2 Name of disease Acute left heart failure
English name acute left heart failure
4 acute left heart failure, alias acute left heart failure; Acute left heart failure
5 Classification Cardiovascular Medicine > Heart Failure
6 ICD number I50. 1
Epidemiology Although the incidence and mortality of some important cardiovascular diseases such as coronary heart disease and hypertension have decreased, the incidence of heart failure is increasing. 5 192 men and women were followed up for 20 years in Framingham area. It was found that the incidence of heart failure was 3.7% in men and 2.5% in women. The National Heart, Lung and Blood Research Center of the United States has diagnosed more than 2 million patients with heart failure, and about 400,000 cases of acute heart failure are newly diagnosed every year.
8 Etiology of acute left heart failure The common causes of acute left heart failure are:
① Myocardial infarction related to coronary heart disease, especially acute extensive anterior myocardial infarction, muscle and tendon rupture, ventricular septal rupture and perforation.
② Acute valve regurgitation caused by valve perforation and chordae tendineae rupture caused by infective endocarditis;
③ Others: hypertension, sharp increase of blood pressure, tachyarrhythmia or severe bradyarrhythmia based on the original heart disease; Transfusion, infusion too much, too fast, etc.
9 Pathogenesis The pathophysiological basis of acute left heart failure is the sudden and severe weakening of myocardial contractility, the sharp decrease of cardiac output, or the acute regurgitation of left ventricular valve, the rapid increase of end-diastolic pressure and poor pulmonary venous return. Due to the rapid increase of pulmonary vein pressure, the wedge pressure of pulmonary capillary also increases, which makes the fluid in blood vessels penetrate into pulmonary interstitial and alveoli, forming acute pulmonary edema.
The principle of fluid exchange in pulmonary capillaries is the same as that in systemic circulation. The colloid osmotic pressure of blood and the pressure of alveolar tissue are the forces to prevent fluid extravasation, while the pressure of pulmonary capillaries is the main force to prevent fluid extravasation, and the colloid osmotic pressure of pulmonary lymphatic vessels is the force to remove extravasated fluid. In the case of little change in colloid osmotic pressure, the level of pulmonary capillary pressure is the main factor to determine whether fluid extravasates. Compared with systemic circulation, pulmonary circulation is a low-pressure system. The average pressure of pulmonary capillaries is 7.5 ~ 1.0 mmHg, while that of colloid osmotic pressure is about 27mmHg, which is beneficial to prevent fluid from extravasating into pulmonary interstitial or alveoli. When left ventricular dysfunction occurs, the left ventricular end-diastolic pressure increases, and the related left atrial pressure and pulmonary capillary pressure also increase accordingly. For example, when the average pulmonary capillary pressure rises to 25mmHg, it will reach a critical value. If it exceeds this value, the fluid oozing from blood vessels can no longer be completely removed by lymphatic vessels, and it begins to accumulate in the interstitial lung, and then penetrates into alveoli to form pulmonary edema.
10 Clinical manifestations of acute left heart failure 10. 1 Dyspnea is the most common and prominent symptom of left heart failure. Breathing exercise is an involuntary activity, but when breathing is difficult, the patient feels breathless and needs to breathe hard and quickly, and the breathing can reach 20 ~ 30 times/minute.
10.1.1(1) Sitting breathing is a unique sign of acute left heart failure. It is characterized by shortness of breath when lying down, and the symptoms can be obviously relieved when lying down. In severe cases, the patient is forced to take a semi-sitting position or a sitting position, so it is called sitting breathing. In the worst case, you often sit on the bed or in an armchair, with your legs drooping and your upper body leaning forward to enhance the function of your breathing muscles. This is a compensatory mechanism to reduce pulmonary congestion. Normal people's lung capacity decreased by 5% on average when lying down, while patients' lung capacity decreased by 25% on average when sitting up and breathing, indicating that lung congestion and lung stiffness were more serious. The mechanisms that cause dyspnea are: ① Increased pulmonary capillary pressure * * * Vagal nerve fibers located beside the blood vessel bed reflexively excite the respiratory center to produce Chueh's reflex, which accelerates breathing. ② With the increase of pulmonary blood, the volume of pulmonary capillary bed increases, the alveolar volume decreases correspondingly, and the lung compliance decreases, that is, more negative pressure is needed to expand the alveoli when inhaling, and more positive pressure is needed to collapse the alveoli when exhaling, so the respiratory muscles need extra work. ③ The increase of pulmonary capillary bed compresses bronchioles and increases ventilation resistance. After the patient was forced to sit up, due to the redistribution of blood, the blood volume in pulmonary circulation decreased and the symptoms were alleviated.
