Physiology
Renal
A 35 year old woman who is 9 weeks pregnant presents to ED with severe persistent morning sickness. What acid-base disturbance would you most expect to see in this patient:
Answer:
Nausea and vomiting occur commonly in the first trimester. Rarely, this may be severe (hyperemesis gravidarum) and intractable vomiting can cause fluid loss and electrolyte disturbances. The acid-base result is typically a metabolic alkalosis due to loss of hydrogen ions but ketosis may also occur if oral intake is poor.Acid-Base Disturbance
Physiology / Renal / Acid-Base Balance
Last Updated: 21st April 2019
Total body pH can be regulated by controlling the ratio of PaCO2 (acid) to [HCO3-] (base) in plasma. Ventilation controls the CO2 level and the kidney controls the HCO3- level. Disorders of acid-base metabolism can therefore arise from either excess acid or base, or from diseases altering CO2 or HCO3- levels.
pH ∝ [HCO3-]/PaCO2
In a respiratory acid-base disturbance, the primary disorder alters the CO2 level whereas in a metabolic acid-base disturbance, the primary disorder alters the HCO3- level either directly, or by the addition of acid or base to the body. In a mixed disorder, there may be both respiratory and metabolic disturbances. When either the HCO3- or CO2 levels change, the pH can be brought back towards normal by altering the other buffer partner in the same direction.
Normal ABG Values
RCEM defines the normal values for blood gases as:
- pH = 7.35 - 7.45
- pO2 (on air) = 11 - 14 kPa
- pCO2 = 4.5 - 6.0 kPa
- HCO3- = 24 - 30 mmol/L
- BE = +/- 2 mmol/L
Acid-base disturbance
| Metabolic Disturbance | Primary Change | Compensatory Change |
|---|---|---|
| Metabolic acidosis (↓pH) | ↓[HCO3-] | ↓PaCO2 (increased ventilation) |
| Metabolic alkalosis (↑pH) | ↑[HCO3-] | ↑PaCO2 (decreased ventilation) |
| Respiratory acidosis (↓pH) | ↑PaCO2 | ↑[HCO3-] (increased renal bicarbonate reabsorption) |
| Respiratory alkalosis (↑pH) | ↓PaCO2 | ↓[HCO3-] (decreased renal bicarbonate reabsorption) |
Base Excess
Base excess is defined as the amount of strong acid that must be added to each litre of fully oxygenated blood to return the pH to 7.40 at a temperature of 37 °C and a pCO2 of 40 mmHg (5.3 kPa).
A base deficit (i.e. a negative base excess) can be correspondingly defined in terms of the amount of strong base that must be added.
The predominant base contributing to base excess is bicarbonate. A typical reference range for base excess is -2 to +2 mmol/L.
The base excess increases (or becomes more positive) in metabolic alkalosis or in compensation for a respiratory acidosis.
The base excess decreases (or becomes more negative) in metabolic acidosis or in compensation for a respiratory alkalosis.
Metabolic Acidosis
Metabolic acidosis arises from the gain of acid or the loss of base as bicarbonate.
This may occur due to:
- increased production of H+ e.g. lactic acidosis, ketoacidosis (DKA, alcohol, starvation)
- ingestion of H+ or of drugs that are metabolised to acids e.g. salicylate overdose, ethylene glycol poisoning
- impaired renal excretion of H+ e.g. acute or chronic renal failure
- loss of HCO3- in the urine e.g. renal tubular acidosis
- loss of HCO3- in the gastrointestinal tract e.g. chronic diarrhoea, ileal conduits, fistulae, small intestinal/pancreatic/biliary drains
The compensatory response to metabolic acidosis is hyperventilation, since the increased [H+] acts as a powerful stimulant of the respiratory centre. The deep, rapid and gasping respiratory pattern is called Kussmaul breathing. At low pH, the blood pressure falls as a result of reduced peripheral resistance and impaired myocardial contractility. Pulmonary oedema and ultimately ventricular arrest can occur.
Metabolic Alkalosis
Metabolic alkalosis arises from addition of bicarbonate to the blood or from loss of H+ ions from the body.
