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CPR Test II > Approach to Acid-base disorders > Flashcards

Approach to Acid-base disorders Flashcards

1
Q

what is arterial pH

A

7.35-7.45

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2
Q

increase in HCO3- does what to pH

increase in PCO2 does what to pH

A

increase pH

decrease pH

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3
Q

increase in RR does what to pH

decrease in RR does what to pH

A

increase in RR = increase CO2 blown off and increase pH

decrease in RR = decrease in CO2 blown off and decrease in pH

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4
Q

what are the two types of Metabolic acidosis

A

High anion gap metabolic acidosis (HAGMA)

Normal anion gap metabolic acidosis (NAGMA)

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5
Q

what are the two types of Metabolic Alkalosis

A 
Saline responsive (hypovolemia)
-aka contraction alkalosis( or chloride deficiency alkalosis)

Saline non responsive (euvolemia of hypervolemia)

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6
Q 
Compensations:
metabolic acidosis?
Metabolic alkalosis?
respiratory acidosis?
respiratory alkalosis?
A

Compensations:
metabolic acidosis = respiratory alkalosis (decreased pCO2 via increased RR)

Metabolic alkalosis = respiratory acidosis (increase PCO2 via decrease RR)

respiratory acidosis = metabolic alkalosis (increase HCO3 via reabsorption and production of HCO3)

respiratory alkalosis = metabolic acidosis
(secretion and decreased production of HCO3)

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7
Q

Compensation formula: Metabolic acidosis

A

Winters formula = PCO2 = 1.5[HCO3] + 8 +/- 2

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8
Q

compensation formula: Metabolic alkalosis

A

PCO2 will increase by .7 mmHg for each 1.0 mEq/L increase from 24 HCO3-

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9
Q

Compensation respiratory acidosis acute and chronic

A

Acute: HCO3- will increase by 1 mEq/L for every 100 mmHg increae in PCO2 from normal (40)

Chronic: HCO3- will increase by 3.5 mEq/L for every 10 mmHg increase in PCO2 from normal (40)

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10
Q

compensation respiratory alkalosis acute and chronic

A

Acute: HCO3- will decrease by 2 mEq/L for every 10 mmHg decrease in PCO2 from normal (40)

Chronic: HCO3- will decrease by 5 mEq/L for every 10 mmHg decrease in PCO2 from normal (40)

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11
Q

how many Acid base disturbances can be present at once in a patient?

A

up to 3

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12
Q 
Normal values:
pH
HCO3-
PCO2
Anion gap
Osmolality gap
A

pH: 7.35- 7.44

HCO3-: 24 mEq/L

PCO2 = 40 mmHg

Anion Gap = 12

Osmolality gap = 10 mosm/kg

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13
Q

How to calculate the anion gap? what is normal? what is it used for?

A

Anion gap = Na+ - (HCO3 + Cl)
- normal AG = 12 +/- 2

help distinguish if the metabolic acidosis is HAGMA or NAGMA

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14
Q

How to calculate the serum Osmolaity? what is considered normal?

what is the osmolar gap? how is it calculated and what is it used for? and what does that tell us?

A

Calculated serum Osmolality = 2(Na) + (glucose/18) + (BUN/2.8)
-normal serum osmolality = 275- 290 mosm/kg

Osmolar Gap = Measured serum osmolality - calculated serum osmolality

  • normal osmolar gap is < 10 mosm/kg
  • if osmolar gap is > 10 mosm/kg suggestive of additional solutes to blood

Clinically useful for screening alcohol ingestions, particularly in HAGMA cases

  • screening for ketoacidosis
  • lactic acidosis
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15
Q

what does a AG of > 20 highly suggestive for?

A

alcohol ingestion

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16
Q

what is the Delta-Delta Gap used for?

A

Used in patients with HAGMA to determine if there is a coexistent NAGMA or metabolic alkalosis present

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17
Q

how to calculate the Delta-Delta gap and delta HCO3

A

Essentially for every increase in AG there should be equal decrease in serum HCO3

Delta gap = calculated AG - normal AG (12)

Delta HCO3 = normal HCO3 (24) - Delta gap

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18
Q

what does it mean if the measured HCO3 value is close to the delta HCO3, greater than or less than?

