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Foundations

Acid–Base Imbalances & ABGs

ABG High-yield Verified · Sep 2026

Acid–base imbalances are disturbances of the homeostasis of plasma acidity — classified into four primary disturbances (metabolic acidosis, metabolic alkalosis, respiratory acidosis, respiratory alkalosis) — with pH below 7.35 defining acidemia and above 7.45 defining alkalemia.

The foundation skill behind DKA, COPD, shock, and sepsis: read a blood gas with the ROME mnemonic and the stepwise method, name the primary disorder and its compensation, and know which pictures are emergencies.

What’s going wrong in the body

The normal physiology, where it fails, and why the body’s compensation backfires.

01 One number, two controllers

Plasma pH is held in a razor-thin band — 7.35 to 7.45, averaging 7.40 — by the bicarbonate buffer system: CO₂ + H₂O ⇌ H₂CO₃ ⇌ HCO₃⁻ + H⁺. Push on either end of that equilibrium and it shifts to resist the change (Le Chatelier’s principle). That single equation is the whole subject: CO₂ is the acid side and bicarbonate the base side, and each has its own controlling organ.

The lungs control CO₂ and work fast — ventilation changes move pH within minutes to hours. The kidneys control HCO₃⁻, reabsorbing bicarbonate and excreting fixed acids, but they are slow — renal compensation takes days to become effective. This two-speed design explains almost every ABG you will ever read: whichever system caused the problem, the other one compensates at its own pace.

The compensation see-saw: lungs adjust the acid (CO₂) side within minutes to hours; kidneys adjust the base (HCO₃⁻) side over days.

02 The four primary disturbances

Every acid–base problem is one of four primary disturbances, named for which side of the equation broke and which direction pH moved. A respiratory problem is a CO₂ problem: respiratory acidosis is failed ventilation with CO₂ accumulating (pH < 7.35 with PaCO₂ > 45 mm Hg), while respiratory alkalosis is hyperventilation blowing CO₂ off (low PaCO₂ with pH > 7.45) — it is almost always induced by some process causing hyperventilation.

A metabolic problem is a bicarbonate problem: metabolic acidosis is increased systemic H⁺ with serum HCO₃⁻ below normal — via increased acid production, decreased acid excretion, acid ingestion, or renal/GI bicarbonate loss — while metabolic alkalosis is pH above 7.45 from an increased serum HCO₃⁻ (classically HCl lost from vomiting or NG suction, leaving a relative bicarbonate excess).

Each primary disturbance triggers the opposite system to compensate: metabolic acidosis drives compensatory hyperventilation (CO₂ falls), metabolic alkalosis drives compensatory hypoventilation (CO₂ rises), respiratory acidosis makes the kidneys retain HCO₃⁻, and respiratory alkalosis makes them generate less of it.

The four-imbalance map: two acidoses, two alkaloses — each named for the side that broke, each answered by the opposite system (dotted arrows).

03 Compensation — and its three grades

Compensation is graded by how far the second system has gotten. Uncompensated: the secondary system’s value is still normal and pH is abnormal — the backup hasn’t engaged yet. Partially compensated: the secondary value is abnormal (the backup is working) but pH is still out of range. Fully compensated: the secondary value is abnormal and pH is back inside the normal range — the backup has won, for now.

The kidneys’ slowness makes the acute-vs-chronic distinction readable on the gas. In respiratory acidosis, HCO₃⁻ rises only about 1 mEq/L per 10 mm Hg of PCO₂ acutely, but about 4 mEq/L per 10 mm Hg once the problem is chronic (days) — which is why a COPD patient can live at a high PaCO₂ with a near-normal pH. Predicted compensation is also checkable: in metabolic acidosis, Winter’s formula gives expected PCO₂ = (1.5 × HCO₃⁻) + 8 ± 2 — the bedside shortcut is that the last two digits of the pH ± 2 approximate the expected PCO₂.

When the numbers refuse to follow the expected pattern, suspect a mixed disorder — two primary disturbances at once. The classic exam example is salicylate (aspirin) toxicity, which drives a respiratory alkalosis (hyperventilation) and a high-anion-gap metabolic acidosis simultaneously.

04 Reading the gas: ROME plus the stepwise method

The ROME mnemonic sorts respiratory from metabolic at a glance: Respiratory Opposite — pH and CO₂ moving in opposite directions (one up, one down) means a respiratory disorder; Metabolic Equal — pH and HCO₃⁻ moving in the same direction means a metabolic one.

