Subscribe
48
Tang Li
Cardiology
About me
Beijing Boai Hospital, Cardiovascular Department, attending physician, has been engaged in clinical work in cardiac internal medicine for many years, with rich clinical experience in the diagnosis and treatment of cardiovascular diseases.
Proficient in diseases
Specializes in the diagnosis of common cardiovascular diseases such as coronary heart disease, hypertension, arrhythmia, atrial fibrillation, paroxysmal supraventricular tachycardia, heart failure, myocarditis, congenital heart disease, cardiomyopathy, and atrial septal defect.
Voices
Is moderate pulmonary hypertension serious?
Pulmonary hypertension is a common clinical condition with complex etiology, which can be caused by various cardiac, pulmonary, or pulmonary vascular diseases. The current diagnostic criteria for pulmonary hypertension are an average pulmonary arterial pressure greater than 25 mmHg at sea level in a resting state, or greater than 30 mmHg during exercise, as measured via right heart catheterization. The severity of pulmonary hypertension can be categorized based on resting average pulmonary arterial pressure levels into mild (26 to 35 mmHg), moderate (36 to 45 mmHg), and severe (greater than 45 mmHg). Echocardiography is the most important non-invasive screening method for pulmonary hypertension. Assessing the severity of moderate pulmonary hypertension not only involves the measurement of average pulmonary arterial pressure but also necessitates identifying its etiology. Since pulmonary hypertension is a disease with a complex etiology, it is crucial to first clarify the cause, and then further determine the patient's cardiopulmonary function status, whether it is in a compensatory or decompensatory stage. Additionally, it is important to determine if there are any related complications, such as pulmonary hypertension stemming from lung-induced conditions. When patients exhibit complications like pulmonary encephalopathy, acid-base imbalance, electrolyte disturbances, arrhythmias, or even shock and gastrointestinal bleeding, the severity of pulmonary hypertension can be extremely severe.
Can atrial septal defect be cured?
Atrial septal defect is a common congenital heart disease. When the defect is small, some patients may heal naturally. In recent years, with the development of interventional technology for congenital heart diseases, most patients with atrial septal defects can be completely cured through interventional treatment, and some through surgical treatment. However, some patients have a large atrial septal defect with significant left-to-right shunting, leading to severe pulmonary arterial hypertension and right heart failure, which generally results in a poor prognosis. Some patients also have complications such as atrial flutter and atrial fibrillation. Certain patients may experience right heart failure due to excessive load on the right ventricle, and these patients often have a poor prognosis.
What are the symptoms of patent ductus arteriosus?
Patients with patent ductus arteriosus may exhibit several clinical manifestations based on the amount of shunting. 1. Small shunt volume: The internal diameter of the patent ductus arteriosus is small, and the patient may exhibit no subjective symptoms. The prominent sign is a continuous machinery murmur heard at the left sternal border at the second intercostal space and below the left clavicle, accompanied by a thrill; pulse pressure may slightly increase. 2. Moderate shunt: Patients commonly experience fatigue, palpitations, shortness of breath, and chest discomfort after exertion. The heart murmur is similar in character to the above but louder, accompanied by a thrill, and widely transmitted. At times, diastolic and mild systolic murmurs caused by left ventricular enlargement, relative mitral valve insufficiency, and stenosis can be heard at the apex, with a positive vascular sign. 3. Large shunt volume: This condition in a patent ductus arteriosus often accompanies secondary severe pulmonary hypertension, leading to a right-to-left shunt. The typical murmur's diastolic component may diminish or disappear, followed by the disappearance of the systolic murmur, and only a diastolic murmur due to pulmonic valve insufficiency can be heard. Patients often exhibit cyanosis and severe clinical symptoms.
How is pulmonary hypertension treated?
The treatment of pulmonary hypertension mainly focuses on identifying the cause. For idiopathic pulmonary hypertension, treatment primarily targets vascular constriction, endothelial damage, thrombus formation, and heart failure. This is to restore the tension, resistance, and pressure of the pulmonary vessels, improve the patient's sexual function, increase cardiac output, and improve quality of life. The main treatments include: 1. Drug therapy, which includes calcium channel blockers, prostacyclin, nitric oxide, endothelin receptor antagonists, and related anticoagulants. Anticoagulants do not improve symptoms, but can slow down disease progression and improve prognosis in some aspects. However, in cases of right heart failure, hepatic congestion, and ascites, cardiotonic diuretics are used, such as digoxin and anti-calcium channel blockers, which can cause adverse reactions like decreased myocardial contractility. But these drugs should be administered under the guidance of a doctor. In advanced stages of pulmonary arterial hypertension, heart-lung transplantation may be considered.
