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Renal - Rao > Acid-Base Physiology > Flashcards

Acid-Base Physiology Flashcards

1
Q

What are the extremes of the pH range that is compatible with life?

A

pH 7.80 and 6.80

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2
Q

What do clinical laboratories measure in arterial samples?

• venous?

A

Arterial
• pH
• Carbon Dioxide
• Oxygen

Venous
• measure total CO2 from which you can calculate Bicarbonate

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3
Q

What is a normal level for total CO2 plus bicarbonate?

• How does Bicarb concentration correspond to this?

A

~25-26 meq/L

• Bicarbonate Concentration Typically 24 mEq/L

So actual CO2 is 1.0 to 1.5 mEq/L

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4
Q

What pH range do you typically see in patients in most clinical scenarios?
• what hydrogen concentration does this correspond to?

A

pH = 7.1 - 7.4

[H+] = 80 at 7.1
[H+] = 40 at 7.4
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5
Q

What is normal pH in a patient?
• normal pCO2
• Normal HCO3-

A

Normal pH:
7.35 - 7.45

Normal pCO2
• 36-44 mmHg (40mmHg)

Normal HCO3-
• 22 - 26 meq/L (24 meq/L)

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6
Q

What is the simplified H/H equation used clinically for acidosis and alkyosis?

A

pH = 24 (CO2)/(HCO3)

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7
Q

What causes Metabolic Disorders of acidosis and alkylosis?

• Respiratory?

A

Metabolic:
Changes in Bicarbonate

Respiratory:
Changes in CO2

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8
Q

What is the Buffer effect?

• is this seen in metabolic or respiratory disorders?

A

Respiratory disorders have buffer effect aka:
• Increased HCO3- with acidosis
• Decreased HCO3- with alkalosis

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9
Q

Where does bicarbonate manifest most of its buffering effects?

A

EXTRACELLULARLY

• Bicarb. is an extracellular Buffer

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10
Q

What is the Isoydric principle?

A

It says that all buffers change in the same direction

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11
Q

If bicarbonate is the main extracellular buffer then what buffers are active in the urine?
• which is the body better at regulating?

A

Phosphate and Ammonia

Body more effectively uses AMMONIA to buffer urine pH

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12
Q

What does it mean if Compensatory (secondary) mechanisms ARE NOT used in acid-base disorders?

A

the Disorder is MIXED

• with both respiratory and renal aspects of buffer system messed up there is no way to compensate

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13
Q

What compensatory mechanisms are used for metabolic and respiratory acidosis and alkylosis?

A

Metabolic Dysfunction = Respiratory Compensation.
• Acidosis = Hyperventilation
• Alkylosis = Hypoventilation

Respiratory Dysfunction = Metabolic Compensation in kidney
• Acidosis = HCO3- reabsorption increased
• Alkylsosis = HCO3- secretion increased

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14
Q

From fastest to slowest what systems react when the H+ and HCO3- balance is thrown off?

A

Immediate:
• Extracellular Fluids
• HCO3- + H+ H2CO3 CO2 + H2O is adjusted

Minutes to Hours:
• Lungs
• BREATHING changes

2-4 Hours:
• Intracellular Fluids
• Phosphate and Protein Buffer Changes

Hours to Days:
• Kidneys
• Hyrogen ion excretion, bicarb reabsorption and Bicarbonate generation

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15
Q

What are the 3 GOLDEN rules of simple acid-base disorders?

A

1) PCO2 and HCO3 always change in the same direction.
2) The secondary physiologic compensatory mechanisms must be present.
3) The compensatory mechanisms never fully correct pH.

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16
Q

What is the general cause of metabolic acidosis?

• what are some things that cause increased acid?

A

General Cause: any increase in acid or loss (failed reabsorption) of bicarbonate

increased acid generation:
Lactic acidosis, Ketoacidosis, ingestion of acids (aspirin, ethylene glycol, methanol), dietary protein intake (animal source)

17
Q

What is the general cause of metabolic acidosis?

• what are some things that cause decreased bicarbonate?

A

General Cause: any increase in acid or loss (failed reabsorption) of bicarbonate

loss of bicarbonate:
Gastrointestinal
•(diarrhea, intestinal fistulas)

Renal: type 2 proximal renal tubular acidosis
• decreased acid excretion (impaired NH4+ excretion)
• Renal failure (reduced GFR) decreased ammonium excretion
• Type I (distal) renal tubular acidosis
•Type 4 renal tubular acidosis (hypoaldosteronism)

18
Q

What is the root cause of Respiratory Acidosis?
• what rapid compensation is always associated with this type of acidosis?
• how effective is this compensation?

A

Induced Hypercapnia (Decreased Alveolar Ventilation)

  • Rapid Increase in Plasma Bicarbonate concentration via Buffer Mechanism
  • only a limited response of ~1-2 mEq/L
19
Q

What is ultimate compensation made in Respiratory Acidosis?

• how long does this take?

A
  • Increasing acid Excretion by NH4+ to GENERATE BICARB

* Takes 2-3 days

20
Q

What is the most common cause of chronic respiratory acidosis?

A

Chronic Obstructive Pulmonary Disease

21
Q

What is the Root cause of Respiratory Alkalosis?

