Pathophysiology of water-salt metabolism. Alterations in Acid-Base Balance.

Functions of water in the body:

1. In a liquid medium, metabolic processes occur
2. Water is a part of saliva, gastric and intestinal juices, blood, lymph
3. Water removes metabolites from the body
4. Water performs a mechanical function
5. Water performs a thermoregulatory function
6. Water performs a transport function
The water content of the newborn is 70% of body weight.
Extracellular water-40% Intracellular water-30%
In adults, the water content is less than 60% of body weight.
Extracellular water-20% Intracellular water-40%
Pathology of water-salt metabolism is associated with a violation of intracellular water
metabolism.
Reducing or increasing it by 10% is dangerous for cells, by 20% - deadly, cells die.

Changes in the water balance in the body manifests in the form of:
I. Negative water balance (hypovolemia, dehydration).
II. Positive water balance (fluid excess)
Negative water balance
Dehydration, hypovolemia.
Basic forms:
1. Hyperosmolar hypovolemia
2. Isoosmolar hypovolemia
3. Hypoosmolar hypovolemia

Hyperosmolar hypovolemia.
Hyperosmolar hypovolemia occurs when limiting the flow of water into the body or its
excessive loss. In this case, there is an accumulation of salts in the intercellular space.
This occurs in the case of an extremely strong and prolonged perspiration, during
prolonged hyperventilation, with insufficient development of ADH (diabetes insipidus).
The general mechanism of ADH deficiency as a result tumors, neuroinfections, traumatic
brain injury, occurs when disturbed hormone production in the supraoptic nucleus of the
hypothalamus. A large amount of low-density water is excreted in the urine.
The peripheral mechanism is associated with reduced reactivity of renal epithelial receptors
to ADH.
In this cases, a decrease in the volume of circulating fluid is accompanied by an increase
in osmotic blood pressure. As a result, water leaves the cells of organs and tissues, i.e. there is
cellular dehydration, which leads to a violation of the vital organs function. The cells increased
protein breakdown, in the blood accumulates ammonia and other toxic products of metabolic
disorders. They affect the cells of the Central nervous system, can cause the development of a
comatose state. Dehydration of the cells of the CNS creates a sense of thirst.

Isoosmolar hypovolemia.
Main causes:
1) loss of fluid through the stomach (gastric exsicosis), Gastric exsicosis occurs when
vomiting. There is a loss of water and salts. A decrease in the content of extracellular and
intracellular fluid.
 2) loss of fluid through the intestine (enteric exsicosis), Enteral exicosis is associated with
the loss of water and sodium through the intestine (cholera, dysentery). Normally, the intestinal
lumen receives up to 8 liters of fluid, but it's reabsorbed. With enteral exsicosis, reabsorption
processes are disrupted, increased intestinal motility, which causes loss of water and salts.
3) loss of fluid during perspiration. Sweating: a person can lose water with salts up to 1.5
liters per hour when overheated, in countries with hot climates.
4) polyuria
5) acute posthemorrhagic anemia.
Dehydration leads to a decrease in the volume of circulating fluid, an increase in
hematocrit and blood viscosity, a drop in the value of blood pressure, a dysfunction in the
microcirculation, tissue hypoxia and a dysfunction of cellular metabolism. First of all, the cells
of the Central nervous system suffer. Their damage is manifested by confusion, hallucinations,
the development of a comatose state. When dehydration reduces renal blood flow, develop of
oliguria and anuria.
Compensation of violations
1.The decrease in the volume of circulating fluid  2.reduction of renal blood flow 
3.enhanced release of renin  4.accumulation of angiotensin II  5 in the blood increased
release of aldosterone 6. increase reabsorption of Na+, the increase in osmotic blood pressure
 7.the release of ADH by the neurohypophysis  water retention in the body.

