5.Fluid and electrolytes imbalance-2.ppt

SARA CHANDIO
LECTURER BCON.
1
FLUID
&
ELECTROLYTES

Objectives:
2
 Homeostasis
 Movement of fluid – Starling forces
 Transport mechanisms
 Tonicity
 Fluid compartments
 Water balance
 Electrolytes - distribution & regulation
 Fluid & electrolytes imbalance

Movement of Body Fluids: Important Concept
3
• Body fluids are not static. Fluids & electrolytes
shift from compartment to compartment.
• Emphasis is always on maintaining homeostasis

Homeostasis
5
 Central concept of physiology
 Physiological systems have evolved to maintain
their internal environment while responding to
both internal and external threats to that stability.
 Disease, by and large, is a failure of homeostasis
 Excessive perturbations result ultimately in death of the
organism.

Homeostasis
6
 The internal environment of the body is tissue
fluid, which bathes all cells making up the body.
 The composition of tissue fluid must remain
constant if cells are to remain alive and healthy.
 Tissue fluid is nourished and purified when
molecules are exchanged across thin capillary
walls.
 Tissue fluid remains constant only if the
composition of blood remains constant.

7
Components of a homeostatic
mechanism
Stimulus Receptors
Control
Center
Effectors
Response

Maintaining Homeostasis
8
 Regulation of homeostasis of body fluids- kidneys,
endocrine system, CV, lungs, GI system.
 Hormones - antidiuretic hormone (ADH), renin-
angiontensin-aldosterone system, atrial natriuretic
factor.

9
 Fluid compartments are separated by membranes that are
freely permeable to water.
 Movement of fluids due to STARLING FORCES :
1. Capillary hydrostatic pressure---tends to move fluid
outward from capillaries to interstitial spaces
2. Capillary colloid osmotic pressure-----(plasma
proteins) fluid movement inward from interstitial spaces to
capillaries

10
03. Interstitial hydrostatic pressure----fluid movement
inward from interstitial spaces to capillaries
04. Tissue colloid osmotic pressure----- tends to move
fluid outward from capillaries to interstitial spaces

12
• the sum of Starling forces usually drives the movement of
water and solutes from interstitium into capillary.
• In favor of moving things from interstitium into capillaries are:
capillary colloid osmotic pressure (Pcap
)
interstitial hydrostatic pressure (PIS
)
• The opposing forces are:
interstitial colloid osmotic pressure (PIS
)
capillary hydrostatic pressure (Pcap
).

13
CLINICAL SIGNIFICANCE:
Edema is the accumulation of fluid within the
interstitial spaces.
Causes:
increased capillary hydrostatic pressure
decreased capillary colloid osmotic pressure
increased capillary membrane permeability

14
Increases Capillary Hydrostatic pressure :
Venous obstruction:
Thrombophlebitis (inflammation of veins)
hepatic obstruction
tight clothing on extremities
prolonged standing
Salt or water retention
congestive heart failure
renal failure

15
Decreased Capillary colloid osmotic
pressure:
↓ plasma albumin (liver disease or
protein malnutrition)
plasma proteins lost in :
glomerular diseases of kidney
hemorrhage, burns, open wounds

16
Increased capillary permeability:
Inflammation
Immune responses

“ WHERE SODIUM GOES, WATER FOLLOWS.”
DIFFUSION – MOVEMENT OF PARTICLES DOWN A CONCENTRATION
GRADIENT.
OSMOSIS – DIFFUSION OF WATER ACROSS A SELECTIVELY PERMEABLE
MEMBRANE
ACTIVE TRANSPORT – MOVEMENT OF PARTICLES UP A CONCENTRATION
GRADIENT ; REQUIRES ENERGY
17
FLUID MOVEMENT:

Osmosis
18
• Movement of water across a semi-permeable membrane from an
area of low solute concentration (lots of water) to an area of high
solute concentration (less water) until even distribution
(homeostasis) is achieved

selectively permeable membrane
19
 A membrane that allows only certain materials to
cross it
 Materials pass through pores in the membrane
 Osmotic pressure: Pressure required to prevent
osmosis

20
 Osmolarity = number of solute particles (milli-
osmoles) in liter of solution
 Normal = 270 – 300 (or 275 – 295) mOsm/l
 Osmolality = number of solute particles (mill-
osmoles) in kilogram of water
mOsm (milliosmoles) = number of particles
in a solution

