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Renal > Acid Base > Flashcards

Acid Base Flashcards

1
Q

Arterial Blood Gases

A
  • arterial pH, carbon dioxide tension (pCO2), oxygen tension (pO2), bicarbonate concentration ([HCO3-]), and percent oxyhemoglobin saturation (SaO2).
  • The pH, pCO2, and the pO2 are measured directly from the sample.
  • The bicarbonate value is calculated from the pH and pCO2 data using the HendersonHasselbalch equation
  • In addition, some laboratories also calculate the percent oxyhemoglobin saturation from the measured pO2 value rather than measuring the saturation directly. This is done using the values obtained from an O2 dissociation curve.
  • At UAMC, oxyhemoglobin saturation is measured directly and values for hemoglobin, methemoglobin and carboxyhemoglobin are also reported routinely.
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2
Q

Basic Metabolic Panel

A
  • Electrolytes (Na+ , K+ , Cl- , CO2**) are usually obtained as part of a “basic metabolic panel” (BMP), which includes creatinine, BUN, glucose and calcium in addition to the basic electrolytes.
  • Electrolytes are also included in a “comprehensive metabolic panel” (CMP) or may be ordered individually.
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3
Q

Acid

A

•a molecule that releases hydrogen ions in solution. Acid: A substance that when added to a solution brings about an increase in [H+]

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4
Q

Base

A

•a molecule that can accept hydrogen ions. Base: A substance that when added to a solution brings about a decrease in [H+]

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5
Q

Buffer

A

•a substance that can reversibly bind hydrogen ions. pH—negative log (base 10) of the hydrogen ion concentration. Acidemia — An arterial pH below the normal range

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6
Q

Alkalemia

A

•An arterial pH above the normal range

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7
Q

Acidosis

A

•A process that tends to lower the extracellular fluid pH (hydrogen ion concentration increases). This can be caused by a fall in the serum [HCO3-] and/or an elevation in pCO2

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8
Q

Alkalosis

A

•A process that tends to raise the extracellular fluid pH (hydrogen ion concentration decreases). This can be caused by an elevation in the serum [HCO3-] and/or a fall in pCO2

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9
Q

Metabolic Acidosis

A

•A disorder that causes reductions in the serum [HCO3-] and pH

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10
Q

Metabolic Alkalosis

A

•A disorder that causes elevations in the serum [HCO3-] and pH

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11
Q

Respiratory Acidosis

A

•A disorder that causes an elevation in arterial pCO2 and a reduction in pH

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12
Q

Respiratory Alkalosis

A

•A disorder that causes a reduction in arterial pCO2 and an increase in pH

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13
Q

Simple Acid Base Disorder

A

•The presence of one of the above four disorders with the appropriate respiratory or renal compensation for that disorder

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14
Q

Mixed Acid Base Disorder

A

•The simultaneous presence of more than one acid-base disorder

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15
Q

Normal pH

A

7.38-7.42

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16
Q

Normal pCO2

A

38-42 mmHg

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17
Q

Normal [HCO3-]

A

22-26 mEq/L

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18
Q

Volatile Acid

A

•Volatile acids are defined as those acids which can be converted into a gaseous form and can thus be eliminated by the lungs. The primary volatile acid of the body is carbon dioxide which is produced in substantial amounts by the processes of cellular respiration

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19
Q

Nonvolatile

A

•A nonvolatile acid (also known as a fixed acid or metabolic acid) is an acid produced in the body from sources other than carbon dioxide, and is not excreted by the lungs. They are produced from e.g. an incomplete metabolism of carbohydrates, fats, and proteins.

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20
Q

Henderson-Hasselbach Equation

A

pH = 6.1 + log HCO3/0.03 x pCO2

Note: pH is defined by the ratio of HC03- to pCO2 and not by the absolute value of either alone

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21
Q

Renal Compensatory Response

A

•the renal compensatory response to respiratory disturbances occurs slowly (taking place over days—usually described as occurring over ~72 hours). Thus, respiratory disorders are divided into “acute” and “chronic” respiratory acidosis or alkalosis. The “acute” response is due to immediate buffering primarily by intracellular proteins. The “chronic” response is due to renal compensation.