Hyposmolar hypovolemia
This form of dehydration is observed with indomitable vomiting, with gastrointestinal
fistulas, intestinal obstruction; with the intestinal form of acute radiation sickness,
mineralocorticoid insufficiency that occurs in infectious processes, intoxication. In all these
cases, there is a decrease in the blood water content, but even more – the concentration of Na+
and CI–.
Reduction of osmotic blood pressure leads to the transition of water from the blood to the
cells. Especially dangerous is the accumulation of water in the cells of the Central nervous
system and brain edema, which can increase vomiting, forming a vicious circle. The feeling of
thirst is absent, because in the cells of the Central nervous system increases the water content.
Positive water balance
I. Generalized (total) hypervolemia.
II. II. Regional (local) hypervolemia.
Generalized hypervolemia is characterized by increasing of water the fact that, the amount of
water increases in all tissues and organs, with different concentrations of osmotic substances,
primarily sodium,
Normally, the salt content in the body is 280-320 mosm / liter.

Distinguish:
1. Hyperosmolar hypervolemia
2. Isoosmolar hypervolemia
3. Hypoosmolar hypervolemia.

Hyperosmolar hypervolemia
develops with transfusion of hypertonic solutions, with the use of sea water.
The increase in the osmotic pressure of the blood leads to dehydration of the cells, and the
flow of fluid into the bloodstream, which exacerbates hypervolemia. Dehydration of cells is
accompanied by a dysfunction of their metabolic processes, appear signs of toxic brain damage.
This condition is characterized by a painful feeling of thirst, due to dehydration of CNS cells.
In this situation, the mechanisms of regulation of sodium and water homeostasis are
ineffective, because the excitation of volumoreceptors of the right atrium leads to increased
 production of aldosterone and retention of Na+. High osmotic blood pressure increases ADH
production, which increases water retention in the body.
Isoosmolar hypervolemia.
Increases intercellular and intracellular water. The plasma osmolarity is approximately 300
mosm / liter.
Causes:
1) transfusion of isoosmolar solutions.
2) alimentary form. This form occurs when excessive consumption of carbohydrates. One
carbohydrate molecule binds 3 water molecules. Often this form is observed in children.
Children loose, pasty; disturbed cellular metabolism.
3)excess of fatty acids and cholesterol in the body. They can form with the water, complexes
"Water+fatty acid", "Water"cholesterol.
Hypoosmolar hypervolemia.
Concentration of osmolar substances in the intercellular space below 270 mOsm / liter.
Hyposmolar hypervolemia occurs in
- massive transfusions of hypotonic solutions,
- if excessive intake of fluid having a low osmotic pressure (water, juices, etc.),
- - if unjustified introduction of large amounts of hypotonic blood and plasma substitutes for
patients with blood loss
- - the consumption of large quantities of water by persons with mental disorders,
- - in violation of renal excretory function in the case of development of acute renal failure etc.
In the development of hypoosmolar hypervolemia plays the role of antidiuretic hormone
(ADH). Hypersecretion of ADH, increases water reabsorption in the renal tubules. Water
accumulates in the intercellular space, and the osmolarity of the interstitial fluid decreases. But
