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Lowering the head of the bed to flat is not the correct initial response to excessive bubbling because bubbling in the water seal indicates an air leak in the drainage system or chest wall, not patient position. Normal respiratory rate is 12–20 breaths per minute, and repositioning does not correct an air leak or system integrity issue. The priority is assessment of the tubing, connections, and patient insertion site before modifying patient positioning, which may worsen respiratory mechanics.

Milking a chest tube is contraindicated as an initial action because it can create dangerously high negative intrapleural pressures, increasing risk of tissue damage and pneumothorax expansion. Contemporary guidelines discourage routine milking; instead, observe for fluctuating water seal and check for kinks or loose connections. If obstruction is suspected, assess and reposition tubing gently, but never milk or strip without specific provider order due to potential for harming lung tissue and altering intrapleural dynamics.

Disconnecting the system and obtaining another is not the first-line action because an open system risks atmospheric air entry into the pleural space, causing or worsening pneumothorax. Instead, clamp technique or bedside assessment for leaks and immediate notification of the provider are preferred. If system failure is confirmed and the patient is unstable, sterile technique to replace the drainage entire apparatus must be executed per protocol, but this step follows assessment and provider direction.

Respiratory alkalosis is characterized by low PaCO2 below 35 mmHg causing elevated pH, typically with pH >7.45; this ABG shows PaCO2 above normal at 47 mmHg and pH at the high-normal limit, inconsistent with hyperventilation. In respiratory alkalosis compensatory metabolic acidosis would lower HCO3− below normal (below 22 mEq/L). Therefore elevated bicarbonate here argues against respiratory alkalosis and supports chronic respiratory acidosis with renal compensation rather than primary respiratory alkalosis.

Metabolic acidosis would present with low HCO3− (below 22 mEq/L) and decreased pH, with respiratory compensation producing low PaCO2. In this case HCO3− is elevated at 32 mEq/L and PaCO2 is high at 47 mmHg, which is opposite to patterns seen in metabolic acidosis. Additionally PaO2 90 mmHg and SaO2 98% are adequate, arguing against hypoxic lactic acidosis. Thus metabolic acidosis is not supported by these arterial blood gas values.

Metabolic alkalosis would show elevated HCO3− above 26 mEq/L and elevated pH, often with respiratory compensation raising PaCO2. While HCO3− is elevated at 32 mEq/L, PaCO2 is also elevated, but the pH is 7.45 (upper-normal) rather than markedly alkalemic. The primary disturbance here is respiratory (high PaCO2) with renal compensation raising bicarbonate; thus labeling this as primary metabolic alkalosis would misidentify the origin of the acid–base imbalance. .

A bland, soft diet is not appropriate as it lacks the high caloric and protein density required to meet the elevated metabolic demands of a COPD client. While some clients may experience fatigue and prefer soft foods, this dietary approach does not address the underlying need for nutritional support to combat muscle wasting and energy deficit caused by the increased work of breathing.

A low-fat, low-cholesterol diet is typically recommended for cardiovascular health, not specifically for COPD. While beneficial for overall health, it does not provide the high caloric and protein content necessary to meet the increased metabolic demands associated with the heightened work of breathing in COPD. The focus for COPD clients is on sufficient energy intake.

A low-sodium, high-calorie diet is partially correct but not the most appropriate choice. While high-calorie intake is necessary, a low-sodium diet is primarily for clients with hypertension or fluid retention. Fluid retention is a later-stage complication of COPD and may require sodium restriction, but the primary nutritional need in the early and moderate stages is a high-calorie, high-protein diet to address energy and muscle mass deficits. *.

Pursed-lip breathing does not directly strengthen the intercostal muscles. Its primary physiological effect is to create back-pressure in the airways, which helps to keep the bronchioles open during exhalation. This back-pressure prevents the collapse of the small airways, reducing air trapping and making the exhalation phase more efficient, which is a key goal in managing conditions like COPD.

Pursed-lip breathing does not primarily promote oxygen intake. Its main purpose is to slow down the exhalation phase, which increases the time for gas exchange and prevents the premature collapse of airways. By reducing air trapping, it allows for more effective exhalation of carbon dioxide, which secondarily creates space for more efficient oxygen intake.

Pursed-lip breathing does not directly strengthen the diaphragm. While it can be used in conjunction with diaphragmatic breathing exercises, its main mechanism is to prolong exhalation and create a physiological back-pressure. The prolonged exhalation period helps prevent dynamic airway collapse, reduces air trapping, and ultimately improves the efficiency of ventilation and gas exchange.

While scattered rhonchi and crackles may be present in a client with COPD, especially during an exacerbation, and a white blood cell count (WBC) may be elevated with an infection (normal range 4,500 to 11,000 cells/mm), these are signs of an acute process, not chronic hypoxemia. Chronic hypoxemia leads to long-term compensatory changes in the body's systems.

Copious amounts of rust-colored sputum are characteristic of bacterial pneumonia, specifically Streptococcus pneumoniae, and not a direct consequence of chronic hypoxemia. While cyanosis is a sign of hypoxemia, it's an acute finding. Rust-colored sputum indicates a different pathological process and is not a long-term expected finding.

Distended neck veins and dependent edema are classic signs of right-sided heart failure (cor pulmonale), which is a late-stage complication of chronic hypoxemia in COPD. While this can occur, it is a consequence of the chronic hypoxemia's effect on the pulmonary vasculature and heart, not a direct finding of the hypoxemia itself. *.

Pleural effusion is the accumulation of fluid in the pleural space. This would cause decreased breath sounds but would typically present with a unilateral dullness to percussion and a non-specific history, not a sudden onset following a fall. A pleural effusion does not cause unequal chest excursion in the same acute manner as a pneumothorax.

Asthma exacerbation is a sudden worsening of asthma symptoms due to bronchospasm. While it causes difficulty breathing and may be triggered by stress, it is not typically associated with a fall or unequal chest excursion. The primary findings would be wheezing and a prolonged expiratory phase.

A pulmonary embolism is a blockage in one of the pulmonary arteries, most often caused by a blood clot. While it can present with sudden chest pain and shortness of breath, it is not typically associated with unequal chest excursion. The risk factors often include immobility or surgery, although a fall could be a precipitating factor. *.

Skipping the next scheduled treatment is an inappropriate response. It withholds a necessary medication that helps with bronchodilation. Albuterol is a short-acting beta-2 adrenergic agonist, and its bronchodilator effects are essential for managing airway obstruction. Withholding the medication could lead to a worsening of the client's respiratory status and is not a safe or correct intervention.

Holding the medication for 24 hours is a potentially dangerous action. It would deprive the client of a critical bronchodilator for a prolonged period, leading to a high risk of respiratory distress or failure. The nurse should not unilaterally decide to hold a prescribed medication for such a duration without a direct order from the healthcare provider, especially for expected side effects.

Requesting a medication for anxiety is unnecessary at this time. The anxiety is a direct pharmacological effect of the albuterol. The focus should be on managing the expected side effects rather than introducing another medication. The client's anxiety is a physiological response to the medication's stimulating properties, not a separate psychological condition requiring an anxiolytic. *.