6. FUNCTION OF BODY WATER
•Transporting nutrients , electrolyte ,
oxygen to blood
•Carry waste product away from cell
•Regulate body temperature
•Lubricate joints and membrane
•Maintain immunity power
16. NORMAL VALUE OF ELECTROLYTE
ELECTROLYTE NORMAL VALUE
ANION
Bicarbonate 22-26meq/l
Chloride 96-106meq/l
Phosphate 2.8-4.5mg/dl
CATION
Potassium 3.5-5.5meq/l
Magnesium 1.5-2.5meq/l
Sodium 135-145meq/l
Calcium 9-11meq/l
17. FLUID VOLUME IMBALANCE
•Fluid volume deficit
Definition
fluid volume deficit is the abnormal loss
of body fluid , inadequate intake or plasma
interstitial fluid shift
18. CAUSES
• Increased insensible water loss
• Diabetic insipidus
• Use of osmotic diuretic
• Haemorrhage
• GI loss
• Inadequate fluid intake
• Burn
• Intestinal obstruction
• Impaired thirst
• Inadequate water intake
28. • Treat underlying causes
• Replace electrolyte and water
• Oral rehydration therapy(sodium chloride 2.6g
,glucose anhydrous 13.5g ,potassium chloride 1.5g
,Trisodium citrate 2.9 g )
• Iv therapy isotonic solution (.9% normal saline and
ringer lactated , 5%dextrose )
• Blood administered (in sever cases of shock)
29. JOURNAL REFERENCE
• Guru c dasari conducted a study on 2019 about incidence of
hypovolemia in preoperative patient
period and correlation with induction of hypotension in
patient with aneurysmal subarachnoid haemorrhage .in
department of anaesthesia in Chandigarh India about 98
patient were analysed
2 were excluded .incidence of hypovolemia was 70.4%in 98
patient,69 patient found to be hypovolemic 29% were
euvolemic correlation between hypovolemia and hypotension
was highly significant with p value 0.001
30. (2) FLUID VOLUME EXCESS
•DEFINITION
accumulation of body fluid both
sodium and water
31. ETIOLOGY
• Excess intake of sodium contain iv fluid
• Excess intake of sodium diet or medication (sodium
bicarbonate )
• Impaired fluid balance regulation (heart failure, renal
failure
SIADH
Cirrhosis of the liver
Cushing syndrome
Pregnancy
36. MANAGEMENT AND
• Removing excess fluid without affecting the electrolyte
• Primary treatment is diuretics administration
• Fluid restriction for patient with heart ,kidney ,liver
problem
• Restriction of sodium intake
• If fluid overload is high may lead to plural effusion and
ascites and it will be managed with thoracentesis
• Check I/O chart
37. RESEARCH REFERENCE
• HOWARD J GREEN CONDUCTED a study in 2019 about
training induced hypervolemia lack of an effect on oxygen
utilization during exercise among 8 male subject (19-24 year
of age)underwent a4 day training programme at an estimated
oxygen 71% maximal estimated aerobic power and ventilation
were not altered .it concluded that hypervolemia induced by
short term exercise not affect
The oxygen consumption either during submaximal or
maximal level
42. PATHOPHYSIOLOGY
Sodium loss from the intravascular
compartment
diffusion of water into interstitial space
sodium in the interstitial space is diluted
decreased osmolarity of ICF
43. water moves into cell as a result of sodium
loss
extra cellular compartment is depleted of
water
clinical symptoms developed
45. DIAGNOSTIC STUDY
• history collection
• Physical examination
• Serum studies
• Neurological assessment ,
• GI motility
• urine osmolality
• Plasma osmolality
46. MANAGEMENT
• Restore NA level to normal and prevent further
complication
• Acute hyponatremia can be treated with 2-3% of
hypertonic saline solution (100ml/hr til NA
concentration improved
• Treat the underline cause of disease (SIADH, kidney
problem ,et )
47. if FVE with hyponatremia can be treated with osmotic
diuretics( mannitol )
Increased oral sodium intake and restrict fluid intake
In severe cases 3% sodium may infused 4-
6ml/kg/h(seizure, hypothermia coma et)
48. JOURNAL PRESENTATION
• Paul Thomas conducted a study on 2019 about the
impact of resolution of hyponatremia on neuro
cognitive and motor performance in geriatric patient
among 150 patient with >70 years of age and serum
sodium less than 130meq/l. the conclusion of the was
hyponatrimic patient have so many neurological
problem and some were died during study age is
more affected to hyponatremia
49. HYPERNATREMIA
•DEFINITION
serum sodium level above 145meq/l
ETIOLOGICAL FACTOR
Excessive sodium intake
Inadequate water intake
Excessive water loss
Excessive use of table sold
diabetic insipidus
50. PATHOPHYSIOLOGY
due to etiological factor
Increased sodium concentration in ECF
Osmolarity raises in the ECF
water leaves the cell by osmosis and enters
into the extracellular compartment
51. dilution of fluid in the extracellular
cell water depleted
clinical manifestation
53. DIAGNOSTIC STUDY
history collection
physical examination with clinical symptoms
