Chap. 54 traditional acid-base Flashcards

1
Q

Traditional acid-base analysis uses:

Blood pH is a measure of:_____ and is dependent on the ratio of _______:_______

PCO2 behaves as an acid in the body and represents

metabolic contribution to acid-base balance

AG is a diagnostic tool that may help identify the cause of

The treatment of most acid-base disorders is focused on resolution of the underlying disease.

Sodium bicarbonate therapy is primarily indicated for:

A

Henderson-Hasselbalch equation to evaluate:
pH as a direct consequence of the PCO2, HCO3, BE

hydrogen ion concentration
ratio of HCO3:PCO2

respiratory contribution to acid-base balance.

Bicarbonate, base excess, and TCO2

metabolic acidosis

tx. of metabolic acidoses w.:
kidney disease
diarrhea-associated loss of bicarbonate

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2
Q

HH equation:

carbonic acid equation:

A

pH = 6.1 (pka) + log ([HCO3]/[0.03xPCO2])
HH equation, pH is consequence ratio HCO3-:PCO2
H2O + CO2 - H2CO3 - H+ + HCO3-

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3
Q

why does CO2 act as an acid in body:

A

bc of ability to react with H2O to produce carbonic acid

H2CO3

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4
Q

major criticisms of using bicarbonate as the measure of the metabolic component

criticisms to trad approach as a whole:

A

not independent of changes in PCO2

=important that changes in bicarbonate concentration are always evaluated in terms of the pH and PCO2

failure to identify individual disease processes that are contributing to the acid-base abnormality

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5
Q

Base excess (BE) is the titratable acidity (or base) of the blood sample. It is defined as:

advantage

A

amount of acid or base that must be added to a sample of oxygenated whole blood to restore the pH to 7.4 at 37° C and at a PCO2 of 40 mmHg

independent of changes in the respiratory system

BE is a parameter calculated by an algorithm programmed into blood gas machines

Herbivores more positive BE
carnivores more negative BE than people

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6
Q

BE can be estimated by

A

estimated by the measured HCO3 - normal HCO3 (22)

in the face of substantial abnormalities in PCO2, the BE is a more reliable measure of metabolic component

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7
Q

TCO2 misleading b/c:

majority of carbon dioxide carried in blood is in what form:

TCO2 will be _____ mmol/L higher than ____

A

represents metabolic acid-base component, not the respiratory

TCO2 is a measure of all the carbon dioxide in a blood sample, and the majority of carbon dioxide is carried as bicarbonate in the blood

1 to 2 mmol/L higher than bicarbonate

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8
Q
Anion Gap
why we calc: 
what is it:
calc.:
normal AG composed of:
false decrease:
A

better define the cause of a metabolic acidosis

electroneutrality requires there to be equal # anions:cations in physiologic systems

no actual AG; the apparent AG exists because more cations in the system are readily measured than anions

AG is a reflection of unmeasured cations and unmeasured anions and is calculated:

[Na] + [k] - [HCO3] - [Cl]

negatively charged plasma proteins, mostly albumin

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9
Q

two common mechanisms of metabolic acidosis

A

loss of bicarbonate: GI or kidneys
involves the exchange of bicarbonate and chloride
=hyperCl metabolic acidosis

gain of acid: DUEL, hydrogen ions will titrate (combine) with bicarbonate, leading to a fall in bicarbonate concentration
- anion that accompanied the hydrogen ion (the conjugate base) will accumulate, maintaining electroneutrality
= increasing the AG

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10
Q

Common acids associated with an increased AG

low AG:

A

lactate, ketone bodies, sulfate, phosphate, and toxins such as ethylene glycol
DUEL
(sulfates, phosphates)

Renal bicarbonate loss
Gastrointestinal bicarbonate loss
Dilutional acidosis
Hypoalbuminemia

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11
Q

metabolic compensatory response to a primary respiratory disorder takes hours to begin and 2 to 5 days

A

espiratory response to a primary metabolic abnormality is rapid in onset and complete within hours

metabolic compensatory response to a primary respiratory disorder takes hours to begin and 2 to 5 days

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12
Q

“overcompensation” assumption is

A

mixed acid-base disorder
changes in the secondary system are not within a range

disturbance of the secondary system preventing appropriate compensation or causing appearance of “overcompensation” (which does not occur)

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13
Q
Metabolic acidosis	
Metabolic alkalosis	
Respiratory acidosis—acute	
Respiratory acidosis—chronic
Respiratory alkalosis—acute	
Respiratory alkalosis—chronic
A

↓ PCO2 of 0.7 mm Hg per 1 mEq/L decrease in [HCO3−] ±3
↑ PCO2 of 0.7 mm Hg per 1 mEq/L decrease in [HCO3−] ±3
↑ [HCO3−] of 0.15 mEq/L per 1 mm Hg ↑ PCO2 ±2
↑ [HCO−3] of 0.35 mEq/L per 1 mm Hg ↑ PCO2 ±2
↓ [HCO−3] of 0.25 mEq/L per 1 mm Hg ↓ PCO2 ±2
↓ [HCO−3] of 0.55 mEq/L per 1 mm Hg ↓ PCO2 ±2