10. 1.2 (2) Paroxysmal dyspnea at night is the clinical manifestation of acute left heart failure with acute exacerbation of pulmonary congestion or chronic pulmonary congestion. Paroxysmal dyspnea can be divided into two categories: ① Acute left heart failure, mainly left heart failure, which is more common. ② Left atrial failure is the main cause of mitral stenosis. But the clinical manifestations are the same. Typical cases occur after lying flat or sleeping for several hours at night, suddenly waking up, forced to sit up, shortness of breath or accompanied by cough. Lighter, it can be relieved in a few minutes after sitting up; Severe cases are accompanied by cough, phlegm and asthma, which is called cardiogenic asthma. The mechanism of paroxysmal dyspnea is that after sleeping 1 ~ 2 hours, the body edema fluid is gradually absorbed, and venous reflux increases, which makes the patient's heart volume load increase, and the respiratory center is insensitive at night, and shortness of breath occurs only when the lung congestion and ischemia reach a certain level. During the attack of cardiogenic asthma, arterial pressure, pulmonary artery pressure and capillary pressure also increase. If the increased arterial pressure suddenly drops, it is a bad omen.
10.2 acute pulmonary edema acute pulmonary edema is the result of the rapid and continuous increase of pulmonary capillary pressure, which is qualitatively different from the above two kinds of dyspnea, that is, a large amount of liquid in the capillary extravasates and cannot be absorbed by lymphatic tissue. First, the fluid infiltrates into the interstitial lung, causing the alveoli to be squeezed, reducing the effective area of gas exchange, and at the same time reducing the compliance of the lungs, causing serious breathing difficulties. The fluid in interstitial lung can also compress bronchioles, further aggravate dyspnea and make wheezing sound similar to asthma, which is called "cardiogenic asthma". When the left ventricular end diastolic pressure, left atrial pressure and pulmonary capillary pressure increase more than 30mmHg, pulmonary edema can occur. According to the development process and clinical manifestations of pulmonary edema, it can be divided into the following five stages:
10.2. 1 (1) The symptoms are atypical at the onset, and the patient is short of breath, sometimes showing anxiety. Physical examination found that the skin was pale, wet and cold, and the heart rate increased. X-ray examination shows that there may be a typical foggy or "butterfly" shadow near the hilum of the lung.
10.2.2 (2) Interstitial pulmonary edema has dyspnea, but no foam sputum. Sitting and breathing, pale skin and frequent cyanosis. In some patients, the jugular vein is dilated, and wheezing can be heard in the lungs, sometimes accompanied by moist rales.
10.2.3 (3) Pulmonary edema has symptoms such as frequent cough, extreme dyspnea and pink foam-like phlegm cough. Both lungs are full of large and medium-sized blisters with wheezing sound.
10.2.4 (4) In shock stage, blood pressure decreased, pulse accelerated, pale skin, cyanosis aggravated, cold sweat dripping, and confusion.
10.2.5 (5) At the end of his life, his breathing and heart rhythm were seriously disordered and he was on the verge of death.
According to the degree, speed and duration of cardiac insufficiency, and the difference of compensatory function, there are the following different manifestations:
10.3 cardiogenic syncope is called cardiogenic syncope, which is a temporary loss of consciousness caused by cerebral ischemia and decreased cardiac output. When syncope attacks last for several seconds, limb convulsions, apnea and cyanosis may occur, which is called Asperger's syndrome. Most seizures are short-lived, and consciousness usually recovers immediately after the seizure. Mainly seen in acute cardiac drainage obstruction or severe arrhythmia.
10.4 Cardiogenic shock The shock of insufficient cardiac output due to low cardiac output function is called cardiogenic shock. When cardiac output suddenly drops significantly, it is too late for the body to compensate by increasing circulating blood volume, but peripheral and visceral blood vessels can contract significantly through nerve reflex, maintain blood pressure and ensure blood supply to the heart and brain. In addition to the general manifestations of shock, it is often accompanied by cardiac insufficiency, increased pulmonary wedge entrapment pressure, jugular vein dilatation and so on.
