Tissue is perfusing, the blood flow (CO) is just inadequate to meet the tissue demand (starved tissue) so therefore, they eat up more O2 than usual, so the returning venous blood has a low SvO2.

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27
Q

Cardiogenic shock therapy has 3 aims:

A

Improve CO (Inotropes)
improve myocardial O2 deliver
Decrease workload of the heart.

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28
Q

A doctor might consider an IABP, LVAD or heart transplant is someone with _________ shock.

A

Cardiogenic

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29
Q

In Cardiogenic shock, there is _____ in EF, ____ in ESV, _____ preload, ______ left atrial pressure, ______ pulmonary capillary hydrostatic pressure, _____ afterload, _____ volume retention by kidneys and _____ pulmonary edema.

A

Decrease
Increase
Increase
Increase
Increase
Increase
Increase

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30
Q

Name that shock:
Severe capillary leak, dilated vessels, decreased SVR, reduced preload.

A

Distributive.

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31
Q

CO is inadequate in distributive shock because:

A

Preload is decreased due to all the fluid 3rd spacing.

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32
Q

Difference between anaphylaxis and anaphylactoid reaction?

A

Anaphylaxis is IgE mediated and results from a sensitizing exposure.
Other than that, they are clinically indistinguishable.

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33
Q

Cell responsible for the anaphylactic response?

A

Mast cells release of vasodilators mediators.

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34
Q

When may epi be contraindicated when treating anaphylactic shock?

A

If patient is taking beta blockers - it could cause severe hypertension due to unopposed alpha stimulation.

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35
Q

Risk factor for death in anaphylactic shock?

A

Delay of epinephrine.

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36
Q

What is the background of neurogenic shock?

A

SNS outflow is disrupted = Un opposed PSNS.

37
Q

What is a hallmark sign of neurogenic shock? Other signs?

A

Very low SVR.
Bradycardia
Poikilothermia.

38
Q

Neurogenic shock is a type of

A

Distributive shock

39
Q

Sepsis diagnosis criteria

A

Suspected/documented infection + 2 or 3 on qSOFA (HAT)
Hypotension SBP<100
AMS GCS <13
Tachypnea >22

OR rise in SOFA score by 2 or more.

40
Q

Severe sepsis dx criteria?

A

Sepsis + vasopressin’s needed for MAP>65 + lactate >2

41
Q

Your patient has decreased BP, pallor, decreased CO, and decreased UOP. What stage of sepsis are they in?

A

Late or Hypodynamic stage.

42
Q

What S/S might a patient display in Early stage that are similar in Late stage sepsis?

A

Confusion, tachycardia, Decreased SVR, increased lactate levels

43
Q

4 fold therapy for sepsis management:

A

Abx to treat infection
Manage hypovolemic state to improve distribution of blood flow
Repair metabolic acid-base imbalance
Correct nutritional deficit.

44
Q

What vasopressor is NOT recommended to be administered in early septic shock

A

Dopamine.

45
Q

Name that shock:
SNS overactivity = vasoconstriction = very high afterload, venous congestion, normal BP but poor perfusion due to decreased blood flow. May have S.S consistent with Rsided HF.

A

Obstructive.

46
Q

Obstructive shock is caused by

A

Circulatory blockage (massive PE, tension pneumothorax or tamponade) that prevent effective cardiac filling and stroke volume.

47
Q

Beck’s triad is associated with what type of shock?

A

Obstructive
Cardia tamponade
Hypotension, muffled heart sounds, JVD

48
Q

Virchow’s triad is associated with what type of shock?

A

Obstructive
PE
Hypercoagulability, venous injury, venostais.

49
Q

Name that shock:
Decreased intravascular volume = Decreased preload, decreased CO, hypotension and decreased tissue perfusion.

A

Hypovolemic.

50
Q

In what classes of Hemorrhagic/hypovolemic shock will you see:
Decreased pulse pressure?
HR over 120?
Normal BP?
30-40% blood loss?

A

Class II, III and IV
Class III and IV
Class I and II
Class III

51
Q

You hypovolemic patient has tachycardia with hypotension, tachypnea, oliguria, anxiety and confusion. What class are they in and how much blood have they lost?

A

III - 30-40% or 1500-2000ml

52
Q

Your hypovolemic patient has a normal pulse and blood pressure but mild anxiety. What class are they in and how much blood have they lost?

A

Class I
<15% or up to 750mls.

53
Q

Are crystalloids or colloids the treatment of choice in hypovolemic shock?
When is it appropriate to give colloids?

A

Crystalloids are 1st line (blood asap)
Colloids (like albumin) if bleeding rapidly or if large amounts of crystalloids are given.

54
Q

If a patient is hemorrhaging, what is important to avoid?

A

Hypothermia.

55
Q

Your patient’s bleeding is controlled. They have an adequate fluid status, however their HCT <24. What should you do?
A: continue to fluid resuscitate with LR
B: give albumin
C: transfuse PRBCs
D: discharge home with a walker.

A

C - if HCT <24 or shock persists despite adequate fluid resuscitation.

56
Q

The amount of blood in the ventricle at the end of diastole = ______

A

Preload.

57
Q

Left atrial pressure is a direct measure of pulmonary capillary occlusion pressure.
____ is a good measure of preload.

A

R atrial pressure.

58
Q

ARDS most commonly associated with ______

A

Septic shock.

59
Q

What is the primary cause of death in ARDS?

A

Multiple organ failure NOT severe hypoxemia.

