Nursing Interventions for Acute Respiratory Failure with Underlying COPD

Case Study Report of “Eddie”: Acute Respiratory Failure with Underlying COPD

Today, approximately 10% of all intensive care unit admissions as well as almost one-quarter (24%) of all patients that require mechanical ventilation, are due to acute respiratory failure (Parcha et al., 2021). The purpose of this case study report is to provide an assessment of “Eddie,” a 50-year-old male recently admitted to the intensive care unit with acute respiratory failure. The case study report begins by providing a brief description of acute respiratory failure, including its pathophysiology, subtypes, causes, and diagnostic criteria. The next section provides a critical analysis of Eddie's presentation on admission to intensive care, linking it to pathophysiology, physical assessment findings, and diagnostic tests, to arrive at a diagnosis of Eddie's acute respiratory failure. In addition, the case study report evaluates and describes the ventilation-perfusion (V/Q) mismatch that was identified in Eddie's diagnosis. In addition, an interpretation of analysis of Eddie's arterial blood gas results and is followed by a discussion concerning two appropriate nursing assessments that would be indicated in Eddie's current condition, together with the physiological rationale, assessment technique, and expected findings. Finally, the case study report discusses the effectiveness of providing fluid to support Eddie's worsening hemodynamics and suggests other evidence-based management strategies that could be initiated to improve Eddie's condition.

Brief description of acute respiratory failure including pathophysiology, subtypes, causes and diagnostic criteria

Acute respiratory failure (ARF) refers to a state in which the respiratory system is unable to sustain adequate gas exchange at normal levels (Anesi et al., 2023). According to Gurka and Balk (2018), ARF is defined as “the inability of the respiratory system to meet the oxygenation, ventilation, or metabolic requirements of the patient” (p. 137). At present ARF is classified according to one of four general types as set forth in Table 1 below:

Table 1

Types of Acute Respiratory Failure

Type

Description

Type 1

Hypoxemic - PO2 < 50 mmHg on room air; usually seen in patients with acute pulmonary edema or acute lung injury because these disorders interfere with the lung's ability to oxygenate blood as it flows through the pulmonary vasculature.

Type 2

Hypercapnic/Ventilatory - PCO2 > 50 mmHg (if not a chronic CO2 retainer); this type of ARF is usually seen in patients with an increased work of breathing due to airflow obstruction or decreased respiratory system compliance, with decreased respiratory muscle power due to neuromuscular disease, or with central respiratory failure and decreased respiratory drive.

Type 3

Peri-operative - this type of ARF is generally a subset of type 1 failure but is sometimes considered separately because it is so common.

Type 4

Shock - secondary to cardiovascular instability.

Source: Adapted from Acute Respiratory Failure Overview (2023)

The causes of ARF include pulmonary diseases, non-pulmonary sepsis, viral or bacterial pneumonia, stroke, surgical complication, cardiogenic edema, cardiac arrest, and trauma (Ghale et al., 2022). The diagnostic criteria for ARF are: 1) pO2 less than 60 mm Hg (or room air oxygen saturation less than or equal to 90%); 2) pCO2 greater than 50 mm Hg with pH less than 7.35; and, 3) signs/symptoms of respiratory distress (Decaro, 2019).

Critical analysis of Eddie's current presentation on admission to intensive care linking to pathophysiology, critically analyse the physical assessment findings and diagnostic tests, and a diagnosis of Eddie's acute respiratory failure

Eddie's admission upon presentation to the intensive care unit suggests that he is suffering from acute respiratory failure, which is most likely caused by the worsening of his underlying COPD. In this regard, Gadre et al. (2018) report that, “Chronic obstructive pulmonary disease is punctuated by recurrent exacerbations and a progressive decline in the patients’ functional status” (p. 2). Likewise, Eddie's tachypnea, tachycardia, and decreased air entry bilaterally indicate the presence of airway obstruction and increased work of breathing and are indicative of ARF exacerbated by COPD. Moreover, the diagnostic tests that were administered to Eddie (pathology, chest X-ray and ECG) ruled out myocardial infarction as the cause of his chest pain and respiratory presentation. In addition, Eddie’s expiratory wheeze and fine crepitations that were identified to the lower bases further support the diagnosis of COPD exacerbation.

Although a myocardial infarction has been ruled out as the cause of Eddie’d chest pain as noted above, Magesh and Karthikeyan (2018) caution that, “Clinically right ventricular myocardial infarction can be suspected when a patient with inferior wall myocardial infarction presents with elevated JVP, positive Kussmaul's sign, hypotension [and] right-sided third or fourth heart sounds” (p. 121). In this regard, Eddie's elevated JVP suggests the presence of right heart failure, a condition that can occur in COPD exacerbations due to increased pulmonary artery pressure. Further, Eddie’s decreased oxygen saturation and concomitant need for high-flow oxygen also support the diagnosis of acute respiratory failure (Ricard et al., 2020). Therefore, aerial blood gas analysis and imaging studies, such as a chest X-ray or CT scan, are needed in order to confirm Eddie’s diagnosis and determine with more specificity the severity of his condition.