Atrial septal defect should be consulted with the Department of Cardiology.
Atrial septal defect is a common congenital heart disease in childhood, and it is also the most common congenital heart disease in adulthood. The incidence rate of atrial septal defects is about 1/1500 live births, accounting for 5%-10% of all congenital heart diseases, and it is more common in females. Most children with atrial septal defect, in addition to being prone to respiratory infections such as colds, may have no obvious symptoms and their activities are not limited. It is generally not until adolescence that symptoms like shortness of breath, palpitations, and fatigue appear. Patients with atrial septal defects should seek treatment in departments such as cardiology, cardiovascular surgery, thoracic surgery, or pediatric cardiology.
How is hypertrophic cardiomyopathy treated?
The treatment of hypertrophic cardiomyopathy aims to improve symptoms, reduce complications, and prevent sudden death. The methods include improving ventricular compliance by reducing outflow tract obstruction, preventing thromboembolic events, and identifying high-risk patients for sudden death. Treatment needs to be individualized, and the main treatments include the following aspects: 1. Medication treatment. Drug treatment is fundamental, and drugs targeting outflow tract obstruction mainly include receptor blockers and non-dihydropyridine calcium channel blockers. For patients with congestive heart failure, targeted treatment is required. Anticoagulation treatment is necessary for patients with atrial fibrillation, and it is worth noting that for patients with chest discomfort, care should be taken to exclude outflow tract obstruction when using nitrate drugs to avoid exacerbation after use. Non-drug treatments include: 1. Surgical treatment: For patients with ineffective drug treatment and heart function class three to four, if there is severe outflow tract obstruction, septal myectomy should be considered. Currently, surgery is listed as the preferred treatment for suitable patients in consensus guidelines in both America and Europe. 2. Alcohol septal ablation; 3. Pacing therapy.
Hypertensive crisis blood pressure values
At any stage of hypertension development and other disease emergencies, severe life-threatening blood pressure increases can occur, requiring emergency treatment. Hypertensive crises include hypertensive emergencies and hypertensive urgencies. Hypertensive emergencies refer to severe blood pressure increases within a short time—hours or days—with diastolic pressure greater than 130 mmHg and/or systolic pressure greater than 180 mmHg, accompanied by severe dysfunction or irreversible damage to critical organs and tissues such as the heart, brain, kidneys, retina, and major arteries. Hypertensive urgencies may present as increased blood pressure but without obvious target organ damage.
What are the infectious causes of pericarditis?
The causes of pericarditis include the following types: first, acute nonspecific; second, tumors; third, autoimmune disorders; fourth, metabolic diseases; fifth, physical factors such as trauma and radiation; sixth, diseases of adjacent organs and tissues, such as acute myocardial infarction, pleurisy, aortic dissection, pulmonary embolism, etc. The infectious causes of acute pericarditis mainly include viruses, bacteria, fungi, parasites, and rickettsiae. Common types of pericarditis include tuberculous pericarditis and purulent pericarditis.
How to treat atrial septal defect
Typical cardiac murmur ECG and X-ray findings may suggest the presence of an atrial septal defect. An echocardiogram can confirm the diagnosis, and it should be differentiated from conditions such as anomalous pulmonary venous return, pulmonary valve stenosis, and small ventricular septal defects. For the treatment of atrial septal defects, in adult patients, if echocardiographic evidence of increased right ventricular volume load is present, the defect should be closed as soon as possible. Treatment options include interventional and open-heart surgical procedures. Before the implementation of interventional surgeries, all cases of simple atrial septal defects that have caused hemodynamic changes, with signs of increased pulmonary blood flow, enlargement of the atria and ventricles, and corresponding ECG findings, should undergo surgical treatment. In older patients with severe pulmonary hypertension, surgical treatment should be approached with caution.
Why does patent ductus arteriosus cause a decrease in diastolic pressure?
In patients with patent ductus arteriosus, since the aortic pressure is significantly higher than the pulmonary artery pressure throughout the cardiac cycle, there is continuous blood flow from the aorta into the pulmonary artery through the open duct, causing a left-to-right shunt. This increases the blood volume in the pulmonary circulation, causing dilatation of the pulmonary artery and its branches. The blood flow returning to the left heart system also increases, thereby increasing the load on the left heart and causing the left heart to enlarge. Due to the diastolic diversion of blood from the aorta to the pulmonary artery, the peripheral arterial diastolic pressure decreases and the pulse pressure increases.