Coronary heart disease in the elderly

Introduction to pulmonary heart disease in the elderly Chronic pulmonary heart disease is caused by chronic tissue lesions in the lung tissue, pulmonary artery or thoracic cavity, resulting in abnormal lung structure and function, increased pulmonary vascular resistance, increased pulmonary artery pressure, expansion of the right heart, hypertrophy, with or without right heart In the case of debilitating heart disease, most patients with pulmonary heart disease in China are based on chronic bronchitis or emphysema. basic knowledge The proportion of sickness: 0.0051% Susceptible people: the elderly Mode of infection: non-infectious Complications: upper gastrointestinal bleeding, renal insufficiency, pulmonary encephalopathy, disseminated intravascular coagulation, chronic pulmonary heart disease, emphysema in the elderly

The cause of pulmonary heart disease in the elderly

(1) Causes of the disease

There are many causes of senile pulmonary heart disease, which can be roughly divided into four categories.

1.COPD: According to the domestic autopsy data of 662 cases of pulmonary heart disease, the COPD accounted for 82.8%; a group of 78853 patients with pulmonary heart disease data analysis, the pulmonary heart disease caused by COPD accounted for 84.01%, it can be seen that CODP is elderly pulmonary heart disease The main cause.

2. Fibrotic lung disease: including idiopathic pulmonary interstitial fibrosis and secondary pulmonary fibrosis, more common pulmonary tuberculosis (5.90%), pneumoconiosis (1.21%) chronic lung infection , lung radiation therapy, etc.

3. Diseases that affect respiratory movements: such as severe thoracic deformity, thoracoplasty, severe pleural hypertrophy, obesity with inadequate pulmonary ventilation, and sleep-disordered breathing.

4. Pulmonary vascular disease: such as pulmonary embolism, primary pulmonary hypertension.

(two) pathogenesis

There are many factors that cause pulmonary hypertension and right ventricular hypertrophy in elderly patients with pulmonary heart disease. Some of them are not very clear. Repeated airway infections and hypoxemia are caused by a series of humoral factors, pulmonary blood vessels and blood changes, making right ventricular blasting. Increased blood resistance, the right ventricle to overcome the increased resistance to pulmonary circulation, strengthen contraction, and produce pulmonary hypertension.

1. Formation of pulmonary hypertension

(1) Body fluid factors: When the alveolar hypoxia, endothelial cells, mast cells, macrophages, platelets, neutrophils, and even vascular smooth muscle cells in the vicinity of pulmonary vascular smooth muscle can release some vasoactive substances and affect the relaxation and contraction of smooth muscle. Function, among which the more important are the arachidonic acid epoxidase product prostaglandin and the lipoxygenase product leukotriene (referred to as leukotriene). The contraction response of pulmonary blood vessels to hypoxia is not completely dependent on a certain vasoconstrictor substance. The absolute amount depends largely on the proportion of local vasoconstrictors and vasodilators. In hypoxia, the active substances that contract blood vessels are relatively increased, causing pulmonary vasoconstriction, increased vascular resistance, formation of pulmonary hypertension, and involvement in hypoxia. Pulmonary vasoconstriction response is still histamine, angiotensin II, platelet activating factor (PAF), endothelium-derived relaxing factor (EDRF) such as nitric oxide and endothelium-derived contractile factor (EDCF) such as endothelin, reactive oxygen species, heart Nasal and so on.

(2) Neurological factors: pulmonary arteries and arterioles with diameters above 30 m are innervated. There are species differences in the amount and function of nerve distribution. Experiments have shown that hypoxia stimulates sympathetic nerves through stimulation of vascular chemoreceptors. The compliance of the elastic artery is reduced, the elastic resistance of the pulmonary blood vessels is increased, and the -blocker can attenuate the pulmonary vasoconstriction caused by hypoxia, indicating the presence of sympathetic nerves in this reaction.

(3) Direct effect of hypoxia on vascular smooth muscle: It was found that a single bovine pulmonary artery smooth muscle cell cultured in vitro can also have hypoxic contraction response. When the oxygen partial pressure of culture medium drops to 3.33 kPa (25 mmHg), smooth muscle cell membrane Shrinkage, increased oxygen partial pressure can restore it, and increased free calcium in smooth muscle cells cultured under hypoxia. These results suggest that pulmonary vascular smooth muscle cells can directly respond to hypoxia, and its mechanism of action is due to hypoxia, smooth muscle cell membrane The calcium ion permeability is increased, the intracellular calcium ion content is increased, and the muscle excitation-contraction coupling effect is enhanced to cause pulmonary vasoconstriction.