the content of salts in the cell is higher, than in the extracellular space, and liquid comes from
the intercellular space to the cell. Intracellular hypervolemia develops. Swelling of cells causes a
violation of all functions of systems and organs. There is a decrease in the activity of enzymes,
hypoxia develops, metabolism is disturbed. Develops swelling of the brain, the phenomenon of
auto-intoxication. All these disorders can be characterized as a syndrome of water poisoning.
Сorrection of water-salt disorders
First of all, it should be remembered that in case of detection of hypo – or hypervolemia in the
patient, it is necessary to determine the concentration of Na+ ions in the blood (plasma
osmolarity).
If hypovolemia:
isoosmolar hypovolemia – introduced isotonic solution;
hyperosmolar - hypovolemia 5% glucose solution;
Hypoosmolar hypovolemia –hypertonic solutions.
If hypervolemia:
Hypoosmola hypervolemia – initially injected hypertonic solution, then the osmotic diuretics –
mannitol, that prevent the development of cerebral edema;
hyperosmolar hypervolemia – diuretics, aldosterone antagonists (aldactone, lasix).
Regional hypervolemia
Regional hypervolemia develops when there is an accumulation of fluid in the intercellular
space. Regional hypervolemia refers to isoosmolar hypervolemia and is characterized by the
development of edema.
Edema is a typical pathological process characterized by a regional increase of water content in
the intercellular space as a result of violations of General (neurohormonal) and local mechanisms
of regulation of water-salt metabolism in the body.
The main types of edema
1. Heart edema (in case of heart failure)
2. Renal edema (nephritic and nephrotic)
3. Allergic edema
 4. Inflammatory edema
5. Neurogenic edema (in neuroses, hysteria-swelling of the larynx, urticaria)
6. Endocrine edema (with myxedema)
7. Toxic edema
8. cachexic edema (fasting , protein deficiency).
If edematous fluid accumulates in the cavities, hydrocele develops. An example of dropsy
is the accumulation of fluid in the abdomen and develops ascites. With the accumulation of fluid
in the subcutaneous fat develops anasarca.
Mechanisms of edema development.
Distinguish:
1. General (neurohormonal) mechanisms
2. Local mechanisms (Starling factors).
General mechanisms of edema development
The accumulation of water in the body occurs by the mechanism of pathological
osmoregulatory reflex. It includes adrenal and hypothalamic-pituitary mechanisms.
Aldosterone retains sodium ions. Increasing the concentration of sodium ions causes
irritation of osmoreceptors. The hypothalamus stimulates the production of ADH. Antidiuretic
hormone increases water reabsorption in the proximal tubules. There is a delay of water in the
body and swelling develops.
Adrenal and hypothalamic-pituitary mechanisms are controlled by the Na-uretic hormone.
When changing (reducing) intracardiac blood volume, which occurs in heart failure, reduced the
activity of sodium-uretic hormone. This leads to hypersecretion of ADH and aldosterone.
Aldosterone delays sodium ions, ADH stimulates reabsorption of water in the renal tubules,
which leads to water retention in the intercellular space and the development of edema
Local mechanisms of edema development.
1. Hydrodynamic factor
2. Disturbance of lymph circulation
3. Osmotic factor
4. Oncotic factor
5. Increased permeability of the vascular wall
6. Hydrophilicity of colloids
7. Reduced tissue backpressure

