Orthopnea

Introduction Sitting breathing: refers to the state in which the patient is forced to take a sitting position or a semi-recumbent position in order to reduce breathing difficulties. This is a more serious manifestation of heart failure, and there is obvious pulmonary congestion in the presence of sitting breathing.

Cause

The mechanism is:

When sitting at the end of the 1st position, the blood is partially transferred to the lower body due to gravity, so that the amount of blood returned to the heart is reduced, thereby reducing pulmonary congestion.

When sitting at the end of 2, the position of the diaphragm is relatively moved downward, the volume of the thoracic cavity is relatively increased, the vital capacity is increased, and the breathing difficulty is relieved, especially in patients with ascites and hepatosplenomegaly. The sitting position allows the squeezed chest cavity to relax and relieve breathing difficulties. .

3 end sitting breathing to reduce the lower body edema fluid absorbed into the blood, reduce lung congestion.

an examination

Related inspection

Pulmonary function test lung biopsy electrocardiogram

The patient sits on the edge of the bed and places both hands on the knee or the bed. At the same time, the diaphragm is lowered under the position, the ventilation of the lung is increased, the symptoms of pulmonary insufficiency are alleviated, and the pain of the patient is relieved, like bronchial asthma. In severe patients, due to lack of ventilation, the patient is sitting and breathing, both hands are supported, the shoulders are high, the forehead is cold and sweaty, and the expression is painful.

Electrocardiogram

It can be found that myocardial infarction, myocardial ischemia, ectopic disease, conduction block, atrioventricular hypertrophy and strain provide an objective basis for the pathology or cause of heart failure.

Differential diagnosis

According to clinical symptoms and mechanisms, dyspnea can be divided into the following types:

Pulmonary dyspnea

It is a ventilatory and ventilation dysfunction caused by respiratory diseases, resulting in hypoxia and/or carbon dioxide retention.

(1) Inspiratory difficulty breathing. It is characterized by inhalation and effort. In severe cases, due to the extreme exertion of the respiratory muscles, the negative pressure in the thoracic cavity increases. When inhaling, the upper sternal fossa, the supraclavicular fossa and the intercostal space are obviously sunken. It is called "three concave sign", often accompanied by dry cough and high-adjusted suction. Gastric throat sounds. The mechanism of occurrence is the narrowing and obstruction of the larynx, trachea and bronchus caused by various causes, such as acute laryngitis, laryngeal edema, throat, diphtheria, laryngeal cancer, tracheal tumor, tracheal foreign body or tracheal compression (gothmoid, lymph node) Swollen or aortic aneurysm) and so on.

(2) Expiratory breathing difficulties. It is characterized by exhalation and effort, and the exhalation time is prolonged and slow, often accompanied by wheezing. The mechanism of occurrence is attenuated alveolar elasticity and/or obstruction of small bronchioles. Common in bronchial asthma, wheezing chronic bronchitis, chronic obstructive emphysema.

(3) Mixed dyspnea. The characteristics are that both inhalation and exhalation are laborious, the respiratory rate is increased and lightened, often accompanied by a weakening or disappearing of the breathing sound, and there may be pathological breathing sounds. The mechanism of occurrence is extensive lung lesions, reduced respiratory area, and affects ventilation function. Common in severe pneumonia, severe tuberculosis, large atelectasis, massive pulmonary infarction, diffuse pulmonary interstitial fibrosis, massive pleural effusion and pneumothorax.

2. Cardiac dyspnea

Mainly caused by left heart and/or right heart failure, the mechanism of the two is different, and the difficulty of breathing caused by left heart failure is more serious.

(1) Left heart failure. The mechanism of occurrence is:

1 pulmonary congestion reduces the gas diffusion function.

2 The alveolar tension is increased, the stretch receptor is stimulated, and the respiratory center is excited by the vagus nerve.

