Acid Base analysis and

disorders
Umair akram
Acid Base Physiology
• PH
• Negative logarithm to the base 10 of hydrogen ion concentration.

• PH= -log10{H+}

• Measure of acidity of a solution

Maintenance of PH
• Enzymes
• Membrane Excitability
• Energy Production
• State of Ionization
• Nervous and Endocrine
Relationship between PH and H ion
conc
• Inverse relation
• Negative Logarithamic scale of PH is non linear
• Reduction by 1 in PH there is 10 times increase activity
• Exapmle;
• PH falls from 7.4->7.3
• the concentration increase from 40->50 nmol/L
PH H nmol/L
6.8 158
6.9 126
7.0 100
7.1 79
7.2 63
7.3 50
7.4 40
7.5 32
7.6 25
7.7 20
7.8 16
7.9 13
8.0 10
Basic Definitions
• Hydrogen Ion
• A hydrogen ion is a hydrogen molecule without electron,which makes it
proton.

• Acid
• A substance that donates a proton e.g HA

• Base
• A substance that accepts a proton e.g A-
Basic Definitions
• Acidosis
• a process that causes acid to accumulate
• Acidaemia
• this is present if pH < 7.36
• Alkalosis
• a process that causes base to accumulate
• Alkalaemia
• this is present if pH > 7.44.
How Body maintain PH?
• PH 7.35-7.45
• H Ion Conc 34-46nmol/L

• Mechansims:
• Buffering
• Compensation
• Correction
What is a Buffer?
• A substance which resist a change in PH by absorbing or releasing H
ions.

• It normally consist of a weak acid and its conjugate base resisting PH

change when a stronger acid or base is added.
Buffer systems in the Body
• Carbonic acid bicarbonate buffer system
• Hemoglobin
• Plasma Proteins
• Phosphate Buffer system
Carbonic acid bicarbonate buffer
system
• Most important buffer in extra cellular fluid.

• CO2 + H2O <--> H2CO3<->H + HCO3

• Increased arterial CO2 stimulate ventilation and respiratory

compensation.
• Due to abundance of Carbonic acid,the ability of lung to excrete CO2
and kidneys to regulate HCO3,this is main buffer system.
Other Buffer systems
• Haemoglobin:
• Other main buffer system for acids in the body.
• Histidine side chains of Hb act as buffer by binding H ions.
• Hb has 38 Histidine residues.
• Deoxygenated Hb is a better buffer than oxygenated Hb
Intraceullar Buffers
• Phosphate:
• Concentration ECF is very low,unimportant buffer
• Phosphate is important buffer of both ICF and urine,as concentration
in higher.

• Proteins:
• Amino acid side chains can buffer both acids and alkalis.
• plasma proteins play a minor role in buffering but intracellular
proteins are higher cons making them important Intraceluular buffer.
Compensatory Mechanisms
• Respiratory
• Renal
Anion Gap
• Difference b/t the measured and cation and anion concentrations in
the plasma.

• Anion Gap = ([Na+] + [K+]) − ([Cl−] + [HCO−3])

• Noraml Anion gap 8-16mmol/L

• Represnts the unmeasured anions present in plasma such as
phosphate,sulphate,acetate and ketones.
• Useful in differential Dx of metabolic acidosis.
Base Excess
• Base excess or deficit is the amount of acid or base required to
restore a liter of blood back to a normal PH at PCO2 5.3 Kpa and tem
37 C.