laboratory studies(k+,na+ca2+) ,glucose ,urea creatine,
plasma osmolality
serum arginine vasopressin in hypothalamus(it tell to
kidney how much water to conserve)
ADH studies
54. MANAGEMENT AND NURSING
DIAGNSIS
• limited a Isotonic solution can be administered only
to stabilize the patient circulatory status
• Hypotonic fluid (.45% normal saline) if unable to
tolerate oral water
• IVF 5% dextrose can be administered
55. • Very rapid correction of hypernatremia lead to brain
edema
(fluid shifting to brain
cell)
Specific treatment such as thiazide diuretic
(chlorthalidone)in CHF
diet therapy
56. JOURNAL REFERANCE
• Mco vas from department of intensive care in
Netherlands conducted a retrospective study the
patient with intraabdominal hypertension, the sample
was 150patient after sodium intake within the 48 hour
of icu admission .99 out of 115 has urine cation
excretion .the study concluded that I AH not explained
by sodium intake or fluid balance
59. ETIOLOGY
• Increased potassium intake( orange juice banana rich
in potassium )
• Renal failure
• Hypoaldosteronism (lead decreased Na and k
exchange in the kidney)
• Fever sepsis
• Cell injury (release so much potassium )
60. • Potassium conserving diuretics(increases the urination
without losing potassium )
• Excessive infusion of potassium
• Acidosis( acidemia will tent to shift k+ out of the cell)
• Drug induced (ACE ,beta blockers et)
65. • History collection
• Physical examination
• Lab result (level of potassium level in blood and urine )
• ECG variation( flat P wave ,wide QRS , prolonged PR
,peaked T ,depressed ST)
66. •MANAGEMENT
Obtain serum potassium level vital sign and ecg if it is
stable repeat SPL test
Severe slp >6.5meq/l or
5.5meq/l with ECG
changes
Mild to moderate
Spl=5.5-6meq/l with no ECG
changes
Establish iv access and
discontinue the causes or
potassium contain
medication
discontinue the potassium
contain medication
Any ECG changes or unstable cardiac
rhythm
•MANAGEMENT
67. Administer calcium
gluconate 10 ml iv.
Re doses iv calcium
(after5mt if ECG
changes )
Administer 10u insulin iv
followed by 25g of
50%dextrose iv. insulin dose
may increase if it is not
improved
If adjunctive treatment
required
Yes No
No
Yes
68. Any kind of failure ,life threatening
hyperkalaemia have treatment method
failure
haemodialysis
Consider a low potassium
diet or adjusting situation
Yes No
Loop diuretics or potassium
binder to remove potassium from
the body
administer nebulized
or iv albuterosol
69. NURSING DIAGNOSIS
• 1) risk for injury related to muscle weakness
• 2) risk for decreased cardiac output related to
dysrhythmia
• 3) ineffective breathing pater related to muscle
weakness and paralysis
70. JOURNAL REFERANCE
• The study was conducted by venu velangpad
department of medicine usa about long term impact of
hyperkalaemia on mortality .he conducted
retrospective , observational case control study
.sample was 287 patient was admitted with
hyperkalaemia .study was on 2017 April .the study
concluded cardiovascular mortality was statistically
more prevalent in hyperkalaemia patient . So risk of
mortality high
72. ETIOLOGY
• Inadequate intake
• Npo
• Renal loses(most common cause is due to excessive
urination by water pill/diuretics)
• hyperaldosteronism
• Magnesium depletion
• Leukaemia(acute myeloid leukaemia)
• Gi loses(diarrhoea ,vomiting)
• Steroid (elevated aldosterone )
74. Low extracellular k+
Increase in the resting membrane potential
The cell become less excitable
Aldosterone is secreted
Sodium is retained in the body
Through reabsorption by kidney tubule
75. Through reabsorption by kidney tubule
Potassium excreted through urine
Develop clinical manifestation
76. •Clinical manifestation
alkalosis (excessive blood alkinity)
shallow respiration
Irritability
confusion
lethargy
threudy pulse
decreased intestinal motility
weakness (Initially it starting from leg muscle)
ECG (ST segment sagging ,T wave depression U wave
elevation )
78. MANAGEMENT
• Administration of od 40-80meq/day iv kcl must always
diluted and never given in concentrated
• Never push directed iv ,it diluted with .9% sodium
chloride (infusion pump)
• Administer with continues monitoring
• Rate of administration should not >10 meq/hr
• Dietary intake is 50-100meq/day
• Diet with high rich potassium( banana ,tomato et)
81. • Decreased oral intake
• Lactose intolerance(unable to digest lactose )
• Decreased vitamin d intake
• End stage of renal disease(decreased calcium
absorption)
• Diarrhoea
• Acute pancreatitis(tetany and hypocalcaemia)
• Hyperphosphatemia
• Immobility
• Removal or destruction of parathyroid gland
82. PATHOPHYSIOLOGY
Due to etiological factors
Fall in serum calcium level
Nerve fibres more excitable may discharge
spontaneously
Causing muscle spasm
Spasm of muscle of larynx
And affect lung muscle
May lead to death
83. CLINICAL MANIFESTATION
• Main two clinical manifestation are
chovostek’sign
it is the contraction of the facial muscle that is
produced by tapping the facial nerve in front of the ear
84. •Trousseau's sign
it is carpal spasm that occur by inflating a
BP s cuff on the upper arm 20mm/hg greater
than systolic pressure over 2-5mt
86. MANAGEMENT
• Manage underlying cause
• Mild to moderate oral supplementation (pregnancy -
1500mg/day)
(children 1000mg/day ,adult 500mg/day)
Iv calcium gluconate( 4.5ml and add 5.5ml nacl 9%)
Monitor ECG(long ST segment )
Administer oral calcium
Give calcium with full class of water( for dissolve and
absorb more quickly)
87. HYPERCALCEMIA
• Definition
calcium level >11mg/dl
Etiological factors
excessive calcium intake
excessive vitamin d intake
renal failure
hyperthyroidism (loss calcium from bone )
malignancy(bone related cancer)
Excessive milk or antacid intake increase
calcium deposit
88. PATHOPHYSIOLOGY
Due to etiological factors
increased level of calcium in the cell
cell membrane become refractory to repolarization
cardiac smooth muscle
activity decreased salt formation in the kidney
shorten Qt segment renal
impairment
93. MANAGEMENT
• Correcting the underlying causes
• Medical management
loop diuretics
calcitonin
bisphosphonate
glucocorticoid drug
isotonic sodium chloride
94. NURSING MANAGEMENT
• Assess stone ,muscle weakness ,anorexia ,et
• Assess the clinical manifestation
• Patient must drink 3000-4000ml of water
• Decrease food high calcium
98. Etiological factor
Alcohol interrupt the absIf calcium level fall in
the blood
Parathyroid hormone
release and calcium and
phosphate release from
bone
Break down the bone
ca2+combined with
phosphate and go to
nephron
Parathyroid hormone
prevent the reabsorption
Calcium reabsorption take
from kidney
Phosphate lost through
the urine
Clinical manifestation
developed
99. CLINICAL MANIFESTATION
• Mild (none)
• Sever muscle weakness , osteomalacia ,altered mental
status
• Stone formation
• Polyuria
• Bone pain
• Constipation
• Depression
• confusion
103. ETIOLOGY
• renal failure
• chemotherapeutic drug
• enemas containing phosphorus
• excessive ingestion of phosphorous
• large vitamin d intake
• Hypothyroidism(parathyroid hormone changes the
phosphate)
104. Etiological factor(kidney failure)
Increase reabsorption of phosphate from
kidney ,calcium lost through the urine
Decreased ca2+ in the blood will release the
Parathyroid hormone again
Reabsorption of calcium from the bone again
Secondary hyperparathyroidism
Again reabsorption of phosphate and
release of calcium
The bone become thin and weak
105. CLINICAL MANIFESTATION
• Mild cases (none)
• Severe cases neurone more excitable (tatani)
• Symptoms of hypocalcaemia (chvosteks sign
,trousseaus sign)
• Cristal form under the skin ,blood vessel , joint,
• Kidney stone
• nephrocalcinosis
107. MANAGEMENT
• Decreased the intake of phosphate contain diet,
medication
• Increase excretion by iv fluid and loop diuretics
• Improve hydration
• Correction hypocalcaemia enhance the excretion of
phosphate
111. PATHOPHYSIOLOGY
Low serum magnesium level
Increased acetylcholine release
Increased neuromuscular irritability
Increased sensitivity to acetylcholine at
the myoneural junction
Diminished
threshold of
excitation for the
motor nerve
Myofibril
contraction
114. MANAGEMENT
• Assess the patient condition
• Mild magnesium corrected by diet alone
• Magnesium salt can be administered
• Vital sign must be assessed frequently
• iv mg2so4
• Check deep tendon reflex
• Maintain urine output
117. Renal failure , excessive iv
infusion of mg
Accumulation of mg in
the body
Altered electrical
conduction
Mg level rises
Slowed heart rate and
av block
Diminished reflex
,drowsiness lethargy
Peripheral vasodilation
Hypotension ,flushing
increased
Severe respiratory
depression
Respiratory arrest may
occur
119. •DIAGNOSTIC STUDY
• Assess the serum mg level
• History collection
• Physical examination
•MANAGEMENT
• Ventilatory support
• Administer iv calcium gluconate(it directly antagonizes
neuromuscular and cardiovascular effect of magnesium
)
120. RESEARCH REFERENCE
• Mekee , conducted a study about analysis of braine
bioavailability of peripherally administered
magnesium sulphate .a study in human with acute
brain injury undergoing prolonged induced hyper
magnesium among 30 patient with acute brain
injury. The conclusion of study was hyper magnesium
produced marginal increase in the total CSF
121. BIBLIGRAPHY
• BOOKS
Lewis ,heitkempet et .medical surgical nursing .1st edition
.
