Acid-Base Balance Introduction
- Human blood has a hydrogen ion concentration [H+] of 35 to 45 nmol/L and it is essential that its concentration is maintained within this narrow range. Hydrogen ions are nothing but protons which can bind to proteins and alter their characteristics.
- All the enzymes present in the body are proteins and an alteration in these enzyme systems can change the homeostatic mechanisms of the body. Hence, a disturbance in acid–base balance can result in malfunction of the various organ systems.
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Table of Contents
Basic Definitions
What is pH?
pH notation is a more common method of expressing the hydrogen ion concentration. It is defined as the negative logarithm to base 10 of the [H+] expressed in mol/L. pH of blood = 7.4.
What is an acid? What is a base? What is a buffer?
- An acid is a substance that dissociates in water to produce H+.
- A base is a substance that accepts H+.
- A buffer is a combination of a weak acid and its conjugate base. By combining with a strong acid or a strong base, they produce the corresponding salt and a weak acid or a weak base, respectively.
For example: A weak acid, such as carbonic acid with its conjugate base, sodium bicarbonate, is called the bicarbonate/carbonic acid buffer system.
- When a strong acid, such as hydrochloric acid, is added to the solution, it combines with the weak alkali (sodium bicarbonate) to form sodium chloride and carbonic acid.
- When a strong base, such as sodium hydroxide is added, it combines with the weak acid (carbonic acid) to form sodium carbonate and water.
- Thus, a strong acid and a strong base are converted into a weak acid and a weak base by the bicarbonate/ carbonic acid buffer system.
The hydrogen ion concentration of blood is maintained within narrow limits because of the presence of buffers in the body.
- These natural buffers are of two types: Extracellular and intracellular. The extracellular buffers are bicarbonate/carbonic acid buffer system, phosphate buffer system and plasma proteins.
- The intracellular buffers are haemoglobin and other proteins. The most important buffer system in the body is the bicarbonate–carbonic acid buffer system. This is because of the ability of the body to maintain or alter the concentrations of its two components separately.
- The concentration of carbonic acid is regulated by respiration wherein the excess carbonic acid is eliminated as carbon dioxide by the lungs. The bicarbonate concentration is independently regulated by the kidneys.
The Henderson And Henderson Hasselbalch Equation
The hydrogen ion concentration is proportional to the concentration of buffer systems of the body. The hydrogen ion concentration, carbonic acid levels and the bicarbonate levels of blood are related according to the following equation:
The amount of carbonic acid in the blood is directly proportional to the partial pressure of carbon dioxide in the blood.
Thus, the carbonic acid concentration is a product of the partial pressure of carbon dioxide in blood and its solubility coefficient. [H2CO3] = α PCO2, where α = solubility coefficient of carbon dioxide in blood and PCO 2 is the partial pressure of carbon dioxide in blood.
α = 0.03 ml/mmHg/100 ml blood and normal PCO2 = 40 mmHg [H2CO3] = α PCO2 = 0.03 × 40 = 1.2 ml/dl. K = 800 for the carbonic acid/bicarbonate buffer system. The normal bicarbonate level of blood is 24 mmol/L.
The Henderson equation can also be written as follows.
From this equation, it is evident that the hydrogen ion concentration increases when the PCO 2 increases or when the [HCO–3] levels decrease.
Similarly, a decrease in hydrogen ion concentration occurs when the PCO 2 decreases or when the [HCO3–] levels increase.
When expressed in logarithmic form, the Henderson equation is written as follows:
This logarithmic version of Henderson equation is called the Henderson-Hasselbalch equation.
The pKa (negative logarithm of the constant K) of the carbonic acid/bicarbonate buffer system is 6.1. pH = 6.1 + log 24/1.2 = 6.1 + log 20 = 6.1 + 1.3 = 7.4
It is important to appreciate that the [H+] and pH are inversely related. When the [H+] rises, the pH decreases and vice versa.
Regulation Of Acid Base Balance
- The normal pH of blood is 7.35–7.45. Acidosis is defined as a pH less than 7.35. Conversely, when the pH is more than 7.45, alkalosis is said to exist. Acidosis and alkalosis are of two types each—respiratory and metabolic.
- An increase in carbon dioxide (CO2) levels increases the plasma [H+] and decreases the pH (respiratory acidosis). Similarly, a decrease in plasma carbon dioxide levels reduces the [H+] and increases the pH (respiratory alkalosis).
- A decrease in [HCO3–] reduces the pH and is called metabolic acidosis. Similarly, an increase in [HCO3–] increases the pH and produces metabolic alkalosis.
