Cardiogenic respiratory distress

Introduction It refers to cardiogenic dyspnea caused by factors such as increased hydrostatic pressure, and is often caused by left ventricular dysfunction caused by cardiogenic pulmonary edema, which leads to respiratory failure. Cardiac dyspnea is mainly caused by left heart and/or right heart failure. The mechanism of the two is different. The dyspnea caused by left heart failure is more serious. The dyspnea caused by left heart failure is characterized by the appearance or aggravation during activities, the reduction or relief at rest, the increase in supine position, and the reduction in sitting position. As the activity increases, the body's oxygen consumption increases; when sitting, the lower body returns to reduce the amount of blood and reduce the degree of pulmonary congestion; while sitting, the position of the sputum is reduced, the diaphragm activity is increased, and the vital capacity can be increased by 10% to 30%. Patients with more severe conditions are often forced to take a semi-sitting position or sitting orthopenea.

Cause

The main cause of dyspnea in left heart failure is pulmonary congestion and decreased alveolar elasticity. The mechanism is as follows: 1 pulmonary congestion, which reduces the gas diffusion function; 2 increased alveolar tension, stimulates stretch receptors, stimulates the respiratory center through vagus nerve; 3 alveolar elasticity declines, its expansion and contraction ability decreases, lung capacity decreases; 4 pulmonary circulation pressure rises Highly reflective stimulation of the respiratory center.

The cause of difficulty in breathing during right heart failure is mainly caused by systemic congestion. The mechanism is as follows: 1 the right atrium and superior vena cava pressure increase, stimulate the baroreceptor to reflect the excited respiratory center; 2 the blood oxygen content decreases, and the acidic metabolites such as lactic acid and pyruvic acid increase, stimulating the respiratory center; 3 congestive liver Swelling, ascites, and pleural effusion restrict respiratory movement and reduce the area of gas exchange in the lungs. Clinically mainly seen in chronic pulmonary heart disease; exudative or constrictive pericarditis, no right heart failure, the main mechanism of dyspnea is due to a large number of pericardial effusion caused by pericardial tamponade or pericardial fibrous thickening, calcification, contraction Narrow, limited diastolic heart, caused by systemic venous congestion.

an examination

Related inspection

Doppler echocardiography chest MRI chest CT examination electrocardiogram dynamic electrocardiogram (Holter monitoring)

The dyspnea caused by left heart failure is characterized by the appearance or aggravation during activities, the reduction or relief at rest, the increase in supine position, and the reduction in sitting position. As the activity increases, the body's oxygen consumption increases; when sitting, the lower body returns to reduce the amount of blood and reduce the degree of pulmonary congestion; while sitting, the position of the sputum is reduced, the diaphragm activity is increased, and the vital capacity can be increased by 10% to 30%. Patients with more severe conditions are often forced to take a semi-sitting position or sitting orthopenea.

In acute left heart failure, paroxysmal dyspnea often occurs, which occurs during nighttime sleep, which is called paroxysmal nocturnal dyspnea. The mechanism is as follows: (1) increased vagal excitability during sleep, coronary artery contraction, decreased myocardial blood supply, decreased cardiac function; 2 small bronchoconstriction, decreased alveolar ventilation; 3 decreased lung capacity in the supine position, increased blood flow to the lower body, resulting in lung Increased congestion; 4 decreased sensitivity of the respiratory center, slow response to mild hypoxia caused by pulmonary congestion, when the degree of congestion increased, hypoxia is obvious, it stimulates the respiratory center to respond. At the time of the attack, the patient often wakes up in the chest and feels awkward and awkward. He is forced to sit up, panic and panic, accompanied by a cough. The symptoms gradually decrease and relieve after a few minutes to tens of minutes. The severe person is highly asthmatic, and his face is blue and purple. Sweat, breathing has a wheezing sound, coughing liquid pink foam-like sputum, the bottom of both lungs has more wet sound, heart rate increases, there is galloping. This type of dyspnea, also known as "cardiac asthma," is common in hypertensive heart disease, coronary heart disease (coronary heart disease), rheumatic heart valve disease, myocarditis, and cardiomyopathy.

Differential diagnosis

Differential diagnosis of cardiogenic respiratory distress:

Acute respiratory distress syndrome: non-cardiogenic pulmonary edema caused by alveolar capillary membrane damage and increased vascular permeability, and therefore must be differentiated from cardiogenic pulmonary edema caused by factors such as increased hydrostatic pressure.

Cardiogenic pulmonary edema: common in hypertensive heart disease, left ventricular heart failure caused by coronary heart disease, cardiomyopathy, and left atrial failure caused by mitral stenosis. They all have a history of heart disease and corresponding clinical manifestations, such as combined with chest X-ray and electrocardiogram, the diagnosis is generally not difficult. Cardiac catheter pulmonary capillary wedge pressure (Paw) increases in left heart failure (Paw > 2.4 kPa), which is more meaningful for diagnosis.

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