1.The hydrodynamic factor.

At the arterial end of the capillary, liquid enters the intercellular space under the influence
of effective filtration pressure equal to 14 mm Hg.
At the venous end of the capillary, the reabsorption pressure is -6 mm Hg. Hg, and the fluid
returns to the vascular bed.
With heart failure, venous pressure increases and part of the transudate does not return to the
vascular bed, but remains in the intercellular space. This mechanism plays a role in the
development of cardiac edema, as well as thrombosis, in pregnant women. With left ventricular
failure, there is a stagnation of blood in the small circle of blood circulation, pulmonary edema
develops.
2.Disturbance of lymph circulation.
Part of the intercellular fluid enters the lymphatic system ("discharge system"). Disturbance
of lymphatic drainage with the obstruction of lymphatic vessels by filarial causes an increase of
pressure in the lymphatic system and leads to the development of edema. This mechanism plays
a role in the development of elephantiasis. Disturbance of lymph flow occurs when the pressure
in the upper Vena cava is high with heart failure.
3.Osmotic factor.
 Development of edema in this case, due to the increase in the content of sodium ions in the
body as a result of secondary hyperaldosteronism, administration of hypertonic solutions, renal
pathology.
4.Oncotic factor.
Oncotic pressure in the blood is 22 mm Hg. If it is reduced, reabsorption is reduced. When
hypoproteinemia occurs, water is retained in the intercellular space. This mechanism plays a role
in the development of nephrotic and cachectic (hungry) edema.
5.Vascular wall permeability.
Increased permeability of the vascular wall occurs with excessive release of biological
active substances (histamine, bradykinin). This mechanism is a trigger in the development of
inflammatory and allergic edema. After exposure of toxic substances increases the permeability
of the vascular wall, and develop toxic edema.
6.Hydrophilicity of colloids.
Colloids are able to bind water, results in increases of tissues hydrophilicity. Acidosis,
myxedema. This mechanism plays a role in the development of endocrine edema.
7.The back-pressure of the tissues.
The development of edema occurs with a decrease in tissue backpressure. Low back-
pressure have: lung tissue, brain (with open craniocerebral trauma), subcutaneous fat. In these
tissues, swelling develops easily.
The spread of edema leads to the development of «edema disease».
Depending on the etiological factors distinguish the following puffiness (edema):
Cardiac edema occurs in heart failure, when cardiac muscle reserve capacity decreases.
The weakening of the force of heart contractions leads to a decrease in the minute volume of
blood (cardiac output), four mechanisms are activated.
First, the intensity of blood flow in the kidneys decreases, as a result of which the cells of
the juxtaglomerular apparatus begin to produce an increased amount of renin. Renin activates
secretion of aldosterone from adrenal glands, which, leads to increased reabsorption of sodium in
the renal tubules.
Secondly, a decrease in cardiac output leads to the excitation of the volumereceptors of
large blood vessels, resulting in a reflex narrowing of the renal arteries, increasing reabsorption
of sodium. This leads to the appearance of extracellular hyperosmia, as a result of which
osmoreceptors of tissues are excited and the secretion of ADH is increased reflexively, which
increases the reabsorption of water in the kidneys, which contributes to its retain in the body and
the development of edema.
Thirdly, as a result of a decrease in the minute volume of blood, circulatory hypoxia
occurs, and the permeability of the capillary walls increases, and the blood plasma begins to flow
into the tissue, which increases edema.
Fourth, venous pressure increases, that is, venous hyperemia develops. The outflow of
lymph from the tissues is disturbed, the filtration of water from the vessels is enhanced, and a
stagnation of blood develops in the liver. In the "stagnant" liver, the synthesis of albumin is
reduced, as a result of which hypoproteinemia develops. Water from the vessels begins to be
filtered in the tissue. Thus, this mechanism, leading to impaired tissue lymphatic drainage,
increased filtration of water in the tissue due to increased venous pressure and causes a decrease
in the protein synthesis function of the liver, and cause a further increase in edema.
Osmotic, membrane, hydrodynamic, lymphatic and oncotic factors play a role in the
development of cardiac edema.
Nephrotic edema. Nephrosis is a kidney disease associated with destruction of the renal
parenchyma (for example, with sublimate poisoning, anaphylactic shock, kidney damage after
blood transfusion, metabolic disorders, etc.).
With nephrosis, the body loses a large amount of protein in the urine. Proteinuria causes
hypoproteinemia. As a result, the filtration of water from the blood vessels into the tissue
increases leads to hypovolemia. Reduced blood flow in the kidneys activates the renin-
aldosterone mechanism, Sodium is retained in the body, ADH secretion and water reabsorption
increase. Oncotic and osmotic mechanisms are involved in the pathogenesis of nephrotic edema.
In allergic and inflammatory lesions of the nephron glomeruli, compression of the renal
vessels occurs by inflammatory edema. Impaired blood supply to the kidneys causes a decrease
in the volume of blood circulating in them, the cells of the juxtaglomerular apparatus are irritated
and the secretion of renin increases. Renin stimulates the adrenal glands, which begin actively to
secrete aldosterone. This leads to a retention in the body's sodium, irritation of the
osmoreceptors of the tissues, as a result of which, the secretion of ADH increases. Water
reabsorption of the renal tubules increases, and water begins to accumulate in the tissues.
Nephritic edema occurs in autoimmune diseases of the kidneys with a predominant diffuse
lesion of the glomerular apparatus.
Circulatory disorders in the cortical layer of the kidneys cause an increase in renin
secretion by juxtaglomerular cells, which in turn activates the renin – angiotensin II –
aldosterone – ADH system. This leads to a retention in the body of Na + and water.
 Diffuse glomerulonephritis is characterized by damage to the microvascular membranes
not only of the renal glomeruli, but also of other organs and tissues. As a result, their
permeability increases and edema spreads. First of all, nephritic edema occurs in the retina, in
the area of the eyelids, in the soft tissues of the face, neck, and then the body.
In addition, during glomerulonephritis, an extra amount of protein enters the glomeruli
ultrafiltrate, which cannot be completely reabsorbed in the renal tubules. As a result, proteinuria
develops, oncotic pressure of the blood decreases, which also contributes to the appearance of
edema.
Allergic edema. In Allergy, a large amount of histamine is released, it causes the expansion of
blood vessels and an increase in the permeability of their walls. The liquid part of the blood
begins to intensively enter the tissue. The basis of allergic edema is membrane factor.
Inflammatory edema. During inflammation, venous hyperemia develops. The hydrostatic
pressure in the vessel rises. The release of biologically active substances increases the
permeability of the vascular wall. Lysosomal enzymes destroy proteins, fats and carbohydrates
of surrounding tissues. Increases hydrophilia of the surrounding tissue The liquid part of the
blood goes to the tissues.
The edema, that occurred, compress the lymphatic vessels and disrupts the lymph flow.
In the pathogenesis of inflammatory edema, hydrodynamic, membrane, osmotic, oncotic and
lymphatic factors play a role.
Hungry (cachexic) edema. It is based on the reduction of oncotic blood pressure (below 5%),
compared with oncotic pressure in the tissues. Such edema can develop during fasting, when the
body begins the breakdown and utilization of own proteins, in the first place - plasma proteins.
As a result, oncotic pressure in the blood drops, and water begins to move toward a higher level
of oncotic pressure — in the tissue. A similar situation arises in hypoproteinemic states of
another etiology, in particular, in cancer cachexia (exhaustion).
Sometimes this type of edema develops with a normal protein content in the blood, but with
severe dysproteinemia, when the albumin-globulin ratio is sharply reduced (normally 2:1), i.e.,
the albumin content is reduced.
Lymphogenic edema is caused by a violation of the outflow of lymph through the
lymphatic vessels, which leads to the accumulation of fluid in the tissues containing a large
amount of protein.
The reasons for the difficulty of lymph outflow may be:
- congenital hypoplasia of lymphatic vessels,
- compression of their by scars (for example, after removal of lymph nodes with radical
mastectomy),
- a growing tumor or metastases.
After some time, in edematous fluid containing protein, connective tissue begins to
actively grow with a possible deformation of the organ – develops of so-called elephantiasis.
 Membranogenic edema due to increased permeability of the vascular wall. Causes:
toxins, poisons of snakes and insects, some bacterial toxins, combat toxic substances, hypoxia
and acidosis, fever, biologically active substances – histamine, bradykinin, serotonin (for
example, in inflammation, allergies, etc.).
Increased permeability of the vascular wall leads to the release into the intercellular space
of a large number of albumins, that bind and retain liquid.
These edemas are local and do not affect the water balance in the whole organism. For the
treatment of such edema using anti-inflammatory, anti-allergic drugs.
Hepatic edema is associated with damage to the liver cells in hepatitis and cirrhosis of the
liver. The main role belongs to the following mechanisms:
- damaged hepatocytes do not synthesize a sufficient amount of albumin, hypoproteinemia
develops and fluid passes into the tissue;
- in case of liver cirrhosis, the connective tissue is actively develop, it compresses the blood
vessels, this leads to portal stagnation, the outflow of blood from the abdominal organs is
hampered, which is accompanied by the development of ascites;
- a decrease in total blood volume, due to a delay of blood by the liver leads to
1) a decrease in the activity of the volumereceptors of the left atrium and an increase in the secretion
of ADH,
2) activation of the volumereceptors of the right atrium and an increase in aldosterone secretion;
Liver with impaired blood flow (stagnant) badly inactivates hormones, including
aldosterone and ADH, which contribute to the retention of salts and water in the body.
The main principles of edema therapy are:
- elimination of the cause of edema, if possible;
- appointment of aldosterone antagonists;
- appointment of diuretics (furosemide, etc.);
- limitation of water and salt intake;
- the impact on the links of pathogenesis, specific to a particular type of edema.

