DIT review - Pulmonary 1 Flashcards

1
Q

What are the 3 openings in the diaphragm (including the structures that pass through and at what level)

A
  • THINK: I ate ten eggs at twelve
    • I ate = “I” for IVC and “ate” for T8
    • Ten eggs = “Ten” for T10 and “eggs” for esophAGus and vAGus
    • At twelve = “At” for AAT (Aorta, Azygous, Thoracic) and twelve for T12
  • Vena caval formamen (caval opening)
    • Contains IVC
    • At level of T8
  • Esophageal hiatus
    • Contains esophagus and anterior and posterior trunks of the vagus nerve
    • At level of T10
  • Aortic hiatus
    • Contains aorta, thoracic duct, azygos vein
    • At level of T12
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2
Q

What nerves innervate the diaphragm

A
  • Diaphragm is innervated by C3, C4, and C5
    • THINK: C3, 4, 5, keeps the diaphragm alive
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3
Q

What is the surfactant ratio used to determine fetal lung maturity in utero

A

Lecithin:Sphingomyelin ratio > 2.0

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4
Q

What are the main components of surfactant

A
  • Lecithin
  • Phosphatidylcholine
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5
Q

What part of the respiratory tree marks the end of the conducting zone and beginning of the respiratory zone

A

Terminal bronchioles are end of the conducting zone

Respiratory bronchioles are beginning of the respiratory zone

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6
Q

Label the lung volume graph

A
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7
Q

What is functional residual capacity?

A

Volume of gas in lungs after a normal expiration

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8
Q

What is the difference between vital capacity and tidal volume

A

Tidal volume = amount of air in a normal, non-labored breath

Vital capacity = max amount of air that can be expired after a maximum inspiration

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9
Q

What are the components of physiologic dead space

A
  • Physiologic dead space (Vd) = Anatomic dead space + functional dead space
    • Anatomic dead space = air in the conduction airways
    • Functional dead space = space that is capable of gas exchange, but no gas exchange is occurring
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10
Q

What is the equation for physiologic dead space

A
  • Vd = Vt x [(PaCO2 – PeCO2) / PaCO2]
    • Vd = physiologic dead space
    • Vt = tidal volume
    • PaCO2 = arterial pCO2
    • PeCO2 = expired air pCO2
  • If there is zero dead space, then PaCO2 = PeCO2, and thus Vd = 0
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11
Q

Describe the difference between perfusion-limited and diffusion-limited pulmonary circulation

A
  • The amount of O2 being received by pulmonary circulation is depending on both perfusion (blood going to lungs) and diffusion (O2 crossing the alveolar barrier)
    • In healthy individuals, the amount of O2 is perfusion-limited
      • Gas equilibrates along the length of the capillary, and increased O2 can only occur via increased blood flow
    • In emphysema and fibrosis, the amount of O2 is diffusion-limited
      • Gas does not equilibrate by the time blood reaches the end of the capillary
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12
Q

What values define pulmonary HTN

A
  • Pulmonary arterial pressure > 25 at rest (normal = 10 mm Hg)
  • Pulmonary arterial pressure > 35 during exercise
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13
Q

Cause of primary pulmonary HTN

A
  • AKA idiopathic pulmonary HTN
  • Associated with abnormalities in BMPR2 (which normally prevents proliferation of vascular smooth muscle)
  • Associated with HIV and Kaposi sarcoma
  • Seen in young adult females
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14
Q

Cause of secondary pulmonary HTN

A
  • Causes:
    • Chronic lung disease
      • Recall that hypoxemia in pulmonary circulation causes vasoconstriction, and thus an increase in pulmonary arterial pressure
    • Mitral stenosis
      • Increased volume in pulmonary circuit
    • Recurrent thromboemboli
    • Autoimmune disease
    • Left-to-right shunts
    • Sleep apnea or high altitude
      • Hypoxic vasoconstriction
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15
Q

Basic premise behind methemoglobin

A
  • Methemoglobin = hemoglobin with oxidized form of Hb (Fe3+) that does not bind to O2 readily but has increased affinity for cyanide
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16
Q

Presentation of methemoglobin

A
  • Cyanosis
  • Chocolate-colored blood
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17
Q

Potential usefulness of methemoglobin

A
  • You can induce methemoglobinemia with nitrites (will oxidize Fe2+ to Fe3+) in order to treat cyanide poisoning
18
Q

Treatment of methemoglobin

A
  • Methylene blue
  • Vitamin C
19
Q

Differentiate between the R and T form of hemoglobin

A
  • Hemoglobin molecule (2a and 2b subunits) exist in 2 forms
    • Taut (T) form
      • Low O2 affinity
      • THINK: Taut in Tissues
    • Relaxed (R) form
      • High O2 affinity
      • THINK: Relaxed in respiratory area
20
Q

What is the basic premise behind carboxyhemoglobin

A
  • Hb bound to CO instead of O2
    • Hb has a 200x increase affinity for CO vs. O2, so will preferentially bind CO
21
Q

