Shock is a serious, often life-threatening condition which merits prompt intervention. It can be defined as circulatory insufficiency with inadequate oxygen delivery resulting in hypoperfusion and tissue hypoxia
In order to understand the pathophysiology, and the subsequent management, of shock two physiological equations are extremely useful (A + B).
(A) 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. One can increase the pressure in the pipe (analogous to the BP) by one of two ways:
(i) increasing the flow of water through the pipe (increasing the CO).
(ii) maintaining the same flow but increasing the resistance to flow by decreasing the pipe diameter (increasing the SVR through vasoconstriction).
We can therefore see that 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).
For low cardiac output states we must also remember that:
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:
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, see figure 2.
Figure 2. The Starling curve.
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 preload (and/or afterload) with vasodilators or diuretics in patients with heart failure improves myocardial function.
2. 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 Starling curve is demonstrated in figure 3.
Figure 3. The Starling curve. Effect of inotropes on contractility and stroke volume.
We can see that an inotrope generates a greater SV for a given preload. One important point to note is that an inotrope is more effective with an adequately filled heart giving substance to the statement that “a sick heart has as much right to be full as a healthy one”.
3. After load: 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.
However, one must also remember that perfusion pressure (BP) is not the only important factor in ensuring adequate oxygen delivery. In order to understand why an “adequate” BP is not always reassuring we must look at a second equation.
Oxygen Delivery = Blood flow X oxygen content of blood
In other words:
DO2 = CO X [oxygen content]
(B) DO2 = CO X ([Hb x arterial oxygen saturations x constant] + a small amount dissolved in plasma)
Here we see that oxygen delivery is dependant on blood flow NOT pressure. We can now look back at equation A 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 (see B) and tissue hypoxia.
You can be shocked with a “normal” blood pressure.
We will come back to these formulae when we consider diagnosis and treatment.