Clinical calculation of PLASMA OSMOLALITY:
21
PLASMA OSMOLALITY (mOsm/kg of water) =
2(Na+
) + [glucose (mg/dl )/18] + [urea mg/dl /2.8]
Roughly: 2(plasma Na+
) = 2 x 145 mEq/L = 290 mOsm/kg of H2O
Na+ biggest determinant of serum osmolality

22
Tonicity of a solution :
Is the effect of solution on the cell volume
determined by conc. of non penetrating
solutes.
Solutes that can penetrate plasma membrane
distribute equally b/w ECF & ICF- do not
contribute to osmotic differences.
Isotonic – same conc. of solutes as body fluids.
Hypertonic – above normal conc.
Hypotonic – below normal.

Isotonic Fluids
example: normal saline 0.9% NaCl
 No net fluid (water)
shifts occur because
the fluids are
EQUALLY
concentrated
23

Hypotonic Fluids
example: 0.45% NaCl
 When a LESS concentrated
fluid is placed next to a MORE
concentrated solution, water
moves to MORE concentrated
solution to equalize the
solutions
 Causes: (over hydration)
 Renal failure
 SIADH
25

26
Cell in a
hypotonic
solution

Hypertonic Fluids
example: 3% NaCl
 When a MORE concentrated fluid
is placed next to a LESS
concentrated solution, water
moves to the MORE concentrated
solution to equalize the solutions
 Causes: (dehydration)
 Insufficient water intake
 Vomiting
 Diarrhea
 Diabetes insipidus
27

28
Cell in a
hypertonic
solution

WATER BALANCE
29
NORMAL WATER CONTENT OF BODY
 75% AT BIRTH
 55-60% YOUNG ADULTS
MEN SLIGHTLY HIGHER THAN WOMEN
(MORE FAT, LESS WATER)
 45% IN ELDERLY, OBESE

WATER BALANCE
30
TOTAL BODY WATER
~40 liters
Fluid compartments
65% (25L)INTRACELLULAR FLUID (ICF)
35% (15L)EXTRACELLULAR FLUID (ECF)
25% interstitial fluid (tissue fluid)---------
8% blood plasma and lymph-------
2% transcellular fluid--------

31
 Interstitial fluid (tissue fluid)---Fluid b/w the cells
 Plasma------noncelluler part of blood
 Lymph-------colorless liquid
 Transcellular fluid--------
synovia,pericardial,peritoneal,plural,inttaocular, CFS.

32
Figure 26-1 Distribution of total body water (TBW). ECF, Extra cellular fluid; ICF,
intracellular fluid; ISF, interstitial fluid; PV, plasma volume .

33
Balance
 Fluid and electrolyte homeostasis is maintained
in the body
 Neutral balance: input = output
 Positive balance: input > output
 Negative balance: input < output

Body Fluid Regulation
34
 Intake should equal output.
 Averages around 2500ml for an adult.
 Average Adult Intake:
 Fluids- 1500ml
 Water in Food- 750 ml
 Water formed from food
metabolism- 250ml

 Average Adult Output 2500ml
 Urine - 1500ml
 Feces - 150ml
 Sweat - 150ml
 Insensible losses:
 Lungs - 350ml
 Skin - 350ml
35
Body Fluid Regulation

ELECTROLYTES
36
 Substance when dissolved in solution separates
into ions & carry an electrical charge
 CAT ION - positively charged electrolyte
 AN ION - negatively charged electrolyte
 # Cat ions must = # Anions for homeostasis
is to exist in each fluid compartment
 Commonly measured in mill equivalents / liter
(mEq/L)

Electrolyte Concentration
37
 Expressed in milliequivalents per liter (mEq/L),
a measure of the number of electrical charges
in one liter of solution

Extracellular and Intracellular Fluids
38
 Each fluid compartment of the body has a distinctive
pattern of electrolytes
 Interstitial fluids are similar plasma (except for the
high protein)
 Sodium is the chief cation
 Chloride is the major anion
 Intracellular fluids have low sodium and chloride
 Potassium is the chief cation
 Phosphate is the chief anion

Extracellular and Intracellular Fluids
39
 Sodium and potassium concentrations in extra and
intracellular fluids are nearly opposites
 This reflects the activity of cellular ATP-dependent
sodium-potassium pumps
 Electrolytes determine the chemical and physical
reactions of fluids

Electrolyte Regulation
40
 Most electrolytes come from dietary intake and
excreted by urine.
 Na+ & Cl- not stored-must be consumed daily.
 K+ & Ca+ are stored in cells and bones.
 When serum levels drop, ions can go from storage
into blood to maintain adequate serum levels.

