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Anesthesia based on Nebuchanedzzer II > ITE Crit Care > Flashcards

ITE Crit Care Flashcards

1
Q

sepsis

A

life threatening organ dysfunction caused by a dysregulated host response to infection

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2
Q

then anterior pituitary secretes ACTH and stimulates the zona glomerulosa of the adrenal cortex to secrete _____

A

aldosterone

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3
Q

humoral response activates ____

A

macrophages, monocytes, neutrophils –> release proinflammatory cytokines

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4
Q

septic shock is diagnosed when a pt has ______

A

sepsis and requires vasopressors to maintain MAP > 65 mmHg and a lactate of > 2 mmol/L
despite adequate fluid recuscitation

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5
Q

pts with septic shock NOT responsive to fluid resuscitation should get ______

A

200 mg IV hydrocortisone

- pt may have adrenal insufficiency

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6
Q

Hydrocortisone inhibits ____

A

nitric oxide synthesis

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7
Q

Phosgene, used as chemical warfare, exposure can cause ______, which can cause significant morbidity and mortality

A

severe pulmonary damage

- targets type I and II pneumocytes

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8
Q

Phosgene is a colorless gas that smells like _____. After dissolving, it spreads _____

A

freshly cut gas,

close to the ground

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9
Q

Dual latency action of phosgene

A

Immediate:
- intense URI irritation

Latent:
- 2-24hrs later, pulmonary edema and circulatory collapse

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10
Q

_______ are typically reported with ABG, but needs to be derived from other measured data

A

base excess
HCO3-
SaO2

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11
Q

ABG directly measures ______

A

pH
PaCO2
PaO2

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12
Q

Neurological sx of hypophosphatemia

A

AMS
sz
central pontine myelinolysis

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13
Q

Hypophosphatemia decreases 2,3 DPG, causing a (Right/Left) shift in the oxyhemoglobin curve, and have poor oxygen release

A

Left

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14
Q

Prolonged QT is associated with (Hyper/Hypo)phosphatemia

A

HYPERphosphatemia

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15
Q

Refeeding syndrome causes:

A 
Hypophosphatemia
Hyponatremia
Hypocalcemia
Hypomagnesemia
Hypokalemia

Hyperglycemia

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16
Q

Why does hypoglycemia with the abrupt stopping of TPN?

A

TPN causes pancreas to secrete excess insulin to prevent hyperglycemia during infusion

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17
Q

(Freshwater/Saltwater) is quickly absorbed by the pulmonary circulation

A

freshwater

- can cause hyponatremia

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18
Q

(true/false) most drowning victims die without aspiration

A

false

- 90% do

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19
Q

_________ is the most common cause of death in hospitalized near drowning pts

A

post-hypoxic encephalopathy

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20
Q

______ is the most common cause of death in drowning pts

A

hypoxic cardiac arrest

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21
Q

large aspiration of fluid in drowning victims result in (4)

A
  1. more V/P mismatch
  2. More surfactant washout
  3. more electrolyte shifts
  4. coagulopathy
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22
Q

Botulinum is a neurotoxin that inhibits ____, which can result in paralysis

A

exocytosis of ACh at autonomic nerve terminals

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23
Q

Key feature of botulism

A

b/l cranial nerve deficits with symmetric weakness

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24
Q

Treatment of botulism in infants < 1 y.o and > 1 y.o

A

< 1 y.o: human-derived immune globulin

> 1 y.o: equine serum antitoxin (contains antibodies to 7/8 of known botulism type)

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25
Q

Treatment for hypermagnesemia

A
  1. accelerated elimination
    - Loop diuretics + D5W
    - dialysis
  2. counteract it
    - calcium*
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26
Q

Why does PaCO2 decrease with sepsis?

A

Sepsis -> lactic acid production -> body compensates with tachypnea -> respiratory alkalosis

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27
Q

Sepsis leads to hypermetabolism, which includes protein (catabolism/anabolism)

A

catabolism

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28
Q

Organism associated with early vs late onset VAP

A

early: MSSA, H influenzae
late: MRSA, pseudomonas, acinetobacter

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29
Q

Orthodeoxia is commonly seen in hepatopulmonary syndrome. what is that?

A

Hypoxia worsens when pt stands and improves when pt lies flat

*standing worsens V/P mismatch since gravity causes increased perfusion and pooling in less ventilated lower lung segments

30
Q

Hepatopulmonary syndrome is defined as _____ and increased A-a oxygen gradient in the setting of ESLD

A

intrapulmonary vascular dilatations (IPVDs)

31
Q

Mean pulmonary artery pressures (PAP) > ___ mmHg is an absolute contraindication to liver transplantation

A

> 50 mmHg

32
Q

Most nosocomial infections arise from ____

A

endogenous flora

33
Q

Use of PPIs (increase/decrease) the incidence of nosocomial infections

A

increase

- gastric acidity inhibits bacterial overgrowth. Use of PPIs allows GNB to migrate into oropharynx

34
Q

Septic shock effects on:

  • TNF-a
  • TF
  • Complement
  • Interferon gamma
A
  • TNF-a: increases
  • TF: increases
  • Complement: increases
  • Interferon gamma: increases
35
Q

The ARDS network states that pts should be ventilated at a tidal volume of 6 mL/kg of PBW and ______

