A 57-year-old male client is brought to the emergency department (ED) by emergency medical services (EMS) with reports of chest pain. Client was mowing his lawn and noticed chest pain presenting as tightness and pressure. The pain continued to increase over about 30 minutes when the client decided to rest. The client's wife called emergency medical services (EMS) when the pain was unrelieved after 20 minutes of rest. Client reports no other incidents of experiencing this pain. His medical history includes hypertension, obesity, and a 20 year history of smoking, having quit about 5 years ago. Takes metoprolol succinate ER 25 mg PO.

Exhibits

For each assessment finding, click to specify if the finding is consistent with angina or myocardial infarction, or both. Each column must have at least one response option selected.

• Pulmonary embolism (PE): The client presents with sudden-onset chest pain, dyspnea, hypoxia (SpO₂ 89% on room air), tachypnea, tachycardia, and cyanosis. These are classic signs of a pulmonary embolism, especially following trauma or immobility, such as after a lower extremity fracture and recent surgery.
• Start continuous cardiorespiratory monitoring: Given the client's compromised respiratory status and cardiac involvement, continuous monitoring is needed to detect worsening hypoxia, dysrhythmias, or hemodynamic instability associated with PE.
• Administer heparin subcutaneous: Anticoagulation with heparin is the standard first-line treatment for PE. It prevents further clot formation and reduces the risk of clot propagation, helping stabilize the client while further evaluation continues.
• Oxygen saturation: Monitoring SpO₂ helps assess the client's respiratory function and the effectiveness of oxygen therapy or anticoagulation. PE impairs gas exchange, so O₂ saturation is a key indicator of clinical progress.
• Cardiac markers: PE can strain the right side of the heart, leading to ischemia. Monitoring cardiac markers helps detect myocardial stress or injury secondary to increased pulmonary vascular resistance.
• Deep vein thrombosis (DVT): While DVT is a risk factor, the client’s acute chest symptoms and hypoxia suggest the clot has embolized to the lungs, indicating PE rather than isolated DVT.
• Myocardial infarct: Although chest pain and increased cardiac workload are seen in both MI and PE, the absence of cardiac history, coupled with low oxygen saturation and recent surgery, makes PE more likely than MI.
• Adult respiratory distress syndrome (ARDS): ARDS involves diffuse alveolar damage and is usually a complication of sepsis or trauma. This client’s symptoms developed suddenly and asymmetrically, favoring PE over ARDS.
• Prepare client for mechanical ventilation: Mechanical ventilation may be needed if the client deteriorates, but his current oxygen saturation and respiratory rate do not yet require intubation.
• Get consent signed for angioplasty: Angioplasty is used for coronary artery occlusion (e.g., in MI), not PE. The client's presentation is not consistent with myocardial infarction requiring catheter intervention.
• Arrange for surgeon to establish artificial airway via tracheostomy: A tracheostomy is not an emergency intervention for acute hypoxia due to PE. Airway is currently patent and oxygenation, while impaired, is being monitored non-invasively.
• Kidney function: While important for general monitoring, it is not the most relevant parameter in assessing PE progression unless complications arise from anticoagulation therapy.
• Presence of petechiae of the thorax: Petechiae is a sign more specific to fat embolism syndrome, particularly after long bone fractures. The client has a lower leg fracture with chest pain but no evidence of petechiae.
• Ventilator settings: The client is not mechanically ventilated, so ventilator settings are not relevant at this point. Monitoring focuses on spontaneous respiratory function and perfusion.

A. Headache with sudden onset: While a sudden headache can be concerning and suggest a neurologic issue, it is not the most immediate sign of hemodynamic instability in the context of atrial fibrillation with hypotension. The priority is assessing cerebral perfusion.

B. Flat jugular vein distention (JVD) at 45 degrees: Flat JVD may reflect low central venous pressure, which is consistent with hypotension but is not as critical as changes in neurologic status. It is a supportive finding rather than a primary indicator to report.

C. Abnormal level of consciousness: Altered mental status indicates reduced cerebral perfusion due to a dangerously low cardiac output from rapid atrial fibrillation and hypotension. This is a critical, life-threatening sign that demands immediate medical intervention to restore adequate perfusion.

D. Nausea with vomiting: These symptoms can occur with hypotension or sympathetic stimulation but are nonspecific and less urgent compared to neurologic compromise. They do not require the same immediate action as a change in consciousness.