Physiopathology 5th lecture:

Hyperchloremic metabolic acidosis:

The anion gap is the difference in the measured cations (positively charged ions) and
the measured anions (negatively charged ions) in serum, plasma, or urine.
The cation usually is measured is Na+, the anions that are measured are HCO3- and ClPlasma anion gap= [Na+]- {[HCO3-]+[Cl-]}
The range of normal values for plasma anion gap is 10-12 mEq/L

Plasma contains unmeasured ion that make up this difference or gap. The
unmeasured anions of lasma include plasma proteins, phosphate, citrate and sulfate.

The plasma inion gap is useful primarily in the differentioal diagnosis of metabolic
acidosis. Metabolic acidosis by definition, associated with a decreas in plasma HCO3concentration. Assuming that the Na+concentration is unchanged. To preserve
electroneutrality of the plasma compartmnt, the concentration of an anion must
increase to replace the lost HCO3-.
That anion gap can be one of the unmeasured anions, or it cn be Cl-. If HCO3- is
replaced by unmeasured anions, the calculated anion gap is increased. If HCO3- is
replaced by Cl-, the calculated anion gap is normal.

Any anion gap could increase if there are unmeasurable anions in the plasma/serum.
As its happening in some intoxications , in accumulation of toxic substances like
sulphate , phosphate and so on.
hyperchloremic metabolic acidosis: occurs when HCO3- is replaced by another
measured anion Cl-, this type of metabolic acidosis is called hypercholermic
metabolic acidosis.

Sub causes for hypercloremic metabolic acidosis:

-

could be exogenous by administering some substances containing Cl- or some

substances which can generate cloric acid, For instance administration or
ingestion of ammoniumchlorid, L-arginine or L-Lysine & Inhalation of
chlorodic gas.

Loss of bicarbonate at the gastrointestinal level. The most common situation is

done by diarrhea , Of course there are also causes for gastrointestinal loses of
bicarbonate.
For example Ileum with intestinal occlusion or fistula , like pancreatic and biliary
fistula and so on.
-

Another way of bicarbonate loss could be the renal way, renal loss of
bicarbonate is due to the proximal renal tubular acidosis .

We will take only one example from this hypercloremic metabolic acidosis and we
will discuss about intestinal loss of bicarbonate done by the DIARRHEA.
Bicarbonate loss by diarrhea: we have to recapitulate the physiology of the ions
transport through the intestinal membrane.
Whats happening through the jejunum level and whats happening in the Ilium
level?
First of all to understand the importance of this transportation we have to remember
that there is a large amout of liquid which is absorbed at theses levels. For instance we
ingest by drinking or by eating a quantity of liquid, almost 1,5-2 liters per day, but
also our gastric secretions produce a large amount of water. So this large amout of
water will be reabsorbed on this way to jejunum and ileum and later in the large colon
a small amount of water will be absorbed.
- In jejunum we reabsorbed 9 liters per 24 hours.
- In ileum we reabsorbe 3 liters per 24 hours.
- And in colon 100 ml per 24 hours . So whats happening with the ions here?
In the lumen of the jejunum we have a predominant of electronegativity, in the lumen
of the ileum we have usually electrical neutrality. And another thing , in the jejunum
we have a sodium-hydrogen transporter similiar to that in the nephrocytes.
so here we will have excretion of hydrogen ions, according to the reabsorption of
sodium. And sodium will attract bicarbonate and reabsorption of bicarbonatesodium will be also associated with absorption of hexosis , aminoacids and ofc
water.
Large amount of water will be absorbed. The absorption of sodium is done in
parallel with the function of ATP-ase , sodium-potassium and the activity of ATPase will be favorized by the electronegativity in this region of the jejunum.
Sodium is able to get out because of the activity of ATP-ase and will be
reabsorbed because of this pump excreting hydrogen ions. And reabsorption of
sodium , attracts reabsorption of bicarbonate , water and other elements.

