Etiology
The etiology of pulmonary heart disease in the elderly can be divided into 4 categories.
1, chronic bronchial and pulmonary diseases are the most common. Chronic obstructive pulmonary disease (COPD) is the most important cause of pulmonary heart disease in China. Others, such as bronchial asthma, severe tuberculosis, bronchiectasis, pneumoconiosis, and interstitial lung disease, can also be secondary to chronic pulmonary heart disease in late stages.
2, severe thoracic deformities such as severe posterior and lateral convexity of the crestal vertebrae, crestal tuberculosis, thoracoplasty, and severe pleural hypertrophy.
3, pulmonary vascular pathology such as pulmonary embolism, idiopathic pulmonary hypertension, etc.
4, other neuromuscular diseases, such as cremasteric palliditis, myotonic dystrophy and obesity with pulmonary hypoventilation, sleep whistling disorder, etc.
Clinical manifestations
The disease is a long-term chronic process, gradually appearing signs of pulmonary and cardiac failure and other organ damage. It is divided according to the compensatory and decompensated phases of function.
1. Pulmonary and cardiac function compensation phase (including remission phase): The main clinical manifestation of this phase is chronic obstructive pulmonary emphysema. The main clinical manifestations of this period are chronic obstructive pulmonary emphysema, cough, sputum, wheezing, palpitation, shortness of breath, fatigue and reduced work endurance after activity. On physical examination, there are obvious signs of emphysema, due to elevated intrapleural cavity pressure and obstruction of vena cava reflux, jugular vein filling, barrel-shaped chest, reduced whistling motion, reduced voice tremor, reduced whistling sounds, prolonged whistling, rales and wet sounds heard at the base of the lungs, narrowing of the cardiac turbinates, distant heart sounds, decreased hepatic turbinates, large liver with pressure pain, positive hepatic jugular reflux, edema and peritoneal effusion, etc. Lower limb edema is common, which is obvious in the afternoon and disappears the next morning. The edema of the lower extremities is common, which is obvious in the afternoon and disappears in the next morning. There may be a hyperactive second heart sound in the pulmonary valve area, suggesting pulmonary hypertension. The presence of a systolic murmur in the tricuspid region or a subxiphoid heartbeat suggests right ventricular hypertrophy. The diaphragm decreases, causing the upper border and lower edge of the liver to move significantly downward, which should be distinguished from the hepatic stasis sign of right heart failure.
2, pulmonary and cardiac function decompensation phase (including acute exacerbation phase)
The main clinical manifestations of this period are mainly whistling failure, or heart failure.
(1) whistling failure
Common causative factors are acute whistling infections, mostly ventilation-impaired whistling failure (type II whistling failure), hypoxemia and hypercapnia coexist. Hypoxemia is manifested by chest tightness, panic, shortness of breath, headache, weakness and abdominal distension. Significant cyanosis occurs when arterial oxygen saturation is below 90%. In severe cases of hypoxia, agitation, coma or convulsions occur. Sedative or hypnotic drugs are contraindicated at this time to avoid aggravating carbon dioxide retention and the occurrence of pulmonary encephalopathy. Hypercapnia is manifested by warm, moist and sweaty skin, dilated superficial veins, flooded veins, bulbar conjunctival congestion and edema, narrow pupils, even protruding eyes, fluttering wing-like tremors of both hands, dizziness, headache, drowsiness and coma. This is the result of vasodilation and increased capillary permeability caused by carbon dioxide retention. When severe whistling failure is accompanied by psychoneurological disorders, excluding other causes, it is called pulmonary encephalopathy.
(2) Heart failure
Pulmonary heart disease in the functional compensation period only pulmonary hypertension and right ventricular hypertrophy and other signs, but no heart failure manifestations. In the decompensated stage, right heart failure, panic, shortness of breath, jugular vein anger, hepatomegaly, lower limb edema, and even generalized edema and peritoneal effusion may appear.
