ACID BASE EQUILIBRIUM,

CLINICAL CONCEPTS AND

ACID BASE DISORDERS
Dr Sajith Damodaran

University College of Medical Sciences & GTB

Hospital, Delhi

Homeostasis
The Interstitial Fluid is the environment of the cells,
and life depends on the constancy of this internal
sea.
Homeostatic Mechanisms : Maintain within a narrow
range.
Tonicity
Volume
Specific ion concentration
Increased Osmolality of ECF
Defence of Tonicity (280-295mOsm/L)
Thirst
Increased
Vasopressin Secretion
Vasopressin secretion
Increased
Inhibitor
Thirst Mechanism
Water Intake
Water Retention
y
Dilution of ECF

Homeostasis
Defence of
Volume:

ECF Na+ - Most

important
Renin-AngiotensinAldosterone System
Vasopressin Secretion:
Volume stimuli override
osmotic regulation
ANP & BNP

Angiotensinogen
Renin

Angiotensin I
ACE

Thirst
Adrenal Angiotensin II
Brain
Cortex

Aldosterone

Vasopressin

Kidney
Na Retention
Water
Retention

Blood Vessel
Vasoconstricti
on

Homeostasis
Defence of Specific Ionic Concentration:
Glucose
Na+ & K+
Ca++ - Mainly by Parathyroid & Calcitonin
Mg++ - Incompletely understood mechanisms
Also dependent on H+ ion
pH is maintained within a narrow range.

Acid Base Equilibrium

What is Acid Base Equilibrium About?
Buffer
s?

Base
Excess/
Deficit?

Fixed
Cation
?

Anion
Gap?

Acid Base Equilibrium

Acid Base Equilibrium is all about
Maintenance of H+ ion
concentration of the ECF.
Source of
H+mEq/d
ion in Body:
12500
CO2 from
metabolis
m

Ingestion of
NH4Cl, CaCl2
Strenuous Exercise
Lactic Acid

H
+
io
n

50 - 100 mEq/d
H+ load from
AA
metabolism
Failure of Kidneys to
Excrete PO4--, SO4--

Diabetic
KA

Some Basic Chemistry

Definitions:
Arrhenius:

Acid: H+ Donor in Solution

Base: OH- donor in Solution

Browsted and Lowry:

Acid: Proton Donor

Base: Proton Acceptor

H20 can be both

Some Basic Chemistry

Simple Rule of Thumb:
Acid Higher conc. Of H+ ion
Base Lower conc. Of H+ ion
Strong Acid/Base Dissociates completely and irreversibly
Weak Acid/Base Dissociates partially and reversibly
Strong Electrolyte: Dissociates completely in solution at
physiological pH
Eg: NaCl, KCl
Weak Electrolyte: Dissociates incompletely in solution at
physiological pH
Eg: CO2 HCO3- System, Proteins

Some Basic Chemistry

pH (Puissant of Hydrogen):
Negative logarithm of H+ ion concentration to the
base of 10
Why pH?
Normal H+ ion conc: 0.00004meq/L or 40nEq/L or
4x10-9 mol/L
pH converts to decimal numbers & takes away
negative sign.
Normal pH: 7.35-7.45
Normal H+ Conc: 0.00002mEq/L 0.0001 mEq/L

Some Basic Chemistry

Pitfalls: Non-linear Negative Logarithmic scale

pH Decreases as [H+] increases.

Each unit change in pH from 7 represents 10 fold
change in H+ ion conc.
Eg:

At pH 4, there are 10 times as much H + than at pH 5, &

100 times as at pH 6

Same numeric change in different portions of the pH

scale implies vastly different nanomolar change in H +
ions
Eg:

pH 56 => 100 times greater change in ionic conc than

when pH 7 8

Body H+ ion conc is not as tightly controlled as the

other ion, though the pH scale implies so.

