Acid Base Disorders Flashcards
acids produced by the body (+source) (4)
- sulfuric, phosphoric and uric acids - metabolism
- ketone bodies - fat oxidation
- lactic acid - anaerobic glucose metabolism
- carbonic acid - dissolved CO2
normal pH of body
7.38-7.42
mechanisms body uses to maintain alkaline pH
- buffer system of blood
- lungs regulate carbonic acid concentration
- kidneys regulate bicarb concentration
normal ratio bicarb/carbonic acid
20 parts bicarb to 1 part carbonic acid
carbonic acid
H2CO3
CO2 + H2O conversion by carbonic anhydrase in kidney
dissociates into H+ and bicarbonate ions
renal control of pH (H+)
H+ ions enter renal tubule in exchange for sodium ions
sodium enters plasma with HCO3
maintains concentration of sodium w/in body and removes acid
metabolic acidosis lab valvues
low pH
low bicarbonate
metabolic alkalosis
high pH
high bicarbonate
respiratory acidosis
low pH
high pCO2
respiratory alkalosis
high pH
low CO2
acidosis symptoms (CNS)
DEPRESSION of CNS
cardiac arrhythmia (hyperK)
alkalosis symptoms (CNS)
EXCITED CNS
altered mental status, spasm, contraction, seizures
acidosis symptoms (cardiac, vascular, pulmonary)
decreased CO, arrhythmias, increased risk of VFib
vasodilation/HoTN
vasoconstriction in lungs, hyperventilation (move blood thru faster and unload CO2)
alkalosis symptoms (cardiac, vascular, pulmonary)
increased contractility (then decrease) refractory ventricular arrhythmia
coronary vasospasm/constriction
vasodilation of pulmonary vasculature, hypoventilation (move blood thru slower)
acidosis symptoms (Neuro, endocrine)
confusion, coma
insulin resistance, inhibitor of ATP synthesis
hyperkalemia
alkalosis symptoms (Neuro, endocrine)
cerebral vasoconstriction – HA, lethargy, tetany, seizures
hypokalemia (all low electrolytes)
stimulation of anaerobic glycolysis/lactic acid production
acid base disturbance with normal ABG
compensatory acid base disorders often develop to counteract
however, the body NEVER overcorrects
2 things req. for diagnosing acid base problems
arterial blood gas
basic metabolic panel
clinical presentation often clues you in
management is focused on correcting UNDERLYING cause
pH values
normal, panic
normal: 7.35-7.45
panic: <7.3, >7.6
pCO2 values
normal, panic
norm: 35-45 mmHg
Panic: <20 or >70
HCO3 values
normal, panic
normal: 22-26
panic: <10, >40
venous blood gas
convert venous sample measurements to arterial if this is what is given
steps in approaching an acid base problem
- academia or alkemia?
- respiratory or metabolic?
- acute or chronic (if respiratory)?
- anion gap? (metabolic acidosis)
respiratory acidosis patho
increased pCO2
lungs fail to excrete carbon dioxide –> retention leads to rise in pCO2 in plasma
increased formation of carbonic acid and lowered pH
compensatory mechanisms of respiratory acidosis
stimulate kidney to make more bicarb
hold onto bicarb and excrete acid
respiratory acidosis lab values (clinical)
pH: low
pCO2: high
HCO3: elevated
causes of respiratory acidosis
sleep apnea
stroke
choking
pneumonia
CNS depressive meds (opioids)
rib fracture/chest wall trauma
respiratory alkalosis
hyperventilation which lowers plasma carbonic acid
respiratory alkalosis compensatory
increasing renal excretion of bicarbonate
respiratory alkalosis labs
pH high
pCO2 low
HCO3 normal to low
causes of respiratory alkalosis
hypoxia (hyperventilation, high altitude)
CNS problems (pregnancy, gram - sepsis)
Pulmonary (PE)
increased amount of plasma bicarb
metabolic alkalosis
often has concomitant K+ depletion and volume contraction
metabolic alkalosis compensatory mechanisms
decreased RR
inefficient bc can’t decrease RR enough to cure the issue
what induces metabolic alkalosis
diuretic therapy
loss of gastric secretions (vomiting or nasogastric suction)
large amounts of exogenous alkali
elevation in plasma bicarbonate concentration can result from
hydrogen loss
hydrogen movement into cells
alkali administration
volume contraction
increased net bicarbonate reabsorption by kidney
volume and potassium depletion
prevents excess bicarbonate from being excreted, worsening alkalosis
why does volume depletion cause increased renal bicarbonate?