Examination
1.Arterial blood gas analysis
Hypoxemia or combined hypercapnia may occur during the pulmonary compensation period of pulmonary heart disease. When PaO2<8kpa (60mmhg), paco2>6.66kPa (50mmHg), it is mostly seen in pulmonary disease due to chronic obstructive pulmonary disease.
2.Blood test
In patients with hypoxic pulmonary heart disease, red blood cells and hemoglobin may be elevated, and hematocrit may be as high as 50% or more. In case of co-infection, the total white blood cell count increases, neutrophils increase, and nuclear left shift phenomenon appears. Serological examination may have renal function or liver function changes, also may appear high potassium, low sodium, low chloride, low calcium, low magnesium and other changes.
3.Other
Pulmonary function tests are meaningful in early or remission stage pulmonary heart disease. Sputum bacteriological examination can guide the selection of antibacterial drugs for acute exacerbation of pulmonary heart disease.
4.X-ray examination
In addition to the features of underlying lung and chest diseases and acute pulmonary infections, there may also be signs of pulmonary hypertension.
①Dilation of the right lower pulmonary artery trunk with a transverse diameter ≥ 15 mm; the ratio of its transverse diameter to the transverse diameter of the trachea ≥ 1.07.
(ii) Protrusion of the pulmonary artery segment or its height ≥3 mm.
(③The central pulmonary artery is dilated and the peripheral branches are slender, both of which are in contrast.
(iv) Significant protrusion of the conus (45° in right anterior oblique position) or “cone height” ≥7 mm.
⑤ Right ventricular hypertrophy sign. Pulmonary heart disease can be diagnosed with one of the above five criteria.
5.Electrocardiographic examination
Right atrial and ventricular hypertrophy changes, such as right-sided electrical axis, frontal mean electrical axis ≥ +90°, severe cis-clockwise transposition (V5: R/S≤1), Rv1+Sv5≥1.05mV, aVR in QR type and pulmonary P wave. Right bundle branch block and low voltage patterns are also seen, which can be used as a reference condition for the diagnosis of pulmonary heart disease. In V1, V2 or even extended to V3, QS waves resembling old myocardial infarction graphics are seen.
6.Electrocardiographic vectorography
It shows the pattern of right atrial and right ventricular hypertrophy. With the increase of right ventricular hypertrophy, the QRS orientation gradually evolves from the normal left downward anterior or posterior to the right, then downward, and finally to the right anterior, but the terminal part is still in the right posterior, and the QRS ring develops from the anticlockwise running or “8” shape to the cisclockwise running in severe cases, and the P ring is mostly narrow, and the amplitude of the P ring increases on the left side and the anterior frontal plane, and the maximum vector The P-loop is more narrow, with increased amplitude on the left side and the anterior frontal plane, and the maximum vector is down, left or right. The more pronounced the right atrial hypertrophy is, the more the P-ring vector is to the right.
7.Echocardiography
The right ventricular outflow tract internal diameter (≥30mm), right ventricular internal diameter (≥20mm), thickness of the anterior wall of the right ventricle (≥5mm), ratio of left and right ventricular internal diameter (<2.0), right pulmonary artery internal diameter or pulmonary trunk and right atrial hypertrophy were measured to diagnose pulmonary heart disease.
Diagnosis
The clinical diagnosis can be made based on the history, clinical manifestations, and relevant examinations confirming the presence of pulmonary hypertension or enlarged right ventricular hypertrophy, with loss of compensation dominated by whistling failure and right heart failure.
Differential diagnosis
Pulmonary heart disease with left ventricular hypertrophy is not uncommon. Pulmonary heart disease can also present with myocardial repolarization abnormalities and ischemic ST-T electrocardiographic changes, especially in the elderly. Left ventricular damage can be caused by high hematocrit, hyperviscosity, hypervolemia, bronchopulmonary vascular shunts, repeated infections with toxemia, hypoxemia, and peripheral vasoconstriction during heart failure in pulmonary heart disease, or it can be caused by coexisting coronary heart disease or hypertensive heart disease, which can be differentiated according to the above-mentioned differential points.
