Learn Haemodynamics

The USCOM and Inotropy

A Guide for Junior Medical and Nursing Staff

Brendan E Smith MB.,Ch.B., FFA, RCS.
Associate Professor, School of Biomedical Science,
Charles Sturt University, Bathurst, New South Wales,
Specialist in Anaesthetics and Intensive Care.
Bathurst Base Hospital, New South Wales,

Basic Science

Clinical studies

Use of    Inotropes

Balancing    Inotropes

Measurement of    Preload
Corrected Flow    Time


So what exactly is inotropy? In a very real sense, inotropy is the power of the heart. In the same way that we talk about the strength of a muscle like the biceps, so we can talk about the strength of a muscle like the heart. In short, when it contracts how powerful is that contraction? Although not strictly the same thing, most clinicians now use the terms inotropy and myocardial contractility interchangeably to mean the power of contraction of the heart.

Inotropy is vitally important in haemodynamics. Cardiac output depends on stroke volume and heart rate. Stroke volume depends on three factors; preload which is the degree of ventricular filling at the start of systole, afterload which is the load the ventricle has to work against and is basically the mean aortic blood pressure, and inotropy. The heart has to respond to changes in preload and afterload to maintain a normal stroke volume and it does this through variations in inotropy. If preload increases, i.e. if more venous blood comes to the heart, then the ventricular fibres are stretched and respond with increased force of contraction and increased stroke volume, so more blood is pumped out of the heart! Similar responses occur if afterload changes. If the SVR rises then the heart has to contract more forcibly to continue ejecting a stable stroke volume. Simple, but crucial.

If the heart could not respond to arterial vasoconstriction for example, then the ventricle would dilate and fail. This is often seen in septicaemia where a very low SVR and blood pressure is treated by a simple vasoconstrictor. The cardiac output may initially be high and ventricular emptying may also be high with a stroke volume of over 75% of the resting end-diastolic volume (ejection fraction > 75%). As the arterial tree is very vasodilated, it is easy for the left ventricle to empty into the aorta. Very little effort is needed if the blood pressure is only 70/40 and the SVR 200! On an echocardiogram, the ejection fraction and cardiac movements may look great and can give a false sense of security.

However, the myocardium is often severely depressed in septicaemia and cannot overcome the increased afterload which follows the use of a vasoconstrictor. The ventricle now has to work much harder to eject the same stroke volume. If it cannot produce that extra power then it fails, sometimes very abruptly.  We have to ensure that the ventricle has sufficient inotropy to cope with the afterload increase. Problem is, how do we know what power it has to start with and how do we know we have given it sufficient power through the use of inotropes to cope with the arterial pressure we aim to expose it to? That’s a tough one!

Similarly, not increasing stroke volume in response to increased preload leads to a backlog of blood in the venous system, increased venous pressure and oedema. This is bad enough in right heart failure with systemic oedema, but even worse in left ventricular failure with pulmonary oedema.

We really have very limited choices. We could reduce the preload by vasodilation, as with nitrates or frusemide (which reduces preload by vasodilation long before we see the first drop of urine!). We could reduce the circulating volume by diuresis, dialysis, fluid and salt restriction or even blood-letting, depending on the urgency. Alternatively, we could reduce the afterload so that the ventricle can empty more easily, so it can take more blood from the venous system and keep it pushed out into the body, an increase in forward flow. This is one of the actions of ACE inhibitors for example, and the reason why they are used in chronic LVF.

But what if the problem is just that the myocardium has insufficient “oomph” to cope at all? Our only choice is to increase inotropy and power the heart up to a more normal level. Problem is, as before, how do we know what power it has to start with and how do we know we have given it sufficient power through the use of inotropes to cope with the demands placed on it?

We have all seen inotropes used clinically, but how do we know when to use them? Which one do we use? How much should we use? What are our clinical targets or therapeutic goals? How do we know when we’ve reached them? How much easier life would be if only we could measure inotropy quickly and easily. Life without guesswork! We could replace questions with logical answers.

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