Acid Base Disorder

Acid Base Disorder

A Stepwise Approach to Acid-Base Interpretation

This approach has three distinct stages.
The first two stages will allow to identify major acid-base abnormalities using only three variables: pH, PaCO2, and
serum HCO3 concentration from arterial blood.
The last stage allows to further investigate cases of metabolic acidosis using commonly measured serum electrolytes.
Stage I: Identify the Primary Acid-Base

Disorder
Consider too the clinical picture.
Ask for:
Known conditions which might lead to an acid-base disorder (diabetes, renal disease, alcoholism, respiratory
disease
Current diarrhoea or vomiting
Localizing features for sepsis (dysuria, cough, abdominal pain)
Drug history e.g. overdose of salicylates, methanol, diuretics

Look for:
Evidence of sepsis fever, tachycardia, hypotension
Dehydration
Respiratory rate
Cyanosis
Respiratory examination (wheeze, creps, dullness or hyper-resonance on percussion)

Basic Definitions:

Acidosis - an abnormal process or condition which would lower arterial pH if there were no secondary changes in
response to the primary aetiological factor.

Alkalosis - an abnormal process or condition which would raise arterial pH if there were no secondary changes in
response to the primary aetiological factor.

Simple (Acid-Base) Disorders are those in which there is a single primary aetiological acid-base disorder.

Mixed (acid-Base) Disorders are those in which two or more primary aetiological disorders are present simultaneously.

Acidaemia - Arterial pH < 7.36 (ie [H+] > 44 nM)

Alkalaemia - Arterial pH > 7.44 (ie [H+] < 36 nM)

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Rule 1: Check arterial pH

The net deviation in pH will indicate whether an acidosis or an alkalosis is present (but will not indicate mixed disorders)
IF an acidaemia (pH < 7.35) is present THEN an acidosis must be present
IF an alkalaemia (pH > 7.45) is present THEN an alkalosis must be present
IF pH is normal (pH 7.35-7.45) THEN either there is no acid-base disorder or there is compensated acid-base disorder.

NB In single acid or base disorder the pH cannot cross the 7.40 mark, i.e. there cant be over-compensation.
For example, in metabolic acidosis with full compensation, the pH generally remains within 7.35-7.4 range.

Rule 2: If the pH and PaCO2 are both abnormal, compare the directional change. If both change in the same direction
(both increase or decrease), the primary acid-base disorder is metabolic, and if both change in opposite directions, the
primary acid-base disorder is respiratory. Remember, CO2 is acid so if CO2 increases the pH should decrease.
Example: Consider a patient with an arterial pH of 7.23 and a PaCO2 of 23 mm Hg. The pH and PaCO2 are both reduced
(indicating a primary metabolic problem) and the pH is low (indicating acidemia), so the problem is a primary metabolic
acidosis.

Rule 3: If either the pH is normal and PaCO2 is abnormal or PaCO2 is normal but pH is abnormal, there is a mixed
metabolic and respiratory acid-base disorder (one is an acidosis and the other is an alkalosis). If the pH is normal, the
direction of change in PaCO2 identifies the respiratory disorder, and if the PaCO2 is normal, the direction of change
in the pH identifies the metabolic disorder.
Example: Consider a patient with an arterial pH of 7.37 and a PaCO2 of 55 mm Hg. The pH is normal, but the PaCO2 is
raised so there is a mixed metabolic and respiratory acid-base disorder. The PaCO2 is elevated, so the respiratory
disorder is an acidosis, and thus the metabolic disorder must be an alkalosis. Therefore, this is a combined respiratory
acidosis and metabolic alkalosis. There is no primary acid-base disorder in this situation; both disorders are equivalent
in severity (which is why the pH is normal).

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Remember that the compensatory responses to a primary acid-base disturbance are never strong enough to correct the
pH, but act to reduce the severity of the change in pH. Therefore, a normal pH in the presence of an acid-base disorder
always signifies a mixed respiratory and metabolic acid-base disorder.

Stage II: Evaluate Compensatory Responses

If a mixed acid-base disorder was identified in Stage I, go directly to Stage III. The goal in Stage II is to determine if the
compensatory responses are adequate and if there are additional acid-base derangements.