Sodium: Na+: 135-145mEq/L
41
 Major ECF cat ion
 Major functions:
 Water balance
 Transmission of nerve impulses
 Regulation controlled at cellular level by sodium-
potassium pump.
 Na+ retention/secretion controlled by aldosterone
 Aldosterone controlled by renin-angiotensin

Potassium: K+: 3.5-5.5mEq/L
42
 Major cation of ICF
 Major function: Electrical conduction of nerve impulses-
cardiac conduction
 Regulation at cellular level by Na-K pump
 Body more sensitive to small changes in serum K+ than
other electrolytes

Calcium: Ca++: 8.5-10.5 mg/dl
43
• Major functions: 1% in ECF
– Normal skeletal muscle, smooth muscle, & cardiac
muscle contraction; blood clotting
• Taken through diet. Needs Vit. D. to be absorbed
• Regulation:
– Parathyroid hormone: triggers Ca release from bone
and/or inhibits renal excretion: raises serum levels
– Calcitonin: thyroid gland; causes ECF levels to decrease
by inhibition of bone resorption (release); inhibits Vit. D
absorption, & increases renal excretion

Chloride: Cl-
44
 Major an ion of ECF
 Functions with Na to regulate serum osmolality and
blood volume
 Major component of gastric juice (HCl).
 Helps regulate acid-base balance.
 Acts as buffer in exchange of O2 & CO2 in RBC’s.

REGULATION OF NaCl & WATER
REABSORPTION
45
 Most important factors:
 Angiotensin II
 Aldosterone: Controls Na+
absorption and K+
loss through kidney
 ADH: Stimulates water conservation
 ANP : Reduce thirst and block the release of ADH and aldosterone
 Sympathetic nerves
 Other factors:
 Dopamine
 Glucocorticoids
 Starling forces & the phenomenon of
glomerulotubular balance.

46
• ANGIOTENSIN II:
• a potent stimulator of NaCl & water reabsorption from
kidney
• Stimulates aldosterone
• The reduction in extracellular fluid volume activates
RENIN-ANGIOTENSIN system which leads to
increased plasma angiotensin II concentration.

48
Renin-Angiotension-Aldosterone System

49
 Patients of Congestive Heart Failure /
Hypertension
treated with angiotensin-converting enzyme (ACE)
inhibitors (e.g., captopril) to lower ECFV & BP
 Inhibition of ACE lowers the convesrion of
angiotensin I to II
lowers plasma [angiotensin II]

50
 ALDOSTERONE:
 Synthesized in adrenal cortex
 Stimulates NaCl reabsorption in distal tubule / collecting duct
 As well as from :
 gut
 sweat glands
 salivary glands
 Also increases water reabsorption in collecting duct secondary to the
increased NaCl reabsorption
 Stimulates K+ secretion in distal tubule / collecting duct
 The two most important stimuli for aldosterone secretion: increased
plasma ANGIOTENSIN II & increased plasma K+

51
Atrial Natriuretic Peptide (ANP):
 Is secreted by cells of atria / kidney
 Secretion is stimulated by increased BP & by
increased ECFV
 Increases urinary NaCl excretion
 also increases urinary water excretion by directly
inhibiting water reabsorption in collecting duct & by
inhibiting ADH secretion

52
 Antidiuretic Hormone (ADH):
 Is the most important hormone that regulates water
balance
 ADH is secreted by posterior pituitary in response to
increased plasma osmolality or decreased ECFV
 ADH increases water permeability in COLLECTING
DUCT, thus conserving body water
 ADH DOES NOT AFFECT URINARY NaCl
EXCRETION

ADH Disturbances
53
 Diabetes Insipidus (dec ADH)
 Posterior pituitary (central) / kidney (nephrogenic)
 Loss of 15 liters of fluid per day
 Treatment: Vasopressin and fluid replacement
 Syndrome of Inappropriate Anti-Diuretic Hormone (SIADH)
(inc ADH)
 Fluid retention (excess)
 Hyponatremia
 Treatment: Diuretics and fluid restriction

