Acute left heart failure in the elderly

Introduction to acute left heart failure in the elderly Acute left heart failure refers to a clinical syndrome caused by a significant decrease in myocardial contractility and/or a significant increase in cardiac load for a certain period of time, resulting in a sharp decrease in cardiac output and a sharp increase in pulmonary circulation pressure. The clinical manifestations are acute pulmonary edema, severe dyspnea, cyanosis, coughing pink foamy sputum, critical illness, rapid onset of cardiogenic shock, coma leading to death. basic knowledge Proportion of the disease: the probability of illness in the elderly is 1.3% Susceptible people: the elderly Mode of infection: non-infectious Complications: shock, arrhythmia, renal failure, acute left heart failure in the elderly, coronary heart disease

The cause of acute left heart failure in the elderly

(1) Causes of the disease

Acute anatomical or functional abnormalities can cause acute left heart failure with a sharp drop in cardiac output and a sudden increase in pulmonary venous pressure. Common causes are:

1. Acute extensive anterior wall myocardial infarction associated with coronary heart disease and primary dilated cardiomyopathy.

2. Acute left ventricular preload overload: senile valvular disease such as mitral regurgitation, aortic regurgitation, mechanical complications of acute myocardial infarction in coronary heart disease, rupture of papillary muscle infarction, perforation of ventricular septum.

3. Acute left ventricular afterload overload: high blood pressure, especially rapid or malignant hypertension, primary obstructive cardiomyopathy, severe aortic stenosis, excessive use of vasoconstrictors.

4. Left atrial failure: mainly seen in severe mitral stenosis, occasionally in the left atrial myxoma or huge thrombus obstruction of the mitral valve.

5. Severe arrhythmia: tachyarrhythmia (such as malignant ventricular arrhythmia) or significant bradycardia.

6. Congenital heart disease: patent ductus arteriosus, ventricular septal, a large number of left-to-right shunts, etc., more common in children, the elderly are rare.

7. Others: such as low cardiac output after surgery, infection, etc.

Characteristics of the onset factors of acute left heart failure in the elderly:

More than 1 cause involved in the onset: the elderly often have several heart diseases at the same time, common coronary heart disease, hypertensive heart disease, degenerative heart valve disease and diabetes, usually one of the main causes of the disease, other Then participate in and aggravate acute left heart failure, making the condition more complicated.

2 Coronary heart disease and hypertension are the most common causes of acute left heart failure in the elderly. This is because of the high prevalence of coronary heart disease and hypertension in the elderly. At present, hypertension is more effective. Coronary heart disease is becoming the most important cause of acute left heart failure in the elderly, especially in acute myocardial infarction. The heart function is already in the edge state of heart failure. In case of sudden increase in myocardial blood discharge function, acute Left heart failure.

3 senile valvular disease, especially acute left heart failure caused by degenerative diseases also account for a certain proportion in the elderly, in addition, the original patients with chronic congestive heart failure, the original elderly patients with asymptomatic heart failure, although There is a decrease in ejection fraction (30% or 35%), but there are no obvious symptoms and signs in the clinic, and acute left heart failure is prone to occur under various inducements.

Common causes of acute left heart failure in the elderly are:

1 infection: respiratory tract infection is the most common, accounting for 68% to 75%, the other is urinary tract infection and intestinal infection, due to infection, the body's metabolism is enhanced, heart rate increases, cardiac load increases, easy to induce acute left heart failure.

2 arrhythmia: such as rapid atrial fibrillation, paroxysmal supraventricular tachycardia, etc., so that the ventricular work suddenly increased, beyond the heart load and acute left heart failure.

3 Infusion and transfusion too much too fast, the elderly heart reserve function is reduced, if the amount of fluid replacement is too fast, the speed is too fast, so that the circulating blood volume suddenly increases, the heart's preload increase is likely to lead to acute left heart failure.