Rule 4: If there is a primary metabolic acidosis or alkalosis, use the table given below (Table 1) to identify the expected
PaCO2. If the measured and expected PaCO2 are equivalent, the condition is fully compensated. If the measured PaCO2
is higher than the expected PaCO2, there is a superimposed respiratory acidosis. If the measured PCO2 is less than the
expected PCO2, there is a superimposed respiratory alkalosis.

Rule 5: If there is a respiratory acidosis or alkalosis, use the PaCO2 to calculate the expected pH using the table given
below. Compare the measured pH to the expected pH to determine if the condition is acute, partially compensated, or
fully compensated. For respiratory acidosis, if the measured pH is lower than the expected pH for the acute,
uncompensated condition, there is a superimposed metabolic acidosis, and if the measured pH is higher than the
expected pH for the chronic, compensated condition, there is a superimposed metabolic alkalosis. For respiratory
alkalosis, if the measured pH is higher than the expected pH for the acute, uncompensated condition, there is a
superimposed metabolic alkalosis, and if the measured pH is below the expected pH for the chronic, compensated
condition, there is a superimposed metabolic acidosis.

Table 1:
Expected PaCO2 = (1.5 X HCO3) + (82) for metabolic acidosis (Equation 1)
Expected PaCO2 = (0.7 X HCO3) + (212) for metabolic alkalosis (Equation 2)
Expected pH = 7.40 - [0008 X (PaCO2- 40)] for an acute respiratory acidosis (Equation 3)
Expected pH = 7.40 - [0008 X (40-PaCO2)] for an acute respiratory alkalosis (Equation 4)
Expected pH = 7.40 - [0003 X (PaCO2- 40)] for an chronic respiratory acidosis (Equation 5)
Expected pH = 7.40 - [0003 X (40-PaCO2)] for an chronic respiratory alkalosis (Equation 6)

Stage III: Use The Anion Gap to Evaluate Metabolic Acidosis

The Anion Gap:
The anion gap is an estimate of the relative abundance of unmeasured anions, and is used to determine if a metabolic
acidosis is due to an accumulation of non-volatile acids. (e.g., lactic acid) or a net loss of bicarbonate (e.g., diarrhea).
The anion gap in plasma is most commonly defined as the difference between the major measured cations and the
major measured anions:
Anion gap = [Na+] - [Cl-] - [HCO3-]
Using normal values, Anion Gap = 140 (104 + 24) = 12mEq/L
Normal range = 8-16 mEq/L (124).

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 Acid Base Disorder

Respiratory Acidosis

pH<7.35
Acidaemia

PaCo2 >45mmHg HCO3 <22 mEq/L

Respiratory acidosis Metabolic acidosis

Inadequate alveolar Overproduction of Increased intake of

ventilation CO2 CO2

Nerve or muscle Lung or chest wall External factors e.g.

Central respiratory Airway disorders e.g.
disorders e.g. OP defects e.g. Pulm inadequate
depression Asthma, larynospasm
poison, snake venom oedema, COPD mechanical vent.

Respiratory acidosis is defined as a primary increase in PaCO 2. This increase drives the reaction

+
to the right, leading to an increase in [H ] and a decrease in arterial pH. For the reasons described above, [HCO 3 ] is
minimally affected.
PaCO2 represents the balance between CO2 production and CO2 elimination:

Carbon dioxide production is a byproduct of fat and carbohydrate metabolism. Muscle activity, body temperature, and
thyroid hormone activity can all have major influences on CO 2 production. Because CO2 production does not
appreciably vary under most circumstances, respiratory acidosis is usually the result of alveolar hypoventilation. In
patients with a limited capacity to increase alveolar ventilation, however, increased CO 2 production can precipitate
respiratory acidosis.

Ask for:
Features s/o hypercapnia e.g. headache, confusion, disorientation
History of trauma to head or neck, or to chest
Drug history (especially sedatives, opiates, anaesthetics, OP poisoning)
Neurological symptoms (s/o Guillain Barre or myasthenia gravis)
Acute onset of chest pain or shortness of breath (s/o pneumothorax, pulmonary oedema, acute exacerbation
COPD)
Known COPD or restrictive lung disease, known asthma, or paraplegia

Look for:
General appearance (warm, flushed and sweating s/o hypercapnia)
Respiratory rate (may be increased or decreased)
Bounding pulse and tachycardia (s/o hypercapnia)
Temperature
Respiratory examination (creps, wheeze, dullness to percussion or hyper resonant)
Focal neurological signs (s/o hypercapnia)

