Acute left-sided heart failure

Introduction to acute left heart failure Acute heart failure is caused by sudden abnormalities in cardiac structure and function, resulting in significant short-term cardiac output, sharp decrease, insufficient perfusion of tissue and organs, and acute venous congestion in the posterior ventricle. basic knowledge The proportion of illness: 0.005% Susceptible people: no special people Mode of infection: non-infectious Complications: Cardiogenic shock Acute cardiac insufficiency Hypokalemia Hyponatremia Metabolic alkalosis Metabolic acidosis Nausea and vomiting

Causes of acute left heart failure

(1) Causes of the disease

Arrhythmia (10%):

Severe arrhythmias, such as ventricular fibrillation, significant bradycardia, etc., cause the heart to pause, and the amount of palpitations is significantly reduced. Infection, excessive physical labor and pregnancy, childbirth and excessive or excessive intravenous blood transfusions, infusions are often the cause.

Acute capacity overload (20%):

Acute volume overload, such as acute myocardial infarction, infective intracardiac inflammation or trauma caused by valve perforation, collateral rupture, papillary muscle dysfunction and other intravenous blood transfusion or input sodium containing liquid too much, too fast.

Acute myocardial damage (25%):

Acute diffuse myocardial damage, such as acute myocardial infarction, acute myocarditis, etc., causes myocardial contractility to decrease, and cardiac output decreases sharply.

Acute mechanical infarction (15%):

Acute mechanical infarction, such as severe hypertension, valvular stenosis, etc., causes the heart to be overloaded and the discharge is blocked.

Ventricular diastolic restriction (10%):

Acute ventricular diastolic restriction, such as acute massive cardiac effusion or hemorrhage caused by acute cardiac tamponade, so that cardiac output decreased, systemic venous congestion.

(two) pathogenesis

The pathophysiological basis of the disease is sudden and severely reduced cardiac contractility, cardiac output decreased sharply, or left ventricular valvular regurgitation, rapid end-diastolic pressure, poor pulmonary venous return, rapid elevation of pulmonary venous pressure, lung The capillary wedge pressure is then increased, allowing intravascular fluid to penetrate into the pulmonary interstitial and alveolar to form acute pulmonary edema.

The principle of fluid exchange between the capillary parts of the lungs and the exchange of capillaries in the systemic circulation is consistent. The colloidal osmotic pressure of the blood and the pressure of the alveolar tissue are the forces that prevent the extravasation of the fluid, while the pulmonary capillary pressure is the main cause of fluid extravasation. Strength, the colloidal osmotic pressure of the lymphatic vessels of the lung is the force to remove the extravasated fluid. Under the condition that the colloid osmotic pressure does not change much, the level of pulmonary capillary pressure is the main factor determining whether the fluid is extravasated. The pulmonary circulation is compared with the systemic circulation. A low-pressure system, the average pressure of the pulmonary capillaries is 7.5 ~ 1.0mmHg, and the colloid osmotic pressure is about 27mmHg, so it is beneficial to keep the fluid from extravasation into the pulmonary interstitial or alveolar, left ventricular dysfunction, left ventricular end diastolic The pressure is increased, and the associated left atrial pressure and pulmonary capillary pressure are correspondingly increased. If the average pressure of the pulmonary capillaries rises to 25 mmHg, the critical value is reached. Above this value, the fluid exuding the extravascular can no longer be lymphatic. When fully removed, it begins to accumulate in the pulmonary interstitial and then extravasively into the alveoli, forming pulmonary edema.

Acute left heart failure prevention

1. Control or eliminate infected lesions inside and outside the heart, control infections such as tonsillitis caused by hemolytic streptococcus; prevent and control rheumatic activities; actively prevent and control infective endocarditis, respiratory infections and other parts infection.

2. Quickly correct arrhythmia: When arrhythmia occurs in a heart patient, it should be corrected quickly, the ectopic heart rhythm should be restored to normal sinus rhythm, or the tachycardia rate of the over-speed and over-speed should be controlled to a safe range to prevent heart failure. occur.

3. Correct water and electrolyte disorders and acid-base balance disorders.

4. Treat anemia and eliminate the cause of bleeding.

5. Avoid excessive infusion, too fast.

6. Disable or use caution with certain drugs that inhibit myocardial contractility.

7. Others: Avoid overwork, emotional, and obese people should control their diet.

Acute left heart failure complications Complications cardiogenic shock acute cardiac insufficiency hypokalemia hyponatremia metabolic alkalosis metabolic acidosis nausea and vomiting

Can be complicated by cardiogenic shock, multiple organ failure, electrolyte imbalance and acid-base balance disorders.

1. Cardiogenic shock: acute left heart failure due to significant short-term cardiac output, rapid reduction, 50% of which are accompanied by severe right ventricular damage that does not respond to volume load, causing blood pressure to drop, peripheral circulation perfusion, and heart Source shock.

