Na & Water Flashcards

1
Q

In a 70kg man, the total body water (TBW) is about _____ and contributes about 60% of the total body weight.
The body’s water is distributed between two compartments;
- extracellular fluid (ECF)
- intracellular fluid (ICF)

A

42L

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2
Q

Of the ECF, approximately ___ is interstitial fluid and ____ is blood plasma

A

80%
20%

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3
Q

About ___ of water is lost daily in sweat and expired air, and less than _____ of sodium a day is lost in
sweat.

A

1 L
30 mmol

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4
Q

The volume of sweat is primarily controlled by skin temperature, although ___ and ____ have some effect on its composition. Water loss in expired air depends on the respiratory rate.

A

ADH
aldosterone

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5
Q

Antidiuretic hormone is a polypeptide with a half-life
of about ____ min that is synthesized in the _______ is secreted
from the posterior pituitary gland

A

20 min
supraoptic and paraventricular nuclei of the hypothalamus and, after transport down the pituitary stalk,

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6
Q

By how much can an increase in extracellular osmolality of 2% affect ADH output?

A

A: It can quadruple ADH output

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7
Q

What happens to ADH secretion if there is an equivalent fall in extracellular osmolality?

A

A: It almost completely inhibits ADH secretion.

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8
Q

How do stretch receptors in the left atrium affect ADH secretion?
.

A

A: They stimulate ADH release in response to low intravascular pressure of severe hypovolemia

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9
Q

If the concentration of solutes outside the cells increases by just 2%, the amount of ADH released by the body increases four times (quadruples).

Conversely, if the concentration of solutes outside the cells decreases by the same amount (2%), ADH secretion almost completely stops.

A
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10
Q

If the concentration of solutes outside the cells (extracellular osmolality) decreases, ADH secretion is inhibited.
This means the body will stop releasing as much ADH when the fluid outside the cells becomes less concentrated, regardless of the cause.

A
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11
Q

Receptors and ADH Secretion:

Stretch receptors in the left atrium of the heart and baroreceptors in the aortic arch and carotid sinus are sensors that detect changes in blood pressure and volume.
When these receptors detect low blood pressure or low blood volume (conditions known as severe hypovolemia), they stimulate the release of ADH to help retain water and increase blood volume.

A
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12
Q

ADH Secretion and High Osmolality:

ADH (antidiuretic hormone) is released when the body detects high extracellular osmolality.
High extracellular osmolality means that there are a lot of dissolved substances (like salt) outside the cells, which can draw water out of the cells and cause them to dehydrate.
When ADH is released in response to this, it is appropriate because ADH helps the body retain water, preventing cells from dehydrating.
ADH Secretion and Low Circulating Volume:

Sometimes, ADH is released in response to a low circulating blood volume (the amount of blood moving through the body).
If the ADH release happens only because the blood volume is low and not because of the high osmolality, this can be considered inappropriate.
Low circulating volume alone does not necessarily mean the body needs more water, so responding with ADH (which retains water) is not the right response in terms of osmolality.

A
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13
Q

Inefficiency in Correcting Hypovolaemia: Hypovolaemia means having a low blood volume. If the body tries to fix this low blood volume by retaining water (due to ADH), it doesn’t efficiently solve the problem. This is because the retained water spreads out into all body compartments, not just the blood vessels where it’s needed to correct the low blood volume.

A
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14
Q

Aldosterone stimulates
sodium reabsorption from the lumen of the distal
renal tubule in exchange for either potassium or
hydrogen ions

A
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15
Q

Effects of Aldosterone:

When aldosterone levels are high and the kidney tubules are functioning normally, the sodium concentration in urine is low.
This means that the body is retaining sodium

A
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16
Q

List the mechanism that CONTROL OF WATER AND SODIUM BALANCE

A

Antidiuretic hormone (arginine vasopressin)
The renin–angiotensin system
Aldosterone
Natriuretic peptides

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17
Q

Where are Natriuretic peptides secreted from and it’s function

A

A peptide hormone (or hormones) secreted from
the right atrial or ventricular wall in response to the
stimulation of stretch receptors may cause high sodium
excretion (natriuresis) by increasing the GFR and by
inhibiting renin and aldosterone secretion

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18
Q

These compartments are:
● intracellular, in which potassium is the predominant
cation,
● extracellular, in which sodium is the predominant
cation, and which can be subdivided into:
– interstitial space, with very low protein
concentration, and
– intravascular (plasma) space, with a relatively
high protein concentration.