In the Ileum we have a reabsorption of sodium and chloride against the

concentration gradient.
In the jejunum , the concentration gradient favorizes the reabsorption of sodium,
because sodium is permanently getting out of the cell because of ATP-ase and
low concentration here attract more and more sodium. But in ileum we have an
active reabsorption of sodium and chloride against the concentration gradient. In
the same time the active reabsorption of chloride is associated with an active
secretion of bicarbonate. The amount of bicarbonate in ileum will be not the
same in colon.
WHY? BECAUSE bicarbonate will be decreased in colon because it will be
consumed , being combined with organic acids produced by the bacterial flora in the
colon, like the pionic acid, mutinic acid? Acetic acid, Lactic acid and so onthese
organic acids will consume the bicarbonate in the colon area.
So this form here in ileum will favorize the bicarbonate secretion. And also the colon
has the ability to secrete potasium, depending on the aldosterone.
whats happening in severe diarrhea? Cholera is an example for an infection
causing dirrhea (The infection with cholera bacilii).
In this situation there is an important disturbance at the electrolyte transport. So this
imbalance will affect the reabsorption of sodium and chloride, which will be
decreased , favorizing the secretion of chloride and sodium.
And responsible for this imbalance is the choleric toxin. Why? because it was noticed
that the coleric toxin has some effects, one of them is to increase the cyclic AMP and
increasing cAMP we have 2 consequenceses:
1. Increased conductility of the luminar membrane for chloride, so will favorize
the secretion of chloride from the cell in the luminal space, and another effect
from cAMP Will be :
2. inhibition of the reabsorption of the sodium and chloride.
So concequences of these 2 effects done by cAMP will be massive loss of
sodium , chloride and water.
Coleric toxin will increase directly the secretion of bicarbonate by the intestinal cells.
So we lose bicarbonate, chloride and sodium and we lose water. In this balance of
loses , the bicarbonate loss is more important than the chloride loss.
So thats why we have hypochloremia, taking into account that we have a high amount
of water loss ( dehydration) . The metabolic acidosis could be explained by the
bicarbonate loss, but the bicarbonate loss is not so important to explain metabolic
acidosis. So might be possible that metabolic acidosis here to be combined. We have
to take into account the hypovolemia, the loss of water in cholera is very important.
The patients are very dehydrated. So we remember what we have discussed in
hypovolemia, and hypovolemic shock.
Hypovolemia driving finally to hypovolemic shock. We have hypovolemia , the
peripheral chemo and baro receptors are signaling the brain, so we will have
discharge of ACTH , noradrenaline and adrenalin,

and finally we will have important vasoconstriction, we can have also peripheral
ischemia, so in conditions of perihperal ischemia we will have an important
production of lactic acids.
So metabolic acidosis is done by loss of bicarbonate, but also by bicarbonate
consumption because of lactic acidosis. And another thing, we have hypovolemia,
we have peripheral ischemia, we also have renal ischemiaso we can have renal
failure, and from here we can say that we have another componet for metabolic
acidosis which is renal acidosis.
So in this situation in important diarrhea, ofc the model is the cholera, choleric toxin,
we will have loss of bicarbonate, lactic acidosis because of hypovolemia with
consumption of bicarbonate and also renal acidosis produced by renal failure in
conditions of vasoconstriction. So 3 types of metabolic acidosis.
About the movement of potasium and hypogenine constipation?
we know that usually metabolic acidosis associated hypercalemia and metabolic
alkalosis associates hypokalemia with some exception especially in renal acidosis
when we can have metabolic acidosis with hypokalemia. Now lets discuss about
metabolic alkalosis.
Metabolic acidosis is caused by a decreased HCO3- in the blood , while
Metabolic alkalosis is caused by an increased HCO3- in the blood .
Metabolic alkalosis primary modification is increased bicarbonate. Increased
bicarbonate rises the PH. The primary increase of the bicarbonate and secondary
increase the PH associating a compensatory increase of carbon dioxide pressure
which is very limited, we know that this type of compensation in metabolic alkalosis
is very limited. WHY?
Beacause increase carbon dioxide above 55-60 mmHg will not inhibit anymore the
respiratory center , will produce hyperventilation which will stimulate the respiratory
center. And of course we have the other type of regulation at the renal level.
Where is the compensation? We have no compensation in metabolic alkalosis. By
respiratory or by renal activity we have no efficiant compensation. But we havet o
discuss about metabolic alkalosis because metabolic alkalosis is among most common
acid base disturbance in hospitalized patients.
How is it possible? The most common acid base balance is metabolic alkalosis,
and why is this possible? Maybe because its limited regulatory capacity. And we can
try a small classification for metabolic alkalosis.
First group:
metabolic alkalosis associated with volemic contraction( hypovolemia): As its
happening here we discussed about vomiting, losing acidity and also fluids, a large
amount of fluids, so we will have metabolic alkalosis with increased bicarbonate
because bicarbonate is not more consumed in buffering as usual, but we have also