Pulmonary heart disease often coexists with coronary artery disease, making the condition and symptoms even more atypical. Pulmonary heart disease combined with coronary artery disease can be diagnosed in patients with one of the following conditions and left ventricular hypertrophy.
1. typical angina pectoris in remission of pulmonary heart disease with electrocardiographic changes of myocardial ischemia.
2, with chest tightness or precordial pain and ECG changes of acute myocardial infarction, with markedly elevated GOT and LDH.
3, ECG with old infarct changes and can exclude pulmonary cool heart infarct graphics.
4, Ⅲ degree atrioventricular block or complete left bundle branch block and can exclude other causes.
5, coronary angiography showing coronary sclerosis meeting the diagnostic criteria for coronary artery disease.
When pulmonary heart disease is combined with pulmonary encephalopathy in the elderly, it should be differentiated from senile dementia, cerebrovascular disease, hypertensive encephalopathy, hepatic encephalopathy, diabetic coma, toxic encephalopathy, etc.
Complications
Common complications of pulmonary heart disease include upper gastrointestinal bleeding, renal insufficiency, pulmonary encephalopathy, DIC, etc.
Treatment
In addition to treating the underlying pulmonary and thoracic diseases and improving pulmonary and cardiac functions, it is important to maintain the functions of all system organs and take measures to save them. Control the infection, ventilate the whistling tract, improve the whistling function, correct hypoxia and carbon dioxide retention, correct whistling and heart failure.
1, active control of pulmonary infection
Pulmonary infection is a common cause of acute exacerbation of pulmonary heart disease, control of pulmonary infection in order to make the condition better. Do sputum culture and drug sensitivity test before applying antibiotics to find the infecting pathogenic bacteria as the basis for choosing antibiotics. Before the results are available, antibacterial drugs are selected based on the infection setting and sputum smear gram stain. Gram-positive bacteria predominate in out-of-hospital infections, while Gram-negative bacteria predominate in in-hospital infections. Or choose antimicrobial drugs that combine both. When selecting broad-spectrum antimicrobials, attention must be paid to possible secondary fungal infections. After the culture results are available, select targeted antibiotics according to the type of pathogenic microorganism. Take 10 to 14 days as a course of treatment, but it is mainly based on the patient’s condition.
2.Clearing the whistle tract
In order to improve the ventilation function, oropharyngeal secretions should be removed to prevent regurgitation of gastric contents into the trachea, frequently change position, and encourage forceful coughing to facilitate sputum discharge. For those who are weak and unable to cough for a long time, pat the patient’s back with your hand when coughing to assist in sputum excretion. If ventilation is severely inadequate, confused, cough reflex is sluggish and sputum is abundant, sticky and obstructs the whistle, an artificial airway should be established and sputum should be aspirated regularly. Moisten the airway and sputum. Mucolytics and expectorants are available. Also apply drugs that dilate the bronchi and improve ventilation.
(1) Bronchodilators
(1) Selective β2 receptor agonists.
②Theophylline drugs.
(2) Elimination of airway nonspecific inflammation Prednisone is commonly used, and beclomethasone (Bicodone) is used as an inhalation drug. The dose of corticosteroids varies from person to person and should not be too large to avoid adverse consequences.
3.Correcting hypoxia and carbon dioxide retention
(1) Oxygen therapy
Oxygen therapy for hypoxia without carbon dioxide retention (type I failure) should be given with high flow oxygen (>35%) to raise PaO2 to 8kPa (60mmHg) or SaO2 to 90% or more. The duration of high concentration oxygen inhalation should not be too long to avoid oxygen toxicity. Oxygen therapy for hypoxia with carbon dioxide retention (type II whistling failure) should be low-flow continuous oxygenation. Oxygen therapy can be used double-lumen nasal tube, nasal catheter or face mask for oxygen inhalation, with an oxygen flow rate of 1 to 2L/min.
(2) Whistle-stimulant drugs
Whistle-stimulant drugs include Niclosamide (Colamine), Lopressor, Doxapram, Dulcolax, etc. Patients who are drowsy can be slowly pushed intravenously first. Closely observe the patient’s lash response, state of consciousness, whistling frequency, and changes in arterial blood gas in order to adjust the dose.
