Pathology disorders of alkaline water electrolyte balance

2021-01-26 12:00 AM

Bicarbonate buffers play a huge role in regulating the body's alkaline balance because both elements of this system can be easily regulated.

Physiology and regulation of electrolyte water

Water distribution in the body

In normal adults, total water volume accounts for about 60% of body weight, of which 40% is intracellular and 20% is extracellular. Of this 20%, 15% is in the interstitial space and 5% is intravascular. The amount of water in the body in women is less than in men and decreases with age. The osmotic concentration between the intracellular and extracellular compartment is usually equal (about 285 osmole / l). The transport of water to and from the cell membrane is due to the differential osmole pressure (osmol), whereas the movement of water through the capillary membrane is dependent on the difference in hydrostatic and colloidal pressure. Intracellular and extracellular water balance disorders result from the imbalance of Bilan Sodium and/or Bilan water.

Mechanisms for regulating electrolyte water, alkaline acidosis

This mechanism is very essential and requires sensitivity and precision to ensure the stability of the homeostasis: it is a necessary condition for life. There is a preference for osmotic equilibrium over homeostasis volumetric equilibrium. The two sides regulate the electrolyte water balance and the acid-alkaline balance that are closely related.

Osmotic balance conditioning:

Mainly due to the mechanism of the anti-diuretic hormone ADH (Antidiuretic Hormone) and thirst mechanism. The stimulation of ADH secretion is an increase in osmotic pressure and a decrease in the volume of the extracellular medium. The thirst centre in the hypothalamus, where there is osmotic pressure receptors, the decrease in volume of the extracellular medium also indirectly stimulates the thirst centre.

Volume regulation of the extracellular medium:

The volume of the extracellular medium is mainly determined by sodium, so the regulation of extracellular volume is mainly due to the regulation of extracellular sodium, the regulation of extracellular sodium mainly through Aldosterone and kidney mediated.

Ion balance conditioning: Sodium ions are listed above:

Extracellular potassium ions are closely related to sodium ions and the pH of the extracellular environment. When pH drops, potassium goes from intracellular to extracellular causing extracellular potassium to increase and be excreted more out if the kidney is normal, or stagnate if kidney failure, alkalization of the extracellular environment has the opposite effect.

Calcium ions are regulated by parathyroid hormone (PTH), vitamin D and closely related to the concentration of phosphorus in the blood.

Balance acid-base balance:

There are buffering systems in the body, which limit the change of pH to some degree to keep the blood pH within normal limits, of which the most important is the Bicarbonate buffers:

H + H2CO3 < = = > H2CO3   < = = > CO + H2O

Bicarbonate buffers play a huge role in regulating the body's alkaline balance because both elements of this system can be easily regulated: HCO3 А by the kidneys and CO2 by the lungs.

Loss of foreign cells


A decrease in volume of the extracellular space, consisting of 2 interstitial and intravascular compartments. Since the loss of sodium ions equates to dehydration, Bilan Sodium is always negative. If purely extracellular dehydration is present, the intracellular osmolality is normal (285 osmoles / l) and the intracellular volume remains constant (indicated by normal serum sodium concentrations).


Causes of renal loss (characterized by sodiumuria <20 mmol / 24 hours):

Loss from the gastrointestinal tract: prolonged vomiting, diarrhoea, gastrointestinal opening, laxatives, ... or dehydration through the skin, mucous membranes: perspiration, extensive burns.

Renal dehydration (sodiumuria> 20 mmol / 24 hours) may be caused by:

Kidney disease: Interstitial kidney disease, end-stage chronic kidney failure with limited salt intake, acute high urinary failure

Extrinsic diseases: due to osmotic diuretic effects: diabetes mellitus, mannitol infusion, hypercalcemia, diuretics, acute adrenal insufficiency.

Dehydration into the "3rd chamber":

Due to the formation of an extracellular fluid compartment: peritonitis, acute pancreatitis, intestinal obstruction, and traumatic striated muscle destruction.


