Shock Overview & Stages of Shock Flashcards

1
Q

What is shock?

A condition that results from some type of cause that leads to decreased tissue perfusion, which causes cell hypoxia

If the cell hypoxia is severe enough, it’ll cause organ dysfunction (MODS) & eventually lead to death

A

Cause of shock depends on what type of shock is presenting

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2
Q

___ shock

Occurs d/t an allergic reaction

A

Anaphylactic

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3
Q

___ shock

Occurs d/t a severe infection

A

Septic

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4
Q

___ shock

Occurs d/t a weak heart

A

Cardiogenic

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5
Q

___ shock

Occurs d/t severe fluid loss

A

Hypovolemic

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6
Q

___ shock

Occurs d/t severe damage to the neuro system (e.g., spinal injury)

A

Neurogenic

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7
Q

Distributive shock includes which 3 types of shock?

A

septic
anaphylactic
neurogenic

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8
Q

Stages of Shock

  • Initial
  • Compensatory
  • Progressive
  • Refractory
A
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9
Q

Initial Stage

✰ CO is low enough to cause the cells to experience ___

Cells switch from aerobic to anaerobic metabolism; the latter will create lactic acid, which’ll accumulate in the blood & lead to lactic acidosis

A

hypoxia

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10
Q
  • Decreased tissue perfusion → LOW CO (HR x SV)
A
  • Normally, body can deal w/lactic acid via the liver, but liver is not functioning @ an optimal lvl b/c of the low amt of O2 its cells are receiving
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11
Q
  • In better circumstances when tissue perfusion is adequate, liver takes lactic acid & converts it to pyruvic acid & then to glucose via gluconeogenesis

! Therefore, lactic acid will start to accumulate in the blood (esp as pt adv to other stages of shock)

A
  • Accumulation of lactic acid causes the blood’s pH lvl to drop (acidosis) & further damages cells
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12
Q

Normal serum lactate lvl < ____ mmol/L

A

1

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13
Q

Abnormal indicating lactic acidosis > ____ mmol/L

A

4

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14
Q

Compensatory Stage

✰ Body systems are coming to the rescue; will try to compensate by using hormonal, neural, & biochemical processes in the body

  • Will try to fight results of anaerobic metabolism; also, will try to increase CO & BP via stimulation of the SNS & RAS, which’ll increase tissue perfusion
A
  • If the cause of shock is corrected during this stage, it’s REVERSIBLE & pt can make a full recovery; if not, next stage
  • Body will succeed @ 1st w/increasing CO & BP via rescue team
  • Will result in an increase in tissue perfusion, BUT body is limited on how long it can maintain rescue effort
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15
Q

How does the body provide compensation?

  • As BP drops, body will sense this (! brain & heart)

1 of the structures to sense this drop in BP is the ____, spec the receptors in the carotid sinus & aortic arch

Will stimulate the SNS to release catecholamines: ___ & ___

A

baroreceptors

epinephrine; norepinephrine

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16
Q
  • Catecholamines will cause vasoconstriction
  • This’ll result in an increase in BP & HR; when this occurs, there’s an increased perfusion to the vital organs
  • Less blood will go to the non-vital organs (GI, renal, skin, lungs) while more will go to the vital organs (heart & brain)
A
  • B/c there was a drop in BP (arterial pressure) there will be a decrease in capillary hydrostatic pressure (the force of pressure the blood creates around the capillary wall)
  • If the BP & CO are low, the force of pressure the blood creates around the capillary wall is definitely low
17
Q
  • This’ll signal the body to try to increase venous blood flow return by shifting fluid from the interstitial compartment to the intravascular compartment
A

How are other systems affected & how do they play a role in the compensatory stage?

18
Q

Kidneys

  • B/c blood flow is dec to the kidneys they activate the renin-angiotensin system
A
  • Renin stimulates angiotensinogen which creates angiotensin I
  • Angiotensin I turns into angiotensin II (a very mighty vasoconstrictor)
  • This substance will cause vasoconstriction in both arterial & venous system
19
Q
  • Constriction in venous system will lead to more blood return to the heart, & constriction in arterial system will incr BP
  • Together, all will lead to an incr in tissue perfusion & the cells will receive more O2
A
20
Q

Presence of angiotensin II will also trigger the release of ____

A

aldosterone

21
Q

Aldosterone

  • Makes the kidneys keep sodium & water → incr blood volume
  • Also, b/c kidneys are incr sodium, it’ll create urine to contain a high amt of sodium, which leads to high osmolality
A
  • High osmolality signals to posterior pituitary gland that body is trying to keep water for some reason, so it releases ADH
  • ADH → prevents water from leaving the kidneys; further incr blood volume
  • By incr blood volume, CO will be incr along w/tissue perfusion
22
Q

GI

  • Perfusion is dec so this system slows down
  • Pt is @ risk for paralysis of intestines in a cond called paralytic ileus
A

Skin

  • Perfusion is dec so blood flow is low, which leads the skin to be cold & clammy

! Is not the case during this stage in septic shock → pt’s skin will be hot & flushed d/t vasodilation presenting

23
Q

Lungs

  • Perfusion is dec so parts of the lung may not be perfused

! Ventilation & perfusion mismatch & O2 lvls become low in blood

A
  • Will lead pt to hyperventilate
24
Q

Progressive Stage

✰ Rescue effort from prev stage has failed, & body can’t compensate anymore; pt is progressing to MODS

  • Is no more compensation in this stage; CO is low, tissue perfusion is low, & cells are NOT receiving O2, which leads to cell hypoxic injury
A
  • Cells will start to swell & CAPILLARY PERMEABILITY is incr
25
Q

Brain

  • Cells to the brain aren’t being perfused; MAP is <60 mmHg
  • This means cerebral perfusion pressure (CPP) is inadequate to maintain perfusion to brain’s cells
A
  • Will start to see major mental status changes
  • Pt will be very slow in their speech, restless, anxious, agitated, & not respond to stimulation
26
Q

Lungs

  • ARDS will develop
  • This occurs d/t incr capillary permeability in the alveoli sacs (where gas exchange occurs); sacs will collapse d/t fluid surrounding them & lung will lose elasticity

! Will need intubation & mech vent to breathe

A
  • Fluid in the lungs (crackles), incr RR, dec O2 lvl, & resp failure
27
Q

Heart

  • Heart cells start to die incl those that play a role in the electrical conduction system of the heart & that help heart contract/pump

! Cardiac dysrhythmias occur along w/death to myocardial tissue

A

GI

  • Gut cells start to die; e.g., cells that protect the lining from its own acid quit working

! Ulcers can develop which can turn into massive GI bleeding (bad b/c clotting abilities are affected d/t liver hypoxia)

28
Q

Liver

  • Dec liver perfusion causes cells to die
  • Will be a build-up of toxic waste products (e.g., bilirubin, ammonia)

! Risk for infection & bleeding

A
29
Q

?

Occurs when small clots form in the vessels, further compromising blood flow to organs

Depletes body’s platelets & clotting stores & leads to massive, uncontrollable bleeding

A

DIC (disseminated intravascular coagulation)

30
Q

____ Stage

  • Unmanageable; cannot be reversed; all organs shut down and fail; death inevitable
A

Refractory