54
Sympathetic Nerves:
( activation caused by hemorrhage or decreased
ECFV)
 Catecholamines released from sympathetic nerves
(norepinephrine) & adrenal medulla (epinephrine)
 stimulate NaCl & water reabsorption in proximal
tubule & thick ascending limb of Henle’s loop

55
2 Rules of Electrolyte Balance
1. Most common problems with electrolyte
balance are caused by imbalance between
gains and losses of sodium ions
2. Problems with potassium balance are less
common, but more dangerous than sodium
imbalance

Common Disturbances Electrolyte Balance
56
Hypernatremia (high levels of sodium)
 (Na > 145)
 Caused by excess water loss or overall sodium excess
 Water moves from ICF ECF
→
 Cells dehydrate
 Causes:
 excess salt intake,
 hypertonic solutions,
 excess aldosterone,
 diabetes – polyuria,
 increased water loss - long term sweating with chronic fever,
 water deprivation (hypodipsia)

Hypernatremia - Clinical manifestations
58
 Thirst
 Dry & flushed skin
 Dry & sticky tongue and mucous membranes
 Lethargy
 Neurological dysfunction due to dehydration of brain
cells
 Decreased vascular volume

Hypernatremia - Lab findings
59
 high serum sodium > 145mEq/L
 high serum osmolality > 295mOsm/kg
 high urine specificity > 1.030

60
Hypernatremia - Management
 Lower serum Na+
 Administration of hypotonic sodium solution [0.3 or 0.45%]
 Rapid lowering of sodium can cause cerebral edema
 Slow administration of IV fluids with the goal of reducing sodium not
more than 08 to 10 mEq/L for the first 48 hrs decreases this risk
 In case of Diabetes insipidus desmopressin acetate nasal spray is used
 Dietary restriction of sodium in high risk clients
60

Hyponatremia (Na < 135)
61
 Overall decrease in Na+ in ECF
 Occurs with net loss of sodium or net water excess
 Causes:
 diuretics
 chronic vomiting
 chronic diarrhea
 decreased aldosterone
 decreased Na+ intake
 increased sweating
 SIADH

62
Hyponatremia - Clinical manifestations
 Neurological symptoms
 Lethargy, headache, confusion, apprehension, depressed
reflexes, seizures and coma
 Muscle symptoms
 Cramps, weakness, fatigue
 Gastrointestinal symptoms
 Nausea, vomiting, abdominal cramps, and diarrhea

Hyponatremia – Lab findings
63
 Serum sodium less than 135mEq/ L
 serum osmolality less than 280mOsm/kg
 urine specific gravity less than 1.010

Hyponatremia - management
64
 Identify the cause and treat
 Administration of sodium orally, by NG tube or
parenterally
 For patients who are able to eat & drink, sodium is easily
accomplished through normal diet
 For those unable to eat, Ringer’s lactate solution or isotonic
saline [0.9%Nacl]is given
 For very low sodium 3%Nacl may be indicated
 water restriction in case of hypervolaemia

65
Hyperkalemia
 Serum K+ > 5.5 mEq / L
 Causes:
 Renal disease
 Massive cellular trauma
 Insulin deficiency
 Addison’s disease
 Potassium sparing diuretics
 Decreased blood pH
 Exercise causes K+ to move out of cells

66
Hyperkalemia - Clinical manifestations
 Early – hyperactive muscles , paresthesia
 Late - Muscle weakness, flaccid paralysis
 Dysrhythmias
 Bradycardia , heart block, cardiac arrest

Hyperkalemia - Lab findings
67
 serum potassium of 5.3mEq/L results in peaked T
wave HR 60 to 110
 serum potassium of 7mEq/L results in low broad P-
wave
 serum potassium levels of 8mEq/L results in no
arterial activity[no p-wave]

70
Hyperkalemia- management
 Dietary restriction of potassium for potassium
 Mild hyperkalemia can be corrected by improving output
by forcing fluids, giving IV saline or potassium wasting
diuretics
 Severe hyperkalemia is managed by
 1.infusion of calcium gluconate to decrease the antagonistic effect
of potassium excess on myocardium
 2.infusion of insulin and glucose or sodium bicarbonate to
promote potassium uptake
 3.sodium polystyrene sulfonate [Kayexalate] given orally or
rectally as retention enema

