Acute heart failure is a disease associated with a high mortality rate and is one of the most common reasons for hospitalisation in the Western world. Heart failure is defined as a condition in which the heart is unable to ensure adequate cardiac output for the body’s current metabolic needs (or can only ensure it by increasing blood filling pressure in the cardiac cavities or by increasing the heart rate). Acute heart failure is distinguished from chronic heart failure by its rapid onset, which prevents the body from successfully adapting to it, or such adaptation is only partial and incomplete. The symptoms and signs of acute heart failure are therefore more prominent and develop at a lower-grade heart dysfunction compared to chronic heart failure.
In Western countries, the annual incidence (number of new cases) of heart failure is approximately 6/1,000. In the United States, there are 900,000 hospitalisations per year due to acute heart failure and more than 80,000 in the UK, with a mean hospital stay of 4.3 days. The rate of hospital re-admissions of discharged patients in the next 30 days is also high, approximately 25%. The severity of the disease is demonstrated by its high mortality, amounting to 6–9% of patients with acute heart failure during hospitalisation, 10% within 30 days from hospital discharge, and up to 30% within a year. Financial projections indicate that in 2030, as much as 80% of all costs for treating heart failure will be attributed to the acute rather than chronic form of the disease. The data above show that acute heart failure is not just an extremely dangerous disease that puts the patient at great risk but also a major public health problem for all of Western society.
Heart function is best described by the left ventricular pumping ability. The main factors affecting cardiac function are: filling of the heart (blood volume and pressure in cardiac cavities), heart frequency, contractility (ability to contract) of the heart muscle and resistance to blood ejection. Sudden changes of any of the above factors might lead to acute heart failure. Therefore, the common causes are sudden changes in heart frequency, severe tachycardia (heart frequency above 100 bpm), bradycardia (heart frequency below 60 bpm), suddenly increased filling of the heart (volume overload), impaired contraction of the heart muscle due to ischaemia (myocardial infarction – the most common cause!) or inflammations and increased resistance to blood ejection (e.g. overload with a sudden increase of arterial blood pressure).
Acute heart failure is clinically manifested in two ways:
Symptoms and signs of increased blood filling pressure:
- The most common signs of increased right ventricular blood filling pressure are swollen neck veins, swellings (oedemas) in the legs and enlarged liver;
- The most common signs of increased left ventricular blood filling pressure are short breath upon exertion (in severe cases even at rest) and the need to lie down or sleep with a raised pillow due to pulmonary oedema.
Consequences of decreased cardiac output:
Rapid and severe fatigue, reduced exercise tolerance, impaired level of consciousness (confusion, drowsiness, disorientation, unresponsiveness …), skin turning blue due to lack of oxygen in peripheral tissues (cyanosis), acute kidney failure …
Even though most patients who come to the emergency department due to acute heart failure are hospitalised, studies have shown that outpatient management of the patient or a short hospitalisation (< 24 hours) can be a safe alternative to the conventional hospital stay lasting for several days, and is not associated with increased mortality.
The fundamental part of therapy for acute decompensated heart failure are loop diuretics (e.g. furosemide, bumetanide) given intravenously in addition to the possibly prescribed oral diuretics, with a trend of increasing the dose until the desired therapeutic effect is achieved. These active ingredients increase urine output and decrease the patients’ volume overload. Early use of high-dose loop diuretics is associated with a lower patient mortality rate (in the long term), faster symptom relief and higher volume loss, but may also cause a transient kidney function impairment. In order to avoid resistance to loop diuretics, they are sometimes used in combination with thiazide diuretics (e.g. chlorothiazide or metolazone). Patients are often instructed to limit their fluid intake, but a significant restriction of fluid intake is limited only to those patients with severe hyponatraemia (too low plasma sodium levels).
Vasodilators (drugs that dilate blood vessels) such as nitroglycerin and nitroprusside are used in patients with acute heart failure and pulmonary oedema (accumulation of fluid in the lungs) without haemodynamically significant hypertension (too low blood pressure) in order to reduce systemic blood pressure, which improves the left ventricular function. The recombinant drugs nesiritide and serelaxine are effective in relieving dyspnoea (difficulties breathing with an unpleasant feeling of breathing muscles effort); however, no effect on long-term cardiovascular outcomes and reduced mortality rate in acute heart failure has been demonstrated.
Guidelines for patients with acute heart failure with signs of systemic hypoperfusion (reduced blood supply to organs and tissues) recommend using positive inotropes (drugs that change the force of the heart muscle contraction), such as dobutamine, dopamine, milrinone and levosimendan. Since these drugs act on beta-adrenergic receptors in the heart muscle, they might lead to the potentially dangerous adverse effects of atrial and ventricular cardiac arrhythmias, which are particularly frequent when the dose given is too high.
Patients with acute heart failure and impaired cardiac output are also candidates for conventional heart failure therapy with ACE inhibitors, angiotensin receptor antagonists, neprilysin inhibitors and beta-blockers, provided they are haemodynamically stable and have no other contraindications.
Patients experiencing cardiogenic shock (acute syndrome caused by insufficient blood supply to the vital organs, which develops due to severe heart failure) who cannot be stabilised with conventional pharmacotherapy (with medicines) can be treated with temporary or permanent mechanical circulation support. The first example of such support is the intra-aortic balloon pump conventionally used in patients in cardiogenic shock following an acute myocardial infarction. By alternating between filling and emptying the balloon catheter in the aorta, this pump reverses blood flow and improves blood supply to coronary arteries supplying the heart and brain. Another example of mechanical circulation support is ECMO (extracorporeal membrane oxygenation), a type of invasive treatment used in intensive care units to pump the blood out of the body using an extracorporeal pump and return the oxygenated blood into the body. ECMO can thus partly or fully replace the function of the impaired heart and/or lungs for a period of a few days to a few weeks.
If patients with acute heart failure have too low a level of oxygen saturation of haemoglobin in their blood, oxygen therapy must be provided (non-invasive mechanical ventilation). In contrast, patients in shock in the ICU can be intubated (placement of a breathing tube into the airway) and invasively mechanically ventilated.
Written by: Jure Bosanac