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PAT401 Advanced Pathotherapeutics > Week 12: Shock > Flashcards

Week 12: Shock Flashcards

1
Q

What is shock?

A

Acute/progressive circ. dysfunction —> poor O2 delivery to body :(

Cell. Metabolism is bad :(

  • more demand/consumption of O2/nutrients
  • decrease removal of waste :0

Body goes into acidosis

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2
Q

What does MODS stand for?

A

Multiple Organ Dysfunction Syndrome (MODS)

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3
Q

In shock, the body’s cellular metabolism is impaired. What type of metabolism does the body shift to?

A

aerobic to ANAEROBIC metabolism.

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4
Q

What are some key features of anaerobic metabolism? (3)

A
  • body goes into ACIDOSIS
  • disruption in making ATP
  • Water loss + edema…swelling :(
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5
Q

During shock, there is an accumulation of _________ & __________ in the cell.

A

sodium and chloride

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6
Q

In shock, _________ leaves the cell. This activates the coagulation pathway, which releases ________________________.

A

Potassium, lysosomal enzymes

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7
Q

In shock, there is impaired ___________ delivery + uptake.

A

glucose

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8
Q

What are the key features of “Impaired glucose delivery + uptake”? (4)

A

Cells shift to:
- glycogenolysis (cell failure)
- lipolysis (cell failure)
- gluconeogenesis (protein breakdown)
—————-
- heart & bones use lactic acid as fuel (temporarily) —> metabolic acidosis

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9
Q

What are the key features of “impaired protein metabolism”? (4)

A
  • organ failure (b/c protein is being used for fuel sooo it’s no longer available to be used for cell structure/function/repair/replication :0)
  • increase in ammonia + urea (thx to protein anaerobic met….disrupt cell function)
  • decrease in albumin —> decrease in circ. V
  • muscle wasting :( (b/c protein breakdown…makes bones and heart muscles weaker)
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10
Q

What are some ways the body compensates during shock?

A
  • SNS increases in symp. flow
  • Increase in E & NE
    —-> stim. alpha & beta receptors (fight or flight)
    ——–> therefore increase in HR and SVR

Kidneys: RAAS; aldosterone & vasoconstriction —> more sodium & water out

**Not all compensatory methods will work for certain types of shock…

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11
Q

Compensatory mechanisms try to maintain ____ & ____

A

Cardiac output (CO) , BP

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12
Q

TRUE or FALSE:
Compensatory mechanisms are effective over the long term, and it is not detrimental if a shock state is prolonged (uncompensated)

A

FALSE
compensatory mechanisms are NOT effective over long term.

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13
Q

In Neurogenic/Vasogenic shock, what are the compensatory mechanisms?

A
  • loss of sympathetic tone prevents compensatory tachycardia
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14
Q

When it comes to cardiogenic shock, what are the compensatory mechanisms?

A

When CO (cardiac output) decreases, compensatory activated!!!
—> renin-angiotensin, SNS…
——–> Fluid retention, sys. vasoconstriction, tachycardia
——–> catecholamines increase contractility & HR

**BUT tachy. & vasoconstriction INCREASE <3 O2 consumption…this is <3 dysfunction…
——-> if this continues, CO & BP drop…soooo organ failure :(

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15
Q

When it comes to hypovolemic shock, what are the compensatory mechanisms?

A

Tachycardia; redistribute blood from skin/gut/kidneys —> brain & heart

  • RAAS (renal sodium & water retention)
  • Secrete ADH (water retention by kidneys)
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16
Q

In obstructive shock, what are the compensatory mechanisms?

A
  • obstruction to blood flow —> low CO & circ. collapse :O
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17
Q

What treatment of shock is the best/necessary in all shock states?

A

Oxygenation!

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18
Q

What are the classifications of shock? (4)

A
  • Distributive
  • Hypovolemic
  • Cardiogenic
  • Obstructive
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19
Q

What are the types of distributive shocks? (3)

A
  • Septic shock
  • Anaphylactic shock
  • Neurogenic/Vasogenic shock
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20
Q

What are the causes of:
- Septic shock
- Anaphylactic shock
- Neurogenic/Vasogenic shock

A
  • septic: cause -infection
  • anaphylactic: cause - hypersensitivity
  • neurogenic/vasogenic: cause - alteration in vas. smooth muscle tone
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21
Q

What are the causes of:
- hypovolemic shock
- cardiogenic shock
- obstructive shock

A
  • Hypovolemic: cause - not enough intravascular fluid (ex. hemorrhage)
  • Cardiogenic: cause - heart failure
  • Obstructive shock: cause - mech. blockage (ex. tamponade, P.E., tension pneumothorax)
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22
Q

In septic shock, what are the key manifestation seen?

