Transcript Document

Metabolic Acidosis/Alkalosis
Jason Corbeill PA-C
Normal values
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From serum (venous) blood:
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CO2 (bicarb) 22-32 mmol/L
Na 135-146 mmol/L
Cl 98-111 mmol/L
From ABG:
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pH 7.35-7.45
pCO2 35-45
Bicarb 21-29
Metabolic Acidosis
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HCO3- excretion is controlled by the kidney
H+ excretion is controlled by the kidney
One H+ buffers one HCO3–
So, an increase in H+ can cause a decrease in
HCO3-
Metabolic Acidosis
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Gain of H+
Loss of HCO3-(bicarb)
Causes of metabolic acidosis due to
gain of acid
Endogenous hydrogen ion production:
ketoacidosis
lactic acidosis
salicylate overdose
Metabolism of toxins
methanol
ethylene glycol
Decreased renal excretion
uremia
renal tubular acidosis (type 1) distal
Causes of metabolic acidosis due to
loss of bicarb
--Renal tubular acidosis type II (proximal)
--GI loss (diarrhea)
Metabolic Acidosis
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Metabolic acidosis can be characterized
based on anion gap
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High anion gap >20
Normal anion gap 7-15 meq/L
AG=Na – (Cl + HCO3-)
Diff Dx of elevated anion gap acidosis
Methanol intoxication (denatured alcohol)
Uremic acidosis
Diabetic ketoacidosis
Paraldehyde intoxication/alcohol intoxication
I INH, infection
Lactic acidosis
Ethylene glycol intoxication
Salicylate intoxication
Elevated anion gap acidosis
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Methanol intoxication
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Ingested methanol is converted in the body to formic acid
leading to metabolic acidosis and high anion gap
Also will have increased osmolal gap
Antifreeze, de-icing solutions, cleaners, solvents
Symptoms include optic neuritis, blindness, pancreatitis
Treatment:
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Give ethanol IV to stop methanol conversion to formic acid
Fomepizole
Dialysis
bicarbonate
Elevated anion gap acidosis
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Uremic acidosis
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Occurs in severe renal failure with GFR <20%
Kidneys unable to excrete H+
Treatment:
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dialysis
Elevated anion gap acidosis
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Diabetic ketoacidosis
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Production of ketoacids due to incomplete fatty acid
oxidation
Presentation
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Acidemia pH 7.15
Hyperglycemia
dehydration
Low k-even if levels appear normal
Urine ketones
Serum ketones (more sensitive)
Tachypnea, polydipsia, polyuria
Elevated anion gap acidosis
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Treatment of DKA
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Insulin
NSS with KCl (250mL/hr)
KCl bolus
No bicarb unless pH less than 7.10
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Ketoacids will be converted to bicarb
Watch K closely
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Serum K driven into cells by insulin in setting of
hyperglycemia
Elevated anion gap acidosis
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Paraldehyde intoxication
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Used in the production of resins
Anti-seizure drug not used much any more
Elevated anion gap acidosis
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Alcohol (Ethanol) intoxication
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Starvation + ethanol = ketogenesis
Occurs after long binge periods
n/v/ abdominal pain
Dehydration, hypoglycemia, GI bleed, pancreatitis
Elevated anion gap acidosis
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Treatment of ethanol intoxication/acidosis
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Do not give glucose until first given thiamine
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Reduces chances for Wernicke’s encephalopathy
“banana bag” or “rally pack” over 4 hrs
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100mg thiamine x 3
Folate 5mg in IVF
MVI in IVF
Mag sulfate 2g
No need for bicarb unless pH < 7.10
Elevated anion gap acidosis
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Lactic acidosis
A—hypotension/tissue hypoxemia
B—sepsis, liver disease, DM, cancer
Elevated anion gap acidosis
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Lactic Acidosis-treatment
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Treat underlying cause
Bicarb, especially if less than 7.10
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Lactic acid will convert to HCO3-
Elevated anion gap acidosis
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Ethylene glycol ingestion
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Similar to methanol intoxication
Usually hx alcohol abuse
Drinking antifreeze/radiator fluid
Causes production of toxic acids
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Acute renal failure
Osmolal gap
Calcium oxalate crystals in urine (oxalic acid)
CNS dysfunction
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Ataxia, confusion, seizures, coma
Elevated anion gap acidosis
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Ethylene glycol ingestion treatment
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Ethanol
Dialysis
Bicarb
Elevated anion gap acidosis
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Salicylate intoxication (aspirin)
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Affects respiratory center and initially causes
respiratory alkalosis
Salicylates causes accumulation of acids
including lactic acid and ketoacids which cause
acidosis
Elevated anion gap acidosis
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Salicylate intoxication-treatment
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Alkalinize the urine with bicarb
May require dialysis
Differential Diagnosis of normal anion
gap acidosis
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Mild renal failure
GI loss of bicarb via diarrhea
Type I (distal) renal tubular acidosis
Type II (proximal) renal tubular acidosis
Normal Anion Gap Acidosis
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Type I Distal RTA
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May be caused by…
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Hyperparathyroidism
Sjorgren’s syndrome
Amphotericin B
Renal tubule unable to eliminate H+
Results in urine pH > 5.3
Calcium phosphate stones
Normal Anion Gap Acidosis
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Type I Distal RTA treatment
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Treat underlying cause
Replace K
Replace bicarb
Normal Anion Gap Acidosis
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Type II (proximal) RTA
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Causes include: multiple myeloma, mercury, lead
Impaired proximal tubular reabsorption of bicarb
May also have a defect in reabsorption of other
solutes such as amino acids, phosphorus, urate,
glucose (Fanconi Syndrome)
Urine pH able to be less than 5.3
Normal Anion Gap Acidosis
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Type II (proximal) RTA treatment
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May require lots of bicarb (K citra)
Replace potassium
Difficult to maintain bicarb levels as reabsorption
threshhold set too low.