Some Basic Chemistry

Water (H2O)
Water dissociates, but to a very low extent.
H2O <====>H+ + OHBut, a glass of water has a billion times more H 2O than H+ & OHAt equilibrium:
[H+] [OH-] = Kw[H2O]
{Kw(Dissociation constant of water) changes with temperature}
Or, [H+] [OH-] = Kw
pH of Water:
Since at neutral pH, [H+] = [OH-]
[H+] = ROOT (Kw)

Acidic solution, [H+] > ROOT (Kw), Basic sol, [H+] < ROOT(Kw)

pH changes with temperature

Acid Base Equilibrium:

Solutions:
When substances are added to water, 3
simple rules have to be satisfied at all
time:
1.
2.
3.

Electrical Neutrality
Mass conservation
Dissociation Equilibrium

ECF is a complex solution with strong ions,

weak ions and CO2 dissolved in water.

Acid Base Equilibrium:

CO2 in Water:

Can Dissolve in water

All these reactions have equilibrium
Can form - Carbonic Acid
Constants and can be solved at equilibrium.
- Bicarbonate ion
- Carbonate ion

CO2(gas) <====> CO2(dissolved)

Rate of Forward Reaction = Kf * PCO2
Rate of Reverse reaction = Kr *[CO2(dissolved) ]
=> [CO2(dissolved)] = Kf /Kr *PCO2
Kf /Kr = SCO2 (Solubility of CO2 ) = 0.03mEq/L/mm Hg at 370 C

Acid Base Equilibrium:

CO2 + H2O <====> H2CO3
=>[CO2][H2O] = K*[H2CO3]
=> [H2CO3] = K*PCO2
H2CO3 <====> H+ + HCO3Henderson Equation:
[H+ ] = K1 [H2CO3]/[HCO3- ]
Modified Henderson Equation:
[H+ ][HCO3- ] = K2 [CO2][H2O]
[H+ ][HCO3- ] = K3 [CO2]
[H+] = K*PaCO2/[HCO3-]

Acid Base Equilibrium:

The Henderson-Hasselbalch Equation:
CO2 + H2O <====> H+ + HCO3=> [H+] = Ka * [CO2]/[HCO3-]
Rearranging:
=>1/[H+] = 1/Ka*[HCO3-]/[CO2]
Taking Logarithm on both sides & Rearranging:
=>

pH= pKa + log10[HCO3-]/0.03*PCO2

Significance:
Includes components of both Met & Resp Acid base disorders
Value of any one variable can be determined if other two known.
Mostly HCO3- is calculated

pH determined by ratio of [HCO 3-]/PCO2 . Maintained at 20.

Increase=> alkalosis, Decrease => Acidosis

Clinical Concepts: The Stewart Approach

Dissociation equations can be solved

mathematically.
When the equations are solved

Independent Variables: SID, [Atot] &

PaCO2

Constants : Dissociation constants

Dependent Variables: [H+], [OH-],
[HCO3-], [CO32-], [A+], [HA], [H2CO3], [CO2
dissolved]

Clinical Concepts: The Stewart Approach

Dissociation equations can be solved

mathematically.
When the equations are solvedIndependent Variables: SID, [Atot] &
PaCO2

Dependent
Variables
Constants : Dissociation constants
canDependent
onlyVariables:
be [Hchanged
], [OH ],
[HCO3 ], [CO3 ], [A ], [HA], [H CO ], [CO
by
changing
the
]
independent

dissolved

2-

Clinical Concepts: The Stewart Approach

SID: Strong Ion Difference
([Na+] + [K+] + [Ca++] + [Mg++]) [Cl-]+ [other Strong Anions]
Normal: 40-44mEq/L with normal protein levels
Change from normal is equivalent to SBE

Dehydration: Increases SID ==> Alkalosis

Dilution, Organic Acids, Hyperchloremia : Decreases SID ==>
Acidosis

[Atot]: Total Amount of Weak Acid in Solution

Albumin is the most important weak electrolyte in plasma.

Other weak acids are Inorganic Phosphates, Plasma proteins.

Hypoproteinemia: Alkalosis
Renal Failure: Accumulation of Phosphate: Acidosis

Clinical Concepts:
Base Excess: Amount of Acid or Alkali required to return
plasma in vitro to normal pH under standard conditions.

Standard BE: BE calculated for Anaemic Blood (Hb = 5Gm

%).
Since Hb effectively buffers plasma & ECF to a large
extent.