The stepwise method makes it systematic. Step 1 — pH: below 7.35 is acidemia, above 7.45 is alkalemia; when pH sits inside the normal range, compare it to 7.40. Step 2 — find the consistent value: whichever of PaCO₂ or HCO₃⁻ moved in the direction that explains the pH is the primary disorder (PaCO₂ > 40 with pH < 7.4 is a respiratory acidosis; PaCO₂ < 40 with pH > 7.4 is a respiratory alkalosis). Step 3 — the inconsistent value is compensation, graded as above. Step 4 — check PaO₂: an acid–base read is not finished until you have assessed oxygenation.

A worked example to calibrate on (StatPearls): pH 7.39 / CO₂ 51 / HCO₃⁻ 30 — pH is normal but below 7.40, CO₂ is the value that fits it, so this is a primary respiratory acidosis; the raised bicarbonate is metabolic compensation that has brought pH back into range (fully compensated). Apply the same two steps to any gas: find the value that matches the pH, then ask whether the other one has moved.

The stepwise ABG read: pH first, then the consistent value names the primary disorder, the inconsistent value grades compensation, and PaO₂ finishes the job.

Causes & risk factors

Modifiable factors are teaching targets — the patient can act on them.

CNS depressants — opioids, sedatives, hypnotics, benzodiazepines, especially combined with alcohol (→ respiratory acidosis) COPD, asthma, bronchitis (→ respiratory acidosis) Neuromuscular disease — myasthenia gravis, Guillain-Barré, ALS, muscular dystrophy (→ respiratory acidosis) Severe obesity, obesity-hypoventilation syndrome, obstructive sleep apnea (→ respiratory acidosis) Anxiety or panic, pain, fear, fever (→ respiratory alkalosis) Sepsis, hypoxemia, pulmonary embolism, high altitude, pregnancy, excessive mechanical ventilation (→ respiratory alkalosis) Ketoacidosis (diabetic, alcoholic, starvation) (→ high-anion-gap metabolic acidosis) Lactic acidosis — shock, sepsis, hypoxia (→ high-anion-gap metabolic acidosis) Renal failure / uremia; toxic ingestions (methanol, ethylene glycol, salicylates) (→ high-anion-gap metabolic acidosis) Severe diarrhea; renal tubular acidosis (→ normal-anion-gap metabolic acidosis) Vomiting or NG suction — gastric HCl loss (→ metabolic alkalosis) Loop and thiazide diuretics; hypokalemia; mineralocorticoid excess (→ metabolic alkalosis) Alkali or calcium-antacid excess — milk-alkali syndrome (→ metabolic alkalosis)

Signs & symptoms

Each finding tied to the mechanism that produces it — and the triage it calls for.

Kussmaul respirations — deep, labored breathing Hold & notify
Why: The signature of metabolic acidosis: the lungs are blowing off CO₂ to compensate. In DKA it pairs with dry mucous membranes and a ketotic "chemical" breath odor.
Anorexia, fatigue, headache, nausea/vomiting early Expected
Why: The nonspecific early face of metabolic acidosis — easy to dismiss until the breathing pattern or a lab draws attention.
Dyspnea, anxiety, wheezing, disturbed sleep early Expected
Why: The early face of respiratory acidosis — the ventilation problem announcing itself before the CO₂ climbs far.
Flushed, warm skin and diaphoresis with rising CO₂ Expected
Why: Hypercapnia is a vasodilator — including in the brain, where cerebral vasodilation drives the neurologic signs that follow.
Drowsiness, lethargy, confusion in a hypercapnic patient late Report immediately
Why: Rising CO₂ depresses the CNS — the CO₂ narcosis picture. A moribund, lethargic, or confused patient in acute respiratory acidosis needs ICU-level monitoring — rising CO₂ can progress to seizures and coma.
Myoclonus, seizures, papilledema (severe hypercapnia) late Report immediately
Why: Severe hypercapnic cerebral vasodilation raises intracranial pressure — the end of the respiratory-acidosis road.
Memory loss, impaired coordination in chronic CO₂ retainers late
Why: Chronic hypercapnia’s sequelae — along with polycythemia, pulmonary hypertension, and heart failure.
Circumoral numbness, tingling hands and feet, carpopedal spasm Expected
Why: The classic respiratory-alkalosis cluster: alkalosis shifts the oxyhemoglobin curve left (impaired O₂ unloading) and drops potassium and ionized calcium, firing up nerves and muscle.
Lightheadedness, dizziness, tremor (hyperventilating patient) early Expected
Why: Low CO₂ from hyperventilation — almost always driven by some identifiable process: anxiety, pain, fever, hypoxemia, sepsis.
Chest discomfort or a new arrhythmia during alkalosis Report immediately
Why: The hypokalemia and hypocalcemia that travel with alkalosis can produce life-threatening arrhythmias — the reason "just hyperventilation" still gets a monitor check.
Muscle twitching, hand tremor, prolonged spasms → tetany Hold & notify
Why: Metabolic alkalosis raises neuromuscular excitability — twitching escalating to tetany tracks how far the pH has climbed.
Slow, shallow breathing in metabolic alkalosis Expected
Why: Compensatory hypoventilation — the lungs retaining CO₂ to fight the alkalemia. Expected physiology, but it costs oxygenation.
Confusion progressing to stupor or coma (alkalosis) late Report immediately
Why: Severe alkalosis decreases cerebral blood flow and impairs peripheral O₂ unloading — a deteriorating LOC in alkalosis is a report-now finding.