Dehydration and salt loss are in an isotonic ratio, leading to a decrease in extracellular fluid volume with no change in osmotic concentration, no change in intracellular fluid volume (plasma osmolality and Normal blood sodium).


Diagnosis is confirmed based on clinical and subclinical examination.

Clinical symptoms:

Lower blood pressure: at first postural hypotension, then while lying down.

Fast heartbeat.

The hypovolemic shock when the fluid loss exceeds 30%.

The superficial veins collapsed.

Primary, anuria.

Weight loss.

Skin pinch mark (Casper) positive.

Dry skin, dry mucosa.

Thirst: C ó but not as much as in intracellular dehydration.

Subclinical symptoms:

There is no test that directly reflects the dehydration of the interstitial fluid compartment, usually, 1 isotonic dehydration in the intravascular compartment: increased blood proetid (> 75g / l), increased Haematocrit (> 50%) without haemorrhagic markers, which may indicate functional acute renal failure due to hypovolemia.

Diagnose the cause:

Usually simple, depending on the context of the disease, the clinical symptoms and the amount of sodiumuria in 24 hours.

Electrolyte dehydration due to non-renal causes:

Primary oliguria.

Sodium urinary <20 mmol / 24 hours.

There is urine concentration phenomenon: Urea / Blood urea> 10; Creatinine urine / Blood creatinine> 40; urinary osmosis> 500 osmole / l.

Dehydration, salt due to renal loss:

Normal or increased urine output (> 1000 ml / 24 hours).

Increased sodium urinary> 20 mmol / 24 hours.

Un-condensed urine: Urea / Blood urea <10; Urinary Creatinine / Blood Creatinine <20.

Strain foreign cells


An increase in the volume of fluid in the extracellular space, especially in the interstitial space, leads to total oedema. Extracellular water retention is usually caused by water and salt retention (in equal amounts), with positive Bilan Sodium.


The three most common causes are heart failure, cirrhosis, nephrotic syndrome.

Other causes in the kidneys: acute glomerulonephritis, acute and chronic renal failure.

External causes: malnutrition, peripheral vasodilation as much as in the case of venous perforation, pregnancy, are being treated with vasodilators.


The transport of water and sodium across the membrane sides of the capillary obeys Startling's law. Usually, oedema is the result of:

Reduced intravascular colloid pressure: seen in severe hypovolemia. Water and sodium go from the intravascular to the interstitial space, reducing the volume of the lumen.

Intravenous hydrostatic hypertension: in this case, the 2 interstitial spaces and the intravascular cavities both increase in volume, usually due to heart failure or a state of water and salt retention due to kidney damage.

Combining many mechanisms: congestive heart failure, reducing blood volume, the kidneys increase the reabsorption of water and salt to increase ejection volume. In cirrhosis: oedema is a consequence of portal hypertension, and also due to vasodilation of the viscera.


Diagnosis is mainly based on clinical practice.

Clinical symptoms of extracellular fluid retention:

Oedema: Peripheral oedema, white, soft, painless, positive concave mark, the possible effusion of membranes (heart-lung-abdomen) or interstitial space.

Signs of lumen: increased blood pressure or acute pulmonary oedema.

Weight gain.

Subclinical is usually poor: blood-thinning (anaemia, decreased blood Protide), constant and no subclinical symptoms to reflect interstitial volume.

Diagnosing the cause is often as simple as analysing the clinical setting and symptoms.

Dehydration in cells


Is decreased extracellular volume due to 1 Bilan negative water with 1 increase in plasma osmolality> 300 osmole / l. This increase in osmolality causes water from the intracellular to the extracellular.

The main manifestation on the test is hypernatremia.

Note: The plasma osmolality can be estimated using the formula: P osmol = [Na + x 2] + Blood glucose = 285 mmol / l.


Intracellular dehydration with hypernatremia:

Decompensated dehydration: Dehydration through the skin, respiratory tract, kidney loss such as in diabetes mellitus, using more mannitol, lost from the digestive tract such as diarrheal, using laxatives.