- The pH is regulated in the human body mainly by two organs: The respiratory system and the renal system. The arterial carbon dioxide levels are regulated by the respiratory system.
- Any increase in carbon dioxide levels stimulates the respiratory centre in the medulla thus augmenting respiration, alveolar ventilation and elimination of extra CO2 levels.
- A decrease in CO2 levels may reduce the stimulus to breathe and cause hypoventilation. This response is limited by hypoxia as the hypoxic drive stimulates the patient to maintain respiration. Respiratory response to changes in CO2 level occurs very fast.
- The plasma bicarbonate levels are regulated by the kidneys. Any decrease in [HCO3–] stimulates the kidneys to retain and synthesise bicarbonate. High [HCO3–] results in elimination of more bicarbonate in urine.
- In general, the pulmonary response to a change in acid–base status is faster and occurs immediately. However, renal regulation takes time, a few hours to days.
- Kidneys filter and reabsorb all the bicarbonate in the urine. When necessary, kidneys can also produce extra bicarbonate through the glutamine pathway.
Acid Base Disorders
- When an acid–base disorder occurs, the initial disturbance that occurs is termed the primary disorder. The body attempts to normalise the pH by certain compensatory mechanisms resulting in a secondary disorder, example primary metabolic acidosis results in an increase in hydrogen ions and a consequent decrease in bicarbonate ions.
- To compensate for this, the patient hyperventilates and reduces the arterial carbon dioxide levels, thus moving the pH back to normal (compensatory respiratory alkalosis). Thus, there are four primary disorders and four secondary disorders.
Primary Disorder – Secondary Disorder
- Respiratory acidosis – Metabolic alkalosis
- Respiratory alkalosis – Metabolic acidosis
- Metabolic acidosis – Respiratory alkalosis
- Metabolic alkalosis – Respiratory acidosis
Respiratory Acidosis
Respiratory Acidosis Causes:
This disorder occurs when the patient’s ability to maintain minute ventilation is compromised. This may be acute or chronic in origin. The causes may be classified as follows:
- Central nervous system: Central nervous system depression due to trauma, tumour, infections, ischaemia or drug overdose. Spinal cord injuries, especially cervical or high thoracic, can cause respiratory muscle paralysis.
- Peripheral nervous and muscular systems: GuillainBarré syndrome, tetanus, organophosphorus poisoning, poliomyelitis, myasthenia gravis.
- Primary pulmonary disease: Asthma, chronic obstructive pulmonary disease, acute respiratory distress syndrome, pneumonia.
- Loss of chest wall integrity: Flail chest.
Respiratory Acidosis Clinical Features:
- The features of the underlying problem predominate the clinical picture.
- If acute, hypoxia and hypercarbia result in tachycardia, hypertension, arrhythmias, confusion, drowsiness and coma. The hypoxia, if untreated, can be fatal.
- If gradual in onset, as in chronic obstructive pulmonary disease (COPD), the patient’s kidneys may compensate by retaining bicarbonate resulting in compensatory metabolic alkalosis.
- Arterial blood gas analysis in these patients typically shows low PaO2, high PaCO2, high bicarbonate levels and a nearnormal pH.
Respiratory Acidosis Treatment:
- Treat the cause.
- Maintenance of oxygenation and ventilation using mechanical ventilatory support till recovery of the primary problem occurs.
Respiratory Alkalosis
This occurs due to an increase in minute ventilation. This increase can be sustained only in abnormal conditions. This may be acute or chronic in origin.
Hyperventilation:
-
- Head injury
- Hydrogen ions (metabolic acidosis)
- Hyperpyrexia
- Hysteria
- High altitudes
Respiratory Alkalosis Causes:
- Supratentorial lesions: Head injury
- Fever
- Pain
- Anxiety, hysterical hyperventilation
- High altitudes
- It may also occur secondarily as a compensation to primary metabolic acidosis.
Respiratory Alkalosis Features:
- Usually, features of the underlying disease predominate the picture.
- Acute severe hypocarbia (PaCO2 <20 mmHg) may cause cerebral vasoconstriction, reduced cerebral blood flow, confusion, seizures and tetany.
- The alkalosis and consequent hypokalaemia can also cause cardiac arrhythmias.
