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BCIT Module 4 > BCIT Module 4 > Flashcards

BCIT Module 4 Flashcards

1
Q

What are the characteristics of ARDS?

A
  • noncardiogenic pulmonary edema
  • severe hypoxemia (often resistant to O2 therapy)
  • characteristic x ray changes (bilateral opacities)
  • decreased lung compliance
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2
Q

What are examples of direct insults that lead to ARDS?

A

Pneumonia, aspiration, pulmonary contusion

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3
Q

What are examples of indirect insults that may result in ARDS?

A

Sepsis, pancreatitis, nonthoracic trauma

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4
Q

Who are the patients most at risk for developing ARDS?

A

Elderly

Severe acute illness

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5
Q

What is the clinical criteria for diagnosing ARDS?

A
  • within 1 week of known clinical insult or worsening respiratory symptoms
  • bilateral opacities on X-ray not fully explained by effusions, lung collapse or nodules
  • respiratory failure not explained by heart failure or fluid overload
  • P:F < 300
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6
Q

What are the 3 phases of ARDS?

A
  1. Exudative phase
  2. Fibroproliferative phase
  3. Resolution phase
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7
Q

What is the exudative phase of ARDS?

A

First 72 hours, mediators (neutrophils, macrophages, platelets) cause injury to pulmonary capillaries leading to micro thromboemboli, increased pulmonary artery pressures and interstitial edema.

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8
Q

What is the fibroproliferative phase of ARDS?

A

Disordered healing in the lungs characterized by fibrosis of the AC membrane resulting in pulmonary hypertension and hypoxemia

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9
Q

What is the resolution phase of ARDS?

A

Structural and vascular remodeling reestablish AC membrane and intraalveolar fluid is transported out of the alveoli back into the interstitium

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10
Q

What kind of V/Q mismatch is characteristic of ARDS?

A

Shunt

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11
Q

What is shunt?

A

Adequate alveolar perfusion with with inadequate ventilation

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12
Q

What causes hypoxemia in ARDS?

A
  • shunt

- impaired diffusion

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13
Q

What is a normal P:F ratio?

A

> 300

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14
Q

How do you calculate P:F?

A

PaO2 / FiO2

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15
Q

What is the P:F in mild, moderate and severe ARDS?

A 
Mild = 200-300 
Moderate = 100-200
Severe = <100
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16
Q

What are typical ABGs in ARDS?

A

Initial = respiratory alkalosis
As fatigue sets in = respiratory acidosis
Progressing = metabolic acidosis (mixed acidosis)

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17
Q

What are the PA catheter changes in ARDS?

A 
Increased PADP (8-15 normal)
Normal PCWP (8-12)
PADP > PCWP by >4 (I.e. pulmonary HTN)
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18
Q

What are typical ARDS ventilation strategies?

A
  • low tidal volumes (6 ml/kg, max PPlat of 30)
  • permissive hypercapnia (PaCO2 < 80, pH > 7.2)
  • use of pressure modes to limit barotrauma
  • PEEP to maintain PO2 > 90%
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19
Q

What are fluid administration strategies in ARDS?

A
  • PCWP 5-8
  • fluid restriction
  • diuretics
  • use vasoactive inotropes to support CO instead
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20
Q

What is static compliance?

A

Compliance that is only influenced by compliance of the lung (represented by PPlat in a no-flow state)

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21
Q

What is dynamic compliance?

A

Compliance that is influenced by flow rate, airway diameter and lung compliance (PIP measures dynamic compliance)

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22
Q

What is one of the consequences of increasing a patient’s respiratory rate to compensate for low tidal volumes?

A
  • higher PPlats (less time to reach PIP = increased flow)

- potential for breath stacking with shortened expiratory time

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23
Q

What are the benefits of using pressure mode ventilation over volume in ARDS?

A
  • allow you to control PPlats to prevent barotrauma

- provides laminar flow which helps to open up collapsed airways

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24
Q

What are the benefits of PEEP in ARDS?

A
  • minimizes alveolar collapse
  • reduces WOB (especially at the beginning of inspiration)
  • thins AC membrane
  • lengthens time period during which gas exchange can occur
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25
Q

`What is a biphasic fluid management strategy?

A

Initial phase with hemodynamic instability from systemic inflammation, give fluids.

Once initial stage has passed, restrict fluids

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26
Q

What are indications for fluid restriction in ARDS?

A
  • worsening hypoxemia
  • rising PPlats & PIPs
  • evidence of increasing pulmonary edema
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27
Q

What are indications for fluid replacement in ARDS?

A
  • influence of inflammatory mediators present

- increases in PEEP (I.e. reduction in preload)

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28
Q

What are the 2 positioning strategies in the management of ARDS?