4 other, such as pulmonary embolism, renal failure, emotional agitation, full meal, difficulty in defecation, etc. can induce acute left heart failure.

(two) pathogenesis

The normal heart has a rich reserve capacity, so that it can fully adapt to the various needs of the body's metabolic state. When the myocardial contractility is reduced and/or the load is too heavy, and the myocardial compliance is reduced, the cardiac reserve is significantly reduced. Compensatory mechanisms, including cardiac hypertrophy, increased sympathetic activity and Frank-Starling mechanism (increased cardiac preload, stretching the heart muscles to increase myocardial contractility), thereby increasing myocardial contractility and heart rate to maintain cardiac output, However, the compensatory mechanism is limited. Once decompensation occurs, heart failure occurs. Under normal circumstances, the principle of fluid exchange between capillary fluid in the pulmonary capillaries and capillary fluid exchange in the systemic circulation is consistent. The colloid osmotic pressure and alveolar tissue of the blood. The pressure is the power to prevent extravasation of the fluid, and the capillary pressure of the lung is the main force of fluid extravasation. The colloid osmotic pressure of the lymphatic lymphatic is the force to remove the extravasated fluid. In the case 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 average pressure of normal human pulmonary capillaries is 0.8-1.3 kPa ( 610mmHg), generally not more than 1.6kPa (12mmHg), and the plasma colloid osmotic pressure is 3.34.0kPa (2530mmHg), so it is beneficial to the reabsorption of water by pulmonary capillaries, and the plasma components of pulmonary capillaries are not. Extravasation into the alveolar and interstitial lung, when acute left ventricular dysfunction, left ventricular end-diastolic pressure (LVEDP) and left atrial mean pressure increased, pulmonary venous pressure increased, when pulmonary capillary pressure is greater than plasma colloid osmotic pressure At the time, the blood fluid can seep from the capillaries to the pulmonary interstitium; at the beginning, the lymphatic reflux increases greatly, and the interstitial fluid can be drained, but the pulmonary capillary pressure continues to increase, and the pulmonary interstitial lymphatic circulation has no ability to drain. When there is too much liquid, the fluid accumulates in the pulmonary interstitial, forming interstitial pulmonary edema around the terminal bronchus and pulmonary capillaries; as the interstitial fluid continues to accumulate, the pulmonary capillary pressure continues to increase, the alveolar wall basement membrane and The capillary endothelium is indirectly destroyed, and the formation of plasma and blood into the alveoli, pulmonary edema occurs, the original chronic heart failure patients, such as mitral stenosis, its pulmonary capillary wall and lung The basement membrane is thickened. When the pulmonary circulation increases and the stenotic mitral valve orifice can not smoothly perfuse blood into the left ventricle, the left atrial and pulmonary circulation pressure rises when the capillary hydrostatic pressure is greater than 4.6 to 5.3 kPa (35). Pulmonary edema occurs when ~40mmHg). The sudden increase of capillary hydrostatic pressure in such patients is caused by temporary physical labor, emotional or ectopic tachycardia, such as paroxysmal supraventricular tachycardia, atrium. The occurrence of fibrillation causes the atria to lose the contractile force that squeezes the blood through the mitral valve orifice. The short heart rate and short diastolic phase are not conducive to blood flow through the narrow mitral valve orifice, when the pulmonary capillary pressure rises above the critical point. Pulmonary edema occurs, and mitral stenosis is less common in the elderly.

In acute left heart failure, hemodynamic changes in the cardiovascular system include:

1 left ventricular compliance decreased, ventricular pressure change rate (dp / dt) decreased, left ventricular end-diastolic pressure (LVEDP) increased (except for simple mitral stenosis).

2 left atrial pressure (LAP) and capacity increase.

3 pulmonary capillary pressure or pulmonary venous pressure increased.

4 pulmonary congestion, acute pulmonary edema in severe cases.

5 peripheral vascular resistance (SVR) increased.

