Acid-Base Disorders

• CSN Vittal

Normal Values

• pH : 7.35 – 7.45• PaCO2 : 35 – 45 mm Hg• PaO2 : > 70 mm Hg• HCO3

- : 22 – 26 mEq/L• BE : -2.0 to +2.0

mEq/L

pH

• Depends on Acid : Base• Proportional to HCO3

- / H2CO3

• pH change to HCO3- is metabolic

• pH change to H2CO3 (CO2) is respiratory

Base Excess

• Difference between patient’s actual buffering capacity and normal buffering capacity

• Normal Values : +/- 2.0 mEq/L• Follows changes in HCO3

-

Primary & Compensatory Chages

Primary Change Compensation

Resp. Acidosis h PaCO2 h HCO3-

Resp. Alkalosis i PaCO2 i HCO3-

Met. Acidosis i HCO3- i PaCO2

Met. Alkalosis h HCO3- h PaCO2

Diagnosis of Acid-Base Disorders

• Consider the history• Look for clues on physical exam• Examine the electrolytes

–pCO2–Potassium–Anion Gap

• Review other laboratory data• Analyze the arterial blood gas

History• Loose Stools and decreased Intake• Polyphagia, Polydipsia of DM• History of Renal Insufficiency• Possibilty of Poisoning in Toddlers• Fever and Increasing Sickness – Sepsis?• Any signs of CNS Disorder• Any Medication History

Examination

• Any Signs of Sepsis• Any Signs of Dehydration• Any Signs of Meningeal irritation• Any Signs of Addison’s Disease• Any Signs of Neuromuscular Disease

Handerson Hasselbalch Equation

pH = pKa + log10

[ A- ]

[HA]

Handerson Hasselbalch Equation

pH = 6.1 + log10

[ HCO3- ]

[PaCO2 x 0.0301]

Vittal

Weak acid/salt systems act as a “sponge” for protons

As acidity tends to increase they take protons up

As acidity tends to decrease they release protons

CHEMICAL BUFFER SYSTEMS

Vittal

Saturation of carbonic acid – bicarbonate

buffer does not occur because carbonic acid

is continuously breaking down into

carbon dioxide and

water.

The 5 Step Approach

1• pH:

• Normal, acid or alkaline?

2• Respiratory component –

• Is it like pH?

3• Metabolic component –

• Normal or Raised Anion Gap?

4• Magnitude of change –

• minor, moderate or major?

5• Recognizing compensation

Step 1pH

Acidemic or Alkalotic?• Acidemic : pH < 7.35• Alkalotic : pH > 7.45

A normal pH does not rule out acid base disorder

Step 2

If the respiratory change is like the pH, i.e., both acid

Respiratory

The exception : when the metabolic component is also acid

Both are contributing to the acid pH.

If the PCO2 is not like the pH, i.e., the PCO2 is low (alkaline)

The primary problem is not respiratory;The low PCO2 is a compensation for the metabolic acidosis.

• Respiratory Component

Step 2If Respiratory, is it Acute or Chronic?

Respiratory AcidosisAcute: pH decrease

= 0.08 X (PaCO2 - 40) / 10

Respiratory AlkalosisAcute: pH Increase

= 0.08 X (PaCO2 - 40) / 10

Chronic: pH decrease

= 0.03 X (PaCO2 - 40) / 10

Chronic: pH Increase

= 0.03 X (PaCO2 - 40) / 10

Step 3

If the Standard Base Excess (SBE) is the component which is

like the pH, i.e., both acid (a negative base excess), then the

cause is …

Metabolic

The exception : when the respiratory component is also acid

Both are contributing to the acid pH.

If the SBE is not like the pH, i.e., the SBE is alkaline

.. then the primary problem is not metabolic; the high SBE is a compensation for the respiratory acidosis.