Quantity of Acid or Alkali required to return plasma in-vivo

to a normal pH under standard conditions

Anion Gap:

AG = [Na+] + [K+] - {[HCO3-] + [Cl-]}

Normal Value: 8-12mEq/L,

Unmeasured Anion: Albumin, Phosphate, sulphate, organic

anions

AG decreases by 2.5mEq/L for every 1mEq/L decrease in

Clinical Concepts:
Acid Base Equilibrium:
Elimination of Acid
Recovery/Regeneration of Base
Mechanisms that keep pH stable
Buffering
Compensation
Correction

Clinical Concepts:
Buffers:
Definition: A substance that can bind or release H +
ions in solution, thus keeping the pH of the
solution relatively constant despite addition of
large amounts of acid or base.
For Buffer HA,
HA <====>H+ + ApH = pKa + log [A-]/[HA]

When [A-] = [HA], pH= pK, buffering capacity is

maximum.
Ideal body buffer has pKa between 6.8 and 7.2

Clinical Concepts:
Most buffers are weak acids (Hbuffer) & their Na Salts (Nabuffer)
Strong Acids Buffered by NaBuffer
HCl

+ NaBuffer <====> H+ + Cl- +Na+ + Buffer <====> Hbuffer + NaCl

Strong Bases buffered by Hbuffer

NaOH

+ H Buffer <====> Na+ + OH- + H+ + Buffer <====> NaBuffer + H2O

Buffer Effectiveness Depends on:

Quanitity

H2CO3 /HCO3- - Most important Extracellular Buffer

Protein Buffers Most improtant Intracellular Buffer

pKa
Buffering capacity maximum when pH=pK a
Function well within 1 pH unit. (Eg: HCO 3- - 5.1-7.1)

Clinical Concepts:
Buffers in ECF:
Carbonate-Bicarbonate Buffer

53%

Plasma (35%)
Erythrocyte(18%)

Hemoglobin 35%
Plasma Proteins 7%
Organic & Inorganic Phosphates5%

Buffers in ICF:
Intracellular Proteins
H PO -HPO - system
2
4
4
Intracellular buffers are responsible for ~85% buffering in Met. Acidosis
and ~35% in met alk and almost complete buffering in respiratory
acidosis and alkalosis

Clinical Concepts:
Bicarbonate Buffer:
HCl

+ NaHCO3- <==>NaCl + H2CO3<==>NaCl + H2O + CO2

useful only for metabolic acid

Hb System:

Both Respiratory & Metabolic Acid in ECF

Forms Carbamino compounds with CO 2
Buffers H+ directly
CO2

+ H2O <====>H2CO3 + KHb <====> HHb + KHCO3

HCO3- diffuses out & Cl- diffuses into cells Chloride

shift
pKa 6.8

Clinical Concepts:
Protein Buffer:
Predominant Intracellular Buffer Large total concentration
pK = 7.4
AA have Acidic & Basic Free radicles
COOH + OH- <====> COO- + H2O
.NH OH + H+ <====> NH + H O
3
3
2
.

Phosphate Buffer:
pK = 6.8
Predominantly Intracellular
Also in renal tubular
HCl + Na2HPO4 <====> NaH2PO4 + NaCl
NaOH + NaH2PO4 <====> Na2HPO4 + H2O

Clinical Concepts:
Compensation:
Pulmonary Compensation
H+ + HCO3-<====> H2CO3 <====>CO2 + H2O

H+ acts on medullary centres.

Increased PaCO2 stimulates ventiallation

Metabolic Acidosis Increased Ventillation
Metabolic Alkalosis Depression of
Ventillation
But,

limited because Hypoxic stimulus can

override Hypercapnia

Clinical Concepts:
Renal Compensatoin:
Mechanisms:
1.

2.
3.
4.