Metabolic Alkalosis
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Results from loss of H+
Results from impaired excretion of HCO3-
Metabolic Alkalosis
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Causes of metabolic alkalosis:
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Potassium depletion
Mineralocorticoid excess (aldosteronism)
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Increases H+ secretion into tubule, loss of K
Dehydration
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Vomiting/NGT suction
Diuretics
Chronic diarrhea
Metabolic Alkalosis
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Treatment of metabolic alkalosis
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Dehydration—NSS IV
Hypokalemia—potassium
Mineralocorticoid excess—treat underlying
disorder.
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No NSS as already fluid overloaded and hypertensive.
Approach to acid/base problems
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1. Identify most obvious disorder
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Look at pH, pCO2 (H+ ) and HCO3- on ABG
If multiple abnormalities, look at which is MORE
abnormal
Approach to acid/base problems
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2. Calculate expected compensation
For metabolic acidosis..
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Expected pCO2 =1.5 x (HCO3-) + 8
For metabolic alkalosis…
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Expected pCO2 =40 + 0.7 x [(measured HCO3-) –
(normal HCO3-)]
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If the degree of compensation is not what is expected by
the above calculation, then there is a respiratory
component involved!
Approach to acid/base problems
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3. Calculate anion gap
AG = Na – (Cl + HCO3-)
CASES:
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1. 40 yo male with shallow respirations,
tachypnea.
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Serum Na 142, K 3.6, Cl 100, bicarb 12
ABG: pH 7.28, pCO2 26, HCO3- 12
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1. metabolic acidosis (pH and HCO3- both low)
2. calculate compensation: exp pCO2 = 26
3. AG = 30
Other labs, questions?
Cases
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2. 20 y/o woman with protracted vomiting,
lethargy, tachypnea, tachycardia, BP 150-98.
Hx IDDM not taking her insulin with variable
glucoses at home. Not eating well.
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Serum Na 142, K 3.6, CL 106, bicarb 16, glu 230,
BUN 70, CR 1.2
ABG pH 7.28, pCO2 34, HCO3- 16
Cases
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Other labs?
How would negative serum ketones and a
creatinine of 12 change your diagnosis?
Cases
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3. 50 y/o male with tachypnea, tachycardia,
BP 90/60
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Serum Na 142, K 3.6, Cl 100, bicarb 12, glu 180,
bun 28,
ABG pH 7.28, pCO2 26, HCO3- 12
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1. problem:
2. expected pCO2 : 26
3. Anion gap: 30
Cases
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Other labs?
Urine shows calcium oxalate crystals
High osmolal gap is present
Cases
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4. Serum Na 135, Cl 114, K 4.5 Bicarb 6
ABG pH 7.15, HCO3- 6, pCO2 18
1. underlying problem
2. expected pCO2? 17
3. AG? 15
Cases
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5. ABG: pH 7.08, HCO3- 10, pCO2 35
Problem
2. Expected pCO2 : 23
3. AG: 14
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Cases
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6. ABG: pH 7.49, HCO3- 35, pCO2 48
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1. underlying problem:
2. expected pCO2 : 48 which equation?
3. AG: 16
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Cases
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7. ABG: pH 7.68, HCO3- 40, pCO2 35
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1. underlying disorder:
2. expected pCO2 : 51 equation?
3. AG: 14
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