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CPR Exam 3 > Approach To Acid-Base Disorders DSA > Flashcards

Approach To Acid-Base Disorders DSA Flashcards

1
Q

Arterial pH: ________

Intracellular pH: _________

A
  • Arterial pH: 7.35 - 7.45
  • Intracellular pH: 7.0 - 7.3
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2
Q

Despite constant production of acidic metabolites, our pH is maintained by intracellular and extracullar buffering systems.

What is the most important extracellular buffering system?

A

Bicarbonate buffer system (HCO3- and CO2)

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3
Q

What is the acid-base equillibrium equation?

A

CA (present in lung alveoli and renal tubular epithelial cells)

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4
Q

What is the Henderson Hassalbalch Equation?

A
  • ↑ HCO3-; ↑ pH
  • ↑ pCO2 (H+); ↓ pH
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5
Q

What are the definitions of:

  1. Acidosis/alkalosis
  2. Acidemia/alkalemia
A
  1. Acidosis/alkalosis= disorder altering H+ levels
  2. Acidemia/alkalemia= prescence of high or low pH in blood
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6
Q

Arterial Blood Gas Levels (ABG)

Normal levels:

  1. pH
  2. HCO3
  3. PCO2
  4. Anion gap
  5. Osmolality Gap
A
  1. pH: 7.35-744
    • Acidosis= pH <7.35
    • Alkalosis= pH >7.44
  2. HCO3
    • 24 mEq/L
  3. pCO2
    • 40 mmHg
  4. Anion gap
    • 12
  5. Osmolality Gap
    • 10 mmol/L
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7
Q

________ regulates pH by altering CO2.

How?

A

Lungs regulate pH by altering CO2.

  • ↑ RR (hyperventilation) = ↑ CO2 blown off = ↑ pH; more basic
  • ↓ RR (hypoventilation) = ↓ CO2 blown off = ↓ pH; more acidic
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8
Q

________ regulates pH by altering HCO3-.

How?

A

Kidneys regulates pH by altering HCO3-.

  • To maintain HCO3- as a buffer in the plasma, the kidneys need to do 2 things:
      1. Reabsorb all filtered HCO3- and generate new HCO3-.
        * If not reabsorbed, makes a alkaline urine.
      1. Excrete H+ protons
        * If excreted, excretes an acidic urine.
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9
Q

•Metabolic Acidosis

  • Low serum ____

•Metabolic Alkalosis

  • High serum ____

•Respiratory Acidosis

  • High _____

•Respiratory Alkalosis

  • Low ____
A

•Metabolic Acidosis

  • Low serum HCO3-

•Metabolic Alkalosis

  • High serum HCO3-

•Respiratory Acidosis

  • High pCO2

•Respiratory Alkalosis

  • Low pCO2
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10
Q

Types of Metabolic Acidosis

A
  1. High anion gap metabolic acidosis (HAGMA)
  2. Normal anion gap metabolic acidosis (NAGMA)
    • AKA hyperchloremic acidosis
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11
Q

Types of Metabolic Alkalosis

A
  1. Saline-Responsive (hypovolemia)
    • AKA contraction alkalosis (or Cl- deficiency alkalosis)
  2. Saline-Non-responsive (euvolemia)
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12
Q

Types of Respiratory Acidosis and Respiratory Alkalosis

A

Acute and Chronic

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13
Q

COMPENSATION:

  • If the kidney caused acidosis/alkalosis, the _____ compensates
  • If the lung caused acidosis/alkalosis, the ______ compensates.
A
  • If the kidney caused acidosis/alkalosis, the lung compensates
  • If the lung caused acidosis/alkalosis, the kidney compensates.
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14
Q

How do we compensate for metabolic acidosis?

A

Induce respiratory alkalosis

  • Hyperventilate (↑ RR) = blow out more CO2 = ↓ pCO2 = respiratory alkalosis ( ↑ pH)
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15
Q

How do we compensate for metabolic alkalosis?

