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ARDS causes shunting of deoxygenated blood through the lungs. Most therapies for ARDS naturally combat this shunting (e.g. opening alveoli with PEEP). However, there is often a limit to which pulmonary shunting is treatable.

Jujitsu is a Japanese martial art based on flexibility and technique, rather than a directly confronting an opponent with force. In the spirit of jujitsu, this post explores how to support ARDS patients without directly confronting lung dysfunction. This is useful in refractory ARDS, when frontal assault has failed.

Basics: systemic oxygen delivery

The amount of oxygen delivered to the body (DO2) is calculated with the equation below. Oxygen delivery results from a synergy of cardiac, pulmonary, and hematologic function:

Oxygen extraction ratio (O2ER) is a ratio of the body’s oxygen consumption (VO2) compared to the systemic oxygen delivery (DO2, formula below). A normal O2ER is ~25%. If oxygen delivery decreases, the O2ER increases as tissues extract more of the delivered oxygen. O2ER is a nice way to describe the adequacy of systemic oxygen delivery.

Shunt oxygenation equations

The core physiologic abnormality in ARDS is shunting of blood through the lungs. We must understand how cardiac, pulmonary, and hematologic variables will affect oxygenation in this situation. Takala 2007 derived equations to describe this: (1)

The associated units and normal ranges are as follows.

Shunt oxygenation equations: Understanding the variables

Let’s start by imagining a typical ARDS patient with baseline values as shown here. The next sections examine the effects of adjusting each variable. Some trends will become apparent:

  • Shunt fraction directly affects arterial oxygen saturation.
  • Optimizing cardiac output, hemoglobin, and VO2 indirectly improves arterial oxygen saturation, secondary to increasing the mixed venous oxygen saturation (if the mixed venous oxygen saturation is higher, then blood shunting past the lungs will contain more oxygen).
do22Cardiac output & Hemoglobin

The figures above show the effect of changing either the cardiac output or hemoglobin on oxygenation. These variables have neighboring positions in the oxygenation equations, so they behave similarly. Cardiac output and hemoglobin both have strong effects on the DO2 and O2ER. Increasing cardiac output and hemoglobin concentration also increases arterial oxygenation saturation, but to a lesser extent.

Systemic oxygen utilization (VO2)

Reducing VO2 causes a mild improvement in arterial oxygen saturation and DO2. However, the strongest effect of VO2 is to directly drive the O2ER:

Shunt Fraction

Most therapies for ARDS focus on reducing the shunt fraction (e.g. PEEP, proning, APRV)(2). The shunt fraction is the variable with the greatest effect on arterial oxygen saturation. However, of all variables, shunt fraction has the weakest effect on the O2ER.

Shunt oxygenation equations: Understanding complex interventions

We can now build on this background, to understand more complex therapies.

Inhaled pulmonary vasodilator

An inhaled pulmonary vasodilator may:

  • improve ventilation-perfusion matching, increasing the arterial oxygen saturation.
  • reduce afterload on the right ventricle, increasing the cardiac output.

This is a win-win, explaining the ability of pulmonary vasodilators to stabilize some crashing ARDS patients.

Increased airway pressure (e.g. increased PEEP, APRV)

This may have positive and negative effects:

  • Increased airway pressures may open alveoli, thereby reducing the shunt fraction (3).
  • Increased airway pressure may reduce cardiac output (due to reduced preload and increased pulmonary vascular resistance)

The balance of these effects is complex. However, it must be recognized that even if increased airway pressures improve the shunt fraction, depression of cardiac output can have a dominant effect on the DO2 and O2ER. For example, if PEEP reduces the shunt fraction from 25% to 10% while reducing the cardiac output from 5 L/min to 4 L/min, the net effect is to reduce systemic oxygen delivery:

shunteqWe’ve all encountered this situation, when increased PEEP improves the patient’s arterial saturation but drops the blood pressure. In this case PEEP appears beneficial, but it is probably reducing systemic oxygen delivery.

Low tidal volume ventilation

The classic ARDSnet 2000 trial demonstrated mortality benefit from 6 ml/kg tidal volume ventilation compared to 12 ml/kg tidal volume ventilation. This led to the religious adoption of 6 ml/kg tidal volume ventilation. However, its unclear why lower tidal volumes improved outcome (low volume? low plateau pressure? low driving pressure?)(4).

Natalini 2013 exposed 16 ARDS patients sequentially to both 6 cc/kg and 12 cc/kg tidal volume ventilation. Low tidal volume ventilation significantly improved O2ER, due to improvements in the cardiac output (figure below)(14). Re-examination of the original ARDSnet study confirms that patients treated with low tidal-volume ventilation experienced more days without circulatory failure (19 vs. 17, p = 0.004). Thus, it’s conceivable that low tidal volume ventilation is beneficial largely because it improves perfusion. If true, this might suggest that we should worry less about tidal volumes and worry more about perfusion.

Oxygenation goals: What are we chasing now?

Oxygenation monitoring is similar to hemodynamic monitoring. Arterial saturation, like blood pressure, is the easiest value to obtain. These measurements are universally obtained on all patients, so we are quite comfortable with them.

Arterial oxygen saturation is a measurement of lung function, but it’s not a good measurement of systemic oxygen delivery (DO2, O2ER). DO2 depends on the trifecta of lung, cardiac, and hematologic function, with lung function (~ arterial saturation) being only one third of this. We have already seen examples where arterial saturation didn’t correlate well with systemic oxygen delivery:

  • Cardiac output, hemoglobin, and VO2 have a strong effects on O2ER, but little effect on arterial saturation.
  • Shunt fraction has a strong effect on arterial saturation, but little effect on DO2 or O2ER.
  • It is possible to improve the arterial saturation despite decreasing the DO2 (e.g. excessive airway pressures).

Systemic oxygen delivery (DO2 and O2ER) has similarities with cardiac output and cardiac index. From a physiologic standpoint, these seem like the most important variables. Unfortunately, they are hard to monitor. Thus, we usually don’t check them. When we do measure them, its unclear exactly what value we are targeting.

Do we pay too much attention to arterial oxygen saturation?

We often focus on minor variations in the arterial oxygen saturation. For example, a saturation of 90% may be regarded as “good” whereas 85% is “bad.” It is commonly believed that if the saturation falls under 88%, the patient will spontaneously burst into flames.

Like any diagnostic test, arterial oxygen saturation requires clinical context. For example, an arterial saturation of 85% on six liters nasal cannula may be a baseline value in a patient with idiopathic pulmonary fibrosis. However, this same oxygen requirement in the context of an acute asthma exacerbation would be alarming.

Excessive focus on arterial saturation may drive excessive use of interventions which reduce the shunt fraction. These interventions carry substantial risks (e.g. increased airway pressures may cause barotrauma and shock, elevated FiO2 may cause lung toxicity).

Oxygen extraction ratio (O2ER): Closer to the truth?

DO2 and O2ER are better measurements of systemic oxygenation, but harder to monitor. O2ER may be the most easily measured (5). Many patients have a central venous catheter placed in the superior vena cava. This can be used to estimate the mixed venous saturation, with debatable accuracy (Beest 2011).

ox3 paired vo2 shuntfr

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