Flashcards in Acid-Base Disorders Deck (51):
Which values on a BMP are important in acid/base disorders? Normal values?
Na 140 mEq/L, K 4.1 mEq/L, Cl 108 mEq/L, CO2 24 mEq/L (bicarb), BUN 10 mg/dL, Creatinine 0.8 mg/dL
Which values on a ABG are important in acid/base disorders? Normal values?
pH 7.35-7.45, pCO2, pO2, calculated bicarbonate
What are the clinical effects of severe acidemia?
depr. cardiac funct., impaired response to catecholamines, arteriolar vasodilation (simultan. venoconstr.), systemic hypotension, pulm edema, insulin resistance, red. hepatic lactate uptake, accel. protein catabolism
What is the homeostatic response to acid/base loads?
chemical buffering by extracellular and intracellular buffers, changes in alveolar ventilation to control pCO2, alterations in renal H excretion to regulate P[HCO3]
How do the kidneys regulate pH?
regulate P[HCO3], formation of titratable acidity, excretion of NH4 in urine; whenever H is secreted from a renal cell into tubule fluid, an intracellular HCO3 is left behind and added to blood
What are the three components of net acid excretion?
titratable acids, ammonium, bicarbonate
What are titratable acids?
secreted H combines with urinary buffers (primarily inorganate P to form H2PO4 and HCO3)
what are the sources of ammonium?
urinary acidification increased by excretion of urinary NH4, tubular cells synthesize NH4 from glutamine, excretion of NH4 leaves behind an intracellular HCO3
what approach do you take to acid-base disorders?
det. electrolyte and ABG values, acidosis/ alkalosis, resp. or met, det. degree of compensation, calculate AG, if elevate Osm gap, if normal UAG
what are the features of metabolic acidosis?
pH decreased due to decrease in serum HCO3 due to either net gain H or net loss of HCO3, lungs compensate inc. ventilation and dec. pCO2
what are the common etiologies of metabolic acidosis?
addition of acid- endog (lactic acid) or exog. (ethylene glycol od), loss of bicarb- GI (diarrhea) or kidney (proximal tubule acidosis=RTA 2), inability to excrete normal daily acid production by kidneys (RTA 1)
What are the causes of high gap acidosis?
MMUDPPILES: methanol, metformin, uremia, diabetic ketoacidosis, propylene glycol, pyroglutamic acid, isoniazid, lactic acid, ethylene glycol, salicylates
How do you treat lactic acidosis?
correct underlying disorder, supportive care for shock: IV fluid (crystalloid or colloid), antibiotics, pressors
what are the causes of lactic acidosis?
type A: tissue hypoperfusion or hypoxia, or B: drugs (metformin, linezolid, propofol, nucleosides), thiamine deficiency, liver failure, malignancy, and D-lactic acidosis
What causes ketoacidosis?
most commonly type 1 diabetes, also alcoholics or starvation
what are the symptoms of salicylate poisoning?
tinnitus, N/V, inc temp, lethargy/excitability, hyperventilation leading to resp. alkalosis, severe toxicity= met. acidosis and seizures
How do salicylates cause acidosis?
stimulate respiratory center directly, early fall in PCO2 and respiratory alkalosis, AG metabolic acidosis due to accumulation of organic acids (lactic and keto)
How do you treat salicylate intoxication?
supportive care and dialysis if elevated level symptomatic
How do methanol and ethylene glycol cause acidosis? What is the treatment?
methanol-> formate + H+, ethylene glycol-> oxalate + H+; fomepizole and dialysis
What is the delta delta gap?
used in high gap metabolic acidosis, decrease in bicarb is equal to the increase in AG
What happens when AG is greater than change in HCO3?
high AG metabolic acidosis with primary metabolic acidosis
What happens when change in HCO3 than change in AG?
either high AG metabolic acidosis with non-AG metabolic acidosis or high AG metabolic acidosis and chronic respiratory alkalosis with compensatory non-AG metabolic acidosis
What are the causes of non-AG acidosis?
Renal or GI; separate based on history and on urinary anion gap
How does urinary ammonium change with urinary anion gap? What does it mean if UAG doesn't change?
