Resp Flashcards

1
Q

V/Q at apex of lung vs. base of lung; V/Q of 0 vs. V/Q of infinity

A

V/Q is high at apex of lung (well ventilated, poorly perfused)

V/Q is low at base of lung (poorly ventilated, well perfused)

Thus V/Q of 0 indicates airway obstruction; V/Q of infinity indicates bloodflow obstruction

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2
Q

Causes of hypoxemia with normal Aa gradient

A

Aa = 5-15

  • High altitude
  • Hypoventilation (e.g. opioid use, obesity hypoventilation syndrome, neuromusc disorders)
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3
Q

Causes of hypoxemia with high Aa gradient (> 15)

A
  • V/Q mismatch (airway obstruction causing shunting, or blood flow obstrxn increasing dead space)
  • Diffusion limitation (e.g. alveolar wall thickening, fibrosis)
  • R to L shunt (cyanotic congenital heart defect)
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4
Q

Anion gap equation

A

Na - Cl - HCO3

normal = 10-14

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5
Q

Stages of salicylate toxicity and acid/base imbalance

A

1: < 15 min (resp alkalosis) - ingestion of aspirin stimulates resp drive, causing you to blow off CO2
2: 3-5 hrs (resp alkalosis and metabolic acidosis) - acid (aspirin) dissociates, so now you also have a met acidosis. pH will start to normalize
3: mixed acidosis - GABA increases, slowing everything down. Decreased resp rate –> CO2 retention –> resp acidosis and metabolic acidosis from the aspirin

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6
Q

Causes of metabolic gap acidosis

A
MUDPILES:
Methanol (formic acid)
Uremia
DKA/starvation
Propylene glycol
INH/Iron tablets
Lactic acidosis
Ethylene glycol (oxalic acid)
Salicylates (late - when aspirin dissociates into an acid)
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7
Q

Causes of metabolic non-gap acidosis

A
HARDASS
Hyperalimentation
Addison disease
RTA
Diarrhea, Acetazolamide (decrease bicarb)
Spironolactone
Saline infusion
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8
Q

Causes of respiratory alkalosis

A
"I start to hyperventilate if i HAS To Pee":
High altitude
Anxiety/panic attack
Salicylates (first 15 min)
Tumor
Pulmonary embolism
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9
Q

Causes of metabolic alkalosis

A

Loop diuretics
Vomiting (decreased K+)
Antacid use (decreased H+)
Hyperaldosteronism (decreased H+ and K+)

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10
Q

Causes of respiratory acidosis

A

Airway obstrxn
Acute or chronic lung disease (if chronic: metabolic compensation -> high bicarb)
Opioids, sedatives (normal bicarb bc acute)
Weakening of resp muscles

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11
Q

O2-induced hypercapnia in COPD

A

COPD pts have poor ventilation, so pulm vasculature constricts and shunts blood to more well-ventilated regions. Giving supplemental O2 gives ventilated regions more O2 and reverses pulmonary vasocontrxn. This will increase dead space and decrease total alveolar ventilation

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12
Q

Type I and II pneumocytes, collapsing P equation

A
  • Type I: 97% of alveolar surfaces; line alveoli. squamous, small, thin for gas xchng
  • Type II: secrete surfactant from lamellar bodies; decrease surface tension, prevent alv collapse, reduce lung recoil, increase compliance. cuboidal, clustered. Proliferate during lung dmg/give rise to type I and other type II cells (stem cells)
  • collapsing P = 2(surface tension)/radius
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