Resp Flashcards
V/Q at apex of lung vs. base of lung; V/Q of 0 vs. V/Q of infinity
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
Causes of hypoxemia with normal Aa gradient
Aa = 5-15
- High altitude
- Hypoventilation (e.g. opioid use, obesity hypoventilation syndrome, neuromusc disorders)
Causes of hypoxemia with high Aa gradient (> 15)
- 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)
Anion gap equation
Na - Cl - HCO3
normal = 10-14
Stages of salicylate toxicity and acid/base imbalance
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
Causes of metabolic gap acidosis
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)
Causes of metabolic non-gap acidosis
HARDASS Hyperalimentation Addison disease RTA Diarrhea, Acetazolamide (decrease bicarb) Spironolactone Saline infusion
Causes of respiratory alkalosis
"I start to hyperventilate if i HAS To Pee": High altitude Anxiety/panic attack Salicylates (first 15 min) Tumor Pulmonary embolism
Causes of metabolic alkalosis
Loop diuretics
Vomiting (decreased K+)
Antacid use (decreased H+)
Hyperaldosteronism (decreased H+ and K+)
Causes of respiratory acidosis
Airway obstrxn
Acute or chronic lung disease (if chronic: metabolic compensation -> high bicarb)
Opioids, sedatives (normal bicarb bc acute)
Weakening of resp muscles
O2-induced hypercapnia in COPD
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
Type I and II pneumocytes, collapsing P equation
- 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