chronic cor pulmonale
Introduction
Introduction to chronic pulmonary heart disease Chronic pulmonary heart disease (chroniccorpulmonale), referred to as pulmonary heart disease, is caused by lung tissue, pulmonary artery or thoracic chronic lesions causing abnormal lung structure and function, resulting in increased pulmonary vascular resistance, increased pulmonary artery pressure, right heart expansion, hypertrophy Heart disease with or without right heart failure. It can happen to the elderly, but most of them are developed from the middle age. Most of the elderly patients with pulmonary heart disease develop from chronic obstructive pulmonary disease (COPD), and its incidence is very high, especially in the smokers, and it is increasing year by year. basic knowledge The proportion of the disease: the incidence rate of the elderly over 60 years old is about 0.03% - 0.05% Susceptible population: occurs in the elderly, most of which are developed from the middle age Mode of infection: non-infectious Complications: heart failure multiple lung infections respiratory failure pulmonary encephalopathy arrhythmia shock diffuse intravascular coagulation upper gastrointestinal bleeding multiple organ dysfunction syndrome
Cause
Causes of chronic pulmonary heart disease
Bronchial and pulmonary lesions (85%)
Chronic obstructive pulmonary disease (COPD) caused by chronic obstructive emphysema is the most common. COPD is the most common cause of senile pulmonary heart disease, followed by bronchial asthma, bronchiectasis, severe tuberculosis, pneumoconiosis, chronic diffuse pulmonary interstitial fibrosis (including idiopathic pulmonary interstitial fibrosis and secondary pulmonary fibrosis) ), pulmonary radiation therapy, sarcoidosis, allergic alveolitis, eosinophilic granuloma, cryptogenic diffuse interstitial pneumonia, alveolar hard rock disease.
Thoracic dyskinesia (5%)
Less common, severe posterior spine, scoliosis, spinal tuberculosis, rheumatoid arthritis, extensive pleural adhesions and severe thoracic or spinal deformities caused by thoracoplasty, severe pleural hypertrophy, obesity with inadequate pulmonary ventilation, sleep breathing Disorders and neuromuscular diseases such as polio can cause thoracic activity limitation, lung compression, bronchial distortion or deformation, resulting in limited lung function, poor airway drainage, repeated lung infection, emphysema, or fiber Chemotherapy, hypoxia, pulmonary vasoconstriction, stenosis, increased resistance, pulmonary hypertension, development into pulmonary heart disease.
Vascular lesions (2%)
Rarely, allergic granulomatosis involving the pulmonary artery, extensive or recurrent multiple pulmonary embolism and pulmonary arteritis, and unexplained primary pulmonary hypertension can narrow and block the pulmonary arterioles. Caused by increased pulmonary vascular resistance, pulmonary hypertension and right ventricular overload, develop into pulmonary heart disease, occasionally in the pulmonary artery and pulmonary vein compression, such as mediastinal tumors, aneurysms, etc., can also be seen in primary pulmonary hypertension.
Other factors (5%)
Repeated pulmonary infection, hypoxemia and toxemia may cause myocardial damage and arrhythmia, and even heart failure; primary alveolar ventilation and congenital oropharyngeal malformations, sleep apnea syndrome, etc. can also lead to pulmonary origin Sexual heart disease; others can be seen after pneumonectomy and high altitude hypoxia, these diseases can produce hypoxemia, increase pulmonary vasoconstriction, leading to pulmonary hypertension, develop into pulmonary heart disease. In addition, sputum poisoning, progressive systemic sclerosis, disseminated lupus erythematosus, dermatomyositis, etc. can also induce the disease.
Pathogenesis
1. Pathogenesis: Pulmonary capillary bed destruction in chronic pulmonary and chest diseases reduces vascular bed area, hypoxia and respiratory acidosis caused by airflow obstruction can cause pulmonary arteriospasm, secondary erythrocytosis caused by chronic hypoxia Factors such as increased blood viscosity can lead to increased pulmonary circulation resistance, pulmonary hypertension, increased right heart load, right ventricular hypertrophy, and development of pulmonary heart disease.
(1) Pulmonary hypertension: pulmonary hypertension (PAH) is an important pathophysiological stage of chronic pulmonary heart disease. In the early stage of pulmonary hypertension, if the cause can be removed in time, or symptomatic treatment is appropriate, it is possible to reverse the lesion or block. Further development of the lesion; in the advanced stage of pulmonary hypertension, the lesion is in an irreversible stage and the treatment is difficult.
