Why does blood pressure have little correlation with cardiac output in the elderly? (Source ATLS student course manual)

2 Answers 2


Cardiac Output (CO) = Heart Rate (HR) X Stroke Volume (SV)

  • Decreases in CO > Decrease BP.
  • Increases in CO > Increase BP.

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With aging CO remains stabilized at rest due to the following:

Heart Rate (HR)

  • (About the Same)

Stroke Volume (SV)

  • Increased Left Ventricular (LV) End Diastolic Volume (EDV) and LV hypertrophy results in increased SV.
  • This SV increase is negated by Peripheral Resistance Increases. Due an increase in LV diameter and increase in Systolic Pressure.
  • Therefore, these combined effects balance each other out resulting no net change in CO, or Systolic BP


  • This is a good answer but too heavy on abbreviations and shorthand. For example, it's not clear how to interpret this: Decreases in CO > Decrease BP. If you could clarify some of your shorthand that would be great.
    – Carey Gregory
    Commented Jul 15, 2017 at 4:12
  • A decrease in cardiac output causes a decrease in blood pressure.
    – Rotterdam
    Commented Jul 18, 2017 at 12:00
  • It is overly simplistic to directly correlate blood pressure and cardiac output as you have completely ignored the compliance of the vasculature. If vascular compliance had no effect on blood pressure then vasopressin and phenylephrine would be completely useless as vasopressors since they directly impact neither heart rate nor stroke volume (although both could indirectly decrease stroke volume by increasing afterload).
    – RudyB
    Commented Jan 28, 2018 at 7:58
  • I am old and frequently measure my BP, I have found almost no correlation between BP and rate / pulse. My cardiologist says he is not surprised. Commented Jan 28, 2018 at 21:11

1) The elderly are the most likely group to be on agents to regulate blood pressure as the incidence of hypertension increases with age.

2) The elderly are the most likely group to have altered large vessel vascular compliance due to atherosclerosis.

Since your question relates to ATLS directly and shock indirectly, let's start from the beginning.

For the first stage of shock, the textbook answer is that the blood pressure is not lowered and the heart rate is not elevated. Urine output is normal. The body compensates by altered vascular tone. With disease or medication, this may be changed. The patient may be on vasodilatory agents for blood pressure that prevent physiologic vasoconstriction.

For the second stage of shock, the textbook answer is that the blood pressure is maintained but the heart rate is elevated, urine output starts to decrease. What if your patient is on a rate-limiting calcium-channel blocker or beta-blocker and cannot mount a tachycardic response? What if they are on diuretics and a decrease in renal blood flow still results in a normal appearing urine output?

For the third stage of shock, the textbook answer is that heart rate is elevated but now blood pressure is low with the urine output compromised. Physiologically (regarding tissue perfusion), a patient on antihypertensives may go from normal right to here. They cannot vasoconstrict or mount a tachycardic response due to multiple antihypertensive agents. One good insult and they are hypoperfused.

For the fourth stage of shock, the textbook answer is that heart rate is significantly elevated, blood pressure is low, and urine output is almost zero. Aside from the elevated heart rate, this could be your end-stage renal disease patient after hemodialysis on a good day.

Numbers are neat when trending over time in one patient, but you are seeing a 90 pound 95 year-old in the trauma bay with a heart rate of 120 and a blood pressure of 84/40 after a motor vehicle collision. You never met her before. She is confused. Is she in shock or is she demented? Is she hypovolemic or is she just anxious and her blood pressure is normal for her? Big picture is you need more data and you need to trend the data you have over time, even if that is a brief amount of time.

The more important thing to remember is that, in general, pediatric trauma patients have much better physiologic reserves than geriatric trauma patients. Older patients crash sooner but you may have more time to intervene. Younger patients seem fine until they aren't, and then at that point they are near death.

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