“Blood pressure” refers to the forces exerted by blood against the vessel walls in the arterial circulation. Correct measurement and interpretation of the blood pressure is essential to all patient management and underlies much of our therapeutic interventions. Despite this, however, our analysis is often reduced to little more than “normal vs abnormal.”
Each component of the blood pressure should be viewed as a specific hemodynamic surrogate, and can help us to craft a detailed picture of the underlying circulatory physiology.
Systolic Blood Pressure (SBP)
SBP is the maximum pressure achieved during contraction of the left ventricle. Pragmatically, SBP can be thought of as the “impulse pressure.” It is the pressure which tears aortas, bursts cerebral blood vessels, and dislodges hemostatic clots. Tight control of the SBP is first order in the resuscitation of most neurologic and vascular emergencies.
Diastolic Blood Pressure (DBP)
DBP is the pressure in the arterial circulation when the ventricles are relaxed and filling and is the pressure responsible for perfusing the coronary arteries. DBP is a surrogate for arterial tone (systemic vascular resistance). It can be particularly useful in helping to differentiate shock states, as it is typically preserved (>50 mmHg) in cardiogenic and hypovolemic shock, and low in vasoplegic (distributive) shock.
Mean Arterial Blood Pressure (MAP)
MAP is the average pressure during the cardiac cycle and can be easily calculated as ⅓ (SBP – DBP) + DBP. The MAP is the most important pressure measurement, particularly in shock states, as it is our closest, and best estimate of organ perfusion pressure. The pressure gradient MAP – CVP more accurately defines organ perfusion pressure, but more on this in the future.
Pulse Pressure (PP)
PP = SBP – DBP and is proportional to the stroke volume (the amount of blood ejected from the left ventricle during systole). PP tends to be low or narrow (<40) in low output states (cardiac failure and hypovolemia) and wide (>40) in high output states (sepsis, anaphylaxis, cirrhosis). Insufficiency of the aortic valve can also cause a wide pulse pressure.
In the words of Mr. Rogers, let’s make believe…
Imagine you have a patient with a BP of 80/55.
- SBP is low. We certainly aren’t going to worry about bursting cerebral blood vessels.
- DBP is preserved (>50). This suggests against vasoplegic pathology. It’s likely, the extremities will feel cool due to preserved arterial tone (high SVR) in the setting of absolute or relative hypotension.
- MAP is 63. Not terrible, provided there isn’t evidence of associated organ hypoperfusion (AMS, increased work of breathing, delayed capillary refill time, decreased UOP, etc). Though probably not ideal either.
- PP is narrow at 25. This also suggests a low output state.
Scrutiny of the blood pressure suggests a low output state with preserved SVR. The next step is to put probe to chest (the ultrasound) and differentiate hypovolemia from cardiac failure.
These hemodynamic surrogates aren’t absolutes, but “60% of the time, this works every time.”
References
- Brown, Gabrielle, and Tricia Desvarieux. “Blood Pressures and Resistances.” Anesthesiology Core Review, by Brian S. Freeman and Jeffrey S. Berger, McGraw-Hill Education Medical, 2014
- de Simone G, Pasanisi F. Pressione arteriosa sistolica, diastolica e differenziale: aspetti fisiopatologici [Systolic, diastolic and pulse pressure: pathophysiology]. Ital Heart J Suppl. 2001;2(4):359-362.
