Acid Base Flashcards
The degree of respiratory compensation expected in a metabolic acidosis can be predicted from the relationship
Paco 2 = (1.5 × [HCO 3 − ]) + 8 ± 2 (Winter’s equation).
_______—defined as independently coexisting disorders, not merely compensatory responses—are often seen in patients in critical care units and can lead to dangerous extremes of pH
Mixed acid-base disorders
The “normal” value for the AG reported by clinical laboratories has declined with improved methodology for measuring plasma electrolytes and ranges from _____mmol/L
6−12
Which of the following can cause a decrease in the anion gap?
A. Hyperlipidemia
B. Uremia
C. Lactic acidosis
D. Salicylate intoxication
A
Metabolic acidosis can occur because of an increase in _____production (such as lactate and ketoacids), loss of bicarbonate (as in diarrhea), or accumulation of endogenous acids because of inappropriately low excretion of net acid by the kidney (as in chronic kidney disease).
endogenous acid
The fall in blood pH is accompanied by a characteristic increase in ventilation, especially the tidal volume (______).
Kussmaul respiration
There are two major categories of clinical metabolic acidosis: ______
high-AG and non-AG acidosis
The p ence of metabolic acidosis, a normal AG, and hyperchloremia denotes the presence of a ______
non-AG metabolic acidosis.
Treatment of metabolic acidosis with alkali should be reserved for _____ except when the patient has no “_____ ” in plasma.
severe acidemia
potential HCO 3 −
Metabolizable acid anion
B hydroxybutyrate, acetoacetate, lactate
patients with a non-AG acidosis (_______)
hyperchloremic acidosis
AG acidosis attributable to a nonmetabolizable anion due to advanced kidney failure (______)
“uremic” acidosis
patients with a non-AG acidosis (hyperchloremic acidosis) or an AG acidosis attributable to a nonmetabolizable anion due to advanced kidney failure (“uremic” acidosis) should receive alkali therapy, either PO (NaHCO 3 tablets or Shohl’s solution) or IV (NaHCO 3 ), in an amount necessary to slowly increase the plasma [HCO 3 − ] to a target value of ______
22 mmol/L.
Bicarbonate therapy in diabetic ketoacidosis (DKA) is reserved for adult patients with severe acidemia _____) and/or evidence of shock.
(pH <7.00
In DKA with severe acidemia bicarbonate therapy:
IV, as a slow infusion of 50 meq of NaHCO3 diluted in 300 mL of a saline solution, over 30–45 min, during the initial 1–2 h of therapy.
A reasonable initial goal in DKA is to increase the [HCO3 − ] to 1____and the pH to approximately _____, but clearly not to increase these values to normal.
0–12 mmol/L
7.20
There are four principal causes of a high-AG acidosis: ______
(1) lactic acidosis
(2) ketoacidosis
(3) ingested toxins
(4) acute and chronic kidney failure
Pyroglutamic acidemia may occur in critically ill patients receiving _____, which causes depletion of glutathione and accumulation of 5-oxyprolene.
acetaminophen
______, which may be associated with jejunoileal bypass, short bowel syndrome, or intestinal obstruction, is due to formation of d-lactate by gut bacteria.
d-Lactic acid acidosis
Alkali therapy is generally advocated for acute, severe acidemia (pH___) to improve cardiovascular function
<7.00
A reasonable approach with severe acidemia is to infuse sufficient NaHCO 3 to raise arterial pH to no more than___ or the [HCO 3 – ] to no more than ____
7.2
12 mmol/L
This condition is caused by increased fatty acid metabolism and the accumulation of ketoacids (acetoacetate and β-hydroxybutyrate).
DKA
Ketoacidosis can occur in patients receiving____ for the same reasons as in classical DKA
SGLT2 antagonists
Ketoacidosis can occur in patients receiving____ for the same reasons as in classical DKA
SGLT2 antagonists
[DKA] If administered, NaHCO should be administered in only limited amounts because of the risk for___
cerebral edema
Patients with DKA are typically volume depleted and require fluid resuscitation with ____
Isotonic Saline
The presence of a high-AG acidosis, in the absence of hyperglycemia, in a patient with chronic alcoholism suggests the diagnosis of ___
AKA
[AKA] As the circulation is restored by administration of IV fluids, the preferential accumulation of β-hydroxybutyrate is then shifted to______.
acetoacetate
Patients with ____ usually present with relatively normal renal function
AKA
[AKA] Extracellular fluid deficits almost always accompany AKA and should be repaired by IV administration, initially, of ________
saline and glucose (5% dextrose in 0.9% NaCl)
[AKA]______ may emerge 12–24 h after admission, exacerbated by glucose infusion, and, if severe, may induce marked muscle weakness, hemolysis, rhabdomyolysis, or respiratory arrest.