The common signs of left heart failure are: ① pulse alternation: the rhythm is normal, and one is strong and one is weak alternately. With the aggravation of heart failure, alternating pulsation can be detected when palpating peripheral arteries. The mechanism is as follows: A. The myocardial fibers involved in ventricular contraction are different. When the pulse is weak, some myocardium is in a relative refractory period, and there are fewer myocardial fibers involved in ventricular contraction, so the myocardial contractility is weak. At the next contraction, all the myocardium is in a reaction period, and many myocardial fibers participate in ventricular contraction, so the pulse is strong. B. due to different degrees of myocardial relaxation. ② Ventricular galloping rhythm: It is a common sign of left heart failure, which is most easily heard when lying on the left side or inside the apex, and enhanced when exhaling. ③ Pulmonary rales: At the beginning, there may be no rales or only wheezing in the lungs, but soon there will be wet rales at the bottom of both lungs, which will spread rapidly to the whole lungs from bottom to top. In severe cases, there will be a coarse rale of the whole lung, like the bubbling sound of boiling water.
1 1 Complications of acute left heart failure may be complicated by cardiogenic shock, multiple organ failure, electrolyte disorder and acid-base imbalance.
1 1. 1 cardiogenic shock Acute left heart failure, due to the obvious and sudden decrease of short-term cardiac output, 50% of them were accompanied by severe right ventricular damage that did not respond to volume load, resulting in blood pressure drop and insufficient peripheral circulation perfusion, thus causing cardiogenic shock.
1 1.2 Acute cardiac insufficiency caused by multiple organ failure, especially cardiogenic shock, can cause acute ischemia, hypoxia and dysfunction of important organs. Kidney, brain, liver and other organs can appear uncompensated multiple organ failure, which further worsens heart function.
1 1.3 electrolyte disorder and acid-base imbalance can lead to hypokalemia, hyponatremia, hypochlorous metabolic alkalosis and metabolic acidosis, due to the use of diuretics, salt restriction, low food intake and frequent nausea, vomiting and sweating.
12 laboratory examination of arterial blood gas analysis: oxygen saturation can be significantly reduced, carbon dioxide content is normal or reduced, and pH is greater than 7.0.
13 auxiliary examination 13. 1 X-ray chest film showed butterfly shadow in hilum of lung and signs of pulmonary edema extending around, enlarged heart boundary and weakened apical pulsation.
13.2 ECG sinus tachycardia or various arrhythmias, myocardial damage, left atrial and left ventricular hypertrophy, etc.
14 diagnosis of acute left heart failure According to the medical history, typical symptoms and signs and auxiliary examination results, it is often not difficult to make a diagnosis of acute left heart failure.
14. 1 has the symptoms of sudden and severe dyspnea, with a breathing frequency of 30-40 times per minute, forced sitting, pale face, cyanosis, sweating, irritability, frequent cough and pink foam sputum. Extremely severe patients may be delirious due to brain hypoxia. In the early stage of pulmonary edema, blood pressure may temporarily increase due to vasoconstriction caused by sympathetic nerve activation; But as the disease continues, blood pressure drops. In severe cases, cardiogenic shock may occur. [ 1]
14.2 signs During auscultation, the lungs were covered with moist rales and wheezing sounds, the first heart sound at the apex of the heart weakened, tachycardia appeared, the galloping rhythm was audible in the early diastolic period, and the second heart sound of the pulmonary valve was hyperactive. [ 1]
14.3 Auxiliary examination (1) Echocardiography showed that atria and ventricles were enlarged and left ventricular ejection fraction was decreased (LVEF
(2) Laboratory examination showed that the level of plasma brain natriuretic peptide (BNP or NTproBNP) increased [1].
(3) Chest X-ray showed enlargement of the heart and pulmonary edema [1].
15 The differential diagnosis of acute left heart failure should be differentiated from bronchial asthma and adult respiratory distress syndrome.
