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Acid-Base
Disorders
JOHN REDEN ROMERO, RMT MD
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DEFINITION

 Bronsted and Lowry’s definition

 ACID: a substance that donates a proton in a reaction

 BASE: a substance that accepts a proton in a reaction

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COMPONENTS OF ARTERIAL BLOOD
GAS
 pH: measurement of acidity and alkalinity, based on H+: 7.35-
7.45

 Pao2: Partial pressure of oxygen dissolved in arterial blood 80-

100 mmHg

 PCO2: Amount of CO2 dissolved in arterial blood : 35-45 mmHg

 HCO3-: Calculated value of the amount of bicarbonate in the

blood: 22-26 mmol/L

 SaO2: Arterial oxygen saturation: >95%

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COMPONENTS OF ARTERIAL BLOOD
GAS

 Buffer base:
 Total quantity of buffers in blood including both volatile
(HCO3) and nonvolatile buffers (Hgb, albumin PO4)

 Base excess/Base deficit

 Amount of strong acid or base needed to restore plasma
pH to 7.40 at PaCO2 of 40 mmHg at 37 C

 Normal value: -2 to +2 mEq/L

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BICARBONATE AND CO2 BUFFER
SYSTEM
 All body buffers are in equilibrium with protons (H+)

 HCO3- and CO2 are the major buffers in the body, therefore pH is
expressed as a function of their ratio expressed by the
Henderson-Hasselbalch equation:

 pH = 6.1 + log HCO3- / pCO2 x 0.03

 This equation indicates that pH increases when the ratio

increases (alkalosis) and pH decreases when the ration
decreases (acidosis)
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BICARBONATE AND CO2 BUFFER
SYSTEM

 increase in HCO3 =metabolic alkalosis

 Decrease in HCO3= metabolic acidosis

 Increase in pCO2= Respiratory acidosis

 Decrease in PCO2= Respiratory Alkalosis

 COMPENSATORY RESPONSE OR
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REGULATION OF PH
 By 3 mechanisms:

 Chemical buffers:
 React instantly to compensate for the addition or subtraction of
H+ ions

 CO2 elimination:
 Controlled by the respiratory system
 Change in pH result in change in PCO2 within minutes

 HCO3- elimination:
 Controlled by the kidneys
 Change in pH result in change in HCO3
 It takes hours to days and full compensation occurs in 2-5
days
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METABOLIC ACIDOSIS

 Results from a reduction of bicarbonate content in the body, with

exceptions including:
 Acidosis resulting from dilution of body fluid by
administration of large amount of saline solution lacking
alkali (DILUTION ACIDOSIS)
 Acidosis from shift of H+ from the cell
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METABOLIC ACIDOSIS

 Primary categories of metabolic acidosis:

 Extrarenal acidosis: primary increase in acid production leading to a
decrease in bicarbonate

 Increased acid excretion

 Renal acidosis: primary reduction in net acid excretion

 Renal acid excretion is normal despite elevated pH

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RENAL ACIDOSIS

Classified into
a) Uremic acidosis: Reduced acid excretion due to reduced
nephron mass or generalized renal dysfunction. Develops when
GFR <20% of normal

b) Renal tubular acidosis (RTA): specific tubular dysfunction in

acid excretory function
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Renal tubular acidosis

 RTA Type I
 Aka classic RTA or distal RTA

 Inability to reduce urine pH below 5.5

 Site of defect: collecting duct

 Etiology: primary disorder or secondary to drug toxicity,

tubulointerstitial disease or other renal diseases
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 RTA type II
 aka proximal RTA

 Characterized by defective proximal bicarbonate reabsorption and a

reduced renal bicarbonate threshold

 Site of defect: proximal tubule

 Etiology: Primary or acquired; Example: Fanconi syndrome:

generalized proximal tubular dysfunction

 Seen with bicarbonaturia, aminoaciduria, GLYCOSURIA, phospaturia

and uricosuria

 *Characteristic finding: HYPOKALEMIA

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 RTA type III

 Hybrid form of type I and II RTA, no longer in use

 RTA type IV
 Caused by aldosterone deficiency leading to impaired renal tubular
potassium excretion - hyperkalemia

 Hyperkalemia induced impairmaent of ammonia production in the

proximal tubule

 MOST COMMON RTA

 Usually caused by HYPORENINEMIC, HYPOALDOSTERNISM, seen in

diabetic nephropathy
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ORGANIC ACIDOSIS

 Overproduction of organic acids primarily LACTIC ACID and

KETOACIDS

 Organic acids react with bicarbonate to form organic anions and

CO2  Increased anion gap
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LACTIC ACIDOSIS

 Formed from pyruvic acid by the enzyme LDH and cofactor NADH

 Increased concentration of pyruvic acid and ratio of NADH/NAD

leads to lactic acid production.

