Acute cor pulmonale

Introduction to acute pulmonary heart disease Acute pulmonary heart disease (acutecorpulmonale) is mainly caused by sudden embolism of the main trunk of the pulmonary artery or its main branches, and most of the pulmonary circulation is blocked, resulting in a sharp increase in pulmonary arterial pressure, acute right ventricular dilatation and right ventricular failure. For patients with massive pulmonary embolism, this section only describes pulmonary embolism and the acute pulmonary heart disease caused by it. basic knowledge The proportion of illness: 0.14% Susceptible people: no specific population Mode of infection: non-infectious Complications: shock, sudden death, pulmonary embolism, cardiogenic shock, pulmonary hypertension

Causes of acute pulmonary heart disease

Age factor (20%):

Pulmonary embolism is not a primary disease. It is a serious complication of many diseases. In the elderly, due to various diseases such as congestive heart failure, atherosclerotic heart disease, malignant tumor, cerebrovascular disease, surgery After major surgery, long-term bed rest and lower limb activity limitation is a high risk factor for thrombosis. The incidence of pulmonary embolism is highest in patients aged 50-65 years. Pulmonary embolism is the common cause of death in the elderly over 70 years old. Pulmonary lobe, small or recurrent pulmonary embolism for timely diagnosis, has a positive effect on reducing the mortality of elderly patients.

Disease factors (35%):

Common risk factors, such as rheumatic heart disease, atherosclerotic heart disease, atrial fibrillation, heart failure, is the basic disease of pulmonary embolism, especially in the past. In addition to cancerous plugs, cancer patients may also have abnormal blood coagulation mechanisms and are prone to pulmonary embolism. 13% to 52% of patients with pulmonary embolism have a history of deep phlebitis, and deep phlebitis of the lower extremities is an important prone factor in the formation of emboli.

Pregnancy factors (15%):

The incidence of thromboembolic disease in women during pregnancy is several times higher than that of women of the same age. Pregnant women with third and multiple births are more susceptible to thrombosis. Amniotic fluid embolism can occur during childbirth, and pelvic vein thrombosis can occur after delivery.

Obesity factor (5%):

Those who are overweight, the incidence of thromboembolic disease is higher.

Drug factor (5%):

Oral contraceptives can cause changes in blood coagulation factors, platelets, fibrinolytic systems and plasma lipoproteins, and are prone to thromboembolism.

Other factors (10%):

Varicose veins of the lower extremities, long-term indwelling intubation and severe trauma, gynecological or surgical, etc., are prone to cause thrombosis. Acute parasitic diseases have a large number of adult or insect eggs entering the pulmonary circulation causing extensive pulmonary arterial embolization.

Pathogenesis

Pulmonary embolism can be single or multiple, the embolism can be from tiny embolism to huge embolism. The embolization site generally has more bilateral lung than unilateral lung, right lung is more than left lung, lower lung is more than upper lung, acute lung In patients with heart disease, a common large embolus or multiple emboli obstructs the trunk of the pulmonary artery and rides across the left and right pulmonary bifurcations (riding over the embolism), causing complete or major embolization of the pulmonary artery and its main branches, sometimes visible embolus Extending to the ventricle and partially obstructing the pulmonary valve, the right ventricle is often enlarged, accompanied by liver congestion, due to right heart failure, decreased cardiac output, shock, reflex coronary artery spasm, etc., causing hypoxia, left ventricular myocardium, especially in the heart Focal necrosis of the submucosal myocardium.

After pulmonary embolism, 38% to 52.9% of patients due to lung tissue ischemia, hypoxia, can cause lung tissue necrosis, known as pulmonary infarction, more common in the lower lobe adjacent to the rib angle, wedge-shaped, the bottom of the lung surface Slightly higher than the surrounding normal tissue, often red, microscopically seen pulmonary interstitial and alveolar hemorrhage, 30% to 40% of pulmonary infarction may be accompanied by pleural effusion, pleural fluid is serous or serous blood, when the thrombus runs to the lungs The size of the effect on the pulmonary circulation, depending on the area of the vascular occlusion, the original reserve capacity of the pulmonary circulation and the degree of pulmonary vasospasm, when the main branches on both sides of the pulmonary artery are suddenly blocked by huge clot emboli and platelet collapse on the surface of the blood clot. The release of humoral factors such as histamine, serotonin, platelet activating factor, various prostaglandins, thromboxane A2, etc. into the pulmonary circulation can cause extensive pulmonary arteriolar spasm, pulmonary arterial pressure rise, or due to a large number of tiny emboli at the same time When pulmonary embolism occurs, the pulmonary circulation cross-sectional area obstructs more than 30%, the pulmonary circulation resistance increases significantly, and the pulmonary artery pressure begins to rise. If more than 50%, the pulmonary artery pressure is urgent. , Right ventricular ejection blocked, right ventricular dilatation occurs with right heart failure, in addition, may be reduced due to a left refluxed effort, blood pressure, coronary insufficiency, etc. Effects of left ventricular function.

