1. Acute Pericarditis
Figure 1. Acute Pericarditis (EmDocs, 2018)
In acute pericarditis, the pericardium surrounding the heart can become inflamed, and while oftentimes is idiopathic, it can be related to a viral or bacterial infection, trauma, MI, or connective tissue disease (McCance and Huether, 2019, p. 1088). The inflammation of the pericardial space can cause an influx of fluids and inflammatory mediators and in turn compress the cardiac tissue and decrease cardiac output (McCance and Huether, 2019, p. 1088). This inflammation, sharp chest pain, tachycardia, and elevated troponin are consistent with clinical manifestations of acute pericarditis (McCance and Huether, 2019, p. 1088). However, this patient is afebrile, and while ST-segment elevation is noted in EKG, it is not widespread like it would be seen in pericarditis (McCance and Huether, 2019, p. 1088). Symptoms of nausea and shortness of breath are generally not symptoms of acute pericarditis. Mr. Smith is not noted to have a friction rub upon auscultation, nor does he have a positive history for connective tissue disease or other reason leading to believe he is experiencing an infectious process (McCance and Huether, 2019, p. 1088).
2. Stable Angina
Figure 2. Stable Angina (A.D.A.M, 2019)
Stable angina is caused by increased myocardial demand typically during exertion (McCance and Huether 2019). The coronary arteries lose their ability to dilate due to progressive atherosclerosis and hardening of the arteries (McCance and Huether, 2019, p. 1079). Pain is typically felt in the chest and can radiate to the jaw, neck, arms, shoulders, or back (McCance and Huether, 2019, p. 1079). Mr. Smith is presenting with chest pain that aligns with stable angina since he has noticed pain during his workouts. He also has a history of atherosclerosis and dyslipidemia which increases his risk for hardening of the coronary arteries. However, stable angina typically resolves with rest when blood flow is restored and results in no true necrosis to myocardial cells (McCance and Huether, 2019, p. 1079). A patient experiencing stable angina would not have elevated troponin or ST elevation on ECG. Nausea is not a typical symptom of stable angina (McCance and Huether 2019).
3. Pulmonary Embolism
Figure 3. Pulmonary Embolism (Mayo Clinic, 2018)
Pulmonary embolism is a result of blockage of the pulmonary artery by an emboli that typically travels from the lower extremities and most commonly begins as a deep vein thrombosis (McCance and Huether 2019, p. 1190). A risk factor for the development of a PE is venous stasis which aligns with Mr. Smith’s long career behind a desk (McCance and Huether 2019, p. 1190). Clinical manifestations of pulmonary embolism can vary depending on the extent of occlusion and can include chest pain, pleuritic chest pain, cough, dyspnea, tachypnea, tachycardia, unexplained anxiety and if large enough even shock (McCance and Huether 2019, p. 1190). In severe cases of pulmonary embolism troponin can be elevated if enough strain is put on the right ventricle (McCance and Huether 2019, p. 1191). When the clot is lodged in the artery, it can cause an influx of inflammatory mediators, catecholamines, histamines and other substances (McCance and Huether 2019, p. 119). This patient is presenting with chest pain, tachypnea, dyspnea, tachycardia, and an elevated troponin and WBC which all align with a pulmonary embolism. However, Mr. Smith’s ECG shows ST elevation which is unique to acute myocardial ischemia, specifically a STEMI (McCance and Huether 2019, p. 1083).