How does the doctor tell whether my blood is too acidic or too alkaline from a test?

A blood gas test — usually taken from a vein (venous blood gas) in a hospital, emergency, or urgent care setting — directly measures blood pH, bicarbonate level, and carbon dioxide. For outpatient assessment, standard blood electrolytes (sodium, potassium, chloride, bicarbonate) allow the GP to calculate an 'anion gap' — a derived number that tells whether acids are accumulating in the blood. The combination of pH, bicarbonate, carbon dioxide, and the anion gap allows the treating team to identify the type of disturbance and narrow down the cause.

What is the anion gap and why does it matter?

The anion gap is a calculated number (sodium minus the sum of chloride and bicarbonate) that identifies whether acids are building up in the bloodstream. A normal anion gap is roughly 8–12 units. A raised anion gap with acidaemia means dangerous acids — such as lactate from shock or sepsis, ketones from diabetic ketoacidosis, or toxins from poisoning — are accumulating faster than the kidneys can clear them. A normal anion gap with acidaemia points instead to bicarbonate loss, most commonly from diarrhoea or kidney tubule problems. The distinction matters because the causes and treatments are different.

When is an acid-base problem an emergency?

Call 000 or go to an Emergency Department when there is severe acidaemia — this typically means a pH below 7.20. Red flags include confusion or loss of consciousness combined with acid-base disturbance; signs of sepsis (high fever, rapid breathing, very fast heart rate, collapse); rapidly worsening breathlessness; muscle weakness that is affecting breathing; suspected poisoning with antifreeze or methanol; or severe kidney failure. Mild, stable acid-base changes in people with known kidney or lung disease may not require emergency care, but always discuss any new symptoms with your GP promptly.

Can medicines cause acid-base problems?

Yes. Metformin (a common diabetes medication) can rarely cause lactic acidosis — particularly when kidney function is reduced, dehydration is present, or contrast dye is being used for a scan. Some anti-seizure medications (topiramate, acetazolamide) cause a mild metabolic acidosis. Long-term high-dose diuretics can cause metabolic alkalosis through electrolyte shifts. Regular review of all medications with your GP, and checking kidney function before radiology procedures, helps prevent drug-related disturbances. If you take metformin and need a CT scan with contrast, tell both your GP and the radiology team — a temporary pause may be recommended.

What does treatment involve?

Treatment is always directed at the underlying cause rather than just the pH number. Diabetic ketoacidosis is treated with insulin and carefully measured fluids. Sepsis is treated with antibiotics and intravenous fluid resuscitation. Severe diarrhoea causing bicarbonate loss is treated with oral rehydration salts and electrolyte replacement. For people with chronic kidney disease whose blood is persistently mildly acidic, oral sodium bicarbonate tablets help preserve kidney function and bone health over the long term. Mild acid-base changes that are secondary to controlled chronic conditions may need no specific acid-base treatment at all.

Acid-base disturbance

Acid-base disturbances: a practical guide for patients and carers

By Dr HB Lo, FACRRM Reviewed 20 July 2026 10 min read

The body maintains blood pH between 7.35 and 7.45. When pH falls below 7.35 (acidaemia) or rises above 7.45 (alkalaemia), this is an acid-base disturbance. Causes are metabolic (kidneys and chemistry) or respiratory (lungs controlling carbon dioxide).

Common metabolic acidosis causes in Australian general practice include diabetic ketoacidosis, sepsis, and kidney failure. Metabolic alkalosis commonly follows prolonged vomiting or diuretic use. Interpretation uses blood gas results with electrolytes; severe acidaemia (pH below 7.20) or suspected toxic poisoning requires urgent Emergency Department assessment.

The body is a remarkably precise acid-base machine. Dozens of chemical processes each day produce acids — from normal metabolism, from exercise, from digestion — and the lungs, kidneys, and blood buffering system constantly work together to keep blood pH between 7.35 and 7.45. Outside that narrow window, enzymes stop working, cellular chemistry breaks down, and organ function deteriorates.

