Now we are going to bring our discussion of shock to the next level and start to explore some patterns that can help us with recognition of shock. Remember, if we no longer define shock as low blood pressure, we need to have some indicators to help us recognize what can be a startlingly subtle yet dangerous state.
But first, a caveat. Imagine you go to the beach one warm summer day. Even though it is a popular beach, you note that there are almost no people there. You notice a purple flag flying over the lifeguard stand. You then notice people running out of the water. Maybe this pattern means that there is something dangerous in the water. Or maybe it is just early in the day, most people haven’t arrived yet, and the people running out of the water were just playing.
The point being that patterns can be helpful, but they can also be limiting. They don’t always hold true, but they can give a framework for what to expect, especially if you have an appreciation for the limitations and exceptions.
That said, let’s consider a pattern commonly seen in shock.
What does shock look like at the bedside?
Imagine you are receiving a patient in the intensive care unit (ICU). The team that is handing him off says, “I’m not sure what is going on with him, but he has us worried. We are thinking he may be in shock.”
What might you expect this patient to look like over the next 12–24 hours assuming he continues to worsen? Not every presentation is the same, but the following is a pattern that is useful to consider ( Fig. 3.1 ).
Let’s consider each of these phases.
Phase 1: cardiac output compensation
Remember that as DO 2 :VO 2 falls, the most ready way that the body can increase this is by augmenting cardiac output. Cardiac output increases when the stroke volume increases (heart squeezes harder) or heart rate increases (heart beats faster). In most people, this can augment CO, and consequently DO 2 several fold (up to 35-fold in some athletes).
Clinically, this can be manifested by tachycardia or by increased pulse pressure (the difference of systole and diastole) ( Fig. 3.2 ).
Ultimately, if DO 2 is not able to keep up with VO 2 requirements, then the DO 2 :VO 2 ratio starts to fall, manifested by lower venous oxygen saturation ( Fig. 3.3 ).
When does this pattern not apply?
There are many reasons other than shock for the heart rate/cardiac output to be augmented in patients in the ICU (agitation, delirium, medication effect, withdrawal, etc.). However, a rise in these parameters should give pause and lead to the consideration that it may be compensation for a drop in DO 2 .
Additionally, a venous oxygen saturation cannot always be used as a surrogate for DO 2 :VO 2 . We remember that if the VO 2 remains constant, a dropping venous oxygen saturation can be a surrogate for a drop in DO 2 :VO 2 .
However, what happens when the cardiac output remains in a high output state, say due to a catecholamine surge or in early sepsis? In this case, the blood may be circulated around the periphery so fast that the oxygen is unable to be extracted. This may lead to a higher than expected venous oxygen saturation, which may not correspond with adequate DO 2 :VO 2 .
In another example, as shock progresses, target organs may begin shutting down, leading to a decreased VO 2 . This will lead to an elevated DO 2 :VO 2 ratio that does not actually mean that the body is adequately delivering oxygen to meet the tissue needs, but rather may have a more ominous meaning ( Fig. 3.4 ).