Diagnostics

Test In this disorder Normal
pH (arterial) Step ① of every ABG. A normal pH does not mean a normal gas — full compensation and mixed disorders both hide behind it < 7.35 = acidemia · > 7.45 = alkalemia; within range, compare against 7.40 for the stepwise read StatPearls 7.35–7.45
PaCO₂ ROME: Respiratory Opposite — CO₂ and pH move in opposite directions when the problem is respiratory > 45 = respiratory acidosis side · < 35 = respiratory alkalosis side — the respiratory (acid) parameter StatPearls 35–45 mm Hg
HCO₃⁻ (bicarbonate) ROME: Metabolic Equal — HCO₃⁻ and pH move in the same direction when the problem is metabolic Below normal in metabolic acidosis · above normal in metabolic alkalosis — the metabolic (base) parameter StatPearls 22–26 mEq/L
PaO₂ / SaO₂ Reference figures per StatPearls; some nursing texts print PaO₂ 80–100 Assessed as step ④ of the read — an ABG interpretation is incomplete without the oxygenation check StatPearls PaO₂ 75–100 mm Hg · SaO₂ 95–100%
Anion gap Correct for albumin: the gap falls ~2.5 mEq/L per 1 g/dL of albumin below normal — a hidden gap in the hypoalbuminemic patient Elevated in ketoacidosis, lactic acidosis, renal failure, and toxic ingestions; normal (hyperchloremic) with diarrhea or renal tubular acidosis StatPearls 8–12 mEq/L (Na⁺ − [Cl⁻ + HCO₃⁻])
Urine chloride (metabolic alkalosis workup) Sorts the alkalosis that will respond to saline + K⁺ repletion from the one that needs its underlying disease treated < 10 mEq/L = chloride-responsive (GI losses, diuretics, post-hypercapnia) · > 20 mEq/L = chloride-resistant (hyperaldosteronism, Bartter/Gitelman) StatPearls —

