Fluids and Electrolytes Compiled Notes.pdf

INFECTIOUS DISORDERS
Figure 6-3 Urinary Tract Infection
An infection (UTI) cause by bacteria, virus, fungus, that occurs in the urinary tract.
Risk for UTI increases when a patient has indwelling catheter, urinary retention,
urinary and fecal incontinence and poor perineal hygiene practices. Other risk factors
are renal scarring from previous infection, decrease ureteral peristalsis, presence of
urinary tract obstruction, being a female, sexual activity. The common causative
microorganisms are escherichia coli , staphylococcus, streptococcus,
enterobacter, klebsiella and aerobacter, pseudoaeriginosa.
Pathophysiology
The epithelilium of the kidneys, ureter and bladder are sterile in healthy
individuals, infection begins when bacteria enters , usually starting at the opening of
the urethra travelling up to the bladder. If the flushing or urinating cannot stop the
bacteria it can move up further to the ureters and kidney. Lower urinary tract
infection( UTI) rarely cause complications but upper UTI if untreated can spread into
the blood stream potential for chronic illness and death .
1. URETHRITIS – is inflammation of the urethra.
Causes
Microorganisms ( Escherichia coli, Chlamydia Trichomonas, Neisseria gonorrhoeae,
and herpes simplex virus type 2),trauma, or hyper-sensitivity to chemicals in products
such as vaginal deodorants, spermicidal jellies, or bubble bath detergents.
Signs and Symptoms
dysuria, frequency, urgency, and bladder spasms. A urethral discharge may
be noticed.
Medical Diagnosis
Based on patient signs and symptoms, urinalysis, and urethral smear
Medical Treatment
Antimicrobials when it is caused by microorganisms. If the patient is sexually
active, the patient and the sexual partner may be treated with antimicrobials to
prevent reinfection.
Nursing Intervention
Sitz baths are soothing and may reduce the pain . Instruct female patients to
wipe from front to back after toileting, and to void before and after sexual intercourse .
Discourage bubble baths and vaginal deodorant sprays. Instruct uncircumcised male

patients to clean the penis under the foreskin regularly. Advise patients to void after
swimming.
2. CYSTITIS - is inflammation of the urinary bladder. The most common
Causes
Bacterial contamination, prolonged immobility, renal calculi, urinary diversion,
indwelling catheters , radiation therapy, and treatment with some types of
chemotherapy.
Signs and Symptoms
urgency, frequency, dysuria, hematuria, nocturia, bladder spasms,
incontinence, and low-grade fever. Urine may be dark, tea colored, or cloudy.
Fever, fatigue, and pelvic or abdominal discomfort and bladder spasms
experienced as pain behind the symphysis pubis.
Medical Diagnosis
Urinalysis, culture, and sensitivity. The presence of bacteria does not mean that
the patient has an infection unless the patient also has white blood cells (WBCs) in
the urine.
Medical Treatment
Antibiotic , mild analgesic such as acetaminophen is useful for relieving
discomfort. Phenazopyridine (pyridium) and Oxybutynin chloride (Ditropan may be
ordered for 2 to 3 days to decrease discomfort and bladder spasms.
Nursing care
advise patient to complete the entire course of antibiotics and take analgesics as
ordered.If phenozopyradine is given, advise patient that the drug causes red-orange
urine Warm sitz bath , oral fluid intake 30m/kg of fluid per day.
To reduce risk of future infection, teach patient to, wear cotton undergraments, avoid
tight-fitting clothing in the perineal area, take shower instead of tub bath, avoid
caffeine drinks, apple, grapefruit, orange these irritates the bladder, maintain high
fluid intake and void often, Wiping from front to back after voiding for female and drink
a glass of water after swimming ,before and after intercourse to flush the bacteria.
3. PYELONEPHRITIS – inflammation of the renal pelvis. It may affect one or both
kidneys.
Cause
Acute pyelonephritis is most often caused by an ascending bacterial infection, but it
may be bloodborne. Chronic pyelonephritis most often is the result of reflux of urine
from inadequate closure of the ureterovesical junction during voiding. It is also
usually caused by long standing UTIs with relapses and reinfections, may even lead
to chronic renal failure .
Signs and Symptoms
High fever, chills, nausea, vomiting, and dysuria. Severe pain or a constant dull ache
in the flank area. The patient with chronic pyelonephritis experience fatigue,
hypertension, increase BUN and creatinine and a slight aching over one or both
kidneys.
Medical Diagnosis
Urinalysis, urine culture and sensitivity, CBC, IVP, cystoscopy
Medical Treatment

Antibiotics, urinary tract anti-septics, analgesics, and antispasmodics . Additional
medications may be needed to treat hypertension. Adults are advised to dink at least
eight 8-oz glasses of fluids daily. Intravenous fluids may be ordered if the patient has
nausea and vomiting. Dietary salt and protein restriction may be imposed on the
patient with chronic disease. follow-up cultures to determine whether the infection
has been resolved.
Nursing Interventions
Record the presence of signs and symptoms, history of previous urinary disorders,
fluid intake at least 8 oz of glasses a day, advise patient to complete the entire course
of antibiotics and take analgesics as ordered. Limit physical activity and exercise ,
protein and salt dietary restrictions if advised by the physician.

KIDNEY TRANSPLANT
- Is the surgical implantation of a human kidney from a compatible donor to a
recipient.
DONOR:
LIVING
1. ABO Screening
2. Tissue specific antigen & human leukocyte antigen histocompatibility
3. Excellent health
4. Full functioning kidneys
5. Emotionally ready
6. Full understanding of the process
CADAVER:
1. Below 60 yrs of age
2. Brain death
3. Normal renal function
4. No metastatic disease, HIV, Hep. B
S/S OF REJECTION
oliguria
fever
pain
tenderness over transplant site
hypertension
creatinine increase
COMPLICATION POST TRANSPLANT
rejection
infection
malignancy (basal and squamous cell carcinoma.-skin,lips, vulva, lungs
cardiovascular – hypertension
IMMUNOSUPPRESSIVE DRUGS

Cyclosporine (Neoral)- blocks interleukin
Azathioprine (imuran) – blocks DNA preventing
lymphocyte proliferation
Corticosteroids (prednisone)- block cytokines
Cyclophosphamide (cytoxan)
Tacrolimus (prograft) – blocks calcineurin and T cell
Mycophenolate (cellcept)- inhibit B & T lymphocyte
OKT 3 - antilymphocyte globulin
NURSING MANAGEMENT FOR RENAL TRANSPLANT
• Maintain fluid balance by monitoring I & O
• Monitor laboratory studies for graft function and electrolyte balance
• Monitor for s/s of graft rejection
• Monitor wound drainage
• Adhere to immunosuppression schedule
• Monitor blood glucose levels related to high glucocorticoids
• Arrange supply of medications prior to discharge to prevent disruption of
immunosupressions
• Arrange post discharge follow - up appointments
NURSING DIAGNOSES POST KIDNEY TRANSPLANT
• Altered nutrition : more than body requirements related to side effects of
immunosuppressant agents
Less than body requirement: related to increased caloric needs after
transplant
• Altered protection and risk for infection related to immunosuppression required after
transplantation
• Effective management of Therapeutic Regimen related to post-transplantation
regimen
• Pain related to transplantation surgery
• Risk for Ineffective Individual Coping after transplantation related to increased stress,
anxiety, fear, and lifestyle changes
• Risk for injury: rejection of transplanted organ related to impaired
immunocompetence
INTERNAL JUGULAR CATHETER
- a central venous catheter inserted through the internal jugular vein.
SUBCLAVIAN CATHETER
- Central venous access via the subclavian vein has several advantages over other
possible locations.
ARTERIOVENOUS GRAFT – artificial graft made of gore-tex or a bovine carotid
artery is used
Risks & Complications in Hemodialysis
• Hypotension
• Blood loss from technical problem
• Muscle cramps
• Disequilibrium syndrome
• Air embolism
• Hypoglycemia

• Cardiac arrythmia
Nursing Care Before and During dialysis
• Check the dialysis order { BFR, duration, bath, UFR, heparin, K+ } * SLED
• Chart client’s weight { DRY WEIGHT}
• Assess vital signs
• Check patency of vascular access
• Withhold antihypertensives
• Ensure bed rest with frequent position change
• Monitor closely for complications
• Monitor blood line connections, arterial and venous and transmembrane pressure
in the dialysis machine
Nursing Care Post Hemodialysis
• Check VS Nursing
• Record post dialysis weight
• Resume all medications
• Apply pressure dressing on decannulated sites
• Protect IJ/subclavian catheter with sterile dressing

REVIEW OF ANATOMY AND PHYSIOLOGY OF THE RENAL SYSTEM
Figure 6-1 Urinary System
The renal system is responsible for maintaining homeostasis in the body by carefully
regulating fluid and electrolytes, acid – base balance, removing wastes, and providing
hormones responsible for red blood cell production, hypertension and bone
metabolism. The renal system is composed of the upper and lower urinary tract.
Lower Urinary System
A. Bladder
The bladder is an extra peritoneal organ that lies behind the symphysis pubis .
Its main function is for storage of urine. As volume of urine increases, starting from
300-500 ml, awareness of the need to void develops. Voluntary voiding is
accomplished by stimulation of the parasympathetic nerve fibers causing coordinated
contraction of the detrusor muscle and the bladder body.
B. Urethra
The urethra drains urine from the bladder to an exterior opening of the body, the
external urethral orifice. In females, the urethra is about 3 to 4 cm. (1.5 in.). In males,
the urethra is about 15 to 20 cm (6 to 8 in.) Micturition, or urination, is the process of
releasing urine from the bladder into the urethra.
Upper Urinary System
Figure 6-2 Structure of the Kidneys

