Heart failure

from Wikipedia, the free encyclopedia
Classification according to ICD-10
I11.0- Hypertensive heart disease with (congestive) heart failure
I13.0- Hypertensive heart and kidney disease with (congestive) heart failure
I50.0- Right heart failure
I50.1- Left heart failure
I50.9 Heart failure, unspecified
R57.0 Cardiogenic shock


ICD-10 online (WHO version 2019)

The heart failure (of insufficiency = insufficiency; in medicine inter alia inadequate performance of an organ ; Insufficientia cordis ) or heart failure is the pathological inability of the heart that needed by the body cardiac output without increase in end diastolic promote pressure. The "pumping weakness" manifests itself in reduced physical and mental performance, one also speaks of forward failure. The symptoms of backward failure are no less relevant : To increase cardiac output, the body increases its water supply , which leads to water retention in the legs when the right heart is weak . If the left heart is weak, water collects in the lungs , which, especially when lying down, becomes noticeable as shortness of breath and in severe cases limits the uptake of oxygen in a life-threatening manner.

Heart failure is the common end of many heart diseases, with longstanding high blood pressure and atherosclerotic narrowing of the vessels supplying the heart ( i.e. coronary heart disease and past heart attacks ) being the most common causes. In addition to the treatment and elimination of underlying diseases and risk factors, certain antihypertensive agents play a major role in therapy , as they have been shown to increase survival time. The advanced heart failure often shows a relapsing course with recurring decompensations , in which the affected persons store a threatening amount of water and thus “overload” their heart. The cardiac decompensation is a common cause of hospital care; it can often be controlled with diuretics and, if necessary, intensive medical treatment, but it can also lead to death from relative health. Heart failure is a common disease with a high mortality rate and is therefore one of the most common causes of death .

Everyday language and double interpretations

The common German term heart failure meets the facts only inaccurate because not only pathologically reduced pump function ( systolic heart failure or heart muscle weakness ), but also an impaired filling of the heart ( diastolic heart failure can lead) with unimpaired pumping function to heart failure. Acute, severe cardiac insufficiency is sometimes referred to as heart failure , although there is no generally accepted definition of this term, which is often used, particularly in death certificates. Critics argue that heart failure is also cited as the most common cause of death because the heart has come to a standstill in every deceased and the actual fatal illness has often not been determined.

The identity of heart failure as too small cardiac output and of the syndrome of too small cardiac output syndrome (English: low cardiac output syndrome ) is often not clear in the specialist literature . Here, cardiac output (CO abbreviated) the English translation of the cardiac output (CO abbreviated). In addition, heart failure is not a disease, but a syndrome , i.e. the symptom of numerous diseases. Also, the heart failure at increased cardiac output ( high output failure ) always a failure with too small cardiac output with increased need of oxygen-rich blood.


Heart failure is classified according to its course (acute or chronic), the predominantly affected half of the heart (right or left, otherwise global) and according to the mechanism.


The acute heart failure develops over a period of hours to days. The causes are:

The chronic heart failure develops over a period of months to years. It is characterized by compensatory processes of the organism (faster heartbeat, thickening of the heart muscle, constriction of the blood vessels, increase in blood volume, etc.), which can compensate for the reduced pumping capacity of the heart for a while. The compensated heart failure shows no or only at greater physical stress symptoms. In the decompensated stage there is pathological accumulation of water ( edema ) and shortness of breath ( dyspnoea ). This occurs even at rest or under low stress.

Special forms of heart failure

Heart failure often does not affect both halves of the heart equally. Regardless of the location of the disorder, the water retention leads to weight gain . During the night (physical rest, elevation of the legs), part of the water retention is mobilized from the tissue and excreted via the kidneys ; this causes increased urination at night ( nocturia ).

Left heart failure

The left ventricular failure (also links insufficiency called) (often resulting in a evidenced by backflow of blood into the pulmonary vessels pulmonary hypertension results) with cough and shortness of breath up to pulmonary edema . The limited pumping capacity of the left ventricle leads to reduced resilience and possibly to low blood pressure.

Right heart failure

In right heart failure (also legal insufficiency called), the contraction failure of the right ventricle and the right atrium, the blood accumulates back into the systemic veins . Due to the increased venous pressure, water can accumulate (as transudate ) in the tissues with edema , especially in the lower body parts (legs), as well as in the abdomen ( ascites ) and in the pleural cavity ( pleural effusion ).