Complications

Warning: CO₂ narcosis — severe acute respiratory acidosis Report immediately
A moribund, lethargic, or confused patient with rising CO₂ needs ICU-level monitoring — and intubation if hypoventilating.
This patient needs ICU-level monitoring. Anticipate CPAP/BiPAP or intubation and mechanical ventilation for hypoventilation — and expect gradual CO₂ correction: rapid alkalization of the CSF can cause seizures. Respiratory stimulants are not effective.
Warning: Severe acidemia (pH < 7.2) — cardiovascular collapse Report immediately
Systemic vasodilation, reduced myocardial contractility and MAP, arrhythmias, hyperkalemia, and diminished responsiveness to catecholamines and vasopressors — severe metabolic acidosis can lead to shock or death.
Treatment is the underlying cause, not the number: fluid resuscitation and electrolyte correction. IV sodium bicarbonate is considered only in severe acidosis (pH < 7.1) — in DKA the 2024 ADA/EASD consensus reserves it for pH < 7.0 — because it carries its own risks: hypernatremia, hypocalcemia, intracellular acidification, increased lactate, reduced contractility.
Warning: Alkalosis extremes — seizures and arrhythmias Report immediately
Respiratory alkalosis is not fatal by itself — the danger is usually its cause — but severe alkalemia (pH above 7.6) can bring confusion, seizures, and arrhythmias, which turn life-threatening with concurrent hypokalemia/hypocalcemia.
Escalate any alkalosis with confusion, seizures, arrhythmias, or hypotension — uncorrected metabolic alkalosis can cause hypotension and cardiac dysfunction.
Caution: The potassium see-saw Hold & notify
Acidemia shifts H⁺ into cells in exchange for K⁺ moving out → hyperkalemia; alkalosis does the reverse and travels with hypokalemia (plus reduced ionized-calcium effects).
Every significant pH move is a potassium event. Check and trend K⁺ with the gas — the cardiac risk often lives in the electrolyte, not the pH itself.
Caution: Mixed disorders — when compensation "doesn’t add up" Hold & notify
If compensation does not follow the expected pattern, a mixed respiratory–metabolic disorder may be present.
The classic: salicylate toxicity, which drives respiratory alkalosis (hyperventilation) and high-anion-gap metabolic acidosis at the same time. A gas that defies the stepwise method is a finding, not a lab error.

Beyond medications

  • Treat the cause, not the number — an abnormal gas signifies an underlying disorder that needs to be corrected: reverse the opioid (naloxone), open the airways (bronchodilators ± corticosteroids for obstructive disease), resuscitate the volume, fix the electrolytes.
  • Ventilatory support for hypoventilation — CPAP/BiPAP, escalating to endotracheal intubation and mechanical ventilation; hypercapnia is corrected gradually because rapid CSF alkalization can cause seizures.
  • Coach the hyperventilating patient — treat the driver (anxiety management, pain control), coach slow breathing, and adjust ventilator settings when the alkalosis is iatrogenic.
  • Skip the paper bag — rebreathing into a bag can cause significant hypoxemia and is no longer recommended; if rebreathing is used at all, monitor oxygen saturation continuously. Coach slow diaphragmatic breathing instead.
  • Replete chloride, potassium, and volume in chloride-responsive metabolic alkalosis (saline-based fluids); chloride-resistant alkalosis needs its underlying condition treated — potassium-sparing diuretics (amiloride, triamterene) have a role.

Nursing considerations

The RN-specific layer — each action paired with the reason it matters.