Alterations in Acid-Base Balance

The terms acidosis and alkalosis describe the clinical conditions that arise as a result of
changes in dissolved CO2 and HCO3- concentrations.
There are four types of acid-base disorders: metabolic acidosis, respiratory acidosis,
metabolic alkalosis, respiratory alkalosis.
A decrease in pH caused by a decrease in bicarbonate is called acidosis, and an elevated
pH caused by increased bicarbonate levels is called alkalosis.

Metabolic Acidosis
Metabolic acidosis involves a primary deficit in base bicarbonate along with a decrease in
plasma pH.,
Causes. Metabolic acidosis can be caused by one of four mechanisms: (1) increased
production of nonvolatile metabolic acids, (2) decreased acid secretion by the kidney, (3)
excessive loss of bicarbonate, or (4) an increase in chloride.
Acute lactic acidosis is one of the most common types of metabolic acidosis. Lactic
acidosis develops when there is excess production of lactic acid or diminished lactic acid
removal from the blood. Most cases of lactic acidosis are caused by inadequate oxygen delivery,
as in shock or cardiac arrest. Neoplasms may produce local increases in tissue metabolism and
lactate production.
Ketoacids produced in the liver from fatty acids. The most common cause of ketoacidosis
is uncontrolled diabetes mellitus, in which an insulin deficiency leads to the release of fatty acids
from adipose cells with subsequent production of excess ketoacids. Ketoacidosis may also
develop as the result of fasting or food deprivation, following prolonged alcohol ingestion, and
vomiting that results in using fatty acids as an energy source.
 Kidney failure is the most common cause of chronic metabolic acidosis. The kidneys
normally conserve HCO3- and secrete H + ions into the urine. In renal failure is retention of
nitrogenous wastes and metabolic acids and loss of bicarbonate rich body fluids. Excessive
losses of HCO3 - ions occur with severe diarrhea; small bowel, pancreatic, or biliary fistula
drainage; ileostomy drainage; and intestinal suction.
Hyperchloremic acidosis occurs when serum Cl - ion levels are increased. Because Cl - and
HCO3 are anions, the serum HCO3 -ion concentration decreases when there is an increase in Cl -
-

ions. Hyperchloremic acidosis can occur as the result of abnormal absorption of chloride by the
kidneys or as a result of treatment with chloride-containing medications. The administration of
intravenous sodium chloride or parenteral hyperalimentation solutions that contain an amino
acid-chloride combination can cause acidosis.
Manifestations
Acidosis typically produces a compensatory increase in respiratory rate with a decrease in
CO2 and H2CO3-.
The manifestations of metabolic acidosis fall into three categories: (1) signs and symptoms
of the disorder causing the acidosis, (2) alterations in function resulting from the decreased pH,
and (3) changes in body function related to recruitment of compensatory mechanisms.
With diabetic ketoacidosis there is an increase in blood and urine glucose and a
characteristic smell of ketones to the breath. In metabolic acidosis that accompanies renal failure,
blood urea nitrogen levels are elevated, and tests of renal function yield abnormal results.
A person with metabolic acidosis often reports weakness, fatigue, general malaise, and a
dull headache, anorexia, nausea, vomiting, and abdominal pain. The skin is warm and flushed,
and there is a decrease in tissue turgor.
The respiratory system compensates for a decrease in pH by increasing ventilation to
reduce PCO2.
Acidosis directly depresses membrane excitability, and decrease neural activity. If acidosis
progresses stupor and coma develops.
When the pH falls to 7.0, cardiac contractility and cardiac output decrease, the heart
becomes less responsive to catecholamines and dysrhythmias can develop.
The respiratory system compensates for a decrease in pH by increasing ventilation to
reduce PCO2.
Chronic acidemia can lead to skeletal problems and symptoms such as anorexia, weight
loss, muscle weakness, and listlessness.
Metabolic Alkalosis
Metabolic alkalosis involves a primary excess of base bicarbonate along with an increased
plasma pH. It can be caused by a gain in HCO3 - or loss of H+ ions. The body compensates for the
increase in pH by decreasing the respiratory rate as a means of increasing PCO 2 and H2 CO3
levels.
Causes. Metabolic alkalosis can occur because of (1) ingestion or administration of excess
NaHCO3 or other alkali, (2) excess H +, Cl-, and K+ loss, or (3) ECF volume contraction.
Excessive alkali ingestion, as in the use of bicarbonate containing antacids or sodium
bicarbonate administration during cardiopulmonary resuscitation, can cause metabolic alkalosis.
Vomiting, removal of gastric secretion through use of nasogastric suction, and low serum
potassium levels resulting from hyperaldosteronism or diuretic therapy are the most common
causes of metabolic alkalosis in hospitalized patients. The binge-purge syndrome, or self-induced
vomiting, is also associated with metabolic alkalosis.
The continued loss of H+ and Cl- ions from the stomach because of vomiting or gastric
suction stimulates continued production of gastric acid and thus the addition of more bicarbonate
into the blood.
Metabolic alkalosis can also result from the use of diuretics and other conditions that cause
excessive loss of potassium in the urine. Hypokalemia produces a compensatory increase in K +
reabsorption and H +secretion by the kidney, along with a simultaneous increase in HCO 3-
reabsorption. The adrenocorticosteroid hormone, aldosterone, increases H+ion secretion as it
increases Na + and HCO3- ions reabsorption.
Manifestations. Persons with metabolic alkalosis sometimes have neurologic signs (e.g.,
hyperexcitability), mental confusion, hyperactive reflexes, tetany, and carpopedal spasm. Severe
metabolic alkalosis also leads to respiratory failure, dysrhythmias, seizures, and coma.

