Renal: Acid Base Flashcards
what three processes must occur everyday in order to maintain acid base balance
- buffering by ICF and ECF buffers
- Alveolar ventilation to control PACO2
- control of serum HCO3 via renal H+ excretion
acid ph=
basic ph=
<7.3 acid
>7.45 alkalosis
PCO2 is high or low with metabolic acidosis and alkalosis
acidosis = LOW PCO2 alkalosis= HIGH PCO2
what is the compensation for acidosis
a reduced CO2 partial pressure (PCO2) that should be predictable
acidosis levels:
- bicarb
- pco2
low biacrb
low PCo2
alklaosis
-PCO2
-Biacarb
levels
bicarb and PCO2 will be high
where is most of the bicarb reabsorbed
proximal tubules MAINLY
little in the distal
why is CO2 increased in metabolic alkalosis
because it is the comepnsatory mechanism done by the lungs
high bicarb=alkalosis state—so to compensate the lungs RETAIN CO2 to bring the pH back down
HIGH BICARB + HIGH CO2= met alkalosis with compensation
same for met acidosis
—>low bicarb—>kidneys want to excrete more CO2 to bring the pH Up
LOW BICARB + LOW CO2= MET ACIDOSIS with compensation
describe amonias role in the kidney buffer system
ammonia NH3 picks up intracellular H+–> now becomes ammonium NH4+ (‘yum’ eats the H+)–>gets secreted into PCT–>excreted into CD
**for each H+ secreted there is a HCO3- gained in systemic circulation
what is the osmolar gap
compares measured and calculated osmolality
Plasma osm (measured) - Plasma osm (calculated)
METABOLIC ACIDOSIS
- values for bicarb and co2 and ph
- three main causes
- types
PH <7.35
- LOW CO2 (bc respiratory compensation=hyperventilation to get rid of CO2 to raise ph)
- LOW BICARB <22
CAUSES
- increased acid production
- decrease acid excretion
- Loss of HCO3 (diarrhea)
**can be HIGH ANION GAP ACIDOSIS or NORMAL ANION GAP ACIDOSIS
Normal anion gap
- define anion gap
- equation
reflects unmeasured anions present in serum
AG= measured cations-measured anions (ECF)
AG= NA- (Cl+HCO3-)
10-12
ways to lose bicarb aka what type of met acidosis?
NON ANION GAP ACIDOSIS
H-->hyperalimentation A-->acetazolamide R-->renal tubular acidosis D-->diarrhea U->ureero-pelvic shunt P-->post-hypocapnia S-->spironolactone
ways to gain acid
-aka causes of type of met acidosis?
HIGH ANION GAP ACIDOSIS
M--> methanol U-->uremia D-->DKA P--> propyelen glycol I-->Isoniazid, infection L-->lactic acidosis E-->ethyelen gycol S--> salicylates
high anion gap acidosis
- *means there is an increase in some other acid (other than Cl-) in the serum
- the H+ is buffered by the HCO3 but the other newly added acid is not buffered
- *increasing the gap
*use winters formula is used to measure the respiratory compensation for met acidosis
{(1.5 X HCO3-) + 8}
MUDPILES= causes
normal anion gap met acidosis
- lab finding
- causes
low ph
low bicarb
low co2
normal AG
*lost bicarb is replaced by CL- so there is no change in AG but there is an accumulation of CL-
OR
*in cases of dirrhea or RTA–> loss of sodium bicarb and kidney tries to preserve volume by retaining NACL
HARDUPS=causes
CM for metabolic acidosis
Cardiovascular
- imparied contractility
- decrease CO
- vasodilation
- Vasocontriction
- arrhythmias
Respiratory
- hyperventilation
- resp muscle fatigue
Metabolic
- hypercalcemia
- hyperK
causes for high osmolar gap >20 mOsm/L
TOXIC ALCOHOL INGESTIONS
- methanol
- ethanol
- isopropanol
- ethylene gylcol
- propylene glycol
- diethyelen glycol
causes for elevated osmolar gap but not >20
alcoholik ketoacidosis
lactic acidosis
renal failure
equation for CALCULATED osmolality
2 (NA+) + (Glucose/18) + (BUN/2.8)
explain why normal AG acidosis can occur
if the acid that accumulates is HCL–>no change in the AG!
also called Hyperchloremic MA
two main causes for normal AG met. acidosis
- Loss of HCO3-
* diarrhea
* proximal RTA (2)
* ketoacidosis - Decreased acid secretion
* kidneys will filter and reabsorb HCO3- at prox tubules
* decr GFR
* distal (type 1) and Type IV RTA
urinary anion gap
-what is it
distinguishes extra renal from renal causes of normal AG MA
what does a large -UAG mean
-cause
metabolic acidosis of extra renal cause
- diarrhea
- assoc with incr excetion of NH4
what does a large + UAG mean
-cause?
metabolic acidosis of renal origin
- NH4 excretion is minimal/impaired
- distal renal tubular acidosis
levels for met alkalosis
-what is this often accompanied by?
HIGH: bicarb, ph and PaCO2
**hypocholoremia and hypoK
**bicarb can sometimes be normal or low
list two causes of elevated HCO3 and LOW CL-
metabolic alkalosis
resp acidosis
**need AGBs and electrolyte pannel to disntinguish the diff
causes of met. alklaosis
- administration of alkali—antacids, citrate in blood transfusions
- Chronic alkali administration—MILK ALKALI SYNDROME–> too much tums
- ->nephrocalcinosis
- ->renal insuff
- ->CA Carbonate
hypoK does what to ammonium excretion
increases it
what is the compensation for met. alk
resp
- hypoxemia
- ***retain CO2
- hyPOventilation
- increase in bicarb
- paCO2 increases 6mmHg for each 10mEq/L increase in HCO3
how to calculate PaCo2
Bicarb + 15
two basic causes of met. alk
- H+ decrease
2. HCO3- increase
causes of H+ decrease aka met alk
- renal loss of H+
- aldosterone causes acid secretion (secretes K and H)
- hyperaldosteronism= incr secretion of acids–leaving behind basic environment - Shift of H+ into cells
* H and K exchanged across cell membrane
* in the state of hypoK–> K+ shifts out of the cells to balance K–>but H+ goes into cell as K+ leaves - vomiting
* loss of H+
Causes of HCO3- increase aka met alk
- increased intake
- loss of acid
* hyperaldosteronism - Volume depletion
*contraction alkalosis
*fluid with low bicarb [ ] is lost, leads to increase in bicarb [ ]
EX: over diuresis
metabolic alkalosis phases
- GENERATION
* acid loss (ie vomiting or prolonged NG tube suction)
* gain HCO3 (Primary hyperaldosteronism) - MAINTENANCE
* kidney is unable to excrete HCO3 and instead absorbs it
CM of met alkalosis
HYPOK–>arrhythmias
HYPOCA–>tremors, muscle cramps, tingling of fingers/toes
hypochloremia
incr anxiety seizures confision HYPOventilation incr irritability