• what are the short term and long term fixes to this problem?

A

• Reduced CO2 due to INCREASED Alveolar Ventilation

Short Term:
• Minimal Change in Buffer to lower serum Bicarb

Long Term (1-2 days):
• More Bicarb excreted
• Less NH4+ excreted

22
Q

What are some diseases that cause Respiratory Alkalosis?

A

ANYTHING that causes HYPOXIA

  • Anxiety, Hysteria
  • Fever
  • Salicylate Intoxication
  • CNS diseases (trauma, stroke, etc.)
  • Congestive Heart Failure
  • Hepatic Insufficiency
  • Pregnant Women
23
Q

Would you expect an acute or chronic respiratory disorder to have a greater change in pH associated with it?
why?

A

Acute, because there is less time for the long term NH4+ excretion compensatory mechanism to kick in

24
Q

Are respiratory or Metabolic Disorders associated with an ion gap?

A

Metabolic disorders is where you will see ion gap

• In respiratory disorders the Cl changes equally and inversely with plasma HCO3

25
Q

T or F: Acid Base disorders cause radical changes in Plasma Sodium

A

False

26
Q

Metabolic Alkalosis
• General Cause
• Specific Causes

A

Processes that raise plasma bicarbonate concentration

Etiology: Loss of hydrogen ion from the GI tract (vomiting) or into the urine (diuretic therapy)

Excessive urinary net acid excretion (primary hyperaldosteronism)

27
Q

Differentiate between a chloride responsive and chloride resistant Alkylosis.

A

Chloride Responsive Metabolic Alkylosis is usually associated with Hypovolemic states

Chloride Responsive:
• Urine Cl less than 20 meq/l (usually less than 10 meq/l) - indcates that the kidney’s are doing what they should and excreting more HCO3- and taking up more Cl- into the serum

Chloride Resistant:
• Urine Cl greater than 20 meq/l (usually more than 50 meq/l) - indicates that you are still taking up a lot of bicarb and excreting a lot of Cl-

28
Q

Differentiate between Acute and Chronic respiratory Acidosis and Alkylosis.

A

Acute Respiratory Acidosis:
HCO3- increases 1 mEq for each 10 mm increase in PCO2

Chronic Respiratory Acidosis:
HCO3- increases 4 mEq for each 10 mm increase in PCO2

Acute Respiratory Alkalosis:
HCO3- decreases 2 mEq for each 10 mm decrease in PCO2

Chronic Respiratory Alkalosis:
HCO3- decreases 5 mEq for each 10 mm decrease in PCO2

29
Q

In what two places in the nephron can you work to correct HCO3- concentrations?

A
  • Proximal Tubule

* Collecting Duct (alpha or beta intercalated cells)

30
Q

In what Acid-Base disorder do we see an ion gap?

• why does this happen/explain the mechanism of the ion gap?

A
  • Strong Acid HA fully dissociates at physiologic pH (into H+ and A-)
  • H+ component is removed via HCO3-
  • A- is either reabsorbed or secreted
  • Reabsorption happens if A- is something that the body doesn’t want to get rid of (e.g. Lactate etc.)

Absorbed anion takes the place of the normal increase in Chloride that would replace decreased HCO3- (w/ less competition in the PT

31
Q

What is the formula for Ion Gap?

• what unmeasured ions may account for this gap?

A

• Ion Gap = Na - (Cl + HCO3-)

  • Protein
  • PO4
  • SO4
  • Organic Acids
32
Q

What are some major causes of an increased ion gap?

A
  • Renal Failure
  • Lactic Acidosis
  • Ketoacidosis
  • Ingestions: Asprin, Ethylene Glycol, Methanol
33
Q

T or F: you can have metabolic acidosis without an ion gap.

A

True, this occurs in situations of Renal Tubular Acidosis, Diarrhea, and some cases of chronic renal failure

34
Q

Where is the main place that bicarbonate is filtered?

A
  • Proximal Tubules

* Final Excretion of ~50-100 meq/d occurs primarily in the collecting duct

35
Q

How is phosphate excretion maintained?

• what role does phosphate play in acid-base balance of urine?

A

Urinary Excretion of Dietary Phosphate

• It is a good urinary buffer especially at low urinary pH (levels can be raised up to 40 mEq/d)

36
Q

Why is Ammonium a better buffer of urinary acid load than phosphate?

A
  • It can be increased to MUCH greater amounts (300 mEq/d) if necessary
  • NH4+ is also Lipid Insoluble and thus is TRAPPED in the Urinary Lumen
37
Q

What is the Urine Anion Gap?

• what is it used for?

A

Urine Anion Gap
• Indirect estimate of NH4+ excretion

Calculation:
• (Na + K) - Cl

38
Q

What values are you looking for with Urine Anion Gap?

A

Probably looking for correction of respiratory acidosis

UAG = (Na + K) - Cl

Normally POSITIVE at ~10 mEq/l, becomes more positive and possibly even negative with increased urinary NH4+ excretion

39
Q

What is the major way the Na and Cl differ when it comes to acid/base disorders?

A

Na ALWAYS remains constant

Cl CHANGES

***If you see a normal Na with messed up Cl then think about acid-base disorders

Renal - Rao (13 decks)

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