Change in stroke volume can be used to determine where a patient lies on the Frank–Starling curve. The curve of a patient with low preload, and hence larger changes with volume, is seen in panel A; changes in preload in a patient who is optimized are seen in panel B. Stroke volume variation (SVV); O indicates the optimal operating point. (Image source Figure 1 from article.)
Change in stroke volume can be used to determine where a patient lies on the Frank–Starling curve. The curve of a patient with low preload, and hence larger changes with volume, is seen in panel A; changes in preload in a patient who is optimized are seen in panel B. Stroke volume variation (SVV); O indicates the optimal operating point. (Image source Figure 1 from article.)

 

Intrathoracic pressure changes during ventilation. Widely appreciated, but less well understood, is how changes in intrathoracic pressure change preload and cardiac output. If you ask a resident what will happen when the ventilator gives a positive pressure breath, you will likely be told that the blood pressure will drop because increased intrathoracic pressure decreases venous return to the heart.  It’s not wrong, just incomplete.

The initial response to a positive pressure breath is that blood is squeezed from the lungs into the left atrium. Think of wringing out a sponge: you squeeze the sponge, and water flows out. That’s what the ventilator does to the lungs. The blood flows into the left atrium, and for a beat or two the preload is increased. Stroke volume and blood pressure acutely rise. It’s true that venous return to the right side of the heart is concurrently decreased, so if you maintain positive intrathoracic pressure† for more than a few seconds blood pressure eventually drops. However, the initial response is an increase in blood pressure and cardiac output from the increased return from the lungs to the left atrium.

What happens when you release pressure? The lungs refill with blood. Refilling the lungs “steals” blood from the left atrium, decreasing preload, cardiac output, and blood pressure for a beat or two. Once the lungs are refilled then the full output of the right side of the heart reaches the left side of the heart. However, with the next positive breath, there will be another transient increase in blood flow to the left atrium, and the cycle will repeat.

Why is this useful to measure volume status? Look back at the Starling curve. There is a steep portion, where small changes in cardiac filling give you big changes in cardiac output, and there is a flat portion where changes in filling have little effect on cardiac output. If the change in preload during the ventilatory cycle produces a big change in blood pressure, then you are directly seeing the heart respond to an increase in volume by increasing blood pressure. On the other hand, if the heart is on the flat part of the Starling curve, and there is no change in blood pressure with the change in preload during ventilation, then you are directly seeing that increasing preload does not affect blood pressure. Through changes in intrathoracic pressure you can interrogate the Starling curve in real time!

This is most easily demonstrated with an arterial waveform, but the photoplethysmogram captured by the pulse oximeter can be used as well. Dr. Paul S. Addison, Respiratory and Monitoring Solutions, Covidien, The Technopole Centre, Edinburgh, Scotland, United Kingdom, reviewed some of the issues involved with using a pulse oximeter to detect changes in left atrial volume. His findings are published in this month’s issue of Anesthesia & Analgesia in the article titled titled “A Review of Signal Processing Used in the Implementation of the Pulse Oximetry Photoplethysmographic Fluid Responsiveness Parameter.”

The pulse oximeter has been used as early as the 1930s as an indicator of intravascular volume status. Changes in the pulse oximetry plethysmographic waveform are expressed as a percentage.   Most authors calculate plethysmographic changes by averaging the signal over 3 respiratory cycles. This signal is best seen when a patient is mechanically ventilated. The article contains summaries of several studies that have examined the validity of pulse oximetry when used to obtain this measure. Manual inspection of the physical traces may not adequately detect subtle differences. Plethysmographic changes can be caused not only by changes in left atrial volume but also depend on the distensibility of vessel walls that result from microvascular tone changes induced by anesthetic events such as temperature, sympathetic nervous system activity, or ischemia/reperfusion-induced changes, or in patients receiving certain drugs such as norepinephrine. Extracorporeal circulation can also later lead to artifacts. Less distortion of the measurement might be seen if the probe is positioned on an earlobe or the forehead compared with the finger. The pulse oximetry signal is already preprocessed and if a raw waveform is used instead, the measurements may be more consistent. If one were to devise their own study, then device-specific, inbuilt signal filtering would have to be understood.

Though some devices might actually calculate plethysmographic changes (one manufacturer has a propriety pulse variability index), the changes in the plethysmogram can be calculated manually by selecting a few optimal respiratory cycles for interrogation. In these instances, the calculation is generally good. As the author notes, “It is precisely this ‘hand-picking’ of the quality data for analysis that is so difficult to automate fully.”

These changes can be seen more easily if the waveform speed is set to the slowest speed, usually 6.25 mm/s. Some of us always do that for big cases where fluid management becomes important. Initially residents say “huh?”  but afterwards they wonder why we don’t always do that.

As Dr. Kirk Shelley, Yale School of Medicine, New Haven, Connecticut, and Dr. Maxime Cannesson, Department of Anesthesiology & Perioperative Care, University of California Irvine, Orange, California, note in their accompanying editorial titled, ““Off-Label” Use of Clinical Monitors: What Happens When New Physiologic Understanding Meets State-of-the-Art Technology” “We are just starting to tap the information in the photoplethysmogram. The next few decades will see further innovations related to this waveform
These advances will be the product of close collaboration among academic anesthesiologists, engineers, physiologists, and industry leaders. The beneficiaries will be our patients.”

Remember also that a large variation in plethysmogram amplitude does not necessarily mean that more fluid should be administered. First, if the patient is not hypotensive, and hemodynamically stable, then fluid is likely not indicated. Additionally, there are other causes of variation in amplitude of the plethysmogram, including airway obstruction. See the AA2day post from Dec 5 for more details.