🔍 What Is Metabolic Acidosis?

Metabolic acidosis is a condition where a cat's blood becomes too acidic due to an excess of acids or loss of base (bicarbonate). It's signified by low blood pH and bicarbonate levels <22 mEq/L and may present with rapid, deep breathing as compensation :contentReference[oaicite:3]{index=3}.

1. Why It Happens – Causes

Three main mechanisms lead to metabolic acidosis in cats:

• 📉 **Excess acid production or ingestion** (e.g., diabetic ketoacidosis, lactic acidosis, ethylene glycol, salicylates) :contentReference[oaicite:4]{index=4}.
• 🩺 **Loss of bicarbonate via GI tract** (e.g., diarrhea, reflux vomiting) :contentReference[oaicite:5]{index=5}.
• 🩽 **Inability of kidneys to excrete acid**, especially in chronic kidney disease (CKD) or renal tubular acidosis (RTA) :contentReference[oaicite:6]{index=6}.

2. At‑Risk Cats

• Senior cats with CKD—up to 80% develop metabolic acidosis :contentReference[oaicite:7]{index=7}.
• Diabetic cats experiencing diabetic ketoacidosis :contentReference[oaicite:8]{index=8}.
• Cats with poisoning (ethylene glycol, aspirin, antifreeze) :contentReference[oaicite:9]{index=9}.
• Cats suffering from severe GI loss (diarrhea/vomiting), sepsis, or shock :contentReference[oaicite:10]{index=10}.
• Cats with RTA due to congenital or acquired renal tubular disorders :contentReference[oaicite:11]{index=11}.

3. Clinical Signs & Physical Findings

• 🧘 Depression, lethargy, weakness, malaise—especially in chronic cases :contentReference[oaicite:12]{index=12}.
• 💨 Tachypnea and deep breathing (compensatory hyperventilation / Kussmaul breathing) :contentReference[oaicite:13]{index=13}.
• 🤢 Vomiting, diarrhea, anorexia, weight loss when GI causes are present :contentReference[oaicite:14]{index=14}.
• 🫀 Tachycardia, hypotension, arrhythmias in more severe cases (e.g., toxin-induced hyperkalemia) :contentReference[oaicite:15]{index=15}.
• 🧠 Confusion, tremors, seizures, coma when pH is severely abnormal :contentReference[oaicite:16]{index=16}.
• Decay of muscle mass, mouth ulcers, and generalized weakness especially with CKD :contentReference[oaicite:17]{index=17}.

4. Diagnostic Work‑Up

1. History & clinical exam: include appetite, fluid intake, toxin exposure, vomit/diarrhea.
2. Blood tests: evaluate acid–base via venous or arterial blood gas—low HCO₃⁻, low pH, compensatory CO₂ reduction :contentReference[oaicite:18]{index=18}.
3. Serum chemistry: look for creatinine, BUN, electrolytes (esp. K⁺, Cl⁻), lactate, glucose, toxins as relevant :contentReference[oaicite:19]{index=19}.
4. Urinalysis: examine kidney function, possible RTA (inappropriately high urine pH) :contentReference[oaicite:20]{index=20}.
5. Imaging: abdominal ultrasound for CKD or identified GI or renal pathology.
6. Special tests: toxin screens (ethylene glycol), blood pressure, ECG (arrhythmias).

5. Categorizing the Acidosis

Use anion gap calculation to distinguish types:

• 🔍 High‑anion‑gap metabolic acidosis (HAGMA): seen in toxin ingestion, ketoacidosis, uremia, lactic acidosis :contentReference[oaicite:21]{index=21}.
• 🔍 Normal‑gap (hyperchloremic) metabolic acidosis: seen in bicarbonate loss or RTA—and chloride rises accordingly :contentReference[oaicite:22]{index=22}.

