Approach To Acid-Base Disorders DSA Flashcards
Arterial pH: ________
Intracellular pH: _________
- Arterial pH: 7.35 - 7.45
- Intracellular pH: 7.0 - 7.3
Despite constant production of acidic metabolites, our pH is maintained by intracellular and extracullar buffering systems.
What is the most important extracellular buffering system?
Bicarbonate buffer system (HCO3- and CO2)
What is the acid-base equillibrium equation?
CA (present in lung alveoli and renal tubular epithelial cells)

What is the Henderson Hassalbalch Equation?
- ↑ HCO3-; ↑ pH
- ↑ pCO2 (H+); ↓ pH

What are the definitions of:
- Acidosis/alkalosis
- Acidemia/alkalemia
- Acidosis/alkalosis= disorder altering H+ levels
- Acidemia/alkalemia= prescence of high or low pH in blood
Arterial Blood Gas Levels (ABG)
Normal levels:
- pH
- HCO3
- PCO2
- Anion gap
- Osmolality Gap
-
pH: 7.35-744
- Acidosis= pH <7.35
- Alkalosis= pH >7.44
-
HCO3
- 24 mEq/L
-
pCO2
- 40 mmHg
-
Anion gap
- 12
-
Osmolality Gap
- 10 mmol/L
________ regulates pH by altering CO2.
How?
Lungs regulate pH by altering CO2.
- ↑ RR (hyperventilation) = ↑ CO2 blown off = ↑ pH; more basic
- ↓ RR (hypoventilation) = ↓ CO2 blown off = ↓ pH; more acidic
________ regulates pH by altering HCO3-.
How?
Kidneys regulates pH by altering HCO3-.
- To maintain HCO3- as a buffer in the plasma, the kidneys need to do 2 things:
-
Reabsorb all filtered HCO3- and generate new HCO3-.
* If not reabsorbed, makes a alkaline urine.
-
Reabsorb all filtered HCO3- and generate new HCO3-.
-
Excrete H+ protons
* If excreted, excretes an acidic urine.
-
Excrete H+ protons
•Metabolic Acidosis
- Low serum ____
•Metabolic Alkalosis
- High serum ____
•Respiratory Acidosis
- High _____
•Respiratory Alkalosis
- Low ____
•Metabolic Acidosis
- Low serum HCO3-
•Metabolic Alkalosis
- High serum HCO3-
•Respiratory Acidosis
- High pCO2
•Respiratory Alkalosis
- Low pCO2
Types of Metabolic Acidosis
- High anion gap metabolic acidosis (HAGMA)
-
Normal anion gap metabolic acidosis (NAGMA)
- AKA hyperchloremic acidosis
Types of Metabolic Alkalosis
-
Saline-Responsive (hypovolemia)
- AKA contraction alkalosis (or Cl- deficiency alkalosis)
- Saline-Non-responsive (euvolemia)
Types of Respiratory Acidosis and Respiratory Alkalosis
Acute and Chronic
COMPENSATION:
- If the kidney caused acidosis/alkalosis, the _____ compensates
- If the lung caused acidosis/alkalosis, the ______ compensates.
- If the kidney caused acidosis/alkalosis, the lung compensates
- If the lung caused acidosis/alkalosis, the kidney compensates.
How do we compensate for metabolic acidosis?
Induce respiratory alkalosis
- Hyperventilate (↑ RR) = blow out more CO2 = ↓ pCO2 = respiratory alkalosis ( ↑ pH)
How do we compensate for metabolic alkalosis?
Induce respiratory acidosis
Hypoventilate (↓ RR) = retain CO2 = ↑ pCO2 = respiratory acidosis
How do you compensate for respiratory acidosis (↑ pCO2)?
Induce metabolic alkalosis
- Kidney will reclaim and regenerate HCO3- = ↑ HCO3- = ↑ in pH
How do you compensate for respiratory alkalosis (↓ pCO2)?
Induce metabolic acidosis
- Kidney will ↓ reclaim and regeneration of HCO3- = ↓ HCO3- = ↑ in pH
Symptoms in patients with acidosis:
- Hyperventilation (trying to blow out CO2)
- Depression of myocardial contractility
- Cerebral vasodilation (increase cerebral blood flow => increase in ICP)
- If high CO2 levels => CNS depression
- Hyperkalemia (high H+ exchanges with K+)
- Shift in oxyHB dissociation curve (Bohr) effect to the R => decreased pH leads to HB releasing more O2 and it is less saturated
Symptoms in patients with alkalosis:
- Hypoventiliation
- Depression of myocardial contractility
- Cerebral vasoconstriction (Decrease in cerebral blood flow),
- Hypokalemia
- Shift in oxyHb dissociation curve to the left
How do we approach acid-base problems?
- Check pH (<7.35 => acidosis; >7.45= alkalosis) to determine if alkalosis or acidosis
- Check HCO3- and pCO2 to determine if metabolic or respiratory
- 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.
- Calculate compensation for primary acid-base disorder
- Compensated => only a simple acid-base disorder is present
- Not compensated =>
- Combined respiratory/metabolic
- 2 metabolic disorders
In most acid base disorders, _____ HCO3 and pCO2 are abnormal.
BOTH. One if is the culprit and other is compensatoery change. You have to figure out which is the problem
What 2 pathologic states can both acidotic and akalotic states occur?
- Vomitting (acidotic)
- Diarrhea (alkalotic)
How do we determine if there are 2 disorders present?
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.
KEY: What is a classic scenario for mixed disorders?
- 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.
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

Is this compensated?

Yes.
Perform Winter’s formula:
Expected pCO2= 22 +/- 2
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
How do we determine is the lungs properly compensates for metabolic alkalosis?

