acid/base disorders Flashcards
acidemia vs. acidosis
Acidemia is a decreased blood pH (normal is 7.36-7.44)
Acidosis is a clinical process in the body that decreases blood pH
alkalemia vs. alkalosis
- alkalemia = increased blood pH
- alkalosis = clinical process in body that increases blood pH
hyperkapnia
increased pCO2 in blood
hypokapnia = low pCO2
minute ventilation
rate by which air reaches alvoli
= RR x Tidal volume
hyperventilation = increased minute ventilation
hyperventilation
= hypokapnia
hypoventilation = hypercapnia
metabolic disorders
follow pH
decrease in pH = decrease in Hco3- = metabolic alkalosis
compensation
resp = w/in hours
metabolic = w/in 2-3 days
- if resp. disorder if over 3 days old, then it it most likely metabolic compensation
- chronic resp. disorders are fully compensated and pH is close to normal after 3 days
- subacute resp. disorders = partially compensated, 2 days
anion gap
A.G.=Na+– HCO3- - Cl-
MUDPILES: Methanol Uremia (End Stage Renal Disease) Diabetic ketoacidosis Paraldehyde Infection, Iron, Isoniazide Lactic acidosis Ethylene glycol (antifreeze), alcohol Salicylates, starvation ketoacidosis
Uremic acidosis
Occurs when renal function is severely decreased (Creatinine clearance is less than 25ml/min)
Due to:
decreased excretion of acids
decreased excretion of H+
Decreased reabsorption/synthesis of HCO3
Accumulation of organic and inorganic anions:
Phosphates
Sulfates
Causes of Lactic Acidosis
caused due to anaerobic metabolism in tissues due to:
- hypoxemia
- hypotension/sepsis
- peripheral vessel blockage
- anemia
- hypoperfusion of vital organs
Medications: METFORMIN!
- Liver failure due to decreased clearance
- Thiamine deficiency in alcoholics
- Hypophosphatemia
- Sepsis (decreased perfusion of tissues, impaired gluconeogensis and poor clearance)
- seizures: due to release of lactate from mm.
diabetic ketoacidosis
insulin deficiency ==> increased lypolysis –> FA delivery to liver –> production of ketones –> acidosis
- associated w/ hyperglycemia
- more often assoc. with Type 1 DM
- may be caused by patients non-compliance w/ insulin, infection and pancreatitis
alcoholic ketoacidosis
ethanol intake –> ketone production
- main difference b/w DM ketoacidosis = NO hyperglycemia
- high osmol gap (normal is less than 10)
osmol gap
(normal is less than 10)
= Difference between measured serum Osmolality and calculated serum osmolality
Calculated Osmolality = 2 (Na+) + (Glucose/18) + BUN/2.8
OG should be equal to Ethanol level/4.6 – if it is more than this, then need to look for other alcohols
If OG more than that, look for other alcohols (alcohols that are in cleaning supplies, etc.)
- used to determine cause of alcoholic ketoacidosis
other alcohol poisoning?
- Ethylene glycol: antifreeze, increased OG, calcium oxalate crystals in urine, acute renal failure common
- Methanol: found in wood alcohol and windshield fluid, causes blindness and acute renal failure, increased OG
salicylate poisoning
usually due to accidental or intentional overdose
may cause metabolic acidosis or respiratory alkalosis
Sx: hemorrhage, fever, nausea, vomiting, diaphoresis, tinnitus, pulmonary edema
normal AG metabolic acidosis
- Diarrhea or illeal drainage with stomach bypasses (due to loss of HCO3)
- Decreased reabsorption of HCO3 by renal tubules (“renal loss”): due to diuretics, or renal tubular acidosis
- increase in anion intakes
- large amount of NaCl (expansion acidosis) - due to dilution of bicarb and decreased renal bicarb reabsorption as result of volume expansion
RTA I
renal tubular acidosis type I (distal) = low pH, kidney stones, hypokalemia
- Decreased hydrogen ions excretion in the collecting ducts leading to alkaline urine and acidic serum
- Increased calcium excretion and decreased citric acid concentration leading to kidney stone formation
- Increased potassium loss leading to hypokalemia
RTA II
Proximal renal tubular acidosis
- acidosis: acidic urine, no kidney stones, hypokalemia
- defect in bicarb reabsorption in proximal tubule, so more bicarb is excreted –> increased bicarb in urine
- increased Ca2+ in urine, doesn’t lead to kidney stones, due to normal citric acid concentration
- distal tubules work OK, ability to acidify urine in response to acidemia is intact, so urine pH is low
- high K+ loss also leads to hypokalemia
RTA IV
distal hyperkalemic acidosis
* see hyperkalemia and metabolic acidosis
- occurs in patients w/ moderate chronic renal failure
- insufficient aldo production
urinary anion gap
UAG = Na + K - Cl
- used to differentiate b/w renal and extrarenal HCO3 loss (RTA vs diarrhea)
- Negative = extra renal loss, diarrhea (bicarb not lost in urine, but kidney increases excretion of ammonia to compensate for acidosis caused by diarrhea)
- due to high level of unmeasured NH4+, excretion of NH4+ by healthy kidneys is compensatory mechanism for acidosis
- Positive = non-existant in renal loss
- due to low level of NH4+ and increased level of HCO3
what causes respiratory alkalosis?
hyperventilation- usually acute pain anxiety Salicylates overdose Fever Sepsis Hypoxia from some pulmonary disorders: CHF Pneumonia PE Mild asthma Mechanical ventilation
what causes metabolic alkalosis?
Vomiting/NG suction
- Due to lose of hydrochloric acid
Contraction alkalosis due to increased HCO3- reabsorption
- Dehydration
- Diuresis (with diuretics other than CAI)
Hypokalemia
- Due to resulting increased mineralocorticoid secretion
Recent correction of chronic respiratory acidosis
- Due to recent metabolic compensation.
Kussmaul breathing
a deep and labored breathing pattern often associated with severe metabolic acidosis, particularly diabetic ketoacidosis (DKA) but also renal failure. It is a form of hyperventilation, which is any breathing pattern that reduces carbon dioxide in the blood due to increased rate or depth of respiration.
what do you see clinically with metabolic acidosis?
Kussmaul breathing, vomiting, arrhtymias and hypotension, confusion, lethargy, coma