After pulmonary embolism, respiratory physiology changes mainly include:

1 The alveolar ineffective cavity is increased. Because the blood flow is blocked, the alveolar with ventilation and no perfusion can not participate in gas exchange, resulting in increased ineffective ventilation and increased physiological ineffective cavity.

2 ventilatory disorders, thrombus can release histamine, serotonin, leukotriene, prostaglandin, platelet activating factor and other inflammatory transmitters, causing bronchial smooth muscle spasm, increased airway resistance, lung infarction due to lung tissue congestion, edema And at the same time, the lung compliance is reduced,

3 ventilatory / blood flow ratio imbalance, blood flow obstruction after pulmonary infarction, alveolar surfactants severely reduced, leading to pulmonary embolism in the pulmonary embolism, local atelectasis and pulmonary edema, pulmonary blood flow through these ventilation is insufficient or no ventilation In the lung area, the pulmonary vein is entered without normal exchange, and the ratio of ventilation/blood flow is reduced and the static-arterial physiology is shunted. In addition, in the case of severe pulmonary hypertension, the pulmonary artery bypass can be opened, and the blood of the pulmonary artery flows directly into the pulmonary vein. These changes are mainly clinically characterized by severe hypoxemia, accompanied by significant dyspnea and cyanosis.

Acute pulmonary heart disease prevention

Actively prevent the occurrence of venous thrombosis or thrombophlebitis, postoperative patients should leave the bed as soon as possible, carry out appropriate physical activity, long-term bed rest should be deep breathing in the bed, flexion or squatting, and often turn over or change Position, in order to maintain venous blood flow, abdominal band or bandage should not be too tight, local compression time should not be too long, so as not to hinder diaphragm activity and lower extremity venous return, timely detection of venous thrombosis and thrombophlebitis, if necessary, oral aspirin Enteric-coated tablets 25 ~ 50mg, once / d, to prevent, if it has occurred, can be treated with anticoagulation.

Acute pulmonary heart disease complications Complications, shock, death, pulmonary embolism, cardiogenic shock, pulmonary hypertension

The disease often has complications such as progressive right heart failure, shock, and sudden cardiac death.

1. Right heart failure due to pulmonary artery thrombosis, by neuroreflex, humoral factors such as histamine, serotonin, bradykinin, platelet activating factor release, pulmonary artery spasm, pulmonary blood flow reduction, alveolar ventilatory, pulmonary surfactant Substance reduction, alveolar atrophy, pulmonary ventilation/blood perfusion ratio imbalance, relative intrapulmonary blood flow, sharp decrease in stroke volume, increased pulmonary artery resistance, pulmonary artery pressure, right ventricular pressure, increased right atrial and venous pressure, right ventricular function loss Compensatory, right heart failure occurred, clinically, about 23.7% of patients with pulmonary embolism developed acute right heart failure.

2. Cardiogenic shock due to obstruction of the pulmonary circulation, blood flow through the pulmonary venous return to the left atrium is reduced, left ventricular end-diastolic filling pressure is decreased, systemic circulation pressure is decreased, heart rhythm and myocardial contractility are increased by excitatory sympathetic nerves to maintain cardiac output The amount is relatively stable. When the heart passes the positive frequency and positive muscle strength, it can not make up for the change caused by the further decrease of blood volume. The blood output of the heart is obviously decreased, the blood pressure is decreased, the visceral blood vessels are contracted, the peripheral circulation resistance is increased, and the shock symptoms appear. Because shock is caused by obstruction of the pulmonary circulation, it is called extracardiac obstructive shock.

3. Sudden cardiac death is caused by pulmonary vascular resistance and pulmonary hypertension caused by embolism of the pulmonary artery, causing serious complications of acute pulmonary heart disease. When the area of pulmonary vascular bed is blocked by about 85%, the so-called "broken" The phenomenon of flow, the pressure of the systemic circulation drops sharply, leading to sudden death.