A

Induce respiratory acidosis

Hypoventilate (↓ RR) = retain CO2 = ↑ pCO2 = respiratory acidosis

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16
Q

How do you compensate for respiratory acidosis (↑ pCO2)?

A

Induce metabolic alkalosis

  • Kidney will reclaim and regenerate HCO3- = ↑ HCO3- = ↑ in pH
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17
Q

How do you compensate for respiratory alkalosis (↓ pCO2)?

A

Induce metabolic acidosis

  • Kidney will ↓ reclaim and regeneration of HCO3- = ↓ HCO3- = ↑ in pH
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18
Q

Symptoms in patients with acidosis:

A
  1. Hyperventilation (trying to blow out CO2)
  2. Depression of myocardial contractility
  3. Cerebral vasodilation (increase cerebral blood flow => increase in ICP)
  4. If high CO2 levels => CNS depression
  5. Hyperkalemia (high H+ exchanges with K+)
  6. Shift in oxyHB dissociation curve (Bohr) effect to the R => decreased pH leads to HB releasing more O2 and it is less saturated
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19
Q

Symptoms in patients with alkalosis:

A
  1. Hypoventiliation
  2. Depression of myocardial contractility
  3. Cerebral vasoconstriction (Decrease in cerebral blood flow),
  4. Hypokalemia
  5. Shift in oxyHb dissociation curve to the left
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20
Q

How do we approach acid-base problems?

A
  1. Check pH (<7.35 => acidosis; >7.45= alkalosis) to determine if alkalosis or acidosis
  2. Check HCO3- and pCO2 to determine if metabolic or respiratory
  3. Determine acid-base disorder
  • Acidosis + low HCO3- = metabolic acidosis
  • Acidosis + high pCO2 = respiratory acidosis
  • Alkalosis + high HCO3- = metabolic alkalosis
  • Alkalosis + low pCO2 = respiratory alkalosis

4.For metabolic acidosis only: calculate anion gap

  • If hypoalbunemia, calculate the the corrected anion gap.
  • If HAGMA is present:
    • calculate the osmolar gap to screen for possible alchol ingestion
    • calculate the delta-delta gap to screen for additional NAGMA or metabolic alkalosis.
  1. Calculate compensation for primary acid-base disorder
  • Compensated => only a simple acid-base disorder is present
  • Not compensated =>
    • Combined respiratory/metabolic
    • 2 metabolic disorders
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21
Q

In most acid base disorders, _____ HCO3 and pCO2 are abnormal.

A

BOTH. One if is the culprit and other is compensatoery change. You have to figure out which is the problem

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22
Q

What 2 pathologic states can both acidotic and akalotic states occur?

A
    1. Vomitting (acidotic)
    1. Diarrhea (alkalotic)
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23
Q

How do we determine if there are 2 disorders present?

A

Determine the expected response by using renal formulas

  • Expected HCO3- for respiratory disorders
  • Expected CO2- for metabolic disorders
    • If actual does not equal expected => a 2nd disorder is present.
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24
Q

KEY: What is a classic scenario for mixed disorders?

A
  • On its own, a body cannot compensate back to a NL pH.
  • Thus, if a patient has a [NL pH with abnormal HCO3- and CO2-], it is a mixed disorder.
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25
Q

How do we determine is the lungs properly compensates for metabolic acidosis?

A
  • Winter’s formula

Tells you the expected CO2 when metabolic acidosis is compensated with respiratory alkalosis
* Actual is not equal to expected = mixed disorder is present

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26
Q

Is this compensated?

A

Yes.

Perform Winter’s formula:

Expected pCO2= 22 +/- 2

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27
Q

Compensated?

A

NO. Right away, we know that there are 2 disorders present because pCO2 is NL. In a metabolic acidosis, pCO2 should be compensating.

Use Winters formula.

Expected pCO2 = 26 +/- 2

pCO2 > expected; concomitant respiratory acidosis

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28
Q

How do we determine is the lungs properly compensates for metabolic alkalosis?

A
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29
Q

How can we determine if the kidney compensate for respiratory acidosis?