Metabolic Acidosis
Metabolic Acidosis Causes:
This is associated with a decrease in bicarbonate ions
due to one of two reasons:
1. Overproduction or retention of non-volatile acids in the body, as in:
- Diabetic ketoacidosis
- Lactic acidosis
- Salicylate poisoning, methanol poisoning
- Renal failure
2. Loss of bicarbonate ions from the body as in
- Diarrhoea
- Intestinal fistulae
Metabolic Acidosis Features:
- Usually features of the underlying disease predominate the picture.
- Hypotension, reduced cardiac output
- Hyperventilation—rapid, deep respirations
- Deep, gasping type of respiration seen in diabetic ketoacidosis is called Kussmaul’s respiration.
- Hyperkalaemia, arrhythmias
- Lethargy, coma
Metabolic acidosis can be of high anion gap or normal anion gap type.
Anion Gap:
- The law of electroneutrality states that the total number of positive charges must be equal to the total number of negative charges in the body fluids. Thus, cations (positively charged ions such as sodium and potassium) must produce a charge exactly balanced by anions.
- However, the concentrations of only sodium, potassium, chloride and bicarbonate ions are routinely measured in clinical practice. The number of the measured cations (Na+) exceeds the sum of measured anions (Cl– and HCO–3) producing a ‘deficit’ called the ‘anion gap’. The normal anion gap is 9–14 mmol/l. This gap is due to the presence of unmeasured anions in the body.
Since the extracellular concentrations of potassium is small, it is often ignored in the calculation of anion gap. Anion gap may be used to distinguish the cause of metabolic acidosis.
Causes of high anion gap acidosis: MUDPILES (methanol, uraemia, diabetic ketoacidosis, paracetamol/ propylene glycol, iron/isoniazid, lactic acidosis, ethylene glycol, salicylate poisoning).
- Anion gap is increased (>14 mmol/L) in metabolic acidosis due to an increase in fixed acid load.
- These acids react with the bicarbonate ions in the plasma lowering its concentration. This results in high anion gap metabolic acidosis (HAGMA).
Causes of normal anion gap acidosis: Diarrhoea, isotonic saline infusion, early renal failure, renal tubular acidosis, ureteroenterostomy.
Anion gap remains unchanged in metabolic acidosis due to loss of bicarbonate ions as the lost bicarbonate ions are replaced by chloride ions. There is no change in the measured anion concentration and thus, the anion gap remains normal. This type of metabolic acidosis is also called ‘hyperchloraemic metabolic acidosis’. Example: Diarrhoea, renal tubular acidosis.
Corrected anion gap: The anion gap (AG) can be falsely low in hypoalbuminaemia, a common clinical condition in the critically ill. Adjust anion gap for albumin as given below: Adjusted AG = Observed AG + 2.5 × [4.5 – measured albumin (g/dl)]
Metabolic Acidosis Treatment:
Identify the cause and treat.
Ensure adequate ventilation.
If pH <7.1 and the patient is unstable, may administer sodium bicarbonate. The chances of life-threatening arrhythmias are reduced when pH is >7.2. Bicarbonate required (mmol/L) = 15 – measured [HCO3–] × 0.6 × Body wt (kg) (Each ml of 8.4% NaHCO3 solution contains 1 mmol of HCO3 . Each ml of 7.5% NaHCO3 solution contains 0.9 mmol of HCO–3).
Half the calculated dose of bicarbonate should be given slowly and should be followed up with repeat blood pH measurements as required.
Metabolic Alkalosis
Metabolic Acidosis Causes:
This may be either due to loss of acid from the body or retention of bicarbonate. It may be due to:
- Loss of gastric hydrochloric acid as in vomiting, prolonged nasogastric drainage.
- Retention of bicarbonate in exchange for loss of chloride ions as in diarrhoea.
- Excessive loss of H+ from kidneys in exchange for K+ in severe hypokalaemia.
- Primary or secondary hyperaldosteronism.
- Excessive exogenous administration of alkali, e.g. indiscriminate use of NaHCO3, antacid abuse.
Metabolic Acidosis Features:
It is one of the common acid–base disorders in the intensive care unit. The underlying problem gives a clue to the cause of metabolic alkalosis. When severe, it can cause hypoventilation and seizures. Associated hypokalaemia can cause arrhythmias and contribute to difficulty in weaning patients off a ventilator.
Metabolic Acidosis Treatment:
- Treat the primary problem.
- Most of the metabolic alkalosis are ‘chlorideresponsive’. Administration of saline and correction of potassium deficits reduce the alkalosis.
- Chloride deficit (mmol) = 0.2 × Body weight (kg) × (100 – serum Cl–)
- The calculated deficit can be replaced over 24 hours using 0.9% saline (contains 154 mmol/L of chloride)
- Chloride unresponsive alkalosis may be due to hypokalaemia or hypomagnesemia. Treat them.
