Cardiogenic respiratory distress is defined as cardiogenic dyspnea caused by factors such as increased hydrostatic pressure and is commonly associated with cardiogenic pulmonary edema due to left heart insufficiency, which in turn leads to respiratory failure. Cardiogenic dyspnea is mainly caused by left and/or right heart failure, and the two occur by different mechanisms, with dyspnea due to left heart failure being more severe. So, how should a patient with cardiogenic respiratory distress be diagnosed? The following is a brief introduction: dyspnea caused by left heart failure is characterized by appearing or worsening during activity, reducing or relieving at rest, worsening in supine position, and reducing in sitting position. Because of the increased load on the heart during activity, the oxygen consumption of the body increases; when sitting, the lower half of the body reduces the amount of cardiac blood return, which reduces the degree of pulmonary stasis; at the same time, the diaphragm position is lowered when sitting, the diaphragm activity increases, and the lung capacity can be increased by 10% to 30%, therefore, patients with severe disease are often forced to adopt a semi-sitting or sitting position breathing (orthopnea). In acute left heart failure, paroxysmal dyspnea often occurs, mostly at night during sleep, called nocturnal paroxysmal dyspnea. The mechanism is: (1) the vagus nerve excitability increases during sleep, the coronary arteries contract, the myocardial blood supply decreases, and the cardiac function decreases; (2) the small bronchi contract, and the alveolar ventilation decreases; (3) the lung volume decreases in the supine position, and the venous blood return to the heart increases in the lower half of the body, resulting in increased pulmonary stasis; (4) the respiratory center is less sensitive, and the response to the mild hypoxia caused by pulmonary stasis is slow, and only when the degree of stasis increases and the hypoxia is obvious does the respiratory center stimulate When the degree of bruising is increased and hypoxia is obvious, the respiratory center is stimulated to respond. During the attack, the patient often wakes up in the middle of sleep with a sudden feeling of breathlessness and is forced to sit up with panic and anxiety, accompanied by coughing, and the symptoms are gradually reduced and relieved after a few minutes to tens of minutes in mild cases; in severe cases, there is a high degree of shortness of breath, blue face, profuse sweating, coughing with croup, coughing plasma pink foamy sputum, more wet rales at the bottom of both lungs, increased heart rate and galloping rhythm. This type of dyspnea, also known as cardiac asthma, is commonly associated with hypertensive heart disease, coronary heart disease, rheumatic heart valve disease, myocarditis, and cardiomyopathy.