WOLLO UNIVERSITY

COLLEGE OF MEDICINE AND HEALTH

SCIENCE
DEPARTMENT OF ANESTHESIA
SEMINAR ON: MANAGEMENTS OF COMMON ACID BASE
DISTURBANCES
By: Asfafaw & Nigussie
ADVISORS:- Sualih M. (assistant professor .) Ayub M. (Msc), & Yechale (Bsc)
DESSIE, ETHIOPIA
DECEMBER 2022
Presentation outline

 Seminar objective

 Introduction

 Simple and mixed acid base disturbances

 compensatory mechanisms

 Management of acid base disturbances

 Anesthesia considerations of acid base disturbances

 Summary

 References

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Seminar objectives

At the end of this presentation you should be able to :

Define acids and bases

Discuss normal compensatory mechanisms

List parameters that are used in acid base diagnosis

Diagnose and treat simple acid base disturbances

Diagnose and treat mixed acid base disturbances

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Managements of common acid base
disturbances

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INTRODUCTION

• Nearly all biochemical reactions in the body are dependent on

maintenance of a physiological hydrogen ion concentration which is
tightly regulated because alterations in hydrogen ion concentration
are associated with widespread organ dysfunction.

• This regulation often referred to as acid–base balance

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Acids & Bases

Brönsted – Lowry definitions

• An acid is chemical species that can act as a proton (hydrogen ion)

donor.

• A base is a species that can act as a proton (hydrogen ion) acceptor.

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 Acids & Bases

Arrhenius’ definitions

• An acid is a compound that contains hydrogen and reacts with water

to form hydrogen ions.

• A base is a compound that produces hydroxide ions in water

• A strong acid is a substance that readily and almost irreversibly gives

up hydrogen and increases hydrogen ion
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Acids & Bases

• A strong base avidly binds hydrogen ion and decreases hydrogen ion.

• weak acids reversibly donate hydroxide ion

• weak bases reversibly bind hydroxide ion

N.B both weak acids and bases tend to have less of an effect on
hydrogen ion for a given concentration of the parent compound than
do strong acids and bases
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 Acidemia and Alkalemia

• A blood pH less than 7.35 is called acidemia

• A pH greater than 7.45 is called alkalemia

• Regardless of the mechanism the underlying process that lowers the

pH is called an acidosis, and the process that raises the pH is known as
an alkalosis.

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 Acidemia and Alkalemia

• patient can have a mixed disorder with both an acidosis and an

alkalosis concurrently, but can only be either acidemic or alkalemic.

The last two terms are mutually exclusive

• Base excess (BE)- is the amount of strong acid (hydrochloric acid for

base excess greater than zero) or

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 Acidemia and Alkalemia

• Strong base (sodium hydrogen for base excess less than zero) required
to return 1 L of whole blood exposed in vitro to a PCO2 of 40 mm Hg
to a pH of 7.4

• Strong Ion Difference is the sum of all the strong, completely or

almost completely dissociated cations minus the strong anions.

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 Acidemia and Alkalemia

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Acid base equilibrium
• Conventionally acid–base equilibrium is described using the
Henderson–Hasselbalch equation
• For a solution containing the weak acid HA, where

• A dissociation constant, K , can be defined as follows:

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Acid base equilibrium
• The negative logarithmic form of the latter equation is called the
Henderson–Hasselbalch equation:

• pH = - log [H+] , Range is from 0 - 14

• If [H+] is high, the solution is acidic; pH < 7
• If [H+] is low, the solution is basic or alkaline ; pH > 7

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Simple Acid Base Disorders

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Mixed Acid Base Disturbances

• Is an independent coexistence of more than one primary disorder

• Mixed disorder occur in very ill and critical patient

• The most common one is metabolic acidosis and respiratory acidosis

• To know hypercloremic (normal anion gap) vs high anion gap

metabolic acidosis we use anion gap (CID SKILL)

• AG =Na – (Cl + HCO3 )

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Mixed Acid Base Disturbances

• We use MOSAD SKILL in increased anion gap to diagnose hidden triple

disturbance

Compare rise in AG with fall in HCO3

If rise in AG =fall in HCO3 pure high anion gap metabolic acidosis

If there fall in HCO3 is low coexistence metabolic alkalosis

If fall in HCO3 is high there is coexisting normal AG metabolic acidosis

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Mixed Acid Base Disturbances

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Compensatory Mechanisms

Physiological responses to changes in [H + ] are characterized by

three phases:

1 immediate chemical buffering,

2 respiratory compensation (whenever possible), and

3 a slower but more effective renal compensatory response

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Bicarbonate Buffer System

• In this system, the base molecule is bicarbonate, and its weak

conjugate acid is carbonic acid.

