These are the physiological effects of infusing one litre of Hartmann's compound sodium lactate into a patient.
This 1 litre of Hartmanns Compound Sodium Lactate contains 131 mmol of sodium, 112 mmol of chloride, 2 mmol calcium, 5mmol potassium and 28 mmol of lactate.
The water distributes rapidly (within about 15 minutes) from the intravascular to the interstitial compartment, and becomes trapped there. All the electrolytes in it (except for the lactate, which doesn’t count) end up trapped in the extracellular space, and the water has nowhere to go. The lactate disappears into the cells (specifically, a good healthy liver can metabolise amazing amounts of it).
Hartmanns is not particularly isoosmotic. Its osmolality (sans lactate) is 248, which is lower than that of the body fluids.
So some of the water shifts into the cells.
Observe my childish attempt to organise the behaviour of the water and electrolytes following the infusion of Hartmanns.
So. Lets ignore the lactate for now. 248 mOsm of electrolytes join the total pool of body electrolytes;
(1015 + 3045 + 8120 + 248) = 12428
1 litre of water joins the total pool of body water.
(1 + 42) = 43
At equilibrium (where the osmolality of the compartments is the same) the mOsm/L concentration will be
12428 / 43 = 289 mOsm/L
But; the osmoles are distributed unequally. Practically none of the 248 mOsm will enter the cells. Thus, more water will be distributed to the extracellular compartment in order to maintain an osmolality of 289 Osm/L.
How much more water will distribute there? Extracellular water volume= (1015 + 3045 + 248) / 289 = 14.9L
Thus, of the 1 litre of Hartmanns, 900ml will distribute to the extracellular compartment and 100ml into the intracellular compartment. Following the 25:75 ratio of intravascular to extravascular spaces, this means about 225ml of Hartmanns will remain to expand the circulating volume.
62 mOsm of the electrolytes end up in the intravascular fluid, and 186 in the extravascular. If we consider that the sodium concentration is initially 140, then it will rise by 0.3 mmol/L. As for chloride – though its concentration in Hartmanns is still higher than in human blood, it will not rise as fast as it would in the case of normal saline.. For every litre of Hartmanns, chloride will rise by 1.5 mmol/L. Thus, a hyperchloremic metabolic acidosis could slowly develop, as the strong ion difference decreases and more hydrogen ions invade the body fluid. This is remedied to some extent by the fact that for every 112 mmol of chloride, 28mmol of lactate are also infused, the metabolism of which consumes 28mmol of hydrogen ions.
Since the osmolality of the compartments decreases by only 1 mmol/L, there is no appreciable osmoreceptor response.
The intravascular compartment volume increases by 225ml – from 5000ml to 5225ml. The increase in intravascular volume is 4.5% - outside the volume receptor sensitivity threshold.
This is explained in detail elsewhere. Essentially, its the response to extra body water which occurs even if there is no response from the osmoreceptors and baroreceptors, and is purely due to the fact that intravascular protein dilution results in diminished water resorption from the proximal tubule.
Well; one can expect that the calcium will remain in the extracellular fluid, because it is a forbidden cation inside cells. The 2mmol of calcium will distribute into the extracellular compartments, and the total concentration will not change dramatically. If it was 2.4 mol/L before, it will become 2.38mmol/L after. This is unlikely to exert a physiological effect.
As for the potassium: this is more complex. The extracellular concentration is tightly controlled, as there is only about 50-60 mmol of extracellular potassium. The body's responsiveness to sudden changes to this potassium occurs via the rapid large-scale movement of potassium into the cells, specifically the muscle cells (which contribute the bulk of your extracellular fluid. This happens within a minute, and is mediated by the activity of Na+/K+ ATPase. Furthermore, this uptake activity is inversely proportional to the extracellular concentration: the more extracellular potassium the less intracellular uptake.
Essentially, the less extracellular potassium there is, the more uptake there will be by cells. A hypokalemic patient will have about 10% of the potassium remain extracellular; a hyperkalemic patient will have about 30% remain extracellular, i.e potassium will distribute more equally into all body fluid compartments.
And then the kidneys will control the total body potassium by selectively excreting an appropriate amount.
One may argue that this has greater relevance when it comes to the act of infusing huge amounts of potassium into people. The humble bag of Hartmanns only has 5mmol of potassium to contribute. Even in a hyperkalemic anephric patient, working on the premise that it distributes into all body fluid compartments equally, when divided among the 43 litres of body fluid this gives us a potassium concentration increase of 0.1 mmol/L after 15 minutes. Of course, in any patient with a normal serum potassium and normal kidneys a piddly 0.5mmol will end up in the extracellular fluid - which gives a rise of 0.035mmol/L, well outside the laboratory error ranges.
But is this actually what happens?
Of course, D.N Lobo again is the champion of responsible fluid physiology. His team compared saline to Hartmanns in a randomised blinded trial; I direct you all to pay special attention to page 21 where the graphs demonstrate changes in electrolyte concentration and osmolality over the hours following the 2 litre infusion.
The serum potassium rises transiently in the Hartmanns group, and then falls as diuresis carries it out with sodium and the extra fluid. So in fact Hartmanns has the potential to induce hypokalemia (by increasing sodium delivery to the distal nephron)
It seems to. The use of "balanced" crystalloids in the resuscitation of sepsis has recently been show to improve mortality. In fact, "Mortality was progressively lower among patients receiving larger proportions of balanced fluids".
Well, actually... yes. Briefly.
The bag of Hartmanns has bold writing on it which recommends we never use it for the treatment of lactic acidosis.
Let us be clear.
The administration of Hartmanns will NEVER cause a lactic acidosis. The lactate in Hartmanns is a conjugate base, the anionic part of lactic acid, in which the role of the hydrogen ion is played by sodium. Such a substance, when infused, will not increase the total body acid content, because no extra hydrogen ions are added (to use the classical interpretation of acid-base balance). Yes, under special conditions the lactate anion will "buffer" hydrogen ions and become an acid - but this happens at and below a pH of 3.86 or so. However. The lactate anion is what the ABG machine measures. So, the rapid infusion of Hartmanns will cause a transient increase in the serum lactate levels, without causing a drop in pH. And, it will confuse your serial lactate measurements.
From the perspective of a Stewart quantitative acid-base analysis, the Hartmanns will actually act as an alkalinising solution, because it has an SID of 29 mEq/L: if the lactate (a strong ion) is completely and rapidly metabolised, it will disappear from the equation, leaving behind volatile CO2 and water. Thus, the only situation in which Hartmanns can cause an acidosis is the total absence of liver function. In patients who have no working liver cells, the lactate cannot be metabolised any more than chloride. Hartmanns will thus not exert any positive alkalinising effect. It will just add to the total body pool of under-metabolised lactate. Indeed, in such a situation - in a totally anhepatic patient - the Hartmanns would act as a fluid with an effective strong ion difference of zero. The effects of infusing it on the acid-base balance would be similar to the effects of other SID=0 fluids, such as normal saline. Unfortunately, a quick lazy search does not reveal any literature in support of this; it does not appear as if anybody has ever performed an experimental Hartmanns infusion during the anhepatic phase of a liver transplant.