1 pulmonary vascular organic changes: repeated peri-bronchitis, interstitial inflammation, which affects the branching of adjacent pulmonary arterioles, resulting in thickening of the arterial wall, stenosis or fibrosis, greatly reducing the area of pulmonary capillary bed, lung circulation resistance Increase, long-term pulmonary circulation resistance increase, can make small arteries hyperplasia, increase pulmonary circulation resistance, resulting in a vicious circle. In the factors affecting pulmonary hypertension, the reduction of pulmonary vascular bed area has a certain effect, but if the degree is light, the range Smaller, the increase in pulmonary artery pressure is not obvious, only when the pulmonary capillary bed area is reduced by more than 70%, the pulmonary artery pressure is significantly increased.
When there is obvious emphysema in severe COPD, the alveoli are over-inflated, and most of the alveolar spaces are ruptured and fused to form a bullous bullous, which also leads to a decrease in the alveolar wall capillary bed, an increase in the alveolar residual gas in the emphysema, and an increase in the alveolar pressure. The capillaries of the alveolar wall are compressed to narrow it. In addition, obstructive emphysema, the patient's expiratory phase is significantly prolonged, up to 5 times the inspiratory phase, and the pressure in the alveoli during exhalation is significantly increased, and the lung wall is compressed. Blood vessels and heart, so that the blood of the pulmonary artery can not be perfused smoothly, can also affect pulmonary artery pressure.
In addition, pulmonary vascular diseases such as primary pulmonary hypertension, recurrent pulmonary vascular embolism, pulmonary interstitial fibrosis, pneumoconiosis, etc., can cause pulmonary vascular stenosis, occlusion, resulting in increased pulmonary vascular resistance, the development of pulmonary hypertension.
2 pulmonary vascular functional changes: hypoxic pulmonary vasoconstriction, which is the most extensive and in-depth mechanism of current research, which can be summarized as the following aspects.
A. Humoral factors: Pulmonary inflammation can activate inflammatory cells including mast cells, eosinophils, basophils and macrophages, releasing a range of inflammatory mediators such as histamine, serotonin (5-HT), Angiotensin 11 (AT-II), and arachidonic acid (AA) metabolites, including leukotrienes, thromboxane (TXA2), prostaglandin F2 (PGF2), prostacyclin (PGl2), and prostaglandin E1 ( PGE1), etc., except for PGl2 and PGE1 causing pulmonary vasodilation, all of the above mediators cause pulmonary vasoconstriction. However, the contraction response of pulmonary vessels to hypoxia depends to a large extent on the proportion of local vasoconstrictor and vasodilator media. If the vasoconstrictor medium increases, the proportion increases, which may lead to pulmonary vasoconstriction.
B. Tissue factors: hypoxia can directly increase the permeability of pulmonary vascular smooth muscle membrane to Ca2, increase Ca2 influx, increase muscle excitability-contraction coupling, cause pulmonary vasoconstriction, and alveolar CO2 partial pressure (PAC02) Ascending can cause local pulmonary vasoconstriction and bronchodilation, in order to adjust the ratio of ventilation/blood flow, and ensure the oxygenation of pulmonary vein blood. There is an imbalance of pulmonary adrenergic receptors after hypoxia, which makes the contraction of pulmonary vessels predominate.
C. Neurological factors: Hypoxia and hypercapnia can stimulate carotid sinus and aortic chemoreceptors, reflexively through sympathetic excitation, increased secretion of catecholamines, and contraction of pulmonary arteries.
3 Pulmonary vascular reconstruction: Pulmonary vascular changes in hypoxic pulmonary hypertension are mainly manifested in the myometrium of less than 60 m non-muscle pulmonary arterioles, thickening of the pulmonary arterioles greater than 60 m, intimal fibrosis, subendometrial The longitudinal muscle bundle appears, as well as the increase of elastic fibers and collagen fibrous matrix, which makes the blood vessels hard and the resistance increases. The structural changes of these pulmonary vessels are called remodeling, and the mechanism may be under the action of stimulating factors such as hypoxia. , a variety of growth factors produced inside and outside the lungs, resulting in a series of changes.
4 increased blood volume and increased blood viscosity: severe COPD can occur chronic chronic hypoxia, increased erythropoietin secretion, resulting in increased secondary erythropoiesis, increased pulmonary vascular resistance, COPD patients also have pulmonary capillary bed area Reduced and decreased pulmonary vascular compliance, the compensatory expansion of vascular volume is significantly limited, and thus pulmonary blood flow can increase, can cause pulmonary hypertension.
