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IM NEPHRO > Acid-Base-Electro > Flashcards

Acid-Base-Electro Flashcards

1
Q

Arterial [H+] is normally

A

40 nEq/L

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2
Q

Normal arterial pH is

A

7.40

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3
Q

is defined as an arterial pH below 7.35.

A

Acidaemia

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4
Q

Alkalaemia is defined as an arterial pH above

A

7.45

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5
Q

The value of pK, is 6.1, and the normal HCO; and PCO) are 24 mmol/L and 40 mmHg, respectively.

A

Henderson—Hasselbalch equation

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6
Q

Physiological responses to changes in [H+] are characterized by three phases:

A

(1) immediate chemical buffering,
(2) respiratory compensation (whenever possible)
(3) a slower but more effective renal compensatory response that may nearly normalize arterial pH even if the pathological process remains present.

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7
Q

Physiologically important buffers in humans include:

A
  • bicarbonate (H2CO3/HCO3-),
  • hemoglobin (HbH/ Hb-),
  • other intracellular proteins (PrH/Pr—),
  • phosphates (H2PO04-/HPO42-),
  • ammonia (NH3/NH4+).
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8
Q

is the most important buffer in the extracellular fluid compartment (effective against metabolic but not respiratory acid—base disturbances.)

A

Bicarbonate

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9
Q
  • though restricted inside red blood cells, also functions as an important buffer in blood.
  • are important urinary buffers.
A
  • Hemoglobin
  • Phosphate and ammonium ions
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10
Q

Has an important role in buffering the pH of the ICF of urine

A

Phosphate buffer system

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11
Q

Contribute to the regulation of pH in the ECF and ICF; interact extensively with the other two buffer systems

A

Protein Buffer System

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12
Q

Is most important in the ECF

A

Carbonic Acid-Bicarbonate Buffer System

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13
Q

The major factors involved in the maintenance of acid-base balance

A
  • Active tissues continuously generate carbon dioxide, which in solution forms carbonic acid. Additional acids, such as lactic acid, are produced inthe course of. normal metabolic operations.
  • Buffer systems can temporarily store H+ and thereby provide short-term pH stability.
  • The respiratory system plays a key role by eliminating carbon dioxide.
  • The kidneys play a major role by secreting hydrogen ions into the urine and generating buffers that enter the bloodstream. The rate of excretion rises and falls as needed to maintain normal plasma pH. As a result, the normal pH of urine varies widely but averages 6.0—slightly acidic.
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14
Q

Classes of acids

  • Do not leave solution
  • Remain in body fluids until kidney excretion
  • Generated during catabolism of amino acids, phospholipids, and nucleic acids
  • Examples: sulfuric and phosphoric acid
A

Fixed acids

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15
Q

Classes of acids

  • Part of cellular metabolism
  • Examples: lactic acid and ketones
  • Most metabolized rapidly so no accumulation
A

Organic acids

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16
Q

Classes of acids

  • Can leave body by external respiration
  • Example: carbonic acid (H,CO3)
A

Volatile acids

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17
Q
  • Changes in alveolar ventilation responsible for it which Paco2 are mediated by chemoreceptors within the brainstem.
  • These receptors respond to changes in cerebrospinal spinal fluid pH.
  • Minute ventilation increases 1—4 L/min for every (acute) 1 mm Hg increase in Paco2.
  • responses are also important in defending against marked changes in pH during
A

respiratory compensation

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18
Q

Renal Compensation During Acidosis (12-24hr): maximal 5 days

A

(1) increased reabsorption of the filtered HCO3-
(2) increased excretion of titratable acids
(3) increased production of ammonia.

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19
Q

Renal Compensation During Alkalosis

A
  • Tremendous amount of HCO3 - normally filtered and subsequently reabsorbed allows the kidneys to rapidly excrete large amounts of bicarbonate, if necessary.
  • Metabolic alkalosis is commonly associated with increased mineralo-corticoid activity
20
Q
  • defined as a primary increase in Paco2.
    T- his increase drives the reaction: H20+CO2 —H2CO3 H+ +HCO3-
  • leading to an increase in [H+] and a decrease in arterial pH.
  • [HCO3-] is minimally affected.
A

RESPIRATORY ACIDOSIS

21
Q

The compensatory response to acute (6—12 h) elevations in Paco2 is limited. Buffering is primarily provided by hemoglobin and the exchange of extracellular H+ for Na+ and K+ from bone and the intracellular fluid compartment The renal response to retain more bicarbonate is acutely
very limited. As a result, plasma [HCO3-] increases only about 1 mEq/L for each 10 mm Hg increase in Paco2 above 40 mm Hg.

