Respiratory Acidosis - Nursing Case Study

Pathophysiology

• Primary mechanism: Respiratory acidosis occurs when the lungs cannot adequately remove carbon dioxide (CO2) from the body, leading to hypercapnia (excessive CO2 in bloodstream). This is often due to hypoventilation or impaired lung function, reducing gas exchange efficacy.

• Secondary mechanism: The excess CO2 combines with water in the body to form carbonic acid, increasing blood acidity (lower pH). The body tries to compensate by increasing bicarbonate production via kidneys, but if respiratory impairment persists, acidosis worsens.

• Key complication: Chronic respiratory acidosis can lead to compensatory metabolic alkalosis, where kidneys overproduce bicarbonate to neutralize acid, but this may disrupt electrolyte balance and result in symptoms like muscle twitching, hand tremors, and nausea.

Patient Profile

Demographics:

65-year-old male, retired coal miner

History:

• Key past medical history: Chronic obstructive pulmonary disease (COPD), hypertension

• Current medications: Albuterol, ipratropium bromide, amlodipine

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Increasing difficulty in breathing, confusion

• Key symptoms: Shortness of breath, lethargy, headache, sleepiness, confusion, tremors

• Vital signs: Blood pressure 130/90 mmHg, pulse rate 95 per minute, respiratory rate 28 per minute, body temperature 37.2 degrees Celsius, oxygen saturation 88% on room air, arterial blood pH 7.28 (low), PaCO2 60 mmHg (high), bicarbonate 24 mmol/L (normal)

Section 1

Change in Patient Status:

Over the next few hours, the patient's condition worsens. His respiratory rate increases to 32 breaths per minute and oxygen saturation drops to 85% on room air. The patient becomes increasingly anxious, with a noticeable tremor in his hands. He complains of increasing difficulty in breathing and appears to be using his accessory muscles for respiration. His skin is cold and clammy to touch, suggesting poor peripheral perfusion. The nurse notes that the patient appears to be retaining CO2, as evidenced by his increased respiratory rate and low oxygen saturation.

New Complications:

The patient's arterial blood gas (ABG) results come back with a pH of 7.24, PaCO2 of 65 mmHg, and bicarbonate of 28 mmol/L. This suggests worsening respiratory acidosis with a compensatory metabolic alkalosis. The patient's electrolyte panel shows hypokalemia with a potassium level of 3.2 mmol/L. The patient's ECG shows U waves and ST depression, which can be associated with hypokalemia. The combination of worsening respiratory status, metabolic alterations, and electrolyte imbalance suggest a complex and deteriorating clinical picture, requiring immediate intervention and close monitoring. This patient is at risk of respiratory failure and cardiac arrhythmias due to the hypokalemia.

Section 2

Change in Patient Status:

Despite initial interventions, the patient's condition continues to deteriorate. His respiratory rate now hovers around 35 breaths per minute, and his oxygen saturation has dipped further to 82% on 2 L of supplemental oxygen. The patient's anxiety has escalated, and he is now experiencing palpitations and a sensation of impending doom. He reports increasing chest discomfort and has developed cyanosis around his lips and fingertips. His capillary refill time has increased to 3 seconds, and his radial pulse is weak and thready at a rate of 110 beats per minute. His blood pressure has dropped to 90/55 mmHg. These signs suggest a decline in the patient's respiratory and cardiovascular status with a possible onset of shock.

New Complications:

Repeat ABG results demonstrate a pH of 7.19, PaCO2 of 72 mmHg, and bicarbonate of 30 mmol/L, indicating a further worsening of the respiratory acidosis and compensatory metabolic alkalosis. The patient's potassium level has dipped further to 2.8 mmol/L. His ECG now shows prominent U waves, flat T waves, and the presence of ventricular ectopic beats, all of which suggest severe hypokalemia and an increased risk of life-threatening arrhythmias. A chest X-ray reveals increased opacities in both lung fields, suggesting possible acute respiratory distress syndrome (ARDS). The combination of severe respiratory acidosis, metabolic alterations, electrolyte imbalance, and potential ARDS paint a critical picture, necessitating immediate and aggressive management.

Section 3

Response to Interventions:

Despite the initial administration of oxygen and bronchodilators, the patient's oxygen saturation levels continue to drop, and his respiratory rate remains significantly high. The patient's anxiety and discomfort are not alleviated with reassurances and non-pharmacologic interventions. Potassium supplementation and adherence to a cardiac diet have not improved his potassium levels, and his ECG changes persist, suggesting an ongoing risk of serious cardiac dysrhythmias.

Change in Patient Status:

The patient's condition continues to worsen. His oxygen saturation has now plummeted to 76% on 4 L of oxygen, and his breathing has become even more labored. He now presents with severe dyspnea and chest tightness and is unable to complete sentences. His blood pressure has further decreased to 86/52 mmHg, and his radial pulse is now barely palpable at 120 beats per minute. Patient's level of consciousness has decreased; he is now disoriented to time and place. These signs indicate a further decline in his respiratory and cardiovascular status and suggest a possible progression to respiratory failure and shock. Immediate corrective measures need to be taken to prevent further deterioration of the patient's condition.

Section 4

New Diagnostic Results:

Further investigations are conducted to ascertain the cause of the patient's deteriorating respiratory status. Arterial blood gas (ABG) analysis reveals a pH of 7.28, indicating acidemia, a PaCO2 of 65 mmHg suggesting hypercapnia, and a bicarbonate (HCO3-) level of 32 mEq/L indicating a compensatory response. These findings confirm the diagnosis of respiratory acidosis, likely secondary to COPD exacerbation.

The patient's blood chemistry shows a persistently low potassium level of 2.7 mEq/L, despite supplementation, which could potentially worsen cardiac dysrhythmias. A chest X-ray reveals hyperinflated lungs, a flattened diaphragm, and possible areas of consolidation, suggestive of a concurrent lower respiratory tract infection exacerbating the patient's COPD. His white blood cell count is elevated at 14,000 per microliter, supporting the suspicion of infection.

These new findings provide a clearer picture of the patient's condition, indicating the presence of severe COPD exacerbation complicated by a possible lower respiratory tract infection and hypokalemia-induced cardiac dysrhythmias. This calls for immediate therapeutic interventions, careful monitoring, and potentially escalation of care.

Section 5

Change in Patient Status:

Overnight, the patient's condition appears to deteriorate further. He becomes increasingly dyspneic despite receiving maximum supplemental oxygen, with a respiratory rate of 32 breaths per minute and an oxygen saturation dropping to 88%. His CO2 retention worsens, with a repeat ABG showing a further rise in PaCO2 to 72 mmHg. Additionally, his heart rate starts to increase to 112 beats per minute, and his blood pressure drops to 100/62 mmHg, perhaps reflecting the combined effects of hypoxemia, hypercapnia, and hypokalemia on his cardiovascular system. His level of consciousness also begins to decrease with a Glasgow Coma Scale (GCS) score dropping to 12 from 15.

New Complications:

Meanwhile, a new complication arises. The patient develops a fever of 38.6 degrees Celsius, and his cough becomes more productive with purulent sputum. A repeat chest X-ray shows increased consolidation in the lower lobes, suggesting a progression of the suspected infection. The sputum culture and sensitivity test confirm the presence of Pseudomonas aeruginosa, a common pathogen in COPD exacerbations, resistant to the initial empirical antibiotics. The elevated WBC count now reaches 17,000 per microliter, indicating an escalating systemic inflammatory response. Collectively, these changes suggest the development of pneumonia superimposed on COPD exacerbation, which is now contributing to a further decline in the patient's respiratory and overall status.