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.
Reference:
Phlebologie
2018; 47: 115–119; https://doi.org/10.12687/phleb2420-3-2018
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