water loss, so we have hypovolemia. Or in diuretic therapy , loss of sodium, loss of

bicarbonate and loss of water ofc.
2nd group of metabolic alkalosis:
metabolic alkalosis with normal volemia or sometimes with hypervolemia. And this
could be possible because of primary or secondary hyperaldosteronism. Another
3rd group:
metabolic alkalosis done by ingestion/treatment by alkaline substances : like its
happening in abusive treatment of duodenal ulcer and gastric ulcer. It is so called
milk Alkali syndrome(Milk-alkali syndrome is a condition characterized by high
levels of calcium in the blood and a disruption in the body's acid/base balance)
Usually to buffer the gastric acidity we can administer some alkaline substances like
bicarbonate-sodium or medicines containing bicarbon formes of bicarbonate but
excessing in this treatment will produce metabolic alkalosis. And because of the
limited compensation , the metabolic alkalosis , already produced, has the mechanism
to be maintained, thats why it is a very common possibility.
For instance , which are the compensatory mechanisms in metabolic alkalosis ?
- Only 2% involvement for the erythrocyte system
- youll remember chloride shift, bicarbonate movement , only 2%.
- 4%of regulation in metabolic alkalosis will be done by the tissue
production of lactate
- organic acids, only 4%.
- Buffering by same proteins only 1%, so the buffering is very low in the
compensation for the metabolic alkalosis , and a much more effective
mechanism is the cellular shift /cellular change, hydrogen ions vs
potasium.
In metabolic alkalosis, we have low hydrogen ion concentration
extracellular, so the potasium will have the tendancy to get into the cell in
exchange with exiting hydrogen ions, so usually the metabolic alkalosis is
associated with hypokalemia,
and this mechanism has an involvement in the compensation around 26%,
and this is the most effective mechanism but this is not enough. In acute
metabolic alkalosis, these are the possibilities.
In chronic metabolic alkalosis, for long term, we have the possibility of bone
compensation, But in long time there is an accumulation of calcium carbonate in
the skeleton, so this is another compensatory mechanism which could absorb the
excess of bicarbonate, but this is on long term.
The kidney not efficient in metabolic alkalosis!!!
The respiratory compensation is very limited, and here we have to discuss a
dangerous situation when the patients have hypercapnea(occurs when there is
too much carbon dioxide in the blood) , done by pulmonary diseases.
We can say that they have pulmonary diseases (chronic pulmonary diseases) , so
they have hypercapnea and this is good for metabolic alkalosis, because of the

increase in carbon dioxide pressure which tends to normalize the ratio of the
HCO3- /CO2 and so in turn to normalize the PH.

But this isnt a good idea because usually patients with COPD , dont have only
hypercapnea, they have also hypoxemia & tissue hypoxia, and this hypoxia can
be very dangerous for these patients!
Renal activity, metabolic alkalosis. Normally everything is filtered, everything
is reabsorbed and could be excreted.
In metabolic alkalosis we have an excessive bicarbonate in plasma , so we will
have also excessive bicarbonate in tubular fluid. And because of this increase
bicarbonate in the tubular fluid, everything is reabsorbed (Bicarbonate will be
reabsorbed also). Because there is a high concentration of bicarbonate in the
filtered fluid. A reabsorption of bicarbonate will associate hydrogen ion
excretion.
And if we take in account that we can have a moderate increase of carbon
dioxide pressure, the carbon dioxide will stimulate the carbonic anhydrase and
again we will have stimulation of hydrogen ion expression and bicarbonate
reabsorption together with sodium.
If we have a moderate hypercapnea, high concentration of carbondioxide will
activate the carbon anhydrase ! In the nephrocytes , and the carbonic acid will
dissociate.
Dissociating hydrogen ion will be excreted, sodium will be reabsorbed attracting
bicarbonate, so well have aggravation of the metablolic alkalosis with the
hydrogen ions loss and bicarbonate reabsorption.
So thats why in metabolic alkalosis , the possibilities of regulation are very
limited. and the cellular shift is the most important.
metabolic alkalosis, By clinical point of view:
- patients are weak,
- neuromuscular weakness,
- stupor hypertension,
- confusion,
- cardiac arrythmia.
Lets see whats happening in metabolic alkalosis. In metabolic alkalosis:
- calcium ions will tend to be bound to the proteins, so the calcium ions
concentration will decrease affecting the neuromuscular transmission.

Potasium will be decreased by the reason that we have already discussed,

so hypokalemia will affect neuromuscular transmission, affecting finally
also the cardiac rythm.and so well have a tendancy to cardiac arrythmias.

Another important effect of metabolic alkalosis is bohr effect: Increasing

the saturation of hemoglobulin with oxygen, but also the movement of the
dissociation curve of the hemoglobin to the left.

That means the hemoglobin will keep its saturated with oxygen, but hemoglobin
fixed this oxygen will not deliver to the tissue as in normal. So we will have
tissue hypoxia, with possibility of lactate production.
You will see there is a metabolic acidosis which will compensate, NO it will not
compensate the metabolic alkalosis, it will aggravate the disturbance , we cannot
read the metabolic acidosis by alkaline because we will aggravate the metabolic
alkalosis, and we cannot read the metabolic alkalosis because we can aggravate the
metabolic acidosis.
So it's a bit to complicated. Now lets see whats happening in metabolic alkalosis by
losing gastric fluid. So done by vomiting.
By vomiting we are not only losing chloridic acid. We are also losing sodium,
potasium and a lot of water.
As you saw, the gastric secretion could be around 10 liters per day, so if you have big
vomiting, you can lose a big amount of water. We will have chloridic acid loss, and so
accumulation of bicarbonate, but associated to this metabolic alkalosis , we will have
hypovolemia, and if we have hypovolemia, what kind of compensatory mechanisms
will be stimulated? The most important renin-angiotensin-aldosterone.
Aldosterone will stimulate the retention of sodium and including water. Retention of
sodium with losing of potasium. Retention of sodium associated with excretion of
hydrogen ions. And ofc reabsorbtion of bicarbonate. So these mechanisms reningangiotensin-aldosterone will aggravate the metabolic alkalosis.
By renal point of view, because of the renal mechanism, we have a possibility to
aggravate and to maintain the metabolic alkalosis, so we have:
Hypovolemia/vasoconstriction/decreased glomerular filtration, and so if we have
decreased glomerular filtration, we will have a tendancy to increase the reabsorption
in general including bicarbonate, chloride.
Because of the hypokalemia, there is another effect of hypokalemia, not only that
cellular??? But also at the renal level, the hypokalemia , will stimulate the ammonium
production, and we know that the most important process for hydrogen ion excretion
is ammonium production. Hydrogen ion secretion as ammonium salt. So hypokalemia
will stimulate this process, again losing acids, again maintaining and aggravating
maybe the metabolic alkalosis. In the distal tubule, the most important mechanism
producing the maintanance and possible aggravation of the metabolic alkalosis is the
aldosterone, stimulated by the hypovolemia, with increased excretion of hydrogen ion
and potassium. So what do you see,you have metabolic alkalosis but the urine is acid
because the hydrogen ions excretion is preserved as ammonium salt and acidity in
general. As u see, metabolic alkalosis with acide urine. This is a particularity of the
metabolic alkalosis by vomiting, by losing gastric fluid.
Lets pass to the respiratory disturbanceIn the respiratory disturbances, we have
the particularity of the renal mechanism as compensatory as regulation in acid base .