A

if the measured HCO3 was close to Delta HCO3 = no additional acid base disorder present

if the measured HCO3 was greater that the Delata HCO3 then there is a metabolic alkalosis present in addition to the HAGMA

if the measured HCO3 was less than 16 then a non-gap metabolic acidosis (NAGMA) is present with the HAGMA

19
Q

what is the HAGMA DDx

A

GOLD MARK

  • Glycols (ethylene and propylene)
  • Oxoproline (Pyroglutamic acid) (acetaminophen toxicity
  • L-lactic acidosis
  • D-Lactic acidosis (seen in short bowel syndromes)
  • Methanol
  • Aspirin
  • Renal Failure
  • Ketoacidosis (alcoholic, diabetic, starvation)
20
Q

what is the treatment and diagnosis of Pyroglutamic acidosis

A

Diagnosis: urinary organic acid screen

Treatment: Discontinue acetaminophen

  • IVF
  • N-acetylcysteine
21
Q

Differential diagnosis of increased Osmolar Gap

A

ME DIE

Methanol
Ethanol’

Diethylene glycol (diuretic Mannitol)
Isopropyl alcohol (rubbing alcohol not associated with MA)
Ethylene glycol

Propylene glycol
ketoacidosis and lactic acidosis (smaller increase in osmolar gap)

22
Q

DDx for Normal anion gap metabolic acidosis (NAGMA)

A

DURHAAM

  • Diarrhea!!!
  • Ureteral diversion (ileal conduit) or fistula
  • Renal tubular acidosis!!!
  • Hyperalimentation (enteral nutrition or total parenteral nutrition, TPN)
  • Acetazolamide (carbonic anhydrase inhibitor)
  • Addisons disease (adrenal insufficiency)
  • Miscellaneous (toluene toxicity - glue sniffing, pancreatic fistula, medications)
23
Q

what does Renal Tubular Acidosis Mean?

A
  • RTA is a condition in which net acid excretion by the kidneys is impaired
  • results in a NAGMA
  • cannot be diagnosed in the setting of AKI

impaired H+ secretion
impaired HCO3- reabsorption

24
Q

what are the three types of RTA

A

RTA type 1 (distal RTA)
-results from decreased net H+ ion secretion in distal tubules and collecting duct

RTA type 2 (proximal RTA)
-results from decreased HCO3 reabsorption in the proximal tubule

RTA type 4 (Hyperkalemic RTA)

  • results from decreased aldosterone secretion or aldosterone resistance
  • leads to decreased net H+ and K+ secretion in collecting duct
25
Q

What to do when suspecting RTA and determining what type it is?

A

measure K+ levels
-Hyperkalemia then it is a type 4 RTA

Hypokalemia determine if their is proximal tubular dysfunction (fanconi syndrome)
-aminoaciduria, phosphaturia, glucosuria, bicarbonaturia, tubular proteinuria, uricosuria

yes to that then it is Type 2 (proximal RTA

no then it is Type 1 (distal RTA)

26
Q

what is the Urine Anion Gap used for and how to calculate it?

A

used to differentiate renal from non renal causes of NAGMA
-its marker is NH4CL excretion

UAG = (UrineNa + UrineK) - UrineCl

27
Q

what does it mean if their is a negative UAG or a Positive UAG

A

Negative indicates appropriate distal nephron urinary acidification = Type 2 RTA
-normal distal renal acidification

indicates inappropriate distal nephron urinary acidification = Type 1 or 4
-abnormal distal renal acidification

28
Q

what is the underlying issue with RTA type 2

A

Proximal RTA there is a decreased capacity to reabsorb HCO3 in PT

  • results in HCO3 loss in the urine
  • causes a decrease in serum HCO3 to stabilize steady state
29
Q

Etiology, Clinical manifestations and diagnosis of Proximal RTA type 2

A

etiology: can be primary or secondary (idiopathic or hereditary)
- children is cystinosis
- adults with Fanconi syndrome have Multiple Myeloma

Clinical manifestations:

  • NAGMA
  • Hypokalemia (mild compared to distal RTA)

Diagnosis: Urine pH can be high or low but urine pH <5.5 (at new steady state)
Urine anion gap is negative

30
Q

what is the underlying issue with RTA type 1

A

Distal RTA patients are unable to acidify their urine

decreased net H+ ion secretion in the distal nephron

  • H+/K+ ATPase or H+ ATPase defect
  • gradient defect due to amphotericin or fungal infections

Lack of net H+ ion secretion prevents urinary acidification and excretion of ammonium
-can prevent HCO3 reabsorption in the distal tubule

31
Q

etiology, Clinical manifestations and diagnosis of RTA type 1

A

Etiology: can be inherited or acquired

  • commonly seen with sjorgens syndrome
  • glue sniffing is another cause due to toulene

Clinical manifestations:
-associated with nephrolithiasis or nephrocalcinosis

Diagnosis:

  • NAGMA
  • Unable to acidify urine pH < 5.5
  • Hypokalemia usually severe
  • UAG is positive
32
Q