Acid-base disturbances are common in hospital medicine and in the general practice management of chronic disease, but they are frequently poorly understood by patients and their families. This page explains what acid-base disturbances are, why they happen, how clinicians assess them, and what the treatment involves.

A. Core clinical — the AU general-practice framework

The four types of acid-base disturbance

There are two directions a disturbance can go — too acidic (pH below 7.35, called acidaemia) or too alkaline (pH above 7.45, called alkalaemia). Each direction can be driven by either the metabolic system (kidneys and body chemistry) or the respiratory system (lungs and carbon dioxide). This produces four primary disturbances:

Metabolic acidosis — too much acid or too little bicarbonate buffering in the blood. The commonest causes in Australian general practice are diabetic ketoacidosis (DKA), lactic acidosis from sepsis or shock, kidney failure, and severe diarrhoea. Lactic acidosis from sepsis is often the first and most dangerous sign of serious infection (Therapeutic Guidelines — eTG).

Metabolic alkalosis — too much bicarbonate in the blood. The commonest causes are prolonged vomiting or nasogastric drainage (hydrochloric acid loss from the stomach), loop diuretic use (potassium and chloride loss), and excessive antacid use.

Respiratory acidosis — carbon dioxide retained by the lungs, making the blood more acidic. Causes include COPD flare, sedative drug overdose, obesity-related hypoventilation, neuromuscular disease (Guillain-Barré, motor neurone disease), and severe asthma. Chronic respiratory acidosis occurs in stable advanced COPD, where the kidneys have compensated by retaining bicarbonate over months (Lung Foundation Australia).

Respiratory alkalosis — carbon dioxide blown off too fast, making the blood more alkaline. Causes include anxiety and hyperventilation, sepsis (often the earliest blood gas finding in serious infection), pulmonary embolism, pregnancy (physiological), and salicylate poisoning.

How the body compensates

The body never accepts an acid-base disturbance passively. Respiratory compensation begins within minutes when the metabolic system is disturbed — breathing rate changes to adjust carbon dioxide. Metabolic (kidney) compensation for respiratory disturbances takes hours to days. Clinicians compare the measured compensation against predicted values (such as Winters’ formula for metabolic acidosis: expected CO₂ = 1.5 × bicarbonate + 8, ± 2 mmHg (Albert Ann Intern Med 1967)) to detect whether a mixed disturbance is present — where two or more processes are operating simultaneously.

The anion gap — the central calculation

The anion gap is the most important derived calculation in acid-base medicine. It is calculated as:

Anion gap = sodium − (chloride + bicarbonate)

A normal anion gap is 8–12 mmol/L in most Australian laboratories. An elevated anion gap means unmeasured acids are accumulating in the bloodstream. The causes cluster under the mnemonic MUDPILES: Methanol, Uraemia (kidney failure), Diabetic or alcoholic ketoacidosis, Propylene glycol toxicity, Iron or isoniazid poisoning, Lactic acidosis, Ethylene glycol, Salicylates.

An important practical point: the anion gap must be corrected for albumin levels. Low albumin — common in hospitalised patients — artificially lowers the measured anion gap and can disguise a significant acid accumulation. For each 10 g/L fall in albumin below normal, add 2.5 mmol/L to the measured anion gap when interpreting the result (Figge Crit Care 2009 — referenced in AMH and eTG clinical frameworks).

A normal anion gap with metabolic acidosis points instead to bicarbonate being lost from the body. Causes cluster under HARDUPS: diarrhoea is the commonest (large bicarbonate loss in gut secretions), followed by renal tubular acidosis (a kidney condition where acid excretion fails), acetazolamide use, and post-urological diversion surgery.

Lactic acidosis — the most urgent metabolic acidosis

Lactic acidosis (elevated blood lactate) results when tissues are not receiving enough oxygen — sepsis, haemorrhagic shock, cardiac failure, severe anaemia — causing cells to switch to inefficient anaerobic metabolism that produces lactic acid as a by-product. It is the most common elevated-anion-gap metabolic acidosis encountered in emergency and intensive care settings.

