Shock Flashcards
Define shock
When the metabolic demand exceeds the body’s ability to deliver oxygen and nutrients
What are the clinical manifestations of shock?
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
2 stages of shock
Compensated
Uncompensated
What is the exception to normal compensatory mechanisms?
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
Markers of uncompensated shock
Acidosis High lactate Altered LOC Oliguria/Anuric Ileus - constipation, decreased GI motility, distention, edema of bowel wall BP falls Multiorgan failure ARDS
Mechanisms of Shock
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
Most common potent initiator of shock
Endotoxin - lipopolysaccharide coat of a Gram neg bacteria
Viral proteins
Teichoic acid
Which bacteria causes more severe septic shock?
Gram NEG - 20-50% mortality
Gram pos - 10-20%
Describe the cascade of septic shock?
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
What needs to happen in the golden hour of septic shock?
Aggressive fluid resuscitation
Ionotropic therapy
Antibiotics
Most common mechanism of shock in kids?
Hypovolemia
- due to diarrheal illness
How does trauma cause shock?
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
Does isolated head trauma cause shock?
No
Not unless there is a large scale scalp laceration
Classes of hemorrhage
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
How can you differentiate between neurogenic and hemorrhagic shock?
Hemorrhagic - rapid and possibly irregular pulse
Neurogenic - slow and regular pulse
Priorities in treatment of shock
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
What are the 4 common pressors and their actions?
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
How should hypovolemic shock be treated?
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.)
How should cardiogenic shock be treated?
Afterload reduction with inotropic support
Low dose epi infusion (0.05 -0.3 mcg/kg/min)
Inodilators (milrinone or amrinone)
How should neurogenic shock be treated?
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
How should septic shock be treated?
Fluid resuscitation
Pressors if needed - ie refractory to fluid resuscitation
- Epi –> NE
Antibiotics
What is the mechanism and use of phenylephrine?
Peripheral vasoconstriction
Causes vasoconstriction without excessive tachycardia
Useful for those whose shock state is caused by vasodilation primarily
Neurogenic shock
What is early, goal-directed therapy?
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
How should anphylactic shock be treated?
IM Epineprhine
What is Toxic shock syndrome (TSS)?
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