WATER & ELECTROLYTES

seminar from pathophysiology

Martin Vokurka
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ICF

ECF

ISF

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IVF

Fluid transfer:
- Capillary Starling balance (ECF): IVF - ISF

- Osmosis driven transfer: ECF - ICF

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Capillary transfers

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Edemas

hypoalbuminemic
hydrostatic
inflammatory
lymphatic = lymphedema

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Consequences of capillary changes

higher filtration on capillary then reabsorption

more fluid in
interstitium

lack of fluid in the vessels

RAAS stimulation

edema

water and sodium

reabsorption
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Low oncotic pressure

hypoalbuminemia
- loss of proteins by urine (nephrotic
syndrome)
- by GIT (exsudative gastropathy,
enteropathy)
- insufficient synthesis low intakde of
proteins (kwashiorkor)
- severe liver disease
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High venous pressure

hydrostatic edema
right sided heart failure
venous insufficiency (lower limbs)
venous thrombosis
portal hypertension

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Ascites

portal hypertension
hypoalbuminemia
increased flow to the splanchnic vessels
exceeding the capacity of lymphatic
drainage

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Inflammatory/allergic edema
increased vessel permeability
inflammatory or allergical mediators
dangerous larynx, intestine

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Lymphedema
disturbance of lymphe drainage
nodulus blockage tumors, surgery,
filariosis
harder, sometimes bizarre
(elephantiasis)

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VOLUME
- total
- intravascular circulation
Changes of IVF (i.e. fluid amount in blood and
vessel) are accompanied by important changes of
circulation CO, BP, HR, organ perfusion

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OSMOLALITY
osmot. concentration in 1 kg of water (mOsm/kg
H2O)

OSMOLARITY
osmot. concentration in 1 L of solution (mOsm/l)

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Osmosis

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Changes of tonicity influence exchange between cells and ISF

as a consequence the cell

volume changes.

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interstitium vessel
1 osmotic chages
2 oncotic pressure (proteins in plasma)

trancellular
fluid
cell
3
1

cell

ISF

cell

ISF

1 (hypotonic ISF)

ICF

ISF

ISF
IVF
(extravascular)

2 (decreased oncotic
plasmatic pressure)

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plasma

Tests

Fluid intake and loss

Body weight (daily)
Skin turgor
Mucosa
Specific weight/osmolality of urine (plasma)
Proteins,
S, U-electrolytes concentrations
Hematocrite

CV system BP, HR, Central venous

pressure
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OSMOLARITY
Transfers between ECF ICF
Measurement (osmometry)
Calculation (estimation of plasma osmolarity)
= 2 (Na+ + K+) + 5
or
= 2 Na+ + glucose + urea
Effective osmolarity
Part of osmolarity caused by non penetrating solutes (glucose,
sodium etc.) differently from solutes penetratign through
membrane, e.g. urea
Its differences cause changes of osmotic pressure:
-isotonicity
-hypertonicity
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-hypotonicity

Regulation of volume and a osmolarity

- antidiuretic hormone (ADH)
- renin-angiontensin-aldosterone system (RAAS)
- natriuretic peptides

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HYPOVOLEMIA

?
osmotic changes

changes on
cellular level

thirst

ADH

volume/circulatory changes

venous return

water retention

preload
cardiac output

e.g. neurologic
changes

shock, collapse

activation of symp.nerves
vasoconstriction

tissue ischemia

kidney hypoperfusion
negative feedback
renin
angiotensin
aldosterone
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ANF

sodium and water retention

Regulation of cell volume

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Volume and osmolarity disturbances

- hypovolemia
- normovolemia
- hypervolemia
- hypoosmotic
- isoosmotic
- hyperosmotic

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HYPOVOLEMIA
Isoosmotic hypovolemia
Loss of isoosmotic fluid
- blood loss
- burns
- 3rd space
- puncture of ascites
- postsurgery drainage
- diarrhea
- diuretics overdose
without changes in osmolarity no transfers of water between ICT and ECT
decrease of effective intravascular volume
circulation disturbances + compensatory mechanisms (RAAS)
urine highly concentrated with high sodium retention (concentration < 10
mmol/l)
increase of hematocrite
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Hyperosmotic hypovolemia
Pure water or hypoosmotic fluid losses
- vomitus, diarrhea
- sweating
- kidney disturbances
- diabetes insipidus
Decrease in pure water intake
osmotic fluid transfers, compensatory mechanisms are efficient:
volume (RAAS) + osmolarity (thirst, ADH)
dry mucosa, decrease in skin turgor, hematocrite not changed
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Hypoosmotic hypovolemia
Greater loss of solutes than water
- ofter from hyperosmotic hypovolemia (diarrhea, osmotic
diuresis) by drinking of pure water w/o electrolytes
- mineralocorticoid deficiency
- kidney disturbances

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HYPERVOLEMIA
Two principle mechanisms
1. water transfer from vessels to the interstitium (IVF-ISF) with
the signalization of underfilling of vessels (decrease of effect.
vessel volume) and RAAS activation (increase of sodium + water
absorption)
secondary hyperaldosteronism
- congestive heart failure
- nephrotic syndrome
- liver cirrhosis and ascites
- hypoalbuminemia
2. primary kidney retention
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Isoosmotic hypervolemia
secondary hyperaldosteronism etc.