• It has a negative value in Acidosis

• It has positive value in Alkalosis
• Give an idea of the severity of the metabolic component of an acid
base derangement.
Comparison of ABG and VBG
Basic type of imbalance
• Metabolic Acidosis
• Metabloic Alkalosis
• Respiratory Acidosis
• Respirtaory Alkalosis
Metabolic Acidosis
• Low arterial blood PH in conjunction with low serum bicarbonate
concentration caused either by increased acid generation/decreased
acid excretion or loss of HCO3
Causes of MA
Osmolal Gap
• osmolal gap = measured osmolality – calculated osmolality
• The concept is similar to the anion gap.
• A raised osmolal gap infers unrecognized/unmeasured osmotically
active molecules within the plasma.
• A raised osmolal gap in conjunction with metabolic acidosis should
immediately raise concern of methanol, ethylene glycol, paraldehyde
or formaldehyde poisoning requiring urgent treatment.
Clinical Effects of MA
• widespread physiological disturbances
• reduced cardiac output,
• pulmonary hypertension,
• arrhythmias,
• Kussmaul respiration and hyperkalaemia
• the severity of the disturbances is related to the extent of the
acidaemia.
Treatment
• identify and reverse the cause.
• If acidaemia is considered to be life-threatening (pH < 7.2, [ ] < 10
mmol L –1 ), measures may be required to restore blood pH to
normal.
• use of sodium bicarbonate may lead to rapid correction of blood pH,
with the risks of tetany and convulsions in the short term and volume
overload and hypernatraemia in the longer term.
How to calculate HCO3?
• HCO3 (mmol) = body weight (kg) × base deficit (mmol L –1 ) × 0.3

• Administration of sodium bicarbonate should be followed by repeated

measurements of plasma and pH.
• Sodium bicarbonate is available as isotonic (1.4%; 163 mmol L –1 )
and hypertonic (8.4%; 1000 mmol L –1 ) solutions.
• Slow infusion of the hypertonic solution is advisable to minimize
adverse effects.
USE of HCO3
• carbon dioxide is generated during the buffering process.
• This may result in a superimposed respiratory acidosis, especially in
those patients with impaired ventilatory reserve or at the limit of
compensation.
• It is also important to distinguish those acidoses associated with
tissue hypoxia (e.g. cardiac arrest, septic shock) from those where
tissue hypoxia is not a factor
Use of HCO3
• exacerbates the acidosis if tissue hypoxia is present. For example, in
patients with type A lactic acidosis, NaHCO3 increases mixed venous
PaCO2 , which rapidly crosses cell membranes resulting in an
intracellular acidosis, particularly in cardiac and hepatic cells.

• Theoretically, this could result in decreased myocardial contractility

and cardiac output and decreased lactate extraction by the liver,
aggravating the lactic acidosis.
Use of HCO3
• Current guidelines for the management of cardiopulmonary arrest no
longer recommend the routine use of sodium bicarbonate.

• However, if the acidosis is not associated with tissue hypoxaemia (e.g.

uraemic acidosis) then the use of sodium bicarbonate results in a
potentially beneficial increase in arterial pH.
Metabolic Alkalosis
increased plasma HCO3, a high pH and an appropriately raised PaCO2 .

The compensatory response of hypoventilation is limited and not very

effective.

For diagnostic and therapeutic reasons, it is usual to subdivide

metabolic alkalosis into the chloride-responsive and chloride-resistant
varieties
Types and Causes of Metabolic
Alkalosis
• Chloride-Responsive (urine chloride < 20 mmol L –1 )
• Loss of acid
• Vomiting
• Nasogastric suction
• Gastrocolic fistula
• Chloride depletion
• Diarrhoea
• Diuretic abuse
• Excessive alkali
• NaHCO3 administration
• Antacid abuse
Types and Causes of Metabolic
Alkalosis
• Chloride-Resistant (urine chloride > 20 mmol L –1 )
• Primary or secondary hyperaldosteronism
• Cushing’s syndrome
• Severe hypokalaemia
• Carbenoxolone
Treatment
• The differential diagnosis of metabolic alkalosis on the basis of the
urinary chloride concentration, is important because of the
differences in treatment of the two groups.