6 pulmonary vascular resistance (PVR) increased.

7 heart rate is accelerated.

8 Cardiac stroke volume (SV), cardiac output (CO), and cardiac index (CI) were all reduced.

9 arterial pressure first increased and then decreased.

10 myocardial oxygen consumption increased.

Acute left heart failure prevention in the elderly

Pulmonary infection caused or induced acute left heart failure is a very common cause and cause of the elderly, so the use of effective antibiotics to control infection is one of the important links to prevent and treat acute left heart failure in the elderly.

Complications of acute left heart failure in the elderly Complications, shock arrhythmia, renal failure, elderly patients with acute left heart failure, coronary heart disease

Mainly complicated by shock, severe arrhythmia, renal failure and so on.

Symptoms of acute left heart failure in the elderly Common symptoms Myocardial infarction arrhythmia Diuretic nose flaps Paroxysmal nocturnal dyspnea Hypertension Diastolic cerebral ischemic coma

Difficulty breathing

Dyspnea is the most common and most prominent symptom of acute left heart failure. The patient feels difficulty breathing, and has difficulty and shortness of breathing. The appearance of the chest muscles is excessive, the frequency is accelerated, and the nose is fanned.

(1) Paroxysmal nocturnal dyspnea: is an early manifestation of acute left heart failure. Most patients are asleep after 1-2 hours of sleep at night. They suddenly wake up due to shortness of breath and shortness of breath. They need to sit up immediately and have frequent cough and wheezing. Cough up the foamy sputum, after taking the sitting position, it can be gradually relieved after a few minutes. Otherwise, it can be a persistent state of cardiac asthma and develop into acute pulmonary edema. Its mechanism:

1 After the patient is lying down, the blood volume of the vein is increased, which exceeds the limit of the left heart load, which aggravates the pulmonary congestion.

After 2 cases, the body venous pressure decreased, and the surrounding subcutaneous edema fluid was gradually absorbed, which increased the circulating blood volume and also aggravated pulmonary congestion.

3 night vagus nerve excitability increased, on the one hand, coronary artery contraction, myocardial blood supply decreased, affecting myocardial contractility, so that left ventricular discharge decreased, so pulmonary congestion increased; on the other hand, bronchial smooth muscle contraction, aggravated lung ventilation Obstruction increases myocardial hypoxia and seriously affects heart function.

4 When lying down, the diaphragm muscles rise, the lung capacity decreases, and the hypoxia is aggravated.

(2) sitting breathing: the patient has difficulty breathing when lying down, often forced to take a sitting or semi-recumbent position, can be relieved or relieved, called sitting breathing, in severe cases, the patient must sit on the bed or chair, The two legs are drooping, the upper body is leaning forward, and the hands are tightly gripped on the edge of the bed or chair to assist in breathing and relieve symptoms. The mechanism is mainly the redistribution of circulating blood in the body.

1 The effect of pulmonary blood volume; in the supine position, the blood in the lower extremities and the intra-abdominal venules, due to changes in body position, more reflux to the heart and pulmonary circulation, can increase the lung blood volume by hundreds of milliliters, while sitting, the upper body The blood is partially transferred to the abdominal cavity and lower limbs due to gravity, and the amount of blood returning to the heart is reduced, and the blood stasis is relieved.

2 changes in vital capacity: in the supine position, due to diaphragmatic elevation, lung capacity decreased significantly (average reduction of 25%), while in the sitting position, lung capacity increased by 10% to 30% compared with lying.

(3) Dyspnea in acute pulmonary edema: Cardiac pulmonary edema in the elderly is the result of acute pulmonary capillary filtration pressure, continuous increase and damage of alveolar capillary membrane, and its dyspnea is due to:

1 pulmonary interstitial edema: a large amount of extravasation of capillaries can not be absorbed by lymphoid tissue, the liquid first extravasated to the pulmonary interstitial, so that the alveoli are squeezed, the gas in the alveoli is difficult to diffuse into the pulmonary capillaries, reducing gas exchange The effective area leads to hypoxemia and severe dyspnea. The interstitial fluid can also compress the bronchioles, making the breathing difficult, and giving out a wheezing sound like asthma, called cardiogenic asthma.

