Acute heart failure – cardial asthma, pulmonary oedema, cardiogenic shock – etiology, pathogenesis, clinical manifestations

01Definition and overview

Acute heart failure is the rapid or gradual onset or worsening of the symptoms and signs of heart failure, severe enough to need urgent care and new or intensified treatment, usually in hospital but sometimes as an outpatient. It is either a first presentation (de novo heart failure, after an infarction or myocarditis, for example) or, more often, a decompensation of known chronic heart failure. European guidance now calls it decompensated heart failure, because the decline is often gradual; the term covers both.

European guidance describes four clinical presentations, which can overlap:

Cardiac asthma, an older term still used, is the wheeze and breathlessness of interstitial and bronchial oedema, typically at night; alveolar pulmonary oedema is the flooding that follows.

The bedside also classifies patients by two questions: are they congested (wet or dry) and are they perfused (warm or cold)? Most are warm and wet; cold and wet is cardiogenic shock.

02Etiology and pathophysiology

Causes and triggers

A new or worsening cardiac problem:

• an acute coronary syndrome, or a mechanical complication of infarction (a ruptured papillary muscle, ventricular septal rupture, free wall rupture);
• arrhythmias: fast atrial fibrillation, ventricular tachycardia, or severe bradycardia;
• a hypertensive emergency;
• acute valve regurgitation, from endocarditis, chordal rupture or aortic dissection, and prosthetic valve thrombosis;
• myocarditis, takotsubo and peripartum cardiomyopathy;
• pulmonary embolism, and cardiac tamponade.

Triggers in a patient with chronic heart failure:

• infection, especially pneumonia;
• poor adherence to drugs, or to advice on salt and fluid;
• drugs that retain salt or depress the heart: NSAIDs, corticosteroids, glitazones, non-dihydropyridine calcium channel blockers, some chemotherapy;
• alcohol and recreational drugs;
• worsening kidney function, anaemia, thyroid disease;
• surgery, pregnancy.

Congestion

1. 1

   Rising filling pressure

   When the left ventricle fails, or the mitral valve leaks or obstructs, the pressure in the left atrium and pulmonary veins rises. Salt and water retention, driven by the renin-angiotensin-aldosterone and sympathetic systems over days, adds to the volume.
2. 2

   Interstitial oedema

   The normal pulmonary capillary pressure is about 8 to 12 mmHg. Above about 18 mmHg, fluid leaves the capillaries faster than the lymphatics can clear it and collects in the interstitium and around the small airways and vessels. The lungs stiffen and the airways narrow: breathlessness, orthopnoea and the wheeze of cardiac asthma.
3. 3

   Alveolar oedema

   Above about 25 mmHg, close to the oncotic pressure of the plasma, fluid floods the alveoli. Gas exchange fails and the patient becomes hypoxaemic, with crackles and frothy, pink sputum.
4. 4

   A vicious circle

   Hypoxaemia, a fast heart rate and the surge of catecholamines raise the afterload and the demand of the heart and reduce coronary perfusion, which worsens the failure.

Patients with chronic heart failure tolerate higher pressures, because their lymphatics have enlarged, while a sudden rise, as in flash pulmonary oedema, floods the lungs at lower pressures. Much acute pulmonary oedema is a redistribution of fluid into the lungs, driven by hypertension and vasoconstriction, rather than a gain of fluid.

Congestion of the body raises the central venous pressure, which reduces the perfusion pressure of the kidneys and the liver. Venous congestion of the kidneys is a main cause of the worsening kidney function in acute heart failure.

Hypoperfusion and shock

In cardiogenic shock the heart cannot maintain the output the organs need. Sympathetic vasoconstriction keeps the pressure up at first, at the cost of the skin, gut and kidneys, and then fails. Lactic acidosis, the release of inflammatory mediators and a fall in coronary perfusion further depress the heart, so shock spirals downwards unless the cause is reversed or the circulation supported. Acute myocardial infarction with loss of a large mass of muscle was the classic cause; decompensated chronic heart failure now accounts for a growing share.

03Clinical features

Symptoms

• Breathlessness, at rest or on minimal exertion, with orthopnoea and paroxysmal nocturnal dyspnoea: waking breathless after an hour or two of sleep and sitting up or going to the window for air, sometimes with wheeze and cough (cardiac asthma).
• In pulmonary oedema, extreme breathlessness, a feeling of drowning, cough with frothy, pink sputum, and sweating and anxiety.
• Swelling of the legs, the abdomen and weight gain in decompensated chronic heart failure.
• Chest pain, palpitations or syncope point to the cause.
• Fatigue, confusion and reduced urine output in low-output states.

