The Vitals: Oxygen Delivery Equation

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Shyam Murali
Shyam Murali
Fellow in Trauma and Surgical Critical Care - University of Pennsylvania, Senior Editor -, Writer -, Saxophonist, EDM remixer, husband, puppy father, and new human father

Wait...there's an equation for oxygen delivery!?

In this post of the Vitals we’ll review the “Delivery of Oxygen Equation” and how to use it at the bedside of a crashing patient.

So, what's the Equation?

Let’s break the equation down and go through the important parts:

  • The cardiac output is determined by stroke volume and heart rate. Normal stroke volume is approximately 60-120mL/beat and normal heart rate is 60-100 bpm. Therefore, a normal cardiac output is approximately 3.6-8L/min.
  • Stroke volume is determined by preload, contractility, and afterload; we will come back to this shortly.
  • Hemoglobin level correlates with how much oxygen can be carried in the blood.
  • SaO2 is the oxygen saturation; look at the monitor and ensure that you have a good waveform.
  • Finally, PaO2 is the partial pressure of O2, found on an arterial blood gas (ABG). Note that the coefficient (AKA plasma diffusion coefficient of oxygen) next to PaO2 is really small (0.003). Changes in PaO2 do not create a significant change in the delivery of oxygen to tissues. However, in certain patients in the ICU who have low hemoglobin and are on 100% FiO2, a significant amount of delivered oxygen may be in the dissolved form.

You’re asking yourself, “why the hell should I care about this equation…?”

Insufficient oxygen delivery leads to anaerobic metabolism and excessive lactic acid production, a hallmark of circulatory shock. Our job is to ensure that the patient maintains sufficient blood flow and perfusion that supports aerobic metabolism necessary for normal organ function. We assess for adequate perfusion by looking at the following (this is not a comprehensive list and there are many non-perfusion factors that can alter these findings):

  • Mental status
  • Peripheral extremity temperature or temperature gradients
  • Capillary refill time
  • Urine output
  • Rising liver enzymes
  • Lactic acidosis or base deficit
  • Mixed and central venous oxygen saturation
  • Heart rate
  • Blood pressure – hypotension is a very late finding

When we notice abnormalities in any of the above clinical findings, we can start to fix the problem by using the equation to improve oxygen delivery:

  1. Stroke volume is dependent on preload, contractility, and afterload. We will dive deeper into stroke volume optimization in future Vitals posts.
    Preload: Fortunately, we have a handy-dandy ultrasound in most of our ICUs to help us determine whether the patient has adequate preload. A quick IVC ultrasound (which is very simple to perform) can show you if the patient is volume-replete or could potentially be volume-responsive. Go one step further and perform a passive leg raise to see if there are improvements in the IVC diameter and collapsibility/distensibility.
    Contractility: Our best friend, the ultrasound, can also help us determine if there is adequate contractility of the heart. Using a parasternal long axis view and an apical four-chamber view, you can calculate the left ventricle outflow tract (LVOT) diameter and the velocity-time integral to estimate the stroke volume. But you can also save some time by just eyeballing it: good squeeze, okay squeeze, or poor squeeze? Use inotropes (epinephrine, dobutamine, milrinone) to improve contractility if your patient has a poorly squeezing heart.
    Afterload: Finally, determine whether the patient has any signs of high afterload (systemic hypertension, aortic stenosis, aortic regurgitation, etc.) and treat the underlying cause.
  2. Too slow or too fast of a heart rate will cause issues with cardiac output, and therefore decrease your organ perfusion. Optimize your heart rate with positive chronotropes (epinephrine, dobutamine, atropine, isoproterenol) or negative chronotropes (metoprolol, diltiazem, digoxin). A heart rate outside of 60-180bpm can have significant effects on cardiac output.
  3. Transfuse to a hemoglobin of 7g/dL. Numerous studies have shown the benefits of restrictive transfusion (target 7g/dL) over liberal transfusion (target 9g/dL or 10g/dL).
  4. Increase your patient’s arterial oxygen saturation (SaO2) to a goal of 92-95%. If your patient is spontaneously breathing, you can do this with supplemental oxygen via NC, NRB, HFNC, or BPAP/CPAP. If they are mechanically ventilated, turn up the FiO2 to achieve the goal saturation.
  5. Attempting to fix the PaO2 has minimal effects on the delivery of oxygen, so don’t worry about that one.

Once you have optimized the components of the Delivery of Oxygen Equation, reassess your patient again and see if they are doing better. If not, then the source of the problem is likely not a problem with tissue oxygenation.

How do you use the delivery of oxygen equation for your sickest patients? Let us know in the comments below. Feel free to also comment on other topics you would be interested in learning about as part of this series.


1. Marino PL. The ICU Book. 4th ed. Wolter Kluwer Health/Lippincott Williams & Wilkins; 2014.
2. Cornwell EE 3rd, Kennedy F, Rodriguez J. The critical care of the severely injured patient–I. Assessing and improving oxygen delivery. Surg Clin North Am. 1996;76(4):959‐969. PMID: 8782482.
3. Hasanin A, Mukhtar A, Nassar H. Perfusion indices revisited. J Intensive Care. 2017;5:24. Published 2017 Mar 14. PMID: 28331621


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