Abstract The patient, female, 64 years old, came to our hospital with the main reason of “active chest tightness and shortness of breath for 1 month, aggravated by chest pain for 7 days”. The patient began to have recurrent chest tightness and shortness of breath one month ago, often with activity, which could be relieved by rest, without chest pain, palpitations, sweating, hemoptysis, fever, or night sweats.
(In the past 7 days, the patient’s chest tightness and shortness of breath worsened, accompanied by persistent chest pain. The patient was previously in good health. Physical examination showed BP 120/80 mm Hg.
The patient had a clear consciousness and poor mental health. The lips were not cyanotic and the jugular veins were filled bilaterally. The breath sounds of both lungs were clear and not heard. There was no significant enlargement of the cardiac turbinate, heart rate was 101 beats/min, rhythmical, and no pathological murmur was heard in each valve auscultation area. Auxiliary examination After admission, the electrocardiogram showed TV1-V5 inversion, SⅠQⅢTⅢ; chest X-ray showed increased and disturbed texture of both lungs, tortuous and calcified aorta. Admission diagnosis Coronary artery disease, unstable angina, cardiac function grade III (NYHA classification) After admission, he was given low molecular heparin calcium, isosorbide mononitrate, enteric aspirin and other drugs, antiplatelet and improve myocardial ischemia treatment. The chest pain symptoms were relieved. On the third day of admission, the results of ancillary tests were returned: cardiac enzymes were in normal range. Blood gas analysis showed a partial pressure of oxygen (PO2) of 66
mm Hg, partial pressure of carbon dioxide (PCO2) 30.5 mm Hg, and oxygen saturation (SO2) 94%. Troponin I <0.1
B-type natriuretic peptide (NT-proBNP) 1150.3 pg/ml. d-dimer 1.5
mg/L, significantly elevated. Blood count showed leukocytes 4.06×109/L, neutrophil percentage 51.6%, erythrocytes 3.51×1012/L, hemoglobin 94.3 g/L, erythrocyte pressure
41.6%. The repeat electrocardiogram showed QIII TIII and SⅠ disappeared. On the fourth day after admission, cardiac echocardiography was performed, and the estimated pulmonary artery systolic pressure (sPAP) was 35 mm
Hg, left ventricular ejection fraction (LVEF) 69%, normal range, right ventricular internal diameter normal range, no indication of ventricular wall segmental dyskinesia. On the 5th day after admission, the superior physician checked the patient and suggested a CT pulmonary arteriogram (CTPA), which indicated that the right upper and lower pulmonary arteries and their branches, and the left pulmonary artery and some of its branches were defective, suggesting bilateral pulmonary artery embolism. The corrected diagnosis was: acute pulmonary embolism, cardiac function grade III (NYHA classification). Warfarin, digoxin and diuretics were added orally, and the patient was hospitalized for 15 days and monitored with an international normalized ratio (INR) of 2.2. Comment: This patient came to our hospital with “active chest tightness and shortness of breath for 1 month, aggravated by chest pain for 7 days”. He had been treated with infusion for coronary artery disease in the local village health office, but the treatment was not effective, so it was the first misdiagnosis; after admission, the receiving physician initially diagnosed the patient with coronary artery disease based on the chest pain and the inverted electrocardiogram TV1-V5.
After admission, the receiving physician made a preliminary diagnosis of coronary artery disease and unstable angina based on the patient’s chest pain and inverted ECG TV1-V5, which was the second misdiagnosis. The lesson to be learned is that it is advisable for the first physician to think broadly and make a good differential diagnosis in the face of a patient presenting with chest pain, if the possibility of coronary artery disease, pulmonary embolism, aortic coarctation, pericarditis, etc. needs to be thought of. The patient was admitted to the hospital with an electrocardiogram that showed T-wave inversion in the chest leads along with SⅠQⅢTⅢ (SⅠ: deepening of S-wave in lead Ⅰ; >1.5
mV is significant; QIII:: Q/q wave in lead III; TIII: T wave inversion in lead III), which is a manifestation of right ventricular compliance with aggravation, and the patient’s bilateral jugular vein filling and tachycardia should be considered as the possibility of pulmonary embolism. Combined with the results of auxiliary examinations after admission, D-dimer
and blood gas analysis were abnormal, and the presence of dynamic changes in the rechecked ECG was highly suggestive of the diagnosis of pulmonary embolism, which was finally confirmed by CTPA. Therefore, the first consulting physician should have a wide range of clinical thinking and avoid the limitation of diagnostic thinking, such as thinking of heart failure when shortness of breath during activity, diagnosing coronary heart disease and subendocardial myocardial infarction when chest pain, palpitations, T-wave inversion in the anterior chest leads of ECG, and elevated cardiac enzymes, and thinking of pneumonia when fever, elevated white blood cells, and shadow on lung X-ray are present. The diagnosis of “preconceptions” or “inertial thinking” should be abandoned.