A
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19
Q

Magnesium and phosphate ions are predominantly ____, and chloride ions ______.

A

intracellular

Extracellular

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20
Q

Distribution of Electrolytes Between Plasma and Interstitial Fluid
Protein Concentration:

Plasma (the liquid part of blood) has a relatively high concentration of proteins.

Interstitial fluid (fluid between cells) has a very low concentration of proteins.

Osmotic Effect and Gibbs–Donnan Effect:

The proteins in the plasma create an osmotic effect, which attracts water.

To balance this effect, the interstitial fluid has slightly higher concentrations of electrolytes (like sodium and chloride ions). This is known as the Gibbs–Donnan effect.

The difference in electrolyte concentration between plasma and interstitial fluid is very small.

Electrolyte Concentrations:

Because the difference is minimal, we can generally assume that the concentration of electrolytes in plasma represents the concentration in the extracellular fluid (ECF) as a whole.

A
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21
Q

Water Distribution Across Membranes:

Water moves across cell membranes based on two factors which are?

A

Hydrostatic Pressure: The pressure exerted by the fluid itself, pushing water out of the blood vessels into the interstitial fluid.
Osmotic Pressure: The pressure due to the concentration of solutes (like proteins and electrolytes) that draws water into the blood vessels from the interstitial fluid.

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22
Q

Break down the fluid distribution in the body

A

Intracellular fl uid compartment
24L
Extracellular fl uid compartment 18L
Interstitial
13L
ntravascular (blood volume) 5L

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23
Q

In healthy individuals, the concentration of sodium and its related anions (negatively charged ions) are key factors influencing the secretion of ADH (Antidiuretic Hormone).
When sodium levels are high, ADH is released to help retain water, diluting the sodium concentration.

A
24
Q

What’s the Response to Increased Extracellular Osmolality

A

When extracellular osmolality rises, two main responses occur:

ADH release is stimulated, reducing water loss by promoting water reabsorption in the kidneys.

Thirst is stimulated, leading to increased water intake.

These actions help dilute the high osmolality, restoring osmotic balance and proper cellular hydration

25
Q

What’s the Relation Between Sodium and Water Homeostasis

A

ADH (Antidiuretic Hormone) and Sodium:

Role of ADH: ADH helps the kidneys reabsorb water back into the bloodstream, reducing the amount of water excreted in urine.

Sodium Influence: When sodium levels in the blood are high, ADH is released to retain more water. This dilution helps to bring sodium levels back down to normal.

Aldosterone and Plasma Volume:

Role of Aldosterone: Aldosterone signals the kidneys to reabsorb sodium and excrete potassium. Retaining sodium helps retain water, as water follows sodium.

Plasma Volume Influence: When blood volume (plasma volume) is low, aldosterone is released to increase sodium (and water) reabsorption, thereby increasing blood volume.

26
Q

SLIDES

A
27
Q

Major factors controlling Na balance

A

The major factors controlling sodium balance are renal blood flow and renin- angiotensin-aldosterone system.
Decreased renal blood flow will lead to the release of renin by the juxtaglomerular apparatus, renin converts circulating angiotensinogen produced by the liver to angiotensin I. Angiotensin I is converted by angiotensin converting enzyme(50% produced by the lungs) to angiotensin II. Angiotensin II serves a number of important action;
potent vasoconstrictor;this helps to maintain bloodpressure
stimulate cells of the zona glomerulosa synthesize and secrete aldosterone; aldosterone increases sodium and water reabsorption by the kidneys.
stimulates the thirst centre and so promotes oral intake.

28
Q

The initial clinical consequences of primary water disturbances depend on changes of extracellular volume and those of primary sodium disturbances depend on changes of extracellular osmolality.
The disorders of water and sodium will therefore be discussed under;

A

a) Volume disorders
b) Tonicity disorders

29
Q

What are theMajor causes of hypovolaemia

A

Extra-renal losses

1) haemorrhage

2) cutaneous losses – sweating , burns

3) gastrointestinal losses – vomiting, diarrhoea, fistulae, tube suction or drainage

Renal losses;

A) hormonal deficit;

1) pituitary diabetes insipidus

2) aldosterone insufficiency

3) addison’s disease

B) output losses

1) nephrogenic DI

2)diuretic diuresis

3) osmotic diuresis

4) chronic renal failure

30
Q

Major causes of hypervolaemia

A

A) Increased plasma sodium

1) massive intake – iatrogenic,excessive intake of beer

2)inadequate sodium excretion – renal failure, heart failure, aldosterone excess

B) increased red blood cell volume; excessive transfusion.