2 Intra-alveolar edema: If no emergency measures are taken during pulmonary interstitial edema, the condition can be further developed, and the fluid is extravasated into the alveoli, so that the alveoli are filled with exudate containing plasma protein, which forms a foam due to respiratory agitation, plus fine The bronchial mucosa is swollen, which can cause obstruction of alveolar and bronchioles, severely affecting gas exchange, aggravating hypoxemia, lowering the surface tension of the alveolar fluid, further reducing lung compliance, and increasing the elastic resistance of lung tissue. Respiratory frequency is accelerated by nerve reflex. In order to assist the lungs to exhale and inhale, the respiratory muscles must increase the workload and forcefully breathe. As a result, the oxygen consumption of the lungs increases, further aggravating hypoxia, and the patient has extreme breathing difficulties.

Cough

In the case of paroxysmal dyspnea and sitting breathing at night, generally only coughing while lying down, while coughing out foam, can be relieved after sitting up, in the acute pulmonary edema, cough frequently, cough up white or pink foam In severe cases, a large amount of thin foamy liquid can be seen from the nose and mouth, which is caused by the infiltration of plasma and red blood cells into the interstitial lung and alveoli during severe pulmonary congestion.

3. Hairpin

In acute left heart failure, there may be hair crests of varying degrees, mostly before the lips, ear lobe and extremities. When there is acute pulmonary edema, there are many persistent cyanosis. This is due to pulmonary congestion, pulmonary interstitial and alveolar edema. The gas exchange of the lungs is insufficient for oxygenation of hemoglobin and the increase of hemoglobin in the blood.

4. Chen-Shi breathing

That is, tidal breathing, regular changes in breathing, speeding up from gradual deepening, and reaching the peak, gradually becoming shallower and slower, until it stops again, more common in acute pulmonary edema, suggesting a poor prognosis, which is due to acute left heart failure. The left ventricle discharges less, making the brain less blood supply, cerebral ischemia and hypoxia, and reducing the sensitivity of the respiratory center. After the respiratory depression is slowed down, the blood carbon dioxide reserves to a certain concentration, so that the respiratory center can be excited. The breathing is deepened faster. After the concentration of carbon dioxide in the blood is lowered, the respiratory center is transferred to the suppression state, and the breathing is weakened and slowed down to stop.

5. Mental state

In acute left heart failure, due to difficulty in breathing, hypoxemia makes the patient very painful. The patient's sitting position is irritated, the expression is extremely anxious, and the complexion is gray. Due to the emergency response of the hypoxic state, the patient may sweat and the skin is damp and cold. If the time is long, the blood pressure will drop due to severe hypoxia and cardiac output, and the pulse will be weak. The mind will turn from waking to confusion, lethargy, and finally coma, and death will occur with cardiogenic shock.

6. Signs

The complexion is gray, bun, sitting and breathing, limbs are cold, the pulse is weak, there may be alternating veins, the heart is enlarged to the left or the left, the heart rate is increased, the apex of the apex is low and blunt, and the diastolic gallop and arrhythmia can be heard. In particular, the emergence of diastolic galloping is an important manifestation of acute left heart failure. It occurs due to excessive left ventricular diastolic load, increased left ventricular diastolic pressure, increased left atrial pressure, and rapid left ventricular filling. Due to obstruction, blood pressure may increase in the early stage, but the duration of this reaction is not long. Due to the serious lack of blood pumping function, the patient is hypotensive, or the blood pressure is completely undetectable. Both lungs can smell blisters and wheezing. When acute pulmonary edema is formed, both lungs are covered with blisters, wheezing sounds and snoring sounds like boiling water. If the voice is limited to one side, especially to the left side, it should be alert to whether it is caused by pulmonary embolism.