Combined Disorders
- In some clinical situations, patients can have combined disorders. HAGMA and NAGMA can co-exist. Similarly, metabolic acidosis and alkalosis can be present in the patient at the same time.
- Hence, whenever a patient presents with HAGMA, check whether there is a co-existing disorder.
- A ‘gap-gap analysis’ helps in identifying whether HAGMA is associated with other disorders. Gap-Gap = (12 – measured anion gap)/24 – measured HCO3–) If the ratio is 1, infer that the patient has HAGMA.
Hagma + Nagma
Hagma + Metabolic Alkalosis
If <1, there is co-existing NAGMA with HAGMA.
If >1, there is co-existing HAGMA and metabolic alkalosis.
Rapid Interpretation Of An Abg Report
Analysis and conclusion of arterial blood gas (ABG) report must always be done in conjunction with history and clinical examination. ABG analysis is done to assess:
- Oxygenation status
- Ventilatory status
- Acid-base status
1. Oxygenation:
The partial pressure of oxygen in arterial blood (PaO2) of a normal, healthy, young adult is usually 90–100 mmHg. While assessing oxygenation, the PaO2 must always be related to inspired oxygen concentration (FIO2).
An easy bedside assessment of oxygenation can be made using a PaO2 /FIO2 ratio. The ratio can also be used to evaluate the response to therapy.
PaO2/FIO2 ratio – Status of oxygenation
- ≥500 – Normal
- 250–500 – Adequate
- 100–250 – Poor
- <100 – Critical
A pulse oximeter is helpful to assess whether the patient’s oxygenation is life-threatening or not. A saturation of 98–100% may be reassuring.
- However, early changes in the oxygenation status may be missed, if one relies on a pulse oximetry and the patient is breathing high concentrations of oxygen.
- This is because of the sigmoid shape of the oxygen dissociation curve where the SaO2 will be 99–100%, whether the PaO2 is 100 mmHg or 500 mmHg. Hence, an arterial blood gas analysis must always be obtained whenever doubt exists about the oxygenation status of the patient.
2. Ventilation:
- The normal PaCO2 is 35–45 mmHg. The PaCO2 must always be related to the alveolar ventilation of the patient. The minute volume of a normal healthy adult at rest would be 100 ml/kg/min. Sixty to sixty-five per cent of this actually ventilates the alveoli, the rest is dead space ventilation.
- If the alveolar ventilation decreases (either due to a decrease in minute volume or an increase in dead space ventilation), the arterial PaCO2 will rise. On the other hand, the arterial PaCO2 may remain normal but the patient’s minute volume may have increased.
- Do not assume that the patient must be well when the PaCO2 is normal. A clinical examination of the patient is necessary to rule out respiratory distress (dyspnoea, tachypnoea, active accessory muscles of respiration, tracheal tug, flaring of alae nasi, etc.).
- The patient may not be able to sustain this increased level of ventilation for a prolonged period of time, is likely to get exhausted and may require mechanical ventilatory support.
3. Acid-Base Status:
- The assessment of acid–base status must be done in three steps and in the following order.
- Assess the pH first: Normal pH—7.35 to 7.45. If the pH is less than 7.35, the patient has acidosis and if it is more than 7.45, the patient is alkalotic. The direction of change in pH shows the primary disorder.
- This is because the compensatory mechanisms never overshoot the requirement of reaching the normal pH. Assess the PaCO2 next: Is the PaCO2 normal? The normal PaCO2 is 35–45 mmHg.
- If the pH is abnormal but the PaCO2 normal, it suggests a metabolic disorder. However, the body usually tries to compensate for a change in pH. The respiratory compensation is early and fast.
- If the changes in pH and PaCO2 are in opposite directions (one is increased and the other decreased), the primary disorder is respiratory. If the changes in pH and PaCO2 are in the same direction (both are increased or decreased), the primary disorder is metabolic.
- For example, if the pH is 7.2 and the PaCO2 is 60 mmHg, the decrease in pH suggests acidosis. The PaCO 2 has moved in the opposite direction (increased) and suggests respiratory acidosis.
- Similarly, if the pH is alkalotic and the PaCO2 is low, it suggests primary respiratory alkalosis. A change in PaCO2 also changes the serum bicarbonate concentration.