A

plateau pressures < 30 cm H2O

36
Q

RASS +4, 0, -4

A

+4: combative violent

0: calm, alert, appropriate
- 4: unconscious, deep sedation

37
Q

_____ electrolyte fluctuations are not commonly seen with TPN.

A

sodium

38
Q

(hyper/hypo) phosphatemia normally results from TPN

A

hypophosphatemia

39
Q

TPN is often administered via _____

A

central line, but peripheral can be used if osm low enough

40
Q

Hepatic steatosis is (common/uncommon) with TPN

A

common

- excess sugar is stored as fat in liver

41
Q

(Hypercarbia/Hypocarbia) commonly occurs with TPN infusion

A

Hypercarbia

- more carbohydrates -> sugar is metabolized to increase CO2 production -> respiratory acidosis

42
Q

Corticosteroid myopathy presentation

A

insidious disease of proximal muscles in upper and lower limb and neck flexors

43
Q

Muscle biopsy of corticosteroid myopathy

A

muscle atrophy without any inflammation

44
Q

If the change in PaCO2 follows the change in pH, the condition is primarily _____

A

metabolic

45
Q

If the change in PaCO2 is opposite the change in pH, the condition is primarily _____

A

respiratory

46
Q

Metabolic disturbance associated with excessive diuresis

A

constriction alkalosis

  • excessive amt of low bicarbonate containing fluid is lost
  • intravascularly depleted
47
Q

Metabolic disturbance associated with salicylate toxicity

A

respiratory alkalosis, + overlying metabolic acidosis

48
Q

Metabolic disturbance associated with pulmonary embolism, PNA, asthma

A

respiratory alkalosis

- inc in minute ventilation

49
Q

Metabolic derrangements seen in respiratory alkalosis

A
  1. hypocalcemia
  2. hypokalemia
  3. hypophosphatemia
50
Q

Metabolic changes during SIRS (4)

A
  1. Hyperglycemia
  2. Proteolysis (catabolism)
  3. Lipolysis
  4. Increased B-2 adrenergic stimulation
51
Q

How does hyperventilation result in hypocalcemia?

A

In response to respiratory alkalosis ->
H+ bound to neg charged albumin is released ->
Ca2+ then binds to albumin
(decreases free/ionized calcium)

52
Q

How does hyperventilation result in hypokalemia?

A

In response to respiratory alkalosis ->
Hydrogen-Potassium transporters pump H+ OUT of cells ->
K+ is pumped INTO cells

53
Q

How does alkalosis cause hypophosphatemia?

A

rising pH ->
stimulates glycolytic pathway ->
triggers cellular uptake of phosphorous

54
Q

_____ is the most common cause of acute liver failure in US

A

acetaminophen toxicity

55
Q

Acute respiratory acidosis

Acute 10mmHg increase in PaCO2 causes a ______ in HCO3-

A

increase of 1 mEq/L

56
Q

Chronic respiratory acidosis

Sustained 10mmHg increase in PaCO2 causes a ______ in HCO3-

A

4-5 mEq/L increase

57
Q

Acute respiratory alkalosis

Acute 10mmHg decrease in PaCO2 causes a ______ in HCO3-

A

decrease of 2 mEq/L

58
Q

Chronic respiratory alkalosis

Sustained 10mmHg decrease in PaCO2 causes a ______ in HCO3-

A

decrease of 5-6 mEq/L

59
Q

What phase of the capnograph is best to analyze for presence of acute or chronic obstructive respiratory pattern?

A

Upstroke phase (B-C)

  • normal: sharp upstroke caused by rapid increase in CO2 detected during expiration
  • obstructive pattern: slower, blunted upstroke
60
Q

What limits the time that jet ventilation can be used?

A

Hypercarbia with respiratory acidosis
(not hypoxemia)
- small tidal volumes used increases dead space ventilation:alveolar ventilation

61
Q

How can jet ventilation cause necrotizing tracheobronchitis (very rare complication)?

A

Dehydration of respiratory mucosa, impaired respiratory cilia fxn

  • high pressure nonhumidified oxygen
  • usually only occurs with prolonged use
62
Q

How does sepsis cause an increase in ETCO2?

A

Increased metabolism (lactic acid and CO2) -> inc CO2 production -> ETCO2

63
Q

Shivering (increases/decreases) ETCO2

A

increases
- enhanced skeletal muscle metabolism

*note: hypothermia -> decreased metabolic activity -> lower ETCO2

64
Q

Hypothermia (increases/decreases) ETCO2

A

Decreases

- decreased metabolic activity -> lower ETCO2

65
Q

How does cardiac arrest affect PaCO2 and ETCO2

A

Increased pathologic dead space
- poor perfusion in setting of adequate ventilation

Increased PaCO2

Decreased ETCO2

66
Q

Which disorders are associated with gradual increase in ETCO2?

A

Thyroid storm

MH

67
Q

metabolic demand for oxygen in an adult

A

3 ml/kg/min * pt weight

68
Q

Why is PT the most useful diagnostic tool in acute abnormalities in hepatic SYNTHESIS?

A

Many coagulants are synthesized in liver

Short half lives

69
Q

Symptoms of HYPERmagnesemia

A

> 7 mg/dL

  1. Hypotension
  2. Bradycardia
  3. Vasodilation
  4. Wide QRS, prolonged PR
  5. Reduced DTR

> 10 mg/dL

  1. Respiratory arrest
  2. Asystole

*depress contractile force of muscles/vessels/myocardium

70
Q

Magnesium sulfate is administered in preeclamptic pts why?

A

Prevent seizure activity through NMDA antagonism in CNS

Anesthesia based on Nebuchanedzzer II (38 decks)

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