Heart failureI50.9

Heart failure is a polyethiological clinical syndrome. It is defined as a pathological inability of the heart to deliver the cardiac output required by the body at normal end-diastolic ventricular pressure (without pressure increase) 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 the cardiac output (CPV):

• Low-output failure: Forward failure with reduction of cardiac output. Cool periphery. The arterio-venous oxygen difference (normally 3.5-5.0ml/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 (normally 3.5-5.0ml/dl) is reduced.

According to the preferred affected chamber:

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 backlog in the large circulation with consecutive organ symptoms (e.g. edema formation).
• Left heart failure (I50.19):
  • With backward failure and backwater into the pulmonary circulation (pulmonary congestion).
  • With forward failure (low output), reduction of cardiac output.
• Global heart failure: Common symptoms in left and right heart failure. Occurs 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 emerged heart failure
• Chronic heart failure

After 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 pumping function and normal ventricle size.
• Combined systolic/diastolic ventricular dysfunction.

functional classification

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

• Forward failure (heart cannot build up sufficient pressure in the arteries)
• Backward failure (backflow of blood in 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 exhaustion, rhythm disturbances, shortness of breath or angina pectoris.
• NYHA II: Slight limitation of physical activity. No complaints at rest. Exhaustion, dysrhythmia, shortness of breath or angina pectoris during everyday physical exertion.
• NYHA III: Severe limitation of physical capacity during usual activity. No complaints at rest. Exhaustion, dysrhythmia, shortness of breath or angina pectoris with little physical strain.
• NYHA IV: Complaints during all physical activities and at rest, bedriddenness.

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, never heart failure symptoms.
• Stage B: Structural heart disease closely associated with the development of heart failure; no heart failure symptoms yet.
• Stage C: Past or present heart failure symptoms 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 transplantation, i.v. 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, heart attack and ultimately heart failure. The prevalence of heart failure is age-related: 5th decade 1%; 6th decade: 3%; 8th decade: 10%;

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Acute heart failure

Develops within hours to days. Causes are:

• tachycardic or bradycardic arrhythmias
• mechanical obstruction of the ventricle filling, e.g. by pericardial tamponade
• Sudden valve insufficiencies due to a rupture of a damaged heart valve
• acute and severe myocarditis
• Pulmonary embolism
• sudden loss of pumping function due to an acute heart attack.

Chronic heart failure

Protracted course over months to years. It is characterized by commensal processes (faster heartbeat, hypertrophy of the myocardium, narrowing of blood vessels, increase in blood volume, etc.). The reduced pumping capacity of the heart is temporarily compensated for (compensated heart failure). Clinically either without symptoms or symptoms only after forced physical exertion. The following diseases are the cause:

• cardiac: coronary heart disease (myocardial infarction or ischemia), dilated cardiomyopathy (primarily cardiac or muscular dystrophy), hypertrophic (obstructive) cardiomyopathy, myocarditis)
• structural/functional: stenosis vitae (e.g. aortic stenosis, mitral stenosis or similar), insufficiency vitae (aortic vitium, mitral vitium or similar), shunt vitae (e.g. large atrial septum defect), myxoma, pericarditis, congenital anomalies, tachycardia (e.g. tachycardic atrial fibrillation), bradycardia (e.g. A.V. block III. degree)
• a.), peripartal cardiomyopathy, immunological cardiomyopathy (rheumatic, collagenosis, sarcoidosis), anaemia, storage diseases (amyloidosis, haemochromatosis, Fabry's disease).

Compensatory mechanisms (decreasing cardiac output leads to reduced perfusion of the organs. This leads to complex compensation 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 (adrenalin/ norepinephrine) leads to an increase in the heart's ability to beat. Blood pressure is increased by constricting the vessels. 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 stimulus for their release is a dilation of the atria (ANP: atrial natriuretic peptides) or ventricles (BNP: brain natriuretic peptides).
• Pathologically/anatomically detectable compensations: Increased volume load of the heart leads to concentric myocardial hypertrophy (remodelling of the heart muscle), fibrotic remodelling of the myocardium, exceeding of the myocardial hypertrophy above the critical limit (>500g) → relative coronary insufficiency with decrease of the cardiac performance, decrease of beta-adrenergic receptors (downregulation). Catecholamines may have a less inotropic effect on the heart, but lead to an increase in afterload via increased vasoconstriction.

The leading symptom of left heart failure is dyspnea, initially occurring as exertional dyspnea, later as resting dyspnea and tachypnea.

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

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

A common symptom in advanced heart failure is nocturnal dyspnea, often in the form of Cheyne-Stokes respiration, characterized by periodic waxing and waning of respiration.

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

The most severe form of heart failure is cardiogenic shock, clinically striking with severe respiratory distress, clouding of consciousness, cold sweat, weak and rapid pulse, and cool hands and feet.

Concomitant diseases

Depending on the cause of heart failure, the following underlying diseases are associated: coronary artery disease (CAD), arterial hypertension, dyslipidemia and/or obesity are among them. The frequency of comorbidities 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 may overlap with the actual heart failure symptoms, are common and increase with the degree of heart failure.