Respiratory acidosis
Respiratory acidosis involves an increase in PCO2 and H2 CO3 along with a decrease in pH.
Causes. Respiratory acidosis occurs in conditions that impair alveolar ventilation and cause
an increase in PCO2. It can occur as an acute or chronic disorder. Because renal compensatory
mechanisms take time to exert their effects, blood pH tends to drop sharply in persons with acute
respiratory acidosis.
Acute respiratory acidosis can be caused by impaired function of the respiratory center in
the medulla (as in narcotic overdose), lung disease, chest injury, weakness of the respiratory
muscles, or airway obstruction. Acute respiratory acidosis can also result from breathing air with
a high CO2 content.
Chronic respiratory acidosis is associated with chronic lung diseases such as chronic
bronchitis and emphysema.
Manifestations. Sudden elevations in arterial CO2 can cause headache, blurred vision, an
increase in heart rate and blood pressure, warm and flushed skin, irritability, muscle twitching,
and psychological disturbances. Carbon dioxide crosses the blood-brain barrier, changes the pH
of brain fluids. Elevated levels of CO2 produce vasodilation of cerebral blood vessels. Paralysis
of extremities may occur, and there may be respiratory depression.

Respiratory alkalosis
Respiratory alkalosis involves a decrease in PCO2 and a primary deficit in carbonic acid
(H2 CO3) along with an increase in pH.
Causes. One of the most common causes of respiratory alkalosis is the hyperventilation
syndrome. Other causes of hyperventilation are fever, hypoxemia, early salicylate toxicity, and
encephalitis. Hyperventilation can also occur during anesthesia or with use of mechanical
ventilatory devices.
Manifestations The signs and symptoms of respiratory alkalosis are mainly associated with
hyperexcitability of the nervous system and a decrease in cerebral blood flow. Alkalosis
increases neuromuscular excitability. The person often experiences light-headedness, dizziness,
tingling, and numbness of the fingers and toes. These manifestations may be accompanied by
sweating, palpitations, panic, air hunger, and dyspnea. Tetany and convulsions may occur.
CONTROL QUESTIONS
1. Functions of water in the body.
2. Hyperosmolar hypovolemia.
3. Isoosmolar hypovolemia. Compensation of violations.
4. Hyposmolar hypovolemia.
5. Hyperosmolar hypervolemia
6. Isoosmolar hypervolemia.
7. Hypoosmolar hypervolemia.
8. Сorrection of water-salt disorders.
9. The main types of edema .
10. General mechanisms of edema development.
11. Local mechanisms of edema development (7).
12. Cardiac edema.
13. Nephrotic edema.
14. Nephritic edema.
15. Allergic edema.
 16. Inflammatory edema.
17. Hungry (cachexic) edema.
18. Lymphogenic edema.
19. Membranogenic edema.
20. Hepatic edema.
21. The main principles of edema therapy.
22. What does the metabolic acidosis mean? Describe the causes of metabolic acidosis.
23. Describe the manifestations of metabolic acidosis.
24. What does the metabolic alkalosis mean? Describe the causes of metabolic alkalosis.
25. What are the manifestations of metabolic alkalosis?
26. What does the respiratory alkalosis mean? Describe the causes and manifestations of
respiratory alkalosis.
27. What does the respiratory acidosis mean? Describe the causes and manifestations of
respiratory acidosis.