DISTURBANCES IN WATER,

ELECTROLYTE AND ACID-BASE

BALANCE

DR. NJAU.N.N.
 1. WATER
• Fluid and electrolyte levels in the body are kept
relatively constant by several homeostatic
mechanisms.

• Water is the most abundant constituent in the

body, comprising approximately 50% of body
weight in women and 60% in men.

• Total body water is divided into two compartments;

2/3 is in the intracellular (ICF) and 1/3 is in the
extracellular (ECF) compartments.
2
• The extracellular fluid comprises both interstitial fluid
(2/3 of the ECF) and intravascular fluid (1/3 of the ECF).

• Water moves freely across the membranes that separate

the compartments.

• To maintain a steady state, water intake must equal water

excretion.

• In healthy individuals fluid intake (2litres/day) occurs

through
- food intake, - fluid intake
- metabolism
3
• ECF: Extracellular Fluid
• ICF: Intracellular Fluid

4
• In sick patients fluid intake may also occur by iv
administration of drugs and fluids.

• In healthy individuals fluid losses occur through

- urine 1.5L/d
- sweating and lungs (1L/d)
- feces (200mls/d)
- skin

• In sick pts fluid losses can occur through diarrhoea,

vomiting, fever, diabetes insipidus, blood loss, burns, etc.

5
• In healthy individuals, volume homeostasis
is regulated by;

1. Antidiuretic hormone (ADH)/vassopressin

- ADH that is secreted by the pituitary
gland, stimulates thirst and reduces
renal excretion of water hence
reduced urine output.

6
2. Renin angiotensin aldosterone system (RAAS)
- Low blood volume leads to the release of renin
enzyme from the kidneys (at the juxtaglomerular
apparatus in the kidney nephrons).

- Renin converts angiotensinogen to angiotensin I.

-Angiotensin converting enzyme (ACE) (found in the

lungs) then converts angiotensin I to angiotensin II
(this conversion occurs in the liver)

7
Angiotensin II;
I. Directly causes blood vessels to constrict,
resulting in increased blood pressure. 

II. stimulates the secretion of the hormone

aldosterone from the adrenal cortex.
Aldosterone causes the distal convoluted
tubule of the kidney nephrons to increase the
reabsorption of sodium and water into the
blood. This increases the volume of fluid in the
body, which also increases blood pressure.

8
iii. Leads to the release of Anti diuretic hormone
(ADH)/vasopressin from the pituitary gland which
leads to the reabsorption of water at the
collecting tubules of the nephrons of the kidneys .
This leads to an increase in blood volume

iv. Leads to the stimulation of the sympathetic

system and an increase in sympathetic outflow
(adrenaline and noradrenaline release) which
leads to increased vasoconstriction resulting in
increased blood pressure

9
 1a. HYPOVOLEMIA
• Generally refers to a state of COMBINED salt and water
loss exceeding intake, leading to ECF volume
contraction.

• Causes include
-increased fluid losses by GIT losses (vomiting,
diarrhoea), skin (fever, burns), blood loss, diuretics,
diabetes insipidus and

- decreased fluid intake(dehydration).

10
• Clinical features include;
- thirst, dry mouth and mucous membranes
- marked hypernatremia
- oliguria, tachycardia, hypotension,
- reduced skin turgor
- bodyweight decreased, apathy,
- coma, death
i.e. features of dehydration

MANAGEMENT: volume replacement

• Adult requirement is 1.5-2.5litres/day hence approx
30mls/kg/day. ORS in mild to moderated dehydration and IV
fluid replacement therapy in severe dehydration
11
• Children need proportionately more fluids.

• Oral fluid therapy is the first line.

- using oral rehydration salts (ORS) according to fluid
loss.

• IV solutions should be approximately isotonic with

plasma to avoid pain and hemolysis of RBCs.

-Half normal (0.45% sodium chloride) to twice normal

(10% dextrose) is acceptable.
12
 IV solutions
1. CRYSTALLOID solutions
• The choice of dextrose or saline depends on the
means of loss.

