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

25
What is the alveolar gas equation
* 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
What is the A-a gradient and what is a normal value?
* 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
Describe the difference between hypoxemia, hypoxia, and ischemia
* Hypoxemia = inadequate oxygen in the blood (decreased paO2) * Hypoxia = inadequate O2 delivery to organs and tissue * Ischemia = inadequate perfusion
28
What are causes of hypoxemia that result in a normal A-a gradient
* Normal A-a gradient (low pAO2 and low paO2) * High altitude * Hypoventilation
29
What are causes of hypoxemia that result in an elevated A-a gradient?
* 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
What are causes of hypoxia
* 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
What are causes of ischemia
* Obstruction of arterial flow * Reduced venous drainage
32
In anemia, what will you see in paO2, saO2, and oxygen content?
* 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
In CO poisoning, what will you see in paO2, saO2, and oxygen content?
SaO2 = decreased (CO competes with O2) PaO2 = normal Total oxygen content = decreased
34
In polycythemia, what will you see in paO2, saO2, and oxygen content?
PaO2 = normal SaO2 = normal Total O2 content = increased
35
What is Virchow's triad
Increased risk for clotting: Stasis, hypercoagulable state, endothelial damage
36
What are the EKG changes seen in pulmonary embolism
* EKG changes: * SIQ3T3 = wide S in lead I, large Q and inverted T in lead III
37
What are the lab values seen in a PE (pO2, pCO2, and pH)
* Low pO2 -- due to PE * Low pCO2 -- due to compensatory hyperventilation (respiratory alkalosis) * High pH -- due to low pCO2
38
Causes of fat emboli
long bone fractures and liposuction
39
Complications associated with amniotic fluid emboli
DIC
40
Causes of air emboli
Caisson disease (nitrogen bubble precipitating during ascent) IV
41
What is the different between a primary spontaneous and secondary spontaneous pneumothorax
* 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
What is a tension pneumothorax
* 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