Shock Flashcards

1
Q

Define shock

A

When the metabolic demand exceeds the body’s ability to deliver oxygen and nutrients

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2
Q

What are the clinical manifestations of shock?

A

Inadequate perfusion and compensation

Inadequate perfusion:

  • BRAIN –> altered LOC
  • kidneys –> decreased U/O

Compensatory mechanisms

  • Tachycardia (out of proportion to fever, distress etc.)
  • Peripheral vasoconstriction –> pale, mottling, cool extremities, delayed cap refill
  • Increased RR
  • BP changes
    • -> higher diastolic pressure = narrow pulse pressure
    • -> systolic falls - LATE sign
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3
Q

2 stages of shock

A

Compensated

Uncompensated

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4
Q

What is the exception to normal compensatory mechanisms?

A

Septic - warm shock
Warm distributive shock

Flushed skin, bounding pulses, hyperdynamic precordium, flash CR

Due to a cascade of inflammatory mediators

Neurogenic shock –> can cause bradycardia in the face of significant hypotension

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5
Q

Markers of uncompensated shock

A
Acidosis
High lactate
Altered LOC
Oliguria/Anuric
Ileus - constipation, decreased GI motility, distention, edema of bowel wall
BP falls
Multiorgan failure
ARDS
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6
Q

Mechanisms of Shock

A

Hypovolemic Shock
Distributive/Vasodilatory Shock
Cardiogenic Shock
Septic Shock

Hypovolemic Shock
- hemorrhage, V/D

Distributive/Vasodilatory Shock
- Neurogenic, Ingestion, Anaphylaxis, Septic shock

Cardiogenic Shock
- Viral myocarditis, hypertrophic cardiomyopathy, myocardial depressant drugs

Septic Shock
- can have features of both distributive and cardiogenic

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7
Q

Most common potent initiator of shock

A

Endotoxin - lipopolysaccharide coat of a Gram neg bacteria
Viral proteins
Teichoic acid

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8
Q

Which bacteria causes more severe septic shock?

A

Gram NEG - 20-50% mortality

Gram pos - 10-20%

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9
Q

Describe the cascade of septic shock?

A

Endotoxin (LPS) is bound to a plasma protein (LBP) –> complex binds to CD14 receptor on macrophages
This stimulates the formation of tumor necrosis factor (TNF) and interleukin which begin the inflammatory cascade

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10
Q

What needs to happen in the golden hour of septic shock?

A

Aggressive fluid resuscitation
Ionotropic therapy
Antibiotics

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11
Q

Most common mechanism of shock in kids?

A

Hypovolemia

- due to diarrheal illness

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12
Q

How does trauma cause shock?

A

Post-traumatic hemorrhage
- kids at high risk of blunt abdo trauma with weak abdo wall
Tension pneumonthorax
- from blunt chest trauma - reduces venous return to cause shock
Cervical spine injury
- can cause neurogenic shock

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13
Q

Does isolated head trauma cause shock?

A

No

Not unless there is a large scale scalp laceration

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14
Q

Classes of hemorrhage

A

Class I - IV

Class I - 15% loss of blood volume
- minimal tachycardia, Axmtc, no treatment

Class II - 15-30% loss

  • tachycardia, tachypnic, narrowed pulse pressure
  • U/O maintained, may have slight altered LOC - fright/anxiety

Class III - 30-40% loss
- compensated signs above +/- uncompensated signs (drop in BP, decreased U/O, confusion)

Class IV - > 40% loss

  • Fatal if untreated
  • may be irreversible shock
  • markedly decreased BP, severe uncompensated shock - extreme tachycardia, complete peripheral vasoconstriction, anuric, altered LOC/unconscious
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15
Q

How can you differentiate between neurogenic and hemorrhagic shock?

A

Hemorrhagic - rapid and possibly irregular pulse

Neurogenic - slow and regular pulse

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16
Q

Priorities in treatment of shock

A

Supportive therapy - supplemental oxygen, assisted ventilation
Fluids - try crystalloid in any shock , blood for hemorrhagic (crystalloids can cause metabolic acidosis, hypothermia etc.), not too much for cardiogenic
Pressors - after fluids - can be dangerous in hypovolemia without giving fluids first

17
Q

What are the 4 common pressors and their actions?

A

Epinephrine
Norepinephrine
Dopamine
Dobutamine

Epinephrine (Alpha-1, Alpha-2, Beta-1, Beta-2)

  • Inotrope (contractility) - Beta-1 / Alpha-1
  • Chronotrope (increases HR) - Beta-1
  • Vasodilation (low dose) - Beta-2
  • Vasoconstriction (high dose)- Alpha-1

Norepinephrine (Alpha 1, Beta 1)

  • Inotrope - Beta-1
  • Vasoconstriction - Alpha-1

Dopamine (Alpha-1, Alpha-2, Beta-1, Beta-2, DA)

  • Inotrope - Beta-1
  • Chronotrop - Beta-1
  • Vasodilation (low dose) - Beta-2
  • Vasoconstriction (high dose) - Alpha-1

Dobutamine (Beta-1, Beta-2)

  • Inotrope - Beta-1
  • Vasodilation - Beta-2
18
Q

How should hypovolemic shock be treated?

A

Replace the volume
NS - 20 cc/kg boluses for fluid loss

Hemorrhagic - 10-15 cc/kg of RBCs - Type O or correct Type after type and screen, massive transfusion (platelets, cryo, FFP etc.)

19
Q

How should cardiogenic shock be treated?

A

Afterload reduction with inotropic support
Low dose epi infusion (0.05 -0.3 mcg/kg/min)
Inodilators (milrinone or amrinone)

20
Q

How should neurogenic shock be treated?

A

Can try fluids initially
But ultimately need pressors - Norepi or Phenyephrine
- powerful alpha agonists
If cardiac output/rate are inadequate (not usually) - try dopamine
If profound bradycardia - use atropine

21
Q

How should septic shock be treated?

A

Fluid resuscitation
Pressors if needed - ie refractory to fluid resuscitation
- Epi –> NE
Antibiotics

22
Q

What is the mechanism and use of phenylephrine?

A

Peripheral vasoconstriction
Causes vasoconstriction without excessive tachycardia
Useful for those whose shock state is caused by vasodilation primarily
Neurogenic shock

23
Q

What is early, goal-directed therapy?

A

Aggressive approach to target indicators of perfusion and vital organ function in the first 6 hours:
- BP: minimal systolic BP:
< 1 mo = 60
1 mo - 10 yr = 70 + 2(age in yrs)
> 10 years = 90
- Strong, distal pulses = to central pulses
- Skin perfusion (warm , CR <2 secs)
- Normal mental status
- U/O > or = 1 ml/kg/hr, once effective circulating volume restored

24
Q

How should anphylactic shock be treated?

A

IM Epineprhine

25
Q

What is Toxic shock syndrome (TSS)?

A

Fever
Erythroderma
Hypotension
Involvement of several other organ systems

Caused by Staph Aureus strains that produce an exotoxin - TSST-1, enterotoxin B and C
Secondary to prolonged tampon use or open skin wounds/abrasions

Exotoxins are profound vasodilators –> cause distributive shock
leaky tissues - loss of intravascular volume
myocardial depression

Can also be due to GAS - Streptococcal pyogenes -associated with scarlet fever