• Metabolic Component

Step 3• Metabolic Component

Anion gap = Na – (Cl + HCO3

-)

Usually 12 + 2

Anion gap Met. Acidosis : AG > 12

Non Anion gap Met. Acidosis : AG < 12

Step 3Is there another metabolic disturbance in increased AG

acidosis?Non AG acidosis or metabolic alkalosis may coexist with an AG metabolic acidosis

Corrected HCO3- = HCO3

- + (AG - 12)

Example 1

• HCO3 10, AG 26

Corrected HCO3 = 10 + (26 -12) = 24No additional disturbance

Example 2

• HCO3 15, AG 26

Corrected HCO3 = 15 + (26 -12) = 29Additional metabolic alkalosis

Step 4• Minor• Moderate• Major

• Magnitude of Disturbance

• Each primary acid base disorder had its own formula for prediction.

• Is the compensation adequate?• If magnitude of the compensation deviates

from the predicted, it indicates additional primary a-b disorder

Step 4

Whenever the pH is normal (7.4) then the PCO2 and the SBE are equal and opposite

.

The slope for BE / PCO2 gives us this ratio:

3 units of change in SBE

= 5 mm Hg change in PCO2.

 AdjectivePCO2

mmHgSBE

mEq/L

Alkalosis

Severe <18 <13

Marked 18 to 25 13 to 9

Moderate 25 to 30 9 to 6

Mild 30 to 34 6 to 4

Minimal 34 to 37 4 to 2

Normal Normal 37 to 43 2 to -2

Acidosis Minimal 43 to 46 -2 to -4

Mild 46 to 50 -4 to -6

Moderate 50 to 55 -6 to -9

Marked 55 to 62 -9 to -13

Severe > 62 to <-13

• Magnitude of Disturbance

Step 4

• Metabolic Acidosis – Winter’s Formula• pCO2 = (HCO3 X 1.5) + (8 + 2)

• Metabolic Alkalosis• Each rise in HCO3 by 1 mEq/L, pCO2 should

rise 0.7 mm Hg, + 2

• If a pt. with a respiratory problem has a high PCO2, e.g., 60 mm Hg (raised by 20 mm Hg) then for "complete compensation" the SBE would have to be about 12

(using the 5 to 3 ratio given above). • If the SBE were zero = "no compensation" -

typical of an acute process of recent onset. Most likely - the patient is somewhere in the middle

(SBE = 6 mEq/L) which is typical for "compensation for chronic respiratory acidosis”.

Step 5

Recognizing compensation

Inverse example:

• If a patient with a metabolic problem has a low SBE, e.g., -12, then the PCO2 would have to be reduced by hyperventilation to about 20 mm Hg to achieve "complete compensation".

• If the PCO2 were still normal --> "no compensation".

Again, far the most likely, the patient is somewhere in the middle (30 mm Hg) which is typical for "compensation for metabolic acidosis".

Step 5

Recognizing compensation

Respiratory Acidosis Acute

The PaCO2 is elevated above the upper limit of the reference range (i.e., > 45 mm Hg) with an accompanying acidemia (i.e., pH < 7.35).

Chronic The PaCO2 is elevated above the upper limit of the

reference range, with a normal or near-normal pH secondary to renal compensation and an elevated serum bicarbonate (i.e., HCO3

- > 30 mEq/L.)

Respiratory Disturbances Is it Acute or Chronic ?

Respiratory AcidosisAcute: pH decrease

= 0.008 X (PaCO2 – 40)

Respiratory AlkalosisAcute: pH Increase

= 0.008 X (PaCO2 – 40)

Chronic: pH decrease

= 0.003 X (PaCO2 – 40)

Chronic: pH Increase

= 0.003 X (PaCO2 – 40)

Respiratory Acidosis - AcuteAbrupt failure of ventilation, h PaCO2

Neuromuscular disorders CNS Depression Brain stem Injury

Musculoskeletal Disorders GBS Myasthenia

Airway Obstructive Disease Asthma Foreign Body Laryngeal Edema Pulmonary Embolism

Drugs Sedatives Barbiturates

Respiratory Acidosis - Chronic

COPD Obesity hypoventilation syndrome

(i.e., Pickwickian syndrome) Neuromuscular disorders

Amyotrophic lateral sclerosis Severe restrictive ventilatory

defects Interstitial fibrosis and Thoracic deformities

Respiratory AcidosisSymptoms: Symptoms of the disease that causes

respiratory acidosis are usually noticeable shortness of breath easy fatigue chronic cough, or wheezing.

