5.1 Airway, Breathing & Oxygen Therapy: Asthma, COPD & Pneumonia

5.1 Airway, Breathing & Oxygen Therapy: Asthma, COPD & Pneumonia

Quick Answer: Oxygen therapy is a prescribed pharmacological intervention aimed at treating or preventing hypoxemia while safeguarding cellular metabolic function. Hypoxemia denotes reduced arterial oxygen tension (PaO2 < 60 mmHg or SpO2 < 90%), whereas hypoxia refers to oxygen deficiency at the tissue and cellular level. Safe oxygen administration requires selecting appropriate delivery devices—ranging from low-flow nasal cannulas to fixed-performance Venturi masks and non-rebreather masks—based on clinical acuity. In chronic hypercapnic conditions such as COPD, nurses must carefully titrate oxygen to maintain SpO2 between 88% and 92% to preserve the hypoxic respiratory drive. Acute respiratory emergencies, including severe asthma exacerbations with the ominous "silent chest" phenomenon and severe pneumonia stratified via the CURB-65 score, demand rapid stepped pharmacology, high Fowler's positioning, chest physiotherapy, and close surveillance for respiratory failure.

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Respiratory Physiology and Gas Exchange

The fundamental physiological role of the respiratory system is to maintain arterial blood gas homeostasis by securing oxygen (O2) for cellular aerobic metabolism and eliminating carbon dioxide (CO2), the primary byproduct of cellular respiration. This life-sustaining process depends on four integrated physiological components:

1. Ventilation: The mechanical movement of atmospheric air into and out of the pulmonary alveoli through cyclic thoracic expansion and diaphragmatic excursion;
2. Diffusion: The passive movement of O2 and CO2 across the alveolar-capillary membrane along their respective partial pressure gradients;
3. Perfusion (Q): The distribution of systemic mixed-venous blood flow through the pulmonary capillary microcirculation;
4. Ventilation-Perfusion Matching (V/Q Ratio): The optimal matching of alveolar ventilation to pulmonary capillary blood flow (ideal normal ratio: ~0.8). Derangements manifest as shunt (perfusion without ventilation, seen in alveolar collapse, atelectasis, or lobar pneumonia) or dead space (ventilation without perfusion, seen in pulmonary embolism).

Hypoxemia vs. Hypoxia

In nursing practice and licensure examinations, clear differentiation between hypoxemia and hypoxia is critical:

• Hypoxemia: A measurable decrease in the partial pressure of oxygen in arterial blood, quantified by an arterial blood gas (ABG) PaO2 of less than 60 mmHg or a pulse oximetry saturation (SpO2) below 90% on ambient room air.
• Hypoxia: Inadequate oxygen availability, delivery, or utilization at the cellular and tissue level, impairing mitochondrial ATP synthesis and driving anaerobic glycolysis, lactic acidosis, and eventual cellular necrosis.

+--------------------------------------------------------------------------+
|                       FOUR ETIOLOGICAL TYPES OF HYPOXIA                  |
+--------------------------------------------------------------------------+
| 1. Hypoxic Hypoxia:       Low arterial PaO2 due to hypoventilation,     |
|                           high altitude, V/Q mismatch, or diffusion      |
|                           barrier (e.g., severe pneumonia, COPD, ARDS).  |
|                                                                          |
| 2. Anemic Hypoxia:        Normal PaO2 but reduced oxygen-carrying        |
|                           capacity of blood (e.g., severe anemia, acute  |
|                           hemorrhage, carbon monoxide poisoning).        |
|                                                                          |
| 3. Circulatory / Stagnant Normal PaO2 and hemoglobin, but inadequate     |
|    Hypoxia:               tissue perfusion and blood flow (e.g., shock,  |
|                           heart failure, arterial occlusion).            |
|                                                                          |
| 4. Histotoxic Hypoxia:    Adequate oxygen delivery to tissues, but cells |
|                           cannot utilize it due to enzymatic poisoning   |
|                           (e.g., cyanide toxicity).                      |
+--------------------------------------------------------------------------+

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Oxygen Delivery Devices: Selection, Flow Rates, and FiO2

Oxygen must be treated as a drug requiring a medical prescription, appropriate dosage, verified administration device, and constant clinical monitoring. Oxygen delivery systems are classified into low-flow (variable performance) and high-flow (fixed performance) devices.

[!CAUTION] Clinical Pearl: Oxygen Toxicity & Absorption Atelectasis Administering high fractions of inspired oxygen (FiO2 > 50%) for longer than 24 to 48 hours carries a significant risk of oxygen toxicity. Hyperoxia generates excess reactive oxygen species (free radicals) that damage alveolar epithelial cells, deplete surfactant, and induce pulmonary edema and fibrosis. Furthermore, breathing 100% oxygen washes nitrogen out of the alveoli ("nitrogen washout"). Because nitrogen normally maintains alveolar patency, its absence allows rapid alveolar collapse, resulting in absorption atelectasis.

