Pulmonary hypertension in children

Introduction to pulmonary hypertension in children Pulmonary arterial pressure exceeds the normal maximum value called pulmonary hypertension. In general, pulmonary systolic blood pressure is higher than 4 kPa (30 mmHg), and the average pressure exceeds 2.7 kPa (20 mmHg). basic knowledge The proportion of illness: 0.1% - 0.3% Susceptible people: young children Mode of infection: non-infectious Complications: respiratory infections pneumonia

Causes of pulmonary hypertension in children

(1) Causes of the disease

Pulmonary hypertension is common in congenital heart disease, neonatal persistent pulmonary hypertension, hypoxic disorders (such as bronchial asthma, infant pneumonia, high altitude heart disease and bronchial dysplasia) and primary pulmonary hypertension.

1. Classification: (1) According to the cause: 1 Primary pulmonary hypertension: The cause of pulmonary hypertension is unknown.

2 secondary pulmonary hypertension: refers to pulmonary hypertension can be found, the most common cause of congenital heart disease in children, especially in the left to right shunt group of large ventricular septal defect, patent ductus arteriosus.

(2) Divided by degree: Generally, the division methods accepted by most scholars are:

1 pulmonary artery systolic pressure: mild to 4 ~ 5.3kPa (30 ~ 40mmHg); 5.3 ~ 9.3kPa (40 ~ 70mmHg) is moderate; > 9.3kPa (> 70mmHg) is more severe, 2 with pulmonary systolic pressure and body The ratio of arterial systolic blood pressure (Pp/Ps) is divided: Pp/Ps0.75 is severe.

(3) According to the hemodynamic characteristics are divided into: 1 passive pulmonary hypertension: due to elevated left atrial pressure and pulmonary venous pressure, pulmonary hypertension caused by pulmonary microvasculature, such as left heart failure, mitral valve disease, three rooms Heart, pulmonary venous obstruction, 2 motility pulmonary hypertension: pulmonary hypertension due to high blood flow in the pulmonary artery, such as left to right shunt congenital heart disease, 3 reactive pulmonary hypertension: pulmonary arteriolar spasm, arterial wall muscle hypertrophy Or contraction causes increased pulmonary vascular resistance, such as pulmonary heart disease, primary pulmonary hypertension, 4 occlusive pulmonary hypertension: mainly due to pulmonary embolism, varying degrees of pulmonary occlusion and pulmonary vascular bed reduction, pulmonary vascular endothelial proliferation, Smooth muscle hypertrophy, collagen accumulation, narrowing of the lumen, is a common pathological manifestation of various pulmonary hypertension.

2. Causes of secondary pulmonary hypertension: According to the principle of fluid mechanics, pulmonary artery pressure is related to pulmonary venous pressure, pulmonary vascular resistance and pulmonary blood flow, which can be expressed as: pa = pv + Rp · Qp, where pa refers to pulmonary artery pressure, pv For pulmonary venous pressure, Rp is pulmonary vascular resistance, Qp is pulmonary blood flow, and all factors that cause an increase in pa, Rp and Qp can cause pulmonary hypertension.

(1) Increased pulmonary blood flow: left-to-right shunt congenital heart disease, such as atrial septal defect, ventricular septal defect, patent ductus arteriosus, atrioventricular pathway, permanent arterial trunk and single ventricle, etc. The high pressure system is caused by an increase in Qp, and (2) pulmonary vascular disease: mainly caused by an increase in pulmonary vascular resistance (Rp).

1 diffuse pulmonary embolism: such as thrombosis, pus, amniotic fluid embolism, primary pulmonary thrombosis of hemoglobin sickle cell disease.

2 pulmonary arteritis: caused by arteritis, Raynaud's syndrome, scleroderma, systemic lupus erythematosus, polymyositis, dermatomyositis, eosinophilic syndrome, nodular arteritis and other pulmonary arteries.

(3) Pulmonary diseases: 1 Chronic obstructive pulmonary disease (COPD): seen in bronchial asthma, emphysema, chronic bronchitis, 2 diffuse interstitial or alveolar diseases: such as idiopathic pulmonary hemosiderin Septic disease, sarcoidosis, granulomatosis, pulmonary interstitial fibrosis, alveolar proteinosis, alveolar microlithiasis, 3 insufficient alveolar ventilation: primary and neuromuscular alveolar ventilation.