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Diagnoses to consider in Respiratory Acidosis:

A: Inadequate Alveolar Ventilation

1. Central Respiratory Depression & Other CNS Problems
Drug depression of resp. center (eg by opiates, sedatives, anaesthetics)
CNS trauma, infarct, haemorrhage or tumour
Hypoventilation due to obesity (eg Pickwickian syndrome)
Cervical cord trauma or lesions (at or above C4 level)
High central neural blockade
Poliomyelitis
Tetanus
Cardiac arrest with cerebral hypoxia
2. Nerve or Muscle Disorders
Guillain-Barre syndrome
Myasthenia gravis
Muscle relaxant drugs
Toxins eg organophosphates, snake venom
Various myopathies
3. Lung or Chest Wall Defects
Acute on COAD
Chest trauma -flail chest, contusion, haemothorax
Pneumothorax
Diaphragmatic paralysis or splinting
Pulmonary oedema
Adult respiratory distress syndrome (ARDS)
Restrictive lung disease
Aspiration
4. Airway Disorders
Upper Airway obstruction
Laryngospasm
Bronchospasm/Asthma
5. External Factors
Inadequate mechanical ventilation

B: Over-production of Carbon Dioxide

Malignant Hyperthermia

C: Increased Intake of Carbon Dioxide

Rebreathing of CO2-containing expired gas
Addition of CO2 to inspired gas
Insufflation of CO2 into body cavity (eg for laparoscopic surgery)

Comments:
Depression of Intracellular Metabolism
As CO2 rapidly and easily crosses lipid barriers, a respiratory acidosis has rapid & generally depressing effects on
intracellular metabolism. The effects described below are the metabolic effects of hypercapnia rather than
respiratory acidosis.

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 Acid Base Disorder

Important effects of Hypercapnia

Stimulation of ventilation via both central and peripheral chemoreceptors
Cerebral vasodilation increasing cerebral blood flow and intracranial pressure
Stimulation of the sympathetic nervous system resulting in tachycardia, peripheral vasoconstriction and sweating
Peripheral vasodilation by direct effect on vessels
Central depression at very high levels of pCO2
Right shift of the oxygen dissociation curve.

Acute Respiratory Acidosis

The compensatory response to acute (612 h) elevations in PaCO2 is limited. Buffering is primarily provided by
+ + +
hemoglobin and the exchange of extracellular H for Na and K from bone and the intracellular fluid compartment (see

above). The renal response to retain more bicarbonate is very limited acutely. As a result, plasma [HCO3 ] increases only
about 1 mEq/L for each 10 mm Hg increase in PaCO 2 above 40 mm Hg.

Chronic Respiratory Acidosis

"Full" renal compensation characterizes chronic respiratory acidosis. Renal compensation is appreciable only after 12
24 h and may not peak until 35 days. During that time, the sustained increase in PaCO 2 has been present long enough

to permit maximal renal compensation. During chronic respiratory acidosis, plasma [HCO 3 ] increases approximately 4
mEq/L for each 10 mm Hg increase in PaCO2 above 40 mm Hg.

Metabolic Acidosis:
pH <7.35
Acidosis

PaCO2 >45mmHg HCO3 < 22mEq/L

Respiratory Metabolic
acidosis acidosis

Normal anion gap

High anion gap (>
(< 16) (loss of
16)
bicarbonate)

Increased
production Renal loss
endogenous acids

Diabetic GIT causes e.g.

ketoacidosis diarrhoea, fistula

Dilutional - fluids
Lactic acidosis
with no
(sepsis)
bicarbonate

Total parenteral
Renal failure
nutrition

Incr intake
Toxins
chloride
(exogenous)
containing acids

Rhabdomyolysis

Metabolic acidosis is defined as a primary decrease in [HCO3-].

There are 3 mechanisms:
1. Consumption of HCO3- by 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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Ask for:
Symptoms are non-specific, and diagnosis can be difficult unless the patient presents with clear indications for
arterial blood gas sampling.
Chest pain, palpitations
Headache, altered mental status such as severe anxiety due to hypoxia
Nausea, vomiting, abdominal pain s/o diabetic ketoacidosis
Altered appetite (either loss of or increased)
Weight loss (longer term),
Known diabetic on insulin s/o diabetic ketoacidosis
Known renal disease
Features s/o sepsis (cough, dysuria, fever, rigors) get increased lactic acid production due to impaired
perfusion
Intake of toxins (e.g. ethylene glycol, methanol, salicylate)
History of bowel surgery
Muscle weakness and bone pains (Longstanding chronic metabolic acidosis leads to osteoporosis and can
cause fractures).