Describe the Hb-O2 dissociation curve in Carboxyhemoglobin

A
  • It decreases O2 bound to Hb but also causes a L shift in the curve
    • Hb bound to O2 is decreased because it is bound to CO instead = the height of curve is lower
      • Decreased O2 content in the blood
    • The heme groups NOT bound to CO have increased affinity for O2 = L shift of curve
      • This makes it more difficult for O2 to be unloaded in tissues
22
Q

Presentation of carboxyhemoglobin

A
  • Headaches, dizziness, and cherry red skin
23
Q

Causes of carboxyhemoglobin

A
  • Fires, car exhaust, gas heaters
24
Q

Treatment of carboxyhemoglobin

A

100% O2

25
Q

What is the alveolar gas equation

A
  • Amount of O2 in the alveoli = amount of O2 in inspired air – amount of O2 consumed
    • pAO2 = pIO2 – (paCO2 / R)
      • pAO2 = alveolar pO2
      • pIO2 = pO2 in inspired air
      • paCO2 = arterial pCO2
    • pAO2 = 150 – (paCO2 / 0.8)
26
Q

What is the A-a gradient and what is a normal value?

A
  • A-a gradient = pAO2 – paO2
    • Normal = 10-15 mm Hg
  • Increased A-a gradient means that there is a problem with O2 equilibrating between alveoli and arteries:
    • Shunting or V/Q mismatch
    • Fibrosis (thickened diffusion barrier)
    • Increased FiO2 (increases pAO2 by flooding alveoli with O2, but there is still a limit as to how much O2 can go into the arteries)
    • Age
27
Q

Describe the difference between hypoxemia, hypoxia, and ischemia

A
  • Hypoxemia = inadequate oxygen in the blood (decreased paO2)
  • Hypoxia = inadequate O2 delivery to organs and tissue
  • Ischemia = inadequate perfusion
28
Q

What are causes of hypoxemia that result in a normal A-a gradient

A
  • Normal A-a gradient (low pAO2 and low paO2)
    • High altitude
    • Hypoventilation
29
Q

What are causes of hypoxemia that result in an elevated A-a gradient?

A
  • High A-a gradient (normal pAO2 and low paO2)
    • Pulmonary fibrosis
    • R-to-L cardiac shunt (blood bypasses pulmonary vasculature and does not get oxygenated)
    • V/Q mismatch
30
Q

What are causes of hypoxia

A
  • Hypoxemia
  • Anemia (decreased O2 carrying)
  • Carbon monoxide poisoning (less O2 bound to Hb)
  • Low cardiac output (blood is oxygenated, but just not getting to tissues)
31
Q

What are causes of ischemia

A
  • Obstruction of arterial flow
  • Reduced venous drainage
32
Q

In anemia, what will you see in paO2, saO2, and oxygen content?

A
  • Recall:
    • PaO2 = saturation of hemoglobin
    • SaO2 = O2 dissolved in blood
  • Oxygen content will be decreased because hemoglobin is decreased
  • SaO2 measures the saturation of the hemoglobin that you do have, so it won’t change since the remaining hemoglobin will be normally saturated
  • PaO2 measures O2 dissolved in blood, which has nothing to do with Hb, so will also be normal
33
Q

In CO poisoning, what will you see in paO2, saO2, and oxygen content?

A

SaO2 = decreased (CO competes with O2)

PaO2 = normal

Total oxygen content = decreased

34
Q

In polycythemia, what will you see in paO2, saO2, and oxygen content?

A

PaO2 = normal

SaO2 = normal

Total O2 content = increased

35
Q

What is Virchow’s triad

A

Increased risk for clotting:

Stasis, hypercoagulable state, endothelial damage

36
Q

What are the EKG changes seen in pulmonary embolism

A
  • EKG changes:
    • SIQ3T3 = wide S in lead I, large Q and inverted T in lead III
37
Q

What are the lab values seen in a PE (pO2, pCO2, and pH)

A
  • Low pO2 – due to PE
  • Low pCO2 – due to compensatory hyperventilation (respiratory alkalosis)
  • High pH – due to low pCO2
38
Q

Causes of fat emboli

A

long bone fractures and liposuction

39
Q

Complications associated with amniotic fluid emboli

A

DIC

40
Q

Causes of air emboli

A

Caisson disease (nitrogen bubble precipitating during ascent)

IV

41
Q

What is the different between a primary spontaneous and secondary spontaneous pneumothorax

A
  • Primary spontaneous pneumothorax
    • Occurs in tall, thin, young males
    • Due to rupture of apical blebs
  • Secondary spontaneous pneumothorax
    • Due to disease lung (e.g. bullae in emphysema, infection) or mechanical ventilation with use of high pressure
42
Q

What is a tension pneumothorax

A
  • Can be any of the above: primary spontaneous, secondary spontaneous, or traumatic pneumothorax
  • Air enters the pleural space but cannot exit, and air continues to build up with each breath
  • Trachea deviates away from the affected lung
  • Needs immediate needle decompression