There are several reasons as to why lactate may rise in haemorrhagic shock; it is a combination of poor tissue oxygenation and increased glycolysis due to a surge of catecholamines.
Lactate rises in shock; tissue perfusion falling is the chief reason for this. In a rat model of haemorrhagic shock, after 4 hours of bleeding the pH fell from 7.37 to 7.07, and the lactate increased from 0.8 to 6.06mmol/l. This study is from the 1970s, and in typical broad strokes the authors measured the whole-body oxygen consumption with the aid of 1-gallon mayonnaise jars. The oxygen consumption after four hours of bleeding decreased to 40% of the baseline value, which I suppose means that a significant proportion of their metabolism has become anaerobic (or their whole-body metabolic demand had been scaled down significantly)
Let's talk about haemorrhagic shock, supposedly the purest model of tissue underperfusion, without weird mitochondrial disabilities or drug-induced metabolic shunting. Yes, this causes some tissues to enter a state of anaerobic glycolysis, due to poor tissue perfusion.
But in addition to this, lactic acidosis can arise by means of aerobic glycolysis in well-oxygenated tissues. Particularly, in the presence of adrenaline, there is a suspected increase of N+/K+ ATPase activity, leading to an increased demand for ATP which drive an increase in aerobic glycolysis. This is predominantly seen in skeletal muscle. The increase in lactate in this situation is more related to the sympathetic overdrive state of trauma, rather than to any tissue hypoxia. Indeed, this is observed directly: when you give these normotensive trauma patients oxygen, it does nothing to reverse their lactic acidosis.
Thus, endogenous catecholamine excess in the context of shock (in any shock state, really) can produce a lactic acidosis. Not to point any fingers, but skeletal muscle is probably almost entirely at fault for this, seeing as it comprises about 40% of all tissue weight, and how saturated with beta-2 receptors it is. Furthermore, the relationship between adrenaline-induced skeletal muscle lactate production and its Na+/K+ ATPase activity has been convincingly demonstrated. Well oxygenated skeletal muscle produced tons of lactate when adrenaline was administered, and an infusion of oubaine (an Na+/K+ ATPase inhibitor) completely abolished its lactate production. Similarly, beta-blockade reverses this effect and causes lactate to decrease. This whole beta-agonist and lactate issue is probably much more complex, but that is the basic flavour of it.
Is this such a tragedy? Is lactate really the enemy? From basic physiology, we know that the metabolic fate of lactate is to ultimately restore homeostasis, to be sucked up into the metabolic pathways and reabsorb the conjugate H+ ion. So lactate in haemorrhagic shock is only a transient concern.
But furthermore, it may actually be beneficial. There is some evidence that it improves cardiac efficiency (two-fold!) in the presence of free fatty acids, and that cardiac work improves by at least 20%. Mind you, the study has flaws. The subjects were extracorporated mouse hearts, beating for 60 minutes while being perfused with unusual mixtures. The measure of cardiac function was also somewhat divorced from clinical practice – the researchers used the physics definition of work, in joules per minute per gram of dry weight.
The ARDS lung becomes an amazing source of lactate, and the magnitude of the hyperlactataemia seems to be proportional to the severity of lung injury. Not only is this the result of hypoxic lung tissue trying to carry on metabolism, but also there is some sort of cytokine-related alteration in the carbohydrate metabolism. In either case, the more ARDSy lung there is, the more lactic acidosis there will be. Is this a tragedy? Perhaps not. There is a growing chorus of opinion in favour of acidosis (both respiratory and metabolic) as a lung-protective feature, and therefore perhaps we should be less aggressive about normalizing the pH in these people.
Lactate increases within 1 hour of onset in mesenteric ischaemia. In spite of this, its very hard to detect ischaemic gut in the critically ill patient. In this situation lactate is viewed as a very sensitive but non-specific marker. This specific study I am linking to has reported a sensitivity of 100% but a specificity of only 42%; Oh’s Manual quotes the same numbers. The chapter authors go on to suggest that in a patient with a raised lactate and no obvious cause, one ought to keep a concerned eye on the abdomen.
A gangrenous leg is full of lactate. Indeed, it is well known that lactic acidosis is the major reason for rigor mortis; anaerobic glycolysis continues in post-mortem tissues and lactate continues to increase; eventually all the ATP is used up and the increased intracellular acidity prevents the actin and myosin from releasing each other, causing the characteristic stiffness of dead muscle.
Similarly, it is well known that an ischaemic limb will be a source of lactate, though admittedly this does not usually become a problem until the ischemic tissue is reperfused (and thus the extracellular fluid is “flushed” with fresh blood, which then carries the lactate into the systemic circulation)
How much lactate is in my gangrenous leg?
Excellent question. The agricultural industry has been more interested in these answers than the medical industry, given that the lactate content significantly contributes to the firmness and texture of meat, as well as acting as a natural deterrent for bacterial growth (too acidic for most pathogenic bacteria to reproduce). And yes, the parameters have been measured, though not in human tissue. The lactate levels seem to peak at 24 hours postmortem, rising to a level of about 110mmol per kilogram of tested muscle tissue. The intracellular pH at this stage is around 5.5. That’s pig muscle we are talking about. Though one cannot ever be completely sure of it, one can reasonably expect one mammalian tissue to be reasonably similar to another in the context of post-mortem anaerobic glycolysis.