Sepsis frequently presents first as rapid breathing and respiratory alkalosis (the body blowing off CO₂), followed rapidly by metabolic acidosis as lactate rises. The combination of raised respiratory rate, fever, and confusion with any acid-base disturbance should trigger urgent assessment for sepsis. Therapeutic Guidelines and Surviving Sepsis Campaign guidance both recommend lactate measurement as a mandatory part of sepsis assessment.

Diabetic ketoacidosis — a preventable acid-base emergency

Diabetic ketoacidosis occurs when profound insulin deficiency leads to uncontrolled fat breakdown, producing ketone acids (acetoacetate, beta-hydroxybutyrate) faster than the kidneys can clear them. It most commonly affects people with type 1 diabetes during illness or insulin interruption. The high anion gap metabolic acidosis is severe, often with pH below 7.20 and breathing that is deep and rapid (Kussmaul breathing) as the body attempts respiratory compensation.

Diabetes Australia provides patient education resources on sick-day rules — particularly the importance of never stopping insulin during illness even if eating less, and knowing the blood glucose thresholds that should trigger urgent medical review.

Chronic acid-base changes in kidney and lung disease

Mild metabolic acidosis is common in chronic kidney disease (CKD), arising when declining kidney function impairs the ability to excrete the daily acid load from diet and metabolism. This chronic low-grade acidosis accelerates bone mineral loss, worsens protein breakdown, and may speed progression of kidney disease itself.

Oral sodium bicarbonate supplementation in CKD with persistent serum bicarbonate below 22 mmol/L has demonstrated slowed progression of kidney disease in randomised trials (de Brito-Ashurst JASN 2009). Kidney Health Australia includes bicarbonate management in its CKD patient education. Dosing is typically sodium bicarbonate 500–840 mg three times daily, with the aim of maintaining serum bicarbonate between 22 and 24 mmol/L.

Chronic respiratory acidosis in stable severe COPD is managed differently. The elevated CO₂ is accompanied by kidney-mediated retention of bicarbonate over months — a compensated chronic respiratory acidosis. These patients tolerate their chronically elevated CO₂ but decompensate acutely during COPD flares. Critically, supplemental oxygen must be delivered cautiously in chronic hypercapnic COPD, targeting oxygen saturation of 88–92% rather than the usual >94%, because excessive oxygen can suppress their respiratory drive and worsen CO₂ retention (Lung Foundation Australia — COPD-X guidelines).

B. Assessment in clinical practice

Venous versus arterial blood gas

For most clinical acid-base assessment, a venous blood gas (VBG) drawn from a peripheral vein is adequate and significantly more comfortable for patients than an arterial blood gas. Studies in Australian emergency settings confirm that venous pH is typically within 0.03 units of arterial pH, venous bicarbonate within 2 mmol/L, and venous potassium within 0.5 mmol/L of arterial values (Kelly Emerg Med Australas 2010). Arterial blood gas is reserved for accurate measurement of oxygen partial pressure (PaO₂) — relevant in respiratory disease management — or when VBG results do not fit the clinical picture.

The clinical five-step interpretation

Interpreting a blood gas follows five sequential steps:

pH — acidaemia or alkalaemia?
Primary process — look at CO₂ (respiratory) and bicarbonate (metabolic) to identify the driving disturbance
Compensation — compare actual values against predicted compensation formulas to detect mixed disturbances
Anion gap — elevated (acid accumulation) or normal (bicarbonate loss)?
Delta ratio (if anion gap elevated) — the ratio of the gap elevation to the bicarbonate fall reveals whether another disturbance is hidden underneath

This framework, systematically taught across Australian medical and nursing education, is summarised in Therapeutic Guidelines and detailed in nephrology and emergency medicine references.

Additional tests

When toxic alcohol poisoning (methanol, ethylene glycol) is possible, the osmolal gap — the difference between measured and calculated blood osmolality — is checked. A gap above 10 mOsm/kg raises concern. The combination of elevated anion gap, elevated osmolal gap, and visual symptoms or renal failure in a patient with altered consciousness is a toxicological emergency requiring the Poisons Information Centre (13 11 26) and urgent specialist input.