Reabsorption of filtered HCO3- (4000-5000

mEq/d)
Generation of fresh bicarbonate
Formation of titrable acid (1mEq/Kg/d)
Excretion of NH4+ in urine

MAJOR RENAL MECHANISMS RESPONSIBLE FOR H +

EXCRETION/HCO3- RETENTION
PERITUBULAR
BLOOD

RENAL
TUBULAR CELL
HCO + H
3

1.
NaHCO3
2.
NaHCO3
3.
NaHCO3

GLOMULAR FILTRATE
Glutamin
e
2+

HCO3- Na+ HPO4

Na+

Na

H2CO3

CO2

CO2 + H2
O

CO
2

H2PO4-

HCO3- + H+
CA

NH4+

HCO3- + H+

H2O

H2PO4-

can be obtained from blood or the tubular fluid

NH4+

NH3

Clinical concepts:
Compensation

ction of Compensatory Responses on Simple Acid Base Disor

Disorder
Disorder

Prediction
Prediction of
of Compensation
Compensation

Metabolic
MetabolicAcidosis
Acidosis

PaCO
PaCO22==(1.5
(1.5xxHCO
HCO33- -))++88
Or
Or
PaCO
PaCO22will
will 1.25mm
1.25mmHg
Hg(1.0-1.5)
per mmol/L
per mmol/L
in [HCO3-in]
[HCO
Or 3- ]
PaCO2 = [HCO3- ] + 15
Or
PaCO2 = [HCO3- ] + 15
Metabolic Alkalosis PaCO2 will 0.75 mm Hg per mmol/L in [HCO3- ]
Or 2 will 0.75 (0.25-1.0) mm Hg per mmol/L in
Metabolic Alkalosis PaCO
PaCO3-2 ]will 6mm Hg per 10 mmol/l
in [HCO3- ]
[HCO
Or
Or
PaCO22 will
= [HCO
+ 15
PaCO
6mm
per 10 mmol/l
in [HCO3- ]
3 ] Hg
Or
Respiratory
PaCO2 = [HCO3- ] + 15, Max 55mmHg
Alkalosis
Respiratory
Acute
Alkalosis
Chronic
Acute
Respiratory
Chronic
Acidosis
Respiratory

[HCO3- ] will 2mmol/L per 10 mmHg

in PaCO2

[HCO3- ] will 4mmol/L per 10 mmHg in PaCO2

[HCO3- ] will 2mmol/L per 10 mmHg in PaCO2
[HCO3- ] will 4mmol/L per 10 mmHg
-

in PaCO2

Acid-Base Nomogram:

Clinical concepts:
Effect of Temp:
pH rises 0.015/0C drop in temp
Effect of PaCO2 on pH:

pH changes by 0.08/10mm Hg change in

PaCO2

Effect of change of [HCO3-] on pH:

pH changes by 0.1/ 6 mEq change in

[HCO -]

Clinical Concepts:
Effect of Electrolytes in Buffering:
Potassium Ion: Intracellular

Hypokalemia - K+ Moves out H+ moves

in
- K+ & HCO3- reabsorption, H+
Excretion

Sodium Ion

Hyponatremia -- Na+ & HCO3- reabsorption

& H+ excretion

Clinical Concepts:
Role of Bones:
Exchange of Extracellular H + for Na+ & Ca++

Acid load Demineralise Bones

Alkaline load Deposition of CO32- in Bones

Time Course of Buffering:

Plasma HCO - ----> Immediate
3

Interstitial HCO3-

-----> 15-20 Min

Intracellular Proteins & Bones ----> 2-4 Hours

Acid Base Disorders

Acidosis/Alkalosis:
Any process that tends to increase/decrease
pH
Metabolic: Primarily affects Bicarbonate
Respiratory: Primarily affects PaCO
2
Acidemia/Alkalemia:
Net effect of all primary and compensatory
changes on arterial blood pH.

