In order to understand the pathophysiology, and the subsequent management, equations of life are extremely useful. Click on each box below to find out more.

Blood Pressure (BP) = Cardiac Output (CO) x Systemic Vascular Resistance (SVR)

This informs us that in order to maintain an adequate perfusion pressure (BP) we need an adequate flow of blood (CO) and adequate vascular tone (SVR). A useful analogy for this is to consider the pressure generated from water flowing through a pipe. The pressure in the pipe (analogous to the BP) can be increased by one of two ways:

1. Increasing the flow of water through the pipe (increasing the CO).
2. Maintaining the same flow but increasing the resistance to flow by decreasing the pipe diameter (increasing the SVR through vasoconstriction).

Hypotension (and resultant hypoperfusion) can be caused by either a low cardiac output (cardiogenic shock, outflow obstruction, hypovolaemic shock) or a low SVR (neurogenic or septic shock) or both (septic shock).

Cardiac output (CO) = stroke volume (SV) x heart rate (HR)

Heart rate is easy to measure, stroke volume is not. However, we can consider the variables that determine stroke volume. Stroke volume – the volume ejected from the heart with every beat is dependent on three variables:

1. Pre-load

If we have two identical elastic bands and fire the first one at the wall, how do we make the second one hit the wall harder? We pull it back more before releasing, i.e. the more we stretch it the more ping we achieve.

The heart muscle is very similar. The more we stretch it the more it pings back. How do we stretch the heart muscle? We increase end-diastolic volume by filling the heart. This will lead to an increase in the stroke volume.

2. Frank-Starling Curve – More information

In the critically ill patient, low pre-load from either hypovolaemia or relative hypovolaemia is probably the most common cause of a low SV and subsequent low CO and reduced perfusion. Fortunately, it can normally be easily rectified by fluid resuscitation. The hypovolaemic patient will attempt to maintain CO and perfusion by mounting a tachycardia.

You’ll also see from figure 2 that it is possible to over stretch the heart. This is why reducing pre-load (and/or afterload) with vasodilators or diuretics in patients with heart failure improves myocardial function.

Cardiac output is dependent on preload, contractility and afterload

1. Contractility

Going back to elastic bands, if we have a range of elastic bands to fire at the wall but can only pull them back a fixed distance, how can we pick an elastic band that will hit the wall harder? We pick a thicker one. This will give us more ping per unit stretch. In the heart this can be achieved by administration of an inotrope. The effect of an inotrope on the Frank-Starling Curve is demonstrated in figure 3.

We can see that an inotrope generates a greater SV for a given pre-load. One important point to note is that an inotrope is more effective with an adequately filled heart ‘a sick heart has as much right to be full as a healthy one’.

2. Afterload

This is the pressure against which the heart has to eject. If you fire an elastic band through air it will hit the wall harder than if fired through water. A high SVR will tend to reduce CO. This has further implications as we will see later.

In low cardiac output states, optimising SV becomes very important to ensuring adequate perfusion.

Delivery of O₂ = CO × ([Hb x arterial oxygen saturations x constant] + a small amount dissolved in plasma)

i.e. DO₂ = CO (l/min) × [Hb (g/l) × 1.34 × SpO₂ × 0.01 + (PO₂ × 0.023)]

Here we see that oxygen delivery is dependent on blood flow not pressure. We can now look back at the equation for BP and see that it could be possible to be in a situation where the blood pressure was in the normal range but this was generated by an extremely high SVR and very low CO. Although perfusion pressure was adequate, a low CO would result in very low oxygen delivery and tissue hypoxia.

You can be shocked with a normal blood pressure.