Kidneys
The two kidneys lie on the posterior wall of the abdomen outside the peritoneal cavity.
Each kidney of the adult human that weighs about 150g is about the size of an
indented region called the hilum through which passes the renal artery and vein,
lymphatic, nerve supply. The outer part is the cortex and inner region called medulla.
The medulla is divided into multiple cone shaped masses called renal pyramids. The
base of each pyramid terminates in the papilla, which projects into the space of renal
pelvis, a funnel shaped continuation of the upper end of the ureter. The outer border
of the pelvic is divided into minor calyces, the walls up the calyces, pelvis that contain
contractile elements that propel the urine toward the bladder, where urine is stored
until it is emptied by micturition.
The functional unit of the kidney is the nephron. Millions of nephrons are present
in each human kidney which aid in the urine production and process of removing
metabolic waste products from the blood. These significant structures extend between
the cortex and the medulla. At one end of the nephron is closed, expanded and folded
into a double-walled cuplike structure called the Bowman’s capsule. This capsule
encloses glomerulus, the nephron’s primary structure in filtering function.
Functions of Kidney
Kidney performs different functions in order to maintain homeostasis in the body
by excreting metabolic waste products and reabsorbing necessary elements for the
body. The following are the functions of the kidney:
1. Formation of urine
The formation of urine happens in three phases which are filtration, reabsorption
and secretion. Each of these processes happens in the body in order to create
homeostasis by removing those metabolic waste products and reabsorbing helpful
substances.
a. Filtration. The filtration process is nonselective, passive process which forms
essential blood plasma without blood protein but both of it is normally too large to
pass through the filtration membrane. If any of the two appeared in the urine, it would
mean that there is a problem in the glomerular filters. The water and solute are
smaller than proteins that are forced through the capillary walls and pores of
Bowman’s capsule into the renal tubule.
b. Reabsorption. Tubular reabsorption is achieved by active and passive transfer
mechanism Sodium, potassium, calcium, phosphate, and uric acid are actively
reabsorbed. Urea, water, chloride, some bicarbonates and some phosphate are
passively reabsorbed. Most reabsorption occurs in the proximal tubule which
conserves needed substances but does not reabsorb metabolic waste products.
c. Secretion. Some of substances such as hydrogen and potassium ion, creatinine,
and ammonia, move from the peritubular capillary blood and secreted by the tubule
cells into the filtration. Excreting nitrogenous waste products , unnecessary and
excess substances .
2. Body’s Water Volume Regulator
Regulation of water in the body contained in the blood is greatly influenced by
antidiuretic hormone (ADH), also called vasopressin. Vasopressin is produced in the
hypothalamus and stored in nearby pituitary gland. Receptors in the brain monitor the
blood’s water concentration causing the release of ADH in the bloodstream if the
amount of salt and other substances is too high. ADH in the bloodstream causes
more water to be reabsorbed into the bloodstream. In the absence of ADH, the
collecting ducts become impermeable to solute and water, making it less
concentrated than plasma and the urine is diluted.
3. Excretion of Metabolic Waste Products
The kidney functions as the body’s main excretory organ, eliminating the body’s
metabolic waste products and serves as the primary mechanism for excreting drug

metabolites. 25g to 30g of urea is produced as the end product of protein breakdown
and excreted daily making it the major waste product of protein metabolism. Other
waste products are creatinine, phosphates and sulfates. Uric acid, formed as a waste
product of purine metabolism, is also eliminated in the urine.
4. Blood Pressure Regulator
Regulating blood pressure is linked to the kidneys' ability to excrete enough
sodium chloride (salt) to preserve normal sodium balance, extracellular fluid volume
and blood volume.
5. Regulation of Acid-Base Balance
The kidney also adjusts the body’s acid-base balance to prevent such blood
disorders as acidosis and alkalosis. It helps maintain normal pH by retaining or
excreting hydrogen ions and regenerating lost buffer. The kidneys excrete acids that
the lungs cannot excrete and they can excrete hydrogen ions or reabsorb bicarbonate
to correct acidosis. They can reverse this process to correct alkalosis. Only renal
mechanisms can remove metabolic acids and excess bases from the body.
6. Regulation of Red Blood Cell Production
Decreasing amount of oxygen in the renal blood flow activates the release of
erythropoietin. Erythropoietin stimulates the bone marrow to produce red blood cells,
thereby increasing the amount of hemoglobin available to carry oxygen.
7. Vitamin D Synthesis
The kidneys are also responsible for the final conversion of inactive vitamin D to its
active form, 1,25-dihydroxychole-calciferol. Vitamin D is necessary for maintaining
normal calcium balance in the body.
8. Secretion of Prostaglandins
The kidneys also produce prostaglandin E and prostacyclin, which have a
vasodilatory effect and are important in maintaining renal blood flow.

DIALYSIS
• A technique in which a substance move from the blood through a semi permeable
membrane into a dialysis solution.
3 PHYSICAL PRINCIPLES (osmosis. Diffusion, ultrafiltration)
Indications of dialysis
1. GFR less than 5 to 1O ml/min
2. Manifestations of uremic syndrome
TWO TYPES
1. Hemodialysis – removal of waste and water by circulating the blood into a
dialyzer through a dialysis machine.
2. Peritoneal dialysis – repeated cycles of instilling dialysate into the peritoneal
cavity.
4 BASIC GOALS OF DIALYSIS
1. Remove waste products from protein metabolism.
2 .Maintain safe concentration of serum electrolytes
3. Correction of acidosis and replenish blood’s bicarbonate system.
4. Removal of excess water
Figure 6-8 Hemodialysis
Components of Hemodialysis
• Dialyzer – Artificial filter containing fine fibers acting as artificial kidney
• Dialysate - Dialysis solution or bath containing sodium, potassium, calcium,
chloride, magnesium, bicarbonate, ph, glucose use to remove toxins , nitrogenous
waste products and excess water from the blood
• Vascular access - direct method of circulating the blood into the dialyzer
• Dialysis machine

Figure 6-9 AVF
External shunt – silastic cannula in the forearm or leg inserted into the artery and the
vein to form an external blood path.
Arteriovenous fistula (AVF) – anastomosis of the artery and the vein
Arteriovenous graft – artificial graft made of gore-tex or a bovine carotid artery is
used
Internal Jugular Catheter – A dialysis catheter containing arterial and venous lumens
inserted in the jugular vein
Complications in Hemodialysis
• Hypotension – Decrease blood pressure as a consequence of reduce cardiac output
secondary to excessive water and sodium removal
114
• Blood loss from technical problem – Blood loss related to blood clotting in the circuit
or blood loss due to loose connections .
• Muscle cramps – Involuntary muscle contraction due to excessive water and sodium
removal

• Disequilibrium syndrome – A neurologic deterioration during dialysis manifested as
headache,nausea,vomiting due to marked decrease of blood urea nitrogen in the
cerebrospinal fluid and brain tissue.
• Air embolism – Obstruction of the circulation by air related to air entry in the blood
circuit
• Hypoglycemia – Low blood sugar concentration related to glucose diffusing out of
the blood
• Cardiac arrythmia- Disturbance in the electrical impulse formation or conduction
related to electrolyte and ph changes during dialysis or underlying heart disease
Nursing Care Before and During dialysis
• Check the dialysis order { BFR, duration, bath, UFR, heparin, K+ } * SLED
• Chart client’s weight { DRY WEIGHT}
• Assess vital signs
• Check patency of vascular access
• Withhold antihypertensives
• Ensure bed rest with frequent position change
• Monitor closely for complications
• Monitor blood line connections, arterial and venous and transmembrane pressure
in the dialysis machine
Nursing Care Post Hemodialysis
• Check VS Nursing
• Record post dialysis weight
• Resume all medications
• Apply pressure dressing on decannulated sites
• Protect IJ/subclavian catheter with sterile dressing
NURSING CARE FOR AVF/GRAFT
• Assess for bruit or thrill
• Assess for bleeding, pain
• May squeeze rubber ball to help in the development of the vessel
• Avoid venipuncture, blood pressure taking on the arm with the vascular access
• Avoid sleeping and wearing of tight fitting clothing on access extremity
• Instruct client not to lift heavy objects using the extremity with the vascular access.
• keep dressing dry
• Keep catheter taped to the skin and prevent pulling of the catheter to prevent
accidental removal
the patient to clamp remaining tail of the catheter and apply direct pressure at
insertion site with occlusive dressing if accidental removal of catheter happens
PERITONEAL DIALYSIS
- repeated cycles of instilling dialysate into the peritoneal cavity and
the peritoneum is the dialyzing membrane.
CYCLES OF PD
1.inflow ( infusion) – the solution is introduced into the peritoneum through a
catheter by gravity
115
• tenckhoff catheter, a siliconized rubber catheter, inserted 3-5 cm below
umbilicus, stabilized by dacron cuffs where fibroblast and blood vessel grow, fixing the
catheter in place, occurring 1-2 weeks after insertion

2. dwell (equilibrium) – solution is retained in the peritoneal cavity for a prescribed
period to allow better exchange and clearance.
3. Drain ( outflow) – process of removing the previously retained solution in the
peritoneal cavity by gravity.
Peritoneal Dialysis Complications
• drainage obstruction – Presence of fibrin or clots in the tubings
• Difficulty of breathing – Dialysis solution in the peritoneum during dwell time may
push the diaphragm
• Bleeding – Bloody dialysate or in the PD catheter insertion site related to the
procedure, manipulation or trauma
• Peritonitis – Microorganism gaining entry into the peritoneum related to poor aseptic
technique during the dialysis procedure
Nursing Responsibilities
•VS and complication monitoring
•Pre warm the solution
•Documentation of the three phases of PD (Solution use, time infused, retain, drain
including the amount, color, appearance )
Table 6-7 Sample Documentation OF Peritoneal Dialysis
Date Vital
Signs
Meds
Added
to
Solution
IN
Solution
OUT
Difference
+ / -
Cumulative
Difference
Remarks
No of
Cycles
BP PR Time
Started
Time
Finished
Vol Time
Started
Time
Finished
Vol
1 Perisol
2.5%
8:30 8:45 1L 10:45 11:00 1200 -200 Slightly
bloody
2 11:00 11:15 1L 1:00 1:25 1300 -300 -500
3 1:25 1:40 1L 340 4:00 800 +200 -300
4 4:15 6:30 11:00 1100 -100 Clear