 2 types of lactic acidosis

 Type A Lactic acidosis- acidosis with associated tissue hypoxia, seen in
shock, cardiac arrest, CO poisoning etc. Most common type of lactic
acidosis

 Type B Lactic acidosis – acidosis without tissue hypoxia. Seen in

antiretroviral drug use and metformin use.
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D-LACTIC ACIDOSIS

 Accumulation of the D isomer of L-lactic acid

 Characterized by severe acidosis accompanied by neurologic

manifestation such as mental confusion and staggering gait

 Mimics ethanol intoxication without elevated plasma levels of

ethanol

 Due to colonic overproduction of D-lactic acid by bacteria due to

increased delivery of carbohydrates to the colon ( seen in
malabsorption syndromes) or proliferation of LDH forming
bacteria in the colon
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KETOACIDOSIS

 Produced flrom Free fatty acid in the liver and metabolized by

extrahepatic tissues (Acetoacetic acid & betahydroxybutyric acid)

 Accumulation of keto acids  leads to acidosis

 Insulin deficiency causes increased mobilization of FFA from

adipose tissue

 Insulin deficiency and glucagon excess are the main stimulus for
the conversion of FFA to ketoacids in the liver


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Approach to diagnosis of metabolic
acidosis
 Calculate serum anion gap

 Na – (Cl + HCO3)

 NV: 12 mmol/L (8-16 mmol/L)

 Increased AG suggests organic acidosis, uremic acidosis or

acidosis due to various toxic alcohols

 Normal AG suggests RTA and diarrheal loss of bicarbonate

 Decreased AG is commonly due to reduction in serum albumin

concentration
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 Check
z for Delta AG/Delta HCO3

 FOR HAGMA
 Delta AG/ Delta HCO3
 IF =1, pure HAGMA
 IF < 1 there is HAGMA + NAGMA
 IF > 1 there is HAGMA + metabolic alkalosis

 FOR NAGMA
 Delta Chloride/ Delta HCO3
 IF =1, pure NAGMA
 IF <1, NAGMA + HAGMA
 IF >1, NAGMA + metabolic alkalosis
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Approach to diagnosis of metabolic
acidosis
 Classification of Extrarenal vs Renal acidosis

 Extrarenal acidosis: Organic acidosis, diarrheal loss of

bicarbonate and acidosis due to toxins

 Renal acidosis: Uremic acidosis (abnormal BUN and Crea)or

RTA
 Hyperkalemic (RTA type IV)

 Hypokalemic: Urine pH below 5.5 = RTA type II

 Hypokalemic: Urine pH above 5.5 even after furosemide

administration= RTA type I
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Compensation for metabolic acidosis

 Achieved by HYPERVENTILATION

 Decreases pCO2, compensation moderately effective

 Maximal compensation is achieved within 12 to 24 hours

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METABOLIC ALKALOSIS
 When renal bicarbonate handling and GFR are normal, high
bicarbonate concentration is diffucult to maintain

 Elevated bicarbonate levels needs two conditions:

 Mechanism to increase plasma bicarbonate
 Administration of alkali, gastric loss of HCL ,
renal regeneration of bicarbonate
 Maintanance of the increased concentration
 Advanced renal failure or renal bicarbonate
threshold is increased (seen in volume depletion
and K depletion)
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Compensation for metabolic alkalosis

 Achieved by HYPOVENTILATION

 Hypoxemia is inevitable when hypoventilatiing, activates

chemoreceptors which increases RR

 This A-B disorder has the most least effective compensatory

mechanism.

 PCO2 does not exceed 60mmHg unless accompanied with

additional respiratory disorder
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Respiratory acidosis

 Elevation of pCO2 usually due to diseases of the lung,

respiratory muscle, respiratory nerve, thoracic cage and airways

 Suppression of respiration by drugs can also cause RA

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Compensation

 Increase in HCO3- concentration attempts to minimize reduction

in pH

 Done by tissue buffering of CO2

 Carbonic acid reacts with KBuff inside cells which leads to an elevated
HCO3 in cells. Increased HCO3 conc inside the cells is regulated by
exchanging with Cl (most notably seen in RBCs with an ubiquitous
anion exhanger)

 Happens within seconds

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Compensation

 Renal compensation
 Increase in renal excretion of acid in the form of NH4.