(4) High altitude pulmonary hypertension.

(5) Pulmonary venous hypertension: It has been mentioned that when pv is elevated, pa is also bound to rise, and the disease causing pulmonary venous hypertension is seen in Sanfangxin, mitral stenosis, complete pulmonary venous drainage and pulmonary venous obstruction.

3. The cause of primary pulmonary hypertension The cause of this disease is unclear, which may be the result of a combination of congenital factors:

(1) Similar to essential hypertension, it belongs to neuro-humoral disease.

(2) Secondary vascular disease of pulmonary arteritis.

(3) Pulmonary vascular changes in collagenous (connective tissue) diseases.

(4) Results of chronic microembolism embolization.

(5) Family hereditary, the literature reported that 63 of the 25 family members had pulmonary hypertension, one thing is certain, there is no congenital heart and lung disease in primary pulmonary hypertension.

(two) pathogenesis

1. Pulmonary artery structure and blood flow

(1) Pulmonary artery structure: The pulmonary artery is divided into three segments from histology:

1 elastic artery segment: outer diameter greater than 1mm, parallel with the bronchus, rich in ring-shaped elastic fibers, less muscle tissue.

2 muscle type arteries: this segment is parallel with the bronchioles, respiratory bronchioles and alveolar ducts. The wall has more muscle tissue, the wall is thin, the lumen is large, and although the wall has contraction and diastolic function, the resistance is not large. , its outer diameter <1mm.

3 small arterial segment: from the alveolar duct, the outer diameter of the alveolar wall is <80m, the muscle layer is absent, leaving only the endothelial cell layer.

(2) Pulmonary blood flow distribution: The main pulmonary artery is short and thick, less than 4cm from the bottom of the right ventricle, that is, divided into two left and right, the right pulmonary artery accounts for 55% of the total blood flow, and the left pulmonary artery accounts for 45%. 2. The pulmonary circulation regulates the pulmonary circulation. A relatively low-pressure, low-resistance and dilatant system, in the regulation of the pulmonary circulation, passive regulation plays a very important position, followed by active regulation and body fluid regulation.

(1) Passive regulation of the pulmonary circulation; the most influential factors are blood hydrostatic pressure and cardiac output.

1 blood hydrostatic pressure: pulmonary blood vessels are divided into 2 categories: one is alveolar vessels, directly under the influence of alveolar pressure, mainly pulmonary capillaries; the other is extra-alveolar vessels, It includes blood vessels in the lung parenchyma and blood vessels outside the lung parenchyma. Among them, the alveolar blood vessels and the blood vessels in the lung parenchyma are affected by the hydrostatic pressure of the blood and the inflated state of the lungs. When the normal person is erect, the tip of the lung is about 30 cm higher than the bottom of the lung. Because of the gravity of the blood, the hydrostatic pressure in the bottom of the lung is 3.1 kPa (23 mmHg) higher than the tip of the lung. This pressure difference makes the blood of the whole lung from the top. And gradually increase, the difference between the upper and lower can reach 5 to 10 times, which will affect the intrapulmonary pressure and its pressure difference with the alveolar pressure and affect the distribution of pulmonary blood flow. According to the results of West in vitro lung perfusion preparation experiments, the lungs were divided into three zones from top to bottom. PA, Pa, and Pv represent alveolar pressure, alveolar arterial pressure and venous pressure, respectively. Under normal circumstances, Pa>PA, the blood push pressure is positive; and whether the alveolar blood vessels can remain unobstructed depends on the trans-wall pressure (Pa-PA), Pa>PA vascular patency, Pa PA, capillary passive expansion, blood Through, in the diastolic phase of the heart, Pa is lowered, PaPv>PA, the transmural pressure is positive, and the alveolar blood vessels are mostly dilated, which is the blood hydrostatic effect caused by gravity.