GLOMERULAR DISORDER
Nephrotic Syndrome - is an alteration of kidney function caused by increased
glomerular basement membrane permeability to plasma protein (albumin). Altered
glomerular permeability result in characteristic symptoms of gross proteinuria,
generalized edema (anasarca), hypoalbuminemia, oliguria, and increased serum lipid
level (hyperlipidemia). It maybe primary, wherein the pathology is the kidney itself or
secondary of which nephrotic syndrome is the renal manifestation of a systemic
disease .Nephrotic syndrome , usually occurs in children between ages 2-6 but may
affect adults , both sexes and any race.
Pathophysiology
Normally large protein cannot pass through the glomerulus. Proteinuria occurs
because of changes to capillary endothelial cells of the glomerulus.The mechanism of
damage to these structures is unknown in primary and secondary glomerular
diseases, but evidence suggests that T cells may upregulate a circulating permeability
factor or downregulate an inhibitor of permeability factor in response to unidentified
immunogens and cytokines. Other possible factors include hereditary defects in
proteins that are integral to the slit diaphragms of the glomeruli, activation of
complement leading to damage of the glomerular epithelial cells and loss of the
negatively charged groups attached to proteins of the GBM.
Figure 6-5 Pathophysiology of Nephrotic Syndrome
Signs and Symptoms
Massive proteinuria , hypoalbuminemia, generalized edema, hyperlipidemia
lipiduria , hypercoagulability and hypertension.
Medical Diagnosis
Urinalysis, serum albumin, renal ultrasound and biopsy. Serologic studies for
infection and immune abnormalities e.g. antinuclear antibody.
Medical/Pharmacologic Management
• Blood-pressure medications , ACE inhibitors and ARBs, which curb the pressure in
the glomeruli and lower the amount of protein in the urine
• Diuretics to reduce swelling
• Cholesterol-lowering drugs
• Blood thinners, or anticoagulants

• Corticosteroids
• Limit salt to reduce swelling and low in saturated fats and cholesterol diet.
• Dialysis if conservative management is not effective .
Nursing Management
1. limit oral fluid intake, low sodium, protein and saturated food sources diet
2. I & O
3. Skin care
4. Reverse isolation, vit c rich diet
5. Monitor lymphocytes & wbc
6. Monitor complications ( pulmonary edema, hypertension, CHF, renal
failure,stroke, )
7. Report fever, malaise & adverse effects of meds
Nursing Diagnoses
a. Fluid Volume
b. Imbalanced Nutrition: Less Than Body Requirements
c. Fatigue
d. Deficient Knowledge
e. Risk For Infection

OBSTRUCTIVE DISORDERS
Figure 6- 4 Renal Calculi ( Urolithiasis )
Renal calculi is the formation of stones in the urinary tract . These are crystalline
structures that form from the components of urine.
Pathophysiology
Most calculi are precipitations of calcium salts (phosphate and oxalate),uric acid,
magnesium ammonium phosphate (struvite) or cystine. These substances are
normally found in the urine.
Factors Fostering Calculi Formation
Concentrated urine
Excessive intake of vitamin D, animal protein, oxalates, sodium, sucrose,
vitamin C, calcium based antacids
Familial history
Immobility, urine stasis, sedentary lifestyle
Altered urine pH
Lack of kidney substance that inhibits calculi formation
Signs and Symptoms
Pain depends on the location of the stone. Nausea, vomiting ,hematuria and
signs and symptoms of UTI
Medical Diagnosis
Urinalysis, urine culture and sensitivity ,IVP, ultrasound
Computed tomography (CT) scan
Medical ,Surgical and Pharmacologic Management
Phases of Stone Management
1. Acute phase
- narcotics, antispasmodic, anti -emetic, warm bath to relieve flank pain
2. Elimination of stone
- Waiting to be passed out
- Mechanical intervention
- Surgical intervention
3. Long term prevention of recurrence
- OFI (3-4l/day), diet, medication

Pharmacologic Management
1.potassium citrate therapy - It attaches to calcium in the urine, preventing the
formation of mineral crystals ; prevents the urine from becoming too acidic .
2.Thiazides – increases urinary Ca excretion
3. Allopurinol – prevents formation of uric acid nidus
FOR SMALL STONES
4. Alpha blockers or α-adrenergic-antagonist - It relax muscle tension in the ureter and
facilitate passage
E.g. tamsulosin
5. Sodium bicarbonate
6. Pain relievers
Surgical and Non-surgical Management of Stone
Often calculi pass spontaneously, if it does not pass and symptoms continues , other
options may be used to destroy or remove the calculus.
Surgical management are indicated if there is progressive renal damage,
obstruction of urine flow , presence of infection and severe pain. The surgical
procedures are Nephrolithotomy (removal of kidney stones) and ureterolithotomy
(removal of stones in the ureters) .
For non-surgical approach, options include ureteral stent placement, lithotripsy,
cystoscopic stone removal, and percutaneous nephrolithotomy.
Ureteral Stent- are small tubes inserted into the ureter to treat or prevent a blockage
that prevents the flow of urine from the kidney to the bladder.
Lithotripsy is a process of eliminating a calculus in the renal pelvis, ureter , bladder
by crushing the stone. It can be accomplished by Extracorporeal shock wave
lithotripsy (ESWL) which utilizing sound, laser, or shockwave energy with a use of a
lithotripter. It is guided by an ultrasound probe, the energy is directed to the stone
through a water-filled cushion.
Table 6-1 Complications of ESWL
Relate d to Shock Fragments Related to Shock waves
colic Bruising /hematoma
Incomplete fragment urosepsis
Blocking of ureters by the multiple stone
fragments
Cystoscopy/Ureteroscopy - use of lighted scope or a tube inserted into the urethra
into the bladder and ureters to remove stone and uses a laser fiber to crush
the stone in the case of ureteroscopy.
Percutaneous nephrolithotomy – The surgeon creates a tunnel directly through the
skin into the kidney and uses ultrasound or electrohydrolysis to break the stone into
pieces. this approach is usually used when stones are large and cannot be broken
with lithotripsy.

Dietary Management
Prevention of stone recurrence is important .Apart from high fluid intake to keep urine
diluted dietary restrictions are also important and the dietary restrictions depend
on the type of stone
Table 6- 2 Recommended Diet for Stone Management
Acid Ash Diet ( To acidify the urine) Alkaline Ash Diet ( To alkalinize the
urine)
Calcium Stones
cranberry, prune juice,meat, egg,
poultry,fish,grapes, whole grains
limit milk and other dairy products
Oxalate Stones
milk, vegetables, fruits except
prunes, cranberry, plums
Avoid tea, chocolate, rhubarb,
spinach
Uric Acid Stones -
Reduce foods high in purine like
liver, brain, kidneys, venison,
shellfish, meat soup, gravies,
legumes
Nursing Management
1. administer prescribed analgesics
2. reassure client that most stones smaller than 4mm can pass out spontaneously
3. provide education to prevent future and recurrence of stone
4. encourage OFI
5. instruct client to avoid foods that contribute to the diagnosed type of stone
Nursing Diagnoses
Acute pain related to renal calculi
Ineffective coping related to anxiety , low activity level and inability to perform
ADL
Impaired urinary elimination related to renal calculi
Risk for infection
Nutrition imbalance, less than body requirements related to nausea

NEUROGENIC BLADDER
- - urinary bladder malfunction due to neurologic dysfunction emanating from internal
or external trauma, disease or injury.
- Interference of the bladder normal mechanism cause by the disruption of the central
and peripheral nervous system
Review of The Neuro Anatomy
- The normal function of the urinary bladder is to store and expel urine in a
coordinated, controlled fashion. This coordinated activity is regulated by the central
and peripheral nervous systems. Normal voiding is essentially a spinal reflex ,
modulated by the central nervous system (brain and spinal cord), which coordinates
function of the bladder and urethra.
The brain receives input via afferent pathways that ascend from the bladder
and provide feedback on how full the bladder is. Higher brain centers then determine
whether it is socially acceptable to void and trigger downstream structures to permit or
suppress the voiding reflex. The pons is a major relay center between the brain and
the bladder. The mechanical process of urination is coordinated by the pons in the
area known as the pontine micturition center (PMC).
The PMC coordinates the urethral sphincter relaxation and detrusor contraction to
facilitate urination. Emotions, experienced in higher brain centers, may exert
downstream effects on the PMC, which is why some people can experience
incontinence with excitement or fear. The spinal cord functions as a long
communication pathway between the brainstem and the sacral spinal cord ( terminal
portion of the spinal cord, situated at the lower back in the lumbar area responsible for
bladder contractions) When the sacral cord receives the sensory information from the
bladder, this signal travels up the spinal cord to the pons and then ultimately to higher
brain centers. a spinal cord injury can lead to urinary frequency, urgency, and urge
incontinence, which may be complicated by difficulty emptying the bladder. This
occurs because the urinary bladder and the sphincter are no longer coordinated
Pathophysiology
Normal bladder function relies on information travelling through neural pathways from
the cerebral cortex, through the spinal cord, and on to the bladder to coordinate
normal micturition and urinary continence. When this pathway is damaged, it can
result in loss of bladder sensation and also the loss of the coordination between
urethral sphincter and its muscles, these muscles may not contract even when the
bladder fills or the person has the urge to void, leading to bladder dysfunction such as
urinary incontinence and retention (Mauk 2012).
TYPES OF NEUROGENIC BLADDER
A. Spastic- Sensory and voluntary control of urination is disrupted partially or totally.
The stimuli generated by bladder filling cause frequent spontaneous detrusor muscle
contraction and involuntary emptying caused by disruption of CNS transmission
above the sacral spinal cord segment.
Causes:
1) Spinal cord injury- most common cause
2) Stroke
3) MS- immune mediated inflammatory disease attacking the myelin and axons
4) CNS lesions

