Summary of medical history
The patient, a 64-year-old female, presented to our hospital with “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 occurring during activity and relieved by rest, without chest pain, palpitations, sweating, hemoptysis, fever, or night sweats, and had been treated with infusion of coronary artery disease at the local village health center (specific medication is not known). He came to our hospital for further treatment. The patient was in good health in the past.
Physical examination
Bp 120/80 mm Hg.
He was mentally clear and mentally poor. The lips were not cyanotic and the jugular veins were filled bilaterally. The breath sounds of both lungs were clear, and no sounds were 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
Post-admission examination: electrocardiogram showed TV1-V5 inversion, SⅠQⅢTⅢ; chest radiography 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
mmHg, partial pressure of carbon dioxide (PCO2) 30.5 mmHg, 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 to monitor the blood internationalization standardized ratio (INR) of 2.2 and was discharged.
Patients with acute chest pain are the most common group of patients in emergency medicine, accounting for about 5%-20% of patients in emergency medicine, and about 20%-30% in tertiary hospitals, and are also frequently encountered as emergencies in primary care hospitals. Most patients diagnosed with cardiac chest pain will have a malignant cardiac event within 30 days, and misdiagnosis of non-cardiac chest pain with good prognosis as serious cardiac chest pain will cause unnecessary psychological stress and economic loss to patients. Chest pain involves several systems, for example, circulatory system diseases such as coronary heart disease and aortic coarctation, respiratory system diseases such as pulmonary embolism, tension pneumothorax and lung cancer, digestive system diseases such as gastroesophageal reflux and esophagitis, neurological system diseases such as intercostal neuralgia, and skeletal muscle system diseases such as thoracic trauma.
Among the various chest pains that require extra attention and rapid judgment are patients with high-risk chest pain, including patients with acute coronary syndrome, aortic coarctation, pulmonary embolism and tension pneumothorax.
The following are the basic treatment measures that should be taken for several common critical and severe chest pains.
I. 20-minute steps to confirm the diagnosis of acute coronary syndrome
Acute coronary syndrome (ACS) is a group of syndromes characterized by coronary atherosclerotic plaque instability as the basic pathophysiological feature and acute myocardial ischemia as a common feature, including unstable angina (UA), non-ST-segment elevation myocardial infarction (NSTEMI) and ST-segment elevation myocardial infarction (STEMI). For patients with suspected ACS, the initial evaluation should be completed within 10 minutes of the patient’s arrival in the ED. 20 minutes to establish the diagnosis: first obtain a history, physical examination, 12-lead ECG, and initial cardiac marker test, and combine these findings to determine if the patient is definitively having ACS. for patients with suspected ACS whose initial 12-lead ECG and cardiac marker levels are normal, 15 minute repeat ECG, and 6 hours after symptom onset, a repeat cardiac marker test may be performed.
The diagnosis of ST-segment elevation myocardial infarction should meet two or more of the following criteria: typical chest pain (angina) lasting more than 20 minutes; elevation of the ST arch in two or more connected leads of the ECG with dynamic changes; elevation of biochemical markers of myocardial necrosis (CK, CK-MB, troponin, etc.) with dynamic evolution. Once the diagnosis is confirmed, early reperfusion therapy is essential to improve ventricular function and increase survival. The goal of treatment is to open the occluded coronary artery within hours to achieve and maintain reperfusion of blood flow at the myocardial level.
The goal of treatment of non-ST-segment elevation acute coronary syndromes is to stabilize ruptured plaque lesions within hours to days, to allow gradual healing of ruptured plaques into stable lesions, to manage risk factors (such as hypertension, hyperlipidemia, smoking and diabetes) and to prevent further plaque rupture. Based on the history typical angina symptoms, typical ischemic ECG changes (new or transient ST-segment depression ≥ 0.1 mV, or T-wave inversion ≥ 0.2 mV) and myocardial injury markers (cTnT, cTnl or CK-MB) measurement, it can be an important reference for the diagnosis of unstable angina versus non-ST-segment elevation myocardial infarction.
For high-risk episodes of ischemia despite intensive treatment, elevated troponin, ST-segment depression, chest pain with signs or symptoms of cardiac insufficiency, positive stress test, cardiac echocardiography showing left ventricular ejection fraction (LVEF) <0.40, hemodynamic instability, persistent ventricular tachycardia, cardiac intervention (PCI) and cardiac bypass surgery (CABG) within 6 months, etc. Patients should be treated with early interventional strategies. Also, intensive statin therapy should be given early for unstable angina and non-ST-segment elevation myocardial infarction, and secondary prevention of coronary artery disease.
Second, aortic coarctation can be diagnosed with the help of CT scan
Aortic coarctation is a tear in the intima of the aorta and blood enters the aortic wall through the tear, causing the middle layer to peel away from the outer membrane, with a high mortality rate. Clinically, it often presents with tear-like pain and a vasovagal-like reaction, such as shock. Sometimes the symptoms of a coarctation tear are associated with an acutely occluded artery, such as a stroke, myocardial infarction, or small bowel infarction, and the compromised blood supply to the spinal cord can cause mild or paraplegia of the lower extremities and limb ischemia, and these manifestations resemble arterial embolism. Imaging tests such as aortic CT scan can establish the diagnosis.
Once the diagnosis of aortic coarctation is established, pharmacological treatment should be started as soon as possible: aggressive sedation and analgesic treatment; rapid control of blood pressure, usually with a combination of sodium nitroprusside and beta-blockers, with the goal of lowering blood pressure to the lowest blood pressure level that maintains adequate cerebral, cardiac, and renal perfusion; and control of heart rate and slowing of the rate of left ventricular contraction, usually with beta-blockers. In addition, all acute entrapment tears of the proximal aorta are indicated for surgery and should be performed as early as possible.
III. Pulmonary embolism-specific electrocardiographic manifestations contribute to the diagnosis
The first manifestation of acute pulmonary thromboembolism (PE) is hypoxemia. The common clinical manifestations of larger pulmonary embolism include severe dyspnea, increased respiration, chest pain, cyanosis, hypoxemia and even syncope. The morbidity, misdiagnosis and mortality rates are high in the acute phase of pulmonary embolism, with 11% sudden death within one hour of onset and 32% total mortality. When acute pulmonary embolism is suspected, electrocardiogram should be done promptly. The typical performance is SⅠQⅢTⅢ (incidence is 25.9%~37.1%), which is mostly presented clinically as one or several performances of SⅠ, SⅠQⅢ, QⅢTⅢ, QⅢ, TⅢ and SⅠQⅢTⅢ, mostly accompanied by dynamic changes. However, more common are often undetected signs of right ventricular strain, such as T-wave inversion in leads V1-V4, new incomplete or complete right bundle branch conduction block, which together with SⅠQⅢTⅢ and each combination of manifestations are meaningful ECG indicators suggesting the presence of pulmonary embolism. At the same time, blood should be drawn for D-dimer, 2D echocardiography and lung-enhanced spiral CT should be done. It should be noted that ECG is a “double-edged sword”, which can be used appropriately to help diagnosis, but inappropriate use can be a tool for misdiagnosis. The case with chest pain as the primary manifestation introduced at the beginning of this paper has the typical ECG manifestation of PE, SⅠQⅢTⅢ, and was misdiagnosed as coronary artery disease twice, so lessons should be learned.
Large pulmonary embolism with hemodynamic instability can be considered for thrombolysis, surgical retrieval of embolus or interventional catheter fragmentation. For patients with recurrent embolism despite anticoagulation therapy or with contraindications to anticoagulation and clear presence of lower extremity deep vein thrombosis (DVT), an inferior vena cava filter may be considered.
If the patient is critically ill and can only undergo bedside diagnostic testing, CT may be considered without immediate CT. # Transesophageal echocardiography can detect pulmonary artery thrombosis in most patients with right ventricular overload and PE, which is eventually confirmed on spiral CT; DVT confirmation and bedside cardiac ultrasound also help in the diagnosis.
Fourth, tension pneumothorax has more typical clinical symptoms
Tension pneumothorax, also known as high-pressure pneumothorax, is usually seen in patients who can form a live valve after the rupture of pulmonary alveoli caused by sharp injuries or previous serious lung diseases (such as emphysema), where the air “only goes in but not out”, which can seriously endanger the cardiopulmonary function. Clinically, patients usually first present with sudden and severe chest pain, dyspnea, and occasionally a dry cough. The pain may radiate to the ipsilateral shoulder, contralateral chest or abdomen and may resemble acute coronary syndrome or acute abdomen. Physical signs may include a percussive chest bulge, diminished or absent palpable fibrillation, and diminished respiratory motion on the affected side. Mediastinal shift may be manifested by a shift of heart murmur and apical pulsation to the healthy side and a marked decrease or absence of breath sounds. The diagnosis can be confirmed if the chest X-ray shows partial air in the periphery of the lung and no lung texture. Rapid air expulsion is a life-saving measure for treatment.
Core tips.
1.If the patient shows pallor, sweating, cyanosis, respiratory distress and life indication, regardless of its cause, it is in critical condition and requires immediate oxygen, cardiac monitoring, establishment of intravenous fluid access and opening of hospital green channel.
2.Whenever a patient with chest pain is encountered, the first thing to think of is the need to exclude these critical illness conditions: acute coronary syndrome, pulmonary embolism, aortic coarctation, tension pneumothorax, etc.