15. 1 bronchial asthma, whether it is cardiogenic asthma or bronchial asthma, has symptoms such as sudden onset, cough, dyspnea and asthma. And their treatment principles are quite different. Bronchial asthma is a reversible obstructive pulmonary disease with increased airway resistance reactivity, and patients often have a long history of recurrent asthma or allergies. Young people are more common. Bronchial asthma cough often has no sputum or sticky white sputum, and when complicated with infection, there are often signs of emphysema. Unless complicated with pneumonia or atelectasis, there is generally no moist rales, and the heart examination is often normal. Pulmonary function examination showed that airway resistance increased and blood eosinophils increased (eosinophil count was often > 250 ~ 400/? l).
15.2 adult respiratory distress syndrome (ARDS) ARDS is also called shock lung, wet lung, pump lung, hyaline membrane disease of adult lung, etc. Dyspnea, cyanosis, lung rales and wheezing are easily confused with acute left heart failure. ARDS generally has no history of lung, and any disease process that can directly or indirectly cause acute lung injury can cause this syndrome. Common diseases include lung trauma, drowning, shock, cardiopulmonary bypass, bacterial or viral pneumonia, toxic pancreatitis and so on. Often on the basis of the primary disease, or 24 ~ 48h after injury, dyspnea is serious but forced to sit and breathe less, hypoxemia is gradually aggravated, and ordinary oxygen therapy is ineffective or ineffective. Although there is asthma with lung moist rales, there is no galloping rhythm, heart enlargement and organic murmur in heart examination. The treatment measures of cardiogenic asthma often have no obvious effect. The floating catheter showed that the wedge-shaped embedded pressure of lung was less than 65438 0.5 mmhg (65438 0.99 kPa). Positive end-expiratory pressure ventilation is effective in adjuvant therapy. ARDS is often complicated with multiple organ failure.
Treatment of acute left heart failure 16 acute left heart failure is a cardiac emergency, and every second should be used for first aid. Specific treatment measures are as follows:
The therapeutic principle of 16. 1 is to remove the inducement, treat the primary disease, reduce the left ventricular filling pressure, increase the left ventricular stroke volume and reduce the circulating blood volume [1].
16.2 general measures (1) immediately ask the patient to take a sitting position or a semi-sitting position, droop or lower his legs, or tie his limbs with a tourniquet, and relax one limb in turn every 15 minutes to reduce venous reflux and pulmonary edema.
(2) Oxygen inhalation: oxygen is immediately given through a large-flow nasal tube, and inhaled through a pure oxygen nasal tube at a speed of10 ~ 20 ml/s. If the patient's condition is particularly serious, put on a mask and apply pressure with an anesthesia machine [1]. If the arterial oxygen partial pressure cannot be maintained at 60mmHg, positive pressure breathing should be added [1].
Immediately supply oxygen and eliminate foam. Oxygen can be humidified with 40% ~ 70% alcohol before inhalation. You can also use 1% silicone solution instead of alcohol, or inhale dimethyl silicone oil defoaming aerosol to reduce the surface tension of foam in alveoli, rupture the foam and improve lung ventilation function. Under normal circumstances, oxygen can be supplied through a nasal catheter, and those with severe hypoxia can also use a mask with high concentration and high dose of oxygen (5 L/min), and after the hypoxia is corrected, conventional oxygen supply can be changed.
(3) Rapid establishment of venous access: ensure intravenous administration and collect blood samples such as electrolytes and renal function. Send a blood gas sample as soon as possible.
(4) ECG and blood pressure monitoring: to deal with all kinds of serious arrhythmia that may exist at any time.
16.3 inject morphine 5 ~ 10 mg subcutaneously or intramuscularly immediately after sedation (directly or slowly intravenously after dilution with normal saline), and inject morphine 5 mg intravenously if necessary; Or pethidine (dolantin) 50 ~ 100 mg intramuscular injection. It has been proved that morphine not only has the functions of calming, relieving patients' anxiety and slowing breathing, but also dilates veins and arteries, thus reducing the front and back load of the heart and improving pulmonary edema.
Intravenous injection of 3 ~ 5 mg morphine can rapidly dilate systemic veins, reduce venous reflux and reduce left atrial pressure [1].
Disabled for patients with respiratory failure [1]. The elderly, asthma, coma, severe lung diseases, respiratory depression and bradycardia, and atrioventricular block should be used with caution or prohibited.
16.4 for rapid diuresis, diuretics with strong quick effect should be selected immediately, and medullary diuretics are commonly used, such as intravenous furosemide (20 ~ 40mg) or bumetanide (butylamide) 1 ~ 2mg, so as to reduce blood volume and cardiac preload.
