bubble_chart Overview Acute heart failure (acute heart failure) is caused by various diseases leading to acute reduction in myocardial contractility and acute ventricular overload, resulting in a sudden decrease in cardiac output. Clinically, acute left heart failure is the most common manifestation. Symptoms include acute pulmonary edema, sudden severe dyspnea, cyanosis, orthopnea, profuse sweating, widespread crackles in both lungs with coughing up large amounts of pink frothy sputum, decreased blood pressure, and rapid pulse.
Acute right heart failure is rare and can be seen in acute cor pulmonale caused by massive pulmonary embolism, or occasionally in acute right ventricular myocardial infarction.
bubble_chart Etiology
disease cause
- Acute myocardial contractility decline is often caused by acute extensive myocardial infarction and acute myocarditis.
- Acute volume overload is commonly due to excessive or rapid fluid infusion, papillary muscle dysfunction caused by acute myocardial infarction, or chordae tendineae rupture.
- Acute mechanical obstruction, such as severe mitral valve stenosis or aortic valve stenosis, left ventricular outflow tract obstruction, leads to excessive cardiac load and impaired blood ejection.
- Acute ventricular diastolic restriction results from rapid ectopic rhythms or acute cardiac tamponade caused by large pericardial effusion or hemopericardium.
bubble_chart Clinical Manifestations
The patient suddenly developed severe dyspnea and orthopnea, accompanied by a sense of fear and suffocation, with a grayish complexion, cyanosis of the lips, profuse sweating, frequent severe coughing with wheezing and expectoration of large amounts of pink frothy sputum. The heart rate and pulse increased, and blood pressure initially rose before dropping below normal. Widespread, varying-sized moist rales could be heard in both lungs, covering more than half of the lung fields, along with wheezing or whistling sounds. In severe cases, due to reduced cardiac output and insufficient blood flow, cardiogenic shock may occur. In the most critical cases, syncope and cardiac arrest may ensue.
bubble_chart Diagnosis The diagnosis is not difficult based on typical symptoms and signs. Auxiliary examinations: (1) X-ray shows dense, foggy shadows extending from the hilum to the mid-lung field, often fan-shaped. (2) The mean pulmonary capillary pressure rises above 4.00 kPa (30.0 mmHg), and the cardiac index drops to 2 L/min·m². A gallop rhythm at the apex and the expectoration of large amounts of pink frothy sputum help differentiate it from bronchial asthma.
bubble_chart Treatment Measures
It is an internal medical emergency, and effective measures should be taken promptly and actively for first aid.
- **Reducing Venous Return** Immediately place the patient in a sitting position with legs dangling or apply tourniquets to the limbs. Method: Use soft rubber tourniquets or pneumatic cuffs (sphygmomanometer cuffs) to constrict the limbs and torso (below the shoulders and groin). The cuff pressure should be inflated to approximately 1.33 kPa (10 mmHg) below the diastolic pressure (or use the diagnostic method where the distal pulse remains palpable while venous engorgement persists), obstructing venous return in the limbs while maintaining arterial blood flow. Rotate the tourniquets every 15 minutes in a specific order (clockwise or counterclockwise), releasing one limb at a time. Each limb should be compressed for 45 minutes and released for 15 minutes to prevent excessive local blood stasis and adverse consequences.
- **Sedation and Reducing Cardiac Preload** (1) Administer morphine 3–5 mg intravenously (over 3 minutes), repeating every 15 minutes as needed, up to 2–3 times. If the condition is less urgent, 5–10 mg may be given subcutaneously or intramuscularly, repeated every 3–4 hours, with a total daily dose not exceeding 60 mg. Alternatively, dissolve 10 mg of morphine in 10 ml of saline, initially administering 5 ml intravenously, followed by 1 ml hourly. If bradycardia is present, atropine may be combined. Administering morphine while the legs are dangling may cause hypotension or collapse, so caution is advised. (2) Meperidine 50–100 mg intramuscularly is suitable for patients with contraindications to morphine and accompanying bronchospasm. Morphine alleviates dyspnea and dysphoria while dilating peripheral veins and reducing venous return. However, it is contraindicated in cases of respiratory depression, unconsciousness, shock, or chronic pneumonia. Elderly or debilitated patients should receive reduced doses.