B. Flaccid- damage to the sacral spinal cord at the level of the reflex arc, cauda
equina, sacral nerve roots leading to loss of detrusor muscle tone resulting to
overdistention, weak and ineffective detrusor muscle contraction.
Causes:
1) Spinal shock phase (6-12 weeks)in SCI
2) Myelomeningocele or meningocele – type of neural tube birth defect wherein the
backbone and spinal canal don’t close before the baby is born; a type of spinal bifida
3) Peripheral neuropathies- DM most common cause ,metabolic derangement of the
Schwann cell results in segmental demyelination and impaired nerve conduction.
4) MS
5) Chronic alcoholism
6) Prolonged overdistention of the bladder
Symptoms of Neurogenic Bladder
Overactive bladder, frequent urination, stress incontinence.urge incontinence ,urinary
retention, underactive bladder ( bladder cannot send signal when full)
Diagnostic Tests
Table 6- 3 Neurogenic Bladder Diagnostics
DIAGNOSTIC TEST PURPOSE PROCEDURE NURSING
RESPONSIBILITY
1) Urine culture,
Urianalysis
Detect UTI Urine sample Midstream clean
catch
2) Creatinine, BUN
* ascending infection,
vesicoureteral reflux in
neurogenic bladder can
damage kidneys
Determine
kidney
damage
Blood extraction Avoid meat
3) Postvoid bladder
scan
*>50mL means
ineffective detrusor
muscle contraction Less
than 50mL PVR is
adequate bladder
emptying
Over 200mL PVR
indicates inadequate
emptying
Children-
More than 20mL PVR is
considered abnormal
Elderly-
50-100 ml PVR is
considered normal
Measures
residual urine
in the bladder
shortly void;
this can be
accomplished
through
ultrasound,
bladder scan, or
by directly
measuring the
urine volume
drained by a
urinary catheter.
Urinary
catheterization is
the gold standard
for measuring the
post-void
residual.
Explain the
procedure
4) Cystometography To evaluate
bladder filling
and detrusor
muscle
function
Shows the
Double lumen
catheter is
inserted into the
bladder, 50 ml is
introduce in one
lumen and
Explain the
procedure

relationship of
intravesical
pressure with
the changing
volume of
urine in the
bladder
pressure is
recorded through
the other lumen
10cms
water for
50-400ml
of urine
5) CYSTOSCOPY To determine
presence of
bladder
lesions
Flexible
cyctoscope
inserted into the
bladder , using
also video system
and irrigating
medium
Explain procedure,
local or GA maybe
use,
Supine or lithotomy
position
MEDICAL MANAGEMENT OF NEUROGENIC BLADDER
GOAL: Maintain continence and avoid complication associated with overfilling or
incomplete emptying of bladder through self-care. Thus, teaching is the primary
intervention.
I. MEDICATIONS
GOAL:
- increase or decrease contractility of detrusor muscle.
- increase/decrease internal sphincter tone.
- relax external urethral sphincter.
Table 6-4 Medications For Neurogenic Bladder
ANTICHOLINERGIC DRUG TO
PREVENT SPASTIC BLADDER
CHOLINERGIC DRUGS TO
STIMULATE MICTURITION
1. Darifenacim (Enablex)
2. Oxybutynin (Ditropan )
3. Solifenacin succinate (vesicare)
4. Trospium (santural)
5. Tolterodine (destrol)
6. Propantheline bromide
(pro-bannthine)
7. Flavoxate hcl (urispas)
*inhibits response to acetylcholine
relaxing the detrusor muscle and
increase sphincter tone
*acetylcholine is a neurotransmitter
causing muscle to contract,activate
pain responses,regulates
endocrine and REM sleep
functions
1. bethanechol chloride (Urecholine)
*stimulates parasympathetic NS
increasing detrusor muscle tone
producing contraction strong enough to
produce micturition

II. NUTRITION
-Moderate to increase OFI to decrease UTI and stone formation
- Diet to acidify urine (cranberry)
III.BLADDER RETRAINING
Measures to stimulate reflex voiding for patients with spastic neurogenic bladder
• Stroke or pinch abdomen, inner thigh, glans penis (trigger points to stimulate
urination)
• Pulling pubic hair
• Tapping suprapubic region
• Inserting gloved finger to rectum and gently stretch anal sphincter
• Crede’s method- applying suprapubic pressure with finger of one or both hands
ALERT: may stimulate SNS causing sudden increase of blood pressure for patients
with SCI (autonomic dysreflexia -medical emergency )
• Valsalva maneuver- bearing down while holding one’s breath
CATHETERIZATION- intermittent for patients with SCI
SURGICAL MANAGEMENT
Maybe required when urination can’t be effectively managed using conservative
measures.
1) Rhizotomy- destruction of the nerve supply to the detrusor muscle or the external
sphincter for patients with hyperreflexia or spasticity.
2) Urinary diversion-
3) Implantation of artificial sphincter
Nursing Management
1. Promote urinary drainage and continence
2. Prevent complication
3. Teach patient and family self-care techniques
Nursing Diagnoses
1) Impaired urinary elimination related to impaired bladder innervation
2) Toileting self-care deficit related to neurologic injury
3) Risk for impaired skin integrity related to urinary incontinence
4) Risk for infection related to impaired urinary reflex

RENAL EXCRETORY STUDY
URINALYSIS - assessed the nature of the urine produce and evaluates the
color,ph and specific gravity, determines the presence of glucose (glycosuria,
protein, blood(hematuria), ketones ( ketonuria) and analyzes sediment for
cells (WBC, called pyuria, casts bacteria, crystals)
Nursing Responsibilities:
Cleanse perineal area, spread labia and cleanse meatus from front to back using
antiseptic sponge, for males, retract foreskin for uncircumcised penis and cleanse
glans antiseptic sponge, must be analyze 1 hour after of collection, For 24 Hour urine
collection ( creatinine clearance) discard the first voided urine, collect all subsequent
urine in a sterile container for 24 hours.
Kidney, ureter ,bladder X-ray (KUB ) - plain film abdominal flat plate x-ray
identifying the number and size of kidneys with tumors, malformations and
calculi ; no special preparations needed
IVP – fluoroscopic visualization of the irinary tract after injection with a
radiopaque dye
Nursing Responsibilities - Test for iodine sensitivity, enema before the procedure, 8
hours, NPO, push fluids after.
ULTRASOUND – non- invasive visualization of the kidney, ureter, bladder
through the use of sound waves
Nursing Responsibilities- Supine position, NPO not required, cleanse conducting
gel from skin after the procedure
CYSTOSCOPY – use of lighted scope to inspect the bladder (CYSTOSCOPE);
maybe use to remove tumors, stones, or other foreign materials or use to
implant radium, place catheters in the ureters.
Nursing Responsibilities Before the Procedure
Explain the procedure will be done under local or general anesthesia, secure consent,
administer sedative as ordered, NPO for general anesthesia, or NPO after light
breakfast for local anesthesia, enema as ordered ,let client assume a lithotomy
position
Post Procedure
Mild analgesic or warm sitz bath to relieve pain, I &O and temperature monitoring,
explain that
hematuria expected post 24-48 hours, assess for clots, burning sensation upon
urination maybe felt, and
force fluids.
RENAL BIOPSY – removal of kidney tissue for microscopic study
Open method promotes better visualization but high risk for infection, close method
none by aspiration with a fine needle and has less risk for infection
Nursing Responsibilities before and during the procedure
Secure consent,NPO after midnight,assess hemoglobin and coagulation
studies ,assist client to assume
Prone position with a pillow below the abdomen, apply pressure for 20 minutes on the
aspirated area after the procedure
Post Procedure
Flat bedrest for 24 hours, monitor for hemorrhage, hypotension, dizziness,
tachycardia ,pallor , back, flank and shoulder pain, avoid strenuous activities,

coughing, sneezing and straining, encourage fluid to avoid urinary retention and clots,
monitor hemoglobin, assess for hematuria and if present should cease 24 hours
after the procedure. Administer analgesics
Blood chemistry and Hemoglobin tests - these tests or panels are groups of
tests that measure many chemical substances in the blood that are released
from body tissues or are produced .For kidney function, creatinine and blood
urea nitrogen .
Nursing Responsibilities – NPO is not required for BUN , hemoglobin and
creatinine , instruct the client not to eat red meat a day prior to creatinine
test ,intake of red meat can affect the result.

RENAL FAILURE
- A condition wherein the kidneys cannot remove the body’s metabolic waste
products or when it cannot perform its regulatory functions. Different causes may lead
to renal failure. There are two types of renal failure, acute renal failure( ARF) or acute
kidney injury (AKI) and chronic renal failure (CRF).
ACUTE RENAL FAILURE
Acute Renal Failure occurs with reversible clinical syndrome wherein there is a
sudden and almost complete loss of kidney function. This type of Renal Failure may
last for days, weeks or even months. Some of the patients with ARF may die and for
some may progress to chronic renal failure.
Categories of AKI
Prerenal - occurs in 60% to 70% of cases which result from impaired blood flow or
if the kidneys do not receive sufficient blood that leads to hypoperfusion of the kidney
and decreases GFR.
intrarenal - This results from parenchymal damage to the glomeruli or kidney
tubules, resulting from prolonged renal ischemia resulting from myoglobinuria
Postrenal ARF is usually the result of an obstruction somewhere distal to the kidney.
Pressure increases in the kidney tubules and eventually the GFR decreases.
Blockage causes urine to back up and harm the kidneys. Common causes are urinary
tract obstruction like calculi, tumors, benign prostatic hyperplasia or an enlarged
prostate, kinked ureter, and blood clots. Increase in blood urea nitrogen and
creatinine are noted in postrenal ARF.
Table 6-5 Causes of AKI

Stages of Acute Renal Failure
1. Initiation period
At this phase the kidney begins with the initial injury and ends when oliguria
develops. Its manifestation is the reduced blood flow to the nephrons. This causes
decreased reabsorption of water, electrolytes, and excretion of protein wastes and
excess metabolic substances. This phase can last from hours to days and is
characterized by urine output at 30 cc per hour or less.
2. Oliguria period
At this period, this is caused by reduction in the glomerular filtration rate. There is
an increase in the serum concentration of creatinine, urea, uric acid, and the
intracellular cations like potassium and magnesium. In this phase the uremic
symptoms first appear and may develop life-threatening condition. Other
manifestations would include hyperkalemia, hypernatremia, hyperphosphatemia,
hypocalcemia, hypermagnesemia and metabolic acidosis. Decreasing renal function
happens with increasing nitrogen retention with urine output of less than 400 ml /24
hours and may last for 1 to 2 weeks.
3. Diuresis period
At this period, there is a gradual increase in urine output, which signals that
glomerulus filtration has started to recover. The laboratory results show an increased
BUN and creatinine result. The urine output ranges from 3 to 5 liters per day due to
partial regenerated tubule’s inability to concentrate urine which lasts for 2 to 3 weeks.
4. Recovery period
This period signals the improvement of renal function and may take 3 to 12
months. Laboratory values return to the patient’s normal value.
Figure 6-6 Pathophysiology of AKI
Pre Intra Post
↓ BLD supply
renal ischemia
tubular damage
↓ GFR
↓ urine output
↑ retention of waste
Precipitation occurs
(CHON/HGB liberated)
Interferes with urine
excretion
kidney swells
necrosis
obstruction
↑intrarenal pressure
↓ GFR
↓ output /retention of
waste

Signs and symptoms
The symptomatology of acute kidney injury depends on the cause.
Figure 6-7 Common Symptoms of AKI
Diagnostic Management
1. History taking , physical exam
2. Identify precipitating cause
3. Creatinine, BUN, Serum electrolytes
4. Urinalysis
Medical Management
1. Treatment of precipitating cause
2. Fluid restriction
3. Dietary management
4. Dialysis
5. Total Parenteral Nutrition (TPN) if indicated
6. Measures to decrease potassiumK (most life-threatening disturbance)
a. administer cation – exchange resin
1. sodium polysterene sulfonate (kayexalate)
2. Calcium Polysterene Sulfonate (Kalimate)
Major site of potassium exchange is the colon if enema is administered and
Intestinal tract for oral administration . Sorbitrol is often administered with kayexalate
to induce diarrhea type effect.
b. IV glucose and insulin – This will cause the potassium to move into the
cell, decreasing the serum potassium serum level .
c. Ca gluconate - Protects the heart from the effects of hyperkalemia
d. Bicarb IV - Corrects acidosis
e . Dialysis - A procedure to remove waste products and excess fluid from
the blood when the kidneys stop functioning properly.
f. Dietary restriction – restrict fruits high in potassium like citrus fruits, banana,
grapes, watermelon ,for protein intake 1 gm /kg during oliguric phase and
sodium 2 g / day.

