A View From Intensive Care

A View From Cardiology

William Withering first described the use of digitalis to treat dropsy in 1785. In the succeeding centuries, we have introduced numerous other inotropes—such as beta-adrenergic agonists, phosphodiesterase inhibitors, and dopaminergic agents—to augment cardiac output in the failing heart.

However, does short-term gain lead to long-term harm? The few randomised studies comparing inotropic to noninotropic therapy for decompensated heart failure have shown or suggested detriment. There is a narrow line between the desire to maintain organ perfusion compatible with survival and avoidably flogging a ‘tired,’ ischaemic myocardium. The decreased contractility associated with myocardial stunning or hibernation could be considered a protective reflex to maintain the bioenergetic supply-demand balance and thus avoid cell death.

Are we disrupting this attempt at cellular self-preservation by our well-intentioned but often misplaced use of inotropes? Should greater efforts be directed at resting the damaged heart by reducing the demands placed upon it, through the use of drugs and devices that optimise preload and afterload, decrease the work of breathing, and augment/assist cardiac performance? And if and when we do have to drive the heart, should we aim to do so as gently as possible?

This is the challenge we face in choosing and titrating optimal therapy.

There may not be a simple ‘Yes’ or ‘No’ answer to the issue of positive inotropy in heart failure. Not that long ago, positive inotropy in heart failure with reduced systolic function seemed like a simple but reasonable approach. However, we have not been able to confirm its benefit. Indeed, the relatively limited data bank suggests a detrimental affect of positive inotropy, a concept apparently supported by recent proven benefit of beta-adrenergic blockade.

As a result we now regularly see the slide of the flogged horse pulling a heavy load up a hill representing positive inotropy, and the obligatory follow-up slide of the happier animal carrying a lighter load, underlining the presently favoured approach of unloading the heart rather than increasing the workload of a damaged pump. Therefore, has positive inotropy seen its day?

Again, it may not be that simple. Rather than look upon inotropy as flogging a tired horse, maybe we should consider the qualifying term of improving cardiac efficiency in circumstances where inotropy may be desired—i.e., improving cardiac function without increasing myocardial oxygen function.

Moreover, if this approach could be coupled with the proven benefit of unloading the heart, then an effective therapy may evolve. This approach needs to be rigorously tested by trusted scientific methods, but it is possible that appropriately used inodilation may make our equine friend even happier.

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