Respiratory acidosis

Metabolic acidosis is a primary fall in serum bicarbonate that is first confirmed with an arterial or venous blood gas, then classified by the serum anion gap into an increased anion gap process (unmeasured organic anion, most often lactate) or a normal anion gap process (bicarbonate loss from the gut or kidney). The urine anion gap and clinical context localize the cause, and management targets the underlying disease, reserving intravenous sodium bicarbonate for severe acidemia (pH less than 7.1-7.2) or specific indications such as chronic kidney disease and renal tubular acidosis.

Respiratory alkalosis is a reduction in arterial Pco2 from increased alveolar ventilation, most often driven by sepsis, hepatic failure, anxiety, hyperventilation, pregnancy, or salicylate toxicity, presenting with tachypnea, lightheadedness, and paresthesia. Diagnosis rests on arterial blood gas confirmation of a primary fall in Pco2 with the expected compensatory drop in bicarbonate, and management targets the underlying driver rather than the blood gas itself, with acetazolamide or controlled hypoventilation reserved for rare severe alkalemia with hemodynamic compromise.

Metabolic alkalosis is a primary rise in serum bicarbonate generated by acid loss or alkali retention (usually vomiting, nasogastric suction, or diuretic use) and sustained by a maintenance state, most often volume contraction, hypokalemia, or mineralocorticoid excess. The urine chloride level is the key diagnostic branch point, separating chloride-responsive (saline-responsive) causes, treated with isotonic saline and potassium repletion, from chloride-resistant causes driven by mineralocorticoid excess, treated with potassium repletion and correction of the underlying endocrine or genetic disorder.

Chronic obstructive pulmonary disease is a persistent, usually progressive airflow obstruction driven mainly by cigarette smoke, confirmed by a postbronchodilator FEV1/forced vital capacity (FVC) ratio below 0.70 and staged by GOLD spirometric grade plus symptom/exacerbation group. Maintenance management is a stepwise ladder of smoking cessation, long-acting bronchodilators, add-on inhaled glucocorticoid, roflumilast, or azithromycin for frequent exacerbators, long-term oxygen for resting hypoxemia, and vaccination, with acute exacerbations managed as a separate protocol.

Obstructive sleep apnea is repetitive upper airway collapse during sleep, diagnosed by an apnea-hypopnea index of 5 or more per hour with symptoms, or 15 or more per hour regardless of symptoms, and treated first with weight loss plus positive airway pressure.

Guillain-Barre syndrome is an acute, post-infectious autoimmune polyradiculoneuropathy causing rapidly progressive ascending flaccid weakness and areflexia. Diagnosis is clinical, supported by albuminocytologic dissociation on CSF and demyelinating changes on electrodiagnostic studies; first-line treatment is IVIG or plasma exchange with close monitoring for respiratory failure.

Myasthenia gravis is an autoimmune disorder of the postsynaptic neuromuscular junction, most often caused by acetylcholine receptor antibodies, producing fluctuating, fatigable weakness of ocular, bulbar, and limb muscles. Diagnosis rests on antibody testing and electrodiagnostics; first-line treatment is pyridostigmine, with glucocorticoids and steroid-sparing immunosuppression for generalized disease and thymectomy for eligible patients.