A

Increased HR, increased immune response

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23
Q

In anaphylactic shock, what are the key manifestations you will see?

A

Difficulty breathing, hives, itchiness

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24
Q

In neurogenic shock, what are the key manifestations seen?

A

low SVR, low HR, low BP

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25
Q

In hypovolemic shock, what are the key manifestations seen?

A

poor skin turgor, THIRST, increases SVR, cool extremities

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26
Q

In cardiogenic shock, what are they key manifestations seen?

A

chest pain, JVD seen

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27
Q

In obstructive shock, what are the key manifestations seen?

A

Depends… low BP, High HR, oliguria

28
Q

Distributive shock is also called:

A

Vasodilatory shock

29
Q

more from slides Manifestations of septic shock include:

A
  • persistent low arterial pressure
  • tachypnea (fast breathing)
30
Q

Septic shock treatment includes: (3)

A
  • CHECK LACTATE LEVELS; obtain blood cultures
  • antibiotics & vasopressors (norepinephrine!)
  • fluid resus. (IV crystalloids; LR or NS)
  • +++ Consider hydrocortisone for adrenal insufficiency.
31
Q

In anaphylactic shock, _________ causes a huge immune and inflammatory response.

A

Allergen

32
Q

more from slides Manifestations of anaphylactic shock include:

A
  • edema (airway, therefore hard time breathing)
  • GI cramps
  • Hives (urticaria)
  • WATCH AIRWAY!!!
33
Q

Anaphylactic shock treatment includes:

A
  • **remove antigen!!!
  • decrease mast cell & basophil degran.
  • admin lactated ringers to reverse hypovolemia
  • O2
34
Q

When is it ideal to give Lactated Ringers?

A

For anaphylactic shock; to reverse relative hypovolemia

35
Q

Define neurogenic/vasogenic shock:

A

Widespread vasodilation happens b/c there’s an imbalance between parasympathetic & sympathetic stimulation.

Causes continuous vasodilation & creates relative hypovolemia
—-> SVR decreases DRASTICALLY

Causes include:
- trauma, severe pain/stress/ anesthesia, depressant drugs

36
Q

What is the treatment for neurogenic shock?

A
  • positioning: RECUMBENT (lay on side); good for venous return…try not to turn head…legs up :)
  • bolus fluids (supports CO)
  • give vasopressors (treats fluid-refractory hypotension)
  • Temp. reg (warm/cool)
  • pain manage
37
Q

Define cardiogenic shock:

A

Heart can’t pump enough blood to tissues & organs :(

  • continuous hypotension & lack of tissue perfusion + left filling pressure problems :(
38
Q

more from slides Manifestations of cardiogenic shock include:

A

dyspnea (+ the ones on my paper)

39
Q

Cardiogenic shock treatments include:

A
  • if there’s a problem with the PUMP, put in an IABP (Intra-aortic Balloon Counterpulsation)
  • in general: mechanical support/surgery/pharm
40
Q

A person develops cardiogenic shock after an acute MI. The nurse understands this will produce a(n):
a) inhibition of the sympathetic nervous system
b) decreased activation of the complement system
c) stimulation of the renin-angiotensin system
d) lowered production of catecholamine system

A

c
** b & d would be right if it said the opposite

41
Q

Define hypovolemic shock:

A

Not enough intravascular fluid volume; loss of blood, plasma, or interstitial fluid

ex. hemorrhage, burns, emesis, diuresis (peeing a lot), diaphoresis (sweating), diabetes

42
Q

more from slide Manifestation of hypovolemic shock is:

A

Low urine output

43
Q

Treatment for hypovolemic shock includes: (4)

A
  • hemorrhage control**
  • fluid replacement
    —–> adults: iso. crystalloids
    —–> kids: iso. crystalloids OR colloids
  • blood replacement
  • monitor for hypervolemia
44
Q