Signs

Congestion:

• a raised JVP and a positive hepatojugular reflux;
• crackles at both bases, rising up the chest as the oedema increases, and wheeze;
• pleural effusions;
• a third heart sound (gallop rhythm);
• pitting oedema of the legs and sacrum, an enlarged, tender liver and ascites.

Perfusion:

• cold, pale, clammy skin and slow capillary refill;
• a narrow pulse pressure, hypotension, a thready pulse;
• confusion and agitation;
• oliguria, under 0.5 mL/kg an hour.

In pulmonary oedema the patient sits bolt upright, breathless, sweaty and often hypertensive, with central cyanosis and crackles throughout the chest. A murmur may reveal acute mitral regurgitation or a ventricular septal rupture after an infarction.

04Diagnosis and management

Immediate assessment

The first minutes identify a patient in shock or respiratory failure, who needs support of the circulation or breathing at once, and the seven causes with their own urgent treatment:

• an acute coronary syndrome, which needs urgent angiography and revascularisation;
• a hypertensive emergency, which needs rapid lowering of the pressure with intravenous vasodilators;
• an arrhythmia or severe bradycardia, which needs cardioversion, rate control or pacing;
• a mechanical cause (acute valve regurgitation, a ruptured septum or free wall, aortic dissection), which often needs surgery;
• pulmonary embolism, which needs anticoagulation or reperfusion;
• infection or inflammation (sepsis, pneumonia, myocarditis), which needs antibiotics or specific treatment;
• tamponade, which needs pericardiocentesis.

Tests

• ECG: ischaemia or infarction, arrhythmias, left ventricular hypertrophy, bundle branch block. A normal ECG makes heart failure less likely.
• Natriuretic peptides: an NT-proBNP below 300 pg/mL or a BNP below 100 pg/mL makes acute heart failure unlikely. Values are higher with age, atrial fibrillation, kidney disease and sepsis, and lower in obesity.
• Blood tests: troponin (often modestly raised in heart failure itself, but a rise and fall suggests infarction), creatinine and electrolytes, full blood count, liver tests, glucose, thyroid function, and a lactate and blood gases in severe cases.
• Chest X-ray: upper lobe venous diversion, Kerley B lines, peribronchial cuffing, fluid in the fissures, bilateral perihilar ("bat wing") shadowing, pleural effusions, and an enlarged heart, though the heart is normal-sized in acute disease without a chronic cause. It also shows pneumonia and other causes of breathlessness.
• Lung ultrasound: multiple B-lines in both lungs show interstitial oedema quickly at the bedside.
• Echocardiography at once in shock and suspected mechanical causes, and during the admission in every new patient: ventricular function, valves, pericardium and filling pressures.
• Further tests for the cause: coronary angiography, CT pulmonary angiography, cardiac MRI.

Management

Management aims to keep the patient alive and relieve symptoms, then to remove the congestion and start the drugs that change the long-term outcome before discharge. The details are in treatment of acute heart failure. In brief:

• oxygen for hypoxaemia, and non-invasive ventilation for respiratory distress;
• intravenous loop diuretics for congestion;
• intravenous vasodilators when the blood pressure is high;
• inotropes, vasopressors and mechanical circulatory support for cardiogenic shock;
• treatment of the cause and of the trigger;
• the long-term heart failure drugs, started or increased before discharge, with early follow-up.

05Epidemiology

Acute heart failure is the commonest cause of unplanned admission in people over 65, accounting for about 1 to 2 per cent of all hospital admissions in Europe. Most patients have known heart failure, and the average age at admission is over 70. About half have a reduced and half a preserved ejection fraction. Readmission is common: about 1 in 4 patients is readmitted within a month or two, often for the same reason. Cardiogenic shock complicates about 5 to 10 per cent of acute myocardial infarctions, and it is the presentation of a few per cent of acute heart failure.

06Prognosis

Acute heart failure marks a turning point in the course of heart failure. In-hospital mortality is about 3 to 10 per cent, about 1 in 4 patients dies within a year, nearly half dies or is readmitted within a year, and more than half dies within 5 years. Older age, low blood pressure, kidney dysfunction, low sodium, high natriuretic peptides and troponin, and persisting congestion at discharge predict a worse outcome. Cardiogenic shock carries the highest mortality, about 40 to 50 per cent in hospital; in a large trial in shock after infarction, about 40 per cent of patients had died by 30 days. Patients with de novo heart failure from a reversible cause, such as myocarditis or takotsubo syndrome, can recover fully.