3 Alveolar elasticity decreases, the ability to expand and contract is reduced, and the lung capacity is reduced.

4 Reflex sensitivity of the pulmonary circulation to the respiratory center.

The difficulty of dyspnea caused by left heart failure is characterized by increased or exacerbated activity, reduced or relieved during rest, increased supine, and reduced sitting position. Because of the reduction in blood volume in the lower body, the degree of pulmonary congestion is reduced. At the same time, the position of the sputum is reduced, the exercise is strengthened, and the vital capacity can be increased by 10% to 30%. Therefore, patients with severe disease are often forced to take a sitting position.

Paroxysmal nocturnal dyspnea often occurs in acute left heart failure. Its mechanism of occurrence is:

1 vagal nerve excitability increased during sleep, coronary artery contraction, myocardial blood supply decreased, reducing heart function;

2 When the supine position is reduced, the lung capacity is reduced, and the blood volume of the lower body is increased, resulting in increased pulmonary congestion. At the time of the attack, the patient suddenly felt awkward and awakened, and was forced to sit up and panic. After a few minutes to tens of minutes, the symptoms gradually disappeared. In severe cases, asthma, cyanosis, sweating, wheezing, coughing pink foamy sputum, wetness at the bottom of both lungs, heart rate increased. This type of dyspnea is also known as cardiogenic asthma, and is common in hypertensive heart disease, coronary heart disease, rheumatic valvular heart disease, myocarditis, and cardiomyopathy.

(2) Right heart failure. The mechanism of occurrence is:

1 The right atrium and superior vena cava pressure rise, stimulating the baroreceptor to reflexively stimulate the respiratory center,

2 blood oxygen content decreased, acidic metabolites increased, stimulating the respiratory center,

3 Congestive hepatomegaly, ascites and pleural effusion, restricting respiratory movement. Clinically, it is mainly seen in chronic pulmonary heart disease.

3. Toxic dyspnea

In uremia, diabetic ketoacidosis and renal tubular acidosis, blood acidic metabolites increase, strongly stimulating the respiratory center, deep and regular breathing, may be accompanied by snoring, called acidosis, large breathing (Kussmaul breathing ). In acute infections and acute infectious diseases, elevated body temperature and the effects of toxic metabolites stimulate the respiratory center and increase respiratory rate. In the case of certain drugs and chemical poisoning such as morphine, barbiturates, and organophosphate poisoning, the respiratory center is inhibited, resulting in slow breathing, which may indicate abnormal breathing rhythms such as Cheyne-Stokess breathing or Biots breathing.

4. Blood-borne dyspnea

Severe anemia, methemoglobinemia or sulphi hemoglobinemia, due to decreased oxygen-carrying capacity of red blood cells, decreased blood oxygen content, resulting in faster breathing, and accelerated heart rate. When hemorrhage or shock, the ischemia and blood pressure drop, stimulate the respiratory center, and also accelerate the breathing.

5. Neuropsychiatric dyspnea

Severe craniocerebral diseases such as craniocerebral trauma, cerebral hemorrhage, encephalitis, meningitis, brain abscess and brain tumors, etc., the respiratory center is stimulated by increased intracranial pressure and reduced blood supply, making breathing slower and deeper, often accompanied There are abnormalities in respiratory rhythm, such as respiratory containment, double inhalation, etc. Patients with rickets may have difficulty breathing due to mental or psychological factors. They are characterized by frequent superficial and frequent frequency, up to 60-100 times in 1 minute, and often cause respiratory alkalosis due to hyperventilation, and there are mouth and limbs. Numbness and hand and foot. The sigh-like breathing patient reported difficulty breathing, but there was no objective manifestation of dyspnea. Occasionally, a deep inhalation, accompanied by a sigh-like exhalation, consciously brisk after sighing, is a manifestation of neurosis.

The patient sits on the edge of the bed and places both hands on the knee or the bed. At the same time, the diaphragm is lowered under the position, the ventilation of the lung is increased, the symptoms of pulmonary insufficiency are alleviated, and the pain of the patient is relieved, like bronchial asthma. In severe patients, due to lack of ventilation, the patient is sitting and breathing, both hands are supported, the shoulders are high, the forehead is cold and sweaty, and the expression is painful.

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