When respiratory acidosis becomes severe, Confusion irritability, or lethargy may be apparent.

Respiratory AcidosisTreatment:

Treat the underlying cause Improve alveolar gas exchange Assisted ventilation

• Bicarbonate must not be infused to treat the acidosis because it generates more CO2

Respiratory AlkalosisHyperventilation, i PaCO2

• Catastrophic CNS Events • Hemorrhage• Hysterical• Assisted ventilation• Drugs• Salicylates (early stages)• Interstitial Lung Disease• Cirrhosis, Liver Failure• Anxiety• Gram negative Septicemia• Hypoxia and severe anemia or high altitude

Respiratory AlkalosisSymptoms

• Tingling and numbness• Parasthesias• Lethargy• Tetany• Unconsciousness• Vasospasm of cerebral vassals -

Hypercapnia

Respiratory Alkalosis

Treatment

• Treat underlying cause

Metabolic Acidosis

• Increased H+ Load

• Increased HCO3- Loss

Metabolic AcidosisWhat is anion gap?Anion gap = (Na+) – (Cl- + HCO3

-) Usually 12 + 2

Major unmeasured anions• albumin• Phosphates• sulfates• organic anions

Anion gap Met. Acidosis : AG > 12Non Anion gap Met. Acidosis : AG < 12

Anion Gap Metabolic AcidosisAccumulation of unmeasured anionsLow HCO3 and h AG

ethanol remia iabetic ketoacidosis araldehyde nfection actic acid thylene glycol alicylates

• M• U• D•

P• I• L• E• S

Na+

Cl-

HCO3-

AG

Na+

Cl-

HCO3-

AG

Differential Dx of high-anion gap acidosis: "SLUMPED":

• Salicylates• Lactic acidosis• Uremia• Methanol intoxication• Paint sniffing (toluene) /

Paraldehyde• Ethylene glycol intoxication• DKA or alcoholic ketoacidosis

High anion gap Metabolic acidosis: ”KULT”

• Ketoacidosis• Uremia• Lactic Acidosis• Toxins (Paraldehyde, Ethylene

glycol, Methanol, Salicylate)

Non Anion Gap Metabolic AcidosisLoss of HCO3 or External acid infusionLow HCO3 AG < 12

• GI Losses of Bicarbonate (Diarrhoea)• Renal Losses

• Renal Tubular Acidosis• Renal Toxins• Carbonic Anhydrase Inhibitors• Ureteral Diversion• Compensation for Resp. Acidosis

• Administration of Acid• HCl or NH4Cl Infusion, TPN

Urine anion gap = [Na+] + [K+] - [Cl-] :• A -ve UAG suggests GI

loss of bicarbonate (eg diarrhea), {neGUTive}

• A +ve UAG suggests impaired renal acidification (ie renal tubular acidosis).

Decrease in Anion Gap Metabolic AcidosisDefined as < 6

P araproteinemias, Multiple myelomaL ithium intoxicationE xcessive Calcium and MagnesiumA lbumin is low (hypoalbuminemia)B romism

Metabolic Acidosis

• Increased work of breathing : Deep rapid breathing (Kussmaul’s)

• Peripheral Vasodilatation, collapse, shock, impaired cardiac function

• Lethargy, drowsiness, confusion, stupor• Hyperkalemia• Nonspecific : Nausea, Vomiting• Chronic Acidosis:

Osteopenia – CaCo3 loss Muscle weakness – Glutamine loss

Clinical Features

Metabolic Acidosis

Principles:• Identify cause• Initial goal : Bring the pH ~ 7.25

(For cardiac contractility & responsiveness to catecholamines)

Sodabicarb : 1-2 mEq/Kg [1 ml of 7.5% NaHCO3 = 0.9 mEq]

Dose : (15 – measured HCO3–) × 0.6 × Body weight OR Body wt.(Kg) X 0.3 X Base excess]   

• Half as bolus• Half as infusion over 12 – 24 hrs.