kidney tries to hold onto Na+ to increase free water
therefore, kidney reabsorbs sodium bicarbonate from tubule and water follows
potassium depletion increases metabolic alkalosis by:
- hydrogen loss
2. H+ movement into cells
hydrogen loss in metabolic alkalosis
potassium depletion causes distal pumps in kidney secrete H+ in exchange for K+
movement of hydrogen into cells worsens metabolic alkalosis by
H+ is moved into cells to move K+ out
intracellular environment is acidotic, so H+ secretion by kidneys increases
also raises plasma bicarb concentration, H+ is no longer in serum suffer
kidney compensation for K+ loss is ba bc
tries to correct volume contraction by absorbing sodium bicarbonate and excreting hydrogen
worsens alkalosis
req. simultaneous correction of K+ def.
etiologies of metabolic alkalosis (6)
- GI acid loss
- renal acid H+ loss
- post-hypercapnia alkalosis
- milk-alkali syndrome
- administration of exogenous alkali
- metabolic contraction alkalosis
metabolic alkalosis from GI acid loss
H+ in stomach is removed (vomiting or suctioning off) but no stimulation to stop producing bicarbonate
therefore:
net hydrogen loss and bicarbonate is still being produced/reabsorbed from kidney (decreased H w/o decreased HCO3)
metabolic alkalosis renal acid loss is caused by which hormone?
aldosterone
high levels of aldosterone cause
- stimulation of H+ secretion in renal tubule
- tubule lumen is more electronegative so Na+ reabsorption is not = to H+ loss
distal K+ secretion is enhanced, resulting in concurrent hypokalemia
renal acid loss metabolic alkalosis
typically presents in pts on loop diuretic or TZD
increase in H+ secretion and volume contraction = metabolic alkalosis
post hypercapnic metabolic alkalosis
COPD/acidosis pts hold onto bicarbonate to control mild respiratory acidosis
the acidosis is rapidly fixed but kidney doesn’t get stimulation to decrease Bicarb causing metabolic alkalosis
metabolic alkalosis due to milk alkali syndrome results when
- increased alkaline load (oral calcium)
- hypercalcemia-mediated constriction of afferent arteriole, induces renal AKI
too much bicarb + increased base going in + kidney can’t get rid of excess
metabolic alkalosis due to administration of exogenous alkali
giving large amounts of sodium bicarbonate or citrate
- blood infusion (>8 units)
- citrate rather than heparin to anticoagulant
- extensive use of crack cocaine
- FFP administration during plasmapheresis
- correction alkalosis
metabolic contraction alkalosis
loos of relatively large volume of bicarbonate free fluid
contraction of extracellular volume around constant quantity of extracellular bicarbonate
what causes metabolic contraction alkalosis
use of IV loop diuretics
underlying electrolyte disorder coupled with high chloride loss
saline responsive metabolic alkalosis patients vitals
normotensive, volume contracted and hypokalemic
saline unresponsive patient vitals
normo or hypotensive
fluid overloaded
causes of saline responsive metabolic alkalosis
renal causes (diuretic use, post-hypercapnia alkalosis)
GI causes (vomiting/suctioning/diarrhea, exogenous alkali)
diuretic use and saline responsive metabolic alkalosis
high NaCl and H2O loss from meds cause contraction of vascular volume and relative concentration of HCO3 increases
treatment of saline responsive metabolic alkalosis
- correction of volume depletion with normal saline
2. correction of potassium depletion
correction of volume depletion in saline metabolic alkalosis
less bicarb and sodium reabsorbed, no longer volume contracted
more bicarbonate secreted by kidney
correction of potassium depletion in saline metabolic alkalosis
K+ moves into cells, H+ moves out
increased extracellular H+ buffers
H+ leaving the cell causes pH to return to normal (stop kidney secretion of H+ and reabsorption of bicarb)
causes of in saline non responsive metabolic alkalosis
hyperaldosteroneism (kidney retains sodium and H+ is excreted)
milk alkali syndrome
treatment of in saline unresponsive metabolic alkalosis
- if pt is hypokalemic, KCl will correct both hypokalemia dn alkalosis
- Acetazolamide (diamox) = inhibits renal sodium bicarb reabsorption and causes diuresis
mechanisms of metabolic acidosis
- increased acid generation (ketoacidosis and lactic acidosis)
- loss of bicarbonate (diarrhea) or bicarbonate precursors (ketoacidosis)
- diminished renal excretion
amount of acid produced exceeds body’s buffering capacity
metabolic acidosis
fall in concentration of bicarbonate bc it is consumed in neutralization of excess acid
etiologies of metabolic acidosis
- intestinal loss of bicarb
- renal tubular acidosis
- excessive acid production/diminshed excretion
- lactic acidosis
- poisons
metabolic acidosis due to intestinal loss of bicarb
too much acid precursor without bicarbonate excretion
metabolic acidosis due to RTA
genetic defect: kidney can’t excrete adequate H+ or reabsorb adequate HCO3
three types (I, II, IV)
hyperchloremic, metabolic acidosis w/o anion gap
normal GFR, no diarrhea
uremia and metabolic acidosis
AKI or late stage CKD
failing kidneys can’t excretion acids from normal metabolism
ketosis and metabolic acidosis
metabolism of fat produces excess ketone bodies and decreases bicarbonate precursors
found in DM, starvation, alcohol
lactic acid is normally produced?