• In chloride responsive alkalosis, the administration of saline causes

volume expansion and results in the excretion of excess bicarbonate;
if potassium is required, it should be given as the chloride salt.
Treatmnet
• In patients in whom volume administration is contraindicated, the use
of acetazolamide results in renal loss of HCO3 and an improvement in
pH.
• H2 -receptor antagonists may be helpful if nasogastric suction is
contributing to hydrogen ion loss.
Treatment
• Severe alkalaemia with compensatory hypoventilation may result in
seizures or CNS depression.
• In life-threatening metabolic alkalosis, rapid correction is necessary
and may be achieved by administration of hydrogen ions in the form
of dilute hydrochloric acid.
• Acid administration requires central vein cannulation, as peripheral
infusion causes sclerosis of veins.
• Acid is given as 0.1 normal HCl in glucose 5% at a rate no greater than
0.2 mmol kg –1 h – 1 .
Respiratory Acidosis
• The cardinal features are a primary increase in PaCO2 , a low pH and
an appropriate increase in plasma bicarbonate concentration.
• The extent of the acidaemia is proportional to the degree of
hypercapnia.
• Buffering processes are activated rapidly in acute hypercapnia and
may remove enough H+ from the extracellular fluid to result in a
secondary increase in plasma HCO3
Clinical features
• Usually, hypoxaemia and the manifestations of the underlying disease
dominate the clinical picture.

• Hypercapnia may result;

• coma
• raised intracranial pressure
• hyperdynamic cardiovascular system (tachycardia, vasodilatation,
ventricular arrhythmias) resulting from release of catecholamines.
 Causes of respiratory acidosis
• Central Nervous System
• Drug overdose, Trauma, Tumour, Degeneration or infection
• Cerebrovascular accident , Cervical cord trauma

• Peripheral Nervous System

• Polyneuropathy , Myasthenia gravis , Poliomyelitis
• Botulism, Tetanus, Organophosphorus poisoning
 Causes of Respiratory Acidosis
• Primary Pulmonary Disease
• Airway obstruction
• Asthma
• Laryngospasm
• Chronic obstructive airways disease

• Parenchymal disease
• ARDS
• Pneumonia
• Severe pulmonary oedema
• Chronic obstructive airways disease
• Loss of mechanical integrity
• Flail chest
Treatment
• reversing the underlying pathology if possible.
• mechanical ventilatory support if required.
Respiratory Alkalosis
• The cardinal features are a primary decrease in PaCO2 (alveolar
ventilation in excess of metabolic needs), an increase in pH and an
appropriate decrease in plasma bicarbonate concentration.

• Usually, hypocapnia indicates a disturbance of ventilatory control (in

patients not receiving mechanical ventilation).
Clinical features
• manifestations of the underlying disease usually dominate the clinical
picture.
• Acute hypocapnia results in cerebral vasoconstriction and reduced
cerebral blood flow and may cause light-headedness, confusion and,
in severe cases, seizures.
• Circumoral paraesthesia, hyperreflexia and tetany are common.
• Cardiovascular manifestations include tachycardia and ventricular
arrhythmias secondary to the alkalaemia.
Causes of Respiratory Alkalosis
• Supratentorial
• Voluntary/hysterical hyperventilation
• Pain, anxiety
• Specific Conditions
• CNS disease
• Meningitis/encephalitis
• Cerebrovascular accident
• Tumour
• Trauma
Causes of Respiratory Alkalosis
• Respiratory disease
• Pneumonia
• Pulmonary embolism
• Early pulmonary oedema or ARDS
• High altitude

• Shock
• Cardiogenic
• Hypovolaemic
• Septic
•
Causes of Respiratory Alkalosis
• Miscellaneous
• Cirrhosis
• Gram-negative septicaemia
• Pregnancy
• IPPV
• Drugs/hormones
• Salicylates
• Aminophylline
• Progesterone
Treatment
• Treatment comprises correction of the underlying cause and thus
differential diagnosis is important.
AnionGap,Delta Gap and Delta Ratio
STEPWISE APPROACH TO ACID-BASE
ANALYSIS
• a structured, rule-based approach to the diagnosis of primary,
secondary, and mixed acid-base disorders using the relationships
between the [H+], PCO2, and HCO3 concentration

• Stage I: Identify the Primary Acid-Base Disorder In the first stage of

the approach, the PaCO2 and pH are used to identify the primary
acidbase disorder.
STEPWISE APPROACH TO ACID-BASE
ANALYSIS
• Rule 1: If the PaCO2 and/or the pH is outside the normal range, there
is an acid-base disorder.