Nursing Management
Nursing goal of treating patients with acute renal failure is to correct or eliminate any
reversible causes of kidney failure. Provide support by taking accurate measurements
of intake and output, including all body fluids, monitor vital signs and maintain proper
electrolyte balance.
1. Precise I/O monitoring
2. Vital signs
3. Dietary management
4. Fluid management base on the clinical manifestation
5. daily weight
6. Assess signs and symptoms of electrolyte imbalance such as mental status,
neuromuscular status and cardiac rate and rhythm.
Nursing Diagnoses
1. Fluid volume excess related to impaired kidney function
2. Decrease cardiac output related to high output renal failure (diuretic phase)
3. Fluid volume deficit related to high output renal failure (diuretic phase)
4. Potential for complications of immobility related to therapeutic restrictions
5. Deficient Knowledge related to condition and treatment
6. Risk for Imbalanced Nutrition: Less Than Body Requirements
CHRONIC RENAL FAILURE
Chronic renal failure (CRF), or End Stage Renal Disease (ESRD), is a progressive,
irreversible deterioration in renal function in which the body’s ability to maintain
metabolic and fluid and electrolyte balance fails, resulting in uremia or azotemia.
The development of uremia happens and adversely affects every system in the body.
The greater the buildup, the greater are the symptoms and are considered fatal.
The pathology of CRF Occurs in 4 stages and the conditions that may contribute to
ESRD include systemic diseases such as diabetes mellitus, hypertension, chronic
glomerulonephritis, pyelonephritis, obstruction of the urinary tract. Hereditary lesions
include polycystic kidney disease, vascular disorders, autoimmune disorders,
infections, medications which are nephrotoxic.
Stage 1. Decreased Renal Reserve
In this stage, the residual renal function is 40-75% than the normal and patient
is asymptomatic with normal BUN and plasma creatinine. Excretory and regulatory
renal functions are undamaged.
Stage 2. Renal Insufficiency
The renal function is 20-40% marked decrease in glomerular filtration rate, solute
clearances, ability to concentrate urine and hormone secretion. The signs and
symptoms include rising BUN, plasma creatinine, mild azotemia, polyuria, nocturia
and anemia.
Stage 3. Renal Failure
Renal function is approximately 5% of normal. Serum urea & creatinine levels rise
rapidly and Urine output is less than 500ml/day .Symptoms of uremia develop
Stage 4 End Stage Renal Disease
End Stage Renal Disease (ESRD) with residual renal function less than 15%
or normal. Its excretory, regulatory and hormonal renal functions are severely
impaired.

111
Unable to maintain homeostasis like fluids and electrolytes imbalance may occur as
well as pH imbalances. Noticeable are elevated BUN and plasma creatinine, anemia,
hyperphosphatemia, hypocalcemia, hyperkalemia, fluid overload, usually oliguria .
Uremic syndrome may occur and all body.
Table 6- 6 Clinical Manifestations of CRF
System Involved Clinical Manifestation
Integumentary Skin
Nails
Hair
Yellow,gray,bronze
pigmentations,pallor,dry
Brittle and thin
dry and coarse
Cardiovascular Hypertension, myocardial dysfunction,
CHF,
Pericarditis
Metabolic Carbohydrate intolerance
Hyperlipidemia
Protein wasting
Skeletal Hypocalcemia
Hyperphosphatemia
Bone demineralization
Pulmonary volume overload, decreased pulmonary
macrophage activity and infections
Gastrointestinal Nausea,vomiting, to gastritis, gastric and
duodenal ulcers
Hematopoietic Anemia, bleeding
Reproductive Diminish fertility
Changes in menstruation
Medical Management
1. Serum studies (nitrogenous wastes, electrolytes)
2. Complete blood count
3. Urinalysis / Culture
4. 24 hour creatinine clearance (to determine GFR
Medical Treatment
Goals:
To prevent further damage to the kidneys
To promote recovery of renal function
To prevent complications
1. Pharmacologic (anti-hypertensive, erythropoletin, iron supplement, phosphate
binding, calcium supplement, anti seizure, ketoanalogues, Sodium Bicarbonate,
Potassium resin exchange (Kayexalate)
2. Nutritional - reduce protein potassium food sources , fluids
3. Blood transfusion to correct anemia
4. Correction of fluid and electrolyte imbalance
5. Dialysis
6. Kidney transplant

SODIUM
(135 to 145 mEq/L)
Sodium is one of the most important elements in the body. It accounts for 90% of extracellular
fluid cations (positively charged ions) and is the most abundant solute in extracellular fluid. The
normal serum sodium levels range from 135 to 145 mEq/L.
The body needs sodium to maintain proper extracellular fluid osmolality (concentration). Sodium
attracts fluids and helps preserve the extracellular fluid volume and fluid distribution in the body.
It also helps transmits impulses in nerve and muscle fibers (Lippincott, 2016).
Sodium imbalances affect the osmolality of ECF and water distribution between the fluid
compartments. When sodium levels are low (hyponatremia), water is drawn into the cells of the
body, causing them to swell. In contrast, high levels of sodium in ECF (hypernatremia) draw
water out of body cells, causing them to shrink (Lemone, 2011).
The kidney is the primary regulator of sodium balance in the body. The kidney excretes or
conserves sodium in response to changes in vascular volume. A fall in blood volume prompts
several mechanisms that lead to sodium and water retention:
HYPONATREMIA
Hyponatremia, a common electrolyte imbalance, refers to sodium
deficiency in relation to the amount of water in the body. It usually results from a
loss of sodium from the body, but it may also be caused by water gains that
dilute extracellular fluid (ECF).
Classifications:
(1) Hypovolemic both sodium and water levels decrease in the extracellular area, but sodium
loss is greater than water loss.
Causes: vomiting, diarrhea, fistulas, gastric suctioning, excessive sweating, cystic fibrosis,
burns, wound drainage, osmotic diuresis,adrenal insudfficiency, diuretic use
(2) Hypervolemic, both water and sodium levels increase in the extracellular area, but the
water gain is more impressive. Serum sodium levels are diluted and edema also occurs.
Causes: heart failure, liver failure, nephrotic syndrome, excessive administration of hypotonic IV
fluids, hyperaldosteronism
(3) Isovolemic sodium levels may appear low because too much fluid is in the body. Patients
may not exhibit signs of fluid volume excess, and total body sodium remains stable.
Causes: glucocorticoid deficiency, hypothyroidism, renal failure
Pathophysiology
Normally, the body gets rid of excess water by secreting less Antidiuretic Hormone
(ADH); less ADH causes diuresis. For that to happen, the nephrons must be functioning
normally, receiving and excreting excess water and reabsorbing sodium.
Hyponatremia develops when this regulatory function goes haywire. Serum sodium level
s decrease, and fluid shifts occur. When the blood vessels contain more water and less sodium,
fluid moves by osmosis from the extracellular area into the more concentrated intracellular area.
With more fluid in the cells and less in the blood vessels, cerebral edema and hypovolemia (fluid
volume deficit) can occur.

Manifestations
The manifestations of hyponatremia depend on the rapidity of onset, the severity, and the cause
of the imbalance. If the condition develops slowly, manifestations are usually not experienced
until the serum sodium levels reach 125 mEq/L. In addition, the manifestations of hyponatremia
vary, depending on extracellular fluid volume.
a. Poor skin turgor
b. Dry mucosa
c. Decrease saliva production
d. Orthostatic hypotension
e. Nausea, abdominal cramping
f. Neurologic changes such as: lethargy, confusion, signs of increase ICP, muscle twitch,
seizure
Laboratory Findings
Serum osmolality less than 280 mOsm/kg (dilute blood)
Serum sodium level less than 135 mEq/L (low sodium level in blood)
Urine specific gravity less than 1.010
Elevated hematocrit and plasma protein levels
Medical Management
• Generally, treatment varies with the cause and severity of hyponatremia.
Hypervolemia/isovolemia
a. Fluid restrictions
b. Oral sodium supplements
Hyponatremia
a. Give isotonic IV fluids (e.g. normal saline)
b. Offer High sodium foods
In SEVERE cases:
a. Infusion of hypertonic saline solution (3% or 5% saline)
Nursing Management
Watch patients at risk for hyponatremia, including those with heart failure, cancer, or GI
disorders with fluid losses. Review patient’s medications, noting those that are associated with
hyponatremia. For patients who develop hyponatremia, take the following actions:
• Monitor and record vital signs, especially blood pressure and pulse, and watch for orthostatic
hypotension and tachycardia
• Monitor neurologic status frequently Report any deterioration in level of consciousness.
• Accurately measure and record intake and output.
• Assess skin turgor at least every 8 hours for signs of dehydration.
• Restrict fluid intake as ordered (fluid restriction is the primary treatment for dilutional
hyponatremia).
• Administer oral sodium supplements as ordered.
• Provide a safe environment for patients with altered thought processes
• Seizure precautions

