What is the likely cause of respiratory alkalosis in a patient with a history of panic attacks, presenting with an increased respiratory rate, normal SpO2, and recent self-harm behavior, with ABG results showing alkalosis and normal CBC and electrolyte levels?

Interpretation: Severe Respiratory Alkalosis from Acute Hyperventilation (Panic Attack)

This patient has severe acute respiratory alkalosis (pH 7.56, PCO2 17.2) from hyperventilation during a panic attack, with compensatory metabolic acidosis (HCO3 19.9) and critically low PO2 (30 mmHg) that requires immediate intervention despite the paradoxically normal SpO2.

Critical ABG Analysis

Primary Disorder: Severe Respiratory Alkalosis

• pH 7.56 indicates significant alkalemia from acute hyperventilation, consistent with panic-induced hyperventilation syndrome 1, 2
• PCO2 17.2 mmHg represents profound hypocapnia (normal 35-45 mmHg), far exceeding typical panic attack levels 2, 3
• The expected compensatory decrease in HCO3 should be approximately 3.6 mEq/L (using 0.2 mEq/L decrease per 1 mmHg PCO2 drop), but the actual decrease is 4.1 mEq/L (from normal 24 to 19.9) 1

Exaggerated Metabolic Response

• Panic disorder patients show exaggerated compensatory responses with HCO3 decreasing by 0.41 mEq/L per 1 mmHg PCO2 drop (versus 0.2 mEq/L in normal subjects) 1
• This exaggerated response is driven by increased lactic acid production during hyperventilation in panic disorder patients, with lactate levels averaging 2.59 ± 1.50 mmol/L 1
• The metabolic acidosis component (low HCO3) is therefore partially from lactate accumulation, not just respiratory compensation 1, 4

Critical Hypoxemia Despite Normal SpO2

• PO2 of 30 mmHg is life-threatening (normal 80-100 mmHg), indicating severe tissue hypoxia 5
• The paradoxically normal SpO2 of 100% is misleading because severe alkalosis shifts the oxyhemoglobin dissociation curve leftward, impairing oxygen release to tissues despite normal saturation 5
• Pulse oximetry alone is insufficient for monitoring as it may appear normal despite dangerous pH or PO2 abnormalities 6

Immediate Management

Airway and Breathing Intervention

• Administer controlled oxygen therapy immediately targeting SpO2 88-92% to correct the critically low PO2, as prevention of tissue hypoxia supersedes CO2 retention concerns 5
• Start with 1 L/min nasal cannula and titrate up in 1 L/min increments while monitoring for adequate tissue oxygenation 6, 5
• Coach the patient to slow their respiratory rate using calm verbal guidance, paper bag rebreathing techniques, or having them breathe through pursed lips 2, 7

Pharmacologic Management

• Administer intravenous benzodiazepines (lorazepam 1-2 mg IV) to abort the panic attack and reduce hyperventilation 8, 2
• This intervention typically produces rapid resolution of clinical and laboratory manifestations without need for invasive measures 2
• Monitor for respiratory depression as benzodiazepines can cause hypoventilation, though this is rarely problematic in acute hyperventilation 8

Serial Monitoring

• Repeat ABG in 30-60 minutes after oxygen and benzodiazepine administration to assess response 6, 5
• Monitor for complications of severe alkalosis including cardiac arrhythmias (tachycardia, ventricular/atrial arrhythmias), tetany from hypocalcemia, and neurologic changes 2, 4
• Check serum lactate levels as they correlate inversely with PCO2 in panic-induced hyperventilation and help confirm the diagnosis 1, 7, 3

Diagnostic Considerations

Confirming Psychogenic Hyperventilation

• Venous blood gas (VBG) could have been used instead of ABG as VBG shows similar respiratory alkalosis and PCO2-lactate correlations in psychogenic hyperventilation, avoiding painful arterial puncture 7
• The history of panic attacks and hesitation cuts (self-harm behavior) strongly supports a psychiatric etiology rather than organic causes 2, 7
• Normal CBC and electrolytes help exclude other causes of hyperventilation such as sepsis, metabolic disorders, or pulmonary embolism 4

Baseline Chronic Hyperventilation

• Low baseline inorganic phosphate levels are associated with patients who panic during stress, potentially reflecting chronic hyperventilation or abnormal intracellular glycolysis 3
• Many panic disorder patients are chronic hyperventilators at baseline, predisposing them to more severe acute episodes 3

Escalation Criteria

When to Consider ICU Admission

• If pH rises above 7.55 despite treatment or patient develops worsening mental status changes 6
• If respiratory acidosis develops (pH <7.35) during treatment, indicating respiratory muscle fatigue requiring non-invasive ventilation 6, 5
• If cardiac complications occur including ischemic chest pain, significant arrhythmias, or hemodynamic instability 2, 4

Non-Invasive Ventilation Indications

• NIV is indicated if respiratory acidosis develops (pH <7.35) despite optimal medical therapy and benzodiazepine administration 6
• However, NIV is not indicated for respiratory alkalosis and would worsen the hyperventilation 9

Key Clinical Pitfalls

Avoid These Common Errors

• Never administer sodium bicarbonate as it will worsen the metabolic alkalosis component 5
• Do not rely solely on SpO2 monitoring as it can be falsely reassuring in severe alkalosis with leftward oxygen dissociation curve shift 6, 5
• Do not ignore the critically low PO2 even with normal SpO2, as tissue hypoxia is occurring 5
• Do not dismiss as "just anxiety" without addressing the life-threatening acid-base and oxygenation abnormalities first 2

Psychiatric Follow-up

• Arrange outpatient psychiatric evaluation for panic disorder management and assessment of self-harm risk (hesitation cuts) after medical stabilization 2, 7
• Consider starting or optimizing SSRI therapy for long-term panic disorder management to prevent recurrent episodes 2