7. Shock

It is the end-stage manifestation of acute pulmonary edema. It is characterized by decreased blood pressure or blood pressure. It is unresponsive to the booster drug until it can not be maintained. The limbs are cold, the urine volume is very little or no urine, the consciousness is blurred, and the breathing is accelerated. The voice of the department can be reduced, but the prognosis is more dangerous. This is due to the lack of pumping function, the reduction of effective circulating blood volume, and the decrease of blood volume. The final heart rhythm and breathing are severely disordered and dying.

According to the difference in cardiac output, acute pulmonary edema is clinically divided into 2 types:

Type I: high-output pulmonary edema, clinically more common, clinical features are blood pressure is often higher than before the onset, and there are cycles of acceleration, increased cardiac output, pulmonary artery pressure and pulmonary capillary pressure significantly increased, etc. Patients are more common in patients with hypertensive heart disease, rheumatic or degenerative valvular disease (aortic valve or mitral regurgitation), syphilitic heart disease, excessive transfusion of blood transfusion, etc., at this time, patients The increase in cardiac output is relative, actually lower than before the onset, but the cardiac output is higher than the normal person in a quiet state.

Type II: low-output pulmonary edema, clinical features are constant or decreased blood pressure, decreased cardiac output, rapid pulse rate, elevated pulmonary hypertension, etc. This type of patient is seen in acute extensive myocardial infarction, diffuse myocarditis, rheumatic heart valve Pulmonary edema caused by disease (severe mitral stenosis and aortic stenosis).

The above classification has important guiding significance for the clinical treatment of acute pulmonary edema. Type I acute pulmonary edema is effective in reducing the preload, such as vasodilators, rapid diuretics, tourniquet ligation, etc. Type II acute pulmonary edema Treatment with the above method may have a temporary effect, but may cause hypotension or even shock.

Examination of acute left heart failure in the elderly

Arterial blood gas analysis

In acute left heart failure, arterial partial pressure of oxygen (PaO2) often decreases to varying degrees; in acute pulmonary edema, when interstitial edema occurs, diffuse obstruction of oxygen into the blood causes PaO2 to drop and hypoxia occurs. Hypertension; further development of alveolar pulmonary edema, in addition to hypoxemia is more obvious, often accompanied by hyperkinetic dysfunction due to dysfunction, and metabolic acid caused by tissue hypoxia, increased anaerobic metabolism Poisoned.

The normal value of PaO2 is generally above 10.6 kPa (mmHg). The value of PaO2 in patients over 60 years old can be estimated by subtracting 80 from the actual age and 60, which is {80-(patient age-60)}. Clinically simple and easy to perform, according to the level of PaO2, usually 7.98 ~ 10.6kPa (60 ~ 80mmHg), 5.32 ~ 7.98kPa (40 ~ 60mmHg) and 5.32kPa (40mmHg) are said to be mild, moderate And severe hypoxemia.

2. Hemodynamic examination

Using the Swan-Garz balloon to the floating catheter, monitoring the patient's pulmonary capillary wedge compression (PCWP) and cardiac index (CI) at the bedside is the most valuable diagnostic method for acute left heart failure. Normal: PCWP is 0.8 to 1.6 kPa. (6 ~ 12mmHg), CI is 2.5 ~ 4.2L / (min · m2), when PCWP> 2.4kPa (18mmHg), CI is normal, suggesting pulmonary congestion; PCWP is 3.3 ~ 4.6kPa (25 ~ 35mmHg), CI is 2.02 ~2.5L/(min·m2), suggesting pulmonary edema; PCWP>2.4kPa (18mmHg), CI<2.0L/(min·m2), suggesting a poor prognosis for cardiogenic shock.