Assessment & monitoring
Assess respiratory rate, depth, and pattern — not just the number — every check on an at-risk patient.
Why: The breathing pattern is the compensation made visible: Kussmaul (deep, labored) breathing means metabolic acidosis being blown off; slow, shallow breathing in a vomiting or diuresed patient means metabolic alkalosis being retained against.
Track level of consciousness closely in any patient with an abnormal gas — and treat new lethargy or confusion in a CO₂ retainer as an emergency.
Why: CNS depression is where both extremes converge: hypercapnia causes drowsiness through CO₂ narcosis, and severe alkalosis drops cerebral blood flow toward stupor. Severe acute respiratory acidosis with a lethargic patient needs ICU-level monitoring.
Check and trend potassium with every significant pH change.
Why: Acidemia pushes K⁺ out of cells (hyperkalemia); alkalosis pulls it in (hypokalemia) — and the alkalotic patient’s arrhythmia risk rides on that potassium and calcium, not the pH alone.
Watch for neuromuscular irritability in alkalotic patients: numbness and tingling, circumoral numbness, carpopedal spasm, twitching, tetany.
Why: These track the alkalosis and its companion hypocalcemia/hypokalemia in real time — escalation from tingling to tetany or arrhythmia is the deterioration signal.
For the ABG draw: radial artery preferred, modified Allen test first, collect anaerobically in a heparinized syringe, eject air bubbles immediately, place on ice and send promptly.
Why: Palm color must return on the Allen test — that proves ulnar collateral flow, and without it radial puncture is unsafe. Air bubbles and delay change the gas values you are about to treat.
When the gas comes back bad
Read it stepwise before acting: pH → the consistent value (primary disorder) → the inconsistent value (compensation grade) → PaO₂.
Why: The method keeps you from treating the compensation as the disease — the elevated HCO₃⁻ of a chronic CO₂ retainer is the kidneys helping, not a second problem.
For the hypoventilating, hypercapnic patient: stay with them, escalate immediately, and anticipate reversal (naloxone if opioid-induced), CPAP/BiPAP, or intubation.
Why: A lethargic or confused patient in acute respiratory acidosis belongs in ICU-level care; CNS depressants — opioids, sedatives, benzodiazepines, especially with alcohol — are a leading reversible cause. Respiratory stimulants are not effective.
For the hyperventilating patient: find and treat the driver (pain, anxiety, fever, hypoxemia), coach slow breathing, and check ventilator settings if the patient is ventilated.
Why: Respiratory alkalosis is almost always secondary to a process causing hyperventilation — the gas normalizes when the driver stops, and excessive mechanical ventilation is a fixable iatrogenic cause.
For the vomiting or NG-suction patient with a climbing bicarbonate: anticipate saline-based fluid with potassium and chloride repletion.
Why: Gastric fluid is highly acidic (pH ≈ 1.5–3.5), so losing it leaves a bicarbonate excess; chloride-responsive alkalosis corrects when chloride, potassium, and volume are restored.
Expect gradual, cause-directed correction — question orders that would normalize the numbers fast.
Why: Rapid hypercapnia correction risks seizures from CSF alkalization, and bicarbonate is reserved for severe acidosis (pH < 7.1; 2024 ADA/EASD consensus: < 7.0 in DKA) because of its own harms.
Patient teaching
Report suspected alkalosis promptly — slowed breathing, new confusion, seizures, palpitations or an irregular pulse, or falling blood pressure.
Why: These are the escalation cues for alkalosis — and the same escalation logic protects the acidotic patient.
Warn patients on opioids, sedatives, or benzodiazepines never to combine them with alcohol.
Why: CNS depression — especially sedatives combined with alcohol — is a leading cause of hypoventilation and respiratory acidosis.
Ask about antacid habits; teach that chronic calcium-antacid excess is not harmless.
Why: Alkali ingestion (milk-alkali syndrome from calcium antacids) is a real cause of metabolic alkalosis.
Teach diuretic users the alkalosis–hypokalemia link and the symptoms to report: muscle twitching, tingling, palpitations.
Why: Loop and thiazide diuretics cause metabolic alkalosis, and hypokalemia both drives and worsens it — the neuromuscular symptoms are the early warning a patient can actually notice.

How a real nurse thinks

The clinical-judgment loop, worked for a typical presentation — reasoning, not reference.

  1. 1
    Recognize cues

    The cues that matter: a previously alert patient now difficult to rouse, RR 9 and shallow, pH 7.26 with PaCO₂ 61, PaO₂ 58, a K⁺ of 5.4 — and an opioid on board in a patient whose COPD already handicaps ventilation. The stable BP and normal temperature are background noise.

  2. 2
    Analyze cues

    Read the gas stepwise. ① pH 7.26 < 7.35: acidemia. ② PaCO₂ 61 is the value consistent with the pH (ROME: pH down, CO₂ up — opposite directions = respiratory): primary respiratory acidosis. ③ HCO₃⁻ 27 is above range — the kidneys are working, but pH is still abnormal: partially compensated. ④ PaO₂ 58 is low: oxygenation is failing too. The declining LOC on top of hypercapnia is the CO₂ narcosis picture — a medical emergency. The K⁺ of 5.4 fits the acidemia: H⁺ moving into cells pushes K⁺ out.

  3. 3
    Prioritize

    Ventilation first — this patient is failing to breathe, and severe acute respiratory acidosis with lethargy is an emergency that needs ICU-level monitoring. Sequence: stay and stimulate → escalate now → reverse the cause → support ventilation. The potassium rides along: it should correct as the acidemia does, but it belongs in the same SBAR.

  4. 4
    Generate solutions

    Stay with the patient, stimulate and reassess responsiveness and airway; call the rapid response/provider immediately; anticipate naloxone for opioid-induced CNS depression, CPAP/BiPAP, and possible intubation if hypoventilation persists; hold further opioid dosing pending provider review; continuous monitoring with a repeat ABG to follow the trend.

  5. 5
    Take action

    Stimulate and position for airway patency while a colleague calls the rapid response. Deliver the SBAR: "COPD patient, post-op day 1, opioid at 1130 — now difficult to rouse, RR 9 and shallow, ABG pH 7.26, CO₂ 61, bicarb 27, PaO₂ 58, K⁺ 5.4. I believe this is opioid-driven respiratory acidosis on chronic lung disease. Requesting immediate evaluation; anticipate naloxone and noninvasive ventilation; I am holding the 1530 opioid pending your review." The trap is treating the number instead of the cause — no gas improves while the drive to breathe stays suppressed.

