What is meant by shock? Let’s return to our two intensive care unit (ICU) patients.
Patient A: BP 100/40, HR 114, UOP < 10 mL
Patient B: BP 80/40, HR 85, UOP 50 mL/hr
Which patient is in shock? Patient A? Patient B? Both?
What is shock?
Often the bias is to define shock simply as a low blood pressure. While this is certainly part of the equation, it is not the whole picture.
Why is low blood pressure usually the first thing we think about when we think about shock? Usually, it is because this is the first parameter that presents itself – the monitor starts beeping, alarms are going off, and people around us start getting concerned. However, we have to remember that a low blood pressure, specifically a low mean arterial pressure (MAP), may or may not mean that a patient is in shock ( Fig. 2.1 ).
What is the difference between low blood pressure and shock?
Shock is defined as circulatory failure causing inadequate delivery of oxygen to meet oxygen consumption requirements, leading to cellular and tissue hypoxia. It all comes back to DO 2 :VO 2 . When DO 2 is not adequate to keep up with VO 2 , shock ensues.
This is an important distinction from blood pressure. A low MAP can be evidence of a low cardiac output and, thus, a deficiency of DO 2 :VO 2 , but it does not mean that the patient is in shock.
Rather, the MAP is an observed value calculated by the systolic and diastolic blood pressure, which is ultimately a factor of cardiac output, central venous pressure (CVP) to a lesser degree, and systemic vascular resistance (SVR) ( Fig. 2.2 ).
We are making this distinction because, ultimately, it does not matter to end organs what the MAP is, but rather how much oxygen is being delivered. It is tempting to chase after specific MAP targets, but these targets only matter to the degree that they are an observed manifestation of cardiac output and ultimately DO 2 .
If you measured the blood pressure of 100 random people, you would notice that there is a vast difference in the overall MAP. Some would have a very high MAP and some may have a very low MAP. The people with the lower MAP likely are not in shock. They may have completely adequate perfusion, normal lacatate levels, great urine output, and overall, adequate DO 2 .
What is the relationship of MAP to cardiac output?
There are certainly some people who if you measured their MAP throughout the course of their normal day (especially during sleep), you might notice a MAP of 65, 60, 55 mmHg, or even below. What is going on with these people? Are we catching shock that would normally go unrecognized?
Clearly not. What we are uncovering here is that MAP only relates to low oxygen delivery to the degree that it is an observable indicator of cardiac output. The reason why some people can maintain adequate oxygen delivery and cardiac output at a lower MAP is SVR.
SVR represents the overall tone of the blood vessels. The normal relation of MAP to SVR is traditionally expressed as:
MAP→CO×SVR
Thus, we can imagine that the same cardiac output, as represented by the green line, could correspond to very different MAPs, based on what the overall SVR is, as illustrated in Fig. 2.3 .
Rather than stating that MAP is a function of CO and SVR, we can consider reframing the relationship as:
CO→MAPSVR
In this regard, we can see that MAP is the observable manifestation of cardiac output as a function of SVR maintained by the blood vessels. SVR is a derived value and MAP is a measured value. Ultimately, both help to describe the cardiac output and, ultimately, the DO 2 .
Reframing how we define shock
Let’s return to our DO 2 :VO 2 relationship. Remember that as DO 2 :VO 2 decreases to below 2:1, we begin to head toward cardiopulmonary and total system collapse ( Fig. 2.4 ).
In order to determine how oxygen is being delivered, we must recognize inadequate delivery of oxygen above all else. If a patient has a normal blood pressure because the SVR is high but oxygen is not being delivered, he or she may be in shock. If a different patient has lower blood pressure because of a lower SVR, but oxygen is being delivered, urine output is adequate, mental status is maintained, and all tissues have evidence of adequate perfusion, shock may not be present, regardless of what the blood pressure is.
How do we classify shock?
Now that we have the framework to recognize shock as a deficiency of oxygen delivery, let’s turn our attention to identifying the cause of shock. You will come to appreciate this as the essential piece to managing a patient in shock. Once you know what you are up against, you will be in a much better position to intervene and improve the outcome for your patient.
The traditional classification of shock is based on the relative contributions of low cardiac output and SVR: cardiogenic, obstructive, hypovolemic, and distributive ( Fig. 2.5 ).
It is often tempting to think of these as fixed classifications, with each patient being assigned a designation when they hit the ICU just as they are assigned a medical record number. Your patient with NSTEMI? Cardiogenic shock. Your patient with urosepsis? Distributive shock.
Unfortunately, it is never this simple – each classification can have a multitude of mechanisms, pathophysiologic processes, and etiologies associated. Pericardial tamponade, pulmonary embolism, and pneumothorax can all cause obstructive shock but obstruct in very different ways. The distributive shock caused by anaphylaxis is very different from distributive shock due to sedation effect or neurogenic shock. Even distributive shock due to sepsis can be very different both clinically and on the cellular level when caused by different pathogens ( Fig. 2.6 ).
These etiologies can often run together, where components of multiple types of shock can be exhibited for a single patient at different points in the clinical course.
Ultimately, classifications are only as useful as their ability to help understand the physiology specific to the patient.
Uncovering the true etiology of shock
The example of distributive shock can be telling. Often when distributive shock is diagnosed, we correctly identify a dysregulation of SVR. However, it is often tempting to think of vascular resistance as the homogenous capability of the blood vessels to provide vascular tone.
However, this lack of tone may be complex in its etiology. Vascular tone is maintained by a vascular endothelium and vascular smooth muscle, with a variety of hormones, neurotransmitters, and vasoactive factors maintaining the endothelium and a host of receptors and cofactors affecting the vascular smooth muscle ( Fig. 2.7 ).