(2) Changes in right heart function: The factors affecting right heart function in chronic lung disease are mainly due to the increase of right heart and back load caused by pulmonary hypertension. After the increase of right ventricular afterload, the myocardial oxygen consumption is increased due to the increase of ventricular wall tension; Increased arterial resistance, decreased blood flow; increased pulmonary vascular input impedance, decreased compliance and impaired right heart function. In addition, hypoxemia has direct damage to the myocardium, right ventricular in the case of chronic stress overload, right The walls of the chamber are hypertrophied to overcome the increased afterload to maintain normal pump function.
When the respiratory tract is infected, the hypoxia is aggravated or other reasons cause the pulmonary artery pressure to increase further than the right ventricle can bear, the right ventricle discharges blood is not complete, the residual blood remaining in the end of systole is too much, and the right ventricular end-diastolic pressure is increased. The right ventricular dilatation is aggravated, eventually leading to heart failure.
2. Pathology
(1) The main primary lesions of the lungs: Although the causes of chronic pulmonary heart disease are various, the main primary diseases of the lungs of chronic pulmonary heart disease in China are chronic bronchitis and obstructive emphysema.
(2) Pulmonary vascular disease: In chronic pulmonary heart disease, it is often observed:
1 The wall of the pulmonary artery is thickened and the lumen is narrowed or occluded.
2 The destruction and reduction of the capillary wall of the alveolar wall is not only a manifestation of chronic pulmonary heart disease, but also an important reason for aggravating and promoting the development of chronic pulmonary heart disease.
3 compression of the pulmonary vascular bed, extensive fibrosis of the lungs, contraction of scar tissue, severe emphysema, etc. can compress the pulmonary blood vessels to make them deform and twist.
(3) Heart disease: In chronic pulmonary heart disease, the main lesions of the heart are increased heart weight, right heart hypertrophy, right ventricular muscle thickening, ventricular cavity enlargement, pulmonary artery conization, apical bluntness, light microscopic observation, common heart Muscle fibers showed varying degrees of hypertrophic changes, characterized by thickening of myocardial fibers, deep nuclear staining, irregular shape, square or rectangular, myocardial fibers with focal sarcoplasmic lysis or focal myocardial fibrosis or fibrosis, between the myocardium Quality edema, inflammatory cell infiltration, fibrosis of the atrioventricular bundle, small infiltration of fat in the form of small pieces, small blood vessel dilation, reduction of conduction beam fibers, extensive pathological edema, hyperemia, focal or punctiform hemorrhage, multiple necrosis Under electron microscope, the cell mitochondria is swollen, the endoplasmic reticulum is dilated, the sarcomere is dissolved or the length is different, and the glycogen is reduced or disappeared.
Prevention
Chronic pulmonary heart disease prevention
1. Since most chronic pulmonary heart disease is a chronic obstructive pulmonary disease (COPD), chronic bronchitis, and bronchial asthma complicated by emphysema, active prevention and treatment of these diseases is a fundamental measure to avoid the occurrence of chronic pulmonary heart disease.
2. Pay attention to hygiene, quit smoking and enhance physical fitness, improve systemic resistance, reduce the occurrence of colds and various respiratory diseases. Respiratory tract infection is a common cause of respiratory failure in patients with chronic pulmonary heart disease and should be treated actively.
3. For patients with chronic pulmonary heart disease, the treatment should be treated separately for the remission period and the acute phase. Remission treatment is the key to prevent the development of chronic pulmonary heart disease.
1 cold water to wipe the body, squat breathing, lip retraction to improve lung ventilation and other cold and rehabilitation exercises.
2 antitussive, expectorant, anti-asthmatic and prevent infections and other symptomatic treatment.
3 drugs to improve the body's immunity such as nucleic acid casein, bronchitis bacterin, immune ribonucleic acid and so on.
4 Chinese medicine treatment: Fuzheng Guben, promoting blood circulation and removing blood stasis, in order to improve the body's resistance and improve lung circulation.
Complication
Chronic pulmonary heart disease complications Complications heart failure multiple lung infection respiratory failure pulmonary encephalopathy arrhythmia shock diffuse intravascular coagulation upper gastrointestinal bleeding multiple organ dysfunction syndrome
Chronic pulmonary heart disease often has heart failure, lung infection, respiratory failure, pulmonary encephalopathy and arrhythmia, shock, diffuse intravascular coagulation, upper gastrointestinal bleeding, multiple organ dysfunction and other complications.
