mechanical ventilation - Nursing Case Study

Pathophysiology

• Primary mechanism: Mechanical ventilation works by using positive pressure to deliver a set volume of air into the lungs. This ensures adequate gas exchange (oxygen and carbon dioxide) when a patient cannot breathe effectively on their own. It can be invasive (through an endotracheal tube) or non-invasive (mask or nasal prongs).

• Secondary mechanism: The ventilator can be set to control either the volume or the pressure of the air delivered. In volume-controlled ventilation, a set volume of air is delivered, while in pressure-controlled ventilation, the machine delivers air until a preset pressure is reached. Both settings aim to maintain adequate lung inflation and oxygenation while minimizing potential lung injury.

• Key complication: The most critical complication is ventilator-associated lung injury (VALI), which can result from high pressures (barotrauma), high volumes (volutrauma), or frequent opening and closing of alveoli (atelectrauma). This can lead to acute respiratory di

Patient Profile

Demographics:

63-year-old female, retired school teacher

History:

• Key past medical history: Chronic Obstructive Pulmonary Disease (COPD), Hypertension, Type 2 Diabetes

• Current medications: Metformin, Lisinopril, Symbicort, Ventolin

• Allergies: Penicillin, Iodine

Current Presentation:

• Chief complaint: Difficulty in breathing, increased lethargy

• Key symptoms: Severe shortness of breath, decreased alertness, cough with purulent sputum, fever

• Vital signs: Blood pressure 160/95 mmHg, Pulse rate 110 bpm, Respiratory rate 28 breaths per minute, Temperature 38.6°C, Oxygen saturation 88% on room air

Section 1

Change in Patient Status:

Our patient has been on volume-controlled mechanical ventilation for the past 48 hours. Despite initial improvements in her oxygen saturation levels, the nursing staff has noticed a progressive increase in peak airway pressures on the ventilator. Concurrently, her oxygen saturation levels have started to decrease, now maintaining at around 90% despite an increase in the fraction of inspired oxygen (FiO2) to 60%. The patient has also developed new onset, bilateral coarse crackles on auscultation, which were not present earlier. She remains febrile with temperatures persistently above 38°C. Her blood pressure has slightly decreased to 150/90 mmHg and her pulse rate has increased to 120 bpm. She remains lethargic, with minimal response to stimuli.

The increase in peak airway pressures along with decreasing oxygen saturation levels and the presence of new crackles on auscultation might suggest the development of a complication such as ventilator-associated pneumonia (VAP) or ventilator-induced lung injury. The persistent fever and increased heart rate could also indicate an ongoing infectious process. This change in patient status requires urgent reassessment and intervention to prevent further deterioration. The next course of action would likely involve obtaining imaging studies and blood cultures, adjusting ventilator settings, and possibly starting empiric antibiotic therapy. The clinical team must consider these developments in the context of the patient's underlying COPD and the potential for exacerbation or secondary infection.

Section 2

Change in Patient Status:

The patient's condition continues to deteriorate. Her oxygen saturation has now dropped to 88%, despite further increases in the FiO2 to 70%. Her blood pressure has also continued to decrease, now at 130/80 mmHg, and her pulse rate has increased to 130 bpm. The patient has become increasingly lethargic, with no response to stimuli. The nursing staff has also noted a new onset of purulent secretions from the endotracheal tube, which were not present before.

The combination of worsening oxygenation, decreasing blood pressure, increasing heart rate, progressively worsening lethargy, and new onset of purulent secretions raises the suspicion of a serious complication such as septic shock secondary to ventilator-associated pneumonia. This could be exacerbated by the patient's underlying COPD, making her more susceptible to severe infections. The clinical team would need to reassess her quickly and consider initiating broad-spectrum antibiotics, obtaining additional cultures, and possibly considering a bronchoscopy to identify the causative pathogen. The team should also anticipate the need for vasoactive medication support if her blood pressure continues to drop. The critical nature of these developments requires immediate action and careful monitoring to prevent further deterioration.

Section 3

New Diagnostic Results:

To further investigate the patient's deteriorating condition, the clinical team decided to conduct a full blood count, blood cultures, and chest x-ray, while the respiratory team performed a bronchoscopy to obtain samples from her lungs. The full blood count showed a significantly elevated white blood cell count at 20,000/mm3, indicative of a severe infection. The blood cultures were sent to the lab for analysis, with results expected in 24-48 hours.

The chest x-ray showed significant infiltrates in the right lung, consistent with the suspected diagnosis of ventilator-associated pneumonia. Bronchial lavage samples obtained from the bronchoscopy were also sent for culture and sensitivity testing. Meanwhile, the patient's oxygen saturation continued to drop, now at 85%, her blood pressure decreased further to 120/70 mmHg, and her pulse rate increased to 140 bpm. As her condition continued to worsen, the clinical team decided to start her on broad-spectrum antibiotics right away while awaiting the culture results. They also prepared for the possible initiation of vasoactive medication support to stabilize her blood pressure. These new diagnostic findings reinforce the initial suspicion and require an urgent response to prevent further deterioration. This stage of the patient's journey demands swift clinical reasoning and careful monitoring of her response to the interventions.

Section 4

New Complications

Despite initial intervention, the patient's condition continued to deteriorate. Her oxygen saturation levels dropped further to 82%, and her heart rate rose to 155 bpm, indicating possible sepsis. Her blood pressure also declined to 110/65 mmHg, further suggesting the need for vasopressor support. Upon reassessment, the patient's skin had become mottled and cool to the touch, especially on her extremities. Her Glasgow Coma Scale score dropped from 15 to 9, indicating a decrease in her level of consciousness.

The patient's deteriorating vital signs and physical assessment findings suggested the development of septic shock, a severe complication that often occurs in patients with ventilator-associated pneumonia. The clinical team ordered a lactate level, which came back elevated at 4 mmol/L, supporting the new suspicion of sepsis. The patient was started on norepinephrine to address the hypotension and improve her perfusion. The team also adjusted the ventilator settings to enhance her oxygenation and decided to conduct an arterial blood gas (ABG) analysis to better understand her respiratory status. The results of these interventions and the ABG findings will guide the next steps in managing this patient's rapidly evolving condition.

Section 5

Change in Patient Status

Upon re-assessment, the patient's condition showed no significant improvement. Her oxygen saturation remained low at 84%, despite adjustments to the ventilator settings. Her heart rate remained high at 160 bpm and her blood pressure further declined to 100/60 mmHg, despite vasopressor support. Her skin continued to be cool and mottled, indicating ongoing poor perfusion. Her GCS score stayed at 9, confirming a persistently decreased level of consciousness.

The arterial blood gas (ABG) analysis revealed a pH of 7.28, PaCO2 of 50 mmHg, and PaO2 of 60 mmHg, indicating respiratory acidosis with hypoxemia. Furthermore, her lactate level increased to 5.5 mmol/L, suggesting worsening sepsis and poor tissue perfusion. These findings underscore the importance of immediate intervention to manage the patient's rapidly deteriorating condition. The clinical team will need to reassess their current management plan, considering more aggressive measures to improve her oxygenation and circulation, and control the source of sepsis.