A
  • Acute
    • ∆[HCO3-]= ∆pCO2/10
      • ​HCO3- will ↑ by [1 mEq/L] for every [10 mmHg] ↑ in PCO2 from NL (40)
  • Chronic
    • ∆[HCO3-]= 3.5 * ∆pCO2/10
      • ​HCO3- will ↑ by [3.5 mEq/L] for every [10 mmHg] ↑ in PCO2 from NL (40)
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30
Q

How do we determine if the kidney compensates for respiratory alkalosis?

A

Acute

  • ∆[HCO3-]= 2* ∆pCO2/10
    • ​HCO3- will ↓ by [2 mEq/L] for every [10 mmHg] ↓ in PCO2 from NL (40)

Chronic

  • ∆[HCO3-]= 5 * ∆pCO2/10
    • ​HCO3- will ↓ by [5 mEq/L] for every [10 mmHg] ↓ in PCO2 from NL (40)
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31
Q
A
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32
Q

How Many Acid-Base Disturbances Can Be Present at Once?

A

Three.

Not 4; bc a person can only breathe fast or slow, not both

33
Q

Anion gap is a _______ concept in clinical medicine and is calculated to _________.

A

fabricated, it does not exist in reality

specify the type of metabolic acidosis (HAG vs NAG)

34
Q

In the body, what is the distribution of anions and cations?

A

all cations (+) and anions (-) equal each other. Thus, there is net neutrality

35
Q

Cations include:

A

Na+, K+, Ca+, Mg+, Protein+ (not many)

36
Q

Anions include:

A

Cl-, HCO3-, Proteins (especially, Albumin-), HPO4-, SO4-2, and organic anions

37
Q

Since we do not routinely measure EVERY cation+ and anion- in the serum, a _______________ exists

Why are anions important?

A

anion gap exists (we only measure Na, Cl- and HCO3-)

Anions are important because they are accompanied by protons (H+ ions), which are buffered by HCO3-

38
Q

Why do you calculate anion gap?

How do you calculate anion gap?

What is a NL AG?

A

With metabolic acidosis, always calculate the anion gap to differentiate between HAGMA or NAGMA.

  • Anion gap = Na+ - (HCO3- + Cl-)
    • NL AG = 12 ± 2
39
Q

What is a trick to differentiate between HAG and NAG?

A

Look at Cl- levels!

  • If high; NAGMA (hyperchloremic)
  • If low/NL; HAGMA
40
Q

What are other uses of anion gap?

A
  • Diagnose paraproteinemias
    • Low anion gap
  • Diagnose lithium, bromide, or iodide intoxications
    • Low or negative anion gap values
  • For quality control monitoring in chemical laboratories
41
Q

In AG acidosis, there is a _____ in HCO3- and a _____ in organ anions, causing a ___ anion gap.

A
  • decrease
  • increase
  • high
42
Q

In hyperchloremic acidosis (NAG), there is a ______ in HCO3- and an _____ in Cl-, causing a ______ anion gap.

A
  • decrease
  • increase
  • NL
43
Q

What conditions result in hyperchloremic metabolic acidosis (NAGMA)?

A
  • 1. RTA (renal tubular acidosis)
  • 2. Diarrhea

HCO3- and Na+ are lost d/t volume contraction. This causes kidney to hold onto NaCl.

44
Q

How does hypoalbuminemia affect the anion gap?

A

falsely ↓ anion gap

45
Q

How do we determine the real anion gap in a patient with metabolic acidosis and hypoalbuminemia, which will falsey lower the AG?

A

[1 g/dL ↓ in albumin] = [↓ AG by 2.5]

resulting in a falsley lowered AG.

Thus, to figure out real AG: for every

1 g/dL ↓ in albumin, we + 2.5 to the calculated AG.

46
Q

Why does the anion gap matter?

A

Determines if we have acidosis as a result of:

  • Primary loss of HCO3-
    • Our body compensates by holding onto Cl-, causing a NAG
  • Primary retention of an acid
    • HCO3- falls w/o ↑ in Cl-, causing an ↑ in AG.
      • Another, unmeasured anion (acids) will ↑ to compensate for the AG.
47
Q

4Calculation of Osmolar Gap

What is it used for?

