Thoracic Anuerysm - Nursing Case Study
Pathophysiology
• Primary mechanism: Thoracic aneurysms primarily occur due to the weakening of the arterial wall in the chest area. This is often caused by atherosclerosis (hardening of the arteries), which leads to the formation of plaque, narrowing the artery and increasing blood pressure.
• Secondary mechanism: Genetic conditions like Marfan syndrome or Ehlers-Danlos syndrome can cause abnormal protein formation in the arterial walls, leading to their degeneration and, consequently, the formation of an aneurysm.
• Key complication: If left untreated, the continued pressure can cause the aneurysm to rupture, leading to potentially fatal internal bleeding. Further, the blood clot formed can dislodge and cause a stroke or organ damage.
Patient Profile
Demographics:
65 years old, Male, Retired construction worker
History:
• Key past medical history: Hypertension, high cholesterol, smoking
• Current medications: Lisinopril, Atorvastatin
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Sharp chest pain and shortness of breath
• Key symptoms: Chest and back pain, difficulty breathing, intense sweating, dizziness, rapid heart rate
• Vital signs: Blood Pressure 160/100, Heart Rate 110 bpm, Respiratory Rate 25 breaths per minute, Temperature 98.6°F, Oxygen Saturation 92% on room air
Section 1
Change in Patient Status:
The patient’s condition started to deteriorate rapidly with his heart rate increasing to 130 bpm and blood pressure rising to 180/110. He also started to experience severe chest pain radiating to his back and was becoming increasingly short of breath. His oxygen saturation dropped to 85% on room air, prompting the need to administer supplemental oxygen.
The patient appeared anxious and was experiencing difficulty in speaking due to extreme shortness of breath. He was also profusely sweating and reported an increase in the intensity of his chest pain. On physical examination, a new diastolic murmur was noted on auscultation of the heart, indicating possible aortic regurgitation secondary to the enlarging aneurysm. This sudden change in his condition suggested that his thoracic aneurysm might be expanding and at risk of rupture, which is a life-threatening situation requiring emergent action.
This change in the patient's status requires immediate clinical reasoning and decision-making. The healthcare team must balance the need to stabilize the patient's vitals while preparing for the potential need for emergent surgical intervention. Furthermore, the new findings increase the complexity of the patient's case, as they may indicate new complications, such as aortic regurgitation or impending aneurysm rupture.
Section 2
Response to Interventions:
Despite being administered supplemental oxygen, the patient's oxygen saturation only improved marginally to 88%, and his respiration rate increased to 28 breaths per minute. He was started on nitroglycerin to manage his chest pain and hypertension, but his blood pressure remained elevated at 175/105. His heart rate also continued to be tachycardic at 125 bpm.
The healthcare team decided to intubate the patient due to his worsening respiratory distress, with his anxiety further limiting his oxygen intake. Post-intubation, his oxygen saturation improved to 92%. However, his blood pressure and heart rate still remained high despite administering labetalol, indicating possible refractory hypertension. The persistence of these symptoms suggests that the interventions may not be fully addressing the patient's condition, and the team may need to explore other treatment options. The healthcare team also considered the possibility of an impending rupture of his thoracic aneurysm, and the need for urgent surgical intervention is becoming increasingly critical.
Section 3
New Complications:
The healthcare team noticed an alarming development in the patient's condition. Despite being intubated and on supplemental oxygen, the patient's oxygen saturation had dropped to 86%, and his respiration rate increased to 32 breaths per minute. His heart rate also spiked to 135 bpm. An EKG revealed the presence of new ST-segment elevations, raising concerns about myocardial ischemia.
Upon auscultation, the team noted a new diastolic murmur suggestive of aortic regurgitation, a complication of thoracic aneurysm. The patient's blood pressure continued to stay elevated at 180/110 mmHg, even after increasing the labetalol dosage. A bedside ultrasound showed an increase in the diameter of the thoracic aneurysm from 5.2 cm to 5.7 cm, indicating rapid expansion. This rapid expansion, coupled with the new cardiac signs, suggested the aneurysm was at a high risk of rupture. The team was now faced with the challenge of managing the patient's refractory hypertension and potential impending rupture of the thoracic aneurysm.
Section 4
Change in Patient Status:
The patient's condition continued to deteriorate. His skin became cold and clammy, and his level of consciousness began to decrease, barely responding to painful stimuli. The patient's pulse was weak and thready, and his blood pressure plummeted to 90/60 mmHg. His heart rate continued to escalate to 150 bpm. His oxygen saturation also fell further to 80%, despite being on 100% supplemental oxygen.
The patient's worsening hypotension, tachycardia, and decreased level of consciousness were indicative of a state of shock, likely cardiogenic due to the thoracic aneurysm's impact on the heart's function. The oxygen saturation drop suggested that the patient's respiratory function was also being compromised. The healthcare team had to act quickly to stabilize the patient and avert a catastrophe. It was clear that the patient's condition was getting critical and the aneurysm was on the brink of rupture. The team had to make rapid decisions regarding immediate surgical intervention versus the risks associated with the patient's unstable condition.
Section 5
Change in Patient Status:
Despite aggressive resuscitation measures, the patient's condition continued to worsen. His blood pressure further dropped to 80/50 mmHg and his heart rate increased to 160 bpm, indicating profound shock. His oxygen saturation also plummeted to 75%, even on 100% supplemental oxygen, suggesting significant hypoxia. The patient became unresponsive to painful stimuli and his skin turned pale and mottled, indicative of peripheral vasoconstriction and poor perfusion.
New Complications:
Suddenly, the patient's monitor began to alarm, showing a rapid drop in heart rate to 40 bpm and a blood pressure of 60/40 mmHg. This bradycardia, coupled with the profound hypotension, suggested a possible rupture of the thoracic aneurysm, resulting in a catastrophic cardiovascular collapse. Concurrently, the patient developed acute respiratory distress with labored breathing and decreased breath sounds on the left side of the chest, raising suspicions of a potential hemothorax secondary to the aneurysm rupture. This development escalated the situation, requiring immediate life-saving interventions, and reinforced the imminent need for surgical intervention.