6. Treatment Approach

i. Correct underlying cause

• Dialysis or specific antidotes for toxins (e.g., fomepizole for ethylene glycol) :contentReference[oaicite:23]{index=23}.
• Treat DKA with insulin + fluids + electrolytes :contentReference[oaicite:24]{index=24}.
• Treat diarrhea or vomiting by providing GI support and fluid therapy :contentReference[oaicite:25]{index=25}.
• Address CKD or RTA with renal diet, blood pressure control, phosphate binders :contentReference[oaicite:26]{index=26}.

ii. Fluid therapy & buffers

• IV balanced crystalloids (e.g., lactated Ringer’s) to correct dehydration and acid–base balance.
• Consider sodium bicarbonate if pH <7.2 or when life-threatening acidosis occurs—administer cautiously :contentReference[oaicite:27]{index=27}.
• In chronic, consider oral alkalinizing agents: potassium citrate or sodium bicarbonate to maintain systemic pH >7.35 :contentReference[oaicite:28]{index=28}.
• Monitor electrolytes—especially potassium—since correcting acidosis can unmask hypokalemia :contentReference[oaicite:29]{index=29}.

iii. Supportive care

• Oxygen therapy for respiratory compensation.
• Antiemetics/gastroprotectants for GI signs.
• Pain relief and appetite stimulants as needed (mirtazapine, maropitant).
• Nutrition: consider assisted feeding in anorexic cats.

7. Prognosis

• Prognosis hinges on the underlying cause. Chronic kidney-related acidosis managed well may have moderate outlook; toxin or shock-related cases vary widely :contentReference[oaicite:30]{index=30}.
• Without treatment, severe acute acidosis often leads to coma or death :contentReference[oaicite:31]{index=31}.
• Long-term alkali therapy in CKD cats reduces progression and supports musculoskeletal health :contentReference[oaicite:32]{index=32}.

8. Prevention & Monitoring

• For CKD: regular bloodwork, early buffer therapy, renal diet adjustments.
• Prevent toxin access (antifreeze, aspirin, chemicals).
• Manage diabetes diligently to prevent ketoacidosis.
• Prompt treatment of GI issues to avoid chronic bicarbonate loss.

9. Ask A Vet Remote Monitoring 🐾📲

• 📸 Upload lab results, blood gas reports, fluid therapy updates for expert review.
• 🔔 Set reminders for fluid feeds, alkali medication dosing, bloodwork rechecks.
• 🧭 Log respiratory rate/depth, appetite, hydration, vomiting/diarrhea frequency.
• 📊 Alerts when critical vital-sign changes or new symptoms (weakness, seizures) occur.
• 👩‍⚕️ Virtual support to guide dose adjustments and follow-up treatment plans.

10. FAQs

Can metabolic acidosis be reversed?

Yes—if underlying cause is treated and buffers restore pH. Chronic cases may require lifelong management.

Is bicarbonate therapy always used?

No—only in severe acidosis (pH < 7.2) or life-threatening electrolyte disturbances due to toxicity or renal failure.

Do I need arterial blood gas?

Not always—venous blood gas combined with clinical signs and chemistry profile often suffices.

How often should acid–base be monitored?

Acute cases: daily until stable. Chronic kidney cats: every 3–6 months with routine labs.

11. Final Take‑Home Tips ✅

• Detect early: monitor at-risk cats (CKD, diabetic, toxin exposure).
• Treat smart: correct fluids, address causes, use buffers when necessary.
• Monitor closely: track vitals, labwork, and side effects.
• Support remotely: leverage Ask A Vet for lab review, alerts, and therapy guidance.

Conclusion

Metabolic acidosis in cats can be a life-threatening but treatable condition with prompt diagnosis and targeted therapy. Understanding causes—especially toxin exposure, GI loss, or renal dysfunction—and managing with fluids, buffers, and supportive care is key. In 2025, integrating remote guidance via Ask A Vet ensures timely intervention, lab interpretation, and medication compliance to improve outcomes 🐾📲.

If your cat shows rapid breathing, weakness, vomiting/diarrhea, exposure history (antifreeze, aspirin), or kidney disease, consult your veterinarian immediately or contact Ask A Vet to begin evaluation and personalized care.