Acid Base Kania Flashcards
normal pH
7.35-7.45
what pHs are incompatible with life
<6.7
>7.7
acidemia is considered what pH
<7.35
HCO3 is what
bicarb
H2CO3 is what
carbonic acid
metabolic disorders involve changes in what
H+ and HCO3 (bicarb)
respiratory disorders involve changes in what
CO2
kidneys compensate what disorders
respiratory
lungs compensate what disorders
metabolic
Henderson hasselbach equation
pH = pKa + log (base/acid)
pKa of carbonic acid
6.1
normal PaCO2
35-45 mmHg (40)
normal HCO3 (bicarb)
22-26 mEq/L (24)
normal PaO2
95-100 mmHg
normal SaO2
95% +
acidemia adverse events cardiovascular
decreased CO
impairment of cardiac contractility
increased pulmonary vascular resistance and arrythmias
hyperventilation
SOB
acidemia adverse events metabolic
insulin resistance
anaerobic glycolysis inhibition
hyperkalemia
acidemia adverse events CNS
coma
altered mental status
alkalemia sx cardiovascular
decreased coronary blood flow
ateriolar constriction
decreased anginal threshold (risk MI)
arrythmias
decreased respirations (hypoventilation)
alkalemia sx metabolic
decreased K+, Ca and Mg
stimulation anaerobic glycolysis
alkalemia sx CNS
decreased cerebral blood flow
lethargy, delirium, stupor
seizures
how is acid generated in us (3)
diet: 1 meq consumed per day
aerobic metabolism glucose
non volatile acids: anaerobic/lactic
4 mechanisms of acid regulation
- buffering systems
- renal regulation
- ventilatory regukation
- hepatic regulation
what is a buffer
ability of a weak acid and its base to resist change in pH with addition of a strong acid or base
what are the three main buffers
bicarb/carbonic acid
phosphate
protein
onset and capacity of bicarb buffer
rapid onset
intermediate capacity
when acid is added to bicarb buffer, what happens with breathing
more exhalations, getting rid of CO2
which buffer is present extracellularly more than any other buffer
bicarb
onset and capacity of phosphate buffer
intermediate onset
intermediate capacity
which types of phosphates more useful
intracellular organic phosphates
onset and capacacity of protein buffer
albumin/hemoglobin
rapid onset
limited capaccity
VERY FAST
two main purposes of kidney in acid regulation
reabsorb filtered HCO3- (hold on to bicarb)
excrete H+ ions released from nonvolatile acids (generate bicarb)
how much bicarb filtered through kidney daily
4,000-4,500 mEq daily
how much bicarb reabsorbed by proximal tubule
85-90%
how much bicarb reabsorbed by distal tubule / collecting duct
10-15%
how much HCO3- in the urine
basically none
what happens if we limits H+ secretion in proximal tubule lumen
bicarb losses in urine
carbonic anhydrase inhibitors do what
block carbonic anhydrase
CO2 and H2O dont get back to tubular cell
losses of bicarb in the urine, metabolic acidosis
bicarb generation onset and capacithy
delayed onset
large capacithy
bicarb generation happens where
distal tubule
describe how bicarb is made from ammoniagenesis
carbonic acid splits into H+ and HCO3
H+ forms ammonium and is excreted
HCO3 gets into bloodstream and is new
how much bicarb is made from ammoniagenesis
40 mEq/day can be increased to 300 mEq/day
how much bicarb made from HPO42 titratable activity
30 mEq/day, cant be increased
how does titratable activity with phos work
HPO4 combines with H+ and HCO3 formed is in bloodstream
distal tubular hydrogen ion secretion makes up what percent of acid excretion
50%
ventilatory regulation, onset and capacity
rapid onset
large capacity
how does ventilatory regulation work
chemoreceptors detect increase in PaCO2 and increase rate and depth of ventilation
hepatic regulation: oxidation of proteins generates what
HCO3- and NH4+
if liver stops urea synthesis, what can happen
metabolic alkalosis
(urea is acidic)
metabolic acidosis primary change and compensation
change: decreased HCO3-
compensation: decreased PaCO2
metabolic alkalosis primary change and compensation
change: increased HCO3-
compensation: increased PaCO2
respiratory acidosis change and compensation
change: increased PaCO2
compensation: increased HCO3-
respiratory alkalosis change and compensation
change: decreased PaCO2
compensation: decreased HCO3-
respiratory compensation speed
rapid
renal compensation speed
3-5 days for max effect
does compensation correct pH?
no, moves it towards normal
types of metabolic acidosis
anion gap
non-anion gap
metabolic acidosis characterized by what 3 things
pH <7.35
PaCO2 decreased (35-45 normal)
decreased HCO3- (<24)
anion gap equation
anion gap = Na - (Cl + HCO3-)
normal anion gap rnage
3-11 mEq/L
patho of non-anion gap metbaolic acidosis
loss of plasma HCO3- replaced by Cl-
non anion gap metabolic acidosis GI bicarb loss causes
diarrhea
pancreatic fistula/biliary drainage (rich in HCO3)
non anion gap metabolic acidosis renal bicarb loss causes
type II renal tubular acidosis (proximal can’t reabsorb H+)
usually from toxins like metals, carbonic anhydrase, drugs)
causes reduced reabsorptive threshold for HCO3 in proximal tubule)
type II renal acidosis occurs where
proximal tubule
can’t reabsorb as much HCO3-
type I renal tubule acidosis occurs where
distal tubule
non anion gap metabolic acidosis renal H+ excretion reduction causes
type I renal tubule acidosis: inc in K+ excretion, hypokalemia
type IV renal tubule acidosis: hypoaldosterone hyperkalemia
chronic renal failure
what is type I renal tubule acidosis
in distal tubule
hypokalemia - increase in K+ excretion
H+ cant be pumped into tubule lumen
what is type IV renal tubule acidosis
in distal tubule
hyperkalemia
hypoaldosteronism (H+ retention)
what happens in chronic renal failure
less H+ secretion
less amonia production
therefore less HCO3 produced
what can acid and chloride administration from TPN or Cl admin cause?