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Acute Asthma Exacerbation: Pathophysiology and Emergency Management

Bronchial asthma is a chronic inflammatory disorder of the conducting airways characterized by bronchial hyperresponsiveness, reversible bronchospasm, and episodic airflow obstruction. Exposure to triggers (allergens, viral respiratory infections, dust, cold air, beta-blockers, nonsteroidal anti-inflammatory drugs) initiates an immediate IgE-mediated mast cell degranulation, releasing histamine, leukotrienes, and prostaglandins.

Pathophysiological Triad

1. Bronchospasm: Acute constriction of bronchial smooth muscle surrounding the conducting airways;
2. Mucosal Edema: Microvascular leakage leading to profound inflammatory swelling of the bronchial mucosa;
3. Mucus Hypersecretion: Production of thick, tenacious, gelatinous mucus plugs that obstruct smaller bronchioles.

+--------------------------------------------------------------------------+
|                       PEAK EXPIRATORY FLOW RATE (PEFR)                   |
+--------------------------------------------------------------------------+
| - Green Zone:   80% to 100% of personal best (Good control; continue    |
|                 routine maintenance therapy).                            |
| - Yellow Zone:  50% to 79% of personal best (Caution; acute flare-up;    |
|                 increase inhaled SABA, contact provider).                |
| - Red Zone:     < 50% of personal best (Medical Emergency; use rescue   |
|                 bronchodilator immediately and seek emergency care).     |
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The "Silent Chest": Ominous Warning of Impending Arrest

Patients experiencing an acute severe asthma attack classically present with tachypnea, prolonged expiratory phase, audible expiratory and inspiratory wheezes, tachycardia, accessory muscle recruitment (sternocleidomastoid retractions), diaphoresis, and pulsus paradoxus (> 10 mmHg drop in systolic blood pressure during inspiration).

[!IMPORTANT] Exam Alert: The Silent Chest Phenomenon If an asthmatic patient who was previously wheezing, tachypneic, and struggling for breath suddenly exhibits diminished or absent breath sounds without audible wheezing, this does NOT indicate clinical recovery. Rather, it signifies a "silent chest"—airflow has become so severely restricted by bronchial obstruction and diaphragmatic exhaustion that the patient cannot generate sufficient velocity to produce musical wheezes. This is a critical indicator of impending respiratory arrest, severe hypercapnia, and acidosis, requiring immediate endotracheal intubation and mechanical ventilation.

Stepped Pharmacological Management

• First-Line / Rescue: Inhaled Short-Acting Beta-2 Agonists (SABA) such as Salbutamol (Albuterol) 2.5–5 mg via jet nebulizer driven by compressed air or oxygen, repeated every 20 minutes for three doses, or continuous nebulization for severe obstruction;
• Anticholinergics: Inhaled Ipratropium bromide 0.5 mg nebulized with salbutamol to block muscarinic receptors, promoting synergistic bronchodilation and inhibiting excessive mucus secretion;
• Systemic Corticosteroids: Early administration of IV Hydrocortisone (100–200 mg) or oral Prednisolone (40–50 mg) to suppress mucosal inflammation, decrease vascular permeability, and upregulate down-regulated beta-2 receptors (onset: 4–6 hours);
• Intravenous Magnesium Sulfate: 1.2–2 g IV infused over 20 minutes for severe, life-threatening asthma refractory to initial nebulization; magnesium inhibits calcium influx into bronchial smooth muscle cells, inducing rapid smooth muscle relaxation;
• Nursing Positioning: Immediately place the patient in a High Fowler's position (seated upright at 90 degrees, leaning slightly forward with arms supported—the "orthopneic / tripod position") to maximize diaphragmatic excursion, optimize thoracic expansion, and decrease venous return to an overloaded right ventricle.

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Chronic Obstructive Pulmonary Disease (COPD)

Chronic Obstructive Pulmonary Disease (COPD) is a progressive, largely irreversible airflow limitation encompassing two major clinical phenotypes, which frequently coexist in varying proportions:

Hypoxic Drive and Controlled Oxygenation

In healthy individuals, the respiratory drive is centrally regulated by chemoreceptors in the medulla oblongata, which respond primarily to increases in arterial carbon dioxide (PaCO2) and hydrogen ion concentration (pH).

In chronic, severe COPD, persistent hypercapnia leads to renal retention of bicarbonate (HCO3-), buffering cerebrospinal fluid pH and desensitizing central medullary chemoreceptors. Consequently, the primary stimulus for ventilation shifts to peripheral chemoreceptors located in the carotid and aortic bodies, which respond to arterial hypoxemia (low PaO2)—a physiological adaptation termed the hypoxic drive.