 Max compensation achieved within 5 days but is 90% complete within

3 days
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Respiratory alkalosis

 Due to stimulation of the respiratory center

 Hypoxic stimulation of the peripheral respiratory center (carotid body
and aortic arch chemoreceptors)

 Stimulation of the pulmonary receptors duting various lung disorders

(Pneumonia, pulmonary congestion, pulmonary embolism)

 Administration of drugs that stimulate the respiratory center

 Progesterone and salilcylate

 HIGHEST LEVELS seen in pyschogenic stimulation due to lack

of time to compensate.
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Compensation

 Tissue buffering: Formation of CO2 by reacting HCO3 with an H

Buff

 Renal compensation
 Reduction in net acid excretion

 Increased excretion of HCO3

 Compensation is most effective in respiratory alkalosis among

all AB disorders (completed within 2-3 days)
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LIMITATIONS OF BLOOD GAS
ANALYSIS

 Blood gas analysis cannot yield a specific diagnosis, a patient

with asthma may have similar values as a patient with
pneumonia

 Analysis also does not reflect the degree of abnormality seen in

the patient. A low PaO2 does not mean tissue hypoxia, nor does
a normal level indicate adequate oxygenation
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VENOUS BLOOD GAS

 Easier to obtain than arterial blood

 The pH, CO2 andHCO3 are similar in arterial blood however

PaO2 is expected to be halved
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Compensation
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Interpretation

 45 y.o male undergoing GB surgery under general anesthesia

(intubated on ventilator support)

 ABG results: pH= 7.48 pCO2=32 mmHg HCO3= 22 meq/L

 Serum elec Na= 136 Cl=101 K=3.6

 INTERPRET!

 Step 1: get the primary disorder

 Since pH is >7.4, disorder is alkalosis

 pCO2 is at alkalotic values therefore respiratory alkalosis

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 Step 2: Predict compensation

 In respiratory alkalosis, for every 1 mmHg fall in pCO2, HCO3

should decrease by 0.2 meq/L to compensate

 In the ABG, there is an 8mmHg fall in pCO2 from normal (40-32

mmHG)

 Therefore 8mmHg x 0.2= 1.6 meq/L

 HCO3 should decrease by 1.6 meq/L from normal to compensate

 HCO3 values in the case is 22 ( 2>1.6 meq/L)= COMPENSATED

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 Step 3. Identify secondary disorder

 Since HCO3 is expected to decrease by 2, there is adequate

compensation and no secondary disorder is noted.

 FINAL INTERPRETATION: COMPENSATED RESPIRATORY

ALKALOSIS
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 CASE 2

 26/M with T1DM, not taking regular insulin, presented with 3

day history of vomiting and increased sleeping time

 ABG results: pH: 7.10 pCO2: 30 mmHg HCO3: 6meq/L

 Blood chem: Corrected Na: 155 meq/L Cl: 110 K: 2.8

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 Step 1. Get primary disorder

 pH <7.4 = ACIDOSIS

 HCO3 (8 meq/L) is at acidic values therefore METABOLIC

acidosis

OR:
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 Step 2. Predict compensation

 In metabolic acidosis, for every 1 meq/L fall in HCO3 there should

be a 1.25 mmHg decrease in pCO2

 There is an 18 meq/L fall (24-6) in HCO3; there should be a

18 x 1.25= 22.5 mmHg fall in pCO2

 An appropriate compensation therefore should be 22.5 mmHg (case

change in PCO2= 10)

 Not compensated
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 Step 3. Secondary disorder

 The decrease in pCO2 is less than calculated appropriate

compensation (10 as compared to 22.5)

 Compensation is LESS than calculated appropriate

compensation

 Patient has concomitant RESPIRATORY ACIDOSIS

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 Step 4. Get anion gap

 Anion gap= Na – (Cl + HCO3)

 155 – (110 + 6) = 39

 NV of AG is 12, therefore we have a high anion gap metabolic

acidosis (HAGMA)

 Get Delta AG/Delta HCO3= (39-12) / (24-6) = 27/18 = 1.5

 Recall that if Delta values in HAGMA is >1, it is HAGMA +

metabolic alkalosis
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 FINAL INTERPRETATION: PRIMARY HIGH ANION GAP

METABOLIC ACIDOSIS WITH CONCOMITANT RESPIRATORY
ACIDOSIS AND METABOLIC ALKALOSIS

 DM caused metab acidosis, decreased sensorium causes

respiratory acidosis and vomiting caused metabolic alkalosis