Condition – PCO2 – [HCO3–]
- Acute respiratory acidosis – 10 mmHg↑ – ↑1 mmol/L
- Acute respiratory alkalosis 10 mmHg↓ – ↓2 mmol/L
- Chronic respiratory alkalosis 10 mmHg↓ – ↓5 mmol/L and acidosis
- Metabolic acidosis: Expected ΔPaCO2 = 1.2 × Δ[HCO3–]
- Metabolic alkalosis: Expected ΔPaCO2 = 0.7 × Δ[HCO3–]
- Metabolic disorders: Changes in serum bicarbonate concentration is accompanied by compensatory changes in PaCO2.
- As described previously, whenever metabolic acidosis is present, calculate anion gap to help diagnose the type of metabolic acidosis (high anion gap or normal anion gap).
- Similarly, when a patient has metabolic alkalosis, assess whether it is chloride responsive or unresponsive type and treat accordingly.
- It must be remembered that these are general guidelines applicable to patients who are breathing spontaneously.
- These are useful for rapid bedside assessment of acid–base status. Occasionally, the patients can present with different combinations of acid–base disorders such as a mixed respiratory and metabolic alkalosis, or a mixed respiratory and metabolic acidosis.
- In critically ill patients with multiorgan failure such as renal and respiratory abnormalities and receiving mechanical ventilation, the physiology can be very complicated.
- Mixed disorders are common in such patients and a more detailed analysis as described previously may be required.
Clinical Notes:
- A 30-year-old man was admitted to the ICU with history of consumption of organophosphorus poisoning 4 hours ago. On admission, he is drowsy, breathing 60% oxygen by face mask and has a bradycardia.
- A blood gas analysis taken half an hour later shows a PaO2 = 100 mmHg, PaCO2 = 60 mmHg and a pH of 7.24.
Analysis:
Oxygenation: The PaO2 on 60% oxygen should have been about 300 mmHg. The PaO2/FIO2 ratio in this patient is 100/0.6 = 167. Thus, although the PaO2 is adequate to sustain life, the patient’s oxygenation status is poor. Ventilation: Raised PaCO2 suggests respiratory acidosis.
Acid–base status: The pH shows acidosis. The pH has decreased, whereas the PaCO2 has increased. Hence, the patient has primary, uncompensated respiratory acidosis.
- A 60-year-old man, a known diabetic since the last 15 years is admitted with diabetic ketoacidosis. He required endotracheal intubation and ventilation with 60% oxygen. An arterial blood gas analysis shows the following:
- PaO2 = 60 mmHg, PaCO2 = 28 mmHg, pH = 7.14 and [HCO3–] = 12 mmol/l Analysis Oxygenation: The PaO2 on 60% oxygen should have been about 300 mmHg.
- The PaO2/FI O2 ratio in this patient is 60/0.6 = 100. Thus, although the PaO2 is just adequate to sustain life, the patient’s oxygenation is poor.
Ventilation: Low PaCO2 suggests respiratory alkalosis. Acid–base status: The pH shows acidosis. The pH has decreased, whereas the PaCO2 has also decreased.
- Hence, it is not respiratory acidosis and must be metabolic. The bicarbonate levels are far below normal and suggest a primary metabolic acidosis.
- The low PaCO2 suggests secondary respiratory alkalosis. The patient has primary metabolic acidosis with partial compensation.
- A 65-year-old man with a 40-year history of smoking, posted for elective herniorrhaphy was sent to the preanaesthetic clinic for evaluation.
- Since, he gave history of poor exercise tolerance as evidenced by breathlessness even on mild exertion, and clinical examination revealed presence of COPD, an arterial blood gas analysis was done while the patient breathed room air.
- The report showed a PaO2 = 55 mmHg, PaCO2 = 60 mmHg, pH = 7.34 and [HCO3–] = 30 mmol/l.
Analysis:
Oxygenation: The PaO2/FIO2 ratio is 55/0.21 = 262. Thus, although the PaO2 /FIO2 ratio seems adequate, the actual PaO2 is less than 60 mmHg and suggests hypoxaemia.
Ventilation: High PaCO2 suggests respiratory acidosis.
Acid–base status: The pH shows acidosis. The pH has decreased, whereas the PaCO2 is high.
- Hence, it is respiratory acidosis. The bicarbonate levels are high which suggests metabolic alkalosis. Since, the pH is acidotic but near normal, the patient must be having primary respiratory acidosis with compensatory metabolic alkalosis.
- He has fully compensated respiratory acidosis. This picture of chronic hypoxaemia and hypercarbia is typical of patients suffering from severe chronic obstructive pulmonary disease.
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