What Are the Most Common Causes of Chest Pain and Dizziness?

Chest pain is a common and life-threatening condition. The causes of chest pain are complex and diverse, including acute coronary syndrome (ACS), aortic dissection, pulmonary embolism (PE), pneumothorax, pericarditis, pericardial tamponade and esophageal rupture Among them, ACS accounts for the highest proportion of these serious life-threatening diseases, the misdiagnosis rate of myocardial infarction (AMI) is 3% to 5%, and the incidence of aortic dissection aneurysms is about 0.5 to 1/10 million people. The misdiagnosis has a mortality rate of more than 90%. The incidence of PE is about 70 / 100,000, the incidence of spontaneous pneumothorax is 2.5 to 18 / 100,000, and the incidence of esophageal rupture is 12.5 / 100,000. In 2009, the Beijing Acute Chest Pain Registration Study included 5666 patients. The results showed that chest pain patients accounted for 4% of emergency patients, of which ACS accounted for 27.4%, aortic dissection accounted for 0.1%, and PE accounted for 0.2%. How to quickly and accurately diagnose and distinguish the causes of ACS and other fatal chest pains has become a difficult and important point in emergency treatment.

Basic Information

English name

chest pain

Visiting department

Cardiothoracic surgery

Common causes

Coronary syndrome (ACS), aortic dissection, pulmonary embolism (PE), pneumothorax, pericarditis, pericardial tamponade, and esophageal rupture, etc.

Common symptoms

Chest pain

Causes of chest pain and common diseases

Causes of chest pain often include the following diseases:

Chest wall disease

Acute dermatitis, subcutaneous cellulitis, shingles, epidemic chest pain, myositis, non-purulent costochondritis, intercostal neuritis, rib fractures, acute leukemia, multiple myeloma, etc.

Cardiovascular disease

Angina pectoris, acute myocardial infarction, myocarditis, acute pericarditis, mitral or aortic valve disease, aortic aneurysm, aortic sinus rupture, dissecting aneurysm, pulmonary infarction: pulmonary hypertension and cardiac neurosis.

3. Respiratory diseases

Pleuritis, pleural tumors, spontaneous pneumothorax, pneumonia, acute tracheobronchitis, lung cancer, etc.

4. Mediastinal disease

Mediastinitis, mediastinal abscess, mediastinal tumor, and esophagitis, hiatal hernia, esophageal cancer, etc.

5. Other

Subdiaphragmatic abscess, liver abscess, spleen infarction, etc.

Differential diagnosis of chest pain

There are many diseases that need to be identified for chest pain. Its accompanying symptoms are more suggestive. The diseases that need to be identified are high-risk diseases such as acute coronary syndrome (ACS), aortic dissection, pulmonary embolism (PE), and tension pneumothorax.

1.ACS (Acute Coronary Syndrome)

ACS includes ST-elevation myocardial infarction (STEMI), non-ST-elevation myocardial infarction (STEMI), and unstable angina (UAs). Among them, the latter two types are collectively referred to as non-ST-segment elevation ACS (NSTE-ACS). Typical angina pectoris is located behind the sternum. It is squeezing, tight, suffocating or burning. It can be radiated to the neck, lower jaw, upper abdomen, shoulder, or left forearm. It usually lasts 2 to 10 minutes, and rests or contains nitroglycerin. Relieves within 3 to 5 minutes. Predisposing factors include fatigue, exercise, full meals, coldness, and emotional excitement. The causes and properties of UA chest pain are the same as above, but the patient's activity tolerance is reduced, or the attack occurs at rest. The duration of chest pain is prolonged, the severity is increased, and the frequency of attacks is increased. The duration of chest pain for myocardial infarction is often> 30 minutes. Nitroglycerin cannot effectively relieve it, and it can be accompanied by nausea, vomiting, sweating, and dyspnea. However, the symptoms of the elderly, diabetes and other patients may be atypical, and they need to be carefully identified in the clinic. Patients with UA generally do not have abnormal clinical signs, and a small number may have heart rate changes or cardiac murmur due to papillary muscle ischemia. Patients with myocardial infarction may also have no clinical signs, and some patients may have pale skin, moist and cold skin, cyanosis, jugular vein filling and anger, hypotension, galloping rhythm, lung murmur, etc. Newly appearing systolic murmur on the left margin of the sternum should be highly vigilant against ventricular septal perforation; some patients may be combined with arrhythmia, bradycardia, atrioventricular block, and tachycardia, especially vigilant ventricular tachycardia and ventricular fibrillation .