HYPERNATREMIA
Hypernatremia, a less common problem than hyponatremia, refers to
excess of sodium relative to the amount of water in the body.
Pathophysiology
The cells play a role in maintaining sodium balance. When serum osmolality increases
because of hypernatremia, fluid moves by osmosis from inside the cell to outside the cell. As
fluid leaves the cells, they become dehydrated and shrink.
Manifestations
Thirst is the first manifestation of hypernatremia. If thirst is not relieved, the primary
manifestations relate to altered neurologic function. Initial lethargy, weakness, and irritability can
progress to seizures, coma, and death in severe hypernatremia. Both the severity of the sodium
excess and the rapidity of its onset affect the manifestations of hypernatremia. You may also
observe the following:
a. Low grade fever
b. Flushed skin
c. Dry mucous membranes
d. Oliguria
e. Orthostatic hypotension
Laboratory Findings
The following laboratory and diagnostic tests may be ordered with the following findings:
Serum sodium levels are greater than 145 mEq/L
Serum osmolality is greater than 295 mOsm/kg
Medical Management
Treatment for hypernatremia varies with the cause. The underlying disorder must be
corrected, and serum sodium levels and related diagnostic tests must be monitored.
Note that the fluids should be given gradually over 48 hours to avoid shifting water into brain
cells.
Nursing Management
•Intravenous fluid replacement (dextrose 5% in water) to return serum sodium levels to
normal
• Sodium intake restrictions
•
Nursing Management
If patient develop hypernatremia, take the following measures:
• Monitor and record vital signs, especially blood pressure and pulse
• Check neurologic status frequently.
• Report any deterioration in the level of consciousness
• Carefully measure and record intake and output.
• Assess skin and mucous membranes for signs of breakdown and infection

• Monitor serum sodium level and report any increase.
• Assist with oral hygiene. Lubricate the patient’s lips frequently.
• Provide a safe environment for confused or agitated patients

PHOSPHOROUS
(1.2 to 3.0 meq/L)
The primary anion, or negatively charged ion, found in the intracellular fluid. It’s
contained in the body as phosphate.
Functions:
a. Integral part of acid base buffer system
b. Regulate ATP use for muscle contraction, nerve transmission, electrolyte transport
c. Regulates 2,3 DPG (diphosphoglycerate) a compound in red blood cells that facilitates
oxygen delivery from the red blood cells to the tissues.
d. Regulates 2,3 DPG (diphosphoglycerate) a substance in RBC affecting oxygen affinity
HYPOPHOSPHATEMIA
Hypophosphatemia occurs when the serum phosphorous level
falls below 1.2 mEq/L. although this condition generally indicates a
deficiency of phosphorous, it can occur under various circumstances
when total body phosphorous stores are normal
Causes:
a. Respiratory alkalosis one of the most common cause of hypophosphatemia, can stem
from a number of conditions that produce hyperventilation
b. Malabsorption syndromes
c. Diuretic use, (Thiazides, Loop diuretics, Acetazolamide)
Pathophysiology
Most effects of hypophosphatemia result from depletion of ATP and impaired oxygen delivery to
the cells due to a deficiency of the red blood cell enzyme 2,3-DPG. Severe hypophosphatemia
affects virtually every major organ system:
Manifestations
a. Muscle weakness, most common symptom
b. malaise, weakened hand grasp, myalgia (pain in the muscles)
c. rhabdomyolysis (skeletal muscle destruction), can occur with altered muscle cell activity
d. Osteomalacia/ Fracture, due to loss of bone density
e. Bruising and bleeding
Laboratory Findings
Diagnostic test results may indicate hypophosphatemia or a related condition:
a. serum phosphorous level less than 1.2 mEq/L
b. elevated Creatinine Kinase level if Rhabdomyolysis is present
c. X-ray studies that reveal skeletal changes typical of osteomalacia or bone fractures
d. Abnormal electrolytes (decreased magnesium levels and increased calcium levels)
Medical Management
Treatment varies with the severity and cause of the condition:
a. Treat the underlying cause
b. Oral and intravenous supplements

Nursing care should focus on careful monitoring, safety measures and interventions to
restore normal serum phosphorous levels.
a. Monitor vital signs.
b. Assess the patient frequently for evidence of decreasing muscle strength, such as weak hand
grasps or slurred speech, and document findings regularly.
c. Assist in ambulation and activities of daily living, if needed, and keep essential objects near
the patient to prevent accidents.
HYPERPHOSPHATEMIA
Hyperphosphatemia is a serum phosphate level greater than
4.5mg/dL. As with other electrolyte imbalances, it may be the result of
impaired phosphate excretion, excess intake, or a shift of phosphate from
the intracellular space into extracellular fluids.
Causes:
a. Renal Failure
b. Hypoparathyroidism impairs less synthesis of parathyroid hormone(PTH), when less PTH
is synthesized, less phosphorous is excreted from the kidneys.
c. Respiratory acidosis
d. Increase tissue breakdown
Pathophysiology
Effects of high phosphorous level are actually due to hypocalcemia; calcium suppresses cellular
excitability.
Manifestations
a. Hyperphosphatemia causes few symptoms (tetany, tissue calcification)
b. Symptoms occurring result from decrease calcium secondary to reciprocity
Laboratory Findings:
The following diagnostic test results may indicate hyperphosphatemia or a related
condition such as hypocalcemia:
a. Serum phosphorous above normal
b. Low serum calcium level
Medical Management:
a. Treat underlying cause
b. Restrict dietary intake
c. Administer phosphate binding antacid, this may decrease absorption of phosphorous in the
gastrointestinal system
Nursing Management
a. Monitor vital signs
b. Monitor intake and output.( if urine output falls below 30 mL/hour, immediately notify the
doctor) Decreased urine output can seriously affect renal clearance of excess serum
phosphorous
c. Monitor serum phosphorous and calcium levels

d. Monitor signs of tetany, such as positive Trousseau’s and Chvostek’s sign

POTASSIUM
(3.5 to 5.0 mEq/L)
A major cation (ion with a positive charge) in intracellular fluid, potassium plays a critical
role in many metabolic cell functions. Only 2% fluid; 98% of the body’s potassium is found in
extracellular fluid. That significant difference affects nerve impulse transmission. The normal
serum (ECF) potassium level is 3.5 to 5.0 mEq/L. To maintain balance, potassium must be
replaced daily through diet. Virtually all foods contain potassium, although some foods and
fluids are richer sources of this element than others.
Aldosterone helps regulate potassium elimination by the kidneys. An increased
potassium concentration in ECF stimulates aldosterone production by the adrenal gland. The
kidneys respond to aldosterone by increasing potassium excretion. Changes in aldosterone
secretion can profoundly affect the serum potassium level.
Potassium directly affects how well the body cells, nerves, and muscles function by:
• Maintaining cells’ electrical neutrality and osmolality
• Aiding neuromuscular transmission of nerve impulses
• Assisting skeletal and cardiac muscle contraction and electrical conductivity
• Affecting acid-base balance in relationship to the hydrogen ion.
HYPOKALEMIA
Hypokalemia is an abnormally low serum potassium level . It
usually results from excess potassium loss, although hospitalized patients
may be at risk for hypokalemia because of inadequate potassium intake.
Pathophysiology
Inadequate intake and excessive output of potassium can cause a moderate drop in its
level, upsetting the balance and causing a potassium deficiency. Potassium shifts from the
extracellular space to the intracellular space and hides in the cells. Because the cells contain
more potassium than usual, less can be measured in the blood.
Causes:
a. Inadequate potassium intake
b. Severe GI losses, e.g. suction, lavage, prolonged vomiting can deplete the body’s potassium
supply as a result potassium levels drop
c. Drug associated, e.g. diuretics,(esp. thiazides and furosemides), corticosteroids, insulin
d. Decrease bowel motility
Manifestations
The signs and symptoms of a low potassium level reflect how important the electrolyte is to
normal body functions.
a. Skeletal muscle weakness, especially in the legs a sign of a moderate loss of potassium.
This also includes paresthesia and leg cramps
b. Decreased bowel sounds, constipation, paralytic ileus
c. Weak and irregular pulse
d. Orthostatic hypotension and palpitations
e. ECG changes, flattened or inverted T wave, prominent U wave

Figure 3-1 (Left) Normal ECG wave ; (Right) Inverted T wave
Laboratory Findings
The following test results may develop to confirm the diagnosis of hypokalemia:
a. Serum potassium level less than 3.5 mEQ/L
b. Increased 24-hour urine level
c. Characteristic ECG changes
Medical Management
a. Identify and treat the cause treatment for hypokalemia focuses on restoring a normal
potassium balance, preventing serious complications, and removing or treating the underlying
causes.
57
b. Oral and IV replacements (40-80 meq/day – Kalium durule or K IV), it can be safely given at
the same time
Nursing Management
Careful monitoring and skilled interventions can help prevent hypokalemia and spare
your patient from its associated complications. The following actions are considered.
a. Monitor vital signs, especially blood pressure hypokalemia is commonly associated with
hypovolemia, which can cause orthostatic hypotension
b. Check heart rate and rhythm and ECG tracings in patients with serum potassium level less
than 3 meQ/L hypovolemia causes tachyarrthymias
c. Assess respiratory rate, depth and pattern hypokalemia may weaken or paralyze
respiratory muscles. Notify the doctor immediately if respirations become shallow and rapid.
d. Monitor serum potassium levels changes in serum potassium level can lead to serious
cardiac complications.
e. Administer potassium infusions cautiously.
HYPERKALEMIA

