Biochemistry Acid-Base Balance Flashcards
Acid-Base Balance is
The regulation of Hydrogen ions
Acid-base metabolism
Production of H+ via metabolism of carbs and fats etc. input into the system buffered by factors and output via the lungs and kidneys.
Carbon dioxide is
The major source of acid in the body
CO2 + H2O = Carbonic Acid (produces acid and base)
Acid produced by the body
- Carbonic acid (from CO2)
- Hydrochloric acid – stomach
- Lactic acid
- Alpha-ketoacids
- Uric acid
- Proteins
Bases produced by the body
- Bicarbonate
- Phosphate
- Proteins
- Ammonia
Buffering System
Bicarbonate = most important Haemoglobin (intracellular) Proteins (extracellular) Phosphate (kidneys) Ammonia (kidneys)
Haemoglobin buffering
CO2 from tissue respiration absorbed in erythrocyte releasing Hco3
See diagrams pg 75
The Henderson – Hasselbalch equation
pH = pKa + log (HCO3)/0.23 x pCO2
pH is proportional to
HCO3-/p CO2
HCO3 =
Base=kidneys=metabolic
Increased Hco3 = increased pH (alkalosis)
Reduced HCo3 = decreased pH (acidosis)
Compensation
A change in pH outside the normal range causes the body to attempt to compensate to return pH towards normal.
Acidosis leads to
Mechanisms that compensate to increase the pH
Alkalosis leads to
Mechanisms that compensate to decrease the pH
If there is no evidence of compensation
Acute process
Over-compensation?
Never an over-compensation
Mixed disorder
Primary disorder my be mixed
Compensation – primary metabolic cause:
Respiratory compensation = Immediate
See slide on 76
Compensation = primary respiratory cause:
Metabolic compensation = Delayed
See slide on 76
pCO2
35-45 mmHg
HCO3-
23-29 mmol/L
Base Excess (BE)
±3 mmol/L
pO2 in the context of acid-base
Is immaterial in this context
Acidosis is a
Process which tends to produce an academia
Alkalosis is a
Process which tends to produce an alkalaemia
pH normal values
7.35-7.45
Acidosis is a
Process which tends to produce an academia
Alkalosis is a
Process which tends to produce an alkalaemia
pH normal values
7.35-7.45
Systematic Approach
- Look at the pH – is the primary acidosis or alkalosis?
- Check the Co2 (respiratory indicator) – is the pH change explained by a rise or fall in pCO2?
- Check the HCO3 – is the ph change explained by a rise or fall in HCO3?
- Is there any evidence of compensation?
- Calculate Anion Gap if metabolic acidosis present
Anion Gap →
→ Calculated difference between the serum anions that are measured in a chemistry profile an the unmeasured anions.
Unmeasured cations (11 mmol/L)
Potassium, calcium, magnesium but they are usually constant.
Unmeasured (23 mmol/L)
Proteins, mostly albumin, organic acids, phosphates, sulphates
AG purpose
Is used in the differential diagnosis of metabolic acidosis.
The body does not generate an AG to compensate for a primary disorder – AG is part of a primary disorder.
Causes of normal anion gap acidosis
HCO3 has been removed from the extracellular space due to renal or GI HCO3 losses:
- diarrhoea
- Pancreatic fistula
- Ammonia or alimentation eg TPN
- Carbonic anhydrase inhibitor
- Renal tubular acidosis
- Ureterosigmoidostomy
- Endocrine – hypoaldosteronism
→ Compensatory hyperchloraemia
AG equation
NA+ - (Cl- + HCO-)
Causes of increased anion gap
Endogenous acidosis
Exogenous acidosis
Endogenous acidosis
Uraemia (renal failure) – no regeneration of HCO3- build up of organic acids normally excreted by the kidney
Ketoacidosis – diabeti or alcoholic
Lactic acidosis
Exogenous acidosis
By intoxication:
- Acetyl-salicylic acid (aspirin)
- Biguanides (metformin)
- Breakdown products of poisons (ethylene glycol and methanol)
Acideamia produces
High K+
Alkalaemia produces
Low K+
Metabolic acidosis
Increased rate of H+ production
Acid ingestion
Reduced renal H+ excretion
Loss of bicarbonate
Metabolic acidosis
Metabolic acidosis
Ketoacidosis
Diabetic or alcoholic lactic acidosis form hypoxia poisoning
Inherited organic acidosis
Metabolic acidosis
Reduced renal H+ excretion causes
Generalised renal failure
Renal tubular acidosis (RTA)
Metabolic acidosis
Loss of bicarbonate
Diarrhoea, pancreatic fistula, RTA
Metabolic alkalosis → Caused by
Gain of HCO3 and maintained by abnormal renal HCO3 absorption.
Metabolic alkalosis → Metabolic alkalosis is almost always due to and examples of this causes
Volume contraction
• Vomiting, gastric aspiration, diuretics
• Profound hypokalaemia
• Renal failure: poor filtration and therefore poor excretion
• Hyperaldosteronism: via increased H secretion and hypokalaemia (Na/K exchanger)
• Excess alkali administration (iatrogenic)
Metabolic alkalosis → Alkalosis tends to
Depress respiration and leads to CO2 retention
Metabolic alkalosis → Compensation
Partial compensation since associated hypoxia overrides this effect and stimulates respiration.
Respiratory Acidosis → Causes
Lung Disease
Mechanical
Neurological
Respiratory Acidosis → Lung disease examples
Fibrosis Oedema Tumours Bronchitis Severe asthma Pulmonary embolism
Respiratory Acidosis → Mechanical
Myopathies
Trauma
Pleural effusions
Pneumothorax
Respiratory Acidosis → Neurological
CNS depression (e.g. drugs) CNS disease
Respiratory Acidosis → Increased H+ due to
CO2 retention, compensated by increased bicarbonate synthesis
Respiratory Alkalosis → Definition
CO2 reduction due to excessive ventilation
Respiratory Alkalosis → Causes
Fall in oxygen (anaemia, CCF, altitude)
Pulmonary pathology (infection, oedema)
Central stimulation (Sepsis, toxins, trauma)
Voluntary, psychogenic, anxiety, pain
Causes of High Osmolar Gap
Isotonic hyponatraemia Glycine infusion Chronic renal failure Ingestions Contrast Media
Isotonic hyponatraemia
Hyperlipidaemia
Hyperproteinaemia
Mannitol
Ingestions
Ethanol
Isopropyl alcohol
Ethylene glycol