A

Kinetic beds (preferred in hemodynamically unstable patients)

Prone positioning (increases perfusion to lung areas that are less likely to be fluid-filled)

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29
Q

What are the common pharmacotherapies used in ARDS?

A
  • antibiotic therapy
  • sedation
  • pulmonary focused drugs
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30
Q

What are the goals of sedation in ARDS?

A
  • optimize ventilation
  • lower oxygen demand (pain, respiratory muscles)
  • RASS goal of -3 to -5
  • short-acting sedatives preferred with daily sedation interruptions
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31
Q

What are the pulmonary-focused drugs used in ARDS?

A
  • broncodilators
  • mucolytics
  • surfactant replacement therapy drugs
  • +/- corticosteroids
  • pulmonary vasodilating drugs (nitric oxide, prostacyclin)
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32
Q

What are the benefits to nitric oxide in ARDS?

A
  • acts on endothelium promoting vasodilation
  • reduces pulmonary vascular resistance
  • improves blood flow to ventilated areas of the lungs (because it is inhaled)
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33
Q

What are the negatives to giving nitric oxide in ARDS?

A
  • Can cause methemogolbinemia and reduce oxygen carrying capacity
  • can also cause renal dysfunction
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34
Q

What are the extra cellular ions?

A

Na
HCO3
Cl
Ca

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35
Q

What are the intracellular ions?

A

K
Mg
HPO4

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36
Q

What is the distribution of ICF to ECF?

A

1/3 ECF

2/3 ICF

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37
Q

What are the forces of water and electrolyte movement?

A 
Osmosis
Hydrostatic Pressure
Oncotic Pressure
Diffusion
Filtration
Active transport
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38
Q

What is osmosis?

A

The movement of water to dilute (equalizes concentrations across membranes)

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39
Q

What is hydrostatic pressure?

A

Force of water/liquid against a membrane (pushes fluid out into interstitium)

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40
Q

What is oncotic pressure?

A

Water drawn to large solutes (pulls fluid in to vascular space)

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41
Q

What is diffusion?

A

Passive movement down concentration gradients

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42
Q

What is filtration and what are the factors that influence it?

A

Renal (glomerular) filtration

Increased blood volume = increased GFR
Increased cardiac output = increased GFR

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43
Q

What is active transport?

A

The movement of ions up the concentration gradient through the use of ATP

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44
Q

What type of fluid is D5W considered?

A

Hypotonic

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45
Q

What is tonicity?

A

Relative osmotic activity between 2 solutions (hypotonic vs hypertonic)

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46
Q

What are the organs/systems that regulate fluids and electrolytes?

A 
Kidneys
Cardiovascular
Lungs
Pituitary
Adrenal gland
Parathyroid
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47
Q

How do the kidneys regulate fluid and electrolytes?

A

Filter plasma (GFR)
RAAS
K+ balance

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48
Q

How does the cardiovascular system regulate F and E?

A

Cardiac output (I.e. through GFR)
Baroreceptors (aortic arch)
BNP/ANP (excretes sodium)

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49
Q

How do the lungs regulate F and E?

A

Loss of fluid through evaporation (I.e. increased RR)

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50
Q

How does the pituitary regulate F and E?

A

ADH osmoreceptors = increased water retention (responds to concentration)

Thirst

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51
Q

How does the adrenal gland regulate F and E?

A

Aldosterone (increased Na, increased H2O, decreased K), responds to concentration AND volume

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52
Q

How does the parathyroid hormone regulate F and E?

A

Calcium balance

53
Q

What are the lab values characteristic of over hydration?

Na, Osm, BUN, HCT

A

Na normal
Osm normal
HCT low (diluted)
BUN normal-low

54
Q

What are the lab values characteristic of dehydration?

A

Na normal
Osm normal
BUN elevated
HCT low if hemorrhage, high if other cause

55
Q

What are causes of over hydration?

A
  • excessive fluid administration
  • heart failure
  • renal failure
  • liver disease
56
Q

What are causes of dehydration?

A 
Hemorrhage
Vomiting
Diarrhea
GI suctioning
Diaphoresis
Decreased oral intake
57
Q

What are hypertonic problems?

A

Hypernatremia: water deficit (common)
Hypernatremia: overhydration (rare)

58
Q

What are hypotonic problems?

A

Hyponatremia: water excess (common)
Hyponatremia: dehydration (rare)

59
Q

What are the causes of hypernatremia: water deficit?

A 
Water deprivation (inability to communicate, immobility) 
Loss of hypotonic solutes (urine, diarrhea, gastric secretions, furosemide, DI)
60
Q

What are the neurohormonal compensatory mechanisms of hypernatremia : water deficit?