• Rule 2: If the PaCO2 and pH are both abnormal, compare the

directional change.
• 2a. If the PaCO2 and pH change in the same direction, there is a
primary metabolic acid-base disorder.
• 2b. If the PaCO2 and pH change in opposite directions, there is a
primary respiratory acid-base disorder.
EXAMPLE
• Consider a case where the arterial pH = 7.23 and the PaCO 2 = 23 mm
Hg.
• The pH and PaCO2 are both reduced (indicating a primary metabolic
disorder) and the pH is low (indicating an acidosis), so the diagnosis is
a primary metabolic acidosis.
STEPWISE APPROACH TO ACID-BASE
ANALYSIS
• Rule 3: If only the pH or PaCO2 is abnormal, the condition is a mixed
metabolic and respiratory disorder (i.e., equal and opposite
disorders).
• 3a. If the PaCO2 is abnormal, the directional change in PaCO2
identifies the type of respiratory disorder (e.g., high PaCO2 indicates a
respiratory acidosis), and the opposing metabolic disorder.

• 3b. If the pH is abnormal, the directional change in pH identifies the

type of metabolic disorder (e.g., low pH indicates a metabolic
acidosis) and the opposing respiratory disorder.
Example
• Consider a case where the arterial pH = 7.38 and the PaCO 2 = 55 mm
Hg. Only the PaCO2 is abnormal, so there is a mixed metabolic and
respiratory disorder. The PaCO2 is elevated, indicating a respiratory
acidosis, so the metabolic disorder must be a metabolic alkalosis.
Therefore, this condition is a mixed respiratory acidosis and metabolic
alkalosis. Both disorders are equivalent in severity because the pH is
normal.
Stage II: Evaluate the Secondary
Responses
• The goal in Stage II is to determine if there is an additional acidbase
disorder.
• Rule 4: For a primary metabolic disorder, if the measured PaCO2 is
higher than expected, there is a secondary respiratory acidosis, and if
the measured PaCO2 is less than expected, there is a secondary
respiratory alkalosis.
Example
• Consider a case where the PaCO2 = 23 mm Hg, the pH = 7.32, and the
HCO3 = 16 mEq/L. The pH and PCO2 change in the same direction,
indicating a primary metabolic disorder, and the pH is acidemic, so the
disorder is a primary metabolic acidosis.
• Using equations PaCO2 is 1.2×(24 – 16) = 10 mm Hg (rounded off),
and the expected PaCO2 is 40 – 10 = 30 mm Hg. The measured PaCO2
(23 mm Hg) is lower than the expected PaCO2, so there is an
additional respiratory alkalosis. Therefore, this condition is a primary
metabolic acidosis with a secondary respiratory alkalosis.
Rule 5
• For a primary respiratory disorder, a normal or near-normal HCO3
indicates that the disorder is acute.
Rule 6
• For a primary respiratory disorder where the HCO3 is abnormal,
determine the expected HCO3 for a chronic respiratory disorder.
• 6a. For a chronic respiratory acidosis, if the HCO3 is lower than
expected, there is an incomplete renal response, and if the HCO3 is
higher than expected, there is a secondary metabolic alkalosis.
• 6b. For a chronic respiratory alkalosis, if the HCO3 is higher than
expected, there is an incomplete renal response, and if the HCO3 is
lower than expected, there is a secondary metabolic acidosis.
PH Electrode
Example 1