Acute care: Circulatory failure and use of inotropes

Back to basics

I bet you never realised that the dry physiology learnt at medical school would turn out to be so important later on. Let us start with blood pressure: Ohm's law has been adapted to demonstrate that blood pressure (BP) is the product of cardiac output (CO) and systemic vascular resistance (SVR)--that is, BP=CO*SVR. Therefore a low blood pressure can be due to a low cardiac output (low flow) or reduced systemic vascular resistance (vasodilatation) or both. Pressure and flow are not the same thing. There is no “normal” blood pressure. What matters is whether a low blood pressure is causing a problem.

Cardiac output

Cardiac output in turn depends on the interrelated factors of heart rate (HR) and stroke volume (SV)--that is, CO=HR*SV. Stroke volume, you will remember, is the volume of blood ejected in a single ventricular contraction. This, in turn, depends on three things--contractility, preload, and afterload.

Contractility is the amount of mechanical work done for a given preload and afterload. It is increased by sympathetic stimulation and inotropes. It is reduced by parasympathetic stimulation, negative inotropes, ischaemia, hypoxaemia, acidosis, and a low serum calcium. Preload is equivalent to the final diastolic volume--how “loaded” the ventricle is just before contraction. Afterload is the tension developed in the ventricular wall during systole--so vasoconstriction increases this.

Treating low blood pressure

To go back to the beginning, what if you have a patient with a low blood pressure that is causing hypoperfusion of vital organs, like the kidneys? The heart rate, preload, afterload then contractility need to be considered in that order (box 1).