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)
-
∆[HCO3-]= ∆pCO2/10
-
Chronic
-
∆[HCO3-]= 3.5 * ∆pCO2/10
- HCO3- will ↑ by [3.5 mEq/L] for every [10 mmHg] ↑ in PCO2 from NL (40)
-
∆[HCO3-]= 3.5 * ∆pCO2/10

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)


How Many Acid-Base Disturbances Can Be Present at Once?
Three.
Not 4; bc a person can only breathe fast or slow, not both
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)
In the body, what is the distribution of anions and cations?
all cations (+) and anions (-) equal each other. Thus, there is net neutrality
Cations include:
Na+, K+, Ca+, Mg+, Protein+ (not many)
Anions include:
Cl-, HCO3-, Proteins (especially, Albumin-), HPO4-, SO4-2, and organic anions
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-

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
What is a trick to differentiate between HAG and NAG?
Look at Cl- levels!
- If high; NAGMA (hyperchloremic)
- If low/NL; HAGMA
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
In AG acidosis, there is a _____ in HCO3- and a _____ in organ anions, causing a ___ anion gap.
- decrease
- increase
- high
In hyperchloremic acidosis (NAG), there is a ______ in HCO3- and an _____ in Cl-, causing a ______ anion gap.
- decrease
- increase
- NL
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.
How does hypoalbuminemia affect the anion gap?
falsely ↓ anion gap
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.
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.
- HCO3- falls w/o ↑ in Cl-, causing an ↑ in AG.
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.
- Calculated serum osmolality= 2Na + (Glucose/18) + (BUN/2.8)
- Clinically used to screen for:
- Ingestion of alcohol, particularly in HAGMA (when >20)
- Ketoacidosis
- Lactic acidosis
When is the Delta-Delta Gap used?
Used in patients with HAGMA to determine if there is a co-existing NAGMA or metabolic alkalosis.
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
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.
GOLD MARK
GOLD MARK is the DDx for HAGMA
- Glycol (ethylene and propylene)
-
Oxoproline (pryroglutamic acid)
- D/t acetominophen toxicity
- L-lactic acidosis
- D-lactic acidosis
- Methanol
- Aspirin
- Renal failure
- Ketoacidosis (alcholic, DB, starvation)
D-lactic acidosis is a common cause of HAGMA.
What can cause D-lactic acidosis?
- Colonic metabolization of glucose, starch, other carbs by bacteria that occurs in short bowel syndromes
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
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)
Acidosis/alkalosis is associated with hyperkalemia
Acidosis
- H+ ions enter the cells and K+ exit the cell
Acidosis/alkalosis is associated with hypOkalemia
Alkalosis
- H+ ions exit cells, K+ enter
DURHAAM
DURHAM is the DDx for non-anion gap metabolic acidosis (NAGMA); primary loss of HCO3-; hold onto Cl-
- Diarrhea***
- Ureteral diversion or fistula**
- Renal tubular acidosis*
- Hyperalimentation (enteral nutrition or total parental nutrition, TPN)
- Acetazolamide (CA inhibitor)
- Addisons disease (adrenal insuffiency)
- Miscellanous (tuloene toxicity – glue sniffing, pancreatic fistula, meds)
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

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+
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+
- H+ ions cannot be secreted into urine via a-intercalated cell either of 2 things:
-
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
What is the purpose of the UAG?
- Used to differentiate renal from non-renal causes of normal anion gap metabolic acidosis.
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
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
When is UAG (-)?
- GI metabolic acidosis (diarrhea)
- Type 2 RTA, where a defect is present in proximal tubule, NOT distal tubule
When is UAG (+)?
- Distal RTA (Kidneys cannot excrete H+ and NH4 and Cl do not increase)
H+ secretion leads to ___________.
HCO3- reabsorption
_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.
- HCO3- filtered load exceeds PT reabsorptive capacity, causing HCO3- loss in urine and low serum HCO3-.
-
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
- Urine pH less than 5.5
-
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 -
- Urine pH can be high or low depending on serum HCO3- levels
- Tx: Sodium Bicarb
What is the only RTA that causes hypERkalemia (high K+)
Type 4
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
- ↓ aldosterone
-
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)
5 most common DDx of Metabolic Alkalosis
- Hypokalemia
-
Vomitting or nasogastric tube suctioning
- GI loss of HCl
- Diuretics (thiazide and loop)
-
Volume depletion
- Contraction alkalosis: volume depletion d/t Cl- depletions => + RAAS and aldosterone secretion, which worsens metabolic alkalosis
- Excess of mineracortcoids
Any factor that ↑ Na+ reabsorption, will do what?
- cause an ↑ in H+ secretion => ↑ HCO3- reabsorption => metabolic alkalosis
What mechanism do excess of mineralcorticoids leads to metabolic alkalosis?
Mineralcorticoids ↑ Na+ reabsorption => ↑ H+ secretion => ↑ HCO3- reabsorption => metabolic alkalosis
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

In a B-intercalated cells, HCO3- made in the cells exits via the ____________ into the lumen.
Cl-/HCO3- exchanger
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-.
DDx Respiratory Alkalosis
Anything that increase RR/tidal volume
- Pneuonia
- PE
- Pulmonary edema
- Pneumothorax
- Pregnany
______ can cause respiratory alkalosis and HAGMA.
Aspirin
DDx for Respiratory Acidosis
-
Anything that ↓ RR/tidal volume, increase dead space or worsens airway obstruction
- PE increases deadspace
- Inadequate ventilator settings
-
Increase in CO2 production
- increased carb diet
- Hyperthermia
- Seizures