(4) Acidic pulmonary vasoconstriction: Carbon dioxide itself is the expansion of pulmonary blood vessels, so that the blood vessels contract the hydrogen ions. If the pH is kept constant, the partial pressure of carbon dioxide will increase the pulmonary blood vessels, and the PaCO2 will increase when hypercapnia occurs. Excessive hydrogen ions, which increase the sensitivity of blood vessels to hypoxic contractions and increase pulmonary arterial pressure.

(5) Remodeling of vascular anatomy: recurrent chronic bronchitis and peribronchial inflammation, interstitial inflammation may involve adjacent pulmonary arterioles, causing vasculitis, vascular smooth muscle hyperplasia, thickening of the wall, stenosis or fiber It is even completely occluded, and it also causes damage to the pulmonary capillary network. When the alveolar capillary bed depletion exceeds 70%, the pulmonary circulation resistance increases, both of which increase pulmonary vascular resistance and produce pulmonary hypertension; when emphysema, Increased alveolar pressure, oppression of the capillary network around the alveoli, causing stenosis or occlusion of the capillary lumen; if the expanded alveolar wall ruptures and fuses, the formation of pulmonary bullae can also cause damage to the capillary network; the pulmonary blood vessels themselves can also Due to chronic hypoxia, the blood vessels contract, and the wall tension can directly stimulate the proliferation of the wall. Under normal circumstances, the pulmonary artery less than 60m has no obvious muscle layer, but hypoxia can transform the surrounding cells of the muscle-free artery into smooth muscle cells. Stenosis of the arterial lumen, increased resistance, and a variety of growth factors (such as polypeptide growth factors), pulmonary arterioles and muscular arterioles in the lungs during hypoxia The smooth muscle cells are hypertrophied, the interstitial cells are increased, the intimal elastic fibers and collagen fibers are proliferated, and the blood vessel wall is thickened and hardened, the lumen is narrow, and the blood flow resistance is increased.

In addition, pulmonary vascular diseases, such as primary pulmonary hypertension, recurrent pulmonary vascular embolism, pulmonary interstitial fibrosis, pneumoconiosis, etc. can cause pathological changes in the pulmonary vasculature, narrowing the vascular lumen, occlusion, and increasing pulmonary vascular resistance. , developed into pulmonary hypertension.

(6) Increased blood volume and increased blood viscosity: Blood volume and blood viscosity of patients with chronic pulmonary heart disease increase, the reasons for which are:

1 Hypoxia reduces the oxygen content in the sensory cells sensitive to oxygen in the kidney, causing activation of a series of enzymes in erythropoietin-synthesizing cells in the glomerulus, eventually leading to increased erythropoietin synthesis, erythrocytosis, blood The viscosity is increased, the hematocrit is more than 0.55~0.60, the blood viscosity is obviously increased, and the blood flow resistance is increased.

2 sympathetic nerves are excited during hypoxia, aldosterone and vasopressin secretion increase, renal tubular reabsorption of sodium water, so that sodium, water retention.

3 hypoxia causes renal arteriolar contraction, renal blood flow is reduced, glomerular filtration rate is reduced, sodium is also increased, water retention, blood volume is increased, blood viscosity is increased and blood volume is increased, and pulmonary artery pressure is increased.

Pulmonary arterial pressure is measured clinically. If the mean pulmonary artery pressure is greater than or equal to 2.33 kPa (20 mmHg) at rest, it is dominant pulmonary hypertension; if the resting pulmonary artery mean pressure is less than 2.33 kPa (20 mmHg), the average pulmonary artery pressure after exercise is greater than > 3.99 kPa (30 mmHg), it is recessive light, moderate pulmonary hypertension.