  6. 6
    Evaluate

    Success looks like: respiratory rate and depth recovering, the patient rousable and staying awake, repeat ABG with PaCO₂ trending down and pH rising toward range, K⁺ drifting back with the pH. Correction should be gradual — and no improvement in LOC or ventilation, or any further CO₂ rise, re-escalates immediately toward BiPAP or intubation.

Scenario — you’re the nurse

Work each question before revealing the answer. Rationales explain the wrong options too.

Med-surg unit · 1400, first rounds after lunch

A 72-year-old woman with COPD, post-op day 1 after hip surgery, receiving scheduled opioid analgesia. The aide reports she "slept through lunch." You find her difficult to rouse, with slow, shallow breathing. A stat ABG is drawn.

1400 vitals — HR 92 · BP 138/78 · RR 9, shallow · SpO₂ 88% on room air · T 37.1 °C
Neuro — arouses briefly to voice and sternal rub, drifts back off; was alert at 0800
Stat ABG — pH 7.26 · PaCO₂ 61 mm Hg · HCO₃⁻ 27 mEq/L · PaO₂ 58 mm Hg
1400 labs — K⁺ 5.4 mEq/L · Na⁺ 138 · glucose 118
MAR — opioid analgesic given 1130 for pain 7/10; next dose due 1530
Q1 Select all that apply
Which findings require immediate follow-up? Select all that apply.
  1. A. Respiratory rate 9 and shallow
  2. B. Increasingly difficult to rouse (alert at 0800)
  3. C. Blood pressure 138/78 mmHg
  4. D. SpO₂ 88% on room air with PaO₂ 58 mm Hg
  5. E. Temperature 37.1 °C
  6. F. Potassium 5.4 mEq/L
Reveal answer & rationale
Answer: A, B, D, F
RR 9 and shallow is failing ventilation — the cause of everything else on the gas. A falling LOC in a hypercapnic patient is the CO₂ narcosis picture, a medical emergency. The PaO₂ of 58 fails step ④ of the read. K⁺ 5.4 is the acidemia shifting potassium out of cells and needs provider awareness. The BP (C) is stable and the temperature (E) is normal — neither changes the plan.
Q2 Multiple choice
The ABG shows pH 7.26, PaCO₂ 61 mm Hg, HCO₃⁻ 27 mEq/L. The nurse interprets this as:
  1. A. Uncompensated respiratory acidosis
  2. B. Partially compensated respiratory acidosis
  3. C. Partially compensated metabolic acidosis
  4. D. Fully compensated respiratory acidosis
Reveal answer & rationale
Answer: B
pH 7.26 = acidemia; CO₂ 61 moved opposite to the pH (ROME: Respiratory Opposite) and explains it — primary respiratory acidosis. HCO₃⁻ 27 is above the 22–26 range, so the kidneys are compensating, but pH is still abnormal: partially compensated (B). Uncompensated (A) would require a still-normal bicarbonate. Metabolic acidosis (C) would need a low HCO₃⁻ moving in the same direction as pH. Fully compensated (D) would require the pH back inside 7.35–7.45.
Q3 Multiple choice
Which factor most likely drove this patient’s respiratory acidosis?
  1. A. Anxiety-driven hyperventilation after surgery
  2. B. Opioid-induced CNS depression on top of chronic obstructive lung disease
  3. C. Bicarbonate loss from postoperative diarrhea
  4. D. Excessive mechanical ventilation
Reveal answer & rationale
Answer: B
CNS depression from opioids is a leading cause of hypoventilation and CO₂ retention, and COPD had already handicapped this patient’s ventilation — the combination is the story the timeline tells (opioid at 1130, unrousable by 1400) (B). Hyperventilation (A) causes respiratory alkalosis — low CO₂, high pH — the opposite gas. Diarrhea (C) causes a normal-anion-gap metabolic acidosis with a low bicarbonate; hers is high. She is not on a ventilator, and over-ventilation (D) also produces alkalosis, not acidosis.
Q4 Put in order
Put the nurse’s first four actions in priority order:
  1. A. Activate the rapid response / notify the provider (SBAR: respiratory acidosis, falling LOC, K⁺ 5.4)
  2. B. Stay with the patient — stimulate her and assess airway and responsiveness
  3. C. Prepare to give naloxone as ordered and anticipate CPAP/BiPAP
  4. D. Hold the 1530 opioid dose pending provider review and document the event
Reveal answer & rationale
Correct order: B → A → C → D
Stay and stimulate first (B) — an unrousable, hypoventilating patient needs a nurse at the bedside protecting the airway before anything else. Escalation (A) comes immediately after, because severe acute respiratory acidosis with lethargy is an emergency needing ICU-level monitoring. Then reversal and ventilatory support as ordered (C) — naloxone targets the reversible cause. Holding the next dose and documenting (D) matters but never precedes stabilizing and escalating. Calling first (A before B) leaves her unattended and hypoventilating while you are on the phone.
Q5 Multiple choice
Two hours after treatment, which finding best indicates the interventions are working?
  1. A. The patient is sleeping quietly and is difficult to wake, but her SpO₂ is now 99%
  2. B. Respiratory rate 14 with easy arousal, and the repeat ABG shows PaCO₂ trending down with pH rising toward range
  3. C. The repeat ABG shows the pH fully corrected to 7.45 within the first hour
  4. D. Potassium has risen to 5.9 mEq/L
Reveal answer & rationale
Answer: B
Success is ventilation restored and the gas following: rate and depth recovering, LOC recovering, CO₂ trending down and pH rising (B). A patient still difficult to wake (A) is still in the CO₂ narcosis picture no matter what the saturation reads — oxygenation and ventilation are separate checks. Very rapid correction (C) is a warning, not a win: hypercapnia is corrected gradually because rapid CSF alkalization can cause seizures. A rising K⁺ (D) is the acidemia logic running backward — potassium should drift down as pH recovers, and 5.9 would be a new problem to report.