When the anion gap is normal and diarrhoea does not explain the metabolic acidosis, the urinary anion gap and urine pH help discriminate between renal tubular acidosis and other causes of bicarbonate loss.

C. When acid-base disturbance becomes an emergency

The following situations require calling 000 or immediate Emergency Department assessment:

Severe acidaemia with pH below 7.20 — enzymes and cardiac function deteriorate rapidly below this threshold
Metabolic acidosis with confusion or altered consciousness — suggests sepsis, DKA, or toxic ingestion
Suspected toxic alcohol poisoning — methanol or ethylene glycol — visual disturbance, renal failure, high anion gap, high osmolal gap; call Poisons Information on 13 11 26 and proceed immediately to hospital
COPD with acute deterioration, worsening breathlessness, or drowsiness — acute-on-chronic respiratory acidosis may require non-invasive ventilation
Neuromuscular respiratory failure — Guillain-Barré syndrome, myasthenia crisis — rising CO₂ from weakening respiratory muscles is life-threatening

In general practice, mild acid-base changes that are clearly linked to a known, controlled chronic condition (stable CKD, compensated COPD) do not usually require emergency transfer, but any unexplained new disturbance warrants urgent assessment and blood tests including electrolytes and lactate.

D. Australian operations

Investigations in general practice

Most acid-base assessment in general practice relies on serum electrolytes — sodium, potassium, chloride, bicarbonate — ordered as a standard chemistry panel. The anion gap can be calculated from these results without a blood gas. TSH, glucose, creatinine, and albumin add clinical context. Lactate and blood gas testing require a setting with point-of-care testing capability or hospital pathology.

MBS-rebated pathology relevant to acid-base assessment includes urea, electrolytes, creatinine (MBS 66512), urine biochemistry (MBS 66509), and serum aldosterone plus renin (MBS 71178) when metabolic alkalosis with hypertension or unexplained hypokalaemia suggests primary hyperaldosteronism.

Chronic management through general practice

Patients with CKD who have persistently low bicarbonate levels benefit from ongoing monitoring, oral sodium bicarbonate supplementation, and dietary review with a dietitian. The GPCCMP (MBS item 965) enables allied health referral for the underlying condition — typically CKD, COPD, or type 1 diabetes — that is driving the chronic acid-base disturbance.

Patients with severe COPD and chronic respiratory acidosis may qualify for home long-term oxygen therapy or non-invasive ventilation. Assessment criteria and treatment are managed through respiratory physician review, with Lung Foundation Australia providing ongoing patient support.

For COPD patients: never stop your inhaled medications during a respiratory illness. Worsening breathlessness, increased sputum, confusion, or drowsiness during a flare are reasons to seek urgent medical care the same day.

E. Special populations

Type 1 diabetes. DKA is the most dangerous acid-base emergency in this population. Sick-day rules — never stopping insulin, knowing when to measure ketones, knowing when to present to hospital — are a core part of diabetes self-management education. Diabetes Australia provides comprehensive sick-day guidance.

Older adults. Age-related decline in kidney function reduces reserve capacity to compensate for acid-base challenges. Drug interactions — NSAIDs worsening kidney function, potassium-sparing diuretics causing hyperkalaemia, loop diuretics causing metabolic alkalosis — are more likely in people on multiple medications. Annual medication review and kidney function monitoring are important preventive measures.

Aboriginal and Torres Strait Islander patients. Higher rates of CKD, type 2 diabetes, and cardiovascular disease in ATSI populations mean acid-base disturbances related to these conditions are more common. Annual health assessments (MBS item 715) provide a systematic framework for monitoring electrolytes, kidney function, and glucose control.

People taking multiple medications. Drug-induced acid-base problems are underappreciated. Metformin accumulation in impaired kidney function causing lactic acidosis; topiramate or acetazolamide causing tubular acidosis; potassium-sparing diuretics causing severe hyperkalaemia — all require awareness and systematic medication review, including before procedures using iodinated contrast.