1. Heart failure: It is one of the main clinical manifestations of cardiac decompensation in chronic pulmonary heart disease. The main cause of right heart failure is acute respiratory infection. Inpatients with chronic pulmonary heart disease and heart failure The incidence rate is 25% to 70%.
2. Pulmonary infection: It is one of the common complications of patients with chronic pulmonary heart disease. It can occur in all seasons. It is the most common cause of acute exacerbation and death in chronic pulmonary heart disease. Streptococcus pneumoniae, influenza bacillus Infection is the main cause of acute exacerbation of chronic pulmonary heart disease.
3. Respiratory failure: refers to a series of pathophysiological changes and clinical manifestations of hypoxia and carbon dioxide retention caused by various diseases caused by pulmonary ventilation and/or ventilatory dysfunction, which may lead to hypoxia and carbon dioxide. Shigosis causes hypercapnia and hypoxemia.
4. Pulmonary encephalopathy: a clinical syndrome characterized by central nervous system dysfunction caused by severe carbon dioxide retention and hypoxia, including hypercapnia and hypoxemia. And brain symptoms caused by hyperventilation, the incidence of pulmonary encephalopathy in patients with chronic pulmonary heart disease respiratory failure is 20%, and the mortality rate is as high as 46%.
5. Arrhythmia: Chronic pulmonary heart disease patients with arrhythmia are more common, the incidence rate is about 17.2% ~ 36.8%, may have atrial premature contraction, ventricular premature contraction, sinus tachycardia, atrial fibrillation, room Ventricular block and so on.
6. Shock: There are not many shock patients with pulmonary heart disease, accounting for 7.4%, but once the prognosis is dangerous, the mortality rate is 72%.
7. Disseminated intravascular coagulation (DIC): often causes bacterial toxins in acidosis, hypoxemia and concurrent bacterial infections, causing damage to capillary endothelium and tissue damage.
8. Upper gastrointestinal bleeding: Pulmonary heart disease complicated with upper gastrointestinal bleeding accounted for about 5.7%, and the mortality rate was as high as 92%.
9. Multiple organ dysfunction syndrome: In the acute attack of pulmonary heart disease, due to pulmonary infection and other factors, resulting in respiratory insufficiency or cardiac insufficiency, multiple organ functions such as brain, kidney, liver, gastrointestinal, etc. may occur simultaneously or sequentially. Incomplete, prone to multiple organ failure, the incidence of multiple organ failure in patients with pulmonary heart disease is 30% to 50%, at this time the condition is more critical, rapid change, the mortality rate is about 50%, is chronic pulmonary heart disease The main cause of death.
Symptom
Symptoms of chronic pulmonary heart disease Common symptoms Arrhythmias, dyspnea, wheezing, confusion, right heart failure, respiratory failure, sitting breathing, wheezing, palpitations, insomnia
Pulmonary heart disease from the basic disease to the formation of pulmonary heart disease, and even the emergence of right heart failure generally takes more than ten years, or even longer, due to the long course of the disease, the basic lesions are different, the severity of the disease is different, and often accompanied by a variety of diseases, so that their symptoms are not Typical, often concealed or confused with other diseases, easily lead to misdiagnosis or missed diagnosis, the disease develops slowly, clinically in addition to the original lungs, chest symptoms of various symptoms and signs, mainly progressive lung, heart failure and other The signs of organ damage are described in terms of the compensatory period and the decompensation period of their functions.
1. Lung, cardiac function compensation period (including remission period)
At this stage, only pulmonary hypertension and right ventricular hypertrophy, but no right heart failure, clinical manifestations are mainly some symptoms and signs of the underlying disease, the most common symptoms are cough, cough, chest tightness, shortness of breath, wheezing, palpitations, due to the elderly Lung degeneration, pulmonary dysfunction, the above symptoms are more significant, more likely to merge with lower respiratory tract infections, fever is not obvious when combined infection, mainly manifested as increased cough, increased sputum, sputum purulent, chest tightness, shortness of breath, wheezing, The heart palpitations are aggravated, the signs are: emphysema sign, auscultation has more respiratory sounds, occasional dry and wet voices or wheezing sounds; heart voiced circles shrink or disappear (often due to emphysema is not easy to find out); heart sounds far away, Pulmonary valve area may have a second heart sound hyperthyroidism, suggesting pulmonary hypertension; systolic murmur in the tricuspid valve area or heart beat under the xiphoid process, suggesting pulmonary hypertension; jugular vein filling, increased intrathoracic pressure due to emphysema , obstruction of vena cava reflow; due to the descending of the diaphragm, the upper and lower margins of the liver are obviously moved underground, which should be distinguished from the hepatic congestion of right heart failure.