Hyperosmotic hypervolemia
sea water, primary hyperaldosteronism, kidney failure etc.

Hypoosmotic hypervolemia
SIADH
kidney failure

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NATRIUM
plasma: 136-148 mmol/l
ICF: 12 mmol/l
total body content: 4000 mmol
functionally non penetrating solute induces water transfer across the
cell membrane
main function: extracellular fluid volume (ECF)
1 mmol of sodium (Na+) 3,6 mL of water
daily intake: 50-300 mmol
daily losses: urine 30-280 mmol
faeces 10 mmol
sweat 10 mmol
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Sodium losses
URINE
osmotic diuresis in chron. kidney failure
mineralocortikoids deficiency
GIT
diarrhea
vomiting
SWEATING
ASCITES
Sodium retention
high intake + usually in combination with the incapacity to
excrete sodium
hyperaldosteronism
- primary (Conn syndrome)
- secondary
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HYPERNATREMIA
Water deficit compared to sodium amount
Sodium stores
- decreased
- normal
- increased
* Mostly caused by loss of water
- loss of pure water (e.g. diabetes insipidus)
- loss of hypotonic fluid (e.g. osmotic diuresis,
vomiting, burns)
RENAL
U-(Na+) > 30 mmol/L
EXTRARENAL
U-(Na+) < 30 mmol/L
* Increased amount (delivery) of hypertonic fluids (often in
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therapy, primary hyperaldosteronism)

Intravascular fluid

Loss of pure water

(ADH deficiency)

hypertonic hypernatremia
with hypersmolality

sodium
potassium
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intravascular volume

HYPONATREMIA
* Hypotonic from dilution
Too much water in relation to sodium
Sodium stores
- Decreased
- normal
- increased
Volume of ECF can be
- normal,
- increased,
- decreased
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1. Impaired capacity of kidneys to excrete water

Decreased volume of ECF
RENAL sodium loss
- Diuretics
- Osmotic diuresis
- Adrenal insufficiency nadledvin
- Nephropathy etc.
U-(Na+) > 30 mmol/l
EXTRARENAL
- Diarrhea
- Vomiting
- Blood loss
- Intensive sweating
U-(Na+) < 30 mmol/L
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Increased volume of ECF

- Secondary hyperaldosteronism
- Kidney failure
Practically normal volume of ECF
- syndrome of inappropriate ADH secretion (tumors,
disturbances of CNS, drugs, pain, intensive nausea etc.)
- hypothyreosis
- thiazide diuretics
2. Excessive water intake
Primary polydipsia, no sodium solutions for irrigations etc.

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EC

IC

Dilution with pure water

(e.g. SIADH)

hypotonic hyponatremia
with hypoosmolality
hypotonic hyponatremia
w/o hypoosmolality

Kidney failure (e.g.

urea accumulation)

hypertonic hyponatremia

accumulation e.g.
glucose in EC

hypotonic hyponatremia
+ water retention

Sodium loss +
water retention
(diarrhea+pure water)

hypotonic hyponatremia
+ sodium retention

sodium
potassium
inperm.solute
Perm. Solut

Retention of water and sodium,

e.g. nephrotic sy

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Clinical symptoms of sodium disturbances

- volume disturbances
- osmotic disturbances
Mainly CNS disorders
Intensive in rapid development
HYPONATREMIA
headache, nausea, vomiting, cramps, lethargy, desorientation,
seizures, coma
Brain edema decreased ventilation, herniation of brain stem
Brain adaptation: rapid / slow
HYPERNATREMIA
Depends on age
hyperpnoe, muscle weakness, koma in infants
Less symptoms in elderly
Decreased brain volume brain hemorhage
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POTASSIUM
plasma: 3,8-5,4 mmol/L
ICF: 120 mmol/L
Total body content: 3500-4000 mmol
Daily intake: 80 mmol (variable)
daily losses:

urine 70 mmol (10-400)

stool 9 mmol
sweat 1 mmol

electrical membrane events, action potential

related to ABB
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HYPOKALEMIA, POTASSIUM LOSSES

- Low intake (elderly, malnutrition)
- Potassium redistribution (from ECF to ICF)
- insulin
- adrenalin
- aldosteron
- katabolism
- long lasting acidemia
- Extrarenal losses
- sweating
- diarrhea
- Renal losses
- More sodium for exchange in kidney tubules
osmotic diuresis, diuretics,
- aldosteron
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Symptoms (< 2.5 mmol/L)

A. General
1. Nausea
2. Fatigue
B. Neurological
1. Weakness
2. Decreased tendon reflexes
3. Paresthesia
4. Cramps
5. Restless leg syndromje
6. Rhabdomyolysis
7. Paralysis
C. Gastrointestinal
1. Constipation
2. Illeus
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materialencefalopathy
3. Exacerbation
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hepatic