Hyperkalemia can result from inadequate excretion of potassium,
excessively high intake of potassium, or a shift of potassium from the ICF
to the ECF. Hyperkalemia affects neuromuscular and cardiac function.
Causes:
a. Increased dietary intake
b. Blood transfusion (stored blood) serum potassium level increases longer the blood is
stored.
c. Rapid IV potassium administration
d. Renal insufficiency
e. Metabolic acidosis, potassium shift to ECF in exchange of H ions
Pathophysiology
Potassium move from the extracellular to the intracellular compartment and increases
cell excitability, so that cells respond to stimuli of less intensity and may actually discharge
independently without a stimulus.
Manifestations
Signs and symptoms of hyperkalemia reflect its effects on neuromuscular and cardiac
functioning in the body.
a. Nausea, abdominal cramping and diarrhea the early signs of hyperkalemia due to smooth-
muscle hyperactivity
b. Muscle weakness that in turn lead to flaccid paralysis
c. Decreased heart rate, irregular pulse, decreased cardiac output, hypotension
d. ECG changes, elevated T wave
Figure 3-2 Elevated T wave
Laboratory Findings
The following test results help confirm the diagnosis and determine the severity of
hyperkalemia:
a. Serum potassium level greater than 5 mEq/L
b. Decreased arterial pH, indicating acidosis

c. ECG abnormalities
Medical Management
Treatment for hyperkalemia is aimed at lowering the potassium level, treating its cause,
stabilizing the myocardium, and promoting renal and gastrointestinal excretion of potassium.
The severity of hyperkalemia dictates how it should be treated.
a. Diet restrictions
b. May administer loop diuretics for mild hyperkalemia to increase potassium loss from the
body or to resolve any acidosis present
c. Sodium polystyrene sulfonate (Kayexalate) a cation-exchange resin (common treatment
for hyperkalemia)
d. Hemodialysis, if patient has renal failure
Patients at risk for hyperkalemia require frequent monitoring of serum potassium and
other electrolyte levels. Take these actions.
a. Assess vital signs.
b. Monitor the patient’s intake and output Report an output of less than 30 mL/hour.
c. Prepare to administer a slow calcium chloride or gluconate IV infusion to counteract the
myocardial depressant effects of hyperkalemia
d. Keep in mind when giving Kayexalate that serum sodium levels may rise. Watch for signs of
heart failure.
e. Monitor ECG changes

FLUIDS AND
ELECTROLYTES
By Amie Perez De Jesus
- NCM 212 CONCEPT LECTURE -

OBJECTIVES OF THE COURSE
After the 45-hour learning provision the learner is expected to:
Identify the different terminologies related to fluid and electrolyte imbalance;
Describe the anatomy and physiology and functions of the affected systems;
Recognize the different causes of disorders that affects fluid and electrolyte imbalance;
Describe the normal variations in assessment findings;
Explain the pathophysiology of the common disease condition affecting fluid and electrolyte
imbalances;
Identify abnormal findings that may indicate alterations in the given disorders;
Illustrate the manifestations of different disorders related to imbalances;
Delineate normal and abnormal findings of specific diagnostic tests related to imbalances;
Discuss specific medical management for clients with problems in fluids and electrolytes;
Appreciate importance of proper holistic nursing care for client’s experiencing such
imbalances;
Recognize the need for self-evaluation and progress completion on this self- learning
module; and
Appreciate the importance of self-learning.

FOUNDATIONAL
CONCEPTS AND
ASSESSMENTS

KEY ELEMENTS UNDERLYING FLUID
AND ELECTROLYTE IMBALANCE
01

THE CELL MEMBRANE
CELL
● smallest autonomous functional unit of the
body
● in its fetal form it is undifferentiated , but as
growth continues the cell differentiates into
specific tissue types, forming organs and
systems.
CELL WALL
● a semipermeable membrane that separates
the intracellular from the extracellular
components, allowing for an exchange in an
effort for the cell to obtain energy, synthesize
complex molecules, participate in electrical
events, and replicate.

COMPOSITION
PHOSPHOLIPIDS
● arranged in one end hydrophilic and the other
end hydrophobic
Hydrophylic head (loving water)
● faces the outside of the membrane, retaining
water and adhering to the neighboring cell
Hydrophobic tail (hating water)
● associates with other fatty groups to exclude
the hydrophilic groups

COMPOSITION
PROTEINS
● second major component of the cell
membrane where most of the functions of
the cellular membrane occur
● They transport lipid-insoluble particles
acting as carriers to pass these
compounds directly through the
membrane. Some proteins form ion
channels for the exchange of electrolytes.
The type of protein involved depends on
the cell’s function.

COMPOSITION
CELL COAT
● long chains of complex carbohydrates make up glycoproteins, glycolipids and lectins that
form the outside surface of the cell. This intricate coat helps in cell-to-cell recognition
and adhesion.

BODY FLUID COMPOSITION
WATER
● primary component of body fluids
● provides a medium for the transport and exchange of nutrients and
other substances such as oxygen, carbon dioxide, and metabolic
wastes to and from cells;
● provides a medium for metabolic reactions within cells
● assists in regulating body temperature through the evaporation of
perspiration.
● constitutes about 60% of the total body weight, but this amount
varies with age, gender, and the amount of body fat
● Total body water decreases from 45% to 50% of total body weight
with obesity and with aging

WATER
● In the person who is obese, the proportion of water
to total body weight is less than in the person of
average weight
● In a person who is very thin, the proportion of water
to total body weight is greater than in the person of
average weight.
● Adult females have a greater ratio of fat to lean
tissue mass than adult males; therefore, they have a
lower percentage of total body water.

WATER
Functions:
1. Temperature regulation
2. Transport of materials to/from the cells
3. Aqueous medium for cellular
metabolism (provides a medium for
metabolic reaction)
4. Assist in food digestion (hydrolysis)
5. Acts as solvent in which solute are
available for cell function
6. Maintain blood volume
7. Medium of waste excretion
8. Cushion body parts from injury

WATER
Factors affecting body water:
1) AGE
Infant 70-80%
Adult 50-60%
Elderly 45-50%
2) SEX
Male - 60%
Female - 50%
3) BODY FATS
-Fat cells contains little H2O
*To maintain normal fluid balance, body water intake and
output should be approximatelyequal. The average fluid
intake and output is about 2500ml over a 24-hour period.

WATER
INSENSIBLE WATER LOSS
● occurs through the skin, lungs and feces
● can increase significantlyduring
a) Exercise
b) High environmental temperatures
c) During illnessesthat respiratory rate, perspiration or GI losses
Table 1-1 Approximate Values Of 24hour Fluid Gain And Loss Of An Adult

ELECTROLYTES
● Body fluids contain both water molecules and chemical
compounds
● Either remain intact in solution or dissociate into
discrete particles
● Substances that dissociate in solution to form charged
particle called ions.
● Cations are positively charged electrolytes; anions are
negatively charged electrolytes
● Electrically charged particles and is expressed in terms
of milliequivalent per liter (meq/L)
*IONS – dissociated electrolyte particles which carry
either (+) (-) charge
(+) charge = cations
(-) charge = anions

4 MAJOR FUNCTIONS OF
ELECTROLYTES:
1. Assisting with regulation of water
balance
2. Regulating and maintaining acid-base
balance
3. Contributing to enzyme reactions
4. Essential for neuromuscular activity
ELECTROLYTES

COMMON ELECTROLYTES
ELECTROLYTE
ION
DISTRIBUTION IN BODY
FLUID
BASIC FUNCTIONS DIETARY
SOURCES
ECF(mEq/L) ICF (mEq/L)
Sodium (Na+) 135-154 15-20 -regulates fluid volume
within ECF compartment
-regulates vascular osmotic
pressure
-controls water distributioj
between ECF and ICF
compartments
-participates in conduction
of nerve impulses
-maintains neuromuscular
excitability
-table salt
-cheese, milk,
processed meat,
poulty, shellfish,
fish, eggs and
foods preserved
with salt (eg ham
and bacon)

COMMON ELECTROLYTES
ELECTROLYTE
ION
FLUID
SOURCES
Potassium 3.5-5 150-155 -regulates osmolality of ICF
-participates in transmission
of nerve impulses
-promotes contraction of
skeletal and smooth
muscles
-regulates acid-base
balance by cellular
exchange of hydrogen ions
-Fruits,
especially
bananas,
oranges, and
dried fruits
-vegetables
-meats
-nuts

COMMON ELECTROLYTES
ELECTROLYTE
ION
FLUID
SOURCES
Calcium 4.5-5.5 1-2 -provides strength and
durability to bones and teeth
-establishes thickness and
strength of cell membranes
-promotes transmission of
nerve impulses
-maintains neuromuscular
excitability
-essential for blood
coagulation
-activates enzyme reactions
and hormone secretions
-dairy products
(milk, cheese,
and yogurt
-sardines, whole
grains and green
leafy vegetables

COMMON ELECTROLYTES
ELECTROLYTE
ION
FLUID
SOURCES
Magnesium 4.5-5.5 27-29 -activates enzyme systems,
mainly those associated
with vit. B metabolism and
the use of potassium
calcium and protein.
-promotes regulation of
serum calcium, phosphorus
and potassium levels
-promotes neuromuscular
activity
-green leafy
vegetables,
whole grains,
fish and nuts

SERUM COMPONENT
SERUM COMPONENT VALUES
CONVENTIONAL SI
Sodium 135-145 mEq/L 135-145 mmol/L
Chloride 98-106 mEq/L 98-106 mmol/L
Bicarbonate 22-26 mEq/L 22-26 mmol/L
Calcium 8.5- 10.0 mEq/L 2.1-2.6 mmol/L
Potassium 3.5-5.0 mEq/L 3.5-5.0 mmol/L
Phosphate/inorganic
phosphorus
1.7-2.6 mEq/L (2.5-4.5 mg/dl) 0.8-1.5 mmol/L
Magnesium 1.6-2.6 mg/dl (1.3-2.1 mEq/L) 0.8-1.3 mmol/L
Serum osmolality 275-295 mOsm/kg 275-295 mmol/kg

BODY FLUID COMPARTMENT
(DISTRIBUTION)
03

Body Fluid is classified by its location
inside or outside the cells. Capillary and
cell membranes separate total body
fluids into two main compartments: the
intracellular and extracellular.
BODY FLUID COMPARTMENT (DISTRIBUTION)

Total body water is the
equivalent of the fluids that exist
in all the fluid compartments.
This approximately 60% of the
body weight of an average adult.
Expressed in kilograms, 1L of
fluid is equivalent of 2.2 lbs (1kg).
*TOTAL BODY WATER*

Intracellular fluid (ICF) is found within
cells. ICF is essential for normal cell
function, providing a medium for
metabolic processes.
• Make’s up 2/3 of the body’s water or
40% of Body weight
• Larger of the two compartments
• Rich in electrolytes, potassium,
magnesium, inorganic and organic
phosphates and proteins
INTRACELLULAR FLUID (ICF) (40%)