2. Lung, cardiac decompensation (including acute exacerbation)
The main clinical manifestations of this period are respiratory failure with or without heart failure.
(1) Respiratory failure: acute respiratory infection is a common cause, bronchial mucociliary epithelial cells shrink, shed, ciliary movement is weakened, synthetic secretory immunoglobulin (SIgA) is reduced, small airways narrow, collapse, mucus secretion increases and retention, In addition to the underlying lesions, patients with pulmonary heart disease are prone to respiratory infections; the elderly are prone to reflux esophagitis, or inhaled infection due to aspiration or feeding of cerebrovascular diseases; elderly patients with pulmonary heart disease often have multiple Diseases such as tuberculosis and diabetes, immune function is easy to secondary infection, respiratory failure is prone to respiratory failure, the number of alveoli in the elderly is reduced, lung compliance is reduced, thoracic elasticity is reduced, diaphragmatic atrophy is thin and fatigue, plus basic diseases, The incidence of respiratory failure increases in elderly patients with pulmonary heart disease. Inappropriate use of sedatives, antitussives and oxygen therapy may induce respiratory failure. Decompensation of senile pulmonary heart disease is most common with respiratory failure, and respiratory failure is mostly type II. The interstitial fibrosis of the disease is mostly type I, and the clinical manifestations are worse than the symptoms and signs of the underlying disease. Mainly due to systemic reactions of hypoxia and/or hypercapnia, elderly patients often have cerebral arteriosclerosis and water-salt balance disorders, prone to neuro-psychotic symptoms, manifested as excitement, irritability, insomnia, headache, apathy, Blindness, lethargy, paralysis, convulsions, flapping tremors, coma, etc., common manifestations of difficulty breathing, sitting breathing, cyanosis and skin flushing and sweating, pulse flooding, rapid heart rate, increased blood pressure, dilated or reduced pupils or The two sides are not equal, the optic disc is edematous, and the vertebral body bundle sign is positive.
(2) heart failure: right heart failure mainly, arrhythmia can also occur, at this time manifested as shortness of breath, palpitation, oliguria, bloating, cyanosis, jugular vein engorgement, pulmonary heart disease 2nd heart sound hyperthyroidism, tricuspid valve Area audible and systolic hairy murmur, liver, liver jugular vein regurgitation positive, lower extremity edema.
In addition, pulmonary heart disease patients often have renal dysfunction, mild manifestations only BUN increased, proteinuria; severe cases of oliguria, no urine, metabolic acidosis, liver damage incidence of about 1/3, mild manifestations only GPT increased, hypoproteinemia, increased jaundice index, severe cases of congestive cirrhosis, hypoproteinemia, ascites, etc., sometimes digestive ulcers or major bleeding, may be stress ulcers or DIC.
3. Other
(1) Cyanosis: Pulmonary heart disease is mainly caused by pulmonary hypertension and intrapulmonary shunt and V/Q imbalance caused by hypoxemia. It is characterized by central cyanosis, earlobe, nose tip, lip, and finger (toe). When concurrent red blood cells In the case of increased disease, the reduced hemoglobin is increased, and even if the arterial oxygen saturation is normal, there is a cyanosis. If there is anemia, it is not easy to express cyanosis in anoxic state.
(2) abnormal tongue diagnosis: the tongue is mostly purpura, dark purple, when the right heart is exhausted, the trunk of the ventral surface of the tongue is full and bulging, the shape is curved or cylindrical, and the ventral surface of the tongue is visible with dark purple abnormal venous branch, which is cystic, range More than 1/2 of the total area.
(3) signs of pulmonary encephalopathy: peripheral blood vessels dilate, skin warm and rosy, sweating, blood pressure rise, muscle twitching, combined with membrane congestion and edema, eyeball convex, pupil diminished in coma, optic disc edema.
