Acute heart failure (AHF) is the sudden onset or exacerbation of heart failure symptoms, and can be manifested by new-onset acute heart failure or acute decompensation of chronic heart failure.
Common causes of new-onset acute heart failure include acute myocardial injury, such as acute coronary syndrome and severe myocarditis, and acute hemodynamic disturbances, such as acute valvular dysfunction, hypertensive crisis, severe arrhythmias, and acute pulmonary embolism.
Classification
Acute left heart failure
Acute left heart failure is characterized by acute or exacerbated left ventricular systolic dysfunction and increased load, leading to a rapid decrease in cardiac output from the left heart, sudden increase in pulmonary circulation pressure, acute pulmonary congestion, pulmonary edema, and potentially inadequate perfusion of organs, even cardiogenic shock. It can be classified into acute decompensation of chronic heart failure, acute pulmonary edema, and cardiogenic shock based on the onset speed and severity. Common causes include acute coronary syndrome, hypertensive crisis, severe arrhythmias, and acute decompensation of chronic heart failure.
Acute right heart failure
Acute right heart failure is manifested by a sudden decline in right ventricular contractility or a sudden increase in right ventricular preload and afterload, leading to a sharp reduction in right heart output and acute systemic congestion, and is often caused by right ventricular infarction or massive acute pulmonary embolism.
Acute heart failure is categorized based on congestion and perfusion status, aiding in assessing severity and guiding treatment. Congestion symptoms and signs include orthopnea/paroxysmal nocturnal dyspnea, pulmonary moist crackles, peripheral (bilateral) edema, jugular venous distention, congestive hepatomegaly, and positive hepatojugular reflux. Low perfusion symptoms and signs include cold and clammy extremities, confusion, oliguria, dizziness, and narrow pulse pressure.
Based on the presence of congestion and perfusion, AHF is classified into four types:
- Warm and dry heart failure: No significant congestion or hypoperfusion, mildest condition
- Cold and dry heart failure: No significant congestion but with hypoperfusion, with prevalence of about 5%, often with hypovolemia
- Warm and wet heart failure: Significant congestion without hypoperfusion, most common condition, often due to acute decompensation of chronic heart failure
- Cold and wet heart failure: Presence of both congestion and hypoperfusion, most severe condition
Clinical manifestations
Sudden onset of dyspnea is the primary clinical manifestation of acute left heart failure. Depending on the severity, it can present with exertional dyspnea, paroxysmal nocturnal dyspnea, or orthopnea. Physical examination may reveal an enlarged heart, early or mid-diastolic gallop rhythm, and pulmonary moist crackles. Early signs can include unexplained fatigue or significantly reduced exercise tolerance, with an increase in heart rate by 15 - 20 beats per minute in patients previously with normal cardiac function.
Acute pulmonary edema is characterized by sudden severe dyspnea, orthopnea, restlessness, and fear of suffocation. Respiratory rate can reach 30 - 50 breaths per minute, with pallor, cyanosis of the lips, diaphoresis, cough, and excessive pink frothy expectoration. Incontinence may occur. Auscultation reveals a rapid heart rate, with an early diastolic gallop often heard at the apex, and widespread pulmonary moist crackles and wheezing.
Cardiogenic shock is manifested by persistent hypotension despite adequate blood volume, with systolic blood pressure ≤ 90 mmHg for over 30 minutes, pulmonary capillary wedge pressure (PCWP) ≥ 18 mmHg, and cardiac index (CI) ≤2.2 L/(min·m2), accompanied by signs of tissue hypoperfusion, including oliguria (urine output < 0.5 ml/(kg·h) or anuria), pallor, cyanosis, cold and clammy extremities, altered consciousness, serum lactate > 2 mmol/L, and metabolic acidosis (pH < 7.35).
Acute right heart failure primarily presents with systemic congestion and reduced cardiac output, such as hypotension, tachycardia, oliguria, cold and clammy extremities, jugular venous distention, positive hepatojugular reflux, hepatosplenomegaly, and edema of the lower limbs and sacral area.