Hypophosphatemia
[Salicylate Induced Acidosis] Vigorous gastric lavage with _____ (not NaHCO ) should be initiated immediately
isotonic saline
[SIA] All patients should receive at least one round of _____ _____ per nasogastric tube (1 g/kg up to 50 g)
Activated charcoal
[SAI] Raising urine pH from 6.5 to ____ increases salicylate clearance fivefold.
7.5
[SAI]_____ should be anticipated with vigorous bicarb therapy and should be treated promptly and aggressively
Hypokalemia
Under most physiologic conditions, sodium, urea, and glucose generate the____ pressure of blood.
Osmotic
[Alcohols] All cause an elevated osmolal gap, but only the first two cause a high-AG acidosis.
ethylene glycol
methanol
The combination of both a high AG and osmolar gap is highly suspicious for____
EG or methanol intoxication
This includes the prompt institution of IV isotonic fluids, thiamine and pyridoxine supplements, fomepizole, and usually, hemodialysis.
Ethylene Glycol Intoxication
The agent of choice and offers the advantages of a predictable decline in EG levels without excessive obtundation, as seen during ethyl alcohol infusion
Fomepizole
[EGI] Fomepizole should be continued until blood pH is _____ or the osmolar gap is <10 mOsm/kg H2O.
Normal
[EGI] Hemodialysis is indicated when the arterial pH is ___, a high-AG acidosis is present, the osmolar gap exceeds 20 mOsm/kg H2 O, or there is evidence of end organ damage such as CNS manifestations and kidney failure.
<7.3
The ingestion of _____ (wood alcohol) causes metabolic acidosis, and its metabolites formaldehyde and formic acid cause severe optic nerve and CNS damage
Methanol
____ is the vehicle used in IV administration of diazepam, lorazepam, phenobarbital, nitroglycerine, etomidate, enoximone, and phenytoin.
Propylene glycol
This form of high-gap acidosis should be considered in patients with unexplained high-gap acidosis, hyperosmolality, and clinical deterioration, especially in the setting of treatment for alcohol withdrawal
Propylene Glycol
With intoxication by propylene glycol, the first response is to______
stop the offending infusion
Ingested isopropanol is absorbed rapidly and may be fatal when as little as ____ of rubbing alcohol, solvent, or deicer is consumed
150 mL
5-Oxoproline accumulation after acetaminophen should be suspected in the setting of an unexplained high-AG acidosis without elevation of the osmolar gap in patients receiving______.
acetaminophen
The non-AG metabolic acidosis of stages 3 and 4 CKD require oral alkali replacement to increase and maintain the [HCO 3 − ] to a value mmol/L.
> 22
Stool contains a higher concentration of HCO 3 − and decomposed HCO 3 − than plasma so that metabolic acidosis develops in diarrhea. T/F
T
Proximal RTA (type 2 RTA) (Chap. 315) is most often due to generalized proximal tubular dysfunction manifested by glycosuria, generalized aminoaciduria, and phosphaturia (______)
Fanconi syndrome
______ occurs as a result of severe pulmonary disease, respiratory muscle fatigue, or abnormalities in ventilatory control and is recognized by an increase in Paco 2 and decrease in pH
Respiratory acidosis
Compensation Mechanisms:
Acute: HCO₃⁻ rises by ___ mmol/L for every 10-mmHg increase in PaCO₂.
Chronic (>24 h): HCO₃⁻ rises by ____ mmol/L for every 10-mmHg increase in PaCO₂ (maximum ~38 mmol
Acute 1
Chronic 4
The most common acid-base d bance in critically ill patients and, when severe, portends a poor prognosis.
Chronic Respiratory Alkalosis
_____ are the most common cause of drug-induced respiratory alkalosis because of direct stimulation of the medullary chemoreceptor
Salicylates
______ is the only acid-base disorder for which compensation can return the pH to the normal value.
Chronic respiratory alkalosis
