Respiratory Acidosis vs Alkalosis — ABG Study Guide
Sources: the Merck Manual Professional pages on respiratory acidosis and respiratory alkalosis, and the StatPearls acid-base reviews. All case numbers below are machine-checked against the Henderson-Hasselbalch relation and the standard compensation rules.
Symbols used: pH is the acid-base scale (7.35 to 7.45 is normal blood). PaCO2 is the partial pressure of carbon dioxide in arterial blood (35 to 45 mm Hg). HCO3 is the bicarbonate concentration (22 to 26 mEq/L). PaO2 is arterial oxygen partial pressure (80 to 100 mm Hg). SpO2 is oxygen saturation on pulse oximetry. mm Hg is millimeters of mercury.
PART 1 — ABG BASICS
1.1 Three numbers run the show
An arterial blood gas (ABG) reports three acid-base numbers: pH, PaCO2, and HCO3. The pH says which way the blood leans. The PaCO2 is the respiratory side: CO2 is an acid, so retained CO2 (high PaCO2) acidifies and blown-off CO2 (low PaCO2) alkalinizes. The HCO3 is the metabolic side, managed by the kidneys: base, so high HCO3 alkalinizes and low HCO3 acidifies.
| Value | Normal range | Controlled by |
|---|
| pH | 7.35-7.45 | The balance itself |
| PaCO2 | 35-45 mm Hg | Lungs (ventilation) |
| HCO3 | 22-26 mEq/L | Kidneys (metabolic) |
PaO2 and SpO2 live on a separate axis: oxygenation, not acid-base. A patient can have a fatal oxygenation problem with a perfectly normal pH, and a severe acid-base disorder with normal oxygenation. Exams check whether you keep the two axes apart.
1.2 Speed: lungs fast, kidneys slow
The lungs adjust PaCO2 in minutes — every breath is a correction. Immediate chemical buffering changes HCO3 within minutes; the kidneys then adjust HCO3 more substantially over hours to days. That timing explains why acute and chronic expected-HCO3 rules differ.
1.3 The one-sentence summary
Respiratory acidosis is too little breathing (CO2 piles up, pH falls). Respiratory alkalosis is too much breathing (CO2 blows off, pH rises). Everything else — causes, symptoms, treatment — follows from that sentence.
1.4 Part 1 checklist
PART 2 — RESPIRATORY ACIDOSIS
2.1 Definition and mechanism
Respiratory acidosis is a primary rise in PaCO2 from inadequate ventilation; pH is usually low in an acute disorder but may be near normal when chronically compensated. The mechanism is hypoventilation — CO2 produced by the body is not exhaled fast enough, so it accumulates and dissolves into carbonic acid. The problem is always ventilation: the pump, the drive, or the pipes.
2.2 Causes, grouped the way exams list them
- Depressed respiratory drive: opioids, sedatives, anesthetics, alcohol, brainstem injury.
- Neuromuscular weakness: Guillain-Barre syndrome, myasthenia gravis, ALS, high spinal anesthesia, muscle fatigue.
- Airway obstruction: COPD exacerbation, late severe asthma, obstructive sleep apnea, obesity hypoventilation.
- Lung and chest wall limits: severe pneumonia, pulmonary edema, flail chest, large effusion, kyphoscoliosis, abdominal distension splinting the diaphragm.
- Iatrogenic: mechanical ventilation set too low for the patient's CO2 production.
2.3 Symptoms: the CO2 narcosis ladder
Rising PaCO2 first gives headache, flushed warm skin, and restlessness; then lethargy, confusion, and drowsiness; then CO2 narcosis — the patient slides toward unresponsiveness, with asterixis (flapping tremor) possible in severe cases. Nurses often see the skin first and the mental change second; the ABG explains both.
2.4 Compensation: the kidney answer
For every 10 mm Hg the PaCO2 rises above 40, immediate nonrenal buffering raises bicarbonate about +1 mEq/L acutely, while renal compensation raises it about +3.5 to +4 mEq/L chronically over days. A COPD patient at PaCO2 70 for weeks therefore runs HCO3 in the mid-30s — and a nearly normal pH. That is compensation, not cure.
2.5 Treatment and nursing actions
Treat the ventilation, then the cause: position upright, clear the airway, encourage deep breathing and coughing, give bronchodilators for obstruction, apply bilevel positive airway pressure or intubation per protocol and provider orders, and reverse the driver when one exists — naloxone for opioid overdose per prescription, sedatives held. Give oxygen for hypoxia: in chronic CO2 retainers titrate toward an SpO2 of about 88 to 92 percent and watch for rising drowsiness — but never withhold oxygen from a genuinely hypoxic patient; hypoxia kills faster than hypercapnia. Reassess ABGs and mental status after every change.
2.6 Part 2 checklist
PART 3 — RESPIRATORY ALKALOSIS
3.1 Definition and mechanism
Respiratory alkalosis is a primary fall in PaCO2 from hyperventilation; pH is usually high in an acute disorder but may be near normal when chronically compensated. The mechanism is hyperventilation — CO2 is exhaled faster than the body makes it, the acid side of the balance drops, and the blood alkalinizes.
3.2 Causes: real sickness hides behind fast breathing
- Anxiety and pain: panic attacks, severe pain, emotional distress.
- Hypoxia-driven: pulmonary embolism (often the first ABG finding), early asthma, pneumonia, heart failure, high altitude.
- Systemic: fever (CO2 production pattern with tachypnea), early sepsis, pregnancy (progesterone-driven), salicylate poisoning (early direct stimulation of the respiratory center), thyrotoxicosis.
- Neurogenic: brainstem injury, meningitis, stroke.
- Iatrogenic: mechanical ventilation set too high.
The exam trap: every panicky-looking hyperventilating patient is not panicking. New dyspnea, pleuritic chest pain, recent long travel, or surgery should put pulmonary embolism and sepsis above anxiety on the differential — assess before you coach breathing.
3.3 Symptoms: the excitability cluster
Alkalosis makes neuromuscular tissue excitable: lightheadedness, dizziness, palpitations, perioral and fingertip tingling (paresthesias), carpopedal spasm, and — severe — tetany. The mechanism is falling ionized calcium: alkalosis shifts calcium onto proteins, so the free, active fraction drops even when total calcium is normal. The patient feels it in the mouth and fingers first.
3.4 Compensation: the kidney answer, reversed
For every 10 mm Hg the PaCO2 falls below 40, immediate buffering lowers bicarbonate about -2 mEq/L acutely, while renal compensation lowers it about -4 to -5 mEq/L chronically (pregnancy and altitude acclimatization are the classic chronic examples). At altitude for a week, a PaCO2 of 30 comes with an HCO3 near 20 and a near-normal pH.
3.5 Treatment and nursing actions
Treat the cause, not the number: oxygen and workup for the hypoxic causes, antipyretics for fever, analgesia for pain, emergency referral for suspected salicylate poisoning or pulmonary embolism. For confirmed anxiety hyperventilation, stay with the patient and coach slow, even breathing. Do not use paper-bag rebreathing: it can worsen hypoxia or interfere with compensation for an unrecognized metabolic acidosis. Safety first: a quiet hyperventilating patient can be sicker than a loud one — assess before assuming anxiety.
3.6 Part 3 checklist
PART 4 — READING AN ABG STEP BY STEP
4.1 Six steps, in order
- pH: below 7.35 = acidemia; above 7.45 = alkalemia; 7.35 to 7.45 is the reference range, but a normal-range pH can also occur in a compensated or mixed disorder, so keep analyzing PaCO2 and HCO3.
- PaCO2: above 45 pushes acid; below 35 pushes alkaline.
- HCO3: above 26 pushes alkaline; below 22 pushes acid.
- Match pH against PaCO2: moving in opposite directions = primary respiratory. Moving in the same direction = primary metabolic (or a mixed picture — flag it).
- Check compensation with the expected-HCO3 rules; an actual HCO3 within a few mEq/L of expected means a single, compensated disorder.
- Read PaO2 and SpO2 as oxygenation — report and treat separately.
4.2 The opposite-direction rule, worked
pH 7.31 (acid) with PaCO2 70 (also on the acid side of its own scale, above 45): the pH and the PaCO2 are pushed the same clinical way? No — read carefully: a HIGH PaCO2 pushes the pH DOWN. So an acid pH with a high PaCO2 means the respiratory system is causing the acidosis: primary respiratory acidosis. The shorthand: high CO2 with low pH = respiratory acidosis; low CO2 with high pH = respiratory alkalosis; low CO2 with low pH would mean the lungs are compensating for a metabolic acidosis — the direction test does the sorting.
4.3 Compensation math on a real case
PaCO2 70 in a COPD regular: rise of 30 above 40, so expected HCO3 = 24 + 3.5 x 3 = 34.5 chronically, or 24 + 1 x 3 = 27 acutely. A measured HCO3 of 34 matches the chronic line — this patient has been retaining CO2 for days to weeks. A measured HCO3 of 27 would fit the expected response to an acute PaCO2 rise. Calling it acute-on-chronic requires evidence of a chronic hypercapnic baseline, such as prior ABGs or a previously elevated bicarbonate. Bicarbonate helps estimate chronicity, but it is not a standalone clock.
PART 5 — FOUR WORKED CASES (all numbers verified)
5.1 Case 1 — the COPD regular (chronic respiratory acidosis)
A 68-year-old with COPD, gradually more breathless for a week, drowsy but rousable. ABG: pH 7.31, PaCO2 70 mm Hg, HCO3 34 mEq/L, PaO2 58 mm Hg. Interpretation: primary respiratory acidosis; expected chronic HCO3 34.5 — matched, so this is chronic and compensated. Nursing path: position upright, start or titrate oxygen toward SpO2 88-92 percent, bronchodilators per orders, watch mental status, prepare for bilevel support if drowsiness deepens.
5.2 Case 2 — the panic attack (acute respiratory alkalosis)
A 22-year-old in the clinic, breathing 30 times a minute after bad news, light-headed, lips and fingers tingling. ABG: pH 7.52, PaCO2 28 mm Hg, HCO3 22 mEq/L. Interpretation: primary respiratory alkalosis; expected acute HCO3 = 24 - 2 x 1.2 = 21.6 — matched, acute and uncompensated beyond the buffer line. Nursing path: stay with the patient, coach slow even breathing, screen for the dangerous mimics (new dyspnea, chest pain, fever, recent travel) before settling on anxiety.