Diagnosis and differential diagnosis
Diagnosis is generally straightforward based on typical symptoms and signs. Patients with acute left heart failure often experience cardiac asthma, which should be differentiated from bronchial asthma and acute exacerbation of asthmatic bronchitis. Cardiac asthma is more common in patients with organic heart disease and requires sitting up during attacks, with dry and wet crackles in the lungs and potentially pink frothy sputum. Bronchial asthma is more common in adolescents with a history of allergies or middle-aged and older patients with chronic bronchitis, with typical wheezing sounds in both lungs during attacks. Measuring plasma BNP/NT-proBNP levels is valuable for distinguishing between acute cardiac asthma and bronchial asthma.
Treatment
Treatment objectives include:
- Stabilizing hemodynamic status, maintaining organ perfusion and function, and alleviating symptoms
- Treatment of etiology and precipitating factors
- Initiating and enhancing evidence-based treatments to improve long-term prognosis
Initial assessment and emergency intervention
Circulatory or respiratory failure needs to be assessed. Patients with cardiogenic shock have the highest risk of acute mortality and require rapid correction of shock, early use of vasopressors, and inotropic agents. If drug treatment is ineffective, early mechanical circulatory support should be considered. In patients with respiratory failure, non-invasive ventilation such as CPAP and BiPAP can be used. If non-invasive ventilation fails, invasive ventilation should be given. It is suggested to correct shock and respiratory failure within one hour.
It is very important to quickly identify clinical situations requiring urgent treatment, such as acute coronary syndrome, hypertensive emergencies, severe arrhythmias, acute cardiac mechanical complications, acute pulmonary embolism, severe infections, and cardiac tamponade. It is crucial to provide appropriate interventions promptly, including emergency revascularization, rapid blood pressure control, cardioversion, emergency surgery, thrombectomy or thrombolysis, anti-infection treatment, and pericardiocentesis.
General measures
The intravenous access should be established, an indwelling urinary catheter should be placed, and ECG, blood pressure, and oxygen saturation should be monitored. For patients with cardiogenic shock, invasive hemodynamic monitoring may be necessary.
High-flow oxygen through nasal cannula should be immediately given.
Patients should be in semi-sitting position or orthopneic position with legs down to reduce venous return.
Administration of 3 - 5 mg of morphine intravenously for sedation can reduce cardiac workload and dilate small blood vessels, reducing cardiac load. It is recommended for patients with acute pulmonary edema. The procedure can be repeated every 15 minutes as needed, up to 2 - 3 times. Reduced dose or intramuscular injection can be used in older patients.
24-hour fluid intake and output should be monitored. For severe volume overload, salt and water intake should be strictly limited, fluid infusion volume and rate should be adjusted, and negative fluid balance should be maintained. Once pulmonary congestion and edema improve, gradual transition to a balanced fluid state should be conducted. In patients with low volume status, appropriate fluid expansion should be considered.
Treatment plan based on clinical classification
In warm and dry heart failure, oral medications can be adjusted.
In cold and dry heart failure, appropriate fluid expansion can be conducted. If low perfusion persists, inotropic agents can be administered.
In warm and wet heart failure, if characterized by hypertension and fluid redistribution, vasodilators are preferred, and followed by diuretics. If characterized by congestion and fluid retention, diuretics are preferred, and followed by vasodilators. For severe diuretic resistance, ultrafiltration can be considered.
In cold and wet heart failure, if systolic blood pressure is ≥ 90 mmHg, vasodilators and diuretics can be used; if ineffective, inotropic agents can be administered. If systolic blood pressure is < 90 mmHg, inotropic agents are preferred; if ineffective, vasopressors can be used. Once low perfusion is corrected, diuretics can be used. For patients unresponsive to medication, mechanical circulatory support should be performed promptly.