• If salt was lost in addition to water, use normal saline

and if only pure water was lost, use 5% dextrose.

1a. Dextrose
• Dextrose is metabolized rapidly (especially dextrose
5%) to water hence the effect of administering
dextrose 5% is to add water to the system.
13
• Rate: desired daily volume infused over 24hrs

• Dextrose 10% and 25% are also used to correct

and prevent hypoglycemia.

• Preparations: dextrose 5%, 10%, 25%, 50%

14
1b. IV normal saline/Sodium Chloride (NaCl)
• Preparations: iv NaCl 0.9% (isotonic), iv NaCl
0.45% (hypotonic), iv NaCl 0.18% and glucose
4%, iv NaCl 1.8%, etc etc.

• IV NaCl 0.9% : Isotonic solution that provides the

most important extracellular ions in near
physiologic concentration.

15
2. COLLOID solutions
• Not usually required unless there has been major
bleeding.

• Used to expand and maintain blood volume.

2a. Colloids of blood origin include; blood, packed

cells/packed red blood cells, albumin.

2b. Colloids of non-blood origin include; haemaccel

(gelatin MW 35,000), dextran (glucose polymer MW
40,000 or 70,000), hetastarch and pentastarch.
16
 2. SODIUM
• Sodium (Na) is the most abundant
EXTRACELLULAR cation in the body and
normal plasma concentrations of sodium
range from 135-145 mmol/L.

• Sodium is actively pumped out of cells by the

Na,K-ATPase pump. As a result, 85 to 90% of
all Na is extracellular.

17
• Sodium excess leads to edematous states while
sodium deficit leads to hypovolemic states.

• Sodium intake is usually higher than requirements.

• Normal volume regulatory mechanisms ensure

that Na loss balances Na gain.

• Na balance is maintained through sodium

excretion by the kidneys.

18
 2a. HYPONATREMIA
• It refers to low sodium levels in the body i.e.
<135mmol/l.

• Symptoms include; lethargy, confusion, weakness,

convulsions, death. Hyponatremia is assymptomatic
in most patients

• Causes are
- Water excess (dilutional hyponatremia):renal
failure, heart failure, excess fluid intake.
- Salt depletion; diuretics, hypoaldosteronism.
19
• Classification involves;
1. Hypovolemic hypotonic
hyponatremia(common in patients
taking thiazide diuretics)

2. Hypervolemic hypotonic hyponatremia

(dilutional hyponatremia)

3. Euvolemic hypotonic hyponatremia(e.g.

SIADH release)
20
MANAGEMENT: Treat cause.

• Dehydrated (hypovolemic hypotonic hyponatremia)

- give 0.9% NaCl as these patients have both
sodium and water deficits)

• Not dehydrated (euvolemic and hypervolemic

hypotonic hyponatremia )
- restrict fluid intake and consider furosemide
(diuretic)
-may consider hypertonic saline (>0.9%NaCl) plus
furosemide.
21
• The hypertonic saline (3% NaCl) more rapidly
manages the hyponatremia

• Furosemide is administered concurrently to

enhance the serum sodium correction by
increasing the excretion of water.

22
 2b. HYPERNATREMIA
• Increased body sodium (>145mmol/l) with or
without water deficiency.

• Causes
- Fluid loss: diarrhoea, vomiting, respiration, burns,
sweat, fever.
- Incorrect iv fluid replacement
- Diuretics
- Drugs; lithium Na, phenytoin Na
23
• Classification involves;
1. Hypervolemic hypernatremia
e.g.mineralocorticoid
excess/hyperaldosteronism

2. Hypovolemic hypernatremia e.g. renal

and GIT losses

3. Isovolemic hypernatremia e.g. diabetes

insipidus
24
• Symptoms
-Thirst, mental confusion, coma.

MANAGEMENT: Treat cause

• Give 5% dextrose to replenish lost fluid/to

replace free water.

**N/B; do not give normal saline**

25
 3.POTASSIUM
• Potassium is the most abundant INTRACELLULAR cation in
the body. The normal serum potassium concentration
range is 3.5 to 5 mmol/L.

• Actively pumped into cells by the Na-K ATPase hence approx

98% of total body potassium is intracellular.

• It is a very dangerous electrolyte and slight alterations can

be fatal.

• Regulatory mechanisms ensure that its tightly controlled by

matching intake with excretion. This is by renal excretion.
26
 3a. HYPERKALAEMIA
• It refers to elevated body potassium above the
normal range i.e 5.3mmol/l. It is life threatening

• Causes are;
 Metabolic acidosis,
 tissue damage,
 renal failure,
 infections,
 dehydration,
 drugs e.g. ACEI’s, ARBs, aldosterone antagonists
 Increased potassium intake 27
• Hyperkalemia is much less common than
hypokalemia. In fact, if all patients with acute and
chronic kidney disease were excluded, the true
prevalence of hyperkalemia would be insignificant.

• The four primary causes of hyperkalemia include;

(1) Increased potassium intake,
(2) decreased potassium excretion,
(3) tubular unresponsiveness to aldosterone, and
(4) redistribution of potassium into the extracellular
space (extreme exercise)
28
• Clinical features include; cardiac arrhythmias
(bradycardia), sudden death,

29
MANAGEMENT: Treat the cause
1. Calcium infusion (calcium
gluconate/calcium chloride) to protect the
heart (cardiac membrane). Calcium
antagonizes the cardiac membrane effect of
hyperkalemia and reverses ECG changes
within minutes

2. Insulin with dextrose (insulin promotes

intracellular K+ movement)

30
3. Beta receptor AGonists e.g. salbutamol
nebulization (promote intracellular K+ movement)

4. Oral/rectal resonium exchange resins. (SPS

(Kayexalate), a cation-exchange resin (enhance K+
excretion)

5. Hemodialysis in severe hyperkalemia (Stage 4 or

5 of Chronic Kidney Disease patients who are non-
compliant with dietary potassium restrictions. It
enhances K+ excretion)

31
 3b. HYPOKALAEMIA
• It refers to low potassium levels in the body
<3.5mmol/l.

• Causes include
 Cushings syndrome,
 Vomiting, diarrhoea.
 Poor intake,
 Drugs; laxatives, steroids, diuretics, B-blockers,
amphotericin B.
32
Features of hypokalemia;
• Muscle weakness, cramping, myalgia,
• malaise
• tachycardia,
• drowsiness
• Dizziness,
• confusion,
• Death.

• n/b; life threatening.

33
MANAGEMENT: Manage the underlying cause

• Give iv/oral potassium replacement therapy

-oral potassium tablets/syrup e.g. kay-cee-L,
sando-K, slow K

- Iv potassium: premixed or not. Given as a

slow iv infusion

34
• Potassium-sparing diuretics (spirinolactone,
triamterene, amiloride)are an alternative to
chronic exogenous potassium
supplementation, especially when patients are
concomitantly receiving drugs that are
known to deplete potassium (e.g. diuretics or
amphotericin B).

35
ACID BASE BALANCE
 INTRODUCTION
• Acid–base disorders are common, and often serious
disturbances that can result in significant morbidity
and mortality.

• Normal body ph ranges from 7.35 to 7.45.

• Cellular metabolism and diet results in the

production of large quantities of hydrogen that
need to be excreted to maintain acid–base balance.

37
• Three homeostatic mechanisms collectively
maintain acid–base balance:

extracellular buffering,

ventilatory regulation of carbon dioxide

elimination, and

renal regulation of hydrogen ion and

bicarbonate excretion.
38
• Extracellular buffering
- Uses bicarbonate/carbonic acid, proteins and
phosphate buffers to regulate the acid-base
balance.