A
  • Osmolar gap= [measured serum osmolality] - [calculated serum osmolality]
    • Calculated serum osmolality= 2Na + (Glucose/18) + (BUN/2.8)
      • NL: 275-290 mOsm/L
    • NL: < 10 mOsm/L
    • If > 10 mOsm/L => solutes were added to blood.
  • Clinically used to screen for:
      1. Ingestion of alcohol, particularly in HAGMA (when >20)
      1. Ketoacidosis
      1. Lactic acidosis
48
Q

When is the Delta-Delta Gap used?

A

Used in patients with HAGMA to determine if there is a co-existing NAGMA or metabolic alkalosis.

49
Q

How to calculate the Delta-Delta Gap?

A

For every ↑ in AG above NL, an equal ↓ in HCO3- should be present.

∆∆= ∆AG/ ∆HCO3-

  • ∆AG= AG-12
  • ∆HCO3-= 24 - [HCO3-]
  • Results
    • ∆∆ ~1= NL
    • ∆∆ <1 = Second, NAGMA is present
      • ​HCO3- is too low.
    • ∆∆ >1= Second, metabolic alkalosis is present.
      • ​HCO3- is too high
50
Q

In a HAGMA, if the AG is 20, what should the HCO3- be?

A

~16

AG is 8 above NL. Thus, HCO3- should be 24-8= 16.

51
Q

GOLD MARK

A

GOLD MARK is the DDx for HAGMA

  1. Glycol (ethylene and propylene)
  2. Oxoproline (pryroglutamic acid)
    1. ​D/t acetominophen toxicity
  3. L-lactic acidosis
  4. D-lactic acidosis​
  5. Methanol
  6. Aspirin
  7. Renal failure
  8. Ketoacidosis (alcholic, DB, starvation)
52
Q

D-lactic acidosis is a common cause of HAGMA.

What can cause D-lactic acidosis?

A
  1. Colonic metabolization of glucose, starch, other carbs by bacteria that occurs in short bowel syndromes
53
Q

Pyroglutamic acidosis occurs due to _______ toxicity and is often seen in __________ or ________.

How is it diagnosed?

A
  • Acetominophen toxicity
  • Malnourished/critically ill
  • Dx: urinary organic acid screen
54
Q

ME DIE + [what else]?

A

ME DIE is the DDx for osmolar gap

  • Methanol
  • Ethanol
  • Diethylene glycol
    • ​D/t mannitol diuretic
  • Isopropyl alchol (rubbing alchol) that is NOT assx with metabolic acidosis
  • Ethylene glycol

Also caused by:

  • propylene glycol
  • ketoacidosis and lactic acidosis (cause smaller ↑ in osmolar gap)
55
Q

Acidosis/alkalosis is associated with hyperkalemia

A

Acidosis

  • H+ ions enter the cells and K+ exit the cell
56
Q

Acidosis/alkalosis is associated with hypOkalemia

A

Alkalosis

  • H+ ions exit cells, K+ enter
57
Q

DURHAAM

A

DURHAM is the DDx for non-anion gap metabolic acidosis (NAGMA); primary loss of HCO3-; hold onto Cl-

  1. Diarrhea***
  2. Ureteral diversion or fistula**
  3. Renal tubular acidosis*
  4. Hyperalimentation (enteral nutrition or total parental nutrition, TPN)
  5. Acetazolamide (CA inhibitor)
  6. Addisons disease (adrenal insuffiency)
  7. Miscellanous (tuloene toxicity – glue sniffing, pancreatic fistula, meds)
58
Q

Renal tubular acidosis causes normal anion gap MA.

How can we differentiate them?

A

Plasma K+ (NL= 3.5-5)

  • Hyperkalemia (more than 5.0)
    • Type 4
  • Hypokalemia (less than 3.5)
    • Type 1; defect in distal tubule
    • Type 2; defect in proximal tubule
60
Q

RTA is a cause of non-anion gap acidosis (NAGMA).
Many patients are asymptomatic and blood work present with low ____ or abnormal ____.