• Chronic renal failure (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 disturbances (difficulty falling asleep, difficulty staying asleep, and lack of nocturnal rest) 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 (proteinnuria), blood gas analysis (hypoxia), drug levels (intoxications, over- or underdoses) if applicable. Brain natriuretic peptide (BNP or NTproBNP): Test procedure that can also be helpful in everyday routine for the diagnosis of heart failure. Depending on the degree of heart failure, there is a moderate to severe increase in BNP or NTproBNP levels. Normal values largely exclude heart failure in an untreated patient.

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

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

Vital signs: Heart rate (tachycardia/bradycardia, pulsus alternans), recording of blood pressure in sitting and standing position, nocturia.

Auscultatory: detection of a 3rd heartbeat; a 4th heartbeat may occur pre-systolically (summation gallop)

Palpatory: enlargement of the liver (hepatomegaly),

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

Detection of diastolic dysfunction 4 stages:

abnormal relaxation,

Pseudo-normalization,

reversible restriction,

irreversible restriction

X-ray thorax (2 planes):

Evidence of an enlarged heart: The concentric hypertrophy of the ventricles due to pressure load cannot be detected in the X-ray image at first. However, eccentric hypertrophy due to volume loading can be detected early on.

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

In left heart failure (signs of pulmonary congestion): Kerley B-lines: horizontal stripes up to 1 cm long in the lower lobes = thickened interlobular septum in interstitial edema, densely congested hilus vessels, widened and congested pulmonary veins (in the hilus region), frosted glass drawing in alveolar pulmonary edema; possible pleural effusion.

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

Cardio-MRI: Supplementary method, no significance in basic diagnostics (effort, availability)

Invasive diagnostics: No significance for basic diagnostics: coronary angiography only in clinical cases of coronary heart disease as the cause of heart failure; right heart catheterization only for special questions (evaluation of coronary arteries, preoperative vitamin diagnostics).

ECG: only non-specific changes; less suitable for the diagnosis of heart failure.

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

Causal therapy (clarification of a cause of heart failure and, if possible, its elimination).

Arterial hypertension: raised blood pressure should be reduced.

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

Obstructive sleep apnoea syndrome (OSA), specialist treatment.

Atrial fibrillation: drug treatment, possibly catheter ablation.

Relevant heart valve defect: if necessary, surgical valve replacement; e.g. mitral valve reconstruction with an annuloplasty ring according to Carpentier-Edwards can lead to an improvement of symptoms in case of valve leakage with poor pumping function.

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

Severe pumping dysfunction: implantation of an "artificial heart" or a left ventricular assist device (LVAD). Used mainly as a bridge to transplantation or in cases of temporary heart failure, e.g. in myocarditis, to recovery ("bridge to recovery").

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

Severe, otherwise untreatable, severe heart failure: heart transplantation.

Reduction of cardiovascular risk factors! Adapted physical activity; in NYHA stages I-III, moderate physical exercise is recommended; in decompensated heart failure, physical rest until bed rest. No travel at high altitudes or in hot and humid climates. Also: weight normalization, reduced saline intake, limited fluid intake (<2 liters/day) and reduction or withdrawal from alcohol and nicotine.

Regulate stool by measures that are as natural as possible (a high-ballast diet, lots of fruit and vegetables). Reduce nocturnal shortness of breath through optimal sleeping conditions. Raise your upper body, comfortable room temperature, fresh air, darkness, no heavy meals before going to bed.

Supporting: Aromatherapy - Vaporization of essential oil of rosemary, rose or nard (Nardostachys jatamansi)

Drug therapy of chronic heart failure

Therapy of acute heart failure

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

Symptomatic therapy (sitting position, sedation, oxygenation, reduction of preload by administration of nitroglycerin, fast-acting loop diuretic e.g. furosemide i.v., possibly positively inotropic beta-receptor antagonists.

Drug therapy of chronic heart failure

Staged scheme for pharmacotherapy of chronic heart failure:

NYHA I-IV (group B in ABCD classification): ACE inhibitors (alternative for intolerance - e.g. cough - to ACE inhibitors AT1 blockers (losartan, candesartan, valsartan)

NYHA II-IV: Beta-blockers (bisoprolol, carvedilol, metoprolol, nebivololol), in hypertension and after heart attack also in NYHA I; creeping dosage, because of the danger of decompensation.

NYHA II-IV: diuretics, in clinically proven fluid retention also in NYHA I

NYHA II-IV: Aldosterone antagonists.

NYHA III-IV: Cardiac glycosides, creeping in and only in stable patients, reserve medication, consider 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

A therapy with phytotherapeutics in combination with chemical-synthetic drugs is usually suitable for the stages NYHAI and NYHAII.

The additional general measures are identical to those of the concomitant measures of traditional therapy (see above).

Hawthorn leaves with flowers are particularly good for the treatment of cardiac insufficiency (NYHA II-III) the optimal dosage is 900-1200mg dry extract.

Camphor is suitable (mostly 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 ointment strand 1-3x/day rub into the heart region.

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
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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.