Principles of treatment

Primary cause of hypervolaemia may be treated

Dietary sodium restriction

Use of diuretics

31
Q

What are the types of hyppnatraemia

A

True Hyponatraemia: Actual low sodium levels due to different reasons.
Pseudohyponatraemia: Appears as low sodium but is due to other factors like high blood fats or sugars.

32
Q

Causes of true hyponatarmia

A

Hyponatremia with Hypovolemia (Low Blood Volume)

Extra-Renal Losses: These are losses of fluid and sodium from the body that do not involve the kidneys.
Examples: Vomiting, diarrhea, and excessive sweating. These conditions lead to a loss of both sodium and water, resulting in hypovolemia and hyponatremia.

Renal Losses: These are losses of sodium through the kidneys.
Examples: Use of diuretics (medications that increase urine production) and aldosterone deficiency (a hormone that helps regulate sodium and water balance).
Hyponatremia with Euvolemia (Normal Blood Volume)

Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH): This condition causes the body to retain water, diluting the sodium in the blood. SIADH can be triggered by various factors such as meningitis, lung disease, and malignant neoplasms.

Hypothyroidism: An underactive thyroid can impair the body’s ability to excrete free water, leading to dilutional hyponatremia.

Psychogenic Polydipsia: Excessive water intake, often due to psychiatric conditions, dilutes the sodium concentration in the blood.

Hyponatremia with Hypervolemia (High Blood Volume)

Oedematous States: Conditions that cause fluid retention and edema can lead to hyponatremia. Examples include congestive cardiac failure, nephrotic syndrome (a kidney disorder causing excessive protein loss in urine), and liver cirrhosis.

33
Q

Pseudohyponatraemia Causes

A

Hyponatremia with Isotonicity

Hyperlipidemia: High levels of lipids (fats) in the blood.
Hyperproteinemia: High levels of proteins in the blood.
Hyponatremia with Hypertonicity

Hyperglycemia: High blood sugar levels can cause a shift of water from inside the cells to the extracellular space, diluting the sodium concentration.
Mannitol Infusion: Mannitol is a medication used to reduce intracranial pressure. It can cause water to move out of cells, leading to dilutional hyponatremia.

34
Q

Treatments of hyponatraemia

A

Principles of Treatment
The treatment of hyponatremia depends on the underlying cause and the patient’s volume status.

Hyponatremia with Volume Depletion

Treatment: Volume repletion with normal saline (0.9% sodium chloride). This helps to restore the fluid and sodium balance in the body.
Hyponatremia with Volume Overload or SIADH

Treatment: Fluid restriction. Limiting fluid intake helps to concentrate the sodium in the blood.
Additional Measures: In patients with edematous states (like heart failure, nephrotic syndrome, or liver cirrhosis), diuretics can be helpful to remove excess fluid.
Severe Hyponatremia Affecting Mental Status

Treatment: Infusion of hypertonic saline (3% sodium chloride). This is a concentrated saline solution used to quickly increase the sodium levels in the blood.
Combination Therapy: Sometimes, hypertonic saline may be combined with diuretics to prevent fluid overload while correcting the sodium deficit.

35
Q

Hypertonicity, an increase in the effective osmolality of body fluids, is usually treated by administering water intravenously, often as 5% dextrose solution or dilute saline solutions. The choice depends on whether there is also a need to administer sodium ions.

How do you correct
Hypervolemia
Hypovolemia
& style of correcting hypertonicity

A

:

Intravenous Water: Administer water through IV as 5% dextrose or dilute saline.

Correct Hypovolaemia: Use IV isotonic saline to correct low blood volume and blood pressure.

Correct Hypervolaemia: Use diuretics to remove excess fluid while treating hypertonicity.

Slow Correction: Slowly correct hypertonicity to prevent brain swelling.

36
Q

Hypovolemia Treatment?

A

Hypovolemia Treatment: If the patient shows signs of hypovolemia (low blood volume), the initial treatment aims to correct hypotension (low blood pressure) by replenishing the plasma volume deficit. This is typically done with IV isotonic saline (normal saline solution), which helps restore the circulating volume without altering the sodium concentration significantly.

