using SvO2 and lactate clearance
Delivery of an adequate amount of oxygen is necessary to meet the body’s metabolic needs. When this doesn’t occur, organ systems start to fail. This is commonly known as shock. As we’ve discussed elsewhere, there are different mechanisms and disease state that produce shock. The final common pathway in all of these is the lack of available oxygen to meet the metabolic needs of the organ systems.
The oxygen carrying capacity of the blood is calculated by this equation:
CaO2 = 1.34 (Hgb) (SaO2) + 0.003(PaO2)
where hemoglobin is expressed in grams/dL. 1.34 is the amount of oxygen, in mL, that can bind to one gram of hemoglobin. The contribution of the PaO2 is so low (even if it’s 300, it adds less than 1 mL of oxygen per dL of blood) that we ignore it unless the patient is profoundly anemic or in a hyperbaric chamber. It just makes the math easier. For a hemoglobin of 15 g/dL and an SaO2 of 100%, the CaO2 is 20.1 mL O2/dL of blood.
Oxygen delivery (DO2) is calculated by this equation:
DO2 = Cardiac Output × CaO2 × 10
The product of the cardiac output and CaO2 is multiplied by 10 because CaO2 is expressed in dL while CO is expressed as L/min. For a “normal” cardiac output of 5 L/min and a hemoglobin of 15 g/dL, the DO2 is about 1000 mL O2/min.
Oxygen consumption (VO2) is the amount of oxygen that the tissues extract per minute. This is normally about 200-250 mL O2/min. During intense exercise, this can go up significantly; in disease states like multisystem trauma or septic shock, it only goes up by about 40-50%. The VO2 can be calculated using the same formula as for DO2, but substituting the SvO2 for the SaO2:
VO2 = Cardiac Output × 1.34 × Hgb × SvO2 × 10
As you can see, normal oxygen delivery is significantly higher than consumption. This makes a lot of sense, physiologically—if your body only delivered exactly what it needed, you would be one fever or pneumothorax or breath-holding spell away from disaster. The reserve of oxygen is why you don’t die immediately if you get something caught in your throat, or hold your breath to swim underwater. Your body also can increase the cardiac output to maintain this reserve. This can be expressed as the DO2/VO2 ratio, and it’s normally 4:1 to 5:1 (if DO2 is 1000 mL O2/min and VO2 is 200-250 mL O2/min). Since many of the factors of both DO2 and VO2 are the same (CO, Hgb, 1.34), the math can be simplified to:
DO2/VO2 = SaO2/SvO2
As oxygen delivery declines, the tissues will extract more and more oxygen to meet their needs (remember, VO2 is constant at this point). This will lower the SvO2. SvO2 is low in low-flow states. These states can include anemia, cardiogenic shock, and hypovolemia. Once the SvO2 reaches 50% (a DO2/VO2 ratio of 2:1), oxygen consumption becomes supply-dependent. That is to say, VO2 will drop as the DO2 drops. This is when anaerobic metabolism begins, and if it’s uncorrected it will rapidly lead to death. This point can be seen on the graph below. The ways to improve DO2 are to increase cardiac output (fluids, inotropes, vasopressors), raise the hemoglobin (transfusion of PRBC), and to maintain adequate arterial oxygenation (increased FiO2, PEEP). VO2 can be lowered by controlling fever, sedation and neuromuscular blockade, and by treating the cause of shock.
The SvO2 is a very useful tool in shock states that are low-flow—hypovolemia, hemorrhagic shock, cardiogenic shock. It’s less useful in high-flow shock states like sepsis. This is because septic shock isn’t characterized by a low cardiac output. Often, the cardiac output (and consequently, oxygen delivery) are high. During the initial resuscitation, the SvO2 may be low because of relative hypovolemia and sepsis-related cardiac dysfunction. After the initial resuscitation, however, the SvO2 may be higher than normal (80-85%). Why?
Two major reasons have been identified. One is the pathologic vasodilation of “shunt channels.” As the patient becomes vasoplegic, dilation of vascular connections between arterioles and venules occurs. Blood flows through these channels, bypassing the capillary beds and thus not unloading oxygen to the tissues. Think of it like a mini-AVM, or short circuit. Blood that’s 100% saturated with O2 will return to the venous system 100% saturated, raising the SvO2.
The other reason is a condition known as “tissue dysoxia.” For some reason that is not well-understood, tissues are not able to extract and use the delivered oxygen. The cardiovascular system gets it there, but the mitochondria can’t take it and use it. This is probably cytokine-mediated and is the subject of extensive research. Autopsies on patients who die of septic shock do not show cellular necrosis or other signs of hypoxemia, unlike the findings in patients who die of hemorrhage or cardiogenic shock.
Since people with septic shock aren’t dying of hypoxia or inadequate oxygen delivery, it doesn’t make a lot of sense to use a test that reflects the balance of oxygen delivery and consumption (i.e. the SvO2 ) as a guide to resuscitation. Better to use a marker of cellular dysmetabolism, like lactate. Lactate clearance has proven to be at least as effective as SvO2 monitoring in patients with septic shock, and a significant percentage of patients who die of sepsis will have normal SvO2 but poor lactate clearance. It’s also easily obtained—you can send a venous sample, but it’s easier and quicker to get a lactate on the ABG.
You can use lactate clearance like this: get an initial ABG with lactate. Resuscitate the patient with fluids, vasopressors, intubation and ventilation, antibiotics, and source control. Six hours later, check another ABG with lactate. If the lactate has fallen by at least 10%, then the resuscitation is going well. If it hasn’t, that means at least one of three things is occurring:
Your resuscitation is inadequate. Make sure that you’ve given enough fluids and that you’re augmenting perfusion as needed with inotropes and vasopressors. Give blood if you need to.
You are missing something. Look for occult sources of infection (dead bowel, abscess). Make sure your antibiotic coverage is adequate.
Your patient has bad genetics and is not responding to your therapy. Nothing you can do about this except revisit numbers 1 and 2.