Medication treatment
Diuretics
The rational use of diuretics is crucial in the treatment of acute heart failure. In patients with evidence of fluid retention, diuretics should be used promptly unless there is uncorrected hypoperfusion. Intravenous loop diuretics such as furosemide, torsemide, and bumetanide are preferred. In patients not on oral diuretics prior to onset, furosemide is commonly used with an initial dose of 20 - 40 mg IV, or torsemide 10 - 20 mg IV. The dose can be adjusted based on urine output and symptoms, with possible IV infusion of 5 - 40 mg/h. The total dose should not exceed 80 mg in the first 6 hours and 160 mg in the first 24 hours for furosemide. In patients on long-term oral diuretics, the initial IV dose should not be less than their usual daily oral dose. In the absence of significant hypovolemia factors such as massive hemorrhage and severe dehydration, negative fluid balance of about 500 - 1,000 ml/day should be maintained; for severe pulmonary edema, negative fluid balance of 1,000 - 2,000 ml/day, possibly up to 3,000 - 5,000 ml/day, should be maintained.
Vasodilators
Vasodilators provide dual benefits by reducing venous tone (preload) and arterial tone (afterload). They are used in AHF patients without tissue hypoperfusion or hypotension and are contraindicated if systolic blood pressure is < 90 mmHg. Blood pressure should be closely monitored during use, and they should be administered slowly in small doses.
Sodium nitroprusside is a vasodilator for both arteries and veins, suitable for severe heart failure, increased afterload, and pulmonary edema. Initial dose is 0.2 - 0.3 μg/(kg·min) IV, increasing by 0.5 μg/(kg·min) every 5 - 10 minutes, not exceeding 10 μg/(kg·min). Infusion rate must be controlled to prevent hypotension. Due to cyanide content, administration should not exceed 72 hours.
Nitrates dilate small veins, reducing venous return, left ventricular end-diastolic pressure, and pulmonary vascular pressure, and are suitable for AHF with hypertension, coronary artery disease, or mitral regurgitation. Common drugs include nitroglycerin and isosorbide dinitrate. Patient tolerance varies. Nitroglycerin is administered initially at 5 - 10 μg/min, increasing by 5 - 10 μg/min every 5 - 10 minutes, with a maximum of 200 μg/min. In emergencies, sublingual nitroglycerin can be used. Isosorbide dinitrate is administered initially at 1 - 2 mg/h, increasing by 1 mg/h every 5 - 15 minutes, with a maximum of 10 mg/h. Nitrate tolerance can develop with continuous use.
α-receptor antagonists selectively bind to α-adrenergic receptors, dilating arteries, reducing peripheral resistance, decreasing cardiac afterload, and increasing cardiac output. They are used for AHF with hypertension or aortic dissection. Common drug is urapidil and the dose is 100 - 400 μg/min IV, and the dose can be adjusted based on blood pressure.
Recombinant human B-type natriuretic peptide (rhBNP) dilates veins and arteries, reducing preload and afterload, lowering PCWP, alleviating pulmonary edema, and improving dyspnea. It also promotes natriuresis and inhibits RAAS and sympathetic nervous system. It can be administered initially at 1.5 μg/kg IV, followed by continuous infusion at 0.0075 - 0.01 μg/(kg·min).
Short-term IV use of inotropic agents can increase cardiac output, raise blood pressure, relieve tissue hypoperfusion, and maintain organ function, but do not improve long-term prognosis. They are suitable for patients with hypotension (systolic BP < 90 mmHg) and/or tissue organ hypoperfusion. They are recommended for early use in indicated patients, and should be discontinued once hypoperfusion improves.
β-receptor agonist dopamine primarily acts on dopamine receptors, selectively dilating renal and mesenteric arteries, promoting diuresis. At low doses (3 - 10 μg/(kg·min)), it stimulates β1 adrenergic receptors with positive inotropic effects; at medium to high doses, it stimulates α-adrenergic receptors with vasoconstrictive effects. It is administered at low doses, gradually increasing.
β-receptor agonist dobutamine primarily acts on β1 adrenergic receptors, slightly reducing systemic vascular resistance and PCWP, increasing stroke volume and cardiac output. It is administered at 2.5 μg/(kg·min), gradually increasing to 20 μg/(kg·min). In chronic heart failure with acute decompensation, long-term, high-dose β-blockers may inhibit cardiac βreceptors, so dobutamine and dopamine are not recommended.