Extracellular fluid (ECF) is located
outside of cells
• contains all the fluid outside the cells
• accounts for 20% of Body weight
• rich in electrolytes: sodium, chloride
and bicarbonate
EXTRACELLULAR FLUID (ECF) (20%)

a) INSTERSTITIAL FLUID (15%)
• located in the spaces between most cells of the body
• accounts for approximately 15% of Body weight
b) INTRAVASCULAR FLUID (5%)
• blood vessel compartments
• called “plasma”, is contained within the arteries, veins, and
capillaries
c) TRANSCELLULAR FLUID (1%)
• includes urine; digestive secretions; perspiration; and
cerebrospinal, pleural, synovial, intraocular,gonadal, and pericardial
fluids
• the transcellular space contributes approximately 1% of the body
fluid, and significant gains and losses do not occur on a daily basis
ECF is further classified by location:

MECHANISM OF FLUID
TRANSPORT
04

Four chemical and physiologic processes control the movement of fluid,
electrolytes, and other molecules across membranes between the
intracellular and interstitial space and the interstitial space and plasma.
These processes are osmosis, diffusion, filtration, and active transport.
MECHANISM OF FLUID TRANSPORT

Active transport allows molecules to move across
cell membranes and epithelial membranes against
a concentration gradient. This movement requires
energy (adenosine triphosphate [ATP]) and a
carrier mechanism to maintain a higher
concentration of a substance on one side of the
membrane than on the other.
Complex sugar, ions, large cells, proteins, and
other particles are transported in this process.
ACTIVE TRANSPORT

Types of Active Transport:
• Primary Active Transport-uses the initial
source of energy to carry the substance
• Secondary Active Transport (cotransport)-
harnesses the energy obtained from the
primary active transport and uses it as a
cotransporter of a secondary substance
ACTIVE TRANSPORT

SODIUM-POTASSIUM PUMP
The sodium-potassium pump moves sodium ions out of and potassium ions into the cell. This
pump is powered by ATP. For each ATP that is broken down, 3 sodium ions move out and 2
potassium ions move in.
EXAMPLES OF PRIMARY ACTIVE TRANSPORT

ENDOCYTOSIS
plasma membrane surrounds the substance being transported and
transport the substance into the cell

• Phagocytosis or cellular eating
Occurs when the dissolved materials enter the
cell. The plasma membrane engulfs the solid
material, forming a phagocytic vesicle.
• Pinocytosis or cellular drinking
Occurs when the plasma membrane folds inward
to form a channel allowing dissolved substances
to enter the cell. When the channel is closed, the
liquid is encircled within a pinocytic vesicle.
• Receptor-mediated endocytosis (RME)
also called clathrin-mediated endocytosis, is a
process by which cells absorb metabolites,
hormones, proteins – and in some cases viruses
– by the inward budding of the plasma
membrane.
MAIN KINDS OF ENDOCYTOSIS

EXOCYTOSIS 11
manufactured substances are pack in the secretory vesicles that fuse
with the plasma and are released outside the cell

Exocytosis Vs Endocytosis
https://www.youtube.com/watch?v=2-icEADP0J4&t=3s

• In these biological process, there is
no need for any energy for
transporting the molecules, as the
biochemicals move from higher to
the lower concentration.
• This process is carried out to
maintain the balance and the
equilibrium level in a cell.
• All the wastes molecules including,
water and carbon dioxide is
separated and moved out of the cell
using passive transport.
PASSIVE TRANSPORT

OSMOSIS
Osmosis is the process by which water moves across a selectively permeable membrane from
an area of lower solute concentration to an area of higher solute concentration. A selectively
permeable membrane allows water molecules to cross but is relatively impermeable to
dissolved substances (solutes). Osmosis continues until the solute concentration on both sides
of the membrane is equal. (Lemone, 2017)
TYPES OF PASSIVE TRANSPORT

OSMOSIS
• the distribution of water from a lesser
area of solute concentration to a higher
area of solute concentration
• the direction is determined by the
concentration of particles on either
side of the cell membrane
• osmosis stops when the concentration
of solutes on both sides of the
membrane becomes equalized
• osmosis the primary process that
controls body fluid movement between
the ICF and ECF compartments

OSMOSIS
OSMOLALITY
• Osmolality, or concentration of a solution, refers to the number of solutes
per kilogram of water (by weight); it is reported in milliosmoles per
kilogram (mOsm/kg). The osmolality of the ECF depends chiefly on sodium
concentration. Serum osmolality may be estimated by doubling the serum
sodium concentration (approximately 142 mEq/L).Glucose and urea
contribute to the osmolality of ECF, although to a lesser extent than
sodium.
• normal serum osmolality is 280-300 mOsm/kg
OSMOLARITY
• The number of solutes per Liter of Fluid
• Expressed as mOsm/L of total solution
• Normal range:
For adults, the normal result range is between 285 and 295.
For children, it’s between 275 and 290.
OSMOLALITY
OSMOLARITY

OSMOTIC PRESSURE
• the power of a solution to draw water
across a membrane
ONCOTIC PRESSURE
• also called colloid osmotic pressure (COP)
• osmotic pressure exerted by plasma
proteins in the vessels (e.g., albumin)
• proteins in the bloodstream exert oncotic
pressure to pull fluid out of the interstitial
space into the intravascular space to
maintain fluid balance and osmolality
• average COP is 28mmHg, a pressure that
remains constant across the capillary
OSMOSIS

refers to the effect a solution’s osmotic pressure has on water movement across the cell
membrane of cells within that solution
TONICITY

ISOTONIC SOLUTION
• have the same concentration of solutes as plasma
• cells placed in an isotonic solution will neither shrink
nor swell because there is no net gain or loss of water
within the cell, and no change in cell volume
HYPERTONIC SOLUTION
• have a greater concentration of solutes than plasma
• in their presence, water is drawn out of a cell, causing
it to shrink
HYPOTONIC SOLUTION
• have a lower solute concentration than plasma
• when red blood cells are placed in a hypotonic
solution, water moves into the cells, causing them to
swell; rupture (hemolysis) of cells may occur with
extremely hypotonic solutions
TONICITY

DIFFUSION
Diffusion is the process by which solute molecules move from an area of
high solute concentration to an area of low solute concentration to
become evenly distributed.

SIMPLE DIFFUSION
Simple diffusion
occurs by the random
movement of particles
through a solution.
Water, carbon dioxide,
oxygen, and solutes
move between plasma
and the interstitial
space by simple
diffusion through the
capillary membrane.
Water and solutes
move into the cell by
passing through
protein channels or by
dissolving in the lipid
cell membrane.
TYPES OF DIFFUSION

FACILITATED DIFFUSION
Facilitated diffusion, also
called carrier-mediated
diffusion, allows large
water-soluble molecules,
such as glucose and amino
acids, to diffuse across cell
membranes.
Proteins embedded in the
cell membrane function as
carriers, helping large
molecules cross the
membrane.
The rate of diffusion is
influenced by a number of
factors, such as the
concentration of solute and
the availability of carrier
proteins in the cell
membrane.
TYPES OF DIFFUSION

SIMPLE DIFFUSION VS FACILITATED DIFFUSION
https://www.youtube.com/watch?v=MS5igwkWKe8

FILTRATION
Filtration is the process
by which water and
dissolved substances
(solutes) move from an
area of high hydrostatic
pressure to an area of low
hydrostatic pressure. This
usually occurs across
capillary membranes.

HYDROSTATIC
PRESSURE
• created by the
pumping action of
the heart and gravity
against the capillary
wall
• filtration occurs in
the glomerulus of the
kidneys, as well as at
the arterial end of
capillaries
FILTRATION
https://www.youtube.com/watch?v=yJEsQcc_Bec

Homeostasis requires
several regulatory
mechanisms and processes
to maintain the balance
between fluid intake and
excretion. These include
thirst, the kidneys, the
renin–angiotensin–
aldosterone mechanism,
antidiuretic hormone, and
atrial natriuretic peptide.
These mechanisms affect
the volume, distribution,
and composition of body
fluids.
FLUID REGULATION

Thirst is the primary regulator of water intake.
Thirst plays an important role in maintaining fluid
balance and preventing dehydration.
The thirst center, located in the hypothalamus, is
stimulated when the blood volume drops
because of water losses or when serum
osmolality increases.
The thirst mechanism is highly effective in
regulating extracellular sodium levels.
Increased sodium in ECF increases serum
osmolality, stimulating the thirst center.
Fluid intake in turn reduces the sodium
concentration of ECF and lowers serum
osmolality.
Conversely, a drop in serum sodium and low
serum osmolality inhibit the thirst center.
(Lemone,2017)
THIRST

NOTE:
The thirst mechanism declines with
aging, making older adults more
vulnerable to dehydration and
hyperosmolality.
Patients with an altered level of
consciousness or who are unable to
respond to thirst, such as intubated
patients and artificially fed patients,
are also at risk.
THIRST
https://www.youtube.com/watch?v=9fzcAqmiK4A&t=68
s

The kidneys are primarily responsible
for regulating fluid volume and
electrolyte balance in the body.
They regulate the volume and
osmolality of body fluids by controlling
the excretion of water and
electrolytes.
In adults, about 170 L of plasma are
filtered through the glomeruli every
day.
By selectively reabsorbing water and
electrolytes, the kidneys maintain the
volume and osmolality of body fluids.
About 99% of the glomerular filtrate is
reabsorbed, and only about 1500 mL of
urine is produced over a 24-hour
period. (Lemone, 2017)
KIDNEYS

• Besides regulating fluid
balance, the kidneys also
contribute to regulation of
electrolyte levels.
• Selectively secreting or
reabsorbing electrolytes
achieves body balance.
• Two important electrolytes
regulated by the kidneys are
hydrogen and bicarbonate.
• Regulation of these two ions
contributes significantly to
the body’s overall acid-base
balance. (Daniels, 2007)
KIDNEYS

• Regulate ECF volume and osmolality
by selective retention and excretion
of body fluids
• Regulation of electrolyte levels in the
ECF by selective retention of needed
substances and excretion of
unneeded substances
• Regulate ph of ECF by retention of
hydrogen ions
• Excretion of metabolic wastes and
toxic substances
Major Functions of Kidneys in maintaining normal
fluid balance

The lungs participate in the maintenance
of fluid balance by excreting moisture
during exhalation.
Under normal conditions, this contributes
about 300ml per 24hