Heart failure I50.9

Heart failure is a polyetiologic clinical syndrome. It is defined as a pathological inability of the heart to pump the cardiac output required by the body at normal end-diastolic ventricular pressure (without an increase in pressure) in the atria. The underlying disease (e.g. coronary heart disease) must be identified in order to be able to treat it as specifically (causally) as possible.

Heart failure can be classified as follows:

According to cardiac output (cardiac output):

• Low-output failure: forward failure with a reduction in cardiac output. Cool periphery. The arterio-venous oxygen difference (normal: 3.5-5.0 ml/dl) is increased.
• High-output-failure: Insufficient blood (_O2) supply to the periphery with increased cardiac output (e.g. in anemia, hyperthyroidism). The arterio-venous oxygen difference is reduced.

According to the chamber preferentially affected:

Left, right, global heart failure

• Right heart failure: Isolated right heart failure (I50.01) is rare (cor pulmonale, right heart attack, arrhythmogenic cardiomyopathy, pulmonary arterial hypertension, pulmonary embolism, etc.). Clinically, it leads to a backflow into the large circulation with consecutive organ symptoms (e.g. edema formation).
• Left heart failure (I50.19):
  • with backward failure and backflow into the pulmonary circulation (pulmonary congestion)
  • with forward failure (low output), reduction in cardiac output
• Global heart failure: common symptoms in left and right heart failure; occurrence in left heart failure + additional right heart failure (due to backflow of blood into the right heart)

According to the time course of heart failure:

• acute decompensated chronic heart failure
• Acute, newly developed heart failure
• chronic heart failure

According to the affected pumping phase of the heart:

• Systolic heart failure: HF-REF (heart failure with reduced ejection fraction < 40 %): Consequence of a contraction disorder of the myocardium
• Diastolic heart failure: HF-PEF (heart failure with preserved ejection fraction ≥ 50 %): Consequence of diastolic dysfunction of the ventricle with preserved systolic pump function and normal ventricular size
• Combined systolic/diastolic ventricular dysfunctionF

Functional classification:

Functionally, a distinction can be made between "forward" and "reverse" failure of the heart:

• Forward failure: The heart cannot build up sufficient pressure in the arteries.
• Backward failure: Blood backs up into the body and pulmonary veins.

Classification of the New York Heart Association (NYHA)

• NYHA I: No physical limitation. Everyday physical exertion does not cause inadequate fatigue, arrhythmias, shortness of breath or angina pectoris.
• NYHA II: Slight limitation of physical capacity. No symptoms at rest. Fatigue, arrhythmia, shortness of breath or angina pectoris during everyday physical exertion.
• NYHA III: Severe limitation of physical performance during normal activity. No symptoms at rest. Fatigue, arrhythmia, shortness of breath or angina pectoris during minor physical exertion.
• NYHA IV: Complaints during any physical activity and at rest, bedridden.

Classification of the American Heart Association (AHA)

• Stage A: High risk of heart failure due to factors strongly associated with the development of heart failure; no structural heart disease, no history of heart failure symptoms.
• Stage B: Structural heart disease closely associated with the development of heart failure, no heart failure symptoms to date.
• Stage C: Previous or current heart failure symptoms with 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 transplantation, intravenous catecholamines, artificial heart).

Heart failure affects > 10 million people in Europe. In 50% of cases, the primary cause is hypertension. Hypertension leads to coronary heart disease, myocardial infarction and ultimately to heart failure. The prevalence of heart failure is age-dependent: 5th decade 1 %; 6th decade: 3 %; 8th decade: 10 %.

m:f = 1.5:1.0

Acute heart failure

Develops within hours to days. Caused by:

• tachycardic or bradycardic cardiac arrhythmia
• mechanical obstruction of ventricular filling, e.g. due to pericardial tamponade
• suddenly occurring valve insufficiencies due to rupture of a previously damaged heart valve
• Acute and severe myocarditis
• pulmonary embolism
• Sudden loss of pumping function due to an acute myocardial infarction

Chronic heart failure

Protracted course over months to years. It is characterized by compensatory processes (faster heartbeat, hypertrophy of the myocardium, constriction of the blood vessels, increase in blood volume, etc.). The reduced pumping capacity of the heart is temporarily compensated for (compensated heart failure). Clinically either asymptomatic or symptoms only appear with forced physical exertion. It is caused by the following diseases:

• cardiac: coronary heart disease (myocardial infarction or ischemia), dilated cardiomyopathy (primary cardiac or in muscular dystrophy), hypertrophic (obstructive) cardiomyopathy, myocarditis)
• structural/functional: stenosis (e.g. aortic stenosis, mitral stenosis, etc.), insufficiency (aortic vitium, mitral vitium, etc.), shunt vitium (e.g. large atrial septal defect), myxoma, pericarditis, congenital anomalies, tachycardia (e.g. tachycardic atrial fibrillation), bradycardia (e.g. AV block III. degree)
• extracardiac: arterial hypertension, metabolic-toxic cardiomyopathy (diabetes mellitus, renal insufficiency, alcohol, drugs such as cocaine, anthracyclines, L-carnithine deficiency, thiamine deficiency, endocrine cardiomyopathy (hyper- or hypothyroidism, pheochromocytoma, etc.), peripartum cardiomyopathy (e.g. hyper- or hypothyroidism, pheochromocytoma, etc.). etc.), peripartum cardiomyopathy, immunological cardiomyopathy (rheumatic, collagenoses, sarcoidosis), anemia, storage diseases (amyloidosis, hemochromatosis, Fabry disease)

Compensatory mechanisms (decreasing cardiac output leads to reduced perfusion of the organs; this leads to complex compensatory processes):

• functional: Frank-Straub-Starling mechanism, staircase phenomenon (increase in contractility as a result of an increase in heart rate), tachycardia
• neuroendocrine activation: sympathetic activation + catecholamine release: the compensatory increased release of hormones (adrenaline/noradrenaline) leads to an increase in cardiac output. Blood pressure is increased by vasoconstriction. Activation of the renin-angiotensin-aldosterone system (RAAS). Vasopressin (ADH) activation leads to water retention and an increase in preload. Natriuretic peptides (ANP/BNP): The trigger for their release is a dilation of the atria (ANP: atrial natriuretic peptide) or ventricles (BNP: brain natriuretic peptide).
• pathologically/anatomically detectable compensations: increased volume load of the heart leads to concentric myocardial hypertrophy (remodeling of the heart muscle), fibrotic remodeling of the myocardium, exceeding of myocardial hypertrophy above critical limit (>500g) → relative coronary insufficiency with decrease in cardiac performance, reduction of beta-adrenergic receptors (downregulation). Catecholamines can have a less inotropic effect on the heart, but lead to an increase in afterload via increased vasoconstriction.

The main symptom of left heart failure is dyspnoea, initially occurring as exertional dyspnoea, later as resting dyspnoea and tachypnoea.

Asthma cardiale: intensification of dyspnoea after lying down; in severe cases leads to threatening nocturnal attacks of breathlessness and coughing (asthma cardiale). Detection of cardiac defect cells (alveolar macrophages containing hemosiderin) in the sputum.

Cardiac pulmonary edema with severe shortness of breath, "bubbling" rales when breathing and foamy sputum.

A common symptom of advanced heart failure is nocturnal respiratory disturbances, often in the form of Cheyne-Stokes respiration, which is characterized by a periodically recurring rise and fall in breathing.

Heart failure leads to fluid retention in the body, in left heart failure in the lungs, in right heart failure mainly in the lower extremities (pretiabial edema, presacral edema in bedridden patients), in the abdomen (ascites), in the liver (indurated atrophic congestive liver, development of cardiac cirrhosis ("cirrhose cardiaque"), in the stomach (congestive gastritis) and in the kidneys (congested kidney with proteinuria).

The most severe manifestation of heart failure is cardiogenic shock. Clinical manifestations include severe dyspnoea, clouding of consciousness, cold sweats, a weak, rapid pulse and cold extremities.

Concomitant diseases

Depending on the cause of heart failure, the following underlying diseases are associated: coronary heart disease (CHD), arterial hypertension, lipometabolic disorders and/or obesity. The frequency of concomitant diseases is related to the patient's age, personal risk factors (e.g. smoking) and the severity of the heart failure itself. Concomitant diseases of other organs, which can overlap with the actual symptoms of heart failure, are common and become more frequent with increasing degrees of heart failure.

• Chronic renal insufficiency (about 50 %)
• Sleep apnea (about 50 %)
• Iron deficiency (> 40 %)
• Anemia (35-40 %)
• Diabetes mellitus (about 30 %)
• Chronic obstructive pulmonary disease (COPD - 30 %)
• Sarcopenia (about 20 %)
• Cachexia (about 10 %)
• Patients with severe sleep disorders (difficulty falling asleep, difficulty sleeping through the night and lack of rest at night) are more likely to develop heart failure.
• Vitamin D and iron deficiency promote heart failure.

Blood count (anemia?), serum electrolytes, urea/creatinine, transaminases, LDH, alkaline phosphatase, bilirubin, albumin, coagulation parameters, urine status (proteinuria), blood gas analysis (hypoxia), medication levels (intoxication, over- or underdosing) if necessary. Brain natriuretic peptide (BNP or NTproBNP): Biomarkers that can also be helpful in everyday routine for the diagnosis of heart failure. Depending on the degree of heart failure, BNP or NTproBNP levels may be moderately to strongly elevated. Normal values largely rule out heart failure in an untreated patient.

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

Inspection: cyanosis, jugular vein congestion, lower leg edema, rales over the lungs, heart enlargement (cardiomegaly, pulmonary congestion)

Vital signs: respiratory rate (tachypnea), heart rate (tachycardia/bradycardia, pulsus alternans), blood pressure in sitting and standing position (nocturia?)

Auscultatory: evidence of a 3rd heart sound; a 4th heart sound may be present presystolically (summation gallop).

Palpation: enlargement of the liver (hepatomegaly)

Ultrasound diagnostics: The most important examination procedure in diagnostics; echocardiography allows a quick and risk-free assessment of the heart muscle function, the heart valves and the pericardium. Determination of the ejection fraction; furthermore, measurement of the tissue velocity in the mitral annulus using tissue Doppler (Eʹ and Aʹ wave). Determination of the quotient E/Eʹ as an indication of the left ventricular filling pressure. Assessment of cardiac output and blood flow (color duplex). Detection of causal factors for heart failure, e.g. vitia, disorders of ventricular wall movement after infarction, pericardial effusion.

Detection of diastolic dysfunction, 4 stages:

abnormal relaxation

pseudonormalization

reversible restriction

irreversible restriction

Chest X-ray (2 planes):

Detection of an enlarged heart: concentric hypertrophy of the ventricles as a result of pressure load cannot initially be recognized in the X-ray image; in contrast, eccentric hypertrophy with volume load can be recognized at an early stage.

Globally enlarged heart with cardiothoracic quotient (HTQ) > 0.5: quotient of maximum heart diameter (in the p.a. image) and thoracic width at the same level > 0.5.

In left heart failure (signs of pulmonary congestion): Kerley B-lines: Horizontal, up to 1 cm long stripes in the lower lobes = thickened interlobar septa in interstitial edema, dense, congested hilar vessels, widened and congested pulmonary veins (in the hilar region), frosted glass pattern in alveolar pulmonary edema, possibly pleural effusion.

In right heart failure: widening of the azygos vein (earliest change), widening of the superior vena cava and the right atrium.

Cardio-MRI: Complementary method, no significance in basic diagnostics (cost, availability)

Invasive diagnostics: No significance for basic diagnostics; coronary angiography only in the case of clinical evidence of CHD as the cause of heart failure; right heart catheterization only for special questions (assessment of the coronary arteries, preoperative ventricular diagnostics)

ECG: only unspecific changes; less suitable for diagnosing heart failure.

Dyspnoea of non-cardiac genesis, cyanosis of non-cardiac genesis, oedema of non-cardiac genesis, nocturia of non-cardiac genesis (e.g. bladder/prostate diseases), jugular vein congestion of non-cardiac genesis (e.g. tumor-induced upper jugular congestion), pleural effusions of non-cardiac origin, ascites of non-cardiac origin, pulmonary edema of non-cardiac origin, circulatory shock of non-cardiac origin (e.g. allergic shock)

Causal therapy (clarification of the cause of heart failure and elimination if possible)

Arterial hypertension: Elevated blood pressure should be lowered.

Coronary heart disease: balloon dilatation if necessary, possibly with stenting; bypass surgery if necessary.

Obstructive sleep apnea syndrome (OSA): specialist treatment

Atrial fibrillation: drug treatment, catheter ablation if necessary.

Relevant heart valve defect: surgical valve replacement if necessary (e.g. mitral valve reconstruction with a Carpentier-Edwards annuloplasty ring can lead to an improvement in symptoms if the valve is leaking with poor pumping function).

Poor pumping function and conduction disorders in the ventricles (e.g. left bundle branch block): Implantation of a three-chamber pacemaker (biventricular pacemaker CRT = cardiac resynchronization therapy). In the case of complete left bundle branch block, the pumping capacity can be improved by up to 20 %.

Severe pumping dysfunction: implantation of an "artificial heart" or a left ventricular assist device (LVAD). Mainly used as a bridge until a heart transplant ("bridge to transplant") or in the case of temporary heart failure, e.g. myocarditis, until recovery ("bridge to recovery").