Look for:
Physical examination occasionally reveals signs of disease, but may be normal.
Cardiac signs of extreme acidaemia: pulse, arrhythmias (ventricular tachycardia), hypotension
Deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic
ketoacidosis.
Neurological signs of extreme acidaemia: lethargy, stupor, coma, seizures.
Dehydration
Cranial nerve abnormalities are reported in ethylene glycol poisoning
Retinal edema can be a sign of methanol (methyl alcohol) intoxication.

Investigations:
Arterial blood gas sampling is essential for the diagnosis.
An ECG can be useful to anticipate cardiac complications.
Electrolytes (including chloride), glucose, renal function and a full blood count.
Urinalysis can reveal acidity (salicylate poisoning) or alkalinity (renal tubular acidosis type I). In
addition, it can show ketones in ketoacidosis
If the pH is low (under 7.35) and the bicarbonate levels are decreased (<24 mmol/l), metabolic acidemia is
present, and metabolic acidosis is presumed.
Due to respiratory compensation (hyperventilation), carbon dioxide is decreased and conversely oxygen is
increased.
Comments
To distinguish between the main types of metabolic acidosis calculate the anion gap.
Anion gap = ( [Na+] - ( [Cl-]+[HCO3-] )
As sodium is the main extracellular cation, and chloride and bicarbonate are the main anions, the result should
reflect the remaining anions. Normally, this concentration is about 8-16 mmol/l (124). An elevated anion gap
(i.e. > 16 mmol/l) can indicate particular types of metabolic acidosis, particularly certain poisons, lactate
acidosis and ketoacidosis.
As the differential diagnosis is made, certain other tests may be necessary, including toxicological screening
and imaging of the kidneys.
It is also important to differentiate between acidosis-induced hyperventilation and asthma; otherwise,
treatment could lead to inappropriate bronchodilation
Metabolic acidosis occurs when the body produces too much acid, or when the kidneys are not removing
enough acid from the body.

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Diagnoses to consider in Metabolic Acidosis:

A. High anion gap acidosis:
1. Increased production of endogenous nonvolatile acids
Renal failure
Ketoacidosis: diabetic, starvation
Lactic acidosis
Mixed : nonketotic hyperosmolar coma, alcoholic
Inborn errors of metabolism
2. Ingestion of toxin
Salicylate
Methanol
Ethylene glycol
Paraldehyde
Toluene
Sulfur
3. Rhabdomyolysis.

B. Normal anion gap:

1. Increased gastrointestinal losses of HCO3-
Diarrhea
Anion exchange resins (cholestyramine)
Ingestion of CaCl2, MgCl2
Fistulas (pancreatic, biliary or small bowel)
Ureterosigmoidostomy or obstructed ileal loop
2. Increased renal losses of HCO3-
Renal tubular acidosis
Carbonic anhydrase inhibitors
Hypoaldosteronism
3. Dilutional
Large amount of bicarbonate free fluids
4. Total parenteral nutrition
5. Increased intake of chloride containing acids
Ammonium chloride
Lysine hydrochloride
Arginine hydrochloride

Compensatory mechanisms
Metabolic acidosis is either due to increased generation of acid or an inability to generate sufficient bicarbonate. The
body regulates the acidity of the blood by four buffering mechanisms.
1. Bicarbonate buffering system
2. Intracellular buffering by absorption of hydrogen atoms by various molecules, including proteins,
phosphates and carbonate in bone.
3. Respiratory compensation
4. Renal compensation

Respiratory compensation during metabolic acidosis

Decrease 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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The pulmonary response to lower PaCO2 occurs rapidly but may not reach a predictably steady state until 12 24
hours; pH is never completely restored to normal.
PaCO2 normally decreases 1 1.5mm Hg below 40mmHg for every 1mEq/L decrease in plasma [HCO3-].