Provides plenty of sodium: in resuscitation, in artificial kidneys.

Decreased water supply: disorders of the hypothalamus in the newborn, the elderly, in a comatose patient.

Intracellular dehydration without hypernatremia:

Secondary hyperabsorption due to disorders of substances with osmotic activities: Glucose, Mannitol, Ethylene glycol.

Substances that diffuse freely into cells such as urea, ethanol, ... will not lead to intracellular water disturbances.


The water bilan remains in balance.

The thirst will regulate water intake and kidney activity to ensure stable permeability between the 2 intracellular and extracellular compartments.

ADH secretion is mainly regulated by changes in plasma osmolality, by lumen volume and by thirst mechanism. When the ADH is inadequately secreted, bilan negative water produces a feeling of thirst.

We can experience 1 Bilan negative water and increased blood osmosis in the following cases:

Dehydration through the kidney: mucosal skin, respiratory tract.

Renal dehydration due to lack of ADH or decreased sensitivity of the kidney to ADH.

A disorder of the thirsty centre or a disorder of the osmotic receptors in the hypothalamus.


Implementing the quadrants:

Clinical symptoms:

Neurological: Nonspecific, associated with hypernatremia.

Lethargic, drowsy.

Feeling exhausted.

Disorders of consciousness in the form of stimulation. Fever.



Cerebral haemorrhage - meningitis

Thirst: A rancid very intense moment.

Dry mucous membranes: A. In particular the inside of the cheek.

Syndrome of drinking a lot, urinating more in the case of kidney causes.

Weight loss.

Subclinical symptoms:

Plasma osmolality> 300 mmol / l.

Blood sodium> 145 mmol / l.


Hydration in cells


An increase in the volume of intracellular fluid due to positive water Bilan in combination with decreased plasma osmolality, decreased blood sodium <135 mmol / l.


Absorbs more water than can be excreted: mental illness drinks more.

Inappropriate excretion of ADH hormone (SIADH).

Due to decreased water excretion in cirrhosis, heart failure, nephrotic syndrome.

In severe chronic renal failure (glomerular filtration rate <20 ml / min).


Clinical symptoms:

Neurological disorders: nonspecific, related to the level of sodium in the blood: nausea, vomiting, loss of appetite, headache, confusion of consciousness, coma, convulsions.

Moderate weight gain.

Not thirsty, on the contrary, he doesn't like to drink water.

Subclinical symptoms:

Plasma osmolality <270 osmole / l.

Blood sodium <135 mmol / l.

Increased blood potassium


Hyperkalaemia is defined as a serum potassium concentration above 5.0 mmol / l. Sudden hyperkalaemia can be life-threatening.


Cardiovascular symptoms:

Is manifested mainly on the electrocardiogram

T waves are tall, pointed and symmetrical.

Abnormal conduction in the atrium (amplitude decrease followed by P wave loss), atrioventricular conduction disorder (Sinus-atrial Bloc, Atrial Bloc).

Then: disturbances of intraventricular conduction: dilated QRS complex.

More severe: ventricular tachycardia, ventricular fibrillation, and cardiac arrest.

Neuromuscular symptoms:

Usually nonspecific: paraesthesia in the extremities and around the mouth. More severe muscle weakness or paralysis may occur in the lower extremities and progress gradually up.


Oversupply with Potassium:

Rarely in the normal person, usually due to intravenous or oral potassium treatment.

Due to Potassium from intracellular to extracellular:

Metabolic acidosis.

Increased cell degradation:

Muscle breakdown and muscle crushing.

Severe burns, heavy haemolysis.

Cancellation of tumour spontaneous or by chemotherapy.

Severe gastrointestinal bleeding.

Heavy physical activity.

Drug causes:

Beta inhibition is not selective.

Digital Poisoning.

Poisoning Fluor and Cyanure.

Decreased renal potassium secretion:

Acute renal failure.

Chronic renal failure.

Lack of mineral corticoids: Adrenal insufficiency.