• Ventilatory regulation of carbon dioxide

elimination
- Both the rate and depth of ventilation can be
varied to allow for excretion of CO2

39
• renal regulation of hydrogen ion and
bicarbonate excretion
- Excretion and reabsorption of H+ and
bicarbonate to regulate acid base
balance.

40
 ACID BASE DISTURBANCES
• A pH < 7.35 is referred to as acidosis

• A pH > 7.45 is referred to as alkalosis

• These disturbances are classified as either metabolic or

respiratory in origin. Hence;
• Metabolic acidosis
• Respiratory acidosis
• Metabolic alkalosis
• Respiratory alkalosis
41
 1. METABOLIC ACIDOSIS
• Metabolic acidosis is characterized by a decrease in pH as the
result of a primary decrease in SERUM bicarbonate
concentration.

• The decrease in HCO3- concentrations is as a result of buffering

or accumulation of acids e.g. lactic acidosis or in renal failure
etc.

• Drugs e.g salicylate overdose can also lead to metabolic acidosis

• Disease states e.g. diabetic ketoacidosis (DKA) and end-stage

kidney failure
42
• Clinical presentation includes; anorexia, nausea,
vomiting, rapid heart rate, coma, dyspnoea,
hyperventilation (Kussmaul breathing)

TREATMENT
• Mild-moderate acidosis: oral alkali replacement;
 Sodium citrate, sodium bicarbonate (baking
soda), potassium citrate (urocit-k), potassium
bicarbonate (k-lyte),

43
• Severe acidosis
 Dialysis
 Treat the underlying cause
 Iv sodium bicarbonate

44
 2. METABOLIC ALKALOSIS
• Alkalosis with ph>7.45 with an increase in
PLASMA bicarbonate.

• Causes: diarrhea, vomiting, drugs (diuretics),

excessive gain of HCO3-.

• Clinical presentation: nausea, vomiting, diarrhea,

dizziness, hypoventilation, arrhythmias etc

45
TREATMENT
Treat the underlying cause

Ventilation of CO2 and oxygen.

Avoid drugs that cause alkalosis.

IV Hcl, ammonium chloride, arginine

monochloride.

46
 3. RESPIRATORY ALKALOSIS
• Respiratory alkalosis is characterized by a primary
decrease in PaCO2 (Partial Pressure of Carbon Dioxide
in Arterial Blood) that leads to an elevation in pH.

• It is the most frequently encountered acid–base

disorder:

• Caused by HYPERVENTILATION: pregnancy, high

altitudes, fever, pain, anxiety, pneumonia, hospitalized
patients etc.
47
• Clinical presentation: light-headedness,
confusion, muscle cramps, nausea, vomiting,
syncope, seizures, hyperventilation.

TREATMENT; Identification and correction of the

underlying cause.
• Usually asymptomatic: no treatment is
usually required.
• A paper bag for re-breathing can be used
• Reduced breathing/respiratory rate.

48
 4. RESPIRATORY ACIDOSIS
• Respiratory acidosis occurs when the lungs fail to excrete
carbon dioxide hence increased CO2 resulting in a lower
pH.

• Causes include; drugs (that lead to respiratory depression

e.g opioids, benzodiazepines), stroke, trauma, heart attack,
asthma, airway obstruction, tumors etc.

• Clinical presentation includes: seizures, stupor, and coma,

headaches, paralysis etc.

49
TREATMENT
• Oxygenation
• Mechanical ventilation
• Treat the underlying cause
• HCO3- administration.

50
 ASSIGNMENT
1. List four ways in which sick individuals lose fluids
2. In healthy individuals volume homeostasis is
regulated by?
3. List the two types of IV solutions giving an
example of each
4. Briefly describe how we manage hyperkalemia
5. Which three homeostatic mechanisms maintain
acid–base balance?

51
 ASSIGNMENT 2
• Hypocalcemia and hypercalcemia
• Hypophosphatemia and hyperphosphatemia
• (to be handed in next week via whatsapp)

52