CRNA Clinical Interview Prep Flashcards

1
Q

SaO2 vs PaO2?

A

SaO2 = oxygen saturation (% of hgb binding sites that are occupied by oxygen)

PaO2= partial pressure of O2 (pressure exerted by oxygen dissolved in arterial blood)

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2
Q

What is MvO2?

A

Myocardial oxygen consumption

quantifies the amount of O2 used by the myocardium and tells us the metabolic demands of the heart - important in HF, CAD

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3
Q

What factors influence the metabolic demand of the heart (MvO2)?

A

heart rate, contractility, and tension in the ventricular walls

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4
Q

Hypoxia vs Hypoxemia?

A

Hypoxemia = low levels of O2 in the blood (measured by PaO2)

Hypoxia = inadequate supply of O2 to the body’s tissues (shock/severe arterial blockages)

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5
Q

What are the 3 stages of ARDS?

A
  1. Exudative
  2. Proliferative
  3. Fibrotic
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6
Q

What occurs during the exudative stage of ARDS?

A

-within the first week of ARDS

-damage to alveolar epithelium and capillary endothelium causes increased capillary permeability

-fluid, proteins, inflammatory cells, and RBCs leak into alveolar and interstitial spaces –> formation of hyaline membrane made of fibrin and cellular debris

-damage to type I alveolar cells (facilitate gas exchange) type II alveolar cells (surfactant production)

-dec surfactant = inc surface tesnsion = alveolar collapse

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7
Q

What occurs during the proliferative stage of ARDS?

A

1-3 weeks after initial lung injury, surviving type II alveolar cells proliferate to repair and replace damaged lung tissue

-increased fibroblast activity causing interstitial fibrosis –> good for wound healing, bad for lung compliance

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8
Q

What occurs during the fibrotic stage of ARDS?

A

3 wks to months after onset, there is extensive fibrosis and collagen deposition in the lungs –> leads to poor compliance and permanent reductions in lung function

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9
Q

Vent settings for ARDS?

A

Low VT = 4-6 mL/kg

limit plateau pressures < 30 cmH2O (pressure at the end of inspiration) to prevent barotrauma

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10
Q

What is the initial trigger for sepsis?

A

Pathogen releases molecules called pathogen-associated molecular receptors (PAMPs), which are detected by the body’s immune cells through pattern recognition receptors (PRR)

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11
Q

Explain the immune response to a pathogen in sepsis.

A

Innate immune cells (neutrophils/macrophages) are activated by the recognition of PAMPs.

Signaling molecules such as cytokines, chemokines, and other mediators are released to help fight the infection and signal other immune cells to join.

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12
Q

List some important cytokines in the inflammatory response

A

interleukin-1 (IL-1), IL-6 & tumor necrosis factor alpha (TNF-a)

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13
Q

What causes hypotension in sepsis?

A

Cytokines released during the innate immune response cause vasodilation to increase blood flow to the area. In sepsis, the response is exaggerated and uncontrolled causing systemic vasodilation, increased vascular permeability and fluid leakage into tissues.

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14
Q

What is cytokine storm?

A

Occurs in severe cases of sepsis when massive and uncontrolled release of cytokines leads to widespread inflammation, tissue damage, and organ failure.

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15
Q

What causes ARDS in septic patients?

A

endothelial cells lining blood vessels are activated and damaged which exacerbates the leakage of fluids and proteins into the tissues

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16
Q

What receptors does norepinephrine act on?

A

Mostly alpha-1 adrenergic receptors

Some beta-1