So we discussed about acute respiratory disturbances, and chronic respiratory

disturbances. Because of this different capacity of regulation, the parameters will be
different and the treatment will be different.
First respiratory acidosis will be produced by the increased carbon dioxide pressure
, this is the primary modification , producing decrease of this ratio and decreased PH,
respiratory acidosis, very logical and very simple. So the respiratory acidosis , is a
hyperkapnic acidosis.
In acute we have no renal compensation, so in acute bicarbonate is not increased,
the bicarbonate concentration cannot be increased because the kidney is not efficient
yet. So the other regulatory mechanisms , the cellular exchange and the buffer
systems, these are the possibilities.
In chronic respiratory acidosis we have hyperkapnea, but also we can have increased
bicarbonate, because the kidney is efficient now and can reabsorb and can economise
the bicarbonate.
Lets see which are the systemic consequenses of the hyperkapnea:
because hyperkapnea will produce:
- acidosis
- Neurological and cardiovascular
By neurological point of view, effect the pathogenesis of the neurological mechanism
is also a vascular complication, hyperkapnea will generate cerebral vasodilation, so if
we have vasodilation in a territory, a hydrostatic pressure in the vessel will be
increased, so it will be the tendency of the water to get out from the vessel/capillary.
And so the water will pass through the capillary membrane in the interstitial space,
producing interstitial edema.
We discussed about cerebral territory, so we will have cerebral edema, we increase
intracranial pressure, and this will affect in general the CNS from sensation of fatigue
to confussion, stupor and late coma.
When carbon dioxide pressure is over 80mm mercury, the coma becomes a reality
by this mechanism of cerebral edema. We will also have headaches ofc.
Cardiovascular effects of the hyperkapnea: Hyperkapnea will stimulate the delivery of
epinephrine and norepinephrine wih well known effects. Increased vasoconstriction,
peripheral vasoconstriction with increased peripheral vascular resistence, with
tacchycardia and so on. But also we will have increased pulmonary vascular
resistence and because of the peripheral vasoconstriction we have decreased renal
flow with decreased glomerular filtration. The severe hyperkapnea will affect also the
myocardial contractility , depressing the myocardial contractility.
Student asks: but we have higher cathecolamines , how come we have low
cardio??
When the hypercapnea is severe the myocardium will not respond anymore to
the the catecholamines
Causes for respiratory acidosis:
- Increased carbon dioxide pressure could be done by increased production of
carbon dioxide or decreased elimination.
- Increased production of carbon dioxide we can describe this only especially by
theoretical point of view because these situation could be possible but very
rare, for instance in intense physical activity or in high fever, hyperthyrodism,
very increaed basal metabolism. So these are some possibilities of increased
carbon dioxide production from the metabolism, but usually the most

important causes for increaed carbon dioxide is the decreased elimination by

hypoventilation, and hypoventilation could be done by disturbances in the
neurological control of the ventilation, so in some neurological diseases
affecting the respiratory center or the responsiveness of the respiratory center
to the stimuli.
-

Other possibilities are mechanical limitations, neuromuscular diseases or

musculo-skeletal diseases of the thoracic cage will affect the respiratory
movement and ofc the respiratory ventilation. And hypoventilation could be
done by coronary diseases or by pulmonary circulation diseases, for instance
increased ventilation of the dead space in the pulmonary vascular obstruction ,
like its happening in the pulmonary thrombi embolism or like its happening in
increased dead space, ventilation of dead space in the total decrease of cardiac
output AGAIN.
And ofc finally the most common causes of hypoventilation are the pulmonary
cause ,obstruction of the airways at different levels, obstuction in upper
airways by foreign bodies, by tumours compressiions and obstruction in lower
airways, in bronchi and alveoli by bronchoconstriction and mucus.

We distinguish between acute respiratory acidosis and chronic respiratory acidosis