Aortic dissection

Aortic dissection is caused by aortic intimal tearing, and blood enters the vessel wall, causing the aorta to detach or rupture. About half of the aortic dissections are caused by hypertension, especially aggressive and malignant hypertension, or refractory hypertension that has been uncontrolled and difficult to control for a long time. Hereditary vascular diseases such as Marfan syndrome, aortic valve malformation, Ehlers-Danlos syndrome, familial aortic aneurysm and / or aortic dissection, and vascular inflammatory diseases including Takayasu arteritis, Behcet syndrome Symptoms and syphilis are high risk factors for aortic dissection. Other factors, such as iatrogenic factors, include interventional catheterization, heart valve and macrovascular surgery injuries, or rupture of the aortic atherosclerotic plaque endometrium. Healthy women's late pregnancy is also the cause of this disease. Patients often complain of sudden and severe chest pain, which is mostly persistent pain, such as knife-cut, tear-like, or acupuncture-like pain, which is intolerable, and may be associated with irritability, pale, sweating, cold limbs, etc. Shock performance. The site of chest pain is closely related to the origin of the dissection. As the dissection hematoma expands, the pain can spread to the proximal or distal end. Other accompanying symptoms and signs of the patient were also related to the site of dissection involvement. Dissection involving the aortic root can cause aortic insufficiency and regurgitation. An aortic valve murmur can be heard on examination: the dissection breaks into the pericardium and causes cardiac tamponade. If the dissection involves the innominate arteries or common carotid arteries, it can cause cerebral blood flow perfusion disorders, and dizziness, drowsiness, aphasia, disorientation, limb paralysis and other manifestations; hematoma compression of the subclavian artery can cause short pulses, bilateral systolic pressure And / or pulse asymmetry. Dissection involves the abdominal aorta or mesenteric artery, which can be accompanied by repeated abdominal pain, nausea, vomiting, melena and other symptoms; when the renal artery is involved, it can cause low back pain, oliguria, anuria, hematuria, and even acute renal failure. There are many types of aortic dissection in clinical practice. DeBakey and Standford are commonly used. Among them, the DeBakey classification classifies those involved in both the ascending aorta and descending aorta as type I, those that only involve the ascending aorta are type II, and those that only involve the descending aorta are type III. The former two are also classified as Standford A type. It is the most common and highest risk type in aortic dissection and requires rapid surgical intervention.

3. Pulmonary embolism

Pulmonary embolism includes pulmonary thromboembolism, fat embolism syndrome, and amniotic fluid embolism. Among them, pulmonary thromboembolism is the most common type, usually referred to as pulmonary thromboembolism. Deep venous thrombosis is the main source of thrombosis that causes pulmonary thromboembolism, which mostly occurs in the lower limbs or deep pelvic veins. Therefore, the risk factors of pulmonary thromboembolism are the same as those of deep vein thrombosis, including primary and acquired risk factors. Dyspnea and shortness of breath are the most common symptoms in patients with pulmonary embolism, which is seen in 80% of patients with pulmonary embolism. In severe cases, irritability, panic and even dying may occur, which may be related to the patient's hypoxemia; syncope or loss of consciousness may be the first or only symptom of pulmonary embolism. A faster breathing rate is the most common sign and can be accompanied by cyanosis of the lips. The signs of the circulatory system are mainly acute pulmonary hypertension, right ventricular dysfunction, and a sharp decrease in left ventricular stroke volume. Common tachycardia, pulmonary heart valve second heart sound (P2) hyperthyroidism or division, jugular vein filling or abnormal pulsation, heart murmur caused by tricuspid regurgitation, right heart galloping law, hepatomegaly, hepatic jugular vein reflux sign, lower limb Signs such as edema. A few patients may have pericardial fricatives. Falling blood pressure and shock suggest a large area of pulmonary embolism. The patient's lower extremity swelling, bilateral asymmetry, and gastrocnemius tenderness suggested that the patient had deep vein thrombosis. Most patients with acute pulmonary embolism have a blood gas analysis with PaO ₂ <80mmHg and a decrease in PaCO ₂ . Plasma D-dimer <500ug / L, which can basically exclude acute pulmonary embolism.

