Tachypnea in a Patient With Asthma

Case Study

A rapid response code was activated for a patient who developed severe dyspnea at rest. On arrival of the condition team, it was found that the patient was a 30-year-old female with a history of asthma who was admitted two days ago for acute cholecystitis. She had undergone laparoscopic cholecystectomy a few hours prior and was successfully extubated without incident. She developed acute severe dyspnea 15 min before the condition was called.

Vital Signs

Temperature: 99.8 °F, axillary
Blood Pressure: 130/90 mmHg
Heart Rate: 120 beats per min (bpm)
Respiratory Rate: 40 breaths per min
Oxygen Saturation: 85% on room air, 95% on 6 L/min O ₂via nasal cannula

Focused Physical Examination

A quick exam showed a young female sitting up in bed in severe respiratory distress. She appeared visibly dyspneic, using accessory muscles of respiration. The patient was alert and oriented. However, she was unable to speak in complete sentences. On auscultation, significant wheezing was present in bilateral lung fields. No crackles were heard. Her cardiac exam showed tachycardia with normal heart sounds. The rest of her physical exam was unremarkable.

Interventions

A cardiac monitor and defibrillator pads were attached. Due to the patient’s new-onset hypoxia and significant work of breathing, emergent intubation was done at the bedside. Once the airway was secured, the patient was given a stat dose of 125 mg intravenous (IV) methylprednisolone and 2 g IV magnesium sulfate. She was also started on albuterol nebulization. A post-intubation chest X-ray (CXR) was obtained, which showed clear lungs, and no acute infiltrates ( Fig. 18.1 ). Arterial blood gas was obtained and showed pH 7.23, pCO ₂ 35, pO ₂ 110, % sat 98% on 100% FiO ₂ . The patient was transferred to the intensive care unit (ICU) for further care.

Final Diagnosis

Acute severe asthma exacerbation in the setting of recent intubation and surgical procedure.

Asthma Exacerbation

Asthma is a chronic disorder of the airways produced by recurring but reversible obstruction of airflow. The pathophysiology of this disorder is complex and involves various inflammatory mediators. The interactions between these mediators collectively result in bronchoconstriction, which is the primary underlying process of the disease. Allergen-mediated IgE-dependent degranulation of mast cells in airways leads to the release of histamine, tryptase, leukotrienes, and prostaglandins, which act directly on the bronchial smooth muscle to cause constriction. Other non-IgE-dependent mechanisms for the release of pro-inflammatory cytokines also exist, as seen in triggers like aspirin and non-steroidal anti-inflammatory drug-induced bronchoconstriction (see Table 18.1 for common triggers of acute asthma exacerbation). Some other important pathophysiological contributors include airway hyperresponsiveness, airway edema, mucous hypersecretion, hypertrophy and hyperplasia of bronchial smooth muscles, and eventual airway remodeling. Fig. 18.2 shows the vicious circle of interaction between mediators of asthma symptoms.

Table 18.1

Common triggers of asthma exacerbation

Type	Examples
Allergic	• Inhaled – animal allergens, dust mites, cockroaches, mold, plant allergens • Food – usually as part of a more widespread allergic reaction • Occupational – toluene, enzymes, wood dust
Irritants	• Cigarette smoke, cannabis smoke • Air pollution and dust • Cleaning products
Miscellaneous	• Respiratory infections • Cold, dry air • Physical activity • Hormonal changes – pregnancy • Medications – beta-blockers, non-steroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitor • Anxiety, stress, gastroesophageal reflux disease • Medication non-compliance