Acid-base Flashcards
What is the name of the equation correlating pH to HCO3 and pCO2? What is the equation?
Henderson-Hasselbalch equation
pH = 6.1 + log (HCO3 / 0.03*pCO2)
What is the carbonic acid equation
CO2 + H2O = H2CO3 = H+ + HCO3-
Define base excess
Base excess is the amount of strong acid that needs to be added to 1L of fully oxygenated whole blood to restore the pH to 7.4 at 37°C with a pCO2 of 40 mmHg
(Calculated based on a human algorithm)
What does total CO2 indicate
The metabolic acid-base component (mostly HCO3). Usually 1-2 mmol/L higher than HCO3
What can falsely decrease the anion gap
Hypoalbuminemia
What is the degree of compensation expected for a metabolic acidosis / alkalosis
- Acidosis: pCO2 decrease of 0.7 mmHg per 1 mmol/L decrease in HCO3 +/- 3 mmHg
- Alkalosis: pCO2 increase of 0.7 mmHg per 1 mmol/L decrease in HCO3 +/- 3 mmHg
What is the expected degree of compensation for an acute / chronic respiratory alkalosis / acidosis
- Acute respiratory acidosis: HCO3 increase of 0.15 mmol/L per 1 mmHg increase in pCO2 +/- 2 mmol/L
- Chronic respiratory acidosis: HCO3 increase of 0.35 mmol/L per 1 mmHg increase in pCO2 +/- 2 mmol/L
- Acute respiratory alkalosis: HCO3 decrease of 0.25 mmol/L per 1 mmHg increase in pCO2 +/- 2 mmol/L
- Chronic respiratory alkalosis: HCO3 decrease of 0.55 mmol/L per 1 mmHg increase in pCO2 +/- 2 mmol/L
Why does hypokalemia contribute to metabolic alkalosis
- Hypokalemia promotes renal acid loss
- Hypokalemia promotes the efflux of K+ from intracellular to extracellular in exchange for H+
What is the prevalence of metabolic alkalosis and metabolic acidosis in cats and dogs
Metabolic acidosis: 43%
Metabolic alkalosis: 15%
What are alternative alkalinizing therapies
- Trishydroxymethyl aminomethane (tromethamine = THAM)
- Equimolar mixture of sodium bicarbonate and sodium carbonate (Carbicarb)
List 6 adverse effects of bicarbonate therapy
- Paradoxical intracellular acidosis
- Increased Hb affinity for O2 (left shift of dissociation curve)
- Hypervolemia
- Hypernatremia, hyperosmolarity
- Ionized hypocalcemia and hypomagnesemia
- Hypokalemia
Explain the paradoxical intracellular acidosis resulting from bicarbonate administration
- HCO3- dissociates to CO2 and H2O
- CO2 crosses the cell membranes and reaches the intracellular space (HCO3- does not)
- In the cell the carbonic acid equation leads to CO2+H2O -> H+ + HCO3-
- H+ accumulation causes intracellular acidosis
What is the bicarbonate deficit equation
HCO3 deficit (mmol) = 0.3 * body weight (kg) * base excess (mmol/L)
or HCO3 deficit (mmol) = 0.3 * body weight (kg) * (normal HCO3 - patient HCO3) (mmol/L)
What is the osmolality of sodium bicarbonate and the appropriate dilution
Osmolality of 2000 mOsm/L
Should be diluted 1:3 to be < 600 mOsm/L for peripheral administration
What point-of-care parameters can be assessed via an IO sample
BUN, TS, bilirubin, Na, Cl, glucose, blood gases (pH, PO2, pCO2) are similar to central venous
K and PCV/Hct not always reliable
What is the effect of body temperature on PO2 and PCO2
Increases in temperature will increase gas partial pressures (hypothermic patients will have lower PO2 and PCO2 in vivo than what is measured)
What can falsely increase / decrease:
- PaO2
- PCO2
- Na
- iCa
- K
- Lactate
- Glucose
- PaO2
- Increase: prolonged pre-analytical time with environmental exposure, air bubbles ; overdilution with liquid heparin
- Decrease: environmental exposure when PaO2 supposed to be >160 (=atmospheric PaO2), leukocytosis - PCO2:
- Increase: -
- Decrease: prolonged pre-analytical time with environmental exposure, air bubbles - Na:
- Increase: hypoproteinemia
- Decrease: hyperlipidemia, hyperglycemia, hyperproteinemia - iCa:
- Increase: hypoproteinemia
- Decrease: excess heparin, alkalemia (including post-sampling) - K:
- Increase: Hemolysis (esp Japanese / arctic breeds), thrombocytosis, leukocytosis
- Decrease: - - Lactate:
- Increase: prolonged pre-analytical time, ethylene glycol metabolites
- Decrease: - - Glucose:
- Increase: -
- Decrease: prolonged pre-analytical time
What are the 3 determinants of acid-base balance in he Stewart approach
- pCO2
- Strong ion difference (SID): Na, Cl (Ca, K, Mg +/- lactate)
- Nonvolatile weak acids (Atot): albumin, phosphate
What are the 5 possible metabolic acid-base abnormalities identified with the Stewart approach
- Increased SID metabolic alkalosis
- Decreased SID metabolic acidosis
- Increased Atot metabolic acidosis
- Decreased Atot metabolic alkalosis
- Increased SIG metabolic acidosis
What is the formula for the simplified SIG in cats and dogs? When does it need to be adjusted?