Common questions

What causes acid–base imbalances & abgs?
Common causes and risk factors include cns depressants — opioids, sedatives, hypnotics, benzodiazepines, especially combined with alcohol (→ respiratory acidosis), copd, asthma, bronchitis (→ respiratory acidosis), neuromuscular disease — myasthenia gravis, guillain-barré, als, muscular dystrophy (→ respiratory acidosis), severe obesity, obesity-hypoventilation syndrome, obstructive sleep apnea (→ respiratory acidosis), anxiety or panic, pain, fear, fever (→ respiratory alkalosis), and others.
What are the early signs of acid–base imbalances & abgs?
Early findings include Anorexia, fatigue, headache, nausea/vomiting, Dyspnea, anxiety, wheezing, disturbed sleep, Lightheadedness, dizziness, tremor (hyperventilating patient).
Which findings should a nurse report immediately in acid–base imbalances & abgs?
Report immediately: Drowsiness, lethargy, confusion in a hypercapnic patient, Myoclonus, seizures, papilledema (severe hypercapnia), Chest discomfort or a new arrhythmia during alkalosis, Confusion progressing to stupor or coma (alkalosis), CO₂ narcosis — severe acute respiratory acidosis, and others. These signal deterioration that needs rapid intervention.
What does ROME stand for in ABG interpretation?
Respiratory Opposite, Metabolic Equal. If pH and PaCO₂ moved in opposite directions (one up, one down), the disorder is respiratory; if pH and HCO₃⁻ moved in the same direction, it is metabolic. Pair it with the stepwise method — pH first, then the consistent value, then compensation, then PaO₂ — and every straightforward gas falls open.
How do I tell uncompensated, partially compensated, and fully compensated ABGs apart?
Look at the secondary system’s value and the pH. Secondary value still normal + abnormal pH = uncompensated. Secondary value abnormal (the backup is working) + pH still abnormal = partially compensated. Secondary value abnormal + pH back in the normal range = fully compensated — then use which side of 7.40 the pH sits on to name the original problem.
Why does potassium change with pH?
Acidemia shifts H⁺ into cells in exchange for K⁺ moving out, producing hyperkalemia; alkalosis does the reverse and is associated with hypokalemia (plus reduced ionized-calcium effects). That is why every significant pH move should trigger a potassium check — the arrhythmia risk often lives in the electrolyte, not the pH itself.

Sources

Reviewed by Hae Suk Lee, RN

Educational summary for nursing students. Scenarios are fictional teaching cases. Always verify against current guidelines and your institution's protocols before acting in practice. Not medical advice.

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