2 changes in cardiac output on the pulmonary circulation: alveolar blood vessels have great compliance, pulmonary artery pressure slightly increased, that is, significant passive expansion; some alveolar blood vessels are not open when the cardiac output and pulmonary artery pressure are normal, but high At cardiac output, a slight increase in pulmonary arterial pressure is sufficient to open this part of the blood vessel and increase the new blood flow path. According to the Poiseuille formula R=P/Q, pulmonary vascular resistance (R) and pulmonary blood flow (Q) In contrast, when pulmonary arterial pressure (P) is constant or slightly elevated, and pulmonary blood flow increases, pulmonary vascular resistance decreases or does not change much. In the early stage of left-to-right shunt congenital heart disease, pulmonary blood flow increases a lot but Pulmonary vascular resistance is associated with normal or slightly elevated pulmonary arterial pressure, and this change is not related to alveolar vascular compliance and vascular opening.

(2) Active regulation of pulmonary circulation: The basis of active regulation of pulmonary circulation is that pulmonary vascular smooth muscle produces a contractile response under the action of nerves, body fluids and chemical factors as well as self-regulation of blood vessels, which causes changes in vascular resistance and pulmonary artery pressure.

1 pulmonary circulatory neuromodulation: A. pulmonary innervation: pulmonary vasculature is mainly dominated by sympathetic nerve and vagus nerve, most of the nerve fibers are located in the outer edge of the muscular layer of vascular smooth muscle 5 ~ 10m, the larger elastic artery has more nerve distribution than the muscle Pulmonary artery; pulmonary artery with an outer diameter of less than 30m has no nerve distribution, so the level of pulmonary arteriole is less likely to affect vascular resistance and change blood flow through neuromodulation. B. Regulation of autonomic nervous system: central nervous system through autonomic nerve The pulmonary circulation is regulated to stimulate the sympathetic nerves of the chest, the cervical sympathetic ganglia and the stellate nerves cause energy-induced pulmonary hypertension, and it is confirmed that this increase is caused by pulmonary vasoconstriction. C. Peripheral chemoreceptors and baroreceptors reflect: Any one of the central efferent and afferent nerves to cut off the carotid body chemoreceptor reflex arc can significantly enhance the pulmonary artery pressure response caused by hypoxia, thus suggesting that the reflex participates in the regulation of pulmonary circulation during hypoxia, and to a certain extent Increased cardiac output, compensates for hypoxia, and delays hypoxic pulmonary artery The role of the development process.

2 Humoral regulation of the pulmonary circulation: Many biologically active substances are activated, inactivated, synthesized or released in the lungs. Many of the biologically active substances play an important role in pulmonary vasomotor, especially in the regulation of pulmonary circulation. In terms of body fluid regulation, humoral regulation plays an important role, and does not require nerve involvement, histamine release; angiotensin II; prostaglandins, especially PGF2a, PGD2, PGE2 and TXA2; leukotrienes, especially LTC4, LTD4, etc. have pulmonary vasoconstriction Role, newly discovered endothelial-derived cells produce and release endothelium-dependent relaxation factor (EDRF), which directly acts on smooth muscle cells, activates soluble cytoplasmic soluble cytosolic cyclase in smooth muscle cells, increases cGMP, and promotes protein phosphorylation. Relaxing vascular smooth muscle and vasodilating, endothelial cells can also release some growth factors, directly stimulate vascular smooth muscle cell hypertrophy and proliferation. 3. The basic mechanism of pulmonary hypertension The basic mechanism of pulmonary hypertension can be explained simply by Ohm's law, Rp= (pa- Pv) / Qp, Rp represents pulmonary circulation resistance; Qp represents pulmonary blood flow; pa represents pulmonary artery mean pressure, pv represents Mean venous pressure, this equation can be collated: pa = pv + Rp × Qp can be seen from the formula, when the pulmonary venous pressure and pulmonary blood flow or pulmonary vascular resistance, pulmonary arterial pressure can be increased.

(1) increased pulmonary venous pressure: various causes of long-term reversible pulmonary venous hypertension caused by pulmonary capillary pressure and pulmonary artery pressure increase, when the pulmonary capillary pressure exceeds the blood colloid osmotic pressure, the intravascular fluid exudates to the interstitial space, making the lung Reduced compliance, resulting in alveolar hypoxia and pulmonary vasoconstriction, aggravating pulmonary hypertension.