This may occur due to:
- loss of H+ in the gastrointestinal tract e.g. vomiting, pyloric stenosis, NGT drainage
- loss of H+ in the kidneys e.g. diuretic therapy
- ingestion of absorbable alkali e.g. sodium bicarbonate, antacid overdose
- increased renal HCO3- reabsorption e.g. primary hyperaldosteronism, secondary to volume depletion, secondary to hypokalaemia
Metabolic alkalosis is associated with hypoventilation and features of hypocalcaemia (due to a decrease in the unbound plasma Ca2+ concentration) and hypokalaemia (due to a shift of potassium into cells) e.g. muscle cramps, weakness, tetany, paraesthesia.
Respiratory Alkalosis
In a respiratory alkalosis, the primary disorder is a decrease in pCO2 resulting from hyperventilation. Respiratory alkalosis is much less common than acidosis, and it is usually acute and uncompensated.
Causes include:
- hysterical overbreathing
- mechanical over-ventilation in a ventilated patient
- raised intracranial pressure
- pregnancy
- thyrotoxicosis
- sepsis
- salicylate overdose
- hyperthermia
- liver failure
- hypoxia-induced e.g. altitude acclimatisation
Clinically, there is neuromuscular irritability, with perioral and extremity paresthesia, muscle cramps, tinnitus, hyperreflexia, tetany and seizures. Cerebral vasoconstriction with reduced blood flow and cardiac dysrhythmias can occur.
Respiratory Acidosis
Respiratory acidosis results from a primary decrease in ventilation as a result of depression of the respiratory centre e.g. opioid overdose, a physical impediment to breathing such as neurological, muscular or chest wall disease, or lung disease or injury e.g. COPD, asthma, pulmonary oedema.
An acute rise in plasma CO2 is usually associated with a fall in oxygen levels, dyspnoea, reduced consciousness, and eventually coma. CO2 causes vasodilation, which may increase cerebral blood flow causing headaches and increased intracranial pressure. Systemic vasodilation reduces blood pressure, and large rises in plasma CO2 levels reduce cardiac contractility.
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- Biochemistry
- Blood Gases
- Haematology
| Biochemistry | Normal Value |
|---|---|
| Sodium | 135 – 145 mmol/l |
| Potassium | 3.0 – 4.5 mmol/l |
| Urea | 2.5 – 7.5 mmol/l |
| Glucose | 3.5 – 5.0 mmol/l |
| Creatinine | 35 – 135 μmol/l |
| Alanine Aminotransferase (ALT) | 5 – 35 U/l |
| Gamma-glutamyl Transferase (GGT) | < 65 U/l |
| Alkaline Phosphatase (ALP) | 30 – 135 U/l |
| Aspartate Aminotransferase (AST) | < 40 U/l |
| Total Protein | 60 – 80 g/l |
| Albumin | 35 – 50 g/l |
| Globulin | 2.4 – 3.5 g/dl |
| Amylase | < 70 U/l |
| Total Bilirubin | 3 – 17 μmol/l |
| Calcium | 2.1 – 2.5 mmol/l |
| Chloride | 95 – 105 mmol/l |
| Phosphate | 0.8 – 1.4 mmol/l |
| Haematology | Normal Value |
|---|---|
| Haemoglobin | 11.5 – 16.6 g/dl |
| White Blood Cells | 4.0 – 11.0 x 109/l |
| Platelets | 150 – 450 x 109/l |
| MCV | 80 – 96 fl |
| MCHC | 32 – 36 g/dl |
| Neutrophils | 2.0 – 7.5 x 109/l |
| Lymphocytes | 1.5 – 4.0 x 109/l |
| Monocytes | 0.3 – 1.0 x 109/l |
| Eosinophils | 0.1 – 0.5 x 109/l |
| Basophils | < 0.2 x 109/l |
| Reticulocytes | < 2% |
| Haematocrit | 0.35 – 0.49 |
| Red Cell Distribution Width | 11 – 15% |
| Blood Gases | Normal Value |
|---|---|
| pH | 7.35 – 7.45 |
| pO2 | 11 – 14 kPa |
| pCO2 | 4.5 – 6.0 kPa |
| Base Excess | -2 – +2 mmol/l |
| Bicarbonate | 24 – 30 mmol/l |
| Lactate | < 2 mmol/l |
