COPD - Nursing Case Study

Pathophysiology

• Primary mechanism: Chronic inflammation - Long-term exposure to noxious gases/particles, particularly tobacco smoke, leads to chronic inflammation in the airways and lung tissue. This inflammation causes structural changes known as 'remodeling', including thickening of the airway walls and destruction of lung tissue, leading to airflow obstruction.

• Secondary mechanism: Oxidative stress - The harmful substances in tobacco smoke also cause oxidative stress, an imbalance between the production of reactive oxygen species (ROS) and the body's ability to counteract their harmful effects. Over time, oxidative stress can further damage lung tissue and impair its function.

• Key complication: Hypoxemia and hypercapnia - As COPD progresses, the impaired gas exchange can lead to low oxygen levels (hypoxemia) and high carbon dioxide levels (hypercapnia) in the blood. This can lead to serious complications such as respiratory failure and heart problems.

Patient Profile

Demographics:

67, male, former coal miner

History:

• Chronic Obstructive Pulmonary Disease (COPD) diagnosed 10 years ago, high blood pressure, high cholesterol

• Albuterol, Tiotropium, Amlodipine, Atorvastatin

• No known allergies

Current Presentation:

• Chief complaint: Increased difficulty in breathing, frequent coughing with phlegm, fatigue

• Key symptoms: Shortness of breath, wheezing, chest tightness, increased mucus production, unexplained weight loss, frequent respiratory infections

• Vital signs: Blood pressure 145/90 mmHg, heart rate 100 bpm, respiratory rate 22 breaths per minute, oxygen saturation 89% on room air, body temperature 98.6°F, BMI 22 kg/m2.

Section 1

Change in Patient Status:

Over the next few days, the patient's condition begins to deteriorate. His oxygen saturation drops to 86% on room air and he reports increased difficulty breathing, even at rest. His respiratory rate increases to 28 breaths per minute, and his heart rate accelerates to 110 bpm. Additionally, he reports increasing fatigue and appetite loss.

Clinical examination reveals increased use of accessory muscles during respiration, decreased breath sounds with rhonchi and crackles, and cyanosis of the lips. His blood pressure is slightly elevated at 150/95 mmHg. Despite his worsening condition, he remains alert and oriented.

These changes may suggest an exacerbation of his COPD and the onset of acute respiratory failure, a common complication in advanced stages of the disease. This situation requires immediate intervention to prevent further deterioration and potential life-threatening complications such as cardiac arrhythmias or a heart attack due to the strain on the heart. It also presents an opportunity for clinical reasoning to determine the cause of the exacerbation, which could include infection, exposure to irritants, or noncompliance with medication.

Section 2

New Diagnostic Results:

Lab results reveal a significant increase in the patient's white blood cell count, suggestive of an infection. His arterial blood gas (ABG) analysis shows a pH of 7.32, PaCO2 of 65 mmHg, and PaO2 of 58 mmHg, indicating respiratory acidosis and hypoxemia. His sputum culture comes back positive for Pseudomonas aeruginosa, a common pathogen in COPD exacerbations. Furthermore, chest X-ray shows hyperinflation of the lungs and increased bronchial markings, consistent with COPD, but there are also new patchy infiltrates, indicating possible pneumonia.

These findings support the hypothesis that an infection, specifically pneumonia, is the cause of the patient's COPD exacerbation. The ABG results confirm the presence of respiratory failure, and the elevated PaCO2 indicates that the patient's ability to expel carbon dioxide is compromised. This is a critical situation that requires immediate medical intervention. The presence of Pseudomonas aeruginosa in the sputum culture suggests that antibiotic therapy should be adjusted to target this specific pathogen. This situation provides an opportunity for clinical reasoning regarding the appropriate pharmacological treatment, the potential need for mechanical ventilation, and strategies to manage his respiratory acidosis and hypoxemia.

Section 3

Change in Patient Status:

Over the next 24 hours, the patient's condition deteriorates. He becomes increasingly dyspneic, with a respiratory rate of 32 breaths per minute and use of accessory muscles noted. His oxygen saturation drops to 88% on 2 liters of nasal cannula oxygen. His heart rate is tachycardic at 110 beats per minute, and his blood pressure is elevated at 150/90 mmHg. The patient also appears more lethargic and is less responsive than previously.

These new findings indicate that the patient's respiratory status is worsening, despite the initial interventions. The increased heart rate and blood pressure may be compensatory mechanisms due to hypoxia. The patient's increased work of breathing and decreased oxygen saturation suggest that he may be failing to maintain adequate oxygenation and ventilation. This change in status requires immediate reassessment of the patient's care plan. Clinical reasoning should be applied to determine whether the patient may benefit from escalated respiratory support, such as BiPAP or potential intubation. Furthermore, the change in the patient's level of consciousness could also suggest increased CO2 retention, a serious complication in COPD patients, necessitating urgent ABG analysis.

Section 4

New Diagnostic Results:

Upon receiving the patient's ABG results, it is found that his pH is 7.28, indicating acidosis. His PaCO2 is 65 mmHg, significantly higher than the normal range of 35-45 mmHg, suggesting hypercapnia. The patient's PaO2 is 55 mmHg, below the normal range of 80-100 mmHg, indicating hypoxia. His bicarbonate level is 30 mEq/L, slightly above the normal range of 22-28 mEq/L, which may be a compensatory response to the chronic hypercapnia. This interpretation of the ABG results confirms that the patient is experiencing acute respiratory failure on top of his chronic COPD.

The elevated CO2 levels and decreased oxygenation are consistent with the patient's increased work of breathing, lethargy, and decreased responsiveness. The patient's elevated bicarbonate level suggests that he has been retaining CO2 for a long period of time, a common occurrence in patients with severe COPD. These results, coupled with the patient's worsening respiratory status, underscore the need for urgent intervention. There may be a need to increase the patient's oxygen delivery and potentially consider invasive ventilation. Moreover, the team should keep an eye out for complications such as acute respiratory distress syndrome (ARDS) and pneumonia.

Section 5

Change in Patient Status:

The patient's condition continues to worsen over the next several hours. His respiratory rate increases to 28 breaths per minute, he becomes increasingly lethargic and is only arousable to vigorous stimuli. His SpO2 declines to 89% on 4 liters of oxygen via a nasal cannula. Additionally, the patient's blood pressure begins to drop, with readings now consistently in the 90/60 mmHg range. On auscultation, the nurse notes coarse crackles throughout the lower lobes of the lungs and diminished breath sounds in the upper lobes. The nurse also observes increased use of accessory muscles and intercostal retractions, suggestive of increased work of breathing.

New Diagnostic Results:

In response to the patient's deteriorating status, the healthcare team orders a chest X-ray, which reveals increased opacity in the lower lobes, indicative of potential pneumonia. A repeat ABG shows a pH of 7.25, PaCO2 of 70 mmHg, and PaO2 of 50 mmHg, suggesting worsening respiratory acidosis and hypoxemia despite the increased oxygen therapy. A CBC reveals an elevated white blood cell count of 15,000/mm3, which further supports the suspicion of a superimposed bacterial pneumonia. While the patient's status is concerning, these findings provide the healthcare team with valuable information for further management and interventions.