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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
How do we determine is the lungs properly compensates for **metabolic acidosis?**
* **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
26
Is this **compensated**?
**Yes.** Perform Winter's formula: **Expected pCO2= 22 +/- 2**
27
Compensated?
**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**
28
How do we determine is the lungs properly compensates for **metabolic alkalosis?**
29
How can we determine if the kidney compensate for **respiratory acidosis?**
* _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)
30
How do we determine if the kidney compensates for **respiratory alkalosis?**
**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)
31
32
How Many Acid-Base Disturbances Can Be Present at Once?
**Three**. Not 4; bc a person can only breathe fast or slow, not both
33
**Anion gap** is a _______ concept in clinical medicine and is calculated to \_\_\_\_\_\_\_\_\_.
**fabricated**, it does not exist in reality specify the type of **metabolic acidosis (HAG vs NAG)**
34
In the body, **what is the distribution of anions and cations?**
all cations (+) and anions (-) **equal each other**. Thus, there is **net neutrality**
35
**Cations** include:
**Na+, K+, Ca+, Mg+, Protein+ (not many)**
36
**Anions** include:
**Cl-**, **HCO3-**, **Proteins** (especially, **Albumin**-), **HPO4**-, **SO4-2**, and **organic anions**
37
Since we do not routinely measure ***EVERY*** cation+ and anion- in the serum, a _______________ exists Why are anions important?
**_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
Why do you calculate **anion gap?** How do you calculate **anion gap?** What is a NL AG?
With metabolic acidosis, always calculate the anion gap to **differentiate between HAGMA or NAGMA.** * **Anion gap = Na+ - (HCO3- + Cl-)** * NL AG = 12 ± 2
39
What is a trick to differentiate between **HAG** and **NAG**?
**_Look at Cl- levels!_** * If high; NAGMA (hyperchloremic) * If low/NL; HAGMA
40
What are other uses of **anion gap**?
* 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
In **AG acidosis**, there is a _____ in HCO3- and a _____ in organ anions, causing a ___ anion gap.
* **decrease** * **increase** * **high**
42
In **hyperchloremic acidosis (NAG),** there is a ______ in HCO3- and an _____ in Cl-, causing a ______ anion gap.
* **decrease** * **increase** * **NL**
43
What conditions result in **hyperchloremic metabolic acidosis (NAGMA)?**
* **1. RTA (renal tubular acidosis)** * **2. Diarrhea** HCO3- and Na+ are lost d/t volume contraction. This causes kidney to hold onto NaCl.
44
How does **hypoalbuminemia** affect the **anion gap**?
**falsely ↓ anion gap**
45
How do we determine the **real anion gap** in a patient with metabolic acidosis and hypoalbuminemia, which will falsey lower the AG?
**[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
Why does the **anion gap** matter?
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
**_4Calculation of Osmolar Gap_** What is it used for?
* **_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) * 2. **Ketoacidosis** * 3. **Lactic acidosis**
48
When is the **Delta-Delta Gap** used?
Used in patients with **HAGMA** to determine if there is a **co-existing** **NAGMA** or metabolic alkalosis.
49
How to calculate the **Delta-Delta Gap?**
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
In a **HAGMA**, if the _AG is 20_, what should the HCO3- be?
**_~16_** AG is 8 above NL. Thus, HCO3- should be 24-8= **16.**
51
**GOLD MARK**
_**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
**D-lactic acidosis** is a common cause of HAGMA. What can cause **D-lactic acidosis?**
1. Colonic metabolization of glucose, starch, other carbs by bacteria that occurs in **short bowel syndromes**
53
**Pyroglutamic acidosis** occurs due to _______ toxicity and is often seen in __________ or \_\_\_\_\_\_\_\_. How is it diagnosed?
* **Acetominophen toxicity** * **Malnourished/critically ill** * **Dx**: urinary organic acid screen
54
**ME DIE + [what else]?**
**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
_Acidosis/alkalosis_ is associated with **hyperkalemia**
**Acidosis** * H+ ions enter the cells and K+ exit the cell
56
_Acidosis/alkalosis_ is associated with **hypOkalemia**
**Alkalosis** * H+ ions exit cells, K+ enter
57
**DURHAAM**
**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
_Renal tubular acidosis_ causes **normal anion gap MA.** How can we differentiate them?
**_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_
59
60
**RTA** is a cause of non-anion gap acidosis (NAGMA). Many patients are **asymptomatic** and blood work present with **low** ____ or **abnormal** \_\_\_\_.
* **Low HCO3-** * **Abnormal K+**
61
**_Type 1 RTA_** * Issue: * Mechanism: * Result: * Key symptoms: * Etiology: * Dx: * Tx:
* **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
What is the purpose of the **UAG**?
* Used to differentiate renal from non-renal causes of **normal anion gap metabolic acidosis.**
63
What is the mechanism by which **UAG** works?
* 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
**_Calculate UAG_** +/- indicates:
**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
When is **UAG (-)**?
1. **GI metabolic acidosis (diarrhea)** 2. **Type 2 RTA,** where a defect is present in proximal tubule, NOT distal tubule
66
When is **UAG (+)?**
1. **Distal RTA** (Kidneys cannot excrete H+ and NH4 and Cl do not increase)
67
**H+ secretion** leads to \_\_\_\_\_\_\_\_\_\_\_.
**HCO3- reabsorption**
68
_**Type 2 RTA (\_\_\_\_)**_ * Issue: * Mechanism: * Result: * Key symptoms: * Etiology: * Dx: * Tx:
**_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
What is the only RTA that causes **hypERkalemia** (high K+)
**Type 4**
70
**_Type 4 RTA_** * Issue: * Mechanism: * Result: * Key symptoms: * Dx: * Tx:
* **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
_5 most common DDx of **Metabolic Alkalosis**_
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
Any factor that **↑ Na+ reabsorption**, will do what?
* cause an **↑ in H+ secretion** =\> **↑ HCO3- reabsorption** =\> **metabolic alkalosis**
73
What mechanism do excess of mineralcorticoids leads to **metabolic alkalosis?**
**Mineralcorticoids** ↑ Na+ reabsorption =\> ↑ H+ secretion =\> ↑ HCO3- reabsorption =\> **metabolic alkalosis**
74
Describe the differences between **alpha** and **beta intercalated cells.**
**_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
In a **B-intercalated cells,** _HCO3-_ made in the cells exits via the ____________ into the **lumen**.
**Cl-/HCO3- exchanger**
76
In **contraction alkalosis (volume depletion d/t ↓Cl)**, what must be given to help secrete HCO3-?
**Cl-,** to power the HCO3-/Cl exchanger that will secrete HCO3-.
77
**DDx Respiratory Alkalosis**
**_Anything that increase RR/tidal volume_** 1. Pneuonia 2. PE 3. Pulmonary edema 4. Pneumothorax 5. Pregnany
78
\_\_\_\_\_\_ can cause **respiratory alkalosis** and **HAGMA.**
**Aspirin**
79
DDx for **Respiratory Acidosis**
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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