A

Increased ADH
Decreased BNP
Increased RAAS
Decreased water and Na excretion

61
Q

What are the common lab values associated with hypernatremia: water deficit?

A

Na high
Osm high
BUN high
HCT high

62
Q

What are the treatments for hypernatremia : water deficit?

A 
Treat underlying problem (I.e. diarrhea)
Hypotonic fluids (water PO, D5W, 1/2 or 1/4 saline)
63
Q

What are some causes of hypernatremia : overhydration?

A

Hypertonic IV solutions, feeding tube solutions
Hyperaldosteronism
Cushing’s syndrome

64
Q

What are the neurohumoral compensatory mechanisms of hypernatremia : overhydration?

A

Decreased ADH
Increased BNP
Decreased RAAS
Increased Na and water excretion

65
Q

What are the common lab values associated with hypernatremia : overhydration?

A

Na increased
Osm increased
BUN decreased
Hct decreased

66
Q

What are some treatments for hypernatremia : overhydration?

A

Treat underlying problem
Diuretics
Possibly hypotonic fluids

67
Q

What are some common causes of hyponatremia : water excess?

A

Polydipsia
Water intoxication
D5W IV in elderly
Flushing tubes/drains with water instead of NS
SIADH
Renal failure, heart failure, liver failure

68
Q

What are common lab values in hyponatremia : water excess?

A

Na decreased
Osm decreased
BUN decreased
Hct decreased

69
Q

What are some treatments for hyponatremia : water excess?

A 
Treat underlying cause
Restrict free water PO
Avoid hypotonic IVs
Maybe diuretics
Maybe hypertonic saline
70
Q

What are some causes of hyponatremia : dehydration?

A 
Inadequate sodium intake
Adrenal insufficiency
Sodium loss (excessive diuretics, vomiting, diarrhea, burns)
71
Q

What are common lab values seen in hyponatremia : dehydration ?

A

Na decreased
Osm decreased
BUN increased
Hct increased

72
Q

What are some treatments for hyponatremia : dehydration?

A

Treat underlying cause
Restrict free water PO
Avoid hypotonic IVs
Maybe hypertonic saline

73
Q

What are the functions of sodium?

A

Regulates water
Affects osmolality
Electrical gradient for cellular function

74
Q

What increases sodium absorption?

A

ADH (indirectly)

RAAS (aldosterone specifically)

75
Q

What causes sodium to be excreted?

A

BNP

ANP

76
Q

What are causes of hypernatremia?

A 
Water deprivation
DI
HT solutions
Hyperaldosterone
Cushings
Diarrhea
Diuretics
77
Q

What are symptoms of hypernatremia?

A 
Confusion
Seizures
Coma
Thirst
Fever
Hypereflexia
78
Q

What are causes of hyponatremia?

A 
Polydipsia
SIADH
Renal failure
Excessive diuretics
GI losses
Burns
79
Q

What are symptoms of hyponatremia?

A

Confusion
Seizures
Coma
Signs of vascular congestion

80
Q

What are the functions of chloride?

A

Fluid, electrolyte, H+ balance

CO2 transport

81
Q

What influences chloride absorption?

A

Follows Na

82
Q

What causes chloride excretion?

A

Follows Na

Presence of bicarbonate

83
Q

What are causes of hyperchloremia?

A

Hypernatremia
Low bicarbonate
Acidosis

84
Q

What are symptoms of hyperchloremia?

A

Acidosis
Tachypnea
Decreased CO
Decreased LOC

85
Q

What are causes of hypochloremia?

A

Decreased Na
Increased bicarbonate
Vomiting (HCl)
Diuretics use

86
Q

What are symptoms of hypochloremia?

A 
Thirst
Dyspnea
Cramps, twitching
Dysrhythmias
Alkalosis
87
Q

What are the functions of potassium?

A

Maintains resting membrane potential
Balances H+
ICF osmolality

88
Q

What causes potassium to be absorbed?

A

Aldosterone

89
Q

What causes potassium to be excreted?

A

Na/K pump (specifically causes a shift from ECF to ICF)

90
Q

What are causes of hyperkalemia?

A

Acidosis (H+ into cell for K+)
Renal failure
Trauma

91
Q

What are symptoms of hyperkalemia?

A

Muscle weakness
Tingling
GI cramps
Decreased HR

92
Q

What are causes of hypokalemia?

A 
Renal losses
Intracellular shifts
Glucose/insulin
GI losses
Diuretics
93
Q

What are symptoms of hypokalemia?

A

Muscle weakness (including respiratory muscles)
Decreased GI motility (nausea, vomiting)
Ventricular irritability

94
Q

What are the functions of calcium?

A

Cardiac impulse transmission

Clotting

95
Q

What are the absorbing factors of calcium?