37
Q

Hypervolemia Treatment:?

A

If the patient shows signs of hypervolemia (excess blood volume), the condition is managed with diuretics to remove the excess fluid. Simultaneously, water replacement is used to treat hypertonicity, ensuring a balanced approach to correcting the fluid and electrolyte imbalance.

Correction Speed: It’s crucial to correct hypertonicity slowly to prevent cerebral edema, which is the swelling of the brain due to rapid changes in osmolality

38
Q

What’s Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

A

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

SIADH is a condition where there is excessive release of antidiuretic hormone (ADH), leading to water retention and hyponatremia (low sodium levels in the blood).

39
Q

Syndrome of Inappropriate Antidiuretic Hormone (SIADH) can occur due to reasons such as?

A

Intracranial Pathology: Conditions such as head injury, hemorrhage, meningitis, encephalitis, or brain tumors can directly stimulate hypothalamic ADH release.

Pulmonary Pathology: Conditions like pneumonia, tuberculosis, or assisted ventilation can cause volume receptors in the pulmonary vascular bed to falsely report a message of vascular depletion to the hypothalamus, prompting ADH release.

Ectopic ADH Production: Tumors, particularly bronchial carcinomas, can produce ADH ectopically.

Cortisol Deficiency: Cortisol and other adrenal hormones antagonize ADH. A deficiency in these hormones results in unopposed ADH action, promoting water retention.

Pain: Pain from trauma or surgery can stimulate ADH release.

Drugs: Various drugs, including antidepressants, narcotics, carbamazepine, sulfonylureas, oxytocin for labor induction, and vincristine for chemotherapy, can stimulate ADH release.

40
Q

What are the Findings in SIADH?

A

Hydration Status: Patients with SIADH are generally overhydrated but not overtly edematous. The retained water is shared between the extracellular fluid (ECF) and intracellular fluid (ICF). Eventually, ECF expansion is limited by the release of atrial natriuretic factor (ANF) from the cardiac atria, promoting saline diuresis.

Hyponatremia: The major problem is hyponatremia, leading to cerebral edema and a consequent depressed level of consciousness. The severity of cerebral edema correlates with the rapidity of hyponatremia onset.

Urine Characteristics: Urine is typically inappropriately concentrated despite low plasma osmolality, and its sodium concentration ([Na+]) is high in the face of hyponatremia, due to the effect of ANF.

41
Q

How can SIADH be managed?

A

Water Restriction: The primary treatment is restricting water intake, which can be sufficient in mild cases.

ADH Antagonism: If symptoms of water intoxication are present, ADH may be specifically antagonized by the drug demeclocycline.

Hypertonic Solutions: In more severe cases, intravenous hypertonic saline (5% NaCl) or mannitol can be administered to rapidly remove intracellular water and correct hyponatremia.

42
Q

What’s Conn’s Syndrome?

A

Primary Hyperaldosteronism is characterized by the autonomous secretion of aldosterone, usually due to an adrenal adenoma (a benign tumor in the adrenal gland). This condition leads to the excessive reabsorption of sodium (Na+) and water in the distal convoluted tubule of the kidney, coupled with the loss of potassium (K+) and hydrogen ions (H+)

43
Q

What are the features of Conn’s Syndrome?

A

Electrolyte Imbalance: Patients typically exhibit hypokalemic alkalosis (low potassium levels and elevated blood pH). Plasma sodium levels can be normal or slightly increased.

Hormonal Levels:

Plasma Renin: Appropriately suppressed due to feedback mechanisms.

Plasma Aldosterone: Elevated and unaffected by changes in posture, salt loading, or the administration of ACE inhibitors.

Clinical Presentation: Patients are usually hypertensive. However, due to the role of atrial natriuretic factor (ANF) in limiting extracellular fluid (ECF) volume expansion, edema is generally not present.

44
Q

How do you treat Conn’s Syndrome?

A

Treatment: The primary treatment is the surgical resection of the adrenal adenoma. It is crucial to exclude Conn’s syndrome as a cause of hypertension, especially in young hypertensive patients.

45
Q

Similar Conditions: Individuals exposed to excess non-aldosterone mineralocorticoids (e.g., from substances like liquorice or hormones like 11-deoxycorticosterone (11-DOC)) present with similar clinical and biochemical features. However, in these cases, plasma aldosterone levels are appropriately suppressed.