Management

Metabolic Acidosis

• Potassium replacement :Serum K+ should be > 3.5 mEq/L before administering HCO3

-

• THAM (tromethamine; tris-hydroxymethyl aminomethane) An amino alcohol

Indication :In partients with CHF who may not be able to tolerate additional Na+ burden if treated with Sodabicarb.

Dose : Body wt. (Kg) X Base excessAdministration: As infusion over 3 - 6 hours

Management – Contd.

Metabolic Acidosis

• DKA• Lactic Acidosis• RTA• Uremia• Salicylate toxicity

Specific Treatment

Metabolic Alkalosis

Very Dangerous:• Shifts O2 dissociation curve to Lt.• Causes vasoconstriction of all

vessels except pulmonary circulation

• Suppresses ventilation• Decreases ionized Ca++ and shifts

K+ into cells – hypocalcemia and hypokalemia

Increase in extra-cellular pH (above 7.45) due to primary increase in plasma bicarbonate

Metabolic Alkalosis

Issues to Ponder over: • What generated the alkalosis?

• What is maintaining the alkalosis – what is preventing kidney from excreting the

alkali ?

Metabolic Alkalosis - Causes• Loss of acid: GI Losses• Vomiting• NG suction• Acid diarrhoea (Congenital

chloridorrhoeas, villous adenomas)

Renal H+ Loss• Diuretics (thiazides,

furosemide)• Bartter’s Syndrome• Mg deficiency• Hyperaldosteronism,

Cushing’s

• Infusion of HCO3:

• Iatrogenic• Milk Alkali syndrome• Massive blood

transfusion (citrated blood)

• Rapid correction of chronic hypercapnia

Metabolic Alkalosis

What’s maintaining1. Volume contraction (Chloride responsive)

NG Suction, vomiting, diuretics2. Potassium deficiency3. Chloride depletion4. Increased mineralocorticoids

(Chloride resistant)

•Metabolic Alkalosis

What’s maintaining• Volume contraction (Chloride responsive)• Adrenal Disorders• Exogenous Steroids• Alkali Ingestion• Licorice• Bartter’s Syndrome

Metabolic AlkalosisClinical Presentation

• Muscle cramps (neuromuscular excitability)

• Weakness• Hypoxia• Arrhythmias• Decreased myocardial contractility• Decreased cerebral blood flow• Mental obtundation, Confusion• Impaired O2 unloading in periphery

Metabolic AlkalosisSaline responsive intravascular volume expansion with normal saline potassium repletion Ammonium chloride / Arginine chloride in resistant cases Acetazolamide ( if NS contraindicated as in CHF) Discontinue diureticsl)

Saline resistant (mineralocorticoid excess) Potassium repletion mineralocorticoid antagonists acetazolamide Hemo or peritoneal dialysis : in severe alkaloses with

hyperosmolar states Discontinue diureticsl) Surgical

Mixed Acid – Base Disorders

• Respiratory Acidosis + Metabolic Acidosis– Resp. Distress Syndrome

• Respiratory Acidosis + Metabolic Alkalosis– Excessive diuretic therapy, Chronic respiratory acidosis

with C.C.F.• Metabolic Acidosis + Respiratory Acidosis

– Hepatic Failure• Respiratory Alkalosis + Metabolic Acidosis

– Salicylate intoxication– Gm – ve sepsis

• Compensatory adjustments fall outside the expected reange

• Vittal