71
Hypokalemia decrease potassium
 Serum K+
< 3.5 mEq /L
 Beware if diabetic
 Insulin gets K+
into cell
 Ketoacidosis – H+
replaces K+
, which is lost in urine
 β – adrenergic drugs or epinephrine
71

72
Causes of Hypokalemia
 Decreased intake of K+
 Increased K+
loss
 Chronic diuretics
 Acid/base imbalance
 Trauma and stress
 Increased aldosterone
 Redistribution between ICF and ECF
72

73
Hypokalemia - Clinical manifestations
 Neuromuscular disorders
Weakness, flaccid paralysis, respiratory
arrest, constipation
 Dysrhythmias, appearance of U wave
 Postural hypotension
 Cardiac arrest

Hypokalemia - Lab findings
74
 K – less than 3mEq/L results in ST depression , flat
T wave, taller U wave
 K – less than 2mEq/L cause widened QRS,
depressed ST, inverted T wave

Hypokalemia - Management
76
 Mild hypokalemia[3.3to 3.5] can be managed by
oral potassium replacement
 Moderate hypokalemia
K-3.0to 3.4mEq/L need 100to 200mEq/L of IV
potassium for the level to rise to 1mEq/L
 Severe hypokalemia K- less than 3.0mEq/L
need 200to 400 mEq/L for the level to rise to l
mEq/L
 Dietary replacement of potassium helps in
correcting the problem[1875 to 5625 mg/day]

77
Calcium Imbalances
 Most in ECF
 Regulated by:
 Parathyroid hormone
↑Blood Ca++
by stimulating osteoclasts
↑GI absorption and renal retention
 Calcitonin from the thyroid gland
Promotes bone formation
↑ renal excretion

78
Hypercalcemia
 calcium plasma level over 11mg/dl
 Causes:
 Hyperparathyroidism
 Hypothyroid states
 Renal disease
 Excessive intake of vitamin D
 Milk-alkali syndrome
 Certain drugs
 Malignant tumors
78

79
Hypercalcemia – Clinical manifestations
 Many nonspecific – fatigue, weakness, lethargy
 Increases formation of kidney stones and pancreatic stones
 Muscle cramps
 Bradycardia, cardiac arrest
 Pain
 GI activity also common
 Nausea, abdominal cramps
 Diarrhea / constipation
 Decreased level of consciousness
79

Hypercalcemia - Lab findings
80
 High serum calcium level 11mg/dl,
 x- ray showing generalized osteoporosis,
 widened bone cavitation,
 urinary stones,
 elevated BUN 25mg/100ml,
 elevated creatinine1.5mg/100ml

Hypercalcemia - Management
81
 1.IV normal saline, given rapidly with Lasix promotes
urinary excretion of calcium
 2.Plicamycin an antitumor antibiotics decrease the plasma
calcium level
 3.Calcitonin decreases serum calcium level
 4.Corticosteroid drugs compete with vitamin D and
decreases intestinal absorption of calcium
 5. If cause is excessive use of calcium or vitamin D
supplements reduce or avoid the same

82
Hypocalcaemia
 It is a plasma calcium level below 8.5 mg/dl
 Hyperactive neuromuscular reflexes and tetany differentiate it
from hypercalcemia
 Convulsions in severe cases
 Caused by:
 Renal failure
 Lack of vitamin D
 Suppression of parathyroid function
 Hypersecretion of calcitonin
 Malabsorption states
 Abnormal intestinal acidity and acid/ base bal.
 Widespread infection or peritoneal inflammation
82

83
Hypocalcemia - Clinical manifestation
 Numbness and tingling sensation of fingers,
 hyperactive reflexes,
 muscle cramps,
 pathological fractures,
 prolonged bleeding time
83

Hypocalcemia -Lab findings
84
 Serum calcium less than 8.5

Hypocalcemia - Management
85
 1.Asymtomatic hypocalcemia is treated with oral
calcium chloride, calcium gluconate or calcium
lactate
 2.Tetany from acute hypocalcemia needs IV
calcium chloride or calcium gluconate to avoid
hypotension bradycardia and other dysrythmias
 3.Chronic or mild hypocalcemia can be treated by
consumption of food high in calcium

Volume Regulation
86
 Since the osmolarity (i.e. concentration) of ECF is
tightly controlled,
 the volume of the ECF is determined by the total
quantity of solute (mainly NaCl),
 so regulation of ECF volume is all about Sodium
Balance