60
Q

ARDS may damage type II pneumocytes. What is the implication of this?

A

These pneumocytes produce surfactant which is essential in health lung compliance.

61
Q

These are low in DIC:
This is high:

A

Platelets, fibrinogen
D-diner - fibrin degradation products.

62
Q

In DIC, platelets can be activated by ________. Excessive _______ release leads to more hemorrhage which leads to compromised ___________ and vascular leakage/edema. _________ is impaired.

A

Cytokines and chemokines
Thrombin
Endothelial barrier function
Anticoagulation

63
Q

Differences between primary and secondary MODS

A

Primary: consequence of insult, <7days, ischemia or impaired perfusion is main cause,

Secondary: due to hosts response to injury, sepsis or septic shock, excessive, destructive immune mechanism, TNFalpha and IL1. Hypermatabolic and hyper dynamic.

64
Q

Highest mortality in burns:

A

<4yo or >60yo, >40%BSA and associated inhalation injury.

65
Q

T/F: the Zone of Stasis is under the Zone of necrosis and above the zone of hyperemia and is sometimes salvageable.

A

True. Depending on adequate resuscitation, infection prevention and appropriate debridement/wound care.

66
Q

Your patient has a burn on her foot that appears mottled. The blisters are flat and dry. What thickness burn do you suspect?

A

2nd Degree Deep partial thickness.
2nd Degree Superficial partial thickness = moist, blisters, red to pale ivory.

67
Q

Painless wounds are associated with what type of thickness burn?

A

Third degree full thickness. Pain nerve endings are destroyed.

68
Q

Victims of high voltage electrical injury often present with ________ degree burns

A

4th degree full thickness with deeper structures.

69
Q

Your patient has all of the back of their left arm burned, and the left leg from the knee down. What BSA% is burned?

A

Back of L arm = 4.5%
L leg knee down = 4.5%
9% total.

70
Q

______ is typically used in the ER to calculate BSA, while _____ is used post debridement for a more accurate calculation of BSA.

A

Rule of 9s
Lund and Browder chart.

71
Q

Your burn patient has carbonaceous sputum, cough and hoarseness. What do you suspect?
T/F: His O2 sats are at 100% on RA, so you do not put him on supplemental O2.
How to measure accurate O2 sats?

A

Inhalation injury.
Inhalation injuries are frequently associated with closed space flames or CO poisoning. His O2 reads could be a false hi. He needs to be on 100% supplemental O2 no matter what his sats are reading.
ABGs

72
Q

Initial burn treatments are wrapping the wounds with sterile dressing. NO wet or topical dressings at this stage.

A
73
Q

In burn patients, After 24hours, fluid replacement is switched from ____ to _____ in order to _____

A

LR to colloid
Replace protein lost during acute burn shock.

74
Q

Your patient weighs 34kgs. They have burns to their entire L arm and R forearm. According to the Modified Brooke formula, How much fluid should they receive in the 1st 8 hours? The next 16hours?

A

2-4ml x 34 x BSA%
Entire L arm = 9%
R forearm = 2.25%
BSA = 11.25%

2-4ml x 34 x 11.25 = 765-1530ml over 24hrs
382-765 over the 1st 8 hours (95ml/hr) and the same amount over the next 16hrs (48ml/hr)

75
Q

Adult adequate UOP?
Peds?

A

30-50ml/hr or 0.5ml/kg/hr
1ml/kg/hr

76
Q

What can happen to cardiac function in burns?

A

Depressed cardiac function that does not respond to adequate fluid resus.

77
Q

Inhalation injury ultimately leads to _______ shock with ____ CO.

A

Hypovolemic shock
Diminished

78
Q

In burns, what can cause kidney failure?

A

Hypovolemia
Excess myoglobin (rhabdo) from tissue breakdown

79
Q

The massive release of Catecholamines with burns causes

A

Hypermetabolism which manifests as tachycardia, increased O2 consumption, hyperglycemia and hyperthermia.

80
Q

Which chemotactic factors are especially important in contributing to pathology of burns?

A

IL1 and TNF alpha.

81
Q

Emergent phase of burn care is defined as ____
What 3 things help accomplish this goal?

A

Time between end of burn shock and closure of wound to <20% TBSA.
Meticulous wound management
Adequate nutritional support
Early surgical excision and grafting of any full thickness wounds.

82
Q

T/F: you prescribe IV antibiotics for your burn victim. Your nurse is right to question this order.

A

True. Burn patients mostly receive topical antibiotics since IV would not be delivered to the appropriate area.

83
Q

What are the main concerns of burn rehabilitation phase?

A

Flexor contractures, excessive scarring and keloid formation.

84
Q

What is an electrical injury usually classified as?

A

4th degree burn.

85
Q

What are some NON-visceral damage that you see in electrical burns?

A

Coagulated blood vessels,
Arrhythmias or cardiac arrest, metabolic acidosis and myoglobinuria.

86
Q

Which chemical burn is more severe and why? Acid or Base?

A

Basic chemical are more severe because it denatures protein and fat which doesn’t limit tissue penetration (liquefaction necrosis)
Acidic chemicals are a coagulative necrosis - the coagulam limits the penetration of the acid.

87
Q

Hydroflouric acid should be treated with _______ and be mindful of _______

A

Copious water irrigation and calcium
Fluoride causes cardiac arrhythmias.

88
Q

Ch 49 pg 1555

A
89
Q

Free Form drawing of Sepsis and DIC patho Phys.

A

Patho (18 decks)

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