5.3 Case 3 — the overdose (acute respiratory acidosis)
An unresponsive patient found with pinpoint pupils and a respiratory rate of 6. ABG: pH 7.17, PaCO2 80 mm Hg, HCO3 28 mEq/L. Interpretation: primary respiratory acidosis; expected acute HCO3 = 24 + 1 x 4 = 28 — matched, acute. Nursing path: airway first, support ventilation, prepare naloxone per prescription and protocol, continuous monitoring, then reassess the ABG.
5.4 Case 4 — the quiet danger (acute respiratory alkalosis)
A 54-year-old, day 4 after hip surgery, sudden breathlessness and sharp chest pain on breathing in. Respiratory rate 28, SpO2 89 percent on room air. ABG: pH 7.49, PaCO2 30 mm Hg, HCO3 22 mEq/L. Interpretation: primary respiratory alkalosis with hypoxia — the classic early pulmonary embolism pattern; expected acute HCO3 = 24 - 2 x 1 = 22 — matched. Nursing path: oxygen per protocol, stay with the patient, elevate the head of the bed, prepare for emergency evaluation — do not treat this as anxiety.
PART 6 — EXAM PATTERNS AND TRAPS
6.1 The five question patterns
- Interpret the ABG: run the six steps; the answer names one primary disorder with compensation status.
- Which patient is at risk: map causes to the two disorders (hypoventilation group vs hyperventilation group).
- Which action first: acidosis = ventilation and airway; alkalosis = find the cause; both = assess before intervening.
- Compensation math: apply the per-10 rules; the answer is the expected HCO3.
- Symptom-to-diagnosis: tingling and tetany point alkaline; drowsiness and flushed skin point acidotic.
6.2 Traps that cost points
- Calling a respiratory disorder metabolic. The direction test settles it: pH and PaCO2 pushed opposite ways is respiratory.
- Waiting for the lungs to compensate for a respiratory problem. The lungs are the culprit; the kidneys compensate.
- Treating panic before excluding pulmonary embolism, sepsis, and salicylate poisoning in a hyperventilating patient.
- Reading PaO2 into the acid-base answer. Oxygenation is graded separately.
- Chasing a normal PaCO2 into a COPD retainer on high-flow oxygen. Titrate toward 88-92 percent, watch for drowsiness — but never leave a hypoxic patient untreated.
- Paper-bag rebreathing. It is not recommended because it can worsen hypoxia or unrecognized metabolic acidosis.
- Treating a normal-range pH as proof of health or full compensation. Abnormal PaCO2 and HCO3 can also indicate a mixed disorder; compare them with the expected-compensation rules.
APPENDIX A — VALUES, RULES, AND KEYWORDS
| Item | Number |
|---|
| Normal pH | 7.35-7.45 |
| Normal PaCO2 | 35-45 mm Hg |
| Normal HCO3 | 22-26 mEq/L |
| Normal PaO2 | 80-100 mm Hg |
| Respiratory acidosis | primary PaCO2 rise; pH usually low acutely but possibly near normal when compensated |
| Respiratory alkalosis | primary PaCO2 fall; pH usually high acutely but possibly near normal when compensated |
| Acute acidosis compensation | HCO3 +1 per 10 mm Hg rise |
| Chronic acidosis compensation | HCO3 +3.5 to 4 per 10 |
| Acute alkalosis compensation | HCO3 -2 per 10 mm Hg fall |
| Chronic alkalosis compensation | HCO3 -4 to 5 per 10 |
| COPD retainer oxygen target | SpO2 about 88-92 percent |
Keyword pairs: flushed and drowsy = CO2 up; tingling and dizzy = CO2 down; recent surgery plus sudden dyspnea = embolism until proven otherwise; pinpoint pupils with a rate of 6 = opioid hypoventilation.
APPENDIX B — TRAP LIST
- Opposite directions means respiratory; say it out loud before choosing.
- Kidneys compensate respiratory disorders; lungs compensate metabolic ones.
- Hypoxia is not an acid-base answer, and a normal pH is not a clean bill of health.
- Anxiety is a diagnosis of exclusion in the hyperventilating patient.
- HCO3 helps estimate whether a respiratory disorder is acute or chronic, but prior values and the expected-compensation range are needed to identify acute-on-chronic or mixed disorders.
- Never withhold oxygen from a hypoxic patient; titrate and monitor instead.
- Salicylate poisoning moves early respiratory alkalosis often becoming a mixed respiratory alkalosis plus metabolic acidosis — the exam loves both halves.
- Tetany is calcium trouble caused by alkalosis, not a calcium lab you will see ordered.
These are original HyNote study notes for nursing and health-science students. They summarize public educational references and all cases are fictional. They are not official materials of any nursing organization, they are not exam questions, and they are not clinical advice. Following the content plan, qualified clinical review is recommended before wider promotion.
