According to a case report published in medical literature, a middle-aged woman in her early 40s presented to an emergency department with atypical symptoms of a massive pulmonary embolism (PE), including dizziness, palpitations, and lethargy, ultimately leading to cardiac arrest and complex multiorgan complications. Early diagnosis of massive PE remains challenging because clinical presentations are highly variable and frequently non-specific, according to underlying medical studies noting that compensatory mechanisms can initially preserve oxygenation and mask the severity of disease.
Atypical Emergency Department Presentation and Clinical Deterioration
The patient arrived at the emergency department complaining of dizziness for approximately seven hours, accompanied by chest discomfort, three episodes of vomiting, and generalized weakness, alongside a three-month history of intermittent palpitations, as stated in the case documentation. Vital signs recorded on arrival included a blood pressure of 100/80 mmHg, a heart rate of 126 beats per minute, a respiratory rate of 30 breaths per minute, and an oxygen saturation of 99% on room air. Initial venous blood gas analysis demonstrated non-anion gap metabolic acidosis with a lactate level of 4.8 mmol/L and a normal hemoglobin level of 136 g/L. Despite the administration of intravenous normal saline boluses, the patient remained tachycardic and tachypneic.
Approximately 30 minutes after arrival, her clinical condition deteriorated as her blood pressure dropped to 80/60 mmHg alongside new-onset central chest pain, according to the clinical timeline. A repeat physical check revealed an inter-arm blood pressure difference, with the right arm measuring 80/60 mmHg and the left arm 100/70 mmHg. A right radial arterial line confirmed persistent hypotension at 84/62 mmHg, prompting clinicians to initiate a norepinephrine infusion at 5 µg/min.
Diagnostic Escalation and Imaging Findings
Roughly two hours after presentation, laboratory results showed markedly elevated troponin-I at 1489.9 ng/L and a D-dimer level exceeding 35.2 mg/L, significantly heightening suspicion for a massive PE or acute aortic syndrome, based on hospital records. Arterial blood gas analysis at that stage revealed worsening metabolic acidosis with a pH of 7.14 and a lactate level of 7.6 mmol/L. Because serum β-ketones tested negative, diabetic ketoacidosis was ruled out. To evaluate for life-threatening causes of shock, clinicians transferred the patient for non-contrast computed tomography (CT) of the head, CT pulmonary angiography (CTPA), and CT angiography (CTA) of the chest and abdomen. Head CT showed no acute intracranial pathology, and CTA of the chest and abdomen confirmed a patent, well-opacified aorta with no evidence of aortic dissection, while the formal CTPA interpretation remained pending.
Cardiac Arrest, Thrombolysis, and Resuscitation
Approximately three hours after initial presentation, while being transferred back from the CT scanner, the patient developed agonal respirations and progressed to cardiac arrest, triggering immediate cardiopulmonary resuscitation (CPR) under Advanced Cardiovascular Life Support (ACLS) guidelines. During ongoing chest compressions, the radiologist provided an urgent verbal report of the CTPA confirming a massive saddle pulmonary embolism with bilateral filling defects in the right and left main pulmonary arteries. Clinicians immediately administered intravenous alteplase as a 50 mg bolus followed by a 50 mg infusion over 20 minutes during active CPR. Return of spontaneous circulation (ROSC) was achieved approximately three minutes later.
Following ROSC, persistent hypotension required escalating vasopressor support from norepinephrine to an epinephrine infusion, which stabilized blood pressure at 125/86 mmHg. Rapid sequence intubation was performed using ketamine and rocuronium, and a right femoral central venous catheter was placed for ongoing hemodynamic monitoring.
Intra-Abdominal Complications and Surgical Intervention
Plans for mechanical thrombectomy were initiated; however, during pulmonary angiography, the patient developed acute hypotension measuring 76/45 mmHg accompanied by a sudden drop in hemoglobin to 4.6 g/L, according to procedural records. A focused assessment with sonography for trauma (FAST) revealed significant pelvic free fluid. This prompted the activation of a massive transfusion protocol, the abortion of the thrombectomy procedure, and urgent CT imaging that demonstrated active anterior upper abdominal venous bleeding.
Transferred to the intensive care unit (ICU), the patient underwent emergency damage control surgery, where approximately 2 to 3 liters of intraperitoneal blood were evacuated, as documented in the surgical notes. Surgeons identified and controlled bleeding from small sub-diaphragmatic veins anterior to the liver using intra-abdominal packing. A planned relook laparotomy was successfully performed two days later for pack removal, hemostasis, and lavage.
Did You Know?
Extended ICU Course and Full Recovery
During her 33-day hospital stay, the patient experienced several additional complications, including right thumb ischemia from a radial artery thrombus that required an open thrombectomy, according to hospital records. Unfractionated heparin was initiated due to high thrombotic risk. She was extubated on day 8 and transitioned off continuous renal replacement therapy (CRRT).
Frequently Asked Questions
What are the classic versus atypical symptoms of a massive pulmonary embolism?
Classic features include dyspnea, pleuritic chest pain, tachycardia, and hypoxemia. However, atypical presentations—such as dizziness, palpitations, lethargy, and vomiting with initially preserved oxygen saturation—frequently occur and can delay timely diagnosis.
Why does massive pulmonary embolism cause sudden hemodynamic instability?
Acute obstruction of the pulmonary vasculature leads to right ventricular strain, reduced cardiac output, and rapid progression to obstructive shock and cardiac arrest, even when compensatory mechanisms temporarily preserve oxygenation.
What are the primary therapeutic options for high-risk pulmonary embolism with cardiac arrest?
According to clinical guidelines and the reported case, systemic thrombolytic therapy administered during ongoing cardiopulmonary resuscitation can achieve a return of spontaneous circulation in life-threatening scenarios.
What complications are associated with thrombolysis during cardiac arrest?
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