Define obstructive shock:

A

Mechanical blockage that blocks blood flow to/from heart.
**commonly duo with cardiogenic shock :0

45
Q

Treatment for obstructive shock includes: (4) **

A
  • restore sys. O2 & perfusion
  • eliminate blockage
  • maintain airway, oxygenate, ventilate
  • bolus fluids
46
Q

Define MODS:

A

Lack of perfusion; massive inflammation b/c multi-organ damage :(

  • happens b/c uncontrolled sys. inflammatory response to severe illness/injury
  • progressive dysfunction of 2+ organs
47
Q

The 2 most common causes of MODS are:

A

Shock and sepsis

**but can be caused by any injury/disease that starts huge sys. inflammation (ex. trauma, burns, etc.)

48
Q

Diffrentiate between the 2 types of MODS:

A

Primary:
- directly because of injury
- 3-7 days after injury

Secondary:
- occurs later
- associated with more organ dysfunctions :(

49
Q

What is primary MODS triggered by?

A

Low perfusion

50
Q

What happens in primary MODS?

A

Neutrophils and macrophages are “primed” by cytokines…prepping WBCs to fight inflammation…

51
Q

What are some key points about Secondary MODS? (3)

A
  • O2 free radicals damage cells; leads to tissue necrosis
  • platelet-activating factor damages endothelium, stim. clot formation, and activate more phagocytes.
  • poor distribution of blood flow & poor perfusion to organs
52
Q

What is the “pathway” of secondary MODS? (5)

A

SHOCK —> inflammation —> neutrophil/platelet —> endothelium —> MODS

53
Q

What are the key manifestations of MODS? (2)

A

renal failure, altered mental status

54
Q

Endothelial cell dysfunction and mediator release in multiple organ dysfunction syndrome produces:
a) a net procoagulant state
b) vasoconstriction
c) a reduction in oxygen free radicals
d) decreased proteases

A

a
**not b since we’re most concerned about VASODILATION
**not c b/c it’s an INCREASE in O2 free radicals
**not d b/c it’s an increase in proteases

55
Q

In secondary MODS, the body goes into ______drive.

A

Overdrive

56
Q

Which MODS is more concerning? Primary or Secondary?

A

Secondary; big clots can disturb blood flow :(

57
Q

What are some manifestations of secondary MODS?

A
  • first 24hrs: low-grade fever, tachy, fast breathing, altered mental status, hyperdynamic/hypermetabolic state
  • 24-72 hrs: start of lung failure :(, potentially ARDS :0
  • 7-10 days: hypermeta/hyperdynamic state intensifies, bacteremia common :0, more organ failure…
  • end: heart & hematologic failure
58
Q

Consequences of MODS include: (5)

A
  1. translocation of bacteria
  2. maldistribution of blood flow
  3. hypermetabolism
  4. imbalance in O2 supply & demand
  5. myocardial depression
59
Q

True or false: vital signs are a reliable when it comes to assessing shock in children

A

FALSE

60
Q

What are some things a nurse should assess for in a child suspected of experiencing shock?***

A
  • extremely irritable
  • lethargy
    —–> LOC is going down
  • decrease response to pain stimuli
    ——> indicates severe heart/lung/neuro compromise :0
  • resps, skin colour
61
Q

In terms of skin colour and shock in children, what are abnormal findings?***(3)

A
  • Mottling
    —> marble/blotchy appearance; but might not be shock if mottling comes from a cold environment
  • Pallor (poor perfusion)
  • Flushed, bright red skin (sepsis!)
62
Q

True or false: In a child, BP may be normal up until the very late stages of shock.

A

True

63
Q

True or false: Liver enzymes (serum lactate) should be assessed for a child who is suspected to be experiencing shock.

A

true

64
Q

Which parameter will the nurse monitor to best determine the systemic perfusion in a child?
a) urinary output
b) partial pressure of arterial oxygen (PaO2)
c) systolic hypotension
d) serum lactate

A

d
**not a; this is good for burn victims
**not b; not an indication of sys. perfusion
**not c; this is late course…BP not a good indicator

65
Q

What is the best indicator of shock?

A

Lactate

PAT401 Advanced Pathotherapeutics (11 decks)

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