Acid/Base Disorder Flashcards by A B

Acidity equation

Acidity = Bicarb/Carbon Dioxide

pH = [HCO3-] / [CO2]

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if HCO3- incr, what is pH change and what disease

incr pH

metabolic alkalosis

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if HCO3- decr, what is pH change and what disease

Decr pH

Metabolic acidosis

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if pCO2 incr, what is pH change and what disease

decr pH

respiratory acidosis

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if pCO2 decr, what is pH change and what disease

incr pH

respiratory alkalosis

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if compensation is not as expected, then…

additional acid base disorder present

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Compensation is ALWAYS in …

same direction as primary change

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Compensation for metabolic acid-base disorders

Compensation for respiratory acid-base disorders

1) change in PCO2 in same direction as bicarb to bring pH back to normal
2) change in bicarb in same direction as PCO2 to bring pH back to normal

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Changes in PCO2 are controlled by …

Changes in HCO3- are controlled by …

1) lungs
2) kidney

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Metabolic acidosis compensation rule

Metabolic alkalosis compensation rule

1) deltaPCO2 = 1 to 1.5 x deltaHCO3-
2) deltaPCO2 = 0.7 x deltaHCO3-

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metabolic-kidney compensation

Respiratory acidosis

acute compensation

chronic compensation

Respiratory alkalosis

acute compensation

chronic compensation

1) deltaHCO3- = incr 1:10 PCO2

deltaHCO3- = incr 4:10 PCO2

2) deltaHCO3- = decr 2:10 PCO2

deltaHCO3- = decr 4:10 PCO2

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Causes of respiratory alkalosis ALWAYS DUE TO

HYPERVENTILATION (breathing too much)

Anxiety, fever, pain
Lung disease
Liver disease
Sepsis
Brain disease
Pregnancy (progesterone)

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Acute respiratory alkalosis is before

Chronic respiratory alkalosis occurs __ after acute

renal compensation

3-5 days

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Case: 21 y/o female in the ER

c/o Shortness of breath, chest pain
Wheezing on exam
pH=7.5; PCO2= 20; HCO3= 20; PaO2=80

(normal: pH: 7.4; PCO2: 40; HCO3 24)

ACUTE OR CHRONIC RESPIRATORY ALKALOSIS

ACUTE COMPENSATION

If acute, HCO3 should ↓ 2 x 2 = 4 and expected

HCO3 is 24-4 = 20

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RESPIRATORY acidosis is due to

breathing too little (CO2 retention)

1) brain injury, narcotics, hypothyroidism,
2) aspiratory of foreign bodies
3) hypokalemia, hypophosphatemia, muscle fatigue
4) pneumonia, COPD, ILD

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21 y/o female in ER

c/o Shortness of breath, chest pain
Wheezing
pH=7.3; PCO2= 50; HCO3= 25; PaO2=58

(normal: pH: 7.4; PCO2: 40; HCO3 24)

acute or chronic?

acute respiratory acidosis

What is expected increase in HCO3 ?
PCO2 has increased by 1 x 10.

If acute, increase in HCO3 is 1 x 1, 24+1= 25

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what does mineralocorticoid normally do?

what does it cause?

mineralocorticoids cause secretion of H+ ion
and reabsorb HCO3-

respiratory alkalosis

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Metabolic alkalosis causes

GENERATION

Addition of HCO3- = (Ringers, packed RBCs, total parenteral nutrition)

Contraction alkalosis = loss of Cl-rich (HCO3- poor fluid) = vomiting, NG suction, diuretics (HCTZ, loop)

Loss H+ (vomiting (HCO3- stays behind), mineralocorticoids and diuretics )

post hypercapneia

hypokalemia

MAINTENANCE

inability to excrete excess bicarbonate (ALWAYS KIDNEY FAULT)

Metabolic alkalosis = Generation

Mineralocorticoids cause H+ excretion via H+ ATPase

and causes HCO3- resorption = mineralocorticoids and diuretics

Causes of excess mineralocorticoids

(incr renal H+ excretion, incr mineralocorticoids)

1) primary hyperaldosteronism

2) Cushing’s syndrome
3) congenital adrenal hyperplasia

4) hyperreninism
5) renal artery stenosis

Maintenance of metabolic alkalosis is ___

Causes?