FLIUD IMBALANCES
87
The five types of fluid imbalances that may
occur are:
 Extracellular fluid Volume deficit (EVFVD)
 Extracellular fluid volume excess(ECFVE)
 Extracellular fluid volume shift
 Intracellular fluid volume excess(ICFVE)
 Intracellular fluid volume deficit(ICFVD)

EXTRACELULLAR FLUID VOLUME DEFICIT
88
 An ECFVD, commonly called as dehydration , is
a decrease in intravascular and interstitial fluids
 An ECFVD can result in cellular fluid loss if it is
sudden or severe

THREE TYPES OF ECFVD
89
 Hyperosmolar fluid volume deficit- water loss is
greater than the electrolyte loss
 Isosmolar fluid volume deficit – equal proportion of
fluid and electrolyte loss
 Hypotonic fluid volume deficit – electrolyte loss is
greater than fluid loss

ETIOLOGY AND RISK FACTORS
90
 Severe vomiting.
 Diaphoresis.
 Traumatic injuries.
 Third space fluid shifts
[percardial, pleural,
peritoneal and joint
cavities]
 Fever.
 Gastrointestinal suction.
 Ileostomy.
 Fistulas.
 Burns.
 Hyperventilation.
 Decreased ADH
secretions.
 Diabetes insipidus.
 Addison’s disease or
adrenal crisis.
 Diuretic phase of acute
renal failure.
 Use of diuretics.

CLINICAL MANIFESTATION
91
 In Mild ECFVD, 1to 2 L of water or 2% of the body
weight is lost
 In Moderate ECFVD, 3 to 5L of water loss or
5%weight loss
 IN Severe ECFVD , 5 to 10 L of water loss or 8% of
weight loss

92
 Thirst
 Muscle weakness
 Dry mucus
 Eyeballs soft and sunken
(severe deficit)
 Apprehension ,
restlessness, headache ,
confusion, coma in
severe deficit
 Elevated temperature
 Tachycardia, weak
thready pulse
 Peripheral vein filling> 5
seconds
 Postural systolic BP falls
>25mm Hg and diastolic
fall > 20 mm Hg , with
pulse increases > 30
 Narrowed pulse pressure,
decreased CVP.
 Flattened neck veins in
supine position
 Weight loss
 Oliguria(< 30 mlper hour)

LABORATORY FINDINGS
93
 Increased osmolality(> 295 mOsm/ kg)
 Increased or normal serum sodium level (> 145mEq/
L )
 Increase BUN (>25 mg / L )
 Hyperglycemia ( >120 mg /dl )
 Elevated hematocrit (> 55%)
 Increased specific gravity ( > 1.030)

MANAGEMENT
94
Mild fluid volume loss can be corrected with oral fluid
replacement
-if client tolerates solid foods advice to take 1200 ml to
1500ml of oral fluids
-if client takes only fluids, increase the total intake to
2500 ml in 24 hours

Management of Hyperosmolar fluid volume
deficit
95
 Administration of hypotonic IV solution , such as 5%
dextrose in 0.2 %saline
 If the deficit has existed for more than 24
hours,avoid rapid correction of fluid [sodium
solution to be infused at the rate of 0.5 to 0.1m Eq/
L/ hr]

If heamorrhage is the cause for ECFVD
96
 Packed red cells followed by hypotonic IV fluids is
administered
 In situations where the blood loss is less than 1 L
normal saline or ringer lactate may be used
 clients with severe ECFVD accompanied by severe
heart , liver, or kidney disease cannot tolerate large
volumes of fluid and sodium

EXTRACELLULAR FLUID VOLUME EXCESS
97
 ECFVE is increased fluid retention in the
intravascular and interstitial spaces (edema)

ETIOLOGY AND RISK FACTORS
98
 Heart failure
 Renal disorders
 Cirrhosis of liver
 Increased ingestion of high sodium foods
 Excessive amount of IV fluids containing sodium
 Electrolyte free IV fluids
 SIADH,Sepsis
 decreased colloid osmotic pressure
 lymphatic and venous obstruction
 Cushing’s syndrome & glucocorticoids

99
 Constant irritating cough
 Dyspnea & crackles in lungs
 Cyanosis, pleural effusion
 Neck vein obstruction
 Bounding pulse &elevated BP
 S3 gallop
 Pitting & sacral edema
 Weight gain
 Change in level of consciousness