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14
Q

compensation in cats:

A

cats do not develop respiratory compensation

extrapolation of the canine calculations of expected metabolic compensation to respiratory disorders should be performed with caution in cats

extrapolation of the canine calculations of expected respiratory compensation to metabolic disorders cannot be recommended in cats

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15
Q

Traditional acid-base analysis identify 4 simple disorders

A
Metabolic acidosis	
Metabolic alkalosis	
Respiratory acidosis
Respiratory alkalosis
mixed
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16
Q

approach:

A
  1. pH - acidemia or alkalemia
  2. CO2 and HCO3:
    influencing pH in same direction is the primary disorder
  3. Calc. compensation
  4. AG if metabolic acidosis (assuming normal albumin)
17
Q

Bicarbonate Therapy
adverse effects of metabolic acidosis:

indications for HCO3-:

controversies:
strict contraindication:

A

Bicarbonate Therapy

  • decreased myocardial contractility
  • arterial vasodilation
  • impaired coagulation
  • decreased renal and hepatic blood flow
  • insulin resistance

controversial, although some consensus has been reached in recent time. There are several concerns with bicarbonate therapy (Box 54-5).
-first is that its use is based on the premise that acidemia has substantial negative consequences to the patient - human studies have demonstrated that a low pH is well tolerated; this includes patients subjected to permissive hypercapnia and patients with DKA

one of the most commonly cited adverse effects of acidemia is decreased myocardial contractility and vascular tone. Investigations have not been able to consistently demonstrate these negative hemodynamic effects

  • studies have failed to demonstrate that bicarbonate administration will improve hemodynamic performance in the face of acidemia (in some studies hemodynamic performance actually deteriorates after bicarbonate administration).
  • another concern is that sodium bicarbonate therapy does not reliably increase pH.
  • after administration, the HCO3- ions rapidly dissociates to CO2 and water
  • ventilation does not increase appropriately, an elevated PCO2 will cause a decrease in pH

=sodium bicarbonate therapy is strictly contraindicated in patients with evidence of hypoventilation

18
Q

HCO3
strict contraindication:
adverse effects CNS acidosis explained:

A

-after administration, the HCO3- ions rapidly dissociates to CO2 and water
-ventilation does not increase appropriately, an elevated PCO2 will cause a decrease in pH
=sodium bicarbonate therapy is strictly contraindicated in patients with evidence of hypoventilation

  • **Of greater concern is paradoxical intracellular acidosis
  • bicarbonate cannot freely cross cell membranes, but the CO2 produced freely enter cells
  • once intracellular, CO2 combines with water, leading H+ release and causing intracellular acidosis

-associated with increases in blood lactate concentration in studies of lactic acidosis, hemorrhagic shock, and DKA - exact mechanism for this response is not known, but left shifting of the oxygen-hemoglobin dissociation curve because of increases in blood pH may play a role

19
Q

HCO3 adverse effects:

A

Increased hemoglobin affinity for oxygen

Increased blood lactate concentration

Paradoxical intracellular acidosis

Hypercapnia

Hypervolemia
Hyperosmolality
Hypernatremia

Hypocalcemia (ionized)

Hypokalemia

Phlebitis

20
Q

WHen to give HCO3:

  • HCO3 is not indicated with:
  • HCO3 is indicated when:
A

If a specific therapy exists for the underlying cause of a metabolic acidosis, this in combination with appropriate IV fluid therapy should be the focus

ventilation inadequate
lactic acidosis
DKA
where bicarbonate therapy has been associated with no improvement in outcome or clinical deterioration despite severe acidemia

diseases causing bicarbonate loss, such as chronic kidney disease and diarrhea (an uncommon cause of metabolic acidosis in small animal patients)

management of patients with acute kidney injury (AKI) is less well defined

management of metabolic acidosis and hyperkalemia is a reasonable option, although caution must be used to avoid volume overload in the oliguric or anuric patient.

21
Q

Hypertonic sodium bicarbonate should never be administered rapidly bc:

diluted to osmolality of less than _____:

or give it by____:

Commercially available 8.4% sodium bicarbonate solution has an osmolality of approximately ____:

so a dilution of 1 part sodium bicarbonate to 3 parts diluent (e.g., sterile water for injection) =

A

can cause vasodilation and increases in ICP, which can be fatal

slow (over 30 minutes or longer) or diluting it with sterile water to make it an isotonic solution

dilution usually results in a significant volume for administration; the rate of infusion should then be governed by the perceived fluid tolerance

less than 600 mOsm/L

central catheter to avoid phlebitis

2000 mOsm/L /3 = 666.6mOsml/L