22
Q

Respiratory Compensatory Response

A

•In contrast, the respiratory compensatory response to metabolic acidosis occurs quickly (usually beginning within minutes). The respiratory compensatory response to metabolic alkalosis is often variable and may take hours (see below for more explanation). Nonetheless, both metabolic acidosis and alkalosis are not separated into acute and chronic phases

23
Q

Metabolic Acidosis

A
  • decrease in pH
  • decrease in [HCO3-]
  • respiratory compensation - Winter’s Formula!

pCO2 = (1.5 x HCO3) + 8 +/- 2

24
Q

Winter’s Formula

A

pCO2 = (1.5 x HCO3) + 8 +/- 2

25
Q

Metabolic Alkalosis

A
  • increased pH
  • increased [HCO3]
  • respiratory compensation

pCO2 = variable increase

or

pCO2 = (0.7 x HCO3) + 20

26
Q

Respiratory Compensation for Metabolic Alkalosis

A

pCO2 = (0.7 x HCO3​) + 20

27
Q

Respiratory Acidosis

A
  • decrease pH
  • increase pCO2
  • renal comlensation
  • acute: HCO3 increases 1 mEq for every 10 mmHg increase in pCO2
  • chronic: HCO3 increases 3.5 mEq/L for every 10 mmHg increase in pCO2
28
Q

Compensation for Acute Respiratory Acidosis

A

HCO3 increases 1 mEq/L for every 10 mmHg increase in pCO2

29
Q

Compensation for Chronic Respiratory Acidosis

A

HCO3 increases 3.5 mEq/L for every 10 mmHg increase in pCO2

30
Q

Respiratory Alkalosis

A
  • increased pH
  • decreased pCO2

*renal compensation

  • acute: HCO3 decreases 2 mEq/L for every 10 mmHg decrease in pCO2
  • chronic: HCO3 decreases 5 mEq/L for every 10 mmHg decrease in pCO2
31
Q

Compensation for Acute Respiratory Alkalosis

A

HCO3 decreases 2 mEq/L for every 10 mmHg decrease in pCO2

32
Q

Compensation for Chronic Respiratory Alkalosis

A

HCO3 decreases 5 mEq/L for every 10 mmHg decrease in pCO2

33
Q

Metabolic Acidosis

A
  • A metabolic acidosis is an abnormal primary process leading to a fall in the plasma bicarbonate. The decrease in the plasma HCO3- can be caused by two mechanisms: a gain of fixed (nonvolatile) acid or loss of base.
  • The fall in plasma bicarbonate with gain of acid is due to titration of HCO3- by H+ . This initial pathophysiology causes a reduction in the serum [HCO3-] producing a decrease in pH.
  • The most common causes are due to excess generation of metabolic acids (e.g., lactic acid and ketoacids), exogenous loss of HCO3- (e.g., loss in stool or urine), reduced kidney excretion of acid (e.g., renal failure).
34
Q

Causes of Metabolic Acidosis - Elevated Anion Gap

A
  • Diabetic Ketoacidosis
  • Alcoholic Ketoacidosis
  • Lactic Acidosis
  • Renal Failure
  • Toxins (ethylene glycol, methanol, ASA)
35
Q

Causes of Metabolic Acidosis - Normal Anion Gap

A
  • Normal tubular acidosis
  • Diarrhea
  • Carbonic Anhydrase Inhibitors

*Admiistration of HCL or NH3Cl

•Acidosis associated with a normal anion gap has a limited number of causes. Basically, the causes are 1) loss of HCO3- through the gastrointestinal tract and 2) renal loss of HCO3- / failure to acidify the urine. Theoretically, normal anion gap acidosis could also occur with administration of HCl or NH4Cl (addition of acid with Cl as the anion), but this is a rare occurrence.