2. Heart disease and heart failure

When the resistance of the pulmonary circulation increases, the right heart is overloaded, which impairs the function of the heart, leading to various compensatory changes such as right ventricular enlargement or ventricular hypertrophy. During the expansion of the heart chamber, ventricular hypertrophy, cardiomyocytes, extracapsular matrix, collagen fibers The net has a corresponding change, that is, the ventricular remodeling process. In the early stage of pulmonary hypertension, the right ventricle can still be compensated, and the end-diastolic pressure is still normal. As the disease progresses, especially during the acute exacerbation period, the pulmonary artery pressure continues to rise and is severe. Exceeding the compensatory capacity of the right ventricle, decompensation of the right heart, decreased blood output of the right heart, increased residual blood volume at the end of systole of the right ventricle, and increased end-diastolic pressure, prompting further enlargement of the right ventricle and right ventricular failure.

Pulmonary heart disease mostly occurs in middle-aged patients. In addition to the right ventricular changes found in autopsy, there are also a few left ventricular hypertrophy, pulmonary heart disease due to hypoxia, hypercapnia, acidosis, increased blood flow and other factors, such as persistence If the sex is aggravated, left and right ventricular hypertrophy may occur, and even left heart failure may occur.

In addition, due to:

1 myocardial hypoxia, lactic acid accumulation, high energy phosphate synthesis decreased, impaired myocardial function.

2 repeated lung infections, toxic effects of bacterial toxins on the myocardium.

3 acid-base balance disorders, arrhythmia caused by electrolyte imbalance.

4 pulmonary hypertension itself can cause heart failure.

5 increased red blood cells, increased blood viscosity, right heart load and other factors, can affect the heart muscle and promote heart failure.

3. Damage to other vital organs

Pathological changes in other important organs such as brain, liver, kidney, gastrointestinal and endocrine systems, and blood systems of hypoxia and hypercapnia cause functional damage of multiple organs, such as mild hypoxia, which may cause attention deficit. Mental retardation, disorientation; although hypoxia is aggravated, arterial partial pressure of oxygen is lower than 6.66 kPa, which can cause irritability, confusion, sputum, below 3.99 kPa, will cause loss of consciousness, and even coma; below 2.66 kPa will occur Irreversible brain cell damage, hypoxia can directly or indirectly damage liver cells to increase alanine aminotransferase, but with the correction of hypoxia, liver function gradually returns to normal.

Elderly pulmonary heart disease prevention

Pulmonary heart disease is a common disease that is easily afflicted by the elderly. It can directly affect the quality of life of elderly patients. The physical activity of patients with pulmonary heart disease with heart failure is obviously limited, and even can not engage in any physical activity, making life difficult to take care of themselves. Prevention and care of pulmonary heart disease is essential, and preventive care can be divided into three levels:

Primary prevention

Also known as the prevention of the cause, mainly by preventing the bronchial, pulmonary, pulmonary and other diseases that can cause the disease, to achieve the purpose of disease-free disease prevention, improve the health knowledge of the population, enhance disease resistance, and actively prevent primary pathogenic factors, such as respiratory tract Infection, various allergens, inhalation of harmful gases and dust, through propaganda and education, promotion of smoking cessation and the application of effective smoking cessation drugs, labor protection and other means have reached the purpose of preventive causes.

2. Secondary prevention

Early diagnosis and early treatment of pulmonary heart disease, through the clinical means, to terminate the further development of pulmonary heart disease, and try to restore the damaged cardiopulmonary function, take effective and effective physical examination means, and timely find that the pulmonary heart function is still in the compensation period Pulmonary heart disease, monitoring the structure and function of the lungs, heart and other organs to prevent the occurrence of a pulmonary heart disease emergency.

3. Three levels of prevention

For patients who have been diagnosed with pulmonary heart disease, take appropriate and appropriate treatment and rehabilitation methods to minimize the degree of damage to the body caused by pulmonary heart disease, protect the lungs, and preserve the function of the heart, and maximize the exertion of the treatment of complications.

Elderly pulmonary heart disease complications Complications upper gastrointestinal bleeding renal insufficiency pulmonary encephalopathy disseminated intravascular coagulation chronic pulmonary heart disease elderly emphysema

Common complications of pulmonary heart disease include upper gastrointestinal bleeding, renal insufficiency, pulmonary encephalopathy, DIC, etc.

Symptoms of pulmonary heart disease in the elderly Common symptoms Dyspnea, respiratory failure, confusion, wheezing, heart failure, lethargy, shortness of breath, short airway, narrowing

The disease has long-term chronic menstruation, and gradually signs of lung, heart failure and other organ damage, according to the functional compensation period and decompensation period.