Acid Base Disorders

The primary
disorders:

Metabolic Acidosis
Metabolic Alkalosis
Respiratory Acidosis

Acute
Chronic

Respiratory Alkalosis

Acute
Chronic

Disorder

Primary
Change

Compensa
tory
Change

Metabolic
Acidosis

HCO3_

PaCO2

Metabolic
Alkalosis

HCO3_

PaCO2

Respiratory
Acidosis

PaCO2

HCO3_

Respiratory
Alkalosis

PaCO2

HCO3_

Acidosis:Clinical Effects
CVS:
Combination of Effects of Direct depression and Catecholamine
stimulation
Heart Rate: Initial Increase then Decrease
Rhythm: Increased Atrial & Ventricular Dysrrhythmias

Due to Changes in S K+
Lower threshold for VF

Contractility: Increased contractility. Depression if pH<7.0

Cardiac Output: Increased

Increased Catecholamines,
Decreased Arterial tone,
Increased Venous Tone
At <7.0, Decreased d/t direct depressant effects
CCF d/t Increased venous tone.

Acidosis:Clinical Effects
Vascular Effects:
Direct Vasodilatation
Vasoconstriction d/t Catecholamines

Respiratory: Vasodilatation predominates

Metabolic: Vasoconstriction
Splanchnic

& Renal Vasoconstriction

Variable effects on Coronary, Cutaneous, Uterine

BP doesnt change till extremes imbalance

Hypotension occurs when pH falls below 7.0

Clinical Effects of Acidosis:

Respiratory System:
Minute Ventilation:
TV

Twice more for RA than MA

Airway Resistance:

Direct: Decrease by Smooth muscle relaxation

Indirect: Increased by Vagal Tone
Vagal

Effect predominates: Increased WoB

Pulmonary Vasculature:

RR

Vasoconstriction
Enhanced HPV

Right shift of ODC:

But tissue hypoxia can occur due to hypotension

Clinical Effects of Acidosis:

GI System:

Variable effects in splanchnic BF

Renal System

Vasoconstriction

Uteroplacental:

CO2 freely diffuses

HCO3- slowly over hours

Similar effects in Fetal systems

Electrolytes:

Calcium: Increased Free Ca++

Potassium: Increased S K+

Clinical Effects of Acidosis:

NeuroEndocrine:

CBF (by PaCO2)

Mental Changes: CNS Depression

Decreased Body Temp

More with RA
Impaired central regulation
Cutaneous vasodilatation
Decreased Cellular Metabolism

Increased secretion of catecholamines

Clinical Effects of Acidosis:

Effect

Direct

Indirect

Clinical

Cerebral blood flow

Heart rate

Cardiac inotropy

Systemic arterial tone

Systemic venous tone

Pulmonary artery tone

Airway tone

Uterine blood flow

Renal blood flow

Ionised calcium

Serum potassium

Respiratory Acidosis:
Primary Increase in PaCO2
Cause:
Production/ Elimination
Produced by:

Carbohydrate and fat metabolism,

muscle activity,
body temp
thyroid hormone activity

Elimination by Lungs.

Immense capacity
CO2 - ventilation compromised

Respiratory Acidosis:
Causes:
Alveolar
Hypoventilation

CNS Depression

Drugs
Cerebral Ischemia/trauma
Sleep Disorders
Pickwickian Syndrome

Neuromuscular
Disorders

Neuropathy
Myopathy

Kyphoscoliosis
Flail Chest

FB/Tumor
COPD/Sever
Asthma

Parenchymal Lung Disease

Pneumothorax
Pleural Effusion

Airway Obstruction

Chest Wall Abnormality

Pleural Abnormality

Pul edema/embolus
Pneumonia
ILD

Ventilator Dysfunction

Respiratory Acidosis:
Causes Contd
Increased CO2 Production:

Large Carbohydrate meal

Malignant Hyperthermia
Intensive shivering
Prolonged seizures
Thyroid Storm
Extensive Burns

Respiratory Acidosis:
pH 7.36
PaCO2 64
HCO3- - 33
pH is acidic, but normal
PaCO2 > 40 => Resp Acidosis
Compensation expected:
HCO3- = 24 + (64-40) x 0.1 = 24+2.4 = 26.4 or
24 + (64-40) x 0.4 = 24 + 9.6 = 33.6
Diagnosis: Chronic Respiratory Acidosis

Metabolic Acidosis:
Causes:
Increased Anion
Gap

Increased
Production of
Endogenous Acid

Ketoacidosis- DM,
Starvation
Lactic Acidosis
Mixed- NKHC, Alcoholic
Abnormal AA Met.
CRF