Global insufficiency

The global heart failure (double-sided heart failure) with contraction insufficiency of the right and the left ventricle shows symptoms of left and right heart failure.

Functional classification

Functionally, one can distinguish between a forward and backward failure of the heart. In the case of forward failure, sufficient pressure cannot be built up in the arteries, while in the case of reverse failure, the blood backlog takes place in the body and pulmonary veins.

High output failure

Heart failure is not always based on a pump failure with a reduction in cardiac output (low output failure). The symptoms of heart failure can also occur if a pathologically increased blood flow requirement of the organs can no longer be met (high output failure):

  • Anemia ( anemia ) - increase because of poor oxygen transport capacity must cardiac output, to ensure a sufficient supply of oxygen to tissues.
  • Overactive thyroid ( hyperthyroidism ) - the pumping capacity of the heart is strongly stimulated, but so is the metabolism and thus the blood flow to the tissues. I.a. the tachycardia can lead to (relative) heart failure.
  • Arteriovenous fistula - a short-circuit connection between arteries and veins causes part of the cardiac output to be consumed without benefit.
  • Sepsis / SIRS - the widening of the small vessels and endothelial barrier disruption associated with the release of inflammatory mediators requires a greatly increased ejection capacity of the heart in order to maintain arterial blood pressure.


Classification of New York Heart Association (NYHA)
NYHA I No physical restriction. Daily physical exertion does not cause inadequate exhaustion, arrhythmias, shortness of breath or angina pectoris .
NYHA II Slight restriction of physical resilience. No complaints in peace. Exhaustion, arrhythmia, shortness of breath or angina pectoris with everyday physical stress.
NYHA III Severe limitation of physical performance during normal activity. No complaints in peace. Exhaustion, arrhythmia, shortness of breath or angina pectoris with little physical exertion.
NYHA IV Discomfort in all physical activities and at rest. Immobility.
Classification of the American Heart Association (AHA)
Stage A High risk of heart failure, as there are factors that are strongly associated with the development of heart failure; no structural heart disease, never heart failure symptoms.
Stage B Structural heart disease, which is closely associated with the development of heart failure, so far no heart failure symptoms.
Stage C Past or current symptoms of heart failure in structural heart disease.
Stage D Advanced structural heart disease and severe heart failure symptoms at rest despite maximum drug therapy (special therapy required, e.g. heart transplant, IV catecholamines , artificial heart).


Heart failure is one of the most common internal diseases with an estimated more than 10 million people in Europe. Almost 10 million more people already have heart muscle weakness without symptoms. Heart failure is one of the most common reasons for advice in a general medical practice in Germany and the most common reason for inpatient hospital admission.

Heart failure incidence per age group

The prevalence and incidence of heart failure are age-dependent. Between the ages of 45 and 55, less than 1% of the population suffer from heart failure, 65 to 75 year olds already suffer from 2 to 5% and over 80 year olds almost 10%. Men are about 1.5 times more likely to be affected than women of the same age. Each year roughly as many patients are diagnosed with heart failure as breast, lung, prostate and colon cancer combined. With increasing age, the proportion of diastolic heart failure increases to more than 30%, in women to more than 40%. People who suffer from type 2 diabetes mellitus are two to six times more likely to develop heart failure. In addition, this group often misinterprets symptoms of heart failure as old age .

In Germany's cause of death statistics from the Federal Statistical Office in 2006, heart failure ranks third, ahead of cancer such as breast, lung or colon cancer. In women, heart failure even ranks second among the most common causes of death with a share of 7.4%.

Pathophysiology and etiology

The human heart

The right heart decreases over the upper and inferior vena cava , the blood from the body and pumps it through the pulmonary artery (pulmonary artery) in the lung (see. The pulmonary circulation ). From there, oxygen- rich blood flows through the pulmonary veins to the left heart, from where it is pumped into the body through the main artery ( aorta ) . This pumping function of the heart can be disturbed for various reasons.

Even without heart disease , heart failure can occur, for example in the case of anemia or if a lung or liver disease reduces the cardiac output. A rare cause of heart failure is the inadequate growth of the donor heart in adolescence after a heart transplant in an infant . Similarly, a cardiac output that is too small in an artificial heart leads to cardiac insufficiency.