by RBCs, skeletal muscles, skin, and brain
metabolized by liver and kidney
when does accumulation of lactic acid occur?
tissue hypoxia (over production) hepatic failure (deficient removal) circulatory collapse
esp. seen in sepsis, bowel or extremity infarction, respiratory failure, seizures
main clinical feature of lactic acidosis?
hyperventilation
this is due to the compensatory mechanisms
this level exceeds 4-5 meq/L
poisons that can cause metabolic acidosis
carbon monoxide cyanide ethylene glycol methanol meds
meds that cause metabolic acidosis (5)
iron
isoniazid
metformin
ibuprofen
salicylates
carbon monoxide
odorless, colorless gas from exhaust, fire
comes from improperly ventilated heater/appliances
CO has a large affinity for HgB 250x that of oxygen – therefore CO never unloads
10-20% carboxyhemoglobin
HA, dizziness, abd pain or nausea
30-40% carboxyhemoglobin
confusion, dyspnea, syncope
50-60% carboxyhemoglobin
HoTN, coma, seizures
survivors may have permanent neurological deficits
treatment of CO poisoning
high flow oxygen
HBO
Cyanide poisoning (patho, symptoms, tx)
cells fail to take up arterial oxygen
HA, nausea, abdominal pain, dizziness, confusion, shock, seizures, death
tx: cyanide antidote package
where is cyanide found?
industry labs apricot pits nitroprusside fires of burning plastics (firefighters)
methanol poising
wood alcohol
organic solvent found in paint remover, industrial cleaners, and perfumes
when does methanol become harmful
metabolized to formaldehyde and then formic acid which accumulates metabolic acidosis and several adverse effects
methanol intoxication occurs byL
children ingesting poisons accidentally
alcoholics substituting methanol for ethanol
bootleg alcohol
inhalation of methanol fumes by factory workers
effects of methanol
rapid retinal edema and permanent vision loss
development of parkinsonism like movement disorder due to accumulation of formic acid in the putamen
methanol toxicity workup
anion gap metabolic acidosis
osmolar gap
methanol levels are detected, but not accurate
if severe symptoms (vision loss) hemodialysis is indicated
ethylene glycol toxicity
found in antifreeze and radiator fluid, taste sweets
occurs due to accidental ingestion, suicide attempts
its appear drunk and develop severe anion gap acidosis, tachypnea, confusion, seizures and coma
ethylene glycol toxicity workup
serum calcium level and UA looking for calcium oxalate crystals
profound anion gap acidosis and hypocalcemia
tx for methanol/ethylene glycol
ethanol - actual booze
fomepizole (antizol or 4MP) - preferred
slow conversion of methanol or ethylene glycol to toxic metabolites, therefore allowing them to be excreted
hemodialysis is also one
anion gap
sorry out cause of metabolic acidosis
represents unmeasured anions in serum sample
Na - (HCO3 + Cl), normal value is 8-16
why is the anion gap useful?
bc irregardless of pH or HCO3 levels
presence of increased anion gap always means there is underlying anion gap metabolic acidosis
decreased anion gap
low level of negative ion charge
BAM
Bromisim
Albumin
Multiple Myeloma
normal anion gap
DURHAM
DURHAM Diarrhea Ureteral diversion Renal Tubular acidosis Hyperalimentation Addison's disease/Acetazolemide Miscellanous
increased anion gap
MUD PILES Methanol Uremia DKA/Drugs (metformin) Phosphate/paraldehyde Ischemia/Iron Lactate Ethylene Glycol Starvation