When to escalate

Escalate from general practice to hospital or specialist care when:

pH below 7.20 on blood gas — Emergency Department
Any metabolic acidosis with lactate elevated above 4 mmol/L — Emergency Department
Suspected toxic alcohol ingestion — Emergency Department, Poisons Information 13 11 26
Metabolic alkalosis with hypokalaemia not responding to oral potassium replacement
Unexplained normal-anion-gap metabolic acidosis — nephrology for renal tubular acidosis assessment
Chronic respiratory acidosis in COPD with worsening hypercapnia — respiratory physician for non-invasive ventilation consideration
Recurrent DKA — endocrinology and diabetes educator review

What this article is and is not

This is general health information drawn from Therapeutic Guidelines (eTG), Australian Medicines Handbook, NPS MedicineWise, Kidney Health Australia, and Lung Foundation Australia. It does not constitute personal medical advice. Acid-base disturbances vary enormously in cause and severity — interpretation and management must be done with a clinician using your actual blood test results.

Consumer resources: HealthDirect, Better Health Channel, Kidney Health Australia, Lung Foundation Australia, Diabetes Australia, Poisons Information 13 11 26.

Sources cited

Frequently asked questions

How does the doctor tell whether my blood is too acidic or too alkaline from a test?

A blood gas test — usually taken from a vein (venous blood gas) in a hospital, emergency, or urgent care setting — directly measures blood pH, bicarbonate level, and carbon dioxide. For outpatient assessment, standard blood electrolytes (sodium, potassium, chloride, bicarbonate) allow the GP to calculate an 'anion gap' — a derived number that tells whether acids are accumulating in the blood. The combination of pH, bicarbonate, carbon dioxide, and the anion gap allows the treating team to identify the type of disturbance and narrow down the cause.
What is the anion gap and why does it matter?

The anion gap is a calculated number (sodium minus the sum of chloride and bicarbonate) that identifies whether acids are building up in the bloodstream. A normal anion gap is roughly 8–12 units. A raised anion gap with acidaemia means dangerous acids — such as lactate from shock or sepsis, ketones from diabetic ketoacidosis, or toxins from poisoning — are accumulating faster than the kidneys can clear them. A normal anion gap with acidaemia points instead to bicarbonate loss, most commonly from diarrhoea or kidney tubule problems. The distinction matters because the causes and treatments are different.
When is an acid-base problem an emergency?

Call 000 or go to an Emergency Department when there is severe acidaemia — this typically means a pH below 7.20. Red flags include confusion or loss of consciousness combined with acid-base disturbance; signs of sepsis (high fever, rapid breathing, very fast heart rate, collapse); rapidly worsening breathlessness; muscle weakness that is affecting breathing; suspected poisoning with antifreeze or methanol; or severe kidney failure. Mild, stable acid-base changes in people with known kidney or lung disease may not require emergency care, but always discuss any new symptoms with your GP promptly.
Can medicines cause acid-base problems?

Yes. Metformin (a common diabetes medication) can rarely cause lactic acidosis — particularly when kidney function is reduced, dehydration is present, or contrast dye is being used for a scan. Some anti-seizure medications (topiramate, acetazolamide) cause a mild metabolic acidosis. Long-term high-dose diuretics can cause metabolic alkalosis through electrolyte shifts. Regular review of all medications with your GP, and checking kidney function before radiology procedures, helps prevent drug-related disturbances. If you take metformin and need a CT scan with contrast, tell both your GP and the radiology team — a temporary pause may be recommended.
What does treatment involve?

Treatment is always directed at the underlying cause rather than just the pH number. Diabetic ketoacidosis is treated with insulin and carefully measured fluids. Sepsis is treated with antibiotics and intravenous fluid resuscitation. Severe diarrhoea causing bicarbonate loss is treated with oral rehydration salts and electrolyte replacement. For people with chronic kidney disease whose blood is persistently mildly acidic, oral sodium bicarbonate tablets help preserve kidney function and bone health over the long term. Mild acid-base changes that are secondary to controlled chronic conditions may need no specific acid-base treatment at all.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.