Causes of Heart Failure

80 to 90% of those affected by heart failure are caused by a dysfunction of the heart muscle, almost two thirds of them in the sense of heart failure. The most common cause of heart failure in Western countries is a circulatory disorder of the heart ( coronary artery disease or CHD) in 54 to 70% of patients, in 35 to 52% accompanied by high blood pressure . In 9 to 20% of cases, high blood pressure (hypertension) is the sole cause of heart failure. Inflammation of the heart muscle ( myocarditis ) manifests itself as (mostly temporary) heart failure in 60 to 70% of affected patients. Vitamin D deficiency promotes heart failure, as does iron deficiency , even without anemia.

In one of the world's largest observational studies with a cohort of around 70,000 adult residents of Norway, it has now also been found that patients with severe sleep disorders ( difficulty falling asleep, staying asleep and lack of nighttime recovery) later develop heart failure significantly more often. It could be ruled out that other risk factors such as obesity, diabetes, sedentary lifestyle, hypertension, nicotine or alcohol led to the increased development of heart failure.


Compensation by increasing the volume in the cardiovascular diagram : The cardiac output can only be maintained by accepting increased central venous pressure .

Due to the decreasing cardiac output in the course of heart failure, there is insufficient blood supply to the organs. In response to this, compensation mechanisms are activated, which are supposed to ensure the supply of the organs with oxygen-rich blood. These include the increased release of hormones such as adrenaline and noradrenaline , which increase the heart's beating power and increase blood pressure by constricting the blood vessels. Angiotensin II and aldosterone , the effector hormones of the renin-angiotensin-aldosterone system , lead to an increase in blood volume and also to an increase in blood pressure. Although the mechanisms mentioned are temporarily necessary to maintain blood flow to organs, they lead to damage to the heart and progression of the disease in the long term. They lead to a thickening of the muscles in the heart ( hypertrophy ). This is initially helpful in order to be able to do more pumping work. In addition, there is increased incorporation of connective tissue ( fibrosis ). Both processes together are also known as cardiac remodeling . The cellular mechanisms underlying remodeling are the subject of intensive research. Among other things, an altered gene expression , the activation of intracellular signaling pathways, e.g. B. MAP kinases , and the change in calcium metabolism and energy metabolism are investigated. More recent studies have also provided indications that epigenetic changes are involved. Aldosterone antagonists such as spironolactone are used in the therapy of heart failure because they counteract remodeling.

As long as the heart can meet the increased demands, one speaks of compensated heart failure . The increase in blood volume causes the heart to fill up more and thus, via the Frank Starling mechanism, a larger stroke volume. However, this mechanism is limited by Laplace's law , according to which a larger heart width requires greater muscle tension. As a result, from a certain point onwards, an increase in heart filling leads to a decrease in stroke volume. While a healthy heart always operates below this point, this reserve is exhausted in the case of untreated heart failure. In the case of decompensated heart failure , the heart is loaded beyond the point of maximum stroke volume, so that the cardiac output can be increased in this case by reducing the blood volume. For a short time, the filling of the heart can be reduced through an upright posture (no shock position !) Or bloodletting . Ultimately, the blood volume must be reduced through therapy with dehydrating drugs .

If the heart is overstretched, it releases natriuretic peptides . These have a vasodilating and diuretic effect and thus represent a counterweight to the renin-angiotensin-aldosterone system. The natriuretic peptides are broken down by the enzyme neprilysin . With the neprilysin inhibitor sacubitril , a drug has recently become available that strengthens the body's own protective mechanism against overloading the heart.


The main symptom of left heart failure is shortness of breath ( dyspnea ) initially during physical exertion (exertional dyspnea ) , in an advanced stage also at rest ( resting dyspnea). The shortness of breath often increases after lying down, which in severe cases can lead to threatening nocturnal attacks of shortness of breath and coughing ( cardiac asthma ). Finally, it may for cardiac pulmonary edema ( "water in the lungs") with severe dyspnea and egress of fluid into the alveoli (alveolar) come recognizable "bubbling" to unwanted noise in the breathing and expectoration frothy.

A common symptom of advanced heart failure are nocturnal breathing disorders, often in the form of Cheyne-Stokes breathing , which is characterized by a periodically increasing and decreasing swelling of the breathing .

Heart failure leads to fluid retention ("water retention") in the body, left heart failure in the lungs (as pulmonary edema or often bilateral pleural effusion ) and right heart failure mainly in the legs ( leg edema ) and in the abdomen ( ascites ). The liver can also be damaged ("cirrhosis cardiaque").

The most severe form of heart failure is cardiogenic shock , which usually manifests itself as severe shortness of breath, clouding of consciousness, cold sweat, weak and fast pulse and cool hands and feet.


