Factors Contributing To Mean Arterial Pressure

In this video, I go over how I approach hypotension/hypertension considering the factors that contribute to mean arterial pressure. Often times, many of these variables affect overall forward flow, so it’s important to have a methodical approach to blood pressure management.

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  1. This is a great video! Are you able to provide an example of how you would think through a hypertensive urgency/emergency using the preload, afterload, contractility, rate/rhythm/valve. I find it more intuitive to think about the hypotensive pt in this manner.

    This next question may not directly apply to this video, however I am wondering if you can comment on what parameter (ie, systolic, diastolic or MAP) is most closely related to the development of hypertensive emergency? I’ve read that the MAP is the most closely related to the risk of hypertensive emergency but do not understand the reasoning as to why?

    • Hey Vanessa,

      Thanks for the questions. I combined them because the answers are somewhat related.

      For HTN urgency and emergency, typically defined as a BP ≥180/≥120 mmHg without and with end-organ damage, respectively, I find that a mixed approach using beta-blockers (affecting heart rate and contractility) as well as calcium channel blockers (affecting primarily afterload) tend to be utilized. I see this situation all the time in patients brought to the CVICU with acute aortic syndromes, and routinely utilize titratable medications like esmolol and nicardipine infusions to achieve BP control. The rate of achieving blood pressure control is debatable and not really based on great data; however, I think it’s fair to be cautious about dropping the MAP too quickly in patients at risk for acute kidney injury, stroke, or myocardial infarction. Quick changes in MAP may be tolerated by an organ’s autoregulatory mechanisms, but these might be chronically altered due to disease, medications, etc.

      In general, I find that most of the cardiovascular patients I care for have poorly compliant vascular tone due to longstanding hypertension, smoking, kidney disease, diabetes, and aging. Therefore, they live and die by afterload – vasodilation might bottom them out whereas potent vasoconstrictor (or stressors like pain/anxiety) can skyrocket their pressure. I’m also utilizing point-of-care ultrasound to gauge how the heart rate and biventricular contractility might be playing into the situation.

  2. Rishi, your video on MAP is very timely as I have been teaching my medics to look at MAP when using the LP15 since that is more accurate than the BP numbers the machine gives. Thanks for the conciseness!

  3. Great, simple video. As a nursing instructor, I often go to the CO equation for them to understand the basics of what you just described; so, I’m pleased I’m on track. I’ve never been clear if pulmonary vascular resistance ties into after load. Seems like it shouldn’t since systole ejects to the systemic system, but that’s the only question that came up for me.

    • No, but it would certainly tie into preload (ie, if the PVR is very high, the right ventricle will have difficulty moving blood into the left side, thereby limiting LV filling).

  4. In regards to monitoring BP/MAP, some coworkers have said if you have an automated cuff and arterial line, the automated cuff is more accurate for MAP and the arterial line is more accurate for SBP/DBP. Thoughts?

    • In general, the automatic cuff is ONLY measuring a MAP directly (via oscillations) whereas an arterial line directly measures a systolic and diastolic blood pressure (and therefore a MAP). By virtue of what they are actually measuring, then yeah, I’m inclined to agree.


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