In sum, Eddie was admitted to the intensive care unit due to acute respiratory failure caused by the exacerbation of his COPD. The presence of airway obstruction and increased work of breathing is indicated by tachypnea, tachycardia, and decreased air entry bilaterally. Diagnostic tests rule out myocardial infarction and suggest COPD exacerbation. Elevated JVP suggests the presence of right heart failure, which can occur in COPD exacerbations, indicating the need for additional diagnostic testing.

3. Assessment and description of the V/Q mismatch

Because Eddie's diagnosis upon admission to the ICU was characterised by V/Q mismatch, it is important to assess its relationship with his underlying COPD. In this regard, Neder et al. (2022) point out that V/Q mismatches are frequently identified in individuals suffering from COPD as a result of their impaired pulmonary gas-exchange efficiency due to abnormal alveolar ventilation, capillary perfusion, or both, which can occur even in early and mild stages of the disease. These abnormalities can lead to significant clinical consequences, including activity-related dyspnea and exercise intolerance (Neder et al., 2022). Likewise, V/Q mismatch is a common cause of hypoxemic respiratory failure in COPD exacerbations which takes place in those cases where there is a mismatch between ventilation (V) and perfusion (Q) in the lungs.

Pulmonary ventilation is the process of inhaling and exhaling air into the lungs. Effective gas exchange occurs in alveoli when they are ventilated and perfused. In this context, ventilation refers to the flow of air, while perfusion refers to the flow of blood to alveolar capillaries. Both V and Q determine the levels of oxygen and carbon dioxide in the blood during gas exchange. For instance, Tiore et al. (2022) report that, “A VQ mismatch is the term used when the ventilation and the perfusion at the alveolar site are not matched. A VQ mismatch is indicative of respiratory distress or failure” (p. 526).

In COPD cases, there is frequently diminished ventilation as a result of obstruction to the airway together with decreased lung compliance; this condition leads to a corresponding increase in dead space ventilation. In this regard, Tiore et al. add that, “Extreme VQ mismatch is the result of an area with perfusion, but no ventilation (V/Q?=?0) termed a ‘shunt’ or an area with ventilation, but no perfusion (V/Q?=?undefined) termed a ‘dead space’” (2022, p. 527). This condition results in an increase in V/Q ratio in affected areas of the lung, leading to decreased oxygenation. Additionally, COPD exacerbations can cause pulmonary vasoconstriction, which leads to an increase in pulmonary vascular resistance and a decrease in perfusion. This increase further exacerbates the V/Q mismatch and may result in hypoxemia. Treatment of V/Q mismatch in COPD exacerbations may include oxygen therapy, bronchodilators, and corticosteroids which are used to improve ventilation and reduce airway inflammation; in severe cases, however, mechanical ventilation may be necessary to improve oxygenation (Tiore et al., 2022).

Interpretation and analysis of the arterial blood gas and two priority nursing assessments indicated in Eddie's current condition

The results of the arterial blood gas test indicate that Eddie is suffering from severe respiratory acidosis, hypoxemia, and hypercapnia. The pH level of 7.28 indicates acidosis, and the high PaCO2 level of 56 mmHg indicates hypercapnia. The low PaO2 level of 50 mmHg and 80% saturations show severe hypoxemia. The HCO3 level of 24 and BE of 1 indicate a partially compensated metabolic alkalosis. These findings suggest that Eddie's respiratory distress has worsened significantly, and his body is struggling to compensate for the accumulation of carbon dioxide and acidic environment. Based on these findings, two priority nursing assessments for Eddie would be:

1. Continuous respiratory assessment: Given the worsening respiratory distress, it is critical to continuously monitor Eddie's respiratory status, including respiratory rate, oxygen saturation, and work of breathing.

2. Assessment of mental status and cognitive function: Eddie was confused to place and person and severe hypoxemia and respiratory distress can lead to altered mental status, confusion, and decreased cognitive function. It is therefore important to assess Eddie's mental status, including his level of consciousness, orientation, and ability to follow commands now and in the future.

Discussion concerning the effectiveness of providing fluid to support the worsening haemodynamics linking to the pathophysiology of Eddie's diagnosis

The medical team prescribed a 500 ml STAT fluid bolus of 0.9% sodium chloride to support Eddie's blood pressure; in the context of Eddie's diagnosis, the effectiveness of fluid resuscitation is limited. As previously discussed, Eddie's acute respiratory failure is characterized by V/Q mismatch, which results in poor oxygenation and impaired gas exchange. Fluid administration can further compromise gas exchange by increasing pulmonary capillary hydrostatic pressure, which can lead to pulmonary edema and exacerbate V/Q mismatch. Some alternative evidence-based management strategies for Eddie's condition include the following:

· Bronchodilators and corticosteroids: Bronchodilators and corticosteroids can improve airway patency and reduce inflammation in patients with COPD which can improve gas exchange and reduce breathing workload (Roland, 2018). Here again, though, the use of these medications should be carefully monitored, as they can cause adverse effects, such as tachycardia, arrhythmias, and hyperglycemia.

· Non-invasive ventilation (NIV): NIV, such as continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP), can improve gas exchange and can also reduce breathing workload in patients with acute respiratory failure. For instance, Kinnear (2023) notes that, “CPAP is employed in patients with acute respiratory failure to correct hypoxemia. It permits a higher inspired oxygen content than other methods of oxygen supplementation, increases mean airway pressure, and will improve ventilation to collapsed areas of the lung” (p. 337).