Ingestion of Toxins

Salicylate
Methanol
Ethylene Glycol
Paraldehyde, Toluene,
Sulphur

Rhabdomyolysis

Metabolic Acidosis:
Causes Contd
Normal
AG(Hyperchloremic)
GI Loss of HCO 3

Diarrhea
Fistula- Pancreatic,
Biliary, Small Intestinal
Ureterosigmoidostomy
Obstructed Bowel Loop
Cholestrylamine, CaCl2,
MgSO4

Renal Loss of Bicarb

RTA
CA Inhibitors
Hypoaldosteronism

Dilutional-

Bicarb free fluid

TPN

Increased Intake of Cl containing Acids

NH4Cl, Lysine
hydrochloride,
Arginine
Hydrochloride

Metabolic Acidosis:

pH 7.36
PaCO2 26
HCO3- - 13

BE - -11
pH Acidic but normal
PaCO2 Decreased => Not Respiratory

HCO3- - Decreased => Metabolic Acidosis

Compensation expected: 40 - (24-13)x1.25 =4013.75 = 26.25
Diagnosis: compensated Metabolic Acidosis

Treatment:
Acute Respiratory
Acidosis

Chronic Respiratory
Acidosis

Correction of the cause Difficult to Correct

Restoration of Adequate Measure to Improve
vent
lung function
Mechanical ventillation
Alkali Therapy:

Indications

Normal AG (Hyperchloremic Acidosis)

Slightly elevated AG (Mixed Hyperchloremic & AG Acidosis)
AG due to Non Metabolisable Anion (Renal Failure)

AG Acidosis due to Accumulation of Organic metabolizable anion, if

pH< 7.2

Goal: To slowly increase plasma HCO 3- to 20-22 mmol/L

Goal: pH to 7.15, Plasma HCO3- ~10mmol/L

Either orally (NaHCO3 / Shohls solution) or IV (NaHCO3)

Carbicarb, THAM

Treatment:
Problems with Bicarbonate Therapy

Cardiac Arrest: Both MA & RA

50mL NaHCO3 Releases 200 mL CO2

Bicarb corrects MA but worsens RA

Intracellular Acidosis

COP increase maybe due to increased intravascular vol

CSF Acidosis

Increased Plasma Osmolarity (3 mmol/50mL)

Extracellular alkalosis - ODC to Left - Decreased Tissue

Oxygenation

Rebound Alkalosis

Decreased Ca++ ---> Myocardial depression

Acidosis: Anaesthetic Considerations:

Potentiation of depressant effects of sedatives

and anaesthetic agents
Exaggerated circulatory depressant effects

Increased opioid penetration into brain

more pronounced with agents that rapidly decrease

symp tone
basic drugs increased non ionised form

Increased arrhytmogenicity of halothane

Respiratory Acidosis augments NDMR delayed
reversal
Succinyl Choline increases Serum K+ further

Alkalosis:
Physiologic Effects:
1. Left shift of ODC
2. Hypokalemia
3. Low ionised Ca++
4. Decreased CBF
5. Depressed
Ventilatoin
6. Respiratory Alkalosis

Bronchoconstriction
Decreased PVR

Effect

Dire
ct

Indir
ect

Clinic
al

Cerebral BF

Heart rate

Cardiac
inotropy

Systemic Art
tone

Syst venous
tone

PA tone

Airway tone

Uterine BF

Renal BF

Ionised Ca++

Respiratory Alkalosis: Primary

Decrease in PaCO2
Causes:

Central Stimulation

Pain
Anxiety
Ischemia
Tumor
Infection
Fever
Drugs: Salicylates,
Progesterone,
Doxapram

Peripheral
Stimulation

Unknown

Hypoxemia
High Altitude
Pulmonary Disease:
CHF, NCPE, PE, Asthma
Severe Anemia
Sepsis, Metabolic
Enceph

Iatrogenic:

Ventilator Induced

Respiratory Alkalosis:

pH 7.5
PaCO2 35
HCO3- - 22

pH Alkalemia
PaCO2 Decrease => Respiratory Alkalosis
Expected Compensation: 24-(40-35)x0.2 = 23 or
24-(40-35)x0.4 = 22
Diagnosis: Chronic Respiratory Alakalosis

