Acid base lecture 2012

Acid-Base Analysis

Ahad Lodhi,M.D.

Outline
 Brief review of acid-base physiology
 Problem-solving
 Differential diagnosis

Overview of Acid-Base Physiology

Net Acid Production = Net Acid Excretion

Daily acid production ~ 1 meq/kg/day

4000 meq HCO3 filtered & reabsorbed daily

Net acid excretion comprised of urinary
titratable acid + ammonium - bicarbonate

Acid Production I
Dietary acid

Endogenous acid production

Urinary and fecal alkali loss

Acid Production II
Dietary acid
– Sulfur containing AA
– Phosphoproteins/Phospholipids
– Neutral organics metabolized to organic acids
– Organic cations

Acid Production III
Dietary acid
Urinary and fecal alkali loss

Acid Production IV
– Breakdown PO4 containing proteins to H2PO4
– Anaerobic metabolism of glucose to lactic acid
– Fat metabolism to organic acids/ketones
– Transporting CO2 as bicarbonate releases H+

Regulation of Acid-Base Status
Chemical buffers
– Works in seconds
– Bicarbonate: main regulation of ECF
– Phosphorous: main regulation of ICF & urine
– Protein
Brainstem respiratory center
– Works in minutes
– Adjust ventilation to retain or expel CO2
Renal mechanisms
– Works in hours to days
– For each H secreted, Na & HCO3 reabsorbed

Ammonium
Ammonium produced by glutamine
metabolism
Each glutamine produces 2 ammonium
and two bicarbonate ions
Bicarbonate returns to bloodstream and
ammonium excreted in urine
Production regulated by acid-base status,
K+ & hormones
Measured indirectly by urinary anion gap

Normal Values

pH ~ 7.35 – 7.45

pCO2 ~ 40

HCO3 ~ 22-26

Step by Step Approach
1) Acidemia or alkalemia?

Acidemia: pH < 7.35

Alkalemia: pH > 7.45


2) Primary disorder: metabolic or respiratory?



3) Calculate anion gap

Anion gap = [Na+] – ( [Cl-] + [HCO3-] )

Pearls:
 Anion gap represents unmeasured anions
 Normally 8-12
 Must correct for albumin. For every g/dL below

 AG ≥ 20 ALWAYS indicates metabolic acidosis
≥ 20 ALWAYS indicates metabolic acidosis
4, must increase AG by 2.5

 Low AG suggestive of paraproteinemia, ↑ Ca, ↑
Low AG suggestive of paraproteinemia,
Mg, Lithium or bromide toxicity
or bromide toxicity




4) Check for appropriate compensation

Compensation
When a primary acid-base disorder exists, the body
attempts to return the pH to normal

Primary Disorder Compensatory Mechanism
Metabolic acidosis Increased ventilation

Metabolic alkalosis Decreased ventilation

↑ reabsorption of HCO3 in the PCT
Respiratory acidosis
↑ excretion of H in the distal tubule
↓ reabsorption of HCO3 in the PCT
Respiratory alkalosis
↓ excretion of H in the distal tubule

Practical Approach

Primary disorder Compensation formula

Metabolic acidosis pCO2 ≈ 1.5 [HCO3-] + 8 +/- 2

Metabolic alkalosis pCO2 ≈ 0.9 [HCO3-] + 16

Acute: Δ pH ~ 0.008 * [pCO2 – 40]
Respiratory acidosis
Chronic: Δ pH ~ 0.003 * [pCO2 – 40]
Acute: Δ pH ~ 0.008 * [40 – pCO2]
Respiratory alkalosis
Chronic: Δ pH ~ 0.003 * [40 – pCO2]




4) Check for appropriate compensation

5) If AG acidosis, delta-delta to assess for
another disorder

Delta-delta: Δ anion gap + measured
HCO3 should be ~ 22-26.
Δ anion gap= anion gap - 10
– If value less than 22, concomitant non-AG
metabolic acidosis.
– If value more than 26, concomitant metabolic
alkalosis

Case 1
44 yo ♀ admitted with 4 day h/o diarrhea
ABG: 7.31/33/16
Na 134 Cl 108 HCO3 16
What is her acid-base disorder(s)?

ABG: 7.31/33/16 Na 134 Cl 108 HCO3 16

1) Acidemic or alkalemic?

ABG: 7.31/33/16 Na 134 Cl 108 HCO3 16

– Acidemic

ABG: 7.31/33/16 Na 134 Cl 108 HCO3 16

– Acidemic
2) Primary disorder?

ABG: 7.31/33/16 Na 134 Cl 108 HCO3 16

– Acidemic
– Metabolic acidosis

ABG: 7.31/33/16 Na 134 Cl 108 HCO3 16

– Acidemic
3)Anion gap?