(2) Increased pulmonary vascular resistance: When liquid flows through a cylindrical tube, its resistance, pressure and flow relationship can be determined by the formula modified by Pois-suille: R = (8) (l/kr4) (), where R is the resistance l is the length of the tube, r is the radius of the tube, and is the viscosity of the liquid. The length of the blood vessel has no significant change before and after the disease. The main factors affecting the pulmonary vascular resistance are the varying viscosity , the lumen radius and the number of blood vessels.

1 viscosity change: viscosity changes are often caused by polycythemia, increased hematocrit increases viscosity, affects pulmonary vascular resistance, pulmonary vascular resistance and red blood cell ratio product is roughly logarithmic.

2 changes in the number of blood vessels: A. Pulmonary vascular bed reserve: When the number of pulmonary vessels is reduced, other pulmonary vessels are compensatoryly dilated and open. According to the study, when the number of pulmonary vessels is reduced by more than 75%, the resting pulmonary artery pressure may rise. Pulmonary vascular bed storage capacity is very large, but in neonates, infants have limited storage of pulmonary vascular beds. This is due to the small number of pulmonary vessels in the newborn, the small number of pulmonary vessels in the baby, and the limited opening of the blood vessels, which restricts the expansion of blood vessels. The pulmonary vascular resistance is increased, and pulmonary hypertension occurs. B. The number of alveolar arteries is reduced: the alveolar arteries accompanying acinar growth are developed until 8 to 10 years old. The alveolar artery is the key vascular segment that controls pulmonary circulation and gas exchange. The ratio of the lower alveolar artery to the alveoli is 1:10. The alveolar artery and alveoli are growing at the same time. The ratio of the two is fixed. In patients with increased pulmonary vascular resistance, the ratio of alveolar artery to alveoli is reduced to 1:30, ie about 2/3 of the alveoli. Development, pulmonary vascular bed is significantly reduced, accelerating pulmonary vascular resistance and pulmonary hypertension.

3 reduction of the inner diameter of the vascular lumen: whether the reduction of the lumen diameter causes an increase in pulmonary artery pressure, which is mainly determined by the number of affected vessels, resulting in a decrease in the lumen diameter: A. External compression or contraction of the blood vessel: pulmonary edema, enlarged left atrium Squeeze the airway, causing alveolar hypoxia and pulmonary vasoconstriction, B. Pulmonary vascular wall thickening: thickening of the pulmonary vascular wall will narrow the vascular lumen, thickened muscle layer or eccentric endometrium caused by thrombosis Thickening, congenital heart disease, pulmonary hypertension and pulmonary vascular resistance are important reasons for hypertrophy of the pulmonary vascular wall, C. increased pulmonary blood flow: when the congenital heart disease is more than twice the normal cardiac output, pulmonary artery pressure There may be no change. This is due to the compensatory dilatation of pulmonary vasculature. When the flow rate is further increased and exceeds the limit of pulmonary vasodilation, dynamic pulmonary hypertension will occur. It should be noted that the increase of pulmonary blood flow itself does not necessarily cause pulmonary hypertension, often As a result of obstruction of the pulmonary arterioles and increased resistance after stenosis, because the pulmonary arteriolar resistance is inversely proportional to the fourth power of the pulmonary arteriole radius, some scholars have observed that large chambers Septal defect often has obvious pulmonary mesenteric hypertrophy and stenosis of the lumen at 2 months after birth.

4. Pathological changes of pulmonary hypertension

(1) The basic pathological changes of dynamic pulmonary hypertension: dynamic pulmonary hypertension can cause plexus pulmonary artery disease, and early stage of plexus pulmonary artery disease is thickening of muscle type pulmonary artery, muscle formation of fine arteries, cell intimal hyperplasia and tube The cavity is narrowed; the lesion develops further, and the collagen and elastic fibers increase, causing the intimal fibrosis of the lamellar arrangement. This kind of concentric lamellar intima fibrosis can completely occlude the lumen, and expandability can occur later. Changes, cellulose-like necrosis, arteritis and plexiform lesion formation.