LAB INVESTIGATION
100
 serum osmolality <275mOsm/ kg
 Low , normal or high sodium
 Decreased hematocrit [ < 45%]
 Specific gravity below 1.010
 Decreased BUN [< 8mg/ dl]

MANAGEMENT
101
 Diuretics [combination of potassium sparing and
potassium depleting diuretics]
 In people with CHF, ACE inhibitors and low dose of
beta blockers are used
 A low sodium diet

EXTRACELLULAR FLUID VOLUME SHIFT:
THIRD SPACING
102
 Fluid that shifts into the interstitial spaces and
remain there is called as third space fluid
 Common sites are abdomen , pleural cavity,
peritoneal cavity and pericardial sac

RISK FACTORS
103
• Crushing injuries, major tissue trauma
• Major surgery
• Extensive burns
• Acid –base imbalances and sepsis
• Perforated peptic ulcers
• Intestinal obstruction
• Lymphatic obstruction
• Autoimmune disorders
• Hypoalbunemia
• GI tract malabsorption

104
 skin pallor
 Cold extremities
 Weak and rapid pulse
 Hypotension
 Oliguria
 Decreased levels of consciousness
LAB INVESTIGATION
 Elevated hematocrit & BUN level

MANAGEMENT
105
Treat the cause
1. For burns and tissue injuries large volume of
isosmolar IV fluid is administered
2. Albumin is administered for protein deficit
3. IV fluid intake is maintained after major surgery
to maintain kidney perfusion
4. Pericardiocentesis if pericarditis is the result
5. Paracentesis for ascitis

INTRACELLULAR FLUID VOULME
EXCESS:WATER INTOXICATION
106
 ICFVE is increase in amount of water inside the
cells.

ETIOLOGY
107
 Administration of excessive amount of hyposmolar
IV fluids[0.45%saline or 5%dextrose in water]
 Consumption of excessive amount of tap water
without adequate nutritional intake
 SIADH
 Schizophrenia[compulsive water consumption]

CLINICAL MANIFESTATIONS
108
 Headaches
 Behavioral changes
 Apprehension
 Irritability, disorientation and confusion
 Increased ICP – papillary changes and decreased
motor and sensory function
 Bradycardia, elevated BP, widened pulse pressure
& altered respiratory patterns, Babinski’s response
flaccidity, projectile vomiting, Papilledema,
delirium, convulsions &coma

LABORATORY FINDINGS
109
 High serum sodium level- 125 mEq/L
 decreased hamatocrit

MANAGEMENT
110
 Early administration of IV fluids containing
sodium chloride cam prevent SIADH
 oral fluids such as juices or soft drinks can be given
orally every hour
 Perform neurologic checks every hour to see if
cranial changes are present
 Monitor fluid intake , IV fluids and fluid output
hourly and weight daily
 Administer antiemetics for food and fluid retention

INTRACELLULAR FLUID VOLUME DEFICIT
111
 Severe hypernatremia and dehydration can cause
ICFVD.
 Relatively rare in healthy adults.
 common in elderly people and in those conditions
that result in acute water loss.
 Symptoms include confusion, coma, and cerebral
hemorrhage.

112
FLUIDS and ELECTROLYTES
Volume Disorders secondary Alteration in Sodium Balance
Expansion
Isotonic Inc N No net change Isotonic fluid
ingestion
Hypertonic Inc Dec ICF  ECF Sea water
ingestion
Hypotonic Inc Inc ECF  ICF Hypotonic IVF
Contraction
Isotonic Dec N No net change Diarrhea
Hypertonic Dec Dec ICF  ECF Diabetes insipidus
Hypotonic Dec Inc ECF  ICF Addison’s disease
Volume ECF ICF Water Conditions
Disorder Vol. Vol. Shift

Medications Likely to Cause F&E
Imbalances
113
 Diuretics
 Metabolic alkalosis, hyperkalemia, hypokalemia
 Steroids
 Metabolic alkalosis
 Respiratory center depressants (narcotic analgesics)
 Respiratory acidosis
 Antibiotics
 Hyperkalemia, hypernatremia
 Calcium carbonate
 Metabolic alkalosis
 Magnesium hydroxide (Milk of Mg)
 hypokalemia

5.Fluid and electrolytes imbalance-2.ppt

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