NH4 excretion increases-> UAG decreases; form of RTA
what is RTA? Causes?
net loss of bicarbonate by the kidneys; Distal RTA (1)- defect in H ion secretion in DT, Proximal (2) defect in PT reabsorption of HCO3, and 4 relative insufficiency of or lack of responsiveness to aldosterone by DT
what are the features of Type 1 RTA?
distal defect->decreased H secretion, H builds in blood, K secreted instead of H, Hypercalciruia, renal stones
What are the causes of RTA 1?
1- idiopathic or familial, 2- hereditary hypercalcemia, hyperthyroidism, vitamin D intoxification
How do you treat type 1 RTA?
1-3 mmol/kg/day HCO3, sodium citrate better tolerated than NaHCO3, potassium citrate if hypokalemic
What are the features of type 2 RTA?
HCO3 wasting, urine pH< 5.5, K low to normal
What are the causes of Type 2 RTA?
Fanconi's syndrome, multiple myeloma, carbonic anhydrase inhibitors, heavy metal poisonings, amyloidosis
What is Fanconi's syndrome?
generalized PT dysfunction, urinary loss of phosphorus, uric acid, glucose, AA
How do you treat Type 2 RTA?
alkali therapy (5-15 mmol/kg/day HCO3), K supplementation, Vit. D replacement
What are the features of type 4 RTA?
impaired function of Na/K/H (cation) exchange mechanism, decreased and K secretion-> plasma build up of H and K hyperkalemia, urine pH < 5.5
What are the causes of type 4 RTA?
decreased renin- diabetic nephropathy, interstitial nephritis, drugs, tubulointerstitial disease
How do you treat Type 4 RTA?
dietary Na restriction, NaHCO3, furosemide= loop diuretic to get rid of K
What are the clinical effects of alkalemia?
cardiac arrhythmias, neuromuscular irritability, tissue hypoxia, cerebral and myocardial blood flow fall and respiratory depression can occur
What are the phases of alkalosis?
generation- loss of H or gain of HCO3, maintenance- prevents kidney from excreting HCO3, Lungs compensate by decreasing ventilation and increasing pCO2
What are some causes of generation of metabolic alkalosis?
loss of acid- vomiting, nasogastric suction, intestinal loss; excessive gain HCO3- oral or enteral intake, lactate or ketone metabolism; renal- persistent mineralocorticoid excess, K deficiency
What mechanisms are responsible for metabolic alkalosis?
decreased renal perfusion, hypermineralocorticoidism, sever hypokalemia, elevated pCO2
What causes impaired HCO# excretion that allows metabolic alkalosis?
ECircV depletion, Chloride depletion (decrease HCO3 secretion), Hypokalemia, Hyperaldosteronism
How do you differentiate causes of metabolic alkalosis?
responsiveness to NaCl, urine Cl < 10mEq/L alkalosis will respond to NaCl, urine Cl > 20 mEq/L
What are the causes of NaCl responsive metabolic alkalosis?
GI loss of H vomiting, gastric drainage or renal loss of H, diuretics, post-hypercapnia, poorly reabsorbable anion
What are the causes of NaCl resistant metabolic alkalosis?
severe K depletion or excess mineralocorticoid activity- hyperaldosteronism, Bartter's and Gitelman's, Cushing's, Excess licorice intake
What are the unclassified causes of metabolic alkalosis?
contraction, exogenous bicarbonate (blood transfusion), milk alkali syndrome, and hypercalcemia with decreased PTH
What are the features of Bartter's syndrome?
metabolic alkalosis, hypokalemia, hypercalciuria, hypomagnesemia, normal BP, gene- loop-durietic sensitive Na/K/Cl cotransporter of thick ascending LOH or apical K channel
what are the features of Gitelman's syndrome?
Metabolic alkalosis, hypokalemia, hypocalcuria, hypomagnesemia, normal BP, genes- thiazide sensitive NaCl cotransporter of distal tubule
What is milk alkali syndrome?
seen in pts with long history of excessive ingestion of milk and antacids, hypercalcemia and vitamin D excess increase, renal insufficiency, develop nephrocalcinosis
What is the diagnostic approach to metabolic alkalosis?
ABG and BMP (pH >7.4, HCO3 > 28, Pco2 > 40), assess compensation (winters), check if chloride responsive (UCl)
what is the treatment for chloride responsive alkalosis?
normal saline (correct volume, replace deficient Cl), replete K deficits
What is the treatment for chloride resistant metabolic alkalosis?
diagnose cause and treat it