A
46
Q

What’s Secondary Hyperaldosteronism

A

Secondary Hyperaldosteronism refers to the excessive secretion of aldosterone in response to elevated renin levels. Unlike primary hyperaldosteronism, the basic issue here is the persistent and inappropriate secretion of renin

47
Q

What are the causes of Secondary Hyperaldosteronism

A

Renin-Secreting Tumor: Although rare, a tumor that secretes renin can cause secondary hyperaldosteronism.

Renal Artery Stenosis: A disturbance in the blood supply to one or both kidneys, such as narrowing (stenosis) of the renal artery, can lead to elevated renin secretion.

Fluid Shifts: An abnormal shift of fluid from the plasma into the interstitial space can lead to a condition where fluid leaks from the vascular bed into tissues. This results in depleted plasma volume, stimulating renin secretion. Despite the reduced plasma volume, the total ECF volume may be grossly expanded. This scenario is the most common cause of secondary hyperaldosteronism.

48
Q

DIABETES INSIPIDUS
Is an uncommon disorder that causes an imbalance of fluids in the body. This causes extreme thirst, and frequent urination
Four types;
Cental DI: lack of ADH (vasopressin)
Nephrogenic DI: failure of the kidneys to respond properly to ADH
Psychogenic DI: excessive fluid intake due to damage to the hypothalamic thirst centre, often occurs in those with psychiatric disorders or on certain medications
Gestational DI which occurs during pregnancy.

Diagnosis is often based on urine test, blood test and Fluid deprivation test.

Plasma: hyponatraemia and hypo-osmolality

Urinalysis: demostrates dilute urine with low specific gravity.

Low urine osmolarity

WATER DEPRIVATION TEST

This test is used in patients presenting with polyuria and low urine osmolality, in which the diagnosis of diabetes insipidus (either hypothalamic or nephrogenic) is being considered. Under medical supervision, patients are deprived of water, serial urines collected, and their osmolalities measured. When urine osmolality plateaus out, (i.e. there is no further increase in osmolality of sequential urine specimens), ADH is administered, and the osmolality of the next urine noted.

A
49
Q

What’s Diabetes Insipidus (DI)?

A

Diabetes Insipidus is an uncommon disorder characterized by an imbalance of fluids in the body, leading to extreme thirst and frequent urination

50
Q

What are the types of DI

A

Central Diabetes Insipidus: Caused by a lack of antidiuretic hormone (ADH), also known as vasopressin.

Nephrogenic Diabetes Insipidus: Occurs when the kidneys fail to respond properly to ADH.

Psychogenic (Primary Polydipsia): Resulting from excessive fluid intake due to damage to the hypothalamic thirst center, often seen in individuals with psychiatric disorders or those on certain medications.

Gestational Diabetes Insipidus: Occurs during pregnancy, often due to the destruction of ADH by an enzyme produced by the placenta.

51
Q

What tests can you use in diagnosing DI

A

Diagnosis

Diagnosis is typically based on a combination of urine tests, blood tests, and the fluid deprivation test.

Plasma Findings:

Hyponatremia: Low sodium levels in the blood.

Hypo-osmolality: Low plasma osmolality, indicating diluted blood.

Urinalysis Findings:

Dilute Urine: Low specific gravity.

Low Urine Osmolality: Indicates the inability to concentrate urine.

Water Deprivation Test

52
Q

How do you perform Water Deprivation Test and how it’s interpreted

A

Water Deprivation Test

The water deprivation test is used to diagnose diabetes insipidus in patients presenting with polyuria (excessive urination) and low urine osmolality. Here’s how it works:

Initial Deprivation: Under medical supervision, patients are deprived of water, and serial urine samples are collected to measure their osmolality.

Plateau Phase: When urine osmolality plateaus (no further increase in osmolality of sequential urine specimens), ADH is administered.

Post-ADH Administration: The osmolality of the subsequent urine sample is noted.

Interpretation:

Normal Subjects and Psychogenic Polydipsia: Urine osmolality rises progressively during water deprivation, typically reaching 700-800 mosmol/kg. Plasma sodium concentration and body weight show negligible changes.

Central Diabetes Insipidus (Neurogenic): After ADH administration, urine osmolality increases, indicating that the kidneys can respond to ADH.

Nephrogenic Diabetes Insipidus: After ADH administration, urine osmolality remains unchanged, indicating that the kidneys do not respond to ADH.