(2) Classification of pathological changes: high-dynamic pulmonary hypertension, Heath et al first proposed a 6-level classification: grade I showed pulmonary hypertrophy; grade II was pulmonary hypertrophy and endometrial cell hyperplasia; grade III showed pulmonary obstructive endometrium Fibrosis; grade IV plexiform lesions; grade V on the basis of the first 4 grades of pulmonary dilatation lesions; grade VI with necrotizing pulmonary arteritis, Department of Pathology, Fuwai Hospital, proposed a four-level classification: Heath describes I, II lesions Classified as Class I (mild); Class II is Class III (moderate) of Heath classification; Class III is Class IV and V (heavy) in Heath classification; Class IV is Class VI of Class of Heath (very severe), It is also suggested that grade I and grade II lesions are reversible; grade III is a critical lesion, and patients have persistent pulmonary hypertension after surgery, but some can almost return to normal, while grade IV, V, and VI have highly fixed pulmonary vascular resistance. Extensive and irreversible obstructive pulmonary vascular disease.

(3) Relationship between lesion grading and mean pulmonary artery pressure and total resistance: According to the study of : the average pulmonary artery pressure is above 6.7 kPa (50 mmHg), the total resistance is >1000 dyn·s·cm -5 belongs to III, grade IV lesions, most of which die. In the complications of pulmonary hypertension, when the mean pulmonary artery pressure is less than 6.7 kPa (50 mmHg), the total resistance is 600-800 dyn·s·cm-5, and the moderate increase is due to reasons other than pulmonary hypertension, and the two-way shunt is proposed. Dividing congenital heart disease to grade III and IV lesions to the right, suggesting that most patients with multi-directional shunt have advanced pulmonary vascular disease.

Pediatric pulmonary hypertension prevention

Secondary pulmonary hypertension is related to congenital heart disease. The current cause of primary pulmonary hypertension is still unclear. The occurrence of congenital heart disease is a comprehensive result of various factors. To prevent the occurrence of congenital heart disease, publicity and education of popular science knowledge should be carried out. Focus on monitoring the age-appropriate population and give full play to the role of medical staff and pregnant women and their families.

1. Get rid of bad habits, including pregnant women and their spouses, such as smoking, alcohol and so on.

2. Actively treat diseases affecting fetal development before pregnancy, such as diabetes, lupus erythematosus, anemia, etc.

Pediatric pulmonary hypertension complications Complications, respiratory infection, pneumonia

Often complicated by respiratory infections, pneumonia and heart failure, Eisenmenger syndrome in the late stage, children often growth retardation, nutritional disorders.

Pediatric pulmonary hypertension symptoms common symptoms arrhythmia bradycardia systolic murmur lifting pulsation heart murmur fatigue labor dyspnea cerebral venous angulation right heart dysfunction

Secondary pulmonary hypertension

(1) Symptoms: In addition to the clinical symptoms of the original underlying diseases, the symptoms of pulmonary hypertension itself are non-specific. The general symptoms of pulmonary hypertension are not obvious in the early stage. Once the clinical symptoms appear, the patients with advanced pulmonary hypertension have reached the stage of advanced disease. Due to decreased cardiac output, oxygen transport is limited, and patients with hypoxia are prone to fatigue and weakness. As pulmonary vascular compliance declines, cardiac output cannot increase with exercise. Patients exhibit labor dyspnea and sudden decrease in brain tissue oxygen supply. Caused by syncope, arrhythmia can also occur, especially bradycardia, due to right ventricular hypertrophy, myocardial insufficiency in patients with blood supply may have angina, if the pulmonary artery dilates the recurrent laryngeal nerve, there may be hoarseness.

(2) Physical examination: As the pulmonary artery pressure increases, it can cause right atrial enlargement and functional failure. Common signs include right ventricular lift pulsation and pulmonary artery pulsation. Palpation can be found in the pulmonary valve area. Cardiac auscultation can find P2 reluctance, systolic jet sounds in the pulmonary valve area and diastolic murmur caused by relative pulmonary regurgitation, and signs of right heart dysfunction such as jugular vein engorgement, liver enlargement, liver neck Venous reflux, edema of both lower extremities.

2. Primary pulmonary hypertension

The clinical symptoms of pulmonary hypertension often occur in childhood, and more than 5 years after birth, symptoms occur, but also occur in infancy, manifested as feeding difficulties, growth and development, shortness of breath, fatigue, fatigue, the main symptoms in childhood is exercise Difficulty breathing, fainting during exercise, pain in the anterior region, due to decreased stroke volume, the disease in the neonatal period due to pulmonary hypertension can cause venous blood flow through the foramen ovale from the right atrium to the left atrium, so that arterial blood Oxygen saturation is reduced, clinically may have cyanosis, this is called continuous fetal blood circulation (PFC), cardiac auscultation is mainly P2 reluctance, most no noise, occasional systolic murmur, may be caused by tricuspid regurgitation, due to right Ventricular ejection resistance increases, systolic load is too heavy, so there may be signs of right heart failure such as hepatomegaly and jugular vein engorgement. The clinical manifestations of left-to-right shunt congenital heart disease depend on the nature of the lesion and the size of the sub-flow. Small flow rate is generally not easy to cause obvious hemodynamic abnormalities, pulmonary vascular resistance is normal, pulmonary hypertension is not easy to occur, so clinically long-term asymptomatic or mild symptoms Divided left-to-right shunt congenital heart disease, especially in children after tricuspid shunt, often have respiratory infections, pneumonia and chronic heart failure. After 1 to 2 years of age, due to elevated pulmonary artery pressure, left to right The flow rate is reduced, the symptoms are gradually relieved, and there are no obvious symptoms in the next few years. The symptoms of Eisenmenger syndrome appear slowly in childhood, which is characterized by shortness of breath after activity, decreased activity, slow growth, cyanosis, and mild symptoms. Finger toe, at this time, arterial oxygen saturation has decreased, the original murmur was found to be relieved during physical examination, P2 was significantly hyperactive with a sense of stimuli, and II-III jet systolic murmurs were often heard in the second intercostal space on the left sternal border.

Examination of pulmonary hypertension in children

Diagnosis is based on medical history, physical examination, X-ray examination and laboratory data. Even if a positive pressure is used to supply 100% oxygen, the child may still have hypoxemia. If the child has primary pulmonary hypertension, the chest X-ray shows that the lung is completely normal, but can show substantial lung disease (such as meconium aspiration syndrome or neonatal pneumonia) or congenital diaphragmatic hernia. Echocardiography was used to evaluate cardiac conditions to rule out congenital heart disease and to determine the presence of pressure in the pulmonary arteries that exceeded the systemic circulation.

Increased pulmonary vascular resistance can lead to pulmonary hypertension and right to left shunt, aggravating hypoxia and acidosis, and improving these symptoms by increasing oxygen partial pressure and pH. Therefore, for any newborn who is close to term and has arterial hypoxemia, the presence of persistent pulmonary hypertension in the neonate should be suspected and treated as early as possible to prevent further progression.

Because such a patient has a large number of right-to-left shunts through an open arterial catheter, the oxygen partial pressure of the right arm artery is higher than the oxygen partial pressure of the descending aorta. If a pulse photo oximeter is placed in both the right hand and the lower extremity, the foot oxygen saturation is shown to be low, demonstrating that the right to left shunt level is in the arterial catheter.

Ultrasound Doppler examination

This method can rule out the presence of congenital heart disease and can assess pulmonary artery pressure.

(1) Indirect signs of pulmonary hypertension

1 The ratio of right ventricular systolic and right ventricular systolic time (PEP/RVET) can be measured by M-ultrasound or Doppler method. The normal rate is generally about 0.35, and the chance of pulmonary hypertension is >0.5.

The Doppler method was used to measure the pulmonary artery blood flow acceleration time (AT) and the acceleration time/right ventricular ejection time ratio (AT/RVET), and the value was reduced, suggesting pulmonary hypertension.

3 Doppler was used to measure the mean blood flow velocity of the left or right pulmonary artery. The decrease of the flow velocity indicated an increase in pulmonary vascular resistance and pulmonary hypertension. The normal value of the above indicators varies greatly, but the series of dynamic observations have certain significance for evaluating the therapeutic effect of PPHN.

(2) direct signs of pulmonary hypertension

1 Two-dimensional color Doppler ultrasound is used to display the open arterial catheter in the high left sternal section. The right to left shunt, bidirectional shunt or left to right shunt can be determined according to the blood flow direction of the catheter. The Doppler sampling point was also placed in the arterial catheter, and the pulmonary artery pressure was calculated by simplifying the Bemoulli equation (pressure difference = 4X velocity ^ 2) according to the flow rate and the reference to the systemic circulation pressure.

2 Using tricuspid regurgitation in children with pulmonary hypertension, continuous flow rate was measured by continuous Doppler to simplify the calculation of pulmonary artery pressure by Bernoulli equation: pulmonary systolic pressure = 4x reflux blood flow velocity ^ 2 CVP (assuming CVP It is 5mmHg). When the pulmonary systolic pressure is 75% of systemic systolic blood pressure, pulmonary hypertension can be diagnosed.

3 by color Doppler direct observation of the atrial level through the right to left shunt of the foramen ovale, if not displayed, you can also use 2 ~ 3m1 saline through the upper limb or scalp vein (better central vein), such as seeing at the same time The "snowflake" shadow is entered into the left atrium by the right atrium, which confirms the right to left shunt.

Diagnosis and diagnosis of pulmonary hypertension in children

diagnosis

Early diagnosis of pulmonary hypertension is quite difficult. Moderate-severe pulmonary hypertension has caused right heart hypertrophy. Workers with strain or right heart failure are more likely to be diagnosed, but the disease has reached the advanced stage of the disease. Therefore, early diagnosis of pulmonary hypertension is very important, complete diagnosis. Should include confirmation of elevated pulmonary arterial pressure, determine the impact of pulmonary hypertension on the heart, respiratory system and the cause of pulmonary hypertension, congenital heart disease and chronic lung disease are common causes of pulmonary hypertension, fatigue, exertional dyspnea and syncope It is often the earliest and only symptom of pulmonary hypertension that cannot be explained. P2 is the main sign of pulmonary hypertension. Heart murmur is helpful in judging congenital heart disease or rheumatic valvular disease, combined with X-ray, electrocardiogram, echocardiography and heart. Catheter examination can confirm the diagnosis of primary PH after congenital heart disease.

Differential diagnosis

Attention should be paid to the identification of primary and secondary PH:

Secondary pulmonary hypertension

Has caused right heart hypertrophy, strain or right heart failure is easier to diagnose PH, but the patient's condition is often critical, has reached the late stage of the disease, treatment is difficult, the prognosis is not good, therefore, early diagnosis of pulmonary hypertension should be done to find pulmonary hypertension The cause, congenital heart disease and chronic lung disease are common causes of pulmonary hypertension. Heart murmur helps to determine congenital heart disease or rheumatic valvular disease, but the original heart murmur may be alleviated or disappeared during pulmonary hypertension. Pulmonary artery High-pressure electrocardiogram is characterized by excessive systolic load in the right ventricle. If left atrial or left ventricular hypertrophy is often the cause of pulmonary hypertension, it may be cardiogenic. X-ray examination is also characteristic, and it is helpful to find the cause of pulmonary hypertension. X-ray diagnosis of lung disease is obvious, large pulmonary venous blood redistribution and Kerleys B line reflect pulmonary venous hypertension. Pulmonary blood increase is mainly seen in left to right shunt congenital heart disease, mitral stenosis, left atrial enlargement Large and valvular calcification can be found, and echocardiography can accurately determine the degree of pulmonary hypertension and changes in cardiac structure. Right heart catheterization can measure the extent of pulmonary hypertension, estimate whether it is reversible, selective pulmonary angiography (including DSA) to find thrombosis, vascular malformation, hypoplasia or stenosis, and lung biopsy for unexplained pulmonary hypertension Further confirm the diagnosis.

2. Primary pulmonary hypertension

Any patient with unexplained exercise dyspnea, fainting during exercise, should be suspected of this disease, if P2 is reluctant, combined with X-ray, ECG, echocardiography and cardiac catheterization, after congenital heart disease can be ruled out Confirmed diagnosis.

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