- **Correcting Hypoxia** Administer high-pressure, high-flow oxygen at 6–8 L per minute. For mask oxygen delivery, place 30–40% alcohol in the humidification bottle, with each session not exceeding 20 minutes. For nasal catheter oxygen delivery, use 70–80% alcohol. If the patient cannot tolerate this, opt for 20–30% alcohol and gradually increase the concentration. Alternatively, start with low-flow oxygen and gradually increase the flow rate once the patient adapts. This method is suitable for conscious patients. For more effective results, place 5 ml of 95% alcohol in a duckbill nebulizer for oxygen-driven inhalation, or use 20–40% alcohol for ultrasonic nebulization, which is more reliable than the aforementioned methods.
- **Rapid Diuresis** Administer furosemide 20–40 mg or ethacrynate sodium 25–50 mg intravenously to induce rapid and substantial diuresis, reducing blood volume and lowering left ventricular filling pressure. For left heart failure complicating acute myocardial infarction, where blood volume is not significantly increased, use with caution to avoid hypotension. Monitor for hypovolemia and hypokalemia, which may lead to cardiac arrest during vigorous diuresis.
- Vasodilators can reduce pulmonary vascular resistance. (1) Sodium nitroprusside 50mg (1 ampoule) is dissolved in 500ml of 5% glucose (concentration 100μg/ml) for intravenous infusion, starting with a small dose, usually 15μg/min or 0.25μg/kg·min. If ineffective, increase the dose every 15-30 minutes by 5-10μg/min until the desired effect is achieved. If no therapeutic effect occurs at a drip rate of 80μg/min, increase by 20μg/min or 0.25μg/kg·min. The maintenance dose is 25-150μg/min, with a maximum dose of 300μg/min. Note that excessive use may cause cyanide poisoning, and blood volume should be replenished before use to prevent excessive hypotension. (2) Phentolamine: For acute left heart failure with pulmonary edema, a larger initial dose can be given, such as 5mg in the first minute, followed by a smaller dose for continuous infusion, or 5-10mg diluted in 20-40ml of 25% or 50% glucose and injected slowly over 5-10 minutes. The usual dose is 1-5μg/kg·min (adults 0.05-0.3mg/min). (3) Nitroglycerin sublingual tablets can rapidly dilate the venous bed and reduce venous return to the heart.
- Cardiotonic drugs such as fast-acting Rehmannia preparations can be administered if no Rehmannia has been used within the past 2 weeks and no digoxin has been used within the past week. For example, cedilanid 0.4mg can be slowly injected intravenously (over 5 minutes or more) with 20–40ml of 50% glucose solution to enhance myocardial contractility and slow the heart rate. After clinical observation, an additional 0.1–0.2mg may be given
- 4 hours later, with the total dose not exceeding 0.25mg. If the heart rate is not rapid (<100 beats/min), strophanthin K can be administered, with an initial dose of 0.25mg slowly injected intravenously with isotonic glucose solution, followed by another 0.25mg after 0.
- 1–2 hours as needed, with the total dose kept below 0.5–0.875mg. Cardiotonic Yaodui is contraindicated for grade III mitral stenosis with acute pulmonary edema accompanied by sinus rhythm. If Rehmannia has been used within the past 2 weeks, cardiotonic drugs should be administered cautiously in small additional doses based on the patient's condition.
- Intravenous injection of 0.25g aminophylline, diluted with 20–40ml of 50% glucose solution and slowly administered, can relieve bronchospasm and alleviate dyspnea. It also enhances myocardial contractility and dilates peripheral blood vessels.
- Other treatments include intravenous injection of 10–20mg dexamethasone, which reduces peripheral vascular resistance, decreases venous return to the heart, and relieves bronchospasm. If pulmonary edema is caused by rapid or excessive blood transfusion or fluid infusion, emergency venipuncture or phlebotomy (300–500ml) can be performed to reduce excessive blood volume. If airway obstruction persists after these measures, an emergency tracheostomy may be performed to suction secretions.
Additionally, precipitating factors should be eliminated, and the primary disease and complications should be treated.