STUDY - Technical - New Dacian's Medicine
Fluid
and Electrolyte Imbalances (1)
Translation Draft
It's evening, I'm fresh from the sea, well fried and very tired. I should have started a short series of fluids and electrolytes today, but... I still have in my eyes and in my mind the sea... From tomorrow I'll move on to recovery...
Let's start with sodium (Na) and water (H2O), addressing the composition of fluids in the human body. Water is the major component of our body (the most abundant constituent of the body), representing about 60-70% of the weight in men and 50-60% in women. This difference is attributed to differences due to the different proportion of fat tissue in men and women. The total amount of water in the body is distributed in two large compartments: 1. between 55-75% intracellular (intracellular fluids - FIC) and 2. 22-45% extracellular (extracellular fluids - FEC). FFS are further divided between intravascular space (plasma water) and extravascular space (interstitial) in a proportion of 1 to 3.
The concentration of solvents and particles in a liquid is known to be its osmolarity and is expressed in milliosmoli/ kg water (mosm/kg). Water crosses cell membranes to achieve osmotic balance (FEC osmolarity = FIC osmolarity). Intra- and extracellular solvents or osmolii are significantly different due to differences in permeability and the presence of active transporters and pumps.
The most important particles in the FEC are Na+ and the accompanying anions, Cl- and HCO3-, while K+ and phosphate seds (ATP, creatine phosphate and phospholipids) are predominantly OSC osmols. Solvents that are limited to FEC or FIC determine the actual osmolarity (or tonicity) of the compartment. Since Na+ is largely limited to the extracellular compartment, the total Na+ content in the body is a reflection of the FEC volume.
So the number of intracellular particles is relatively constant and a change in FIC osmolarity is often due to a change in the CONTENT of FIC in water. However, in certain situations, brain cells may vary the number of intracellular solvents to defend against large water exchanges. This process of osmotic adaptation is important in protecting cell volume and occurs in hyponatremia and chronic hypernatremia. Certain solvents, such as urea, do not contribute to water exchanges in the cell membrane and are known as inefficient osmoles.
The movement of fluids between intravascular and interstitial space occurs at the capillary wall and is determined by Starling forces (capillary hydrostatic pressure and osmotic colloid pressure). The transcapillary hydrostatic pressure gradient exceeds the corresponding oncotic pressure gradient and thus favors the passage of ultrafiltered plasma into the extravascular space. The return of fluids to the intravascular space is achieved through lymphatic flow.
Now, a few things about water balance. Normal plasma osmolarity is between 275 and 290 mosm/ kg and is kept within these tight limits by mechanisms capable of detecting 1-2% changes in tonicity. In order to maintain a stable situation it is necessary that the ingestion of water is equal to the excretion. Disorders of water homeostasis cause hypo or hypernatremia. Normal individuals have mandatory water loss through urine, stool and water evaporation in the skin and respiratory tract.
Gastrointestinal excretion is usually a minor component of total water balance, except for patients with high vomiting, diarrhoea and enterostoma. Evaporation or insensitive water loss is important in regulating the central body temperature. Mandatory loss of water at the renal level is required by the minimum excretion of solvents required to maintain the equilibrium state. Normally about 600 mosm should be excreted daily and, since the maximum urinary osmolarity is 1200 mosm/ kg, a minimum urine production of 500 ml/ day is required for the balance of neutral solvents.
In terms of water intake, the first stimulant for water intake is thirst, mediated both by increasing effective osmolarity and by increasing the volume of The FEC or lowering blood pressure. Osmoreceptors, located in the anterolateral hypothalamus, are stimulated by increased tonicity. Ineffective osmoli, such as urea and glucose, do not play a role in stimulating thirst. The average osmotic threshold for the appearance of thirst is around 295 mosm/ kg and varies from individual to individual. Under normal conditions, daily water intake exceeds physiological needs.
As for water excretion, in contrast to water intake, it is strictly regulated by physiological factors. The main determinant of renal water excretion is anginin vasopressin (AVP), also called the antidiuretic hormone, a polypeptide synthesized in the supraoptic and paraventricular nucles of the hypothalamus and secreted by the posterior pituitary gland. Linking AVP to V2 receptors in the basolateral membrane of the collector duct cells activates adenylcyclase and initiates a sequence of events that leads to the insertion of water channels into the luminal membrane.