Renal compensation:
By 3 mechanisms:
1. Increased reabsorbtion of the filtered HCO3-,
2. Increased excretion of titratable acids, and
3. Increased production of ammonia.
These mechanisms are probably activated immediately; their effects are generally not appreciable for 12 24 hours
and may not be maximal for up to 5 days.

Respiratory Alkalosis:

pH > 7.45 Alkalosis

PaCO2 < 35mmHg

HCO3 > 26mEq/L
Respiratory
Metabolic alkalosis
alkalosis

Central cause Pulmonary cause Iatrogenic

Hypoxaemia e.g. asthma, pulm (excessive
e.g. Drugs oedema ventilation)

A respiratory alkalosis is a primary acid-base disorder in which arterial PCO falls to a level lower than expected.
+
Increased removal of CO2 is caused by hyperventilation, so there is a fall in PaCO2 and [H ].

Ask for:
History of head trauma or CVA
Drug history e.g. salicylates, methanol
Cough and fever s/o pneumonia
Increased shortness of breath s/o pulmonary oedema
Is the patient on a ventilator?

Look for:
Pulse, Blood pressure, temperature, pulse oximetry
Respiratory rate
Creps or wheezing in chest

Diagnoses to consider in Respiratory Alkalosis:

1. Central Causes (direct action via respiratory centre)
Head Injury
Stroke
Anxiety-hyperventilation syndrome (psychogenic)
Other 'supra-tentorial' causes (pain, fear, stress, voluntary)
Various drugs (eg analeptics, propanidid, salicylate intoxication)
Various endogenous compounds (eg progesterone during pregnancy, cytokines during sepsis, toxins in patients
with chronic liver disease)
2. Hypoxaemia (act via peripheral chemoreceptors)
Respiratory stimulation via peripheral chemoreceptors

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3. Pulmonary Causes (act via intrapulmonary receptors)

Pulmonary Embolism
Pneumonia
Asthma
Pulmonary oedema (all types)

4. Iatrogenic (act directly on ventilation)

Excessive controlled ventilation

Compensation:
The compensatory response is a fall in bicarbonate level.
As can be seen by inspection of the Henderson-Hasselbalch equation (below), a decreased [HCO3-] will counteract the
effect of a decreased pCO2 on the pH. Mathematically, it returns the value of the [HCO3]/0.03 pCO2 ratio towards
normal.
pH = pKa + log {([HCO3]/ 0.03 pCO2 }

Key points regarding compensation in respiratory alkalosis:

Physicochemical effect: Initially there is an immediate physicochemical change which lowers the bicarbonate
slightly.
Role of Kidney: The effector organ for compensation is the kidney.
Slow Response: The renal response has a slow onset and the maximal response takes 2 to 3 days to be
achieved.
Outcome: The drop in bicarbonate results in the extracellular pH returning only partially towards its normal
value.

Compensation in an ACUTE Respiratory Alkalosis

Not really compensation as there is insufficient time for the kidneys to respond. Thus only slight decrease in HCO3. (ie
2mmol/L per 10mmHg decrease of PaCO2).

Compensation in CHRONIC Respiratory Alkalosis

Maximal response takes 2 to 3 days.
Renal compensation by retention of acid causes a further fall in plasma bicarbonate (4 mmol/L per 10mmHg).

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 Acid Base Disorder

Metabolic Alkalosis:

pH > 7.45 Alkalosis

PaCO2 < 35 mmHg

HCO3 > 26mEq/L
Respiratory
Metabolic alkalosis
alkalosis

Expanded effective Renal failure with Contracted

arterial blood Transient ingestion effective arterial
volume exogenous alkali blood volume

GI loss chloride e.g.

Renin/aldosterone Intravenous Milk alkali
vomiting, NG
changes bicarbonate syndrome
suction, diarrhoea

Renal loss chloride

Corrected Bicarbonate
or potassium e.g.
hypercapnia ingestion
drugs

Metabolic alkalosis is defined as a primary increase in plasma [HCO3 ]. Most cases of metabolic alkalosis can be divided
into
(1) those associated with NaCl deficiency and extracellular fluid depletion, often described as chloride sensitive, and
(2) those associated with enhanced mineralocorticoid activity, commonly referred to as chloride resistant

Ask for:
Dietary intake (licorice, alkali)
History of massive blood transfusion (citrate in stored blood is metabolized)
Severe vomiting (chloride and potassium loss)
Profuse diarrhoea (chloride and potassium loss)
Drug history (especially diuretics, laxative abuse)