Phosphodiesterase inhibitors have both positive inotropic effects and reduce peripheral and pulmonary vascular resistance. Risks of hypotension and arrhythmias should be vigilantly considered
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Levosimendan enhances myocardial contractility by binding to cardiac troponin C and dilates coronary and peripheral vessels through ATP-sensitive potassium channels. Its metabolites are bioactive, with a half-life of 75 - 80 hours, and effects can last 7 - 9 days after discontinuation. It can be administered with a loading dose of 6 - 12 μg/kg IV (>10 minutes), followed by an infusion of 0.05 - 0.2 μg/(kg·min) for 24 hours.
Digitalis glycosides slightly increase cardiac output and reduce left ventricular filling pressure. They are mainly indicated for atrial fibrillation with rapid ventricular rate (>110 bpm). Lanatoside C can be administered at 0.2 - 0.4 mg IV for 10 minutes, with a dose of 0.2 mg in 2 - 4 hours if needed. They should be avoided in the first 24 hours post-acute myocardial infarction, severe myocardial ischemia, or early severe myocarditis with significant myocardial damage. Potassium and magnesium levels should be monitored to prevent digitalis toxicity, as hypokalemia and hypomagnesemia can increase risk.
Vasoconstrictors such as norepinephrine and epinephrine have significant vasoconstrictive effects on peripheral arteries, redistributing blood flow but increasing left ventricular afterload to elevate blood pressure and ensure vital organ perfusion. They are suitable for patients with tissue hypoperfusion or significant hypotension unresponsive to inotropic agents. Norepinephrine is preferred in cardiogenic shock. Blood pressure, heart rhythm, heart rate, hemodynamics, and clinical status should be monitored closely during use, and they should be discontinued as soon as tissue perfusion is restored.
Hospitalized AHF patients have a significantly increased risk of thromboembolism. Anticoagulation is indicated for patients at high risk of deep vein thrombosis and pulmonary embolism without contraindications.
Non-medication treatment
Mechanical ventilation, including non-invasive ventilation and intubation mechanical ventilation, is used in patients with severe respiratory failure that cannot be improved with conventional treatment and in cardiopulmonary resuscitation patients.
Continuous renal replacement therapy (CRRT) is used for the removal of metabolic waste and fluids to maintain homeostasis in case of high volume overload resistant to diuretics, severe renal impairment, and hyperkalemia.
Mechanical circulatory support devices can be considered when acute heart failure does not significantly improve with conventional drug treatment, especially in drug-resistant cardiogenic shock.
Intra-aortic balloon pump (IABP) can be used in patients with coronary artery disease and acute left heart failure to improve myocardial perfusion, reduce myocardial oxygen consumption, and increase cardiac output.
Extracorporeal membrane oxygenation (ECMO) provides extracorporeal cardiopulmonary support when the heart cannot maintain systemic perfusion or the lungs cannot perform adequate gas exchange. It is mainly used for heart failure caused by low cardiac output after cardiac surgery, cardiogenic shock, acute fulminant myocarditis, acute myocardial infarction, and rejection after heart transplantation, and can also be used as a means of extracorporeal resuscitation to improve resuscitation success rates.
Left ventricular assist device (LVAD) can be used in acute heart failure to maintain peripheral perfusion and reduce myocardial oxygen consumption by assisting ventricular pumping, thereby alleviating myocardial damage. It is mainly suitable for refractory heart failure and cardiogenic shock due to various causes, especially as bridging therapy for heart transplantation.
Long-term management
After the condition stabilizes, a comprehensive assessment of the etiology, precipitating factors, and complications of heart failure is needed. It is important to prevent the recurrence of acute heart failure. In patients with acute heart failure accompanied by underlying heart disease, proper prevention, treatment, and rehabilitation of the primary disease should be implemented.
In patients with decompensated chronic heart failure, the chronic heart failure treatment regimen should be restored or initiated, medication therapy should be optimized to the greatest extent, and the indications for device therapy should be evaluated.
Patients and their family education should be strengthened, and follow-up plans should be formulated.