ABG: 7.31/33/16 Na 134 Cl 108 HCO3 16

– Acidemic
3)Anion gap?
– AG = 134 – (108 + 16) = 10

ABG: 7.31/33/16 Na 134 Cl 108 HCO3 16

– Acidemic
3)Anion gap?
– AG = 134 – (108 + 16) = 10
4) Appropriate compensation?

ABG: 7.31/33/16 Na 134 Cl 108 HCO3 16

– Acidemic
3)Anion gap?
– AG = 134 – (108 + 16) = 10
– Exp pCO2 = 1.5 [HCO3] + 8 +/- 2 = 30-34

Hyperchloremic (non-gap) metabolic
acidosis secondary to diarrhea

Hyperchloremic acidosis
Diarrhea
Renal failure
RTA
Ureteral diversion
Pancreatic/biliary/duodenal secretions
Carbonic anhydrase/aldosterone inhibitors
Saline administration
Hyperalimentation
Administration of inorganic acids
Recovery phase of ketoacidosis

Use urinary anion gap to narrow down
differential of hyperchloremic acidosis

UAG = UNa + UK – UCl
UAG negative if GI losses
UAG positive if renal process
Only useful if UNa > 25

Anion Gap Metabolic Acidosis I
L-Lactic acidosis
– Type I: Tissue hypoxia
– Type II: Medications
D-Lactic acidosis (not measured by lab)
– Short gut syndrome
Ketoacidosis
– Diabetes
– Alcoholic

Anion Gap Metabolic Acidosis II
Severe renal failure
Rhabdomyolysis
Intoxications
– Ethanol
– Ethylene glycol
– Methanol
– Acetylsalicylic acid
– Paraldehyde
– INH

Complications of Acidemia
Renal stones from hypercalciuria/hypocitraturia
Bone disease: inhibits formation/resorption
Enhanced interstitial fibrosis
Muscle wasting from protein catabolism
↓ myocardial contractility → ↓ CO → ↓ BP
Sensitized myocardium to arrhythmias
Pulmonary venoconstriction
↓ binding of norepinephrine to receptors
Affects ATP generation, FA biosynthesis
Drug effects

Case 2
70 yo ♂ with h/o CHF admitted with SOB
ABG: 7.24/60/52
Na 135 Cl 100 HCO3 27

7.24/60/52 Na 135 Cl 100 HCO3 27


7.24/60/52 Na 135 Cl 100 HCO3 27

– Acidemic

7.24/60/52 Na 135 Cl 100 HCO3 27

– Acidemic
– Respiratory acidosis

7.24/60/52 Na 135 Cl 100 HCO3 27

– Acidemic

7.24/60/52 Na 135 Cl 100 HCO3 27

– Acidemic
– AG = 135 – (100 + 27) = 8

7.24/60/52 Na 135 Cl 100 HCO3 27

Acute resp acidosis
– Δ pH = 0.008 * (pCO2 - 40)

Chronic resp acidosis
– Δ pH = 0.003 * (pCO2 - 40)

7.24/60/52 Na 135 Cl 100 HCO3 27

Acute resp acidosis
– Δ pH = 0.008 * (pCO2 – 40)
– Δ pH = 0.008 * (20) = 0.16

– Δ pH = 0.003 * (pCO2 - 40)

7.24/60/52 Na 135 Cl 100 HCO3 27

Acute resp acidosis
– Δ pH = 0.008 * (pCO2 – 40)
– Δ pH = 0.008 * (20) = 0.16
– 7.4 – 0.16 = 7.24
– Δ pH = 0.003 * (pCO2 - 40)

7.24/60/52 Na 135 Cl 100 HCO3 27

Acute resp acidosis
– Δ pH = 0.008 * (pCO2 – 40)
– Δ pH = 0.008 * (20) = 0.16
– 7.4 – 0.16 = 7.24
– Δ pH = 0.003 * (pCO2 - 40)
– Δ pH = 0.003 * (20) = 0.06

7.24/60/52 Na 135 Cl 100 HCO3 27

Acute resp acidosis
– Δ pH = 0.008 * (pCO2 – 40)
– Δ pH = 0.008 * (20) = 0.16
– 7.4 – 0.16 = 7.24
– Δ pH = 0.003 * (pCO2 - 40)
– Δ pH = 0.003 * (20) = 0.06
– 7.4 – 0.06 = 7.34

7.24/60/52 Na 135 Cl 100 HCO3 27

– Acidemic
– AG = 135 – (100 + 27) = 8
– ACUTE RESPIRATORY ACIDOSIS

Respiratory Acidoses
Parenchymal: Pneumonia, pulm edema, COPD, ARDS
Reduced perfusion: PE, cardiac arrest
Airway obstruction
Restrictive lung disease: Obesity, ascites
Musculature: MG, restrictive lung disease, ↓ K, ↓ PO4
Neurologic:
– CNS: Sedatives, neurologic lesions, drugs, myxedema, severe CHF
– Peripheral: Paralyzing agents, cord injury, ALS, polio
Thorax: Hemothorax, PTX, flail chest