A

Parathyroid hormone

96
Q

What are the excreting factors of calcium?

A

Calcitonin

Phosphate

97
Q

What are causes of hypercalcemia?

A

Increased PTH
CA with bone mets
Renal dysfunction
Acidosis (increased [H] kicks Ca off albumin increasing serum levels of Ca)

98
Q

What are symptoms of hypercalcemia?

A

Weakness
Lethargy
Shortened QT

99
Q

What are causes of hypocalcemia?

A 
Blood transfusion (binds with citrate)
Alkalosis (increased Ca binding with albumin)
Vitamin D deficiency
Thyroid injury
Loop diuretics
100
Q

What are symptoms of hypocalcemia?

A

Tentany (signs)
Prolonged QT
Decreased cardiac contractility

101
Q

What are the functions of phosphate?

A

Required to produce ATP

Forms 2,3 DPG (right O2D curve shift)

102
Q

What are absorbing factors of phosphate?

A

GI

Calcium

103
Q

What are excreting factors of phosphate?

A

Insulin (=shift to ICF)
Increased Ca
Kidney perfusion

104
Q

What causes hyperphosphatemia?

A

Massive cellular lysis
Renal dysfunction
PTH dysfunction

105
Q

What are the symptoms of hyperphosphatemia?

A

Same as hypocalcemia

106
Q

What are causes of hypophosphatemia?

A 
Inadequate intake
GI losses
Alkalosis (resp)
Diuretics
Sepsis
Burns
107
Q

What are symptoms of hypophosphatemia?

A

Weakness
Fatigue
Difficult vent weaning (L O2D curve shift due to decrease in 23DPG)

108
Q

What are the functions of magnesium?

A

DNA formation
ATP reactions
Helps move Ca into muscle

109
Q

What causes Mg to be absorbed?

A

Low Ca

Increased albumin

110
Q

What causes Mg to be excreted?

A

High Ca

Low albumin

111
Q

What are causes of hypermagnesemia?

A

Renal failure

High intake

112
Q

What are symptoms of hypermagnesemia?

A 
Hyperkalemia
N/V
Weakness
Hypotension (vasodilation, flushing)
Bradycardia
Hypoactive reflexes
113
Q

What are the causes of hypomanesemia?

A

Renal losses (loop diuretics)
GI losses
Poor diet

114
Q

What are the symptoms of hypomagnesemia?

A 
Neurological depression
Confusion
Tetany
Ataxia
Anorexia
115
Q

What are the management strategies for electrolyte imbalances?

A

Correct underlying causes
Consider influencing factors
Alleviate the imbalance

116
Q

What are the factors that influence electrolyte balance?

A

H+ exchanged for K+
Glucose/insulin take K and phosphate inside the cell with them
H+ and Ca compete for binding sites on albumin (bound Ca is inactive)
The negative charge of Cl and bicarbonate are used to balance ion excretion in the renal tubules (I.e. excessive bicarbonate excretion is balanced by excessive Cl reabsorbtion)

117
Q

What are the effects of acidosis?

A 
Decreased myocardial contractility
Arterial vasodilation
Pulmonary vasoconstriction (increased dead space)
Decrease response to vasoactive drugs (pH<7.2)
Increased likelihood of dysrhythmias
Decreased LOC
R O2D shifts
Increased inflammatory response
Decreased ATP production
Decreased response to insulin
118
Q

What are the key functions of the liver?

A

Metabolism (carbohydrates, proteins, lipids)
Storage (fats, vitamins, iron, copper, blood)
Filtration (bacteria, antigens, worn RBCs)
Detoxification (inactivated hormones, drugs, alcohols, toxins)

119
Q

What are the tests for liver function?

A

AST (like CK to cardiac)
ALT (like troponin to cardiac)
Albumin (more for chronic injury)
PT (early marker for dysfunction)

120
Q

What is TPN?

A

Total parenteral nutrition - feeding a person intravenously

121
Q

What are the complications of TPN?

A

Glucose intolerance

Electrolyte imbalances

122
Q

What is refeeding syndrome?

A

Feeding after starvation can lead to increased insulin production creating an anabolic environment which leads to cellular shifts of phosphorus, potassium and magnesium into cellular space (with ATP)

123
Q

What is the target bG with feeding?

A

7-9 (both EN and TPN)

124
Q

What is normal RA/CVP?

A

2-6

125
Q

What are normal PAS/PAD?

A

20-30/8-15

126
Q

What is normal PCWP?

A

8-12

127
Q

What is normal CO?

A

4-8

128
Q

What is normal SVR?

A

800-1400

129
Q

What is normal SvO2?

A

60-80

BCIT Module 4 (1 decks)

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