Heart failure rarely occurs alone. Rather, it is often associated with accompanying diseases, which, depending on the cause of the heart failure, include coronary artery disease , high blood pressure , lipid metabolism disorders or obesity . An atrial fibrillation can be both a consequence and a cause of heart failure. The frequency of comorbidities is related to the age of the patient, personal risk factors (e.g. smoking) and the severity of the heart failure itself, so that it is also referred to as a multi-system disease. Concomitant diseases of other organ systems are also common. These include chronic kidney failure and sleep apnea , both of which affect almost half of heart failure patients, iron deficiency (more than 40%), anemia (35 to 40%), diabetes mellitus (around 30%), chronic obstructive pulmonary disease ( COPD , about 30%), sarcopenia (about 20%), and cachexia (about 10%) as well as some others. The symptoms of comorbidities can overlap with the actual heart failure symptoms and can sometimes be difficult to separate.


Heart failure is diagnosed when typical symptoms (see above) and corresponding objective findings coincide.

Physical examination

Even during the physical examination , some clinical signs may indicate heart failure. These include jugular vein congestion , rattling noises over the lungs, an enlarged heart ( cardiomegaly ), a third heart sound, lower leg edema, an enlarged liver ( hepatomegaly ), pleural effusions , nocturia and an accelerated pulse ( tachycardia ).

Laboratory diagnostics

Since the beginning of the 21st century, a laboratory test for routine diagnostics has been available to determine the plasma concentration of the brain natriuretic peptide (BNP or NTproBNP). Its particular benefit is that low normal BNP or NTproBNP levels largely rule out heart failure in an untreated patient. Depending on the extent of the heart failure, the values ​​are moderately to strongly increased; the normal range depends on age and gender. The measurement of the BNP for the differential diagnosis and follow-up of heart failure has meanwhile been incorporated into the guidelines of the German Society for Cardiology and Pediatric Cardiology. Elevations in BNP or NTproBNP are a diagnostic criterion for heart failure with a slightly reduced or preserved ejection fraction.

Blood tests are also done to identify the causes, complications, or complicating factors of heart failure (such as diabetes mellitus , kidney failure , electrolyte imbalances , anemia, or hyperthyroidism ) and possible side effects of the therapy.


The electrocardiogram is hardly suitable for diagnosing heart failure, but it can show underlying diseases, such as past heart attacks or cardiac arrhythmias. In addition, other therapy recommendations may arise if there is no sinus rhythm or bundle branch block.

Ultrasound diagnostics

The most important examination method for heart failure is an ultrasound examination of the heart ( echocardiography ). It allows a quick and risk-free assessment of the heart muscle function, the heart valves and the pericardium. On the one hand, the suspected diagnosis of heart failure can be confirmed or ruled out, on the other hand, essential causes can already be determined.

An essential measured variable in echocardiography is the ejection fraction of the left ventricle. The ejection fraction is defined as the proportion of the stroke volume in the end diastolic volume and thus describes how completely the heart empties when beating. A lower ejection fraction is associated with a poorer prognosis. Falls below the ejection fraction 40%, is in the presence of symptoms, a heart failure with reduced ejection fraction (English Heart Failure with reduced ejection fraction , HFrEF) ago. The HFrEF is the “classic”, well-researched and comparatively easily treatable heart failure, as it typically occurs in men with circulatory disorders of the heart. An ejection fraction of at least 50% defined along with some other criteria, the heart failure with preserved ejection fraction ( heart failure with preserved ejection fraction , HFpEF) for age, female gender, hypertension and diabetes are major risk factors. Heart failure with preserved ejection fraction can worsen in the further course to heart failure with reduced ejection fraction. Due to advances in the treatment of circulatory disorders of the heart, HFpEF is now more common than HFrEF in developed countries. A HFmEF (heart failure with mid-range ejection fraction) is defined between HFrEF and HFpEF . Since the recommended therapy is based on the ejection fraction, a correct determination is particularly important.

X-ray examinations

The chest x-ray (chest x-ray ) shows u. a. the heart and lungs off. In milder forms of heart failure, it usually still shows normal findings. If the heart is widened to more than half the width of the chest, one speaks of cardiomegaly ; By expanding the left ventricle, the heart can take on a characteristic “wooden shoe shape”. A backlog of the blood in the pulmonary circulation shows up as increased vascular markings. A pulmonary edema shows up as a shadow in the center ("butterfly edema"); in interstitial pulmonary edema, Kerley lines appear on the edge . A pleural effusion can also be clearly seen in the chest X-ray.