A
  • Low HCO3-
  • Abnormal K+
61
Q

Type 1 RTA

  • Issue:
  • Mechanism:
  • Result:
  • Key symptoms:
  • Etiology:
  • Dx:
  • Tx:
A
  • Issue: Distal nephron cannot acidify urine
  • Mechanism:
    • H+ ions cannot be secreted into urine via a-intercalated cell either of 2 things:
      • Defect in [H/K ATpase] or [H+ ATPase pump], causing acidemia
      • Secreted H+ ions flow back into tubular cells due to abnormally permeable DT and CD, caused by amphotericin or funal infection
    • Cannot reabsorb K+, thus, more is excreted (hypokalemia), causing us to hold onto H+
  • Result:
    • Very low HCO3- (less than 10)
    • Urine pH is high (>5.5)
  • Key symptoms:
    • Chronic kidney stones (sometimes bilateral)
    • Nephrocalcinosis (acidosis causes increase in Ca2+ from bones) and suppresses resorption (high Ca2+ in urine)
    • Rickets
    • Growth failure in kids)
  • Etiology:
    • AI diseases (Sjrogens, RA)
    • Glue sniffing (Toluene)
  • Dx:
    • NAGMA
    • Urine pH is above high (above 5.5)
    • Severe hypokalemia
    • UAG is +, indicating that the distal nephron cannot acidify urine
  • Tx:
    • Sodium bicarb
62
Q

What is the purpose of the UAG?

A
  • Used to differentiate renal from non-renal causes of normal anion gap metabolic acidosis.
63
Q

What is the mechanism by which UAG works?

A
  • In acidosis, kidneys get rid of acid by excreting NH4.
  • However, NH4 (acid) cannot be measured directly. When NH4+ is secreted, it leaves with Cl-. Thus, UAG is a marker of ammonium excretion via NH4Cl
64
Q

Calculate UAG

+/- indicates:

A

UAG= Urine (Na + K - Cl).

When body is excreting NH4, Cl rises, causing UAG to become (-) when acid (H+) is being excreted

  • - UAG: distal nephron is acidifying urine appropriately
  • + UAG: distal nephron is acidifying urine inappropriately
65
Q

When is UAG (-)?

A
  1. GI metabolic acidosis (diarrhea)
  2. Type 2 RTA, where a defect is present in proximal tubule, NOT distal tubule
66
Q

When is UAG (+)?

A
  1. Distal RTA (Kidneys cannot excrete H+ and NH4 and Cl do not increase)
67
Q

H+ secretion leads to ___________.

A

HCO3- reabsorption

68
Q

_Type 2 RTA (____)_

  • Issue:
  • Mechanism:
  • Result:
  • Key symptoms:
  • Etiology:
  • Dx:
  • Tx:
A

Proximal RTA (Type 2)

  • Issue: Proximal tubule cannot reabsorb HCO3-
  • Mechanism:
    • HCO3- filtered load exceeds PT reabsorptive capacity, causing HCO3- loss in urine and low serum HCO3-.
      • As serum HCO3- decreases, the resorptive capacity of PT, TAL and DT are not overwhelmed. Thus, there is no further HCO3- loss in the urine and serum HCO3- stabilizes at a lower level, creating a new steady state.
  • Result:
    • Urine pH less than 5.5
      • Initially, pH may be high due to increase HCO3- excretion because PT cannot reabsorb HCO3-.
      • However, distal intercalated cells are NL and DT will excrete H+ ions and urine becomes acidic.
    • Low HCO3- (12-20)
    • Hypokalemia (more mild than type 1)
      • Loss of HCO3- resorption causes diuresis => volume contraction => increase in aldosterone => Increase in K excretion => hypokalemia
  • Key symptoms:
    • ​No kidney stones
  • Etiology:
    • ​Primary or secondary
    • Cystinosis (children)
    • _Fanconi syndome (_adults)
      • ​Can cause multiple myeloma => type 2 RTA
      • Can directly cause Fanconi
  • Dx:
    • ​Urine pH can be high or low depending on serum HCO3- levels
      • ​If in a new steady state, urine pH is less than 5.5
    • UAG can be + or -
  • Tx: Sodium Bicarb
69
Q

