The Oxygen Challenge On ECMO
THE OXYGEN CHALLENGE OR HYPEROXIA TEST ON ECMO
The oxygen challenge or hyperoxia test for respiratory ECMO patients makes it easy to evaluate the lungs ability to transfer oxygen. The FiO2 on the ventilator is increased to 100% for 5 minutes. At the end of 5 minutes an arterial blood gas is drawn to test the response. The FiO2 is then returned to a lower level.
The ECMO flow diagram below is of a septic patient on ECMO for respiratory failure over a period of about 6 days. The solid black line represents the arterial pCO2. The red line represents the ECMO blood flow. The green line represents the patient’s arterial pO2. The yellow line represents the FiO2 on the patient’s ventilator. Each yellow spike indicates when the ventilator FiO2 is increased to 100%. This is the ventilator FiO2, not the sweep gas FiO2. This maneuver is called an ‘oxygen challenge’.
The patient’s poor response in the early days to 100% FiO2 clearly indicates the poor degree of oxygen exchange capacity by the lungs. The low arterial pO2 values at the beginning of ECMO indicate that the heart is expelling lots of de-saturated blood which, even when mixed with the high pO2 blood from the ECMO pump, remains below 75 mmHg for the first 2 days.
As the days progress the patient’s pO2 value gradually increases when the ventilator FiO2 is increased to 100% during the oxygen challenge. On the first day, the pO2 increases to barely over 100 mmHg, but by the 6th day the pO2 has increased to over 250 mmHg. The dotted black line represents the trend in improvement over the 6 days. Typically, when the patient can achieve an oxygen challenge of 250 mmHg under these circumstances, weaning is appropriate.
The ECMO flow diagram below is of a meconium aspiration patient on ECMO for respiratory failure over a period of about 4 days. The oxygen challenge is over 300 mmHg on every day. However, the arterial pO2 values between the oxygen challenge tests show a gradual decrease in the arterial pO2 over the four days on ECMO. This represents the resolution of ‘cardiac stun’ which was probably the occult reason the patient was placed on ECMO.
Cardiac stun occurs when a heart is depleted of its high energy ATP molecules or when it is damaged by reperfusion injury, or both. This can happen just prior to ECMO, as in this example, or just after ECMO starts when oxygenated ECMO blood reperfuses the hypoxic heart to cause reperfusion damage, as in the example discussed below.
During ECMO, the heart pumps de-saturated blood into the aorta where it mixes with the ECMO blood. If there is very little blood coming from the heart, the blood in the aorta will be mostly blood from the ECMO pump which has a high pO2 (~250+ mmHg). As the cardiac stun resolves, the heart will pump increasing amounts of de-saturated blood into the aorta to mix with the ECMO pump blood. This causes the blood in the aorta to have lower and lower pO2 values. In this patient the cardiac stun resolved after 3 days. The patient was weaned off on the fourth day of ECMO.
The third diagram (below) illustrates a complete cardiac stun cycle. Soon after the initiation of ECMO the patient’s arterial pO2 value gradually increases from 100 mmHg to 250 mmHg at ECMO hour 26. There after the arterial pO2 gradually falls back to 80 mmHg by hour 50, signaling the resolution of the cardiac stun cycle. During this time period the ventilator was maxed out to 100% only at hours 14 and 42, but otherwise set at 30% or less FiO2. The two oxygen challenges have no perceptible effect on the arterial pO2. Between ECMO hours 50 and 96, the arterial pO2 remains low at less than 100 mmHg and does not respond to the oxygen challenges at hours 66 and 88, indicating a persistent pulmonary hypertension. Between hour 97 and 146 the arterial pO2 is reactive to an increase in the FiO2 indicating readiness to wean from ECMO.
Unlike many cardiac patients, respiratory patients with cardiac stun may still display pulsatility because the ECMO blood flow is less than normally needed in cardiac patients. Although the respiratory patient’s heart is still contracting, it lacks vigor and has little reserve while in stun.
The oxygen challenge is not usually useful in patients with a primary cardiac diagnosis with the exception of a biventricular cardiac patient with pulmonary hypertension. The oxygen challenge in univentricular patients probably does not provide any useful information. The last diagram (below) represents a cardiac surgery patient (complete AV canal repair) who failed to wean from CPB. After being placed on ECMO the arterial pO2 remains at about 250 mmHg through most of the ECMO time period, with no reaction to the oxygen challenges as represented by the yellow spikes. This is because the ECMO blood flow is very high and does not allow very much blood to pass through the lungs to react with the oxygen. The high pO2 values are strictly representative of blood emerging from the ECMO pump. Pulsatility is absent during most of the time at high ECMO blood flow. Once the ECMO blood flow is reduced during weaning, the lungs receive more blood flow, pulsatility returns and the arterial pO2 reacts appropriately to the oxygen challenge.