4.Tensile pneumothorax

Tensile pneumothorax refers to a large lung bubble rupture or a large and deep lung laceration or bronchial rupture. The slit is connected to the pleural cavity and forms a one-way valve. It is also called high-pressure pneumothorax. When inhaling, the air enters the pleural cavity through the cleft, and the valve closes when exhaling. The air in the cavity cannot be expelled, which causes the pressure in the pleural cavity to continuously increase, compressing the lungs to gradually collapse, and pushing the mediastinum to the healthy side. Squeezing the healthy side of the lungs creates severe disturbances in breathing and circulation. If the high-pressure air in the pleural cavity is squeezed into the mediastinum, it spreads to the subcutaneous tissue, forming subcutaneous emphysema in the neck, face, and chest. Clinically, the patient has extreme difficulty breathing and sits and breathes. In severe hypoxia, cyanosis, irritability, coma, and even suffocation. On physical examination, the injured chest is full, the intercostal space is widened, the breathing range is reduced, and subcutaneous emphysema may be present. Percussion was highly drummed. Auscultation breath sounds disappeared. A chest X-ray showed a large amount of gas in the pleural cavity. The lungs can collapse completely, and the trachea and heart shadow shift to the healthy side. The pleural cavity is punctured with high-pressure gas flushing out. Symptoms improved after inspiratory symptoms, but they became worse soon, and this performance also helped diagnosis. Severe chest injuries, such as rapid signs of tension pneumothorax, may cause bronchial rupture, and should be promptly rescued, or even a thoracotomy. Tension pneumothorax should be vented immediately to reduce the pressure in the pleural cavity.

Chest pain check

Myocardial injury markers

Traditional myocardial injury markers include cTn, CK-MB, myoglobin and other biomolecules that reflect myocardial cell necrosis. In recent years, a variety of new biomarkers such as ischemic modified proteins and heart-type fatty acid binding proteins have also been gradually applied to the clinic. Myoglobin rises within 2 hours after onset, and peaks within 12 hours; it returns to normal within 24 to 48 hours. Troponin I (cTnI) or T (cTnT) increased 3 to 4 hours after the onset, cTnI peaked at 11 to 24 hours, normalized at 7 to 10 days, and cTnT peaked at 24 to 48 hours, 10 ~ 14 days to normal. The increase of these myocardial structural proteins is a sensitive indicator for the diagnosis of myocardial infarction. Creatine kinase isoenzyme CK-MB increased. Increased within 4 hours after onset, peaked in 16 to 24 hours, and returned to normal within 3 to 4 days. The degree of increase can more accurately reflect the scope of infarction.

The measurement of myocardial necrosis markers should be comprehensively evaluated. If myoglobin appears earliest after AMI, it is also very sensitive, but the specificity is not very strong; cTnT and cTnI appear slightly delayed, and the specificity is very high. If it is negative within 6 hours after the symptoms appear, it should be re-applied after 6 hours Re-examination has the disadvantage that the duration can be as long as 10 to 14 days, which is not good for chest pain during this period and judging whether there is a new infarction. Although CK-MB is not as sensitive as cTnT and cTnI, it has important value for the diagnosis of early (<4 hours) AMI.

2.D-dimer

D-dimer is a soluble degradation product produced by cross-linked fibrin under the action of fibrinolytic system. It is a specific marker of fibrinolytic process and can be used as a screening indicator for acute pulmonary embolism. D-dimer <500ug / L, can basically exclude acute pulmonary thromboembolism.

3. ECG

All patients undergoing chest pain need an electrocardiogram. The first electrocardiogram should be completed within 10 minutes of receiving the patient. Electrocardiogram is an important method to diagnose ischemic chest pain.

4. Echocardiography

Echocardiography is also an important non-invasive test for diagnosing patients with chest pain. If new contradictory motions of the wall are found, free endometrial flaps appear in the aorta, the right heart is dilated and the left ventricular septum is "D" shaped, etc. Assist in the diagnosis of acute myocardial infarction, aortic dissection and acute pulmonary embolism. For other non-fatal chest pains, such as stress cardiomyopathy and pericardial effusion, echocardiography also has important diagnostic value.

5. Cardiac stress test

Cardiac stress tests include treadmill exercise tests, stress echocardiography, and myocardial nuclide perfusion imaging. Various stress tests can help to diagnose ischemic chest pain. However, heart stress tests are contraindicated for hemodynamic disorders, fatal chest pain, severe aortic stenosis, and obstructive hypertrophic cardiomyopathy.

6. Chest radiograph

Chest radiographs are suitable for screening patients with chest pain of respiratory origin. The diseases that can be found include pneumonia, mediastinal and lung tumors, lung abscesses, pneumothorax, thoracic spine and rib fractures. Changes in the contours of the heart and large blood vessels can sometimes prompt patients with diseases such as aortic dissection and pericardial effusion, but they lack specificity.

7.CT

Common chest and abdomen CT scans are widely used in clinical work, and their clear imaging can provide intuitive diagnosis for most chest and abdominal diseases. Contrast-injection selective CT angiography has become the first choice for diagnosis of chest pain-related diseases such as aortic dissection and acute pulmonary embolism, and it has also become an important method for screening coronary heart disease.

Chest pain treatment principles

Corresponding treatment is given according to different causes.