2. Multiple organ failure: acute cardiac insufficiency, especially cardiogenic shock, can cause acute ischemia, hypoxia and dysfunction of important organs. Kidney, brain, liver and other organs can not compensate for multiple organ failure. Multiple organ failure further worsens cardiac function.

3. Electrolyte disorders and acid-base balance disorders: due to the use of diuretics, limited salt, eating less and patients often have nausea, vomiting, sweating, etc., can lead to hypokalemia, hyponatremia, low chloride metabolic base Poisoning and metabolic acidosis.

Acute left heart failure symptoms Common symptoms Dyspnea, shortness of breath, shortness of heart, blood discharge, obstruction, cardiac output, skin, pale heart failure, shock, alternating jugular vein, stagnation

Difficulty breathing

Dyspnea is the most common and prominent symptom of left heart failure. Respiratory exercise is an unconscious voluntary activity. However, when breathing is difficult, the patient feels suffocating and needs to use force and speed to breathe. Breathing can reach 20-30. Times / min.

(1) sitting breathing: is a unique sign of acute left heart failure, manifested as shortness of breath when lying down, symptoms can be significantly relieved in the reclining position, in severe cases, the patient is forced to take a semi-sitting or sitting position, so called sitting breathing The most serious case, often sitting on the bedside or on the backrest chair, the legs are drooping, and the upper body is bent forward to enhance the function of the respiratory muscles. This is a compensatory mechanism for relieving pulmonary congestion. When normal people are lying down, The average lung capacity decreased by 5%, while in patients with squat breathing, the lung capacity decreased by 25% on average, indicating that pulmonary congestion and lung stiffness are more severe. The mechanism of dyspnea is:

1 Increased pulmonary capillary pressure stimulates the vagus nerve fibers located next to the vascular bed, and reflexively excites the respiratory center to produce a Churchill-Cope reflex, which increases breathing.

2 pulmonary blood increases, the volume of the pulmonary capillary bed increases, the volume of the alveoli decreases correspondingly, the compliance of the lung decreases, that is, the need for greater negative pressure during inhalation can expand the alveoli, and the demand for exhalation is greater. The positive pressure can cause the alveoli to collapse, so the respiratory muscles need extra work.

3 The enlargement of the pulmonary capillary bed, oppression of the small bronchus, increased ventilation resistance, after the patient was forced to sit up, due to the redistribution of blood, the blood volume of the pulmonary circulation decreased, and the symptoms were relieved.

(2) Paroxysmal dyspnea at night: It is a clinical manifestation of acute exacerbation of acute left heart failure with pulmonary congestion or chronic pulmonary congestion. Paroxysmal dyspnea is divided into two categories:

1 caused by acute left heart failure, mainly left heart failure, more common.

2 caused by mitral stenosis, mainly left atrial failure, but the clinical manifestations are the same, typical occur in the night after lying down or a few hours after sleeping, suddenly awakened, forced to sit up, shortness of breath or accompanied Cough, light, a few minutes after sitting up can be relieved; severe with cough, cough foam and asthma, called cardiogenic asthma, the mechanism of paroxysmal dyspnea occurs after 1 ~ 2 hours of sleep, body edema Gradually absorbed, increased venous return, the patient's cardiac volume load is aggravated, and the respiratory center is not sensitive at night. When the blood stasis and ischemia reach a certain level, the rapid breathing occurs. When the cardiogenic asthma attacks, the arterial pressure rises. High, pulmonary artery pressure and capillary pressure are also elevated, and if the elevated arterial pressure drops suddenly, it is a bad omen.

2. Acute pulmonary edema

Acute pulmonary edema is the result of a sharp and continuous increase in pulmonary capillary pressure. It has a qualitative change compared to the above two types of dyspnea, that is, a large amount of extravasation of capillaries can not be absorbed by lymphoid tissues, and the fluid first infiltrates into the lungs. Interstitial, the alveoli are squeezed, reducing the effective area of gas exchange, while reducing lung compliance, leading to severe dyspnea, the interstitial fluid can also compress the bronchioles, further exacerbating dyspnea, sending out asthma The wheezing sound, called "cardiac asthma", can cause pulmonary edema in patients with left ventricular end diastolic pressure, left atrial pressure and pulmonary capillary pressure increased by more than 30 mmHg. According to the development process and clinical manifestations of pulmonary edema, It can be divided into the following five periods:

(1) Incidence period: The symptoms are atypical, the patient's shortness of breath, sometimes manifested as anxiety and anxiety, physical examination shows that the skin is pale and cold, heart rate increases, X-ray examination can see a typical misty or "butterfly" shadow near the hilar.

(2) Interstitial pulmonary edema: there is difficulty in breathing, but no foaming, sitting breathing, pale skin, often with cyanosis, some patients can see jugular vein engorgement, the lungs can smell and wheezing, sometimes accompanied by Fine wet voice.