To diagnose and treat coronary artery disease as the cause of heart failure, a cardiac catheter examination with coronary angiography ( coronarography ) is often performed. The pressure conditions in and on the heart can be measured directly, and narrowing of the coronary arteries can be assessed and treated with stents.


Assessment of the anatomy of the heart and large vessels in the case of complex congenital vitia and cardiomyopathies, evidence of vitality before any planned restoration of blood flow (cardiac catheter, bypass operation), stress test with dobutamine or adenosine to assess and identify relevant constrictions (stenoses) in the area Blood flow to the heart (coronary arteries)

A new study shows that magnetic resonance spectroscopy can help to better estimate the risk of heart failure.


Causal therapy

Whenever possible, the cause of the heart failure should be eliminated after the first general therapeutic measures:

Non-drug therapy

A reduction in cardiovascular risk factors is desirable. Non-drug therapy includes weight normalization, reduced salt intake, limitation of fluid intake (<2 liters / day) and alcohol and nicotine reduction or abstinence. Moderate physical training is recommended in NYHA stages I-III, and physical rest until bed rest in case of decompensated heart failure. Travel to high altitudes and hot and humid climates should be avoided. Attending a heart school can be useful for a permanent lifestyle change .

In the case of respiratory failure caused by heart failure , ventilation may be necessary. If possible, a non-invasive form of ventilation should first be used to avoid endotracheal intubation .

Medical therapy

Step-by-step scheme for pharmacotherapy of heart failure with reduced ejection fraction
ACE inhibitors / AT1 antagonists a indexed indexed indexed indexed
Beta blockers after myocardial infarction or in hypertension indexed indexed indexed
Aldosterone antagonists - indexed b indexed indexed
Sacubitril / valsartan - instead of ACE inhibitor / AT1 antagonist c instead of ACE inhibitor / AT1 antagonist c instead of ACE inhibitor / AT1 antagonist c
Diuretics - with fluid retention indexed indexed
Cardiac glycosides - - Reserve funds d Reserve funds d
with uncontrollable tachyarrhythmic atrial fibrillation
a AT1 antagonist as an alternative if ACE inhibitors cannot be tolerated. b If symptoms occur despite treatment with ACE inhibitors / AT1 antagonists and beta blockers. c If symptoms occur despite treatment with ACE inhibitors / AT1 antagonists, beta blockers and aldosterone antagonists. d Only with sinus rhythm, low target serum level.

In the drug therapy of heart failure, a distinction is made between drugs with a confirmed prognostic indication and those with a symptomatic indication.

Interventional and operative therapy

  • Cardiac resynchronization therapy: In the event of poor pump function and conduction disorders in the heart chambers, e.g. B. a left bundle branch block , the implantation of a three-chamber pacemaker ( biventricular pacemaker ) improves symptoms and mortality.
  • The mitral valve repair for example with an annuloplasty ring to Carpentier -Edwards can result with poor pumping function for the relief of symptoms associated with leakage of the valve.
  • An implantable cardioverter defibrillator (ICD) is recommended if there is a high risk of sudden cardiac death, e.g. B. after a ventricular arrhythmia with haemodynamic instability or with chronically low pumping capacity of the heart ( NYHA stage II-III and ejection fraction below 35%). If necessary, also in combination with a biventricular pacemaker.
  • The cardiac contractility modulation (engl. Cardiac contractility modulation , CCM ) is a new method for the treatment of moderate to severe left ventricular systolic heart failure (NYHA II-IV), the medium contractility and the pumping performance of the heart and long-term can improve. Cardiac contractility modulation is particularly suitable for the treatment of heart failure patients with a normal QRS complex , for whom no established interventional treatment option has previously existed below the highly stressful implantation of an artificial heart or a heart transplant.
  • An " artificial heart " or left ventricular assist system (LVAD) can be used for severe pumping disorders. In particular, it serves as a bridge to a heart transplant ("bridge to transplant") or in the case of temporary heart failure, e.g. B. in myocarditis, until recovery ("bridge to recovery").
  • A heart transplant should be sought in patients with intractable, severe heart failure.

See also


Web links

Wiktionary: Heart failure  - explanations of meanings, word origins, synonyms, translations

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  33. a b Chapter "Diagnostics" of the NVL Chronic Heart Failure 2019
  34. Chapter "Epidemiology, Risk and Prognosis Factors" of the NVL Chronic Heart Failure 2019
  35. a b Chapter "Definition and Classification" of the NVL Chronic Heart Failure 2019
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