because of the different compensatory possibilities.
Acute respiratory acidosis we will have decreased PH with decreased carbon
dioxide with no increased bicarbonate or maybe the bicarbonate could be decreased.
Bicarbonate could be decreased because of the buffering the acids , the hydrogen ions
in excess. What kind of acute causes will lead to acute respiratory acidosis?
- Drops, depressing the respiration like barbituris
- The obstruction of other respiratory ways by foreign bodies or by
angioneurotic edema or by glottic edema,
- spontaneous pneumothorax
- depressed the pulmonary tissue
The acute decompensation of a neuromuscular disease , like a neuromuscular disease
affecting the respiratory movements or the status asthmaticus. You know about
asthma, you know about asthma crisis, but the most severe for of asthma crisis is
status asthmaticus which could be finalized with death! Why it is so severe? Because
it is not only bronchoconstruction, it is also high production of mucus, and mucus will
obstruct the lower respiratory ways so the patient is obstructed in this territory, acute
respiratory acidosis and a very big emergency.
Chronic respiratory acidosis, the most common disease producing chronic respiratory
acidosis is the obstructive chronic lung disease. Another group of causes is
represented by neuromuscular diseases like poliomyelitis, multiple sclerosis ,
myasthenia gravis, poliomyositis and so on. Whats happening in chronic
respiratory acidosis? We have hypercapnea with low PH but hypercapnea is
associated with increased concentration of bicarbonate because in chronic stage the
kidney had time to compensate the increased acidity by reabsorbing bicarbonate. The
decreased PH is compensated in respiratory acidosis in general by the erythrocyte
involvement, by the chloride shift phenomen. the erythrocytes in this process could be
considered as a producer of bicarbonate.

So if we have hypercapnea, the carbonic anhydrase in the erythrocytes is stimulated,

and being stimulated the bicarbonate will be dissociated (will get out )form the cell
in exchange for the cloride. And so in this situation the erythrocytes could be
considered as a producer of bicarbonate. And the compensation could be taken into
account, it is not very important but it exists!!!!!
Respiratory alkalosis:
In respiratory alkalosis we have hypocapnea (loss of carbon dioxide or low
production of carbon dioxide) and increased PH.
Again bicarbonate will be moved(modified), if the respiratory alkalosis is acute or
chronic , only when it is CHRONIC renal compensation is able to decrease the
problem.
whats happening if we have hypokapnea,near respiratory alkalosis , we have also
systemic consequences done by hypocapnea.
Hypocapnea will increase the neuromuscular excitability , and will stimulate the
vasoconstriction in the arterial territory.
Because of the vascoconstriction, in the brain the blood flow will be decreased,
producing cerebral ischemia. Hypocapnea with respiratory alkalosis will move the
dissociation curve of the hemoglobin to the left, increasing the affinity of the
hemoglobin for the oxygen, so the delivery of the oxygen will be impaired. Again
hypoxia( tissue hypoxia) !
Because of the vasoconstriction, the vasoconstriction is not only in the brain, it will be
also in the myocardial territory, so we will have disturbances in the myocardial
function with arrhytimias and other. We have alkalosis , we have hypokalemia.
Hypokalemia will aggravate the neuromuscular excitability disturbances and the
cardiac arrhythmias.
Causes of respiratory alkalosis : acute or chronic.
- The first group will be increased alveolar ventilation, hyperventilation could
be done by anxiety or by some drugs producing excitability of the respiratory
center with aqua ventilation?? Hypoxemia could also produce a stimulation of
the chemoreceptors in the carotid region, producing hyperventilation. The
most common cause of hyper ventilation is done by a defective control of the
ventilatory apparatus , mechanical ventilation is used to assist the patients.
Low production of carbon dioxide causing rare situation could be done by
paralysis , by low basal metabolism, like its happening in hypothermia
Now we finished with the acid base balance!!!
We will pass to the next chapter

Fluids and electrolytes:

The fluids electrolytes balance is very well interconnected with acid base balanc. We
discussed them separated first. metabolic acidosis, metabolic alkalosis and
respiratory.
And now we will discuss about fluids and electrolytes disturbances. They are not
separated. They are always together.
- When you have a discturbance in acid base balance , you have to have
associated disturbance in electrolytes and maybe in fluids.
- If u have a disturbancy in electrolytes , usually you have a disturbancy in
water.
- If you have a disturbancy in water , you obligatory have a disturbance in
electrolytes, and all of them are related with acid base balanse. They are not
separated.
So the balance of fluids and electrolytes is maintained by an integration of renal ,
hormonal and neural function. Changes in the electrolytes composition will affect
the electrical potentials for instance. So will affect the excitability of the cells and
especially the excitatory cells. The changes in electrolytes composition will affect
also the shifts of fluid from one compartment to another , so in the extracellular
compartment we will see about this. In extracellular compartment , the
composition in electrolytes is modified, the water could pass form a compartment
to another according to this change, ACCORDING to the tonicity loss.
Fluids modifications, fluid fluctuations affect blood volume ofc and the cellular
function, SO water going out of the cells or going into the cells will affect the
cellular metabolism and will affect also the PH. Alterations in the PH will affect
the cellular functions and the enzymes functions/enzyme systems.
From physiology :the distribution of body fluids,
- The total water in our body is around 60%, from the body weight(in childhood
or newborn it is around 80%). So the children are very exposed/vulnerable to
the dehydration.
- Extracellular fluid 1/3 from total body water
- Intracellular fluid 2/3 from total body water