A

Acute Respiratory Acidosis

22
Q

“Full” renal compensation characteristics
- Renal compensation is appreciable only after 12-24 hr and may not peak until 3-5 days.
- plasma [HCO3-] increases approximately 4 mEq/L for each 10 mm Hg increase in Paco2 above 40 mm Hg.

A

Chronic Respiratory Acidosis

23
Q

defined as a primary decrease in [HCO3-]

A

Metabolic acidosis

24
Q

Pathological processes can initiate metabolic acidosis by one of three mechanisms:

A

(1) consumption of HCO3- by a strong nonvolatile acid
(2) renal or gastrointestinal wasting of bicarbonate
(3) rapid dilution of the extracellular fluid compartment with a bicarbonate-free fluid.

25
Q

Pulmonary compensatory response in a simple metabolic acidosis characteristically does not reduce Paco2 to a level that completely normalizes pH but can produce marked hyperventilation

A

Kussmaul’s respiration

26
Q

major plasma cations — major plasma anions

A

Anion gap

27
Q

The anion gap decreases by ___ mEq/L for every 1 g/dL reduction in plasma albumin concentration.

A

2.5

28
Q

Metabolic acidosis with an increased anion gap is characterized by an increase in relatively strong

A

nonvolatile acids

29
Q

Endogenously produced organic acids are normally eliminated by the kidneys in urine. Glomerular filtration rates below 20 mL/min (renal failure) typically result inprogressive metabolic acidosis from the accumulation of these acids.

A

Failure to Excrete Endogenous Nonvolatile Acids

30
Q

Severe tissue hypoxia following hypoxemia, hypoperfusion (ischemia), or an inability to utilize oxygen (cyanide poisoning) can result in lactic acidosis. Decreased utilization of lactate by the liver, and, to a lesser extent by the kidneys, is less commonly responsible for lactic acidosis; causes include hypoperfusion, alcoholism, and liver disease.

A

Increased Endogenous Nonvolatile Acid Production

31
Q

An absolute or relative lack of insulin can result in hyperglycemia and progressive ____ from the accumulation of B-hydroxybutyric and aceto- acetic acids.
- may also be seen following starvation and alcoholic binges.

A

Ketoacidosis

32
Q

Ingestion of large amounts of salicylates frequently results in

A

metabolic acidosis

33
Q

rapidly accumulate and produce a high anion gap acidosis.

A

Salicylic acid and other acid intermediates

34
Q

Metabolic acidosis associated with a normal anion gap is typically characterized by

A

hyperchloremia

35
Q

increases to take the place of the HCO3- ions that are lost.

A

Plasma [Cl-]

36
Q

most commonly results from abnormal gastrointestinal or renal losses of HCO3-, or from excessive intravenous administration of 0.9% NaCl solution.

A

Hyperchloremic metabolic acidosis

37
Q

can potentiate the depressant effects of most sedatives and anesthetic agents on the central nervous and circulatory systems.

A

Acidemia

38
Q

Because most opioids are ___, acidosis can increase the fraction of the drug in the nonionized form and facilitate penetration of the opioid into the brain.

A

weak bases

39
Q

is defined as a primary decrease in Paco2. Mechanism is usually an inappropriate increase in alveolar ventilation relative to CO2 production.

A

Respiratory alkalosis

40
Q

Defined as a primary increase in plasma [HCO3-].

A

Metabolic alkalosis

41
Q

Most cases of metabolic alkalosis can be divided into:

A

(1) those associated with NaCl deficiency and extracellular fluid depletion (often described as chloride sensitive)
(2) those associated with enhanced mineralocorticoid activity, commonly referred to as chloride-resistant

42
Q

DX OF ACID-BASE DISORDERS

A
  1. Examine arterial pH: Is acidemia or alkalemia present?
  2. Examine Paco2: Is the change in Paco2 consistent with a respiratory component?
  3. If the change in Paco2 does not explain the change in arterial pH, does the change in [HCO3-] indicate a metabolic component?
  4. Make a tentative diagnosis.
  5. Compare the change in [HCO3-] with the change in Paco2. Does a compensatory response exist?
43
Q

Disorder:

Primary Change: high PaCO2
Compensatory Response: high HCO3-

A

Respiratory Acidosis

44
Q

Disorder:

Primary Change: low PaCO2
Compensatory Response: low HCO3-

A

Respiratory Alkalosis

45
Q

Disorder:

Primary Change: low HCO3-
Compensatory Response: low PaCP2

A

Metabolic Acidosis

46
Q

Disorder:

Primary Change: high HCO3-
Compensatory Response: high PaCO2

A

Metabolic Alkalosis

IM NEPHRO (7 decks)

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