These water channels, which are specifically activated by AVP, are encoded by the acondensin gene 2. The network effect is represented by the passive reabsorption of water, as a result of the osmotic gradient between the lumen of the collector duct and the hyperton medullary interstitial. The major stimulus for AVP secretion is hypertonicity. Since the major solvents in the FEC are represented by Na+ salts, the actual osmolarity is mainly determined by the concentration of Na+ in the plasma. An increase or decrease in tonicity is detected by hypothalamic osmoreceptors as a decrease or increase in cell volume leading to an increase or decrease in AVP secretion.
The osmotic threshold for AVP secretion is 280-290 mosm/ kg, and the system is sensitive enough to detect a variation in plasma osmolarity of no more than 1-2%. Nonoosmotic factors that regulate aVP secretion include actual circulating volume (arterial), nausea, pain, stress, hypoglycaemia, pregnancy, numerous medications. The hemodynamic response is mediated by the baroreceptors of the carotid sinus. The sensitivity of these receptors is significantly lower than that of osmoreceptors. In fact, enough blood volume delet to result in a decrease in average blood pressure causes a VP of AVP secretion, while small changes in circulating blood volume have low effects. Within hypovolemia, osmotic regulation by AVP remains unchanged.
However, the osmotic threshold for AVP secretion is low and sensitivity is increased. To maintain homeostasis and normal plasma concentration of Na+, ingestion of water without solvents may result in the loss of an equal volume of water without electrolytes. Three steps are necessary for the kidney to secrete an excess of water: 1. filtration and transport of water (and electrolytes) to the dilution sites of the nephron, 2. active reabsorption of Na+ and Cl- without water in the ascending thick branch of the Henle ansa and, to a small extent, in the distal nephron and 3. maintenance of diluted urine due to waterproofing of the water collector duct in the absence of AVP. Abnormalities in any of these three stages may cause an alteration in the excretion of free water and possibly hyponatry.
Now, a few "things" about sodium balance. Na+ is actively removed from the cell by the ATP pump Na+ - K+. As a result, 85-95% of all Na+ is extracellular and therefore the FEC volume is a reflection of the total amount of Na+ in the body. Normally, volume-regulating mechanisms strike a balance between loss and intake of Na+. if this does not happen, excess or na+ deficiency manifested as edema or hypovolemic states, respectively. It is important to distinguish between disturbances of osmolar adjustment and disturbances of volemy adjustment, since water balances and Na+ are independently adjusted. Changes in Na+ concentration generally reflect disturbances in water homeostasis, while alterations in Na+ content manifest as expansions or contractions of the FEC and imply an abnormal na+ balance.
Sodium balance is a matter of intake and elimination. In the case of Na+ intake, individuals on a typical Western diet consume about 150 mmol NaCl/ day. This consumption exceeds the physiological requirements. As has already been seen, Na+ is the main extracellular cation. Thus, the ingestion of Na+ causes an expansion of the FEC volume which in turn favors the increase of renal excretion while maintaining the Na+ balance. Adjusting Na+ excretion is multifactorial and is the main determinant of Na+ balance. A deficit or excess of Na+ manifests itself as a decrease or increase in actual circulating volume respectively. Changes in actual circulating volume tend to lead to changes in the same sense in the glomerular filtration rate (RFG).
However, tubular reabsorption of Na+ and not RFG is the main mechanism that controls Na+ excretion. Almost 2/3 of the filtered Na+ is reabsorbed into the proximal contorted tube, this process being electrically neutral and isoosmotic. Additional reabsorption (25-30%) appears in the thick ascending branch of the Henle ansa through the apical countertransporter Na+ - K+ - 2Cl-, an active process and also electrically neutral. The meter tube reabsorbs 5% of Na+ via the Na+ - Cl- thiazide-sensitive co-transporter. The final reabsorption of Na+ occurs in the cortical and medullary collecting ducts, the amount excreted being almost equivalent to that ingested daily.
Ready for this post! I'll continue addressing hypovolemia, then hyponatremia, hypernatremia, potassium, hypopotasemia and hyperpotasemia. Most likely it will be two more posts... Acidosis and alkalose (related to Na+ - K+ balance and electrolytes) will follow with three more posts and, aba after this, we finish with all this primary chemistry of the human body...
