Introduction to acid base disturbances Flashcards
what is the systematic method for diagnosis of simple and mixed acid base disorders
1) measure the arterial blood gas and electrolyte concentrations simultaneously
- determines if acidemic or akalemic
2) Compare the [HCO3-] obtained on the electrolyte panel with the calculated value from the arterial blood gas analysis
3) is the overriding disturbance respiratory of metabolic
4) estimate the compensatory response for either carbon dioxide pressure or plasma [HCO3-]
5a) if respiratory disturbance is it acute or chronic
5b) if metabolic acidosis, calculate the anion gap (AG)
6) Appreciate the major causes of high AG acidosis HAGMA
- GOLDMARK
7) Appreciate the major causes of non-AG acidosis (NAGMA)
- HARDUPS
8) look for mixed disorder by examining compensation relative to expected compensation. compare the change in AG and the change in HCO3-, urine anion gap, osmolar gaps
9) If metabolic alkalosis
- is compensation appropriate or is it a mixed disorder
- chloride (saline) sensitive or chloride insensitive
Respiratory acidosis, what is the primary defect and primary response
primary defect: Alveolar hypoventilation
- increase in PaCO2
- decrease in pH
Compensatory response: increase renal HCO3- reabsorbtion
- limits of compensation: HCO3- 38mEq/L
- chronic 45 mEq/L HCO3-
Respiratory alkalosis, what is the primary defect and what is the compensatory response
Primary defect: Alveolar hyperventilation
- decrease in PaCO2
- increase in pH
Compensatory response: decrease in renal HCO3- reabsorbtion
- limits: HCO3- is 18 mEq/L
- if chronic: 15 mEq/L
Metabolic acidosis, what is the primary defect and what is the compensatory response
Primary defect: Loss of HCO3- or gain of H+
-decrease in pH
compensatory response: Alveolar hyperventilation to increase pulmonary CO2 excretion
- decrease in PaCO2
- limit is 10 mmHg
Metabolic alkalosis what is the primary defect and what is the compensatory response
Primary Defect: Gain of HCO3- or loss of H+
-increase pH
Compensatory response: Alveolar hypoventilation to decrease pulmonary CO2 excretion
- increase in PaCO2
- 55 mmHg
What is the Serum Anion Gap
[Na+] - ([Cl-] + [HCO3-] = 11-12 (normal range is 8-16)
-if high means other solutes in plasma (alcohols, lactic acidosis, ketoacidosis
used to determine if other solutes are in there
what is the Osmolal Gap
Serum Osm - [2x([Na+] + [K+]) + glcose/18 + BUN/2.8] = 0
if greater than 10 then that means other solutes in plasma (alcohol, lactic acidosis, ketoacidosis)
used to determine if their are other solutes in there
- if greater than 0 can be because of unmeasured osmotic particles such as NH4+
- 200 to 300 mean chronic severe metabolic acidosis
- less than 75 suggests renal tubular acidosis
what is the Urine Anion Gap
[Na+] + [K+] - [Cl-] = 20-90 in healthy people largely due to unmeasured NH4+
- becomes negative 20 to -50 in metabolic acidosis due t loss of HCO3- since excretion of unmeasured NH4+ increases
- surrogates for urinary NH4+ excretion
What is the Delta-Delta Gap
Change Gap = Calculated Anion Gap - normal anion Gap (12)
Delta [HCO3-] = normal HCO3- - Change Gap
if measured HCO3- is the same as the Delta HCO3- then it is a simple acid base disorder
if the measured HCO3- is greater than the delta HCO3- then it is metabolic alkalosis plus HAGMA
if measured HCO3 less then the Delta HCO3- then non-gap metabolic acidosis + HAGMA
what is the Delta AG/Delta HCO3 Ratio represent
used in somebody with a HAGMA if cause is unclear from history or in checking for mixed disorder
1:1 then simple HAGMA
less then 1 then losing HCO3 else where like diarrhea or kidneys are rapidly eliminating anion via ketoacidosis or D-lactate
greater then 1 to 2 suggests lactic acidosis
- need maintaince of lactate levels because L lactate is being reabsorbed
- intracellular buffering of H+ so HCO3 doesnt fall as much
ratio close to or gereater than 2
- metabolic alkalosis
- baseline HCO3 is elevated due to chronic respiratory acidosis
What are acute and chronic causes of respiratory acidosis and associated symptoms
Acute: CANS
- CNS depression
- Airway obstruction
- Neuromuscular disorders
- Severe pneumonia, embolism, edema
symptoms: headache, confusion, anxiety, drowisness, stupor tremors, convulsions, coma
Chronic:
- COPD
- anything chronic leading to impaired ventilation
symptoms: memory loss, sleep disturbances, excessive daytime sleepiness, and personality changes
- gait disturbances, tremor, blunted deep tendon reflexes, myoclonic jerks
Predicted delta HCO3- as compensation for respiratory induced delta PaCO2
for every increase of 10mmHg in PaCO2 (respiratory acidosis)
- increase HCO3 of 1 in acute
- increase HCO3 of 3.5 for chronic
For every decrease of 10mmHg of PaCO2 (respiratory alkalosis)
- decrease HCO3 by 2 acute
- decrease HCO3 by 5 for chronic
Causes of Respiratory Alkalosis and symptoms of both acute and chronic
Respiratory alkalosis: CHAMPS
- CNS disease-hyperventilation
- Hypoxia
- Anxiety
- Mechanical Ventilators
- Progesterone
- Salicylates/Sepsis
symptoms of acute: lightheadness, confusion, peripheral and circumoral paresthesias, cramps, and syncope
- thought to be due to change of cerebral blood flow and pH
- Tachypnea or hyperpnea
- carpopedal spasm due to hypocalcemia
symptoms of chronic respiratory alkalosis: usually asymptomatic
Causes of Metabolic Acidosis via High anion metabolic acidosis
HAGMA: GOLDMARK
- GLycols (ethelene or propylene)
- Oxoproline (pyroglutamic acid intermediate of acetaminophen toxicity
- L lactate
- D Lactate
- Methanol
- Asprin
- Renal failure
- Ketoacidosis
Causes of Metabolic Acidosis via no anion gap metabolic acidosis
NAGMA: HARDUPS
- Hyperalimentation
- Acetazolamide
- Renal Tubular Acidosis
- Diarrhea
- Ureterosigmoid fistula, colon wastes HCO3-
- Posthypocapnia (pancreatic fistula wastes HCO3-)
- Spironolactone