• The enzyme carbonic anhydrase, present in the endothelium,

erythrocytes, and kidneys, catalyzes this reaction to greatly accelerate
the formation of carbonic acid and make this the most important
buffering system in the human body

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Hemoglobin Buffer

• Hemoglobin is rich in histidine, which is an effective buffer from pH

5.7 to 7.7 (pKa 6.8). Hemoglobin is the most important noncarbonic
buffer in extracellular fluid

• capable of buffering both carbonic (CO2 ) and noncarbonic

(nonvolatile) acids

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Respiratory Compensation

• Mediated by chemoreceptors within the brainstem with receptors

respond to changes in cerebrospinal spinal fluid pH.

• lungs are responsible for eliminating the approximately 15 mEq of

CO2 produced every day as a byproduct of carbohydrate and fat
metabolism.

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Respiratory Compensation

During Metabolic Acidosis- Decreases in arterial blood pH stimulate

medullary respiratory centers. The resulting increase in alveolar
ventilation lowers Paco2 and tends to restore arterial pH toward
normal.

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Respiratory Compensation

During Metabolic Alkalosis- Increases in arterial blood pH depress

respiratory centers.

• Paco2 does not increase above 55 mmHg in response to metabolic

alkalosis because it is limited by activation of oxygen-sensitive
chemoreceptors so , it is less effective

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Renal Compensation

Compensate by-

• bicarbonate reabsorbed from filtered tubular fluid and form new

bicarbonate, and

• eliminate hydrogen ion in the form of titratable acids and ammonium

ions allows them to exert a major influence on pH during both
metabolic and respiratory acid base disturbances.
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Renal Compensation

• kidneys are responsible for eliminating the approximately 1 mEq/kg

per day of sulfuric acid, phosphoric acid, and incompletely oxidized
organic acids that are normally produced by the metabolism of
dietary and endogenous proteins, nucleoproteins, and organic
phosphates (from phosphoproteins and phospholipids).

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Renal Compensation

Renal Compensation During Acidosis- have 3-fold:

1 increased reabsorption of the filtered bicarbonate

2 increased excretion of titratable acids and

3 increased production of ammonia.

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Renal Compensation

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Renal Compensation During Alkalosis

• If necessary tremendous amount of bicarbonate can normally filtered

and subsequently reabsorbed allows the kidneys to rapidly excrete
large amounts of bicarbonate

• The kidneys are highly effective in protecting against metabolic

alkalosis which therefore generally occurs only in association with
concomitant sodium deficiency or mineralocorticoid excess.

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Rules Of Compensations

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 Respiratory Acidosis

Causes - Alveolar hypoventilation

- Increased CO2 production

• Buffering is primarily provided by hemoglobin and the exchange of

extracellular for + and from bone and the intracellular fluid
compartment

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Treatment of Respiratory Acidosis

• Treat the underling causes

• Increasing alveolar ventilation by controlled mechanical ventilation

bronchodilation, reversal of narcosis, or improving lung compliance (diuresis)

• Measures aimed at reducing CO2 eg, dantrolene for malignant hyperthermia,

muscle paralysis for tetanus, antithyroid medication for thyroid storm, and

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Treatment of Respiratory Acidosis

• Reduced caloric intake in patients receiving enteral or parenteral

nutrition

• Severe acidosis (pH <7.20), CO2 narcosis, and respiratory muscle

fatigue are indications for mechanical ventilation.

• An increased inspired oxygen concentration is also usually necessary,

as coexistent hypoxemia is common.