Examine
Examination of chronic pulmonary heart disease
Laboratory inspection
Pulmonary heart disease is caused by different lung diseases. The early and late stages of the disease are sensitive to various examination methods, and should be selected according to the specific conditions of the patients. The following describes several methods with practical diagnostic significance:
Pathogen examination
Repeated pulmonary infection is the main cause of deterioration of pulmonary heart disease and heart failure. Timely diagnosis of pathogens is the key to controlling infection. The cultivation of sputum bacteria is convenient and easy, but it is susceptible to bacterial contamination of oropharynx. In recent years, the use of protective brush to remove the respiratory specimens, or the removal of respiratory specimens by the ring-shaped membrane puncture method for bacterial culture as a basis for pathogen diagnosis, targeted antibiotics based on sensitive tests, facilitate early control Infection, the patient is often a resident of the upper respiratory tract during the remission period, and the disease is caused by low immunity of the bacteria invading the lower respiratory tract, such as hemolytic streptococcus, influenza bacillus, pneumococcus, staphylococcus, enterococci and Neisseria. Increased Gram-negative bacilli, such as Alcaligenes, Klebsiella, and Pseudomonas aeruginosa, can produce Staphylococcus aureus, Escherichia coli, influenza bacillus, and P. aeruginosa in the acute exacerbation of pulmonary infection Bacteria and fungi.
2. Determination of serum electrolytes
The incidence of electrolyte disorder in pulmonary heart disease is high and changes rapidly. It should be measured and guided in time. Respiratory acidosis is often caused during acute exacerbation of pulmonary heart disease. Blood potassium is often elevated. When ventilation is improved, diuretics are used, and basic drugs are prone to occur. Respiratory acidosis combined with metabolic alkalosis and hypokalemia, hypochloremia, comprehensive clinical analysis of 6997 cases of pulmonary heart disease clinical analysis of electrolyte imbalance in the order of low chloride (48.04%), low sodium (35.74%), low potassium (22.4%), high potassium (14.05%), high sodium (8.1%), high chlorine (3.2%) and calcium, magnesium, phosphorus disorders.
3. Blood gas analysis
There are many causes of pulmonary heart disease, and the mechanisms of hypoxemia and hypercapnia are different, but the basic reasons are insufficient alveolar ventilation, dysregulation of ventilatory/blood flow, diffuse dysfunction and shunt, and the degree and type of blood gas change can guide treatment. , estimated prognosis, blood gas analysis purposes:
(1) can understand the severity of pulmonary heart disease: early pulmonary heart disease, PaO2 mildly decreased, generally >60mmHg; PaC02 mildly increased, generally 50mmHg, A-aDO2 slightly increased when inhaling air, after aspiration of pure oxygen A- aDO2 is about 30mmHg, Qs/Qt is about 15%; pulmonary heart disease compensation period: PaO2 is more than 57mmHg, PaCO2 is above 48mmHg; pulmonary heart disease decompensation period PaO2 is about 42mmHg, PaCO2 is about 60mmHg; pulmonary heart disease is no heart failure PaO2 averaged 53mmHg, PaO2 averaged 40mmHg in patients with heart failure, PaO2<50mmHg and PaCO2>50mmHg in patients with pulmonary encephalopathy. When PaO2<40mmHg often showed arrhythmia, oliguria or liver function damage, blood gas analysis can accurately reflect low The degree of oxytemia is not affected by the amount of hemoglobin, such as PaO2 51 ~ 60mmHg for mild hypoxemia, PaO2 31 ~ 50mmHg for moderate hypoxemia, PaO2 30mmHg for severe hypoxemia, but also according to Blood gas analysis distinguishes type I respiratory failure (ie, PaO2 <60 mmHg) and type II respiratory failure (ie, PaO2 is reduced by <60 mmHg, accompanied by PaCO2 >50 mmHg).
(2) According to the change of blood gas judgment mechanism and type: PaO2 and PaCO2 change and after exercise, the change after inhalation of pure oxygen can be identified as insufficient alveolar ventilation, ventilatory/blood flow imbalance, diffuse function reduction or intrapulmonary shunt .
