Abstract

Descriptions of the pathophysiology of heart failure have gone through a substantial evolution in the last 50 years. It is now recognised that heart failure can occur in the presence and also in the absence of a reduction in left ventricular function. In the former situation, this classically has been described to lead to hypotension and secondary salt and volume retention by the kidneys, further aggravating cardiac function. In the latter, this has been described to lead to pulmonary congestion because of impaired cardiac diastolic filling. These concepts have further evolved in the discrimination of 'acute vascular' versus 'acute congestive' heart failure. The current paper builds the argument from numerous smaller observational studies that irrespective of the clinical presentation of heart failure, fluid congestion is the key. If left ventricular function is preserved, fluid retention is probably due to the inability of damaged kidneys to excrete the large amounts of salt ingested with modern diet. In the extreme of end-stage renal disease requiring haemodialysis, heart failure is frequent, but can be prevented almost entirely by strict volume control. Unfortunately, the absence of systematic studies describing fluid volumes and renal haemodynamic and reabsorptive function in patients with acute heart failure precludes the final proof of our concept. This paper therefore is a strong call for mechanistic research in this area.

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