Look for:
Pulse (rate and rhythm can get arrhythmias), blood pressure look for evidence of volume depletion
Dehydration
Mental status (get confusion and coma)- due to reduced cerebral blood flow
Respiratory rate (hypoventilation due to respiratory response to metabolic alkalosis)

Diagnoses to consider in Metabolic Alkalosis

A: Addition of Base to ECF (transient or with associated renal failure)

Milk-alkali syndrome
Excessive NaHCO3 intake
Recovery phase from organic acidosis (excess regeneration of HCO3)
Massive blood transfusion (due metabolism of citrate)

B: Contraction of effective Arterial blood volume

GI - Chloride Depletion
Loss of acidic gastric juice eg vomiting due to pyloric stenosis or obstruction, NG suction
Excess faecal loss (eg villous adenoma): increase excretion of bicarbonate
Laxative abuse
Renal loss
Diuretics eg frusemide, thiazide
Post-hypercapnia*

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C: Changes in renin/aldosterone balance leading to Potassium Depletion

Primary hyperaldosteronism
Cushings syndrome
Secondary hyperaldosteronism
Some drugs (eg carbenoxolone)
Kaliuretic diuretics
Excessive licorice intake (glycyrrhizic acid)
Bartter's syndrome
Severe potassium depletion

D: Other Disorders
Severe hypoalbuminaemia

Comments:
* Post hypercapnia metabolic alkalosis is a common occurrence in mechanically ventilated patients, especially in COPD
patients with chronic CO2 retention (respiratory acidosis). Imagine a COPD patient with pH 7.10 and pCO2 110mmHg,
HCO3 40, is kept in ventilator. The PCO2 level instantly drops down and HCO3 remains the same as renal compensation
takes some time as mentioned above. Then the arterial blood gasses would look like pH 7.50, pCO2 30, HCO3 40
(metabolic alkalosis)

Pathophysiology
Whenever the plasma bicarbonate rises above 24mmols/l, bicarbonate is excreted by two renal processes:
Tubular reabsorption of nearly all of the large daily filtered load of bicarbonate
Excretion of the net daily production of the fixed acid (which results in regeneration of the titrated plasma
bicarbonate)
This response is reasonably prompt and effective so a metabolic alkalosis will be rapidly corrected. The persistence of a
metabolic alkalosis requires an additional process which acts to impair renal bicarbonate excretion and prevent the
return of the elevated plasma level to normal.
Chloride deficiency causes the kidney to reabsorb more bicarbonate anion than usual because there is not sufficient
chloride anion present. Reabsorption of an anion is necessary to maintain electroneutrality as Na+ & K+ are reabsorbed
so the deficiency of chloride leads to a resetting upwards of the maintained plasma bicarbonate level. Chloride and
bicarbonate are the only anions present in appreciable quantities in extracellular fluid so a deficiency of one must lead
to an increase in the other because of the strict requirement for macroscopic electroneutrality.
Potassium depletion occurs with situations of mineralocorticoid excess. Bicarbonate reabsorption in both the proximal
and distal tubules is increased in the presence of potassium depletion. Potassium depletion decreases aldosterone
release by the adrenal cortex
The effects of the alkalosis are often difficult to distinguish from the effects of associated problems such as
hypovolaemia, potassium and chloride depletion. This makes it more difficult to characterize the effects of the alkalosis
itself.
Hypoxaemia may occur and oxygen delivery to the tissues may be reduced. Factors involved in impaired arterial oxygen
content are:
Hypoventilation (due respiratory response to metabolic alkalosis)
Pulmonary microatelectasis (consequent to hypoventilation)
Increased ventilation-perfusion mismatch (as alkalosis inhibits hypoxic pulmonary vasoconstriction)
Peripheral oxygen unloading may be impaired because of the alkalotic shift of the haemoglobin oxygen dissociation
curve to the left. The bodys major compensatory response to impaired tissue oxygen delivery is to increase cardiac
output but this ability is impaired if hypovolaemia and decreased myocardial contractility are present.

Compensatory response
The peripheral chemoreceptors alone acted as the initial sensor responding to the rise in blood pH and the
hypoventilation causes a compensatory rise in arterial PCO2.

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