Film degree exam
Electrocardiogram
The pathological basis of electrocardiogram diagnosis of pulmonary heart disease is right ventricular hypertrophy caused by pulmonary hypertension. It can be normal in early or remission period. Because emphysema is common, and the left ventricle is thicker than the right ventricle in adults, slight changes are difficult to show from the electrocardiogram. Only when the right ventricle is obviously hypertrophic or the right ventricular activation intensity exceeds the left ventricle, the electrocardiogram changes only, so the ECG positive rate in pulmonary heart disease is only about 30%, which is characterized by variability, acute heart attack due to hypoxia, acidosis Electrolyte disorder can cause various arrhythmia and other obvious changes. When the cause is relieved, the arrhythmia can disappear by itself after the condition is relieved, and the P and QRS groups are also greatly improved. The main changes are: the right atrium is large, and the P wave is high. The apex angle is >70, the average electric axis is 90°, the amplitude is 2mm; the right ventricle is large, the electric axis is right-biased, the aVR is QR type (R/Q1), and the right chest lead is R-type (V1R/S>1) The left chest lead is rS type (V5R/S<1); severely clockwise transposition, V1 ~ V5 are rS type; right bundle branch block pattern, arrhythmia).
2. Heart vector diagram
The heart vector map of the diagnosis of pulmonary heart disease is more sensitive than the electrocardiogram, and the positive rate is 80% to 95%. The electrocardiogram of the same group is only 38% positive. The heart vector can accurately record the direction, size and size of the instantaneous integrated vector of each stage of cardiac activation. The exercise program can reflect the changes of quality and quantity in the process of cardiac depolarization and repolarization, so it can understand the changes of left and right ventricular voltage and potential, which has certain value for early detection of right ventricular hypertrophy.
3. Echocardiography
The early pathological changes of pulmonary heart disease are pulmonary artery dilatation, right ventricular outflow tract, clinical symptoms are not obvious, and ECG is not easy to show. Echocardiography can directly detect right ventricular outflow tract and right ventricular diameter and right pulmonary artery diameter, and the positive rate is higher. According to the literature, the compliance rate of 648 patients with pulmonary heart disease is 60.6%-87%, which is higher than that of ECG and X-ray. The pulsed Doppler echocardiography provides a non-invasive assessment of pulmonary heart disease. A promising method for directly responding to pulmonary blood flow, more direct than ECG, X-ray, M-mode and 2D echocardiography, pulmonary impedance blood flow map, and correlation between main parameters and pulmonary artery pressure it is good.
4. X-ray inspection
Pulmonary heart disease X-ray examination can show the characteristics of the primary disease of the lung and the shape of the heart, changes in pulmonary blood vessels.
(1) X-ray changes of chest lesions: Pulmonary heart disease is caused by chronic bronchitis with obstructive emphysema. Chest X-ray shows increased lung texture, distortion, deformation or interstitial fibrosis. Emphysema changes to lung perfusion. The luminosity is enhanced, the diaphragm is lowered, the thoracic cage is enlarged, the lateral anteroposterior diameter is increased, and the lung texture is reduced or sparse.
(2) Pulmonary vascular X-ray changes: the right lower pulmonary artery is dilated, its transverse diameter is 15mm, the right lower pulmonary artery transverse diameter and tracheal ratio is >1.07, the posterior anterior pulmonary artery segment is >3mm, the central pulmonary artery segment is dilated and the peripheral branch is slender. .
(3) X-ray changes of the heart: the apex is upturned or rounded, the right anterior oblique slice shows the conus of the pulmonary artery, and the lateral slice shows that the anterior border of the heart protrudes forward. The size of the heart is related to the primary disease of the lung, such as The ratio of cardiothoracic value in patients with emphysema is often <0.4, while the ratio of pulmonary tuberculosis to pulmonary fibrosis is often >0.5.
Diagnosis
Diagnosis and diagnosis of chronic pulmonary heart disease
diagnosis
Most of the pulmonary heart disease is caused by the development of chronic chest and lung diseases. The symptoms of the respiratory system and the symptoms of the circulatory system are often staggered. It is difficult to be sure whether there is heart disease in the early stage. Before the occurrence of heart failure, the diagnosis mainly relies on comprehensive judgment, that is, collection. Complete medical history, combined with physical signs, electrocardiogram, X-ray diagnosis.
Differential diagnosis
1. Identification with coronary heart disease
Coronary heart disease and pulmonary heart disease are more common in middle-aged and above, heart enlargement, arrhythmia and heart failure can occur, the heart murmur is not obvious, pulmonary heart disease ECG has similar myocardial infarction pattern, causing difficulty in diagnosis, identification points:
1 patients with pulmonary heart disease often have chronic bronchitis, history and signs of emphysema, and no typical angina or myocardial infarction.
2 Pulmonary heart disease ECG ST-T wave changes are not obvious, similar to myocardial infarction pattern occurs in the acute exacerbation of pulmonary heart disease, with the improvement of the condition, these patterns can disappear, pulmonary heart disease can also appear a variety of arrhythmia, more after the incentive is removed Normal, short-term and variability is characteristic. Coronary heart disease often has atrial fibrillation and various conduction blocks, which is constant and long-lasting compared with pulmonary heart disease.