Note: Do not overdo it when using diuretics, especially pay attention not to cause hypokalemia [1].
16.4. 1 furosemide 20 ~ 40 mg intravenous injection, completed within 2 minutes, 10 minutes effective, lasting 3 ~ 4 hours, repeated after 4 hours [1]. In addition to diuresis, this medicine also has the function of dilating veins, which is beneficial to the relief of pulmonary edema [1].
16.5 simple vasodilator emergency treatment, sublingual nitroglycerin 0.5mg, 5 ~ 10min/ time, up to 8 times. If the curative effect is not obvious, it can be changed to intravenous infusion of vasodilator. Commonly used preparations are nitroglycerin, sodium nitroprusside and phentolamine. If the blood pressure is lower than 90/40 mmHg (12/5.3 kPa) during the application of vasodilators, dopamine can be added to maintain blood pressure, and the dosage or dripping speed of vasodilators should be reduced as appropriate.
Note: When using vasodilators, pay attention to prevent blood pressure from falling too fast [1].
The tolerance of nitroglycerin patients to 16.5. 1 varies greatly, starting at 5 ~ 10μ g/min, and then adjusting 1 time every 10 minute, and increasing by 5 ~10 μ g/each time.
Nitrate drugs, such as nitroglycerin, are prone to drug resistance after continuous intravenous drip for more than 72 hours. Pay attention to changing other vasodilators or using them intermittently [1].
16.5.2 Sodium nitroprusside was injected intravenously with a concentration of 50mg/500ml and a rate of 0.5μ g/(min kg), and the dosage was gradually adjusted according to the treatment response. The usual dose is 3 μ g/kg per minute and the maximum dose is 10 μ g/kg per minute.
The adverse reactions of sodium nitroprusside are [1]: ① the blood concentration of this product is high, and the rebound blood pressure may increase when the drug is stopped suddenly; ② Blood pressure drops too fast and too fast, causing dizziness, sweating, headache, muscle twitching, nervousness or anxiety, irritability, stomachache, reflex tachycardia or arrhythmia. The occurrence of symptoms is related to the speed of intravenous administration, but has little to do with the total amount. Reducing the dose or stopping the drug can improve it; ③ Thiocyanate poisoning can cause dyskinesia, blurred vision, delirium, dizziness, headache, loss of consciousness, nausea, vomiting, tinnitus and shortness of breath. Drug administration should be stopped and symptomatic treatment should be given.
Matters needing attention in the use of sodium nitroprusside [1]:
(1) is sensitive to light. The infusion solution should be freshly prepared, and the infusion bottle should be wrapped in black paper to avoid light quickly.
(2) Other drugs should not be added to the solution. The prepared solution can only be slowly infused intravenously, and it is best to use a micro infusion pump, so that the administration speed can be accurately controlled.
(3) During the application of this product, blood pressure should be measured frequently, preferably in the monitoring room.
(4) If the renal function is not complete, and the product has been used for more than 48 ~ 72 hours, cyanide or thiocyanate in the plasma shall be determined every day, and the thiocyanate shall not exceed100μ g/ml; Cyanide does not exceed 3μmol/ml.
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16.6 Positive inotropic drugs Positive inotropic drugs are suitable for patients with acute left heart failure and hypotension, and can be used alone or in combination. Generally speaking, they should start with a small dose and gradually increase the dose as needed. If the blood pressure is obviously reduced, they can be used in combination with m- hydroxylamine (alamin) for a short time to quickly raise blood pressure and ensure blood perfusion in the heart and brain.
(1) Dopamine: Low dose of dopamine (2μg/kg per minute) can increase myocardial contractility and cardiac output. It can be used for patients with pulmonary edema and hypotension. [ 1]
(2) Dobutamine: the initial dose is 2 ~ 3 μ g/kg per minute, and the highest dose can reach 20 μ g/kg per minute [1].
(3) Phosphodiesterase inhibitor (PDEI): Milrinone is a type III PDEI, which has a positive inotropic effect and reduces peripheral vascular resistance. Inject 25μg/kg at 10 ~ 20 minutes, and then drip at the rate of 0.375 ~ 0.75 μ g/(kg min). [ 1]
16.7 cardiotonic drugs: 0.4 ~ 0.8 mg can be injected intravenously for the first dose, and 0.2 ~ 0.4 mg can be injected as appropriate after 2 hours [1].