Dogs: SIG = albumin x 4.9 - AG
Cats: SIG = albumin x 7.4 - AG
In case of abnormal phosphorus, AG needs to be adjusted in the formula: AGp = AG + (2.52 -5.58*phosphorus)
What is the general formula for SIG
SIG = SID - (HCO3 + Atot)
How will SIG change with the addition of unmeasured anions? How about the simplified SIG?
SIG will increase (become more positive)
Simplified SIG will become more negative (because for some reason the formula is negative??)
What are the parameters included in the semi-quantitative approach of metabolic acid-base disorders
- Free water effect (Na)
- Chloride effect
- Albumin effect
- Phosphorus effect
- Lactate effect
In the semi-quantitative approach, is a positive effect associated with alkalotic or acidotic influence
Alkalotic
What are the simplified formulas of effects for the the semi-quantitative approach of metabolic acid-base disorders
- Free water effect = (Na - mid-normal Na)/4
- Chloride effect = mid-normal Cl - corrected Cl ; corrected Cl = Cl * (mid-normal Na / measured Na)
- Phosphorus effect = (mid-normal P - P)/2
- Albumin effect = 4*(mid-normal albumin - albumin)
- Lactate effect = -1*lactate
Unmeasured ion effect = base excess - sum of effects
What is the limitation of including lactate in the acid-base calculations
Lactate is not always associated with acidosis (when it is not due to anaerobic metabolism)
What are possible unmeasured anions in the semi-quantitative approach
Ketoacids, sulphuric acid, ethylene glycol, salicylic acid, propylene glycol, metaldehyde
What is the definition of a buffer
A molecule that can accept or donate protons and minimize a change in pH when H+ ions are added or removed from a solution
Name physiologic buffers
Extracellular:
- Bicarbonate
- Phosphate - most important urinary buffer
Intracellular:
- Organic phosphates (2,3 -DPG, AMP, ATP, ADP)
- Proteins (ex: hemoglobin)
What is the normal anion gap in dogs and cats
Dogs: 12-24 mEq/L
Cats: 13-27 mEq/L
What are the mechanisms of metabolic acidosis in hypoadrenocorticism
- Dilutional acidosis (hypoNa)
- Decreased renal H+ excretion:
- decreased aldosterone -> lack of activation of H+ transporter
- decreased aldosterone -> decreased Na+ reabsorption -> positive tubular lumen -> inhibited H+ excretion
- hyperK -> decreases NH4+ excretion)
- Lactic acidosis
- Hyperphosphatemia (from hypovolemia / decreased GFR)
What are clinical scenarios where bicarbonate therapy is indicated? Not indicated?
Indicated: HCO3- loss (GI with diarrhea / renal with RTA)
Not indicated: DKA, lactic acidosis
What were the results of the BICAR-ICU trial on the use of bicarbonates in critically ill patients with metabolic acidosis
- No benefit of using NaHCO3 on 28-day mortality except for patients with AKI
- Decreased need for RRT and vasopressors in patients receiving NaHCO3
- More alkalosis, hypernatremia, and hypocalcemia in patients receiving NaHCO3 but no life threatening complications
What is the name of the ventilation pattern caused by severe metabolic acidosis
Kussmaul breathing
In the kidney, which mechanisms regulate HCO3 reabsorption?
- Increase in filtered HCO3 –> increased reabsorbed HCO3
*** in metabolic alkalosis, filtered load may exceed reabsorptive capacity - Hypercapnia –> more H+ secreted => more HCO3 reabsorbed
- Hypocapnia –> less H+ secreted => less HCO3 reabsorbed
- ECF contraction –> renin –> aldosterone –> H+ secretion –> HCO3 reabsorption
- ECF expansion –> decreased HCO3 reabsorption
- Angiotensin II –> increases HCO3 reabsorption
In the kidney, which mechanisms regulate H+ secretion?
- Aldosterone –> increases H+ secretion via the H+-ATPase pump in the intercalated cells
- Diffusion trapping: H+ combines with NH3 in the lumen and is excreted as NH4+
** in acidosis, there is an adaptive increase in NH3 synthesis - Hyperkalemia inhibits NH3 synthesis –> decreased H+ excretion
- Hypokalemia stimulates NH3 synthesis
How can IV fluid therapy resolve alkalosis?
By adressing contraction alkalosis
Volume contraction activated RAAS system and aldosterone promotes reabsorption of HCO3 in the renal tubule –> contraction alkalosis
How can respiratory alkalosis can cause signs of hypoacalcemia.
H+ and Ca2+ compete for binding sites on plasma proteins.
Decreased [H+] causes increased protein binding of Ca2+ and decreased free ionized Ca2+.
What is the difference between base excess and standard base excess
Standard base excess is calculated for a Hgb of 5 g/dL (anemic blood) to account for the fact that Hgb has to buffer both the intravascular space and extravascular space.
SBE is supposed to be more representative of the acid-base status of the whole extra-cellular fluid vs. only blood.
What are the major unmeasured ions in the normal animal?
Albumin & phosphorus
- Anion Gap not reliable with abnormal albumin
List 5 adverse effects of metabolic acidosis
- Decreased myocardial contractility
- Arterial vasodilation
- Impaired coagulation
- Increased work of breathing
- Decreased renal and hepatic blood flow
- Insulin resistance
- Altered CNS function
Why should sodium bicarbonate be administered slowly?
If administered rapidly, may cause vasodilation and increase ICP
What is the advantage of SIG over AG?
SIG is independent of changes in albumin and is therefore more reliable in hypoalbuminemia
What is the corrected chloride formula?
Measured Cl x (normal Na/measured Na)
What is a limitation of the non traditional approaches to acid/base disturbances?
Do not recognize compensatory changes to respond disorders –> all changes are considered pathologic
