L11 Classification Of Acid/Base Status Flashcards
The three lines of defense against acid/base disturbances:
Buffers (mainly HCO3-, Hb and phosphate to lesser extent)
Respiratory compensation - adjusts CO2 levels, very fast but usually incomplete; always active when primary problem is metabolic
Renal compensation - adjusts HCO3- levels, slow but potent; compensates for respiratory problems and metabolic problems if they do not involve the kidney
What are normal acid/base values?
pH: 7.35-7.45 (mean = 7.40)
Plasma HCO3-: 22-26 mEq/L (mean = 24)
PaCO2: 35-45 mmHg (mean = 40)
Use these average values for all acid/base assessments
How would you classify a condition if the patient has:
pH = 7.52
HCO3- = 22
PCO2 = 28
1) It’s an alkalosis (pH > 7.4)
2) There is a respiratory component (PCO2 is less than 35)
3) Expected HCO3- = 22 (PCO2 is 12 mmHg below normal, which will depress [HCO3-] by 2 mEq/L due to mass action)
4) Actual HCO3- = 22, so there is no renal compensation
Result: It’s an uncompensated (pure) respiratory alkalosis
How would you classify a patient with
pH = 7.43
HCO3- = 18
PCO2 = 28
The pH is normal, but the other conditions suggest alkalosis
Primary disturbance is respiratory
Expect [HCO3-] = 22. Actual [HCO3-] = 18; therefore, 4 mEq/L HCO3- has been removed from kidneys
Result: this is completely compensated respiratory alkalosis
How would you classify a patient with
pH = 7.25
HCO3- = 12
PCO2 = 28
This is an acidosis (pH < 7.4)
There is a respiratory alkalosis; not primary factor (PCO2 < 40)
Expected HCO3- = 22, actual = 12; a primary metabolic acidosis has therefore reduced [HCO3-] by 10 mEq/L
This is a partly compensated metabolic acidosis
How would you classify a patient with
pH = 7.30
HCO3- = 25
PCO2 = 52
This is an acidosis (ph < 7.4)
There is a respiratory acidosis factor (PCO2 > 40)
Expected HCO3- = 25 and it is!
Therefore, this is uncompensated (pure) respiratory acidosis
Metabolic alkalosis is defined as
H+ loss or HCO3- gain
Typical causes:
- Ingestion of alkali (ie antacids)
- Hyperaldosterone ( ie - Conn syndrome)
ECF volume contraction:
Vomiting (lose HCl, fluid, and K+)
Nasogastric suction (same as above)
Loop or thiazide diurects (lose fluid and K+)
ECF volume contraction due to vomiting or extensive use of diuretics can _______ metabolic alkalosis
Maintain
ECF volume contraction increases H+ loss via RAAS:
• Angiotensin II stimulates Na+/H+ antiporter and HCO3- reabsorption
• Aldosterone stimulates secretion of H+ (H+ ATPase) from type A intercalated cells and K+ from principal cells
These factors can maintain alkalosis even when vomiting has stopped. Critical factor is markedly elevated aldosterone.
Treatment for metabolic alkalosis
Administer saline (NaCl or KCl) • Corrects saline-responsive forms of metabolic alkalosis
MOA for the saline:
Correction of fluid volume deficit —> adjusts the RAAS
Results in excretion of bicarbonate
What about saline-resistant metabolic alkalosis?
Due to aldosterone excess (secreting tumor)
—> ECF volume is increased, administering saline does not help as the patient is already volume expanded
Excess aldosterone increases H+ secretion and Na+ reabsorption
Example: Conn Syndrome
Treatment: remove tumor, or aldosterone antagonist (spironolactone)
What is the definition of metabolic acidosis
Gain of H+ or loss of HCO3-, typically due to ingestion of acids or acid-forming compounds (salicylate, methanol)
HCO3- is lost from the body (ie from diarrhea)
Non-volatile acid accumulation (lactic acid)
Renal HCO3- recovery is reduced, or excretion of titratable acid and NH4+ is reduced
NOTE: some metabolic acidosis are associated with an increase in teh anion gap
In the body, the concentration of anions must equal…
The concentration of cations
Major anions: Cl- (100) and HCO3- (24) = 124
Major cations: Na+ = 140
Anion Gap = [Na+] - [Cl-] - [HCO3-]
Normal gap = 8-16 mM
Why does the anion gap exist?
Due to the omission of several anions from routine blood chemistry analysis (ie sulphate, phosphate etc). K+ also typically omitted from the anion gap calculations.
Anion gap is often normal in acidosis due to …
Simple bicarbonate loss
Cl- increases to meet the drop in HCO3- (maintains the anion balance), ex: diarrhea, RTAs
The anion gap _______ in acidosis where there is an excess of other non-volatile (fixed) acids
Increases
Fixed acids liberate H+ which is buffered by HCO3- w/o changing Cl- levels; this increases the anion gap.
Disorders that increase the anion gap generate _________ which reduce HCO3- concentrations.
Non-volatile acids (ie lactic acid, oxalic acid)
Anions associated with these acids (lactate, oxalate) take the place of HCO3-; Cl- levels do not change
Metabolic acidosis from diminished tubular H+ secretion
Renal Tubular Acidosis (RTA)
Three types: Type I (distal) - H+ ATPase activity is reduced Type II (proximal) - Na+/H+ antiporter activity is reduced Type IV - reduced formation of NH4+, often due to hyperkalemia secondary to aldosterone deficiency; inhibits enzymes that degrade glutamine
How does Distal/Type I RTA happen?
Due to impaired H+ secretion by H+ ATPase in the distal nephron, or generalized failure of type A intercalated cells
Presenting symptoms are metabolic acidosis and HYPOkalemia
Anion gap is NORMAL
How does Proximal/Type II RTA happen?
Due to defect in Na+/H+ exchanger in the proximal convoluted tubule —> leads to impairment of H+ secretion and bicarbonate recovery (reabsorption)
Several causes (ie - toxins, hereditary conditions etc)
Results in loss of bicarbonate (less H+ in lumen)
Anion gap is NORMAL
Which is usually more severe, Type I or Type II RTA?
Type I (distal)
Type IV RTA includes several disorders w/ these common features:
- Impaired bicarbonate generation
- Metabolic acidosis
- Hyperkalemia
Defect in urinary acidification due to inhibition of renal glutamine season which impairs formation of NH4+
Correlated w/ aldosterone deficiency —> leads to hyperkalemia (inhibits renal glutaminase)
Anion gap is NORMAL
Which type of RTA is correlated with aldosterone deficiency?
Type IV RTA
What are some examples of metabolic acidoses with INCREASED anion gap?
Lactic acidosis (due to lactic acid)
Ketoacidosis (ie diabetic - due to acetoacetic acid)
Renal failure (due to accumulation of phosphoric, sulphuric, and other non-volatile metabolic acids)
Salicylate poisoning (aspirin)
Ethylene glycol poisoning (converted to glycolic and oxalic acids)
Methanol poisoning (converted to formic acid)
Respiratory alkalosis is due to a …
Decrease in PaCO2 via increased alveolar ventilation
Causes:
High Altitude
Anxiety
Hypoxemia
In some cases, the lack of oxygen leads to increased production of lactic acid, which partially counters the respiratory alkalosis
Respiratory acidosis is due to…
Impaired pulmonary excretion of CO2
Chronic respiratory acidosis occurs when alveolar ventilation is reduced by:
Impairment of central respiratory regulation
Chest wall dysfunction
Impaired airway mechanics
Impaired gas exchange
Focus of treatment is to correct underlying ventilators disorder