Digitalis drugs are most suitable for patients with atrial fibrillation with fast ventricular rate and known ventricular enlargement with left ventricular systolic dysfunction [1]. Digitalis has a good therapeutic effect on cardiogenic pulmonary edema caused by pressure overload, such as aortic stenosis and hypertension. It is more life-saving for acute pulmonary edema caused by mitral stenosis with rapid atrial fibrillation.
Digitalis should not be used in patients with acute myocardial infarction within 24 hours [1]. Patients with severe mitral stenosis and sinus rhythm are prohibited [1].
Erioside C (Ceylon) is often the first choice. For those who have no recent medication history, dilute 0.4 ~ 0.6 mg and inject slowly intravenously. For left atrial failure caused by rapid atrial fibrillation or supraventricular tachycardia, lanatoside C should be the first choice, and β receptor blockers can also be used as appropriate.
16.8 treatment of bronchospasm according to typical symptoms and signs, attention should be paid to the differentiation between acute dyspnea and bronchial asthma. Coughing pink foam sputum and apical diastolic rhythm are helpful to diagnose pulmonary edema and distinguish cardiogenic shock complicated with pulmonary edema from shock caused by other reasons. [ 1]
0.25g aminophylline plus normal saline or glucose solution, intravenous drip, can relieve the dyspnea caused by bronchospasm [1].
250mg is added to 20 ml of 5% glucose solution for slow intravenous injection, or 500mg is added to 250 ml of 5% glucose solution for intravenous drip, which is especially suitable for patients with obvious wheezing, and can relieve bronchospasm and strengthen diuretic effect.
16.9 inducement and etiology treatment After the acute symptoms are relieved, the inducement and basic etiology should be treated [1].
Hypertensive patients should correct rapid ectopic arrhythmia if they take antihypertensive measures; Patients with mitral stenosis receive emergency balloon mitral valvuloplasty or mitral valvulotomy.
16. 10 adrenocortical hormone has anti-allergic, anti-shock, anti-exudation and stress relieving effects. Dexamethasone 10 ~ 20 mg is generally used for intravenous injection or intravenous drip. For patients with active bleeding, this product should be used with caution or disabled. If it is acute myocardial infarction, it is generally not used routinely unless it is complicated with heart block or shock.
16. 1 1 mechanical auxiliary ventilator mask method for continuous positive airway pressure oxygen inhalation can be used for severe acute left heart failure of various reasons, which is safe and effective.
16. 12 notes: ECG and hemodynamics should be monitored during treatment.
17 prognosis the short-term prognosis of acute heart failure is related to the basic cause, the degree of cardiac function deterioration and whether the rescue is timely and reasonable. Acute left heart failure caused by rapid increase of blood pressure, severe arrhythmia, excessive and rapid infusion and other factors is easy to control and has a relatively good prognosis. The mortality of acute heart failure and cardiogenic shock caused by acute myocardial infarction is high. The mortality rate of valvular heart disease complicated with acute left heart failure is high. 62% patients with mitral stenosis died of acute heart failure. 70% patients with aortic stenosis died of acute left heart failure. After acute left heart failure, most myocardial diseases gradually develop into refractory heart failure with poor prognosis.
18 prevention of acute left heart failure 1. Timely control or eliminate infectious lesions inside and outside the heart, and control infectious lesions such as tonsillitis caused by hemolytic streptococcus; Prevention and control of rheumatic activities; Actively prevent and control infective endocarditis, respiratory tract infections and infections in other parts.
2. Quickly correct arrhythmia? When arrhythmia occurs in patients with heart disease, it should be corrected quickly, and the ectopic rhythm should be restored to normal sinus rhythm, or the ventricular rate of bradycardia and tachycardia should be controlled within a safe range to prevent the occurrence of heart failure.
3. Correct water-electrolyte imbalance and acid-base balance.
4. Treat anemia and eliminate the cause of bleeding.
5. Avoid too much and too fast infusion.
6. Stop using or use some drugs that inhibit myocardial contractility with caution.
7. Others? Avoid overwork and emotional excitement. Obese people should control their diet.
19 related drugs