Chest X-ray examination

It is valuable for the diagnosis of acute left heart failure.

The X-ray features of interstitial pulmonary edema are increased lung texture, thickening, disorder, and more obvious lung tip; lung field transillumination is reduced, and uneven density of patchy water or reticular shadow; uneven hilar shadow The contours are blurred; the Kerley A and B lines are often located in the interstitial space or the interlobular space. In the case of alveolar pulmonary edema, the cloud-like shadows with unclear borders extend from the hilum to the surrounding, and the typical large shadows are outward from the hilum. Butterfly-like distribution, large cloud-like appearance in the lungs, large nodules, small shadows, small nodules and miliary, blurred edges.

According to the severity of pulmonary edema on the X-ray, Kigler et al. divided it into 3 degrees:

1 Mild: The lungs and pulmonary vascular congestion and interstitial pulmonary edema caused by blurred lung texture or Kerley B line.

2 Moderate: Small patchy shadows caused by alveolar pulmonary edema, and the total area of dense shadows is estimated to be more than 1/2 of the total area of each lung field.

3 Severe: Large villi-like dense shadows caused by alveolar pulmonary edema, the total area of which exceeds 1/2 of the lung field.

2. ECG examination

Have the performance of the original basic heart disease, as well as help to understand the presence or absence of arrhythmia, acute myocardial ischemia and other manifestations.

3. Echocardiography

Left ventricular end-diastolic diameter increased, ventricular wall motion amplitude was extremely weakened, left ventricular ejection fraction was significantly reduced, and basic heart disease performance.

Diagnosis and diagnosis of acute left heart failure in the elderly

Diagnostic criteria

According to clinical symptoms, signs and various auxiliary examinations can make a diagnosis of acute left heart failure.

1. There is a basis for heart disease that causes acute left heart failure, such as patients with previous coronary heart disease, acute myocardial infarction, hypertension, senile valvular disease and other medical history.

2. Sudden severe breathing difficulties, sitting breathing; coughing and coughing a lot of white or pink foam , heart rate increased, there are galloping horses, both lungs full of blisters and wheezing sounds.

3. X-ray examination showed thickening of the bronchial and vascular shadows, showing the kerley B line, alveolar edema with cloud-like butterfly wing shadows on both sides of the hilum.

4. PVWP > 4.0 kPa (30 mmHg).

Differential diagnosis

1. Bronchial asthma.

2. Tracheal or bronchial lung cancer

Cancer can cause tracheal and bronchoconstriction. If accompanied by secondary infection, it may have symptoms such as shortness of breath and cough. It should be differentiated from acute left heart failure. The history of cancer patients is shorter, and there is no obvious seizure in shortness of breath. Wheezing is limited to a certain part, more obvious when exhaling, no history and signs of heart disease, X-ray can find signs of lung cancer.

3. Chronic bronchitis complicated by emphysema

When the elderly patients are more common, the asthma is increased, and the wheezing is increased. However, the general condition is longer, the air urgency is progressively aggravated, the amount of sputum is more, the mucus is the same, and there is no characteristic of nocturnal paroxysmal episodes. The swelling sign, although there is enlargement of the right ventricle, there is no left ventricular enlargement and pathological murmur. X-ray examination has signs of emphysema and rough lung texture.

4. Old age, debilitation, obesity and severe anemia, etc., can produce labor dyspnea, but no other signs of acute left heart failure, pulmonary dysfunction caused by chronic pulmonary heart disease, but also dyspnea, but chronic bronchus, The past history of lung and thoracic diseases, signs of emphysema, heart enlargement is mainly left ventricle, cyanosis is more difficult than breathing, such as blood gas analysis and lung function test, it is more conducive to identification, but should pay attention to elderly patients It is not uncommon for patients with chronic pulmonary heart disease and coronary heart disease to coexist at the same time. If it is not easy to rule out acute left heart exhaustion, the treatment should be considered.

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