1. Lung, cardiac function compensation period (including remission period)

This period is mainly the performance of chronic obstructive emphysema, which can be manifested as cough, cough, wheezing, after the activity can be palpitations, shortness of breath, fatigue and labor endurance, can also be manifested as cardiogenic asthma, sitting breathing, Acute pulmonary edema and other symptoms of left heart failure, physical examination may have obvious signs of emphysema, due to increased intrapleural pressure, obstruction of vena cava reflow, visible jugular vein filling, chest appearance of barrel chest, respiratory movement weakened, speech tremor Decreased, breathing sound is reduced, exhalation is prolonged, sometimes wheezing sounds and wet squeaks are heard at the bottom of the lungs, heart sounds are narrowed, heart sounds are far away, liver dullness is declining, liver is accompanied by tenderness, hepatic jugular venous reflux is positive, edema and ascites Etc., lower extremity edema is common, lower extremity edema is obvious in the afternoon, and disappears in the morning. In addition, the pulmonary heart valve area may have a second heart sound hyperthyroidism, suggesting pulmonary hypertension, systolic murmur in the tricuspid region or heart beat under the xiphoid process. It is suggested that there is right ventricular hypertrophy. Because of the decrease of sputum, the upper and lower margins of the liver should be clearly removed and differentiated 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, mostly dyspnea-type respiratory failure (type II respiratory failure), hypoxemia and hypercapnia occur simultaneously, the main manifestations of hypoxemia are chest tightness, palpitation Shortness of breath, headache, fatigue and bloating, etc. When the arterial oxygen saturation is less than 90%, obvious blemishes may occur. Those with severe hypoxia may experience restlessness, coma or convulsions, but avoid sedation or hypnotics at this time. In order to avoid aggravation of carbon dioxide retention, pulmonary encephalopathy occurs. The main manifestations of hypercapnia are warm and wet skin, superficial vein dilatation, flood veins, conjunctival congestion and edema, dilated pupils, and even eyeballs. Dizziness, headache, lethargy and coma, which is the result of increased blood vessel dilation caused by carbon dioxide retention, increased capillary permeability, and severe respiratory failure associated with psychiatric disorders and other causes can be called pulmonary encephalopathy.

(2) Heart failure performance: pulmonary heart disease in the functional compensation period only pulmonary hypertension and right ventricular hypertrophy and other signs, but no heart failure performance, decompensation period, right heart failure, palpitation, shortness of breath, jugular vein engorgement, liver Large, edema of the lower extremities, and even systemic edema and ascites, a small number of patients may also be associated with clinical manifestations of left heart failure, and arrhythmias may also occur.

In patients with pulmonary heart disease, if pulmonary heart failure occurs, the diagnosis is generally not difficult, but for early patients, the diagnosis must be combined with medical history, symptoms, signs, and various auxiliary examinations for comprehensive analysis and comprehensive judgment. The following items can be used as a diagnosis of pulmonary heart disease. Reference: history of lung and chest diseases such as chronic bronchitis; signs of underlying diseases such as chronic obstructive emphysema or chronic pulmonary interstitial fibrosis; and the aforementioned electrocardiogram, X-ray findings, and reference to ECG vector diagram Echocardiography, pulmonary impedance blood flow map, pulmonary function or other tests that can make a diagnosis, lung, heart decompensation patients have clinical signs of respiratory failure and right heart failure and blood gas changes.

Elderly pulmonary heart disease examination

Arterial blood gas analysis

Pulmonary heart disease lung function compensation period may occur hypoxemia or hypercapnia, when PaO2 <8kPa (60mmHg), PaCO2>6.66kPa (50mmHg), this is more common in chronic obstructive pulmonary disease caused by lung disease.

2. Blood test

In patients with pulmonary heart disease with hypoxia, red blood cells and hemoglobin can be increased, hematocrit can be as high as 50% or more, whole blood viscosity and plasma viscosity can be increased, red blood cell electrophoresis time is often prolonged, and total white blood cells are increased when combined infection, neutral particles When the cells are increased, there may be a left shift of the nucleus. Some patients may have changes in renal function or liver function, and may also have changes in high potassium, low sodium, low chlorine, low calcium, and low magnesium.

3. Other

Pulmonary function tests are meaningful for patients with early or remission pulmonary heart disease, and sputum bacteriological examination can guide the selection of antibiotics for acute exacerbation of pulmonary heart disease.