Etiology of Hyperkalemic RTA (type 4)

A

Characterized by distal nephron dysfunction from impaired renal excretion of H+ and K+ causing NAGMA and hyperkalemia

Deficiency of circulating aldosterone:

  • DM
  • Drugs: NSAIDS, B-blockers, ACEi/ARB and heparin

Aldosterone resistance in collecting ducts

  • interstital renal disease: SCD, SLE
  • drugs: amiloride, triamterene, spirnolactone, trimethoprim

results inmpaired Na reabsorption by principle cells and leads to negative CD which impairs acidification as a result of decreased driving force H+ secretion leading to hyperkalemia

33
Q

Clinical manifestations and diagnosis of Hyperkalemic RTA (Type 4)

A

Clinical manifestations:

  • usually asymptomatic
  • NAGMA
  • Hyperkalemia
  • history of diabetes or CKD

Diagnosis:

  • variable urine pH usually >5.5
  • UAG is positive
34
Q

What is the relationship between acidosis/alkalosis and serum potassium

A

acidosis is associated with hyperkalemia
-H+ into the cell and K+ out

alkalosis is associated with hypokalemia
-H+ out of the cell and K+ into

35
Q

what are some main Metabolic alkalosis DDx

A

Hypokalemia

Vomiting or nasogastric tube
-loss of HCL

Diuretics (thiazide and loop diuretics)

Volume depletion( in the setting of Cl- depletion and the activation of RAAS

Mineralcorticoid excess

Brtter, Gitelman syndrome, liddle syndrome,

Hypercalcemia/milk-alkali syndrome

36
Q

what are the main factors that lead to Metabolic alkalosis?

A

Factors that stimulate Na reabsoroption, secondarily increase H+ secretion and thus stimulate HCO3 reabsorption

37
Q

what is Bartter syndrome and what are the clinical manifestations

A

typically affects prenatal or neonatal patients resulting death

Clinical manifestations:

  • severe hypokalemia
  • metabolic alkalosis (saline non responsive)
  • low to normal blood pressure
  • hypercalciuria and nephrocalcinosis

caused by inactivating mutations if thick ascending loop transporters
-lead to NaCl loss causing volume depletion and leading to secondary hyperaldosteronism

38
Q

what is the net result of Bartter syndrome

A

similar to using a loop diuretic

39
Q

epidemiology, clinical manifestations, and pathophysiology of Gitelman syndrome

A

rare autosomal recessive
-typically seen in late childhood or adulthood

Clinical manifestations:

  • Severe hypokalemia
  • metabolic alkalosis (saline non-responsive)
  • low to normal blood pressure
  • hypocalciuria
  • hypomagnesemia

Pathophysiology:

  • incativated mutations of NaCl co transporter (NCCT)
  • increased RAAS and increased collecting duct Na reabsorption and H+ and K+ secretion
  • down regulation of Mg channel TRPM6 in DCT
40
Q

what does Bartter syndrome act similar too?

A

Thiazide diuretics

41
Q

epidemiology, clinical manifestations, pathophysiology of Liddle syndrome

A

Rare autosomal dominant disease
-patients typically present at young age with HTN and electrolyte abnormalities

Clinical manifestations:

  • Resistant HTN
  • Hypokalemia
  • Metabolic alkalosis

Caused by mutations in the Na Channel (ENaC) in collecting duct
-results increase Na reabsorption and K+ and H+ secretion

42
Q

Diagnosis and Treatment of Liddle Syndrome:

A

Diagnostic: Genetic testing, Low aldosterone levels and renin levels

Treatment:

  • amiloride, or triamterene (block sodium channel
  • low salt diet
  • spironolactone is not effective due to this not being a RAAS issue
43
Q

what causes a Respiratory alkalosis DDx:

A

anything that increases respiratory rate

  • Pneumonia
  • PE
  • pulmonary edema
  • Pregnancy
  • elevated altitude
  • CHF
  • Sepsis
  • excercise
44
Q

what causes a Respiratory acidosis DDx:

A

Anything that lowers respiratory rate/vidal volume, increases dead space or worsens airway obstruction

  • Respiratory muscle weakness
  • Hypokalemia and hyperkalemia (diaphragm muscle weakness)
  • ARDs
  • COPD
  • Asthma
  • interstitial lung disease
  • Fractured ribs
  • Central brainstem lesion
  • Drugs (opiates, barbiturates, benzodiazepines)

Inadequate ventilator settings

Increases in CO2 production
-Increased carbohydrate diet, hyperthermia, seizures

CPR Test II (6 decks)

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