What is the only RTA that causes hypERkalemia (high K+)

70
Q

Type 4 RTA

  • Issue:
  • Mechanism:
  • Result:
  • Key symptoms:
  • Dx:
  • Tx:
A
  • Issue:
    • DT does not respond to aldosterone due to either aldosterone deficiency/resistance, causing impaired excretion of H+ and K+
  • Mechanism/Etiology:
    • ↓ aldosterone
      • Dt: DM, Drugs (NSAIDS, ACE-I/ARBS, high dose of heparin)
    • CD is resistant to aldosterone
      • Dt: Interstitial renal disease (sickle cells nephopathy, obstructive, lupus) or drugs (amiloride, triamterene, spironolactone, trimethoprim, etc)
    • Both causes ↓ Na+ reabsorption by prinicple cells => ↓ luminal negativity of CD => ↓ driving force for H+ secretion
    • Aldosterone def/resistance => ↓ excretion of K+ => retention of K+ => Hyperkalemia
      • hyperkalemia causes pH of cells in PT to ↑ => prevent ammoniagenesis => less excretion of NH4+ => acidosis
  • Result:
    • Urinary pH is more than 5.5.
    • Hyperkalemia
  • Key symptoms:
    • Most are asymptomatic
    • 50-70s with a history of DB or CKD
  • Dx:
    • Variable urine pH, usually > 5.5
      • UAG
  • Tx:
    • Fludrocortisone (mineralcorticoid)
71
Q

5 most common DDx of Metabolic Alkalosis

A
  1. Hypokalemia
  2. Vomitting or nasogastric tube suctioning
    1. GI loss of HCl
  3. Diuretics (thiazide and loop)
  4. Volume depletion
    • Contraction alkalosis: volume depletion d/t Cl- depletions => + RAAS and aldosterone secretion, which worsens metabolic alkalosis
  5. Excess of mineracortcoids
72
Q

Any factor that ↑ Na+ reabsorption, will do what?

A
  • cause an ↑ in H+ secretion => ↑ HCO3- reabsorption => metabolic alkalosis
73
Q

What mechanism do excess of mineralcorticoids leads to metabolic alkalosis?

A

Mineralcorticoids ↑ Na+ reabsorption => ↑ H+ secretion => ↑ HCO3- reabsorption => metabolic alkalosis

74
Q

Describe the differences between alpha and beta intercalated cells.

A

Mirror images of one another

  • Alpha intercalated cells
    • Apical (lumen): H+/K+ antiporter & H+ ATPase
    • BL: HCO3-/Cl- exhanger
  • Beta intercalated cells
    • Apical (lumen): HCO3-/Cl- exchanger
    • BL: H/K antiporter & H+ ATPase
75
Q

In a B-intercalated cells, HCO3- made in the cells exits via the ____________ into the lumen.

A

Cl-/HCO3- exchanger

76
Q

In contraction alkalosis (volume depletion d/t ↓Cl), what must be given to help secrete HCO3-?

A

Cl-, to power the HCO3-/Cl exchanger that will secrete HCO3-.

77
Q

DDx Respiratory Alkalosis

A

Anything that increase RR/tidal volume

  1. Pneuonia
  2. PE
  3. Pulmonary edema
  4. Pneumothorax
  5. Pregnany
78
Q

______ can cause respiratory alkalosis and HAGMA.

79
Q

DDx for Respiratory Acidosis

A
  1. Anything that ↓ RR/tidal volume, increase dead space or worsens airway obstruction
    • PE increases deadspace
  2. Inadequate ventilator settings
  3. Increase in CO2 production
    • increased carb diet
    • Hyperthermia
    • Seizures

CPR Exam 3 (10 decks)

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