Acid-Base disorders Flashcards
Acidosis vs acidemia
acidemia is a blood pH<7.36
Acidosis is the clinical process that leads to a decreased blood pH (does not always succeed in creating acidemia)
Ventilation
process that brings inhaled air tot he alveoli (does not include the process of gas exchange)
*influences pCO2, not pO2
Minute ventilation
rate by which air reaches alveoli
L/min
=RRxTV
reflected by hyper or hypoventilation
General causes of met. acidosis
over production or accumulation of acid
loss of base
under excretion of acid
General causes of met. alk.
loss of acid
underexcretion of base
Chronic respiratory disorders
fully compensated (pH is close to normal) likely 2-3 days old
sub-acute or acute respiratory disorders
occur w/in 2 days of initiation of disorder
uncompensated (resulting acidemia or alkalemia)
or paritally compensated
**ability to compensate depends on chronicity
compensation for metabolic disorders
can be fully or partially compensated at time of presentation (depending on amount of acid/alkalemia and LUNG FUNCTION)
Causes of respiratory acidosis
Hypoventilation: decreased RR (decreased drive- drugs, coma stroke) decreased TV (NMJ disorders, kyphoscoliosis, airway obstruction, COPD, OSA)
High AG metabolic acidosis
Methanol uremia DKA paraldehyde infection, iron, isoniazide lactic acidosis Ethylene glycol, ETOH Salicylates, KA
uremic acidosis
when renal function is severely decreased ( decreased excretion of H+, decreased bicarb reabs )
lactic acidosis
anaerobic metabolisms (hypoxemia, circ failure, vessel bloackage, anemia=decreased muscle perfusion
meds:
metformin, HIV meds, Isoniazide
liver failure, thiamine deficiency, sepsis, seizures
DKA
increased lipolysis d/t lack of insulin
increases production of ketones
associated with hyperglycemia
more often of type I DM (presentaiton)
alcoholic ketoacidosis
idiopathic increase in ketone production in the liver after large ETOH consumption, normal blood glucose
high osmolar gap (>10)
Osmolar gap
difference bw measure serum Osm and calculated serum osm
calculated=2(Na)+(Glu/18)+(BUN/2.8)
should =ETOH leve/4.6
used to Identify other alcohols
ethylene glycol
found in antifreeze metabolites are toxic increases OG calclium oxalate crystals are often found in urine can cause ARF
Salicylate posioning
usually a result of OD
may cause metabolic acidosis and/or respiratory alkalosis
hemorrhage, fever, nausea, vomiting, tinnitus, edema
Causes of normal AG (hyperchloremic) acidosis
Diarrhea
decreased renal bicarb reabs (CAi) or RTA
increased anion intake (parenteral feeding)
large amount of NaCl consumption
Renal Tubular Acidosis type I
decreased H+ excretion in CD
alkaline urine and acidic serum
increased Ca excretion and decreased citric acid concentration leading to kidney stone formation**
increase K loss= hypokalemia
RTA type II
proximal
defects in bicarb reabs= decreases serum pH and inc urine pH
increases Ca in urine, but normal citrate= stones are rare
hypokalemia
distal tubules work, so you are still able to acidify urine later
acidic urine
RTA IV
occurs in pt with moderate CRF
lack of ald or ald resistance
decreased K+ excretion= hyperkalemia
decreased H+ excretion= acidmeia
acidic urine
Urinary anion gap
used to differentiate bw renal (RTA) and extrarenal (diarrhea) causes of acidosis
Urine (Na+K)-Cl-
negative urine anion gap
Extra renal loss
d/t high levels of unmeasured NH4+
(excretion of NH4 by normal kidneys is compensatory mechanisms)
Positive or non-existent uAG
renal loss
d/t low levels of NH4 and high levels of HCO3-