D. Cardiovascular
1. Orthostatic hypotension,
vasodilatation
2. Arrhytmias
3. ECG
a. flattened T waves
b. prominent U waves
c. ST depression
E. Renal
1. Metabolic alkalosis (intracellular
acidosis)
2. Polyuria, polydipsia
3. Decrease of GFR
4. Glucose intolerance
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HYPERKALEMIA AND POTASSIUM RETENTION

Decreased excretion by kidneys
Kidney failure
Inhibitors of prostaglandin synthesis (inhibition of renin)
Hypoaldosteronism
Redistribution (from ICF to ECF)
Acidosis
Insulin deficiency (diabetes mellitus)

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K+mmol/l
8
7
6

H+

H+

K+

K+

3
D

2
1

A: Normal
6,9 7,0 7,1 7,2 7,3 7,4 7,5 7,6 7,7 7,8 pH

H+

H+

H+

H+

H+

H+

+
K

K+

K+

K+

K+

K+

B: Acidosis
exchange K+ for H+

C: Long
term
acidosis
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depletion of K+

D: Fast alkalization exchange H+ for K+ dangerous hypokalemia

Potassium intake and delivery

A. P.o. or i.v. potassium substitution
B. Blood transfusion etc.
C. Endogennous
1. Tumor lysis
2. Burns
3. Crush sy
F. Massive hemolysis
G. Surgery
H. Gastoinestinal bleeding
Pseudohyperkalemie
A. Blood clotting
B. Hemolysis in the sample
C. Delayed analysis
D. Severe thrombocytosis
E. Severe leucocytosis

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Symptoms (> 6.5 mmol/L)

A. Neurological
1. Weakness
2. Paresthesia
3. Areflexia
4. Ascending paralysis
5. Respiratory failure
B. Cardiovascular
1. Bradycardia or even asystolia or ventricular fibrillation
2. Prolongation of AV conduction

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Diagnostics: ECG
A. Early
1. Peaked T waves
B. Further
1. ST depression
2. AV block I. degree
3. QRS widening
C. Terminal
1. Biphasic QRS and fusion with T wave
2. Threat of cardiac arrest
D. Changes more pronounced in:
1. Hyponatremia
2. Hypokalcemia
3. Acidosis
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4. Hypermagnesemia

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Hyperkalemia
ECG changes suggestive of an effect of hyperkalemia
on cardiac conduction include the following (in order of
appearance
Peaked T waves
Prolongation of the PR interval
Widening of the QRS (as seen in the image below)
Widened QRS complexes in a patient whose serum
potassium level was 7.8 mEq/L.
Loss of the P wave
Sine wave pattern
Sinus arrest
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eMedicine

Hyperkalemia peaked T waves

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eMedicine

Hyperkalemia prolongated QRS

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eMedicine

Hyperkalemia
Kalium cca > 6 mmol/l: Tall peaked symmetrical
T waves in all leads, mainly visible in V2-4. The
QT interval is shorter.
Kalium cca 7 - 8 mmol/l: Prolongation of the PQ
interval, flattening of the P wave.
Kalium cca 8 - 10 mmol/l: QRS complex
deformities (widening), resulting in asystole or
more rarely in ventricular fibrillation.

Prof. Widimsk: Hypokalemia and the heart

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Normalized ECG

Hyperkalemic ECG
K+ = 7.8. This ECG demonstrates peaked T waves, loss of
P wave amplitude and widening of the QRS complex. A
baseline waveform is provided for comparison.

K+ = 8.1. This ECG demonstrates peaked T waves, loss of P

wave amplitude, minimal widening of the QRS complex and
profound bradycardia.

K+ = 8.7. This ECG demonstrates peaked T waves, loss of P

wave amplitude and widening of the QRS complex. The
following EKG shows the same patient after treatment.

K+ = 8.8. This ECG demonstrates peaked T waves, loss

of P wave amplitude and widening of the QRS complex.
The patient was subsequently treated with two amps of
bicarb and the following ECG was obtained.

Hyperkalemia
Written By: David Lane MD
Georgetown University Hospital and Washington Hospital Center
Washington, DC
Edited By: Dave Wald
Temple University School of Medicine
http://www.cdemcurriculum.org/ssm/endo/hyperkalemia/hyperkalemia.php Philadelphia, Pennsylvania

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Hypokalemia
Kalium cca 3,0 3,8 mmol/l: Flattening or
inversion of T waves
Kalium cca 2,3 3,0 mmol/l: Q-T interval
prolongation (longer duration of the T wave),
visible U wave, mild ST depression (0,5 mm),
ventricular extrasystoles
Kalium cca < 2,3 mmol/l: torsades de pointes,
ventricular fibrillation.

Prof. Widimsk: Hypokalemia and the heart

unofficialAn
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material
article
from the E-Journal of the ESC Council for Cardiology Practice

Prof. Widimsk: Hypokalemia and the heart

unofficialAn
study
material
article
from the E-Journal of the ESC Council for Cardiology Practice

K+ influence on cardiac conductivity

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