53
Q

Some electrolyte-containing fluids for intravenous infusion
1) Saline ;
‘Normal’(physiological 0.9%)- [Na+] = 154 mmol/L, [Cl-]=154 mmol/L
Twice ‘normal’(1.8%)- [Na+] = 308 mmol/L [Cl-]= 308 mmol/L
Half ‘normal’ (0.45%)- [Na+]= 77mmol/L [Cl-]= 77mmol/L
2) ‘Dextrose’ saline (5%, 0.45%)- [Na+]= 77mmol/L, [Cl-]= 77 mmol/L, glucose= 278 mmol/L
3)Sodium bicarbonate
1.4%- [Na+]= 167mmol/L, [HCO3-]=167mmol/L
8.4% - [Na+]= 1000mmol/L, [HCO3-]=1000mmol/L

A
54
Q

List the common Saline Solutions used in practice

A

Normal Saline
Twice Normal Saline
Half Normal Saline
Dextrose Saline
Sodium Bicarbonate Solutions
8.4% Sodium Bicarbonate
Complex Solutions
Ringer’s Solution
Hartmann’s Solution (Lactated Ringer’s)

55
Q

List the composition and the reason why of the common Saline Solutions used in practice

A

Saline Solutions

Normal Saline (0.9% NaCl)

Sodium (Na+): 154 mmol/L

Chloride (Cl-): 154 mmol/L

Why: Normal saline is called “0.9% NaCl” because it contains 9 grams of sodium chloride per liter of water. This concentration is isotonic with human blood, meaning it has the same salt concentration as cells and blood, making it suitable for fluid replacement and intravenous hydration without causing cells to shrink or swell.

Twice Normal Saline (1.8% NaCl)

Sodium (Na+): 308 mmol/L

Chloride (Cl-): 308 mmol/L

Why: This solution has double the concentration of NaCl compared to normal saline. It is hypertonic, meaning it has a higher salt concentration than blood. It’s used in specific medical situations where a higher salt concentration is needed to draw water out of cells or to treat hyponatremia (low sodium levels in the blood).

Half Normal Saline (0.45% NaCl)

Sodium (Na+): 77 mmol/L

Chloride (Cl-): 77 mmol/L

Why: This solution has half the salt concentration of normal saline. It is hypotonic, meaning it has a lower salt concentration than blood. It can be used when cells need to absorb water, such as in dehydration with high sodium levels.

  1. Dextrose Saline (5% Dextrose in 0.45% NaCl)

Sodium (Na+): 77 mmol/L

Chloride (Cl-): 77 mmol/L

Glucose: 278 mmol/L

Why: This solution combines the properties of dextrose and saline. The dextrose provides energy while the saline maintains hydration and electrolyte balance. It is used for patients who need both fluid and caloric supplementation.

  1. Sodium Bicarbonate Solutions

1.4% Sodium Bicarbonate

Sodium (Na+): 167 mmol/L

Bicarbonate (HCO3-): 167 mmol/L

Why: This solution is used to correct acidosis, a condition where there is too much acid in the body fluids. Bicarbonate acts as a buffer to neutralize excess acids.

8.4% Sodium Bicarbonate

Sodium (Na+): 1000 mmol/L

Bicarbonate (HCO3-): 1000 mmol/L

Why: This highly concentrated solution is used in emergency situations to quickly correct severe acidosis. Due to its high concentration, it must be administered carefully to avoid complications.

  1. Complex Solutions

Ringer’s Solution

Sodium (Na+): 147 mmol/L

Potassium (K+): 4.2 mmol/L

Chloride (Cl-): 156 mmol/L

Calcium (Ca++): 2.2 mmol/L

Why: Ringer’s solution contains multiple electrolytes that closely mimic the composition of body fluids. It is used for fluid replacement in patients with electrolyte imbalances or dehydration.

Hartmann’s Solution (Lactated Ringer’s)

Sodium (Na+): 131 mmol/L

Potassium (K+): 5.4 mmol/L

Chloride (Cl-): 112 mmol/L

Calcium (Ca++): 1.8 mmol/L

Bicarbonate (as lactate): 29 mmol/L

Why: This solution is similar to Ringer’s but also contains lactate, which is metabolized to bicarbonate in the liver, helping to correct metabolic acidosis. It is often used in surgery, trauma, or severe dehydration cases.