It's evening, I'm fresh from the sea, well fried and very tired. I should have started a short series of fluids and electrolytes today, but... I still have in my eyes and in my mind the sea... From tomorrow I'll move on to recovery...
Let's start with sodium (Na) and water (H2O), addressing the composition of fluids in the human body. Water is the major component of our body (the most abundant constituent of the body), representing about 60-70% of the weight in men and 50-60% in women. This difference is attributed to differences due to the different proportion of fat tissue in men and women. The total amount of water in the body is distributed in two large compartments: 1. between 55-75% intracellular (intracellular fluids - FIC) and 2. 22-45% extracellular (extracellular fluids - FEC). FFS are further divided between intravascular space (plasma water) and extravascular space (interstitial) in a proportion of 1 to 3.
The concentration of solvents and particles in a liquid is known to be its osmolarity and is expressed in milliosmoli/ kg water (mosm/kg). Water crosses cell membranes to achieve osmotic balance (FEC osmolarity = FIC osmolarity). Intra- and extracellular solvents or osmolii are significantly different due to differences in permeability and the presence of active transporters and pumps.
The most important particles in the FEC are Na+ and the accompanying anions, Cl- and HCO3-, while K+ and phosphate seds (ATP, creatine phosphate and phospholipids) are predominantly OSC osmols. Solvents that are limited to FEC or FIC determine the actual osmolarity (or tonicity) of the compartment. Since Na+ is largely limited to the extracellular compartment, the total Na+ content in the body is a reflection of the FEC volume.
So the number of intracellular particles is relatively constant and a change in FIC osmolarity is often due to a change in the CONTENT of FIC in water. However, in certain situations, brain cells may vary the number of intracellular solvents to defend against large water exchanges. This process of osmotic adaptation is important in protecting cell volume and occurs in hyponatremia and chronic hypernatremia. Certain solvents, such as urea, do not contribute to water exchanges in the cell membrane and are known as inefficient osmoles.
The movement of fluids between intravascular and interstitial space occurs at the capillary wall and is determined by Starling forces (capillary hydrostatic pressure and osmotic colloid pressure). The transcapillary hydrostatic pressure gradient exceeds the corresponding oncotic pressure gradient and thus favors the passage of ultrafiltered plasma into the extravascular space. The return of fluids to the intravascular space is achieved through lymphatic flow.
Now, a few things about water balance. Normal plasma osmolarity is between 275 and 290 mosm/ kg and is kept within these tight limits by mechanisms capable of detecting 1-2% changes in tonicity. In order to maintain a stable situation it is necessary that the ingestion of water is equal to the excretion. Disorders of water homeostasis cause hypo or hypernatremia. Normal individuals have mandatory water loss through urine, stool and water evaporation in the skin and respiratory tract.
Gastrointestinal excretion is usually a minor component of total water balance, except for patients with high vomiting, diarrhoea and enterostoma. Evaporation or insensitive water loss is important in regulating the central body temperature. Mandatory loss of water at the renal level is required by the minimum excretion of solvents required to maintain the equilibrium state. Normally about 600 mosm should be excreted daily and, since the maximum urinary osmolarity is 1200 mosm/ kg, a minimum urine production of 500 ml/ day is required for the balance of neutral solvents.
In terms of water intake, the first stimulant for water intake is thirst, mediated both by increasing effective osmolarity and by increasing the volume of The FEC or lowering blood pressure. Osmoreceptors, located in the anterolateral hypothalamus, are stimulated by increased tonicity. Ineffective osmoli, such as urea and glucose, do not play a role in stimulating thirst. The average osmotic threshold for the appearance of thirst is around 295 mosm/ kg and varies from individual to individual. Under normal conditions, daily water intake exceeds physiological needs.
As for water excretion, in contrast to water intake, it is strictly regulated by physiological factors. The main determinant of renal water excretion is anginin vasopressin (AVP), also called the antidiuretic hormone, a polypeptide synthesized in the supraoptic and paraventricular nucles of the hypothalamus and secreted by the posterior pituitary gland. Linking AVP to V2 receptors in the basolateral membrane of the collector duct cells activates adenylcyclase and initiates a sequence of events that leads to the insertion of water channels into the luminal membrane.