ALWAYS KIDNEY’S FAULT (INABILITY TO EXCRETE HCO3-)

1) excess mineralocorticoid activity

2) hypovolemia
3) chloride depletion and K+ depletion –> impairs HCO3 excretion

Maintenance of metabolic alkalosis

causes

Hypovolemia causes … Na+ resorption

Na+ resorption causes …HCO3- and Cl- resorption

Excess mineralocorticoid activity

Metabolic alkalosis

if urine Cl is low < 20

described as metabolic alkalosis chloride responsive

with hypovolemia as maintenance factor

1) contraction alkalosis
2) addition of bicarb
3) GI H+ loss
4) Renal H+ loss

metabolic alkalosis

if urine Cl is high > 20

chloride resistant
= chloride depletion with hypovolemia is not the maintenance factor

1) hypertensive = excess mineralocorticoid activity
2) normotensive= intracellular H+ loss

Compensation for metabolic alkalosis by body

PCO2 incr by hypoventilation max PCO2 = 55 in acute and 60-70 in chronic deltaPCO2 = 0.7 x deltaHCO3-

July 4th picnic, vomiting x 24 hrs, BP 90/40, HR125 c/o dizziness, nausea, can’teat/drink pH7.5; PCO2:50 ;HCO3-:34 (nl:7.4/40/24) UrineNa: 25; UrineCl: 9 what does she have how do you treat her compensation?

primary disorder = metabolic alkalosis with appropriate respiratory compensation ALWAYS GET URINE CHLORIDE) Because urine chloride \< 10 --\> chloride responsive --\> give her NS since low BP and vomiting deltaPCO2 = 0.7 x 10= 7 pCO2 = 40 + 7 = 47

metabolic acidosis Each day the kidney has to deal with ___ mEq of H+ which consumes ___ of HCO3-

60 mEq of H+ consumes 60 mEq of HCo3- drives reaction to H2O and CO2

handling daily acid load in proximal tubule... in distal tubule...

1) reabsorb HCO3- 2) secrete H+, make HCo3-, acidify urine, excrete daily acid load (want to get H+ ion into lumen and reabsorb HCO3-) secrete 60 H+ means make 60 HCO3-

Proximal tubule reabsorption mechanisms

Glucose reabsorbs using energy from Na/K atpase so don't pee out

Fate of secreted H+ 2 mechanisms for neutralizing acid

1) TA- HPO4- + H+ --\> H2PO4- 2) Ammonia trapping- NH3 + H+ = NH4+

Failure of kidney to handle daily acid load --\> \_\_\_\_ Proximal = Distal =

metabolic acidosis = renal tubular acidosis proximal = failure to reabsorb HCO3- distal = failure to secrete H+ and make HCO3-

urine anion gap is positive when \_\_\_

distal kidney problem = failure to secrete H+ and reabsorb HCO3-

if metabolic acidosis problem is renal, then urine anion gap is \_\_\_\_ if metabolic acidosis problem is GI (diarrhea, surg drains, fistulas), urine anion gap is \_\_\_

1) positive 2) negative

Normal anion gap calculation Adjust down by 2.5 for every \_\_\_

Na - HCO3- - Cl- = 9 +/- 3 1 mg/dL decr in albumin

With the loss of HCO3-, compensate by

incr Cl- so UAG is same

4th of July picnic, diarrhea for 3 days ! pH: 7.2; PCO2: 26; HCO3- : 10 ! Serum Na: 140; Cl: 120; HCO3- : 10 ! Urine Na: 10; Urine K: 10; Urine Cl: 40 serum anion gap = ? urine anion gap = ? deltaPCO2 = ?

serum anion gap = 10 (normal) urine anion gap = -20 (negative = GI cause) deltaPCO2 = 1 to 1.5 x deltaHCO3- = 26

Bicarbonate loss causes anion gap to be \_\_\_ addition of acid causes anion gap to be \_\_\_

to be normal to be increased

Causes of H+ anions to be added

! Ketones(Metabolism) – Starvation (ketones) – DKA (ketones) ! AspirinandotherToxins/Ingestions – Ethylene glycol (-\> -\> glycolic acid -\> -\> oxalic acid) – Methanol (formaldehyde -\> formic acid) – Ethanol (ketones) – Aspirin (Acetylsalicylic acid -\> salicylic acid) ! Renalfailure(sulfate,urate,phosphate,hippurate) ! Lacticacid(Hypoxia)

normal values pH pco2 HCO3-

7.40 40 24

compensation resp alkalosis 2 steps compensation resp acidosis 2 steps metabolic alkalosis

1) cell H+ release (acute 2) renal H+ retention (chronic \_\_\_ 1) cell buffering = H+ abs by cell buffers 2) renal H+ excretion--\> makes new HCO3

in appropriately compensated resp acidosis, pH does not fall below \_\_\_

7.20