non-anion gap metabolic acidosis
causes of anion gap metabolic acidosis
M - methanol intoxication
U - uremia
L - lactic acidosis
E - ethyleneglycol
P - aldehyde ingestion
A - aspirin / salicylates
K - ketoacidosis
I - infection
what is the delta gap equation
difference between patient’s anion gap and the normal anion gap
when do we measure delta gap
only in anion gap above normal
how do we use delta gap
add it to the pts HCO3, it should be in normal range
- if HCO3 isnt in normal range after adding then they have a metabolic alkalosis as well
what is the most common cause of anion gap acidosis
lactic acidosis
what causes lactic acidosis (9)
shock
drugs/toxins
seizures
leukemia
hepatic failure
renal failure
diabetes
malnutrition
rhabdomyolysis
drugs that cause lactic acidosis
ethanol
metformin
linezolid
propofol
topirimate
propylene glycol
NRTIs
what does salicylate toxicity present as?
respiratory alkalosis - respiratory drive stimulation
metabolic acidosis - organic acid accumulation
methanol/ ethylene ingesetgion from what substances
cleaning supplies
paint
lactic acidosis symptoms
Kussmaul respirations - breathing fast and deep
flushing, tachycardia
N/V
lethargic / coma
hyperkalemia
bone demineralization in chronic RTAs
when do we use bicarb therapy
treat underlying cause
pH < 7.1
hyperkalemia
overdose
in a code
does bicarb therapy reduce morbidity and mortatlity
no evidence
bicarb therapy how to calculate dose
(o.5 x IBW) x (12- HCO3-) mult by 1/3-1/2
IBW = 50+ 2.3 (in over 60)
how much bicarb given during cardiac arrest
1 mEq/kg
what might we need to supplement in cardiac arrest
K+
what happens with Hg if we have too much bicarb
Hg saturation increases
oxygen not released to tissues
decreased cerebral blood flow
what happens with bicarb overload
hypernatremia
CSF acidosis
hypokalemia
hypocalcemia
chronic bicarb therapy / metabolic acidosis therapy dose
average 1-3 mEq/kg
is veverimer used
no, FDA denied
metabolic alkalosis marked by what
pH >7.45
high HCO3-
high PaCO2 compensatory hypoventilation
metabolic alkalosis rise in HCO3 comes from what
loss of acid from GI tract
administration of bicarb
contraction alkalosis (loss Cl- rich fluid and HCO3 poor fluid)
metabolic alkalosis kidney impairment
renal impairment in HCO3 excretion
volume and chloride depletion
decrease in blood volume
proximal tubule capcity increases so we hang on to more bicarb
types of metabolic alkalosis
saline responsive
saline resistant
saline responsive alkalosis Cl level
Cl in urine < 10-20 mEq/L
saline responsive alkalosis causes (3)
diuretics
vomiting / NG suction
bicarb administration
how do diuretics cause alkalosis
aldosterone release increases bicarb reabsoption and generation
hypokalemia because K moves out
hypo chloremic state because bicarb absorbed instead with Na
in alkalosis and diuretics, without Cl - Na is reabsorbed with ____
bicarb
what is an example of exogenous bicarb administration
blood transfusion - citrate breaks down into bicarb
in metabolic alkalosis, what happens with Na
reabsoprtion increased in distal and proximal tubule
saline resistant alkalosis urinary chloride level
> 20 mEq/L
key difference with saline resistant alkalosis vs saline responsive
no chloride depletion
causes of saline resistant alkalosis
increased mineralocorticoid activity
hypokalemia
renal tubular chloride wasting (Bartters)
symptoms of metabolic alkalosis
muscle cramps
dizziness
hypoxia, confusion, seizures
arrythmias
treatment of metabolic alkalosis
treat underlying cause
fluid replacement
carbonic anhydrase inhibitor
HCl acid
ammonium chloride
use fluid replacment for alkalosis with caution in what pts
HF
renal / hepatic failure
who should get carbonic anhydrase inhibitors in metabolic alkalosis
sodium responsive pts who cant tolerate fluids / sodium
carbonic anhydrase drug, dose and what it should be given with
acetazolamide 250-375 mg
given with potassium
when should HCl be given
metabolic alkalosis sodium responsive
- cant tolerate sodium
- severe bicarb
- severe HF
- others not working
who should not get ammonium chloride
hepatic / renal failure
treatment for saline resistant alkalosis
decrease mineralocorticoid
supplement potassium
potassium sparing diuretic: spironolactone
respiratory acidosis classified by what
pH < 7.35
CO2 increased
HCO3 increased compensatory
causes of respiratory alkalosis
not breathing out
asthma
choking
aspiration
overdose
sleep apnea
trauma
CNS infection
PE
mechanical vent
Guillian-Barre syndrome
symptoms of respiratory acidosis
SOB
dyspnea
drowsiness
tachycardia
coma / seizure
treatment of respiratory acidosis
correct underlying cause
mechanical vent or oxygen
respiratory alkalosis characterized by what
pH >7.45
decreased PaCO2
decreased HCO3
causes of respiratory alkalosis
anxiety
trauma
salicylate intoxication
high altitude
symptoms of respiratory alkalosis
lightheadedness
decreased cerebral blood flow
N/V
treatment of respiraotry alkalosis
underlying cause
sedation
paralysis
vent