Elsevier mosby publication,new deli; 2011
Erb’s ,kozier. Fundamental of nursing .9th edition .doling
Kindersley publication, new Delhi India pvt limited 2014
suddarth’s ,brunners .medical surgical nursing .12th
edition
wolters Kluwer publication .pvt new deli india ; 2012
Preload (end of ventricular filling during diastole)
Mean arterial pressure (average pressure in the arteries during cardiac cycle)
Tissue perfusion (oxygen and nourishment to tissue capillary level )
Increased pulse rate
Decreased urine out put
Increased respiratory rate
Weakness
Wight loss
Seizure
Coma
isotonic hypovolemia is (losing both water and electrolyte in equal amount)
Hypertonic (losing more fluid than solute )
Hypotonic (losing more solute than fluid ,decreased solute concentration in the body)
History of haemorrhage , gi problem injury
Hypotensio ,drowsiness
Elevated blood urea nitrogen (decreased renal blood fluid and dehydration ,formation hematicrite )
elevated urine specific gravity
Sodium bicarbonate is-salt of sodium
Heart failure –right ventricular heart failure (heart cant blood pump)
renal failure (kidney not to excrete water)
Cirrhosis of the liver (canot properly store fluid ,retention in abdominal area)
Cushing syndrome (it produce excessive cortisol and ACTH level to very low )
Bounding puls (when a person feel their heart beating harder or more vigorously
Weight gain (2% in mild ,5%mederate, 8%severe)
Dyspnoea (shortnes of breth)
Muscle spasm
Gfr (increased extracellular volume and decreased intracellular volume)
Blood investigation blood sodium ,other electrolyte
Sodium is high in kidney patient
Consult doctor if swelling without showing any reason present in the body
(1) Gi loss , sweating , use diuretics
(2) by using diuretics
(3)Burns ,wound drainage
4)SIADH, heart failure ,
(5) primary hypoaldosteronism (induse ADHand it may cause hyper volemia and hyper natremia)
(6) Hypotonic tube feeding , excesive drinking of water
So many study shows that Na and water correlated with severity of PH (POSTURAL HYPOTENTION )
Previous history ,family history ,history of disease past and present
Tremors ,muscle twitching ,and all clinical manifestation
NA level DECREASED
FVE FLUID VOLUME EXCESS
NURSING DIAGNOSIS
IV FLUID HYPERTONIC ,NACL,EXCESSIVE ISOTONIC SOLUTION
UNCONCIUSNESS ,COGNITIVE IMPAIRMENT
INCRESED INSENSIBLE WATERLOSS
USE OF OSMOTIC DIURECTICS
DRY OR STICKY MUCUS MEMBRANE
RUBBERY TISSUE TURGURE
WEIGHT LOSS
RESTLESSNESS
INCREASED B P
WEAKNESS LETHARGY
RESTLESSNESS
SEIZURE
COMA
RISK FOR INJURY RELATERD TO ALTERD SENSORIUM AND SEIZURE SECONDARY TO ABNORMAL CNS FUNCTION
POTENTIAL COMPLICATION OF SEIZURE
normal range is 3.5 -5.5mg/dl
Decreased potassium excretion
K is inner cellular cation
Aldosterone help the kidney to secrete the potassium
DECREASED B P
History ( renal failure ,injury ,hormonal problem excessive banana intake)
p/e clinical manifestation )
Electrolyte study k na cl
ECG chages of ecg
Albuterosol (beta adrenergic –it stimulate intracellular shift of potassium )
Calcium gluconate is the emergency medicin
(increased aldosterone's produce lead to lowered level of potassium
Mg associated with hypokalemia
History collection
Physical examination
Serum electrolyte (k na
ECG changes
Parathyroid hormone control the calcium level
Calcium needed for transmission of nerve impulse and regulate muscle contraction
Sign of latent tetany
Hyper reflexia of carpel region
History collection
Phisical examination
Serum study
Magnesium level increased in urin
Deposition of calcium salt in the renal parenchyma lead to