Respiratory Alkalosis:
Treatment:

Treatment of Underlying cause

Ventilator adjustments
Reassurance, Rebreathing from paper
bag

Metabolic alkalosis:
Causes:
ECF Contraction,
Normotension,
K+ Deficiency & 20
Hyperreninemic
Hyperaldosteronism

Gastrointestinal

Vomiting
NG suction
Villous Adenoma

Renal

Diuretics
Mg++ Deficiency
Chronic Hypokalemia
Hypercalcemia/Hyperp
ara.
Post Hypercapnic State
Barters syndrome

Sweat

Cystic Fibrosis

Metabolic alkalosis:
Causes:
ECF Expansion,
Hypertension, K+
Deficiency &
Mineralocorticoid Excess
High Renin

Low Renin

Renal Artery Stenosis

Accelerated HTN
Primary Aldosteronism
Adrenal Enzyme defects
Cushings Syndrome

Other

Liquorice

Exogenous HCO- Loads:

Massive Blood Transfusion

Acetate containing colloids

Alkali therapy + Renal Failure

Milk-Alkali Syndrome

Metabolic Alaklosis:

pH 7.58
PaCO2 48
HCO3- - 44

BE - +19
pH Alkalemia
PaCO2 Increased => Not Respiratory

HCO3- - Increased => Metabolic Acidosis

Expected Compensatoin: 40+(44-24)x0.8 = 56
Diagnosis: Partially compensated Metabolic
Alkalosis

Metabolic Alkalosis:
Treatment:

Correction of underlying stimulus for HCO3- generation:

Remove factors that sustain HCO3- Reabsorption

ECF contraction NaCl administration

K+ deficiency KCl administration

Acetazolamide

Correction of cause of 10 Hyperaldosteronism

Reduction of Gastric secretions: H2 Blockers, PPI
Reduction of Renal loss of H+ : Discontinue Diuretics

But can cause K+ loss

Dilute HCl (0.1N HCl)

Oral NH4Cl

Alkalosis:
Anaesthetic considerations:

Increased protein binding of opioids

prolonged respiratory depression
Decreased cerebral blood flow Cerebral
Ischemia
Atrial and Ventricular dysrhythmias with
hypokalemia
Potentiation of NDMR due to
hypokalemia

Acid Base Disorders:

PO2 90.6

PCO2 53.8

pH 7.484
K+ - 3.7
Na+ - 151
HCO3- (A) 37.7

HCO3- (S) 34.3

BE 13.9
SBE 14.1
SO2 97.3

pH Alkalemia
PCO2 Increased =>
Metabolic Alkalosis
Expected Compensation:
PaCO2 =
40+(13.7x0.75) = 50.2
Body never
overcompensates
Diagnosis:
Metabolic Alkalosis +
Respiratory Acidosis

Summary:

Acid Base Homeostasis is all about maintenance of normal H +

concentration.
Changes in acid base status of ECF have profound and often
unpredicatble clinical and laboratory effects, more so during anaesthesia.
pH scale is a negative logarithmic scale with its inherent counterintutive
results.
The three independent variables which affect acid base status are SID,
[Atot] & PaCO2.
SBE as a measure for Metabolic acid base disturbance is most accurate
and clinically validated.
Anion gap must always be calculated, and effect of Plasma Albumin
considered to decipher more accurately the complex acid-base disorders
in critically ill patients.
Bicarbonate therapy must be used with caution in view of its various
deleterious effects.

References:

Millers Anesthesia, 7th Edition

Wylie And Churchill Davidsons A Practice of Anaesthsia,
7th Edition
Morgan Michael &
Clinical Application of Blood Gases, Shapiro, 5th Edition
Harrisons Principles of Internal Medicine, 16th Edition
Ganongs Review of Medical Physiology, 20th Edition
Acid-Base tutorial. Prof. Alan W Grogono, MD, FRCA
www.acid-base.com
A Basic Approach to body pH
www.anaesthetist.com/icu/elec/ionz/Findex.htm#Stewart
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