36
Q

Renal Causes of Hyperchloremic Acidosis

A

•The renal causes of hyperchloremic acidosis can be divided into 4 major categories:

  1. Primary defects in ammoniagenesis
  2. Hypoaldosteronism
  3. Disorders of the proximal tubule
  4. Disorders of the distal tubule
37
Q

“MUDPILES” - Metabolic Acidosis with Elevated Anion Gap

A

Methanol

Uremia

DKA

Propofol / Propylene Glycol

Iron / Isoniazid

Lactic Acidosis

Ethylene Glycol

Salicylates

38
Q

“MUDPALES” - Metabolic Acidosis with Elevated Anion Gap

A

Methanol

Uremia

DKA

Propofol / Propylene Glycol

Alcoholic Ketoacidosis

Lactic Acidosis

Ethylene Glycol

Salicylates

39
Q

Metabolic Alkalosis

A
  • A metabolic alkalosis is a primary disorder that causes the plasma HCO3- to rise, usually initiated by gastric loss of H+ (vomiting or nasogastric suction) or diuretic therapy.
  • The pathogenesis of metabolic alkalosis requires both the generation and maintenance of this process.
  • Regardless of the process generating the increase in HCO3- , the process must include a maintenance stage in which renal excretion of HCO3- is reduced.
  • GI H+ Loss

– Vomiting

– Nasogastric Suction

• Renal H+ Loss

– Diuretics

  • Loop
  • Thiazide

– Primary Mineralocorticoid Excess

– Bartter’s, Gitelman’s, & Liddle’s Syndromes

• Alkali Administration

40
Q

Causes of Metabolic Alkalosis

A

•The most common causes of metabolic alkalosis (vomiting, nasogastric suction, loop or thiazide diuretic use) are due to Cl depletion/deficiency and have low urinary Cl- . These types of metabolic alkalosis rapidly respond to Cl replacement (usually as infusion of “normal saline” in hospitalized patients [normal saline = 0.9% NaCl solution]).

41
Q

Respiratory Acidosis

A

•The underlying pathophysiology (most often alveolar hypoventilation causing hypercapnic respiratory failure) increases the pCO2 because volatile acid (CO2) is not removed by lung ventilation

42
Q

Respiratory Alkalosis

A

•The initial process is a decrease in the pCO2 due to an increase in ventilation (hyperventilation). Several (of many) causes are hypoxemia, anxiety, pregnancy, liver failure, mechanical ventilation, progesterone, salicylate poisoning, and pain.

43
Q

Anion Gap

A

Total Cations = Total Anions

Anion gap = measured cations – measured anions

44
Q

Normal Anion Gap

A

8-12 mEq/L

45
Q

Formula to Calculate Anion Gap

A

AG = Na- (Cl + HCO3)

correct for albumin

AGcorrected = AG + 2.5(4 - measured albumin)

•If there is a significantly elevated anion gap, there is a primary metabolic acidosis.

46
Q
A
47
Q

Net Renal Acid Excretion

A
  • Net Renal Acid Excretion = Titratable acidity + NH4 + - urinary HCO3 -
  • HCO3 - Reabsorption
  • Titratable Acid
  • Ammoniagenesis and NH4 + excretion
48
Q

HCO3 Reabsorption

A
  • ~4300 mEq/day filtered
  • 80% reabsorbed proximal tubule
49
Q

HCO3 Reabsorption Proximal Tubule

A
50
Q

HCO3 Reabsorption Collecting Duct

A

•principal cells respond to

  • ADH –> more H2O reabsorption (aquaporins)
  • aldosterone –> reabsorbing NaCl —> more H2O reabsorption (water flows where Na goes!)

•intercalated cells secrete or reabsorb H+

51
Q

Titratable Acid

A
52
Q

Ammoniagenesis and NH4 + excretion

A

•Ammoniagenesis: in proximal tubule metabolism of glutamine produces NH4+ and HCO3-

Renal (26 decks)

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