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NSER 7210 - Theory > Module 2 - Distributive Shock, ETOH, Immunocompromise > Flashcards

Module 2 - Distributive Shock, ETOH, Immunocompromise Flashcards

1
Q

What is SIRS?

A

Systemic Inflammatory Response Syndrome
- overwhelming, unregulated, inflammatory response

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2
Q

What are the effects of SIRS?

A
  • uncontrolled coagulation
  • widespread vessel leakage
  • poor distribution of circulating volume
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3
Q

What are conditions outside of infection that cause SIRS?

A
  • Trauma
  • Pancreatitis
  • Burns
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4
Q

How is septic shock different from hypovolemic shock?

A
  • total fluid volume may be normal
  • circulating volume is low b/c of leaky vessels
  • coagulation system malfunctions EARLY, clotting factors are depleted - leading to bleeding
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5
Q

What is the definition of Sepsis?

A

Dysregulated host response to infection causing life threatening organ dysfunction

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6
Q

What are the two clinical requirements for definition of Septic Shock?

A
  1. Vasopressor requirement to maintain MAP > 65 mmHg
  2. Serum lactate > 2 mmol/L
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7
Q

What are the three systems most affected by sepsis and septic shock?

A
  • Lungs
  • Kidneys
  • Cardiovascular
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8
Q

How is sepsis managed?

A
  • Fluid resuscitation
  • Blood cultures
  • Antibiotics
  • Serum lactate level (increase represents tissue hypoxia)
  • Vassopressors to maintain MAP > 65
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9
Q

What are indicators of organ dysfunction that nurses can use to identify potential sepsis in patients RAPIDLY?

A
  • Altered LOC
  • Hypotension
  • Poor cap refill
  • Tachypnea
  • Tachycardia
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10
Q

How does sepsis negatively affect cardiac output?

A

Decrease preload
- decrease circulating volume
- leaky vessels, decreased vascular tone
- HR will increase to maintain CO, but if beats too fast (less filling time and increased myocardial demand)

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11
Q

How does sepsis decrease a patient’s oxygen supply?

A
  1. Decreased diffusion causing impaired alveolar gas exchange
  2. Decreased preload causing decreased cardiac output
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12
Q

Why is alveolar gas exchange impaired in sepsis?

A

Leaky vessels will cause fluid to shift out of the intravascular space to the interstitial space (including the lungs)
- decrease diffusion of O2
- increase RR and tidal volume to attempt to compensate for decreased oxygen supply and increased demand
- RR will eventually decrease as patient tires out and brain becomes hypoperfused

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13
Q

What 4 things increase a septic patient’s oxygen demand?

A
  • Fever
  • Pain
  • Stress
  • Anxiety
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14
Q

What are symptoms of Alcohol Withdrawal Syndrome?

A
  • Agitation
  • Tremor
  • Fever
  • Diaphoresis
  • Tachycardia
  • Confusion
  • HTN
  • Irritability
  • Anxiety
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15
Q

What is the onset of Delirium Tremens?

A

48 - 72 hours after last drink

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16
Q

When is the onset of minor withdrawal symptoms (ETOH)?

A

6 - 12 hours after last drink

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17
Q

When is the onset of Alcohol Withdrawal Seizures?

A

24 - 48 hours after last drink

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18
Q

What are the signs and symptoms of Delirium Tremens?

A
  • Delirium
  • Psychosis
  • Hallucinations
  • Hyperthermia
  • Malignant HTN
  • Seizures
  • Coma
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19
Q

Why is Thiamine given to ETOH?

A

Prevention of Wernicke’s Encephalopathy

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20
Q

What can precipitate or worsen Wernicke’s Encephalopathy?

A

Administration of glucose
- give Thiamine BEFORE glucose!

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21
Q

What is the gold standard treatment for AWS (ETOH)?

A

Benzodiazepines

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22
Q

What are the drugs of choice for ETOH?

A
  1. Lorazepam
  2. Diazepam
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23
Q

Why would Lorazepam be chosen over Diazepam?

A

Lorazepam is shorter-acting (prevent respiratory depression)
- Good for patients over 75
- Better for patients with advanced liver disease

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24
Q

When is the IV route preferred over the oral route for treatment of ETOH?

A

IV: for moderate to severe forms of AWS
PO: for milder forms of AWS

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25
Q

How is oxygen transported to tissues (two forms)?

A
  1. Dissolved in plasma
  2. Bound with hemoglobin
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26
Q

How is the concentration of oxygen dissolved in plasma represented?

A

PaO2
(Partial pressure of oxygen)

27
Q

How is the concentration of oxygen bound to hemoglobin represented?

A

SaO2
(Oxygen saturation)

28
Q

If the oxygen curve is shifted to the LEFT, what happens to oxygen affinity?

A

High Affinity
- Holds onto the oxygen and doesn’t let go

29
Q

If the oxygen curve is shifted to the RIGHT, what happens to the oxygen affinity?

A

Low Affinity
- Oxygen is slippery, hard to pick up and hard to hold onto

30
Q

Why is pre-oxygenation so important prior to RSI?

A

Increasing levels of PaO2 prior to intubation provides enough time to paralyse patients (stop breathing) in order to insert ETT without drastic falls in saturation levels

31
Q

What are things that pulse oximetry CAN’T tell you?