X-ray inspection

In addition to lung, chest disease and acute lung infections such as enhanced lung transmission, widening of intercostal space and increased lung texture, there may be signs of pulmonary hypertension:

1 The right lower pulmonary artery is dilated, its transverse diameter is 15mm; the ratio of its transverse diameter to tracheal transverse diameter is 1.07.

2 pulmonary artery segment is prominent or its height is 3mm.

3 The central pulmonary artery dilation and the peripheral branch slenderness are in sharp contrast.

4 The conical portion is significantly convex (45° in the right front oblique position) or cone height 7 mm.

5 right ventricular hypertrophy (combined with different body position judgment), the above five criteria, with one can diagnose pulmonary heart disease, individual heart failure can be seen after the control of heart failure has been reduced.

2. ECG examination

The main manifestations are right atrium, changes in ventricular hypertrophy, such as the right deviation of the electric axis, the average frontal electric axis +90 °, severe clockwise transposition (V5 R / S 1), Rv1 + Sv5 1.05mV, aVR It is a QR-type and pulmonary-type P wave. It can also be seen as a right bundle branch block and a low-voltage pattern. It can be used as a reference condition for the diagnosis of pulmonary heart disease. At V1, V2 or even V3, a QS wave resembling an old myocardial infarction pattern can appear. Should pay attention to identification.

3. ECG vector chart check

Mainly manifested as right atrium, right ventricular hypertrophy, with the degree of right ventricular hypertrophy aggravated, QRS orientation gradually evolved from normal left lower front or back to right, then downward, finally turned to the right front, but the terminal is still right After that, the QRS ring runs from the inverse clock to the running or "8" shape to the clockwise operation, the P ring is narrow, the amplitude of the P ring on the left side and the frontal surface increases, and the maximum vector goes down, left or right. In general, the more obvious the right atrial hypertrophy, the more the P-ring vector is to the right.

4. Echocardiography

By measuring the right ventricular outflow tract inner diameter ( 30mm), right ventricular diameter ( 20mm), right ventricular anterior wall thickness ( 5mm), left and right ventricular diameter ratio (<2.0), right pulmonary artery diameter or pulmonary trunk and Right atrial hypertrophy and other indicators to diagnose pulmonary heart disease.

5. Pulmonary impedance blood flow map and its differential map examination

Analysis of the rise time, amplitude, wave area and maximum rate of rise in the pulmonary impedance blood flow map can reflect the filling intensity of blood flow in the pulmonary blood vessels and the time required for it, and the amplitude and differential of the pulmonary impedance blood flow map in pulmonary heart disease The wave value is reduced, the QB (equivalent to the right ventricular ejection) time is prolonged, the BY (equivalent right ventricular ejection period) time is shortened, and the QB/BY ratio is increased. It has reference significance for the diagnosis of pulmonary heart disease, and predicts pulmonary artery pressure. There is a significant correlation between predictive and recessive pulmonary hypertension after exercise, which has certain reference value.

Diagnosis and diagnosis of pulmonary heart disease in the elderly

According to the medical history, body film, related examination confirmed pulmonary hypertension or right ventricular hypertrophy; decompensation is mainly respiratory failure and right heart failure, the differential diagnosis of senile pulmonary heart disease is generally not difficult.

Older pulmonary heart disease often coexists with coronary heart disease, which makes the condition confusion and symptoms more atypical. Patients with pulmonary heart disease in the elderly have one of the following conditions and left ventricular hypertrophy can be diagnosed as pulmonary heart disease with coronary heart disease: 1 typical angina pectoris occurs during remission of pulmonary heart disease There is also an electrocardiogram change of myocardial ischemia. 2 ECG changes in chest tightness or precordial pain and acute myocardial infarction, GOT and LDH were significantly increased. 3 ECG has old myocardial infarction changes and can exclude the heart of the heart like a heart stalk. 4 III degree atrioventricular block or complete left bundle branch block and can exclude other causes. 5 coronary angiography showed that coronary atherosclerosis meets the diagnostic criteria for coronary heart disease.

Older pulmonary heart disease with pulmonary encephalopathy should be differentiated from senile dementia, cerebral vascular disease, hypertensive encephalopathy, hepatic encephalopathy, diabetic coma, and toxic encephalopathy.

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