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Treatment of Respiratory Acidosis

• Intravenous NaHCO3 is rarely necessary, unless pH is <7.10 and HCO3

is <15 mEq/L.

• Buffers that do not produce CO 2 , such as Carbicarb (mixture of 0.3 M

sodium bicarbonate and 0.3  M sodium carbonate) or tromethamine
(THAM), are theoretically attractive alternatives

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Treatment of Respiratory Acidosis

• Buffering by this mixture mainly produces sodium bicarbonate instead

of CO2 .

• Tromethamine has the added advantage of lacking sodium depletion

effect and may be a more effective intracellular buffer

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Metabolic Acidosis

Caused by

1 consumption of HCO3 − by a strong nonvolatile acid

2 renal or gastrointestinal wasting of bicarbonate or

3 rapid dilution of the extracellular fluid compartment with a

bicarbonate free fluid.

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Anion Gap

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Treatment of Metabolic Acidosis

• Treat the underling causes

• Any respiratory component of the acidemia should be corrected.

• Respiration should be controlled, if necessary a PaCO2 in the low 30s

may be desirable to partially return pH to normal

• If arterial blood pH remains below 7.20 alkali therapy, usually in the

form of a 7.5% NaHCO3(1 mEq/kg) solution may be necessary
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Treatment of Metabolic Acidosis

• Raising arterial pH above 7.25 is usually sufficient to overcome the

adverse physiological effects of the acidemia.

• Profound or refractory acidemia may require acute hemodialysis with

a bicarbonate dialysate.

• If large amounts of NaHCO3 in treating cardiac arrest Paradoxical

intracellular acidosis may occur.
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Treatment of Metabolic Acidosis

• for diabetic ketoacidosis replacement of the existing fluid deficit

insulin, potassium, phosphate, and magnesium

• for lactic acidosis adequate oxygenation and tissue perfusion.

• salicylate poisoning alkalization of the urine with NaHCO3

• for ethanol or ethylene glycol intoxication include ethanol infusion or

fomepizole administration
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Anesthetic Considerations In Patients With
Acidosis
• potentiate the depressant effects of most sedatives and anesthetic
agents on the central nervous and circulatory systems.

• depressant effects of both volatile and intravenous anesthetics can

also be exaggerated.

• Halothane is more arrhythmogenic in the presence of acidosis.

• Avoid succinylcholine in acidotic patients with hyperkalemia.

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Respiratory Alkalosis

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Treatment of Respiratory Alkalosis

• Correction of the underlying process is the only treatment for

respiratory alkalosis.

• For severe alkalemia (arterial pH >7.60), intravenous hydrochloric

acid, arginine chloride, or ammonium chloride may be indicated.

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Metabolic Alkalosis

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Treatment of Metabolic Alkalosis

• Correct the underlying disorder.

• decreasing minute ventilation to normalize PaCO2 .

• for chloride-sensitive metabolic alkalosis is administration of

intravenous saline (NaCl) and potassium (KCl).

• H2 -blocker therapy is useful when excessive loss of gastric fluid is a

factor.
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Treatment of Metabolic Alkalosis

• Acetazolamide in edematous patients.

• mineralocorticoid activity readily responds to aldosterone antagonists

(spironolactone).

• When arterial blood pH is greater than 7.60, treatment with

intravenous hydrochloric acid (0.1 mol/L), ammonium chloride (0.1
mol/L), arginine hydrochloride, or hemodialysis should be considered.

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Anesthetic Considerations In Patients With
Alkalemia
• Cerebral ischemia can occur from marked reduction in cerebral blood
flow during respiratory alkalosis, particularly during hypotension.

• The combination of alkalemia and hypokalemia can precipitate

severe atrial and ventricular arrhythmias.

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Summary

• Only three factors independently affect acid-base balance, the arterial

partial pressure of carbon dioxide (PaCO2), the strong ion difference
(SID), and the total concentration of weak acids (ATOT).

• Most acid-base disorders are treated by reversal of the cause.

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References
Morgan 7th edition
Basics of anesthesia, 6th edition

P.Barash 6th edition

MILLER 7th Edition

www. nicky.oosthuizen@up.ac.za.com

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 Thank you!

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