(3) Alveolar pulmonary edema period: frequent cough, extreme breathing difficulties, coughing pink foamy sputum and other symptoms, both lungs full of large and medium bubble sound with wheezing sound.

(4) Shock period: blood pressure drops, pulse speed is fine, skin is pale, hair becomes aggravated, cold sweat is dripping, and consciousness is blurred.

(5) dying period: serious disturbance of breathing and heart rhythm, dying of death.

Depending on the degree of cardiac dysfunction, the difference in speed and duration, and the difference in compensatory function, there are the following differences:

3. Cardiac syncope

As the heart's own blood loss function is reduced, the heart discharge is reduced to cause brain ischemia, and a short-term loss of consciousness occurs, called cardiogenic syncope. When the syncope episode lasts for a few seconds, there may be limb convulsions, apnea, cyanosis, etc. For A-S syndrome, the episodes are mostly short-lived, and the consciousness often recovers immediately after the attack, mainly in the acute cardiac discharge obstruction or severe arrhythmia.

4. Cardiogenic shock

Because of the low blood circulation of the heart, the shock caused by insufficient cardiac output, called cardiogenic shock, when the cardiac output is reduced suddenly and significantly, the body does not have time to compensate by increasing circulating blood volume, but through nerve reflex The peripheral and visceral blood vessels are significantly contracted to maintain blood pressure and ensure blood supply to the heart and brain. In addition to the general shock performance, clinical manifestations are associated with cardiac insufficiency, elevated pulmonary wedge pressure, and jugular vein engorgement.

Common signs of left heart failure are:

1 alternating pulse: normal rhythm alternates with a strong and weak pulse. As heart failure worsens, alternating veins can be detected when palpating peripheral arteries. The mechanism of occurrence is: A. Myocardial fibers involved in ventricular contraction How many different, weak pulse is due to partial myocardial in the relative refractory period, less myocardial fiber involved in ventricular contraction, myocardial contractility is weak, and the next contraction, all myocardium is in the reaction period, more myocardial fibers involved in ventricular contraction The stroke volume is large, so the pulse is strong, B. Due to the varying degrees of myocardial relaxation.

2-ventricular galloping horse: It is a common sign of left heart failure. It is most easily heard on the apex or apex of the apex in the left lateral position, and is enhanced when exhaled.

3 lung voice: at the beginning, the lungs may have no arpeggios or only wheezing sounds, but soon there is a wet voice at the bottom of both lungs, and the lungs are quickly covered from bottom to top. There is a thick voice, like a bubbling sound of boiling water.

Acute left heart failure examination

Arterial blood gas analysis: There may be a significant decrease in oxygen saturation, normal or decreased carbon dioxide content, pH > 7.0.

X-ray

It can be seen that the hilar has a butterfly-like flaky shadow and a sign of pulmonary edema that spreads to the periphery, the heart is enlarged, and the apex beats are weakened.

2. ECG

Sinus tachycardia or various arrhythmias, myocardial damage, left atrium, left ventricular hypertrophy, etc.

Diagnosis and diagnosis of acute left heart failure

It is often difficult to make a diagnosis of acute left heart failure based on the history and typical symptoms and signs combined with the results of the auxiliary examination.

Differential diagnosis

Bronchial asthma

Cardiac asthma and bronchial asthma have sudden onset, cough, dyspnea, asthma and other symptoms. There is a big difference between the two principles. Bronchial asthma is a reversible obstructive pulmonary disease with increased airway resistance. Often have a long history of repeated asthma or allergies, more common in young people, bronchial asthma, cough, often no sputum or sticky white sputum, cough jaundice with infection, often signs of emphysema, unless pneumonia or atelectasis, generally Non-wet vocalization, cardiac examination is normal, pulmonary function tests have increased airway resistance, blood eosinophilia (eosinophil count is often >250 ~ 400 / l).

2. Adult respiratory distress syndrome (ARDS)

ARDS is also known as shock lung, wet lung, pump lung, adult hyaline membrane disease, etc., when the onset of breathing difficulties, cyanosis, lung wet voice, wheezing sound and so on and confusion with acute left heart failure, ARDS generally no lung disease History, the disease can directly or indirectly cause acute lung injury can cause the syndrome, common diseases are lung trauma, drowning, shock, cardiopulmonary bypass, bacterial or viral pneumonia, toxic pancreatitis, etc., often in the original Onset on the basis of onset, or onset 24 to 48 hours after injury, severe dyspnea but less forced to sit breathing, hypoxemia is progressively worse, ordinary oxygen therapy is ineffective or poor, although there is asthma with lung wetness Cardiac examination without galloping and heart enlargement and cardiac organic murmur. Cardiovascular asthma treatment often has no obvious effect. Floating catheter shows pulmonary fibrillation pressure <15mmHg (1.99kPa), positive end-expiratory pressure ventilation Adjuvant therapy is effective, ARDS often combined with multiple organ failure.

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