ABG - Nursing Case Study

Pathophysiology

• Primary mechanism: Altered ventilation can lead to respiratory acidosis or alkalosis. Hypoventilation causes CO2 retention, increasing carbonic acid and decreasing blood pH (acidosis), while hyperventilation expels CO2 excessively, reducing carbonic acid and increasing pH (alkalosis).

• Secondary mechanism: Metabolic processes can result in metabolic acidosis or alkalosis. In metabolic acidosis, there's an accumulation of non-volatile acids or loss of bicarbonate (e.g., in kidney failure). In metabolic alkalosis, excessive bicarbonate or loss of hydrogen ions (e.g., vomiting) increases blood pH.

• Key complication: Compensatory mechanisms may mask underlying issues. For example, in chronic respiratory acidosis, kidneys retain bicarbonate to normalize pH, potentially delaying diagnosis and treatment of the primary respiratory disorder.

Patient Profile

Demographics:

45-year-old female, office worker

History:

• Key past medical history: Hypertension, Type 2 Diabetes

• Current medications: Metformin, Lisinopril, Aspirin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Shortness of breath and fatigue

• Key symptoms: Dizziness, headache, palpitations, mild confusion

• Vital signs: Blood pressure 150/95 mmHg, heart rate 110 bpm, respiratory rate 24 breaths per minute, temperature 37.8°C, oxygen saturation 90% on room air

Section 1

As the clinical team proceeds with the initial assessment, they note that the patient’s respiratory distress appears to be worsening. The patient is now exhibiting increased work of breathing, with accessory muscle use and nasal flaring. Her respiratory rate has increased to 28 breaths per minute, and her oxygen saturation has further decreased to 88% on room air. Auscultation of the lungs reveals diminished breath sounds bilaterally with faint crackles at the bases, suggesting potential fluid accumulation or atelectasis.

An arterial blood gas (ABG) analysis is performed to better understand the underlying acid-base disturbance. The results reveal a pH of 7.32, PaCO2 of 55 mmHg, and HCO3- of 26 mEq/L, indicating primary respiratory acidosis without significant metabolic compensation. These findings align with the clinical picture of hypoventilation and CO2 retention, possibly exacerbated by the patient’s underlying comorbidities of hypertension and Type 2 Diabetes, which may contribute to poor respiratory muscle function or fluid overload.

The patient is placed on supplemental oxygen via nasal cannula at 2 L/min, and her oxygen saturation improves slightly to 92%. However, her heart rate remains elevated at 115 bpm, and she continues to report dizziness and mild confusion, suggesting that the underlying issue may not be fully addressed. The clinical team considers the possibility of a more complex interplay of respiratory and metabolic imbalances, perhaps involving an element of metabolic acidosis secondary to poor perfusion or renal impairment. Further diagnostic tests, including chest X-ray and metabolic panel, are ordered to investigate potential causes such as pulmonary edema or renal dysfunction, which could complicate the existing respiratory acidosis and require adjustment of the treatment plan.

Section 2

As the clinical team reviews the new diagnostic results, the chest X-ray reveals bilateral infiltrates suggestive of pulmonary edema, which may be contributing to the patient's respiratory distress and hypoxemia. The metabolic panel shows a serum creatinine of 2.1 mg/dL, indicating acute kidney injury, likely secondary to hypoperfusion and possibly exacerbated by underlying diabetes mellitus. Blood urea nitrogen (BUN) is elevated at 45 mg/dL, further supporting compromised renal function. These findings raise concerns about fluid overload contributing to both respiratory and metabolic complications.

In response to these results, the team decides to initiate diuretic therapy with furosemide to address potential fluid overload and improve pulmonary function. The patient is also reassessed for volume status, with careful monitoring of urine output and electrolyte balance. Meanwhile, the supplemental oxygen is adjusted to a simple face mask at 5 L/min to optimize oxygenation, as her saturation remains borderline despite initial interventions. The clinical team continues to monitor the patient's respiratory status closely, watching for signs of improvement or further deterioration.

Despite these interventions, the patient exhibits new signs of increased respiratory effort, with a respiratory rate now at 32 breaths per minute and persistent use of accessory muscles. Her level of confusion has worsened, and she is less responsive to verbal stimuli, raising concerns about worsening respiratory acidosis or possible cerebral hypoxia. Repeat ABG shows a pH of 7.29, PaCO2 of 58 mmHg, and HCO3- of 27 mEq/L, indicating a deepening respiratory acidosis without adequate compensation. The team must now consider more aggressive interventions, such as non-invasive ventilation or transfer to a higher level of care, to address the escalating severity of her condition.

Section 3

As the clinical team evaluates the situation, the patient's status continues to change, prompting a reassessment of her condition and immediate priorities. The patient's blood pressure has decreased to 88/54 mmHg, indicating potential hemodynamic instability. Her heart rate remains elevated at 112 beats per minute, and her skin is cool and clammy, suggesting worsening perfusion. These changes raise concerns about the adequacy of cardiac output and the possibility of worsening shock, likely due to the combination of fluid overload, acute kidney injury, and potential cardiac dysfunction.

Given the new developments, the team immediately initiates a discussion about the need for non-invasive ventilation to support the patient's breathing effort and improve carbon dioxide clearance. A CPAP (Continuous Positive Airway Pressure) machine is quickly set up to provide positive pressure support, aiming to reduce the work of breathing and enhance oxygenation. While the diuretic therapy with furosemide continues to be titrated, the team also considers starting a low-dose inotropic agent to support cardiac function and improve renal perfusion, balancing the risks of further fluid shifts and electrolyte imbalances.

The latest lab work, including repeat electrolytes, shows a new potassium level of 3.2 mEq/L, indicating hypokalemia, likely secondary to the diuretic effect. This finding necessitates prompt intervention to avoid potential cardiac arrhythmias. The clinical team decides to administer potassium replacement cautiously, alongside close monitoring of the patient's cardiac rhythm and electrolyte levels. As the patient's condition remains precarious, the team continues to reassess her response to these interventions, ready to escalate care by potentially transferring her to the intensive care unit if her status does not stabilize.

Section 4

As the team closely monitors the patient's response to the interventions, a new set of arterial blood gas (ABG) results reveals concerning changes. The ABG shows a pH of 7.28, PaCO2 of 55 mmHg, and HCO3- of 24 mEq/L, indicating a mixed respiratory and metabolic acidosis. This result highlights the inadequate clearance of carbon dioxide despite the CPAP support, suggesting that the patient's respiratory effort is insufficient to meet her metabolic demands. Coupled with her low blood pressure and elevated heart rate, these findings point toward worsening respiratory failure and the need for enhanced ventilatory support.

Furthermore, the patient develops new-onset confusion and restlessness, raising concerns about cerebral perfusion in the setting of declining hemodynamics. Her oxygen saturation, which was initially stable at 92% on CPAP, has now dropped to 88%, underscoring the urgency of the situation. The team discusses the potential need for transitioning to a more invasive form of ventilation, such as BiPAP or even intubation, to stabilize her respiratory status and ensure adequate gas exchange.

Simultaneously, the patient's renal function shows further deterioration, with a serum creatinine level now at 2.3 mg/dL, up from 1.9 mg/dL earlier in the day. This trend, along with the persistent hypokalemia, suggests that her acute kidney injury is worsening. The clinical team recognizes the need for a delicate balance in managing her fluid status, as aggressive diuresis may further compromise renal function, yet fluid overload could exacerbate her respiratory distress. With these complexities in mind, the team remains vigilant in reassessing her condition and is prepared to escalate to ICU care, where more intensive monitoring and interventions can be administered.

Section 5

As the clinical team deliberates the next steps in managing the patient's deteriorating condition, they decide to initiate BiPAP therapy to provide more robust ventilatory support. Shortly after implementing this intervention, a new set of diagnostic results arrives, providing further insights into her evolving clinical picture. A repeat arterial blood gas analysis reveals a pH of 7.25, PaCO2 of 60 mmHg, and HCO3- of 26 mEq/L, confirming the persistence and worsening of respiratory acidosis despite the change in ventilatory strategy. The patient's oxygen saturation remains concerning at 86%, even with the increased support, indicating that her respiratory system is struggling to meet the body's demands.

In addition to the respiratory challenges, the patient's cardiovascular status also shows signs of compromise. Her blood pressure has decreased further to 85/50 mmHg, and her heart rate remains elevated at 120 beats per minute. These hemodynamic changes, coupled with her altered mental status, suggest that she may be entering a state of shock, possibly septic or distributive in nature. The team considers the potential for underlying infection or systemic inflammatory response as contributing factors, given her acute kidney injury and respiratory failure. Blood cultures and a broad-spectrum antibiotic regimen are initiated to address any infectious cause while fluid resuscitation is cautiously administered to stabilize her blood pressure without exacerbating her respiratory distress.

The patient's renal function continues to decline, with a serum creatinine level now at 2.6 mg/dL. This progression underscores the delicate balance required in her management, particularly concerning fluid status and renal perfusion. As her condition remains precarious, the decision is made to transfer her to the ICU for closer monitoring and potential escalation to invasive mechanical ventilation if her respiratory status does not improve. The team remains vigilant in reassessing her response to interventions and is prepared to adjust the treatment plan as new information becomes available, recognizing the complexity and interconnection of her respiratory, cardiovascular, and renal issues.