A
  • Hemoglobin level
  • Identify non-functional hemoglobin
  • What hemoglobin is saturated with (carbon monoxide)
32
Q

What can shift the oxy-hemoglobin curve to the right?

A
  • Increased temperature
  • Acidosis
  • Exercise
  • Increased partial pressure of arterial carbon dioxide (PaCO2)
33
Q

What can shift the oxy-hemoglobin curve to the left?

A
  • Increased blood pH (alkalosis)
  • Decreased temperature
  • Decreased PaCO2 levels
34
Q

Why could the SpO2 give an abnormally high value for a patient near respiratory failure?

A
  • Patient may be hyperventilating (trying to increase oxygenation)
  • Resulting in respiratory alkalosis
  • Shifts the curve to the left, increasing affinity (Hgb hanging onto the O2 instead of releasing it)
35
Q

What happens during an allergic response?

A

Immunoglobin (IgE) triggers the release of histamine and other vasoacrtive substances from mast cells and basophil cells

36
Q

How is anaphylaxis different than an allergy?

A

Anaphylaxis has a two system involvement

37
Q

What are some signs and symptoms of anaphylaxis?

A
  • Difficult breathing
  • Rash
  • Nausea / Vomiting / Diarrhea
  • Stridor
  • Headace
  • Dizziness, syncope, hypotension
38
Q

What signals impending respiratory failure?

A

Decreased effort and rate of breathing

39
Q

What is the drug of choice for anaphylaxis?

A

Epinephrine

40
Q

What is the dose of epinephrine for adults in anaphylaxis?

A

0.3 - 0.5 mg

41
Q

What is the dose of epinephrine for children in anaphylaxis?

A

0.01 mg/kg
(max 0.5 mg)

42
Q

What are other medications used in the treatment of anaphylaxis?

A
  • H2 blockers (GI symptoms) - Famotidine
  • Steriods (anti-inflammatory)
  • H1 blockers (symtom control): Benadryl
43
Q

What is the concentration of Epinephrine used in anaphylaxis? ACLS?

A

Anaphylaxis = 1mg / 1mL
ACLS = 1 mg / 10 mL

44
Q

What is the best route of Epinephrine in anaphylaxis>?

A

IM
- lateral thigh

45
Q

What cells does HIV target?

A

CD4 (T-helper cells)

46
Q

Describe the patho of HIV

A
  1. HIV fuses to the surface of the CD4 and implants RNA
  2. Infected CD4 cells die and release more replicated copies of HIV
  3. HIV takes over more CD4 cells
  4. Fewer and fewer CD4 cells left to fight infection
  5. Progression to AIDs
47
Q

What is a normal CD4 count?

A

500 - 1500

48
Q

What is the CD4 count of AIDS?

49
Q

What is the goal number for viral load of HIV?

50
Q

What is the most common AIDS defining illness?

A

PCP
Penumocystis Pneumonia

51
Q

What are some example of immunocompromised patients in the ED?

A
  • HIV+
  • Cancer patients
  • Rheumatoid arthritis
  • Lupus
  • Active chemotherapy
  • Anti-rejection drugs
  • Newborns / Neonates
52
Q

Why does fever happen in SIRS?

A

Body is fighting off infection
- increases temperature to create inhospitable environment
- increases oxygen demand
- decreased oxygen affinity (shift to the RIGHT)

53
Q

What are the consequences of giving Tylenol to the Oxy-hemoglobin curve?

A

Increases affinity of oxygen
- shifts the curve to the LEFT
- might hinder getting O2 to the tissues b/c Hgb won’t release the O2

54
Q

Why does an increased RR happen in SIRS?

A

There is a decreased O2 supply, affinity has changed
- increased RR to increase supply
- body is trying to bring in more oxygen to the tissues
- trying to blow off CO2

55
Q

What are the SIRS Criteria?

A
  1. HR > 90
  2. Temp > 38 or < 36
  3. RR > 20 or PaCO2 < 32 mmHg
  4. WBC >12,000 or < 4,000
56
Q

Why is the body initially in a state of Respiratory alkalosis and progresses to acidosis in Shock?

A
  1. Increase RR compensation to increase oxygenation
  2. Blows off CO2 - alkalosis
  3. Shifts curve to the LEFT, increases affinity of oxygen (doesn’t release as readily)
  4. Worsens hypoxemia
  5. Leads to organ dysfunction
  6. Cells switch to anaeorbic metabolic
  7. Byproduct is lactate produced
  8. Shifts curve to the right
  9. Results in metabolic acidosis
  10. May show respiratory acidosis if CO2 is climbing
57
Q

What is mild hypoxemia?

58
Q

What is moderate hypoxemia?

59
Q

What is severe hypoxemia?

60
Q

Why is a high CO2 an acidic state?

A

CO2 + water = carbonic acid
(More CO2 equals more carbonic acid)

61
Q

Why is a low HCO3 an acidic state?

A

HCO3 is a buffer
If you don’t have a lot of buffer, you have more H+ in the blood = acidic state

62
Q

Why is there an increased HR in SIRS and sepsis?

A

Increased HR trying to compensate for decrease in stroke volume

63
Q

Why is there an elevated WBC or > 10% immature neutrophils?

A
  • High WBC = early onset of infection
  • Low WBC = immunocompromised
  • Immature neutrophils = all mature neutrophils are dying, so send in the CHILDREN!

NSER 7210 - Theory (6 decks)

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