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Decompensated heart failure is considered a contraindication for compression therapy and lymphatic drainage. Since the treatment is usually prescribed by phlebologists, dermatologists and GPs, and less often by cardiologists, it is important to understand the correlation between compression and heart failure, and to establish the significance of the latter. According to the European Society of Cardiology, heart failure is characterised by a shortness of breath, peripheral oedema, palpitations and reduced cardiac output. Underlying primary diseases include CHD, hypertension, valvular heart disease and post-inflammatory changes. Decompensated heart failure is classified under NYHA stages III and IV in which the symptoms mentioned above appear even at low levels of physical activity or when the body is at rest. The contraindication for using compression therapy with decompensated heart failure is based on the idea that blood volumes in the extremities shift towards the heart causing a volume overload in the pulmonary circulation and possibly resulting in a pulmonary oedema. Scintigraphy and air-plethysmography reveal the displacement of regional blood volumes when medical compression stockings (MCS) are used. This is compensated for in healthy heart patients. Structural cardiac disease has been shown to change the behaviour of myocardial regulation processes. An increased volume in the right atrium produces a local rise in pressure and an increased expression of natriuretic peptides. However, studies have shown that this increase is temporary and is not accompanied by clinically relevant haemodynamic changes. Thus MCSs pose no threat at NYHA stages I and II. Invasive measurements of patients suffering from heart failure NYHA stages III and IV have also identified that haemodynamic changes caused by compression are compensated for after a few minutes and usually only have minor clinical impact. Nevertheless, drainage therapy on patients with decompensated heart failure should be strictly monitored due to its prognostic implications.


Phlebologie 2018; 47: 115–119;