High risk of sudden cardiac death: implantable cardioverter defibrillator (ICD), e.g. after ventricular arrhythmia with haemodynamic instability or with chronically reduced cardiac pumping capacity (NYHA stage II-III and ejection fraction < 35%); possibly also in combination with a biventricular pacemaker.

Severe, otherwise untreatable heart failure: heart transplantation

Reduction of cardiovascular risk factors! Adapted physical activity; moderate physical training is recommended in NYHA stages I-III; in the case of decompensated heart failure, physical rest until bed rest. No travel to high altitudes or to hot and humid climates. Furthermore: normalize weight, reduce salt intake, limit fluid intake (< 2 litres/day) and reduce or abstain from alcohol and nicotine.

Regulate bowel movements as naturally as possible (high-fiber diet, plenty of fruit and vegetables). Reduce shortness of breath at night through optimal sleeping conditions: elevate upper body, pleasant room temperature, fresh air, darkness, no heavy meals before going to bed.

Supportive: Aromatherapy - vaporization of essential rosemary oil, rose oil or nard oil (Nardostachys jatamansi)

Drug therapy for chronic heart failure

Treatment of acute heart failure

Causal therapy of the underlying cause (hypertensive crisis, acute coronary syndrome, pericardial tamponade, bradycardic arrhythmia, tachycardic arrhythmia)

Symptomatic measures include seated positioning, sedation, O₂ administration, preload reduction with nitroglycerin, rapid diuresis using loop diuretics (e.g. furosemide i.v.) and - in the case of advanced decompensation - the use of positive inotropic catecholamines (e.g. dobutamine).

Drug therapy for chronic heart failure

Step-by-step scheme for the pharmacotherapy of chronic heart failure:

NYHA I-IV (Group B in ABCD classification): ACE inhibitors (alternatively AT1 blockers (losartan, candesartan, valsartan) in case of intolerance - e.g. cough - to ACE inhibitors)

NYHA II-IV: beta-blockers (bisoprolol, carvedilol, metoprolol, nebivolol), also for NYHA I in the case of hypertension and after a heart attack; gradual dosage as there is a risk of decompensation.

NYHA II-IV: diuretics, also for NYHA I in the case of clinically detectable fluid retention

NYHA II-IV: Aldosterone antagonists

NYHA III-IV: Cardiac glycosides, gradually and only in stable patients, consider reserve medication in case of beta-blocker intolerance and sinus rhythm (low target serum level)

NYHA II-IV: If channel blocker (ivabradine), improves prognosis in systolic heart failure and sinus rhythm > 70/min.

Therapy with phytotherapeutics in combination with synthetic agents is generally suitable for stages NYHA I and NYHA II.

The additional general measures are identical to those of the accompanying measures of the traditional therapy (see above), in particular, order therapy, nutrition therapy with reduction of excess weight and exercise therapy.

for cardiac insufficiency (NYHA I-II):

Crataegi folium cum flore(HMPC, ESCOP and Commission E monographs); Convallariae majalis herba (positive Commission E monograph and empirical medicine).

see also under Adonidis herba and Scillae bulbus (for both Commission E monographs, HMPC and ESCOP not processed), but these are no longer recommended today. see also under Adonis herb + lily of the valley herb + sea onion + oleander leaves, only described in empirical medicine for heart failure: Armoraciae rusticanae radix

Foxglove without monograph. Oleandri folium: negative monograph from Commission E.

Camphor is suitable (usually 10-20% as a combination preparation with rosemary, menthol, benzyl nicotinate) in the form of ointments or liniments as a circulatory tonic therapeutic agent (e.g. Praecordin® S ointment) 1-2cm long strand of ointment rubbed into the heart area 1-3x/day(Commission E monograph).

1. EMA/HMPC: European Union herbal monograph on Crataegi folium cum flori-Final, Apr 5, 2016. htpp//www.a-turl.de/?k=urba
2. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012 of the European Society of Cardiology and Commentary of the German Society of Cardiology of 2013
3. Graefe KH et al. heart failure. In: Graefe KH et al (Eds) Pharmacology and Toxicology. Georg Thieme Publisher Stuttgart S.513
4. Hellenbrand N et al (2015) Isolation and quantification of oligomeric and polymeric procyanidins in leaves and flowers of Hawthorn (Crataegus spp.). Fitoterapia 104:14-22.
5. National Care Guideline Chronic Heart Failure of the German Medical Association, the National Association of Statutory Health Insurance Physicians and the AWMF (valid until 12/2014).
6. Guideline Chronic Heart Failure in Childhood and Adolescence of the German Society for Pediatric Cardiology.