But usually the water is not pure, it contains electrolytes! So if there is a movement of
electrolytes it will affect the water movement and when there is a chane in water it
will affect the electrolytes repartition.
whats happening for instance if we have modifications of the water?( especially
water in the extracellular space).
For instance if u have a dehydration( water loss), where from I will lose water? First
from the extracellular space by vomiting, urine, diarrhea, hemorrhage , plasmolagia,
or by any movement type we are losing water.

This water isnt pure. This water will contain electrolytes, BUT we will take into
account the example when the water has a low content in electrolyte, i mean the loss
is predominant in water. And so what remains in the extracellular space? It will
remain a hypertonic liquid with high concentration of sodium which is the most
important ion of the extracellular space. It is one of the determinants of the osmolality
and of the tonicity. The most important determinants of the osmolarity of the
extracellular fluids are the glucose, the sodium, and the urea!!!
NOw from this constitutient, these 2( glucose & sodium) are important also for the
tonicity of a space. Urea is not important for the tonicity, it will not modify the
tonicity, why? Because the modification of the concentration of urea in a
compartment will be rapidly passed to the other compartment, why? Because urea is
diffusable, diffuses through the membrane. So urea could modify the osmolarity but
cannot modify the tonicity, because if we have high urea here, urea will transvers the
membrane and establish a balance between these 2 spaces.
But glucose and sodium will not transverse the membranes. So if we lose more
water than electrolytes , we have an important loss of water , that means here we have
a hypotonic dehydration! and whats happening with the water between these 2
compartments? The water will be moved , a certain quantity of water will move
form the intracellular space to the extracellular space , so we will have a double
dehydration: extracellular and intracellular, when we have hypotonic extracellular
dehydration!!!! And this movement of the water from the intracellular space to the
extracellular space , partially compensates the loss of water from this space.
So by hemodynamic point of view, the hypotonic dehydration is not so severe
because of this mechanism of transport of transport of water from intracellular space
to extracellular space.
For the treatment we have to know how much water did the patient lose, So we can
calculate deficiency of water taking into account the actual concentration of sodium
compared to a normal concentration of sodium around 140mEq/L . and so the
deficiency of water will be calculated from the total body water (60%) multiplied with
1 minus normal concentration of sodium divided with actual concentration of sodium.

This is lower THAN the actual. We can also demonstrate this formula but this is not
our job today.
If we have another type of loss from the extracellular space, loss of water but
especially a very important loss of electrolytes .
which is the most important extracellular electrolyte? sodium!!
So if we have a big deficiency of sodium. We have also dehydration but sodium is
much more lost than the water, so this space, the extracellular space is dehydrated but
remains hypotonic, so this is a hypotonic dehydration.
- The concentration of sodium here(the actual concentration), is lower than
normalHYPOTONIC dehydration.
Now for the restoration of the equilibrium, we have to know how much sodium did
the patient lose. So we will calculate the deficiency of soidum. The deficiency , the
mili equivalents of sodium could be calculated : total body water multiplied with the

difference between concentration of normal sodium minus concentration of actual

sodium.

So here we have liters and mEq/L.

you will obtain mEq . Not concentration, quantity of soidum that you have to
administer!!!
You will give the patient water charged with sodium , maybe hypertonic fluids
in such volume to cover the quantity of sodium which was lost. Very
important for this stage to estimate approximately how much is the water loss
in this case and how much is the sodium loss.
And ofc we can talk about hyperhydration. And again hyperhydration is not alone,
must be taken into account with electrolytes , less or more.
The most important /common are dehydrations so we will discuss about that later
on!!!!