Symptoms of acute pulmonary heart disease Common symptoms Irritability, difficulty breathing, chest pain, chest tightness, suffocation, blood pressure, post-sternal pain

Symptom

Small pulmonary embolism can be asymptomatic, or have fever, shortness of breath, chest pain, palpitations and decreased blood pressure. When a large or multiple pulmonary infarction occurs, patients often have difficulty breathing, obvious cyanosis, suffocation, palpitations, severe cough and Hemoptysis, when the lesion involves the pleura, severe chest pain can occur, due to the significant decrease in left ventricular discharge, resulting in a sharp drop in blood pressure, irritability, pale face, sweating, cold limbs, and even shock, due to insufficient blood supply to the coronary arteries To severe myocardial hypoxia, often chest tightness and post-sternal pain, more moderate fever, severe cases often cause sudden death, or death due to heart failure, shock, cardiac arrest or ventricular fibrillation.

2. Signs

Pulmonary infarction area percussion dullness, respiratory sounds weakened or accompanied by wet voice, such as lesions involving the pleura may appear pleural friction sound or signs of pleural effusion, heart rate increased, heart sound tone expansion, sternal left edge 2 to 3 ribs In the inter-pulmonary artery segment, the voiced sound is widened, the pulsation is enhanced, the second sound of the pulmonary valve area is hyperthyroidism, and the systolic and diastolic murmurs can be heard. The tricuspid valve area can also smell systolic murmur and diastolic galloping. Tachycardia, premature beats, atrial flutter, tremors and other arrhythmias, right heart failure, heart dullness enlarges, jugular vein engorgement, hepatomegaly and pain and tenderness, jaundice can occur, acute lower extremity edema is not very obvious.

According to the sudden onset of severe chest pain, dyspnea that is not commensurate with lung signs, cyanosis and shock, especially in long-term bed rest, surgery or childbirth and heart failure patients, combined with pulmonary hypertension characteristics, ECG, ECG vector and X-ray examination The results can be initially diagnosed, and high-resolution CT and/or radionuclide lung perfusion scans and selective pulmonary angiography can confirm the location and extent of embolization.

Examination of acute pulmonary heart disease

1. Blood examination The number of white blood cells can be normal or increased, and the blood sedimentation rate increases.

2. Serum lactate dehydrogenase is often increased, serum bilirubin can be increased.

3. ECG and ECG vector diagrams. Typical changes in ECG often show a significant right deviation of the motor axis, extreme clockwise transposition and right bundle branch block, I lead S wave depth, ST segment depression, III lead Q The wave is significantly and the T wave is inverted, showing the SIQIIITIII waveform. The actual SIQIII TIII is only 18%, and disappears quickly. The T wave pattern of the aVF lead is similar to the III lead. The R wave of the avR lead is often increased. V1, V2T wave inversion, P wave high tip is lung type P wave, ECG vector diagram shows QRS ring initial electrical axis left slightly forward direction, after which QRS main body part is mainly upward, right and rear shift, there is obvious direction The right end of the ring, but no conduction delay performance, T ring backwards, up and to the left, P ring is more vertical, amplitude increases, the above ECG and ECG vector changes, can be on the onset 5 ~ Appeared at 24h, and most of the recovery after a few days.

4. X-ray examination of the lungs may appear in the lower lobe of the oval or triangular infiltration shadow, the bottom of the ligament and pleura, there may be pleural effusion shadow, one side of the hilar vascular shadow deepening and ipsilateral diaphragm elevation, bilateral pulmonary artery When embolized, the infiltrating shadow is similar to bronchial pneumonia. In severe cases, the pulmonary artery segment can be prominently prominent, the heart shadow is enlarged, and the azimuth and superior vena cava shadows are widened. For selective pulmonary angiography, the location of the embolization can be accurately understood. The scope provides a basis for surgical treatment.

5. CT and radionuclide lung perfusion scan is a method to diagnose pulmonary embolism without trauma and high positive rate.

Diagnosis and diagnosis of acute pulmonary heart disease

Acute pulmonary heart disease should be differentiated from congestive heart failure, acute myocardial infarction, acute exacerbation of chronic pulmonary heart disease, adult respiratory distress syndrome, atelectasis, and spontaneous pneumothorax.

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