(3) Mechanical ventilation In patients with severe whistling failure, early mechanical ventilation should be performed.
4.Correct acid-base imbalance and electrolyte disorders
Acid-base imbalance and electrolyte disorders are easily seen during acute exacerbation of pulmonary heart disease, and are commonly seen in whistling acidosis, whistling acidosis combined with metabolic acidosis or metabolic alkalosis. The treatment of whistling acidosis lies in improving ventilation. When whistling acidosis combined with metabolic acidosis, pH is obviously reduced, when pH <7.2, treatment should pay attention to improving ventilation, but also according to the situation of static sodium bicarbonate solution, while treatment and observation. When whistling acidosis combined with metabolic alkalosis, most of them are related to low blood potassium and low blood chloride, attention should be paid to supplementing potassium chloride. Triple acid-base imbalance may occur in critically ill patients. Electrolyte disorders should be monitored continuously and treated in a targeted manner. In addition to monitoring electrolytes such as potassium, sodium, chloride, calcium and magnesium, attention should also be paid to the problem of hypophosphatemia.
5.Lowering pulmonary artery pressure
Oxygen therapy is one of the measures to treat pulmonary hypertension. Targeted drug therapy for pulmonary hypertension should be based on the type of pulmonary hypertension.
6.Control of heart failure
The treatment of heart failure in pulmonary heart disease is different from the treatment of heart failure in other heart diseases because heart failure in patients with pulmonary heart disease usually improves after aggressive control of infection and improvement of whistling function. However, diuretic and positive inotropic drugs can be used appropriately for patients who are ineffective after treatment or are more severe.
(1) Diuretics Eliminate edema, reduce blood volume and reduce right heart load. The principle of application is to apply a small number of doses.
(2) Positive inotropic drugs Correct hypoxia and prevent hypokalemia before use to avoid toxic reactions to digitalis drugs.
Indications for application are.
(1) those with heart failure in which the infection is controlled, hypoxemia has been corrected, and recurrent edema cannot be obtained with diuretics with good efficacy.
(ii) Those with right heart failure as the main manifestation without obvious infection.
(iii) those who present with acute left heart failure.
④ Combined supraventricular tachyarrhythmias, such as supraventricular tachycardia, atrial fibrillation with rapid ventricular rate.
7. Cerebral edema
Pulmonary heart disease is often combined with pulmonary encephalopathy due to severe hypoxemia and hypercapnia, and clinical manifestations such as neuropsychiatric symptoms, intracranial hypertension and cerebral edema appear. Intracranial pressure should be reduced as soon as possible to reduce cerebral edema and control its neuropsychiatric symptoms.
①Dehydration drugs
Choose 20% mannitol for rapid intravenous infusion, 1~2 times/day. Pay close attention to blood electrolyte changes during the drug administration period.
②Corticosteroids
They must be used in combination with effective antibiotics and drugs to protect the gastric mucosa, such as bismuth potassium citrate (Deloitte) and compound bismuth aluminate (Gastric Biocide), to avoid worsening of the whistling infection and inducing upper gastrointestinal bleeding. Most use dexamethasone, aminophylline and niclosamide in 5% glucose solution intravenous drip, depending on the severity of the disease, give 1 to 3 doses per day, when the symptoms of pulmonary encephalopathy relief, cerebral edema reduction, can be reduced to discontinued.
8.Strengthen nursing care
Closely observe changes in the condition, it is advisable to strengthen the monitoring of cardiopulmonary function. Turning and patting the back to exclude whistling secretions is an effective measure to improve the ventilation function.
Prognosis
It varies depending on the primary disease and is closely related to the status of cardiopulmonary function at the time of remission and whether it is managed by active and correct remission therapy. The mortality rate has been decreasing year by year with the development of medical technology. Pulmonary heart disease decompensated patients without critical comorbidities still have a good prognosis after active and reasonable rescue treatment; those with combined pulmonary brain, gastrointestinal hemorrhage, DIC, and multi-organ failure have a poor prognosis.