Due to drugs: non-Steroid anti-inflammatory, cyclosporine A, Heparin, ACE inhibitors, Angiotensin II receptor inhibitors.


All suspected cases of hyperkalaemia must be electrocardiogram, electrolyte. Conduction disorders must be diagnosed early for emergency treatment.

Lower blood potassium


Called hypokalaemia when blood potassium levels are below 3.5 mmol / l. It can be life-threatening because it causes cardiovascular disorders.



Delayed repolarization of the ventricles due to prolonged inert period.

Symptoms of the electrocardiogram depend on the degree of hypokalaemia.

The ST segment is concave.

T wave inversion.

Increase U wave amplitude.

Lasts about QU.

Subsequent QRS relaxation is associated with supraventricular or ventricular arrhythmias (extrasystoles, ventricular tachycardia, torsional apex, ventricular fibrillation.)

Muscle symptoms:


Muscle pain.

Muscle weakness, paralysis.

When severe, it can destroy rhabdomyolysis.

Gastrointestinal symptoms: fertilization (due to paralysis).

Renal Symptoms: Severe chronic hypokalaemia can be:

Manifestations 1 urinary syndrome drink a lot.

Metabolic alkalosis.

Chronic interstitial kidney disease.


Reduce potassium supply.

Transfer of Potassium from extracellular to intracellular:

Metabolic or respiratory alkalosis.

Insulin treatment in diabetes.

Stimulants β Adrenergic:


Salbutamol, Dobutamine, poisoning Theophylline.

Family cycle paralysis.

Losing too much potassium:

Through the digestive tract: diarrhoea, small intestine probe.

Loss through the kidneys:

Loop Diuretics and Thiazide.

Increased secretion of Adrenal Steroids, Primary and Secondary Aldosterone Enhancement.

Interstitial kidney disease.

Toxic tubular disease: Amphotericin B, Aminoxide.


Definitive diagnosis: based on blood potassium and electrocardiogram.

Diagnosis of the cause: dysbiosis, must be based on clinical background, personal history, family history and potassium.

Metabolic acidosis


Arterial blood pH is below 7.38.

HCO3- less than 22 mmol / l.

PCO2 is reduced secondary to compensated ventilation.



Increased ventilation.

Then severe respiratory failure.


Reduced output of the heart, kidneys, liver.


Hypersensitivity to Catecholamine.


R amniotic disturbances of consciousness, coma.


Increased blood potassium

Metabolic alkalosis


Arterial blood pH above 7.4.

HCO3- blood above 27 mmol / l.

Secondary (compensatory) PCO2 increase.


Too much alkali in the treatment.

Disorders of alkaline excretion of the kidneys.

Due to hypovolemia, stimulates the Renin-Angiotensin system: often combined with hypokalaemia and secondary hyperaldosteronism.

Due to primary hyperaldosteronism, Cushing's syndrome ...


Nervous: Headache, drowsiness, confusion, convulsions.

Cardiovascular: Ventricular or supraventricular arrhythmias, easy Digital poisoning.

Respiratory: Decreased ventilation.

Neuromuscular: Chwostek (+), Trousseau (+), muscle weakness.

Laboratory tests: decrease in blood K +, decrease in blood Ca, decrease blood magnesium, decrease blood phosphate, or increase blood pH above 7.42; HCO3- above 27 mmol / l.

Kidney: Urine a lot, thirst a lot, urine concentration disorder.

Respiratory acidosis

Cause: emphysema, acute pulmonary oedema, decreased activity of the respiratory centre.

Clinical manifestations: Purple, shallow tachypnoea, headache, limb tremor, psychosis.

Diagnosis: Mainly based on the clinical setting with appropriate etiologic and blood ion test.

Respiratory alkalosis

Causes: Histeria, damage to the central nervous system (encephalitis, Salisilat poisoning ...) breathing exertion.

Clinical manifestations: Rapid, deep breathing, disturbed consciousness.

Diagnosis: Based on a blood test.