Pulmonary heart disease with coronary heart disease is difficult to diagnose, and often missed diagnosis, foreign reports of pulmonary heart disease with coronary heart disease misdiagnosis rate of 8% to 38%, missed diagnosis of 12% to 26%, because the two together in the presence of symptoms cover each other, it can not be applied The diagnostic criteria for pulmonary heart disease or coronary heart disease should be combined with clinical comprehensive diagnosis. The following points support the diagnosis of pulmonary heart disease with coronary heart disease:
(1) due to long-term hypoxia and emphysema: typical angina symptoms are less, such as pre-cardiac discomfort, chest tightness increased, taking nitroglycerin 3 ~ 5min relieved.
(2) The second sound of the aortic valve is larger than the second sound of the pulmonary valve: the apical systolic murmur of the apex 2/6 or above indicates the dysfunction of the papillary muscle.
(3) X-ray shows that the left and right chambers are enlarged: the aortic arch is distorted, prolonged, calcified, and the heart is enlarged. The shape is aortic, and the aorta-mitral valve and left ventricle are large.
(4) ECG changes: myocardial infarction pattern can exclude patients with myocardial infarction, complete left bundle branch block, left anterior block and / or double bundle branch block, left ventricular hypertrophy or strain can be excluded Blood pressure, two to three degrees of atrioventricular block, the power axis is severely left (<-300 °) and can exclude high blood pressure.
(5) Echocardiography showed a decrease in the amplitude of the posterior wall of the left ventricle: the difference in the diameter of the left ventricular end-systolic phase was <10 mm.
2. Identification with Rheumatic Heart Disease
Rheumatic mitral stenosis can cause pulmonary hypertension, right heart involvement, myocardial contraction in heart failure is not easy to hear typical murmur, easy to be confused with pulmonary heart disease, pulmonary heart disease tricuspid valve relatively closed, heart reversal, in the original The mitral valve area can smell 2/6~3/6 grade air-conditioning murmurs. Pulmonary valve regurgitation has a diastolic murmur in the pulmonary valve area. Right ventricular hypertrophy and pulmonary hypertension are easily mistaken for rheumatic heart disease.
(1) Pulmonary heart disease is more common in middle-aged and above, but more common in rheumatic heart disease.
(2) Pulmonary heart disease has a history of respiratory diseases for many years, respiratory function is reduced, heart failure often occurs on the basis of respiratory failure; rheumatic heart disease often has a history of rheumatism, rheumatism and fatigue are often the cause of heart failure.
(3) Pulmonary heart disease murmur is enhanced after heart failure, while rheumatic heart disease can be weakened.
(4) Pulmonary heart disease often shows right heart failure, and rheumatic heart disease often shows left heart failure.
(5) X-ray changes: pulmonary heart disease is mainly caused by right ventricle, and rheumatic heart disease is mainly mitral valve heart changes.
(6) Blood gas analysis: Pulmonary heart disease often has a decrease in PaO2 or an increase in PaCO2, and rheumatic heart disease can be normal.
(7) Electrocardiogram: Pulmonary heart disease has pulmonary P wave and right ventricular hypertrophy, while rheumatic heart disease has mitral P wave.
3. Identification with constrictive pericarditis
Constrictive pericarditis is insidious, clinical manifestations are palpitations, shortness of breath, cyanosis, jugular vein engorgement, hepatomegaly, ascites, ECG low voltage and pulmonary heart disease, but no history of chronic bronchitis, pulse pressure becomes smaller, X-ray The heart is straightened, the heart beats weakly or disappears, and the pericardial calcification is seen, and there is no emphysema and pulmonary hypertension, which can be differentiated from pulmonary heart disease.
4. Identification with primary cardiomyopathy
Primary cardiomyopathy, heart enlargement, weak heart sound, murmur caused by relative atrioventricular valve dysfunction and right hepatic failure, ascites, lower extremity edema and pulmonary heart disease, pulmonary heart disease has a history of chronic respiratory infection and emphysema Signs, X-rays have pulmonary hypertension changes, electrocardiogram has right axis deviation and clockwise transposition, while cardiomyopathy is characterized by extensive myocardial damage, echocardiography shows "large ventricle, small opening", blood gas changes are not obvious, possible There is mild hypoxemia.
