B-type natriuretic peptide (BNP) is a 32 aminoacids peptide that is synthesized and released predominantly from the ventricular myocardium. The triggers for BNP release are increased ventricular preload and/or afterload. Circulating BNP possesses several physiological activities including vasodilation, inhibition of the renin-angiotensin-aldosterone system (RAAS), inhibition of sympathetic nervous activity as well as promoting natriuresis and diuresis. Together these activities not only counteract the deleterious effects of the RAAS and sympathetic system in heart failure but also reduce the ventricular preload and afterload. The potential therapeutic effect of BNP was tested when a recombinant hBNP (nesiritide) was released. The outcomes of nesiritide therapy in heart failure have so far been positive. BNP has also been promoted as a diagnostic tool for cardiac failure. Given the wide range of cardiac diseases encountered in the intensive care setting, and the recent observations that BNP levels could be affected by age and gender, its use as a diagnostic tool for cardiac dysfunction in this particular setting should however be cautioned. Nevertheless, this should not discourage the use of BNP in the intensive care unit, in particularly the potential use of nesiritide in acute heart failure and the use of plasma BNP as an index in guided therapy.