Respiratory Alkaloses
Anxiety Sepsis
Pain Pregnancy
Hypoxia Hepatic
Drugs encephalopathy
– Salicylates Mechanical ventilation
– Progesterone CNS disease
– Catecholamines
– Xanthines
– Thyroxine

Case 3
45 yo diabetic presents to ER with emesis
and abdominal pain
ABG: pH 7.42 pCO2 35
Na 140 Cl 90 HCO3 24
What (if any) disorders does pt have?
Can patient be discharged home from
ER?

pH 7.42 pCO2 35 Na 140 Cl 90 HCO3 24


pH 7.42 pCO2 35 Na 140 Cl 90 HCO3 24

– Neither

pH 7.42 pCO2 35 Na 140 Cl 90 HCO3 24

– Neither
2) Primary disorder

pH 7.42 pCO2 35 Na 140 Cl 90 HCO3 24

– Neither
2) Primary disorder
– pH, pCO2 & HCO3 all in normal range!

pH 7.42 pCO2 35 Na 140 Cl 90 HCO3 24

– Neither
2) Primary disorder

pH 7.42 pCO2 35 Na 140 Cl 90 HCO3 24

– Neither
2) Primary disorder
– AG = 140 – (90 + 24) = 26

pH 7.42 pCO2 35 Na 140 Cl 90 HCO3 24

– Neither
2) Primary disorder
– AG = 140 – (90 + 24) = 26
– Exp pCO2 ~ 1.5[HCO3] + 8 +/-2 ~ 42 - 46

pH 7.42 pCO2 35 Na 140 Cl 90 HCO3 24

– Neither
2) Primary disorder
– AG = 140 – (90 + 24) = 26
– Exp pCO2 ~ 1.5[HCO3] + 8 +/-2 ~ 42 – 46
– Resp alkalosis

pH 7.42 pCO2 35 Na 140 Cl 90 HCO3 24
– Neither
2) Primary disorder
– AG = 140 – (90 + 24) = 26
– Exp pCO2 ~ 1.5[HCO3] + 8 +/-2 ~ 42 – 46
– Resp alkalosis
5) Delta-delta: HCO3 + Δ AG

pH 7.42 pCO2 35 Na 140 Cl 90 HCO3 24
– Neither
2) Primary disorder
– AG = 140 – (90 + 24) = 26
– Exp pCO2 ~ 1.5[HCO3] + 8 +/-2 ~ 42 – 46
– Resp alkalosis
5) Delta-delta: HCO3 + Δ AG = 24 + 14 = 38

pH 7.42 pCO2 35 Na 140 Cl 90 HCO3 24
– Neither
2) Primary disorder
– AG = 140 – (90 + 24) = 26
– Exp pCO2 ~ 1.5[HCO3] + 8 +/-2 ~ 42 – 46
– Resp alkalosis
5) Delta-delta: HCO3 + Δ AG = 24 + 14 = 38
Metabolic alkalosis

pH 7.42 pCO2 35 Na 140 Cl 90 HCO3 24

Normal pH, pCO2 & HCO3, BUT:
TRIPLE ACID-BASE DISTURBANCE

Metabolic Alkalosis - Pathophys
Generation Phase
– Loss of acid
– Gain of bicarbonate
Maintenance Phase: Kidney unable to
excrete bicarbonate normally
– Volume contraction
– Reduced GFR
– Cl or K depletion
– Increased PCO2
– Hyperaldosteronism

Metabolic Alkalosis - DDx
Chloride responsive Chloride resistant
Urinary Cl < 20 Urinary Cl > 20
 Vomiting  Current diuretic use
 NG suctioning  Mineralocorticoid
 Villous adenoma excess
 Prior diuretic use  Low K+ or Mg++
 Post-hypercapnia  Alkali excess
 CF  Bicarbonate, citrate,
acetate
 Refeeding alkalosis
 Bartter’s/Gitelman’s

DDx Hypokalemic Alkalosis –
Low-Normal BP
GI
– Vomiting
– NG suction
GU
– Diuretics
– Bartter’s
– Gitelman’s

DDx Hypokalemic Alkalosis –
↑ Renin, ↑ Aldo
High BP
– RAS
– Renin-secreting tumor
↓ Renin, ↓ Aldo
– AME: Deficiciency/Inhibition of 11B-hydroxysteroid dehydrogenase
– Liddle’s
– Cushings
– CAH
↓ Renin, ↑ Aldo
– Primary hyperaldosteronism
– GRH: Aldosterone synthase regulated by ACTH

Acid base lecture 2012

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