Chronic Hypercapnia (High PaCO2) 
       |
       v
Desensitized Central Medullary Chemoreceptors
       |
       v
Peripheral Chemoreceptors take over (Triggered by Low PaO2)
       |
       v
*Uncontrolled High-Flow O2 Administered*
       |
       v
Sudden Elevation of PaO2 abolishes Hypoxic Drive
       |
       v
Acute Alveolar Hypoventilation -> CO2 Narcosis, Coma & Respiratory Arrest

[!IMPORTANT] Target SpO2 in COPD: Nurses must titrate oxygen therapy to achieve and maintain an SpO2 of 88% to 92% using a controlled Venturi mask (at 24% or 28% FiO2) or low-flow nasal cannula (1–2 L/min). Never withhold life-saving oxygen during severe hypoxemic arrest, but closely monitor arterial blood gases, mental status, and respiratory depth for signs of CO2 narcosis (somnolence, confusion, flapping tremor / asterixis).

Pursed-Lip Breathing Technique

Pursed-lip breathing is a core behavioral nursing intervention in COPD rehabilitation. The patient inhales slowly through the nose for 2 counts, puckers their lips as if whistling or extinguishing a candle flame, and exhales gently and slowly through pursed lips for 4 counts (1:2 ratio).

• Physiological Rationale: Prolonged exhalation against positive resistance creates positive end-expiratory pressure (PEEP) inside the airways, which splints smaller bronchioles open, prevents premature dynamic airway collapse during expiration, promotes alveolar emptying, and reduces dynamic hyperinflation and air trapping.

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Community-Acquired vs. Hospital-Acquired Pneumonia

Pneumonia represents an acute infection of the pulmonary parenchymal tissue (alveoli and interstitial spaces) leading to inflammatory exudation, consolidation, and impaired gas diffusion.

Etiological Classification

• Community-Acquired Pneumonia (CAP): An acute pulmonary infection acquired outside of a healthcare facility or diagnosed within < 48 hours of hospital admission. The predominant bacterial pathogen worldwide and in Ghana is Streptococcus pneumoniae (pneumococcus), followed by Haemophilus influenzae, Mycoplasma pneumoniae, and Chlamydia pneumoniae.
• Hospital-Acquired Pneumonia (HAP / Nosocomial): Pneumonia occurring >= 48 hours after hospital admission that was not incubating at the time of admission. Common pathogens include multidrug-resistant Gram-negative bacilli (Pseudomonas aeruginosa, Klebsiella pneumoniae, Escherichia coli) and Gram-positive organisms such as Methicillin-Resistant Staphylococcus aureus (MRSA).

Clinical Assessment and Diagnostic Workup

• Clinical Signs: Pyrexia, shaking chills (rigors), pleuritic chest pain aggravated by deep inspiration or coughing, tachypnea, productive cough with rust-colored or purulent sputum, dullness to thoracic percussion, increased tactile fremitus, bronchial breath sounds, and inspiratory crackles (crepitations) over the consolidated zone.
• Diagnostics: Chest radiograph (confirms lobar or patchy bronchopneumonic consolidation), baseline pulse oximetry, arterial blood gas, complete blood count with leukocytosis and left shift, and sputum Gram stain and blood cultures collected PRIOR to starting empirical antibiotic therapy.

CURB-65 Severity Score for Pneumonia

The CURB-65 criteria provide an objective, validated clinical tool to determine the site of care and 30-day mortality risk in adult patients with community-acquired pneumonia:

CURB-65 SCORING & DISPOSITION GUIDELINES:
- Score 0 to 1:  Low mortality risk (0.7%–2.1%) -> Safe for OUTPATIENT management with oral antibiotics.
- Score 2:       Moderate mortality risk (9.2%) -> INPATIENT hospital ward admission recommended.
- Score 3 to 5:  High mortality risk (about 14%–57%) -> URGENT INPATIENT admission; evaluate for ICU escalation.

Respiratory Nursing Interventions

1. Empirical Antibiotic Administration: Prompt administration of prescribed empirical antimicrobial agents (e.g., amoxicillin-clavulanic acid plus azithromycin, or respiratory fluoroquinolones) within 4 hours of arrival;
2. Chest Physiotherapy (CPT) and Postural Drainage: Utilization of gravity-assisted body positions combined with rhythmic thoracic clapping (percussion) and manual vibration over affected lung segments to dislodge tenacious secretions into major central airways for expectoration. Contraindicated in severe osteoporosis, rib fractures, hemoptysis, and unstable angina;
3. Incentive Spirometry: Prescribed to prevent and reverse secondary atelectasis. The patient seals their lips around the mouthpiece, inhales slowly and deeply (sustained maximal inspiration), holds their breath for 3 to 5 seconds, and exhales passively. Target: 10 breaths every hour while awake;
4. Systemic Hydration: Maintenance of adequate fluid intake (2 to 3 liters per 24 hours, unless contraindicated by heart failure or renal dysfunction) to liquefy viscous bronchial mucus, facilitating easier mucociliary clearance.