These water channels, which are specifically activated by AVP, are encoded by the acondensin gene 2. The network effect is represented by the passive reabsorption of water, as a result of the osmotic gradient between the lumen of the collector duct and the hyperton medullary interstitial. The major stimulus for AVP secretion is hypertonicity. Since the major solvents in the FEC are represented by Na+ salts, the actual osmolarity is mainly determined by the concentration of Na+ in the plasma. An increase or decrease in tonicity is detected by hypothalamic osmoreceptors as a decrease or increase in cell volume leading to an increase or decrease in AVP secretion.
The osmotic threshold for AVP secretion is 280-290 mosm/ kg, and the system is sensitive enough to detect a variation in plasma osmolarity of no more than 1-2%. Nonoosmotic factors that regulate aVP secretion include actual circulating volume (arterial), nausea, pain, stress, hypoglycaemia, pregnancy, numerous medications. The hemodynamic response is mediated by the baroreceptors of the carotid sinus. The sensitivity of these receptors is significantly lower than that of osmoreceptors. In fact, enough blood volume delet to result in a decrease in average blood pressure causes a VP of AVP secretion, while small changes in circulating blood volume have low effects. Within hypovolemia, osmotic regulation by AVP remains unchanged.
However, the osmotic threshold for AVP secretion is low and sensitivity is increased. To maintain homeostasis and normal plasma concentration of Na+, ingestion of water without solvents may result in the loss of an equal volume of water without electrolytes. Three steps are necessary for the kidney to secrete an excess of water: 1. filtration and transport of water (and electrolytes) to the dilution sites of the nephron, 2. active reabsorption of Na+ and Cl- without water in the ascending thick branch of the Henle ansa and, to a small extent, in the distal nephron and 3. maintenance of diluted urine due to waterproofing of the water collector duct in the absence of AVP. Abnormalities in any of these three stages may cause an alteration in the excretion of free water and possibly hyponatry.
Now, a few "things" about sodium balance. Na+ is actively removed from the cell by the ATP pump Na+ - K+. As a result, 85-95% of all Na+ is extracellular and therefore the FEC volume is a reflection of the total amount of Na+ in the body. Normally, volume-regulating mechanisms strike a balance between loss and intake of Na+. if this does not happen, excess or na+ deficiency manifested as edema or hypovolemic states, respectively. It is important to distinguish between disturbances of osmolar adjustment and disturbances of volemy adjustment, since water balances and Na+ are independently adjusted. Changes in Na+ concentration generally reflect disturbances in water homeostasis, while alterations in Na+ content manifest as expansions or contractions of the FEC and imply an abnormal na+ balance.
Sodium balance is a matter of intake and elimination. In the case of Na+ intake, individuals on a typical Western diet consume about 150 mmol NaCl/ day. This consumption exceeds the physiological requirements. As has already been seen, Na+ is the main extracellular cation. Thus, the ingestion of Na+ causes an expansion of the FEC volume which in turn favors the increase of renal excretion while maintaining the Na+ balance. Adjusting Na+ excretion is multifactorial and is the main determinant of Na+ balance. A deficit or excess of Na+ manifests itself as a decrease or increase in actual circulating volume respectively. Changes in actual circulating volume tend to lead to changes in the same sense in the glomerular filtration rate (RFG).
However, tubular reabsorption of Na+ and not RFG is the main mechanism that controls Na+ excretion. Almost 2/3 of the filtered Na+ is reabsorbed into the proximal contorted tube, this process being electrically neutral and isoosmotic. Additional reabsorption (25-30%) appears in the thick ascending branch of the Henle ansa through the apical countertransporter Na+ - K+ - 2Cl-, an active process and also electrically neutral. The meter tube reabsorbs 5% of Na+ via the Na+ - Cl- thiazide-sensitive co-transporter. The final reabsorption of Na+ occurs in the cortical and medullary collecting ducts, the amount excreted being almost equivalent to that ingested daily.
Ready for this post! I'll continue addressing hypovolemia, then hyponatremia, hypernatremia, potassium, hypopotasemia and hyperpotasemia. Most likely it will be two more posts... Acidosis and alkalose (related to Na+ - K+ balance and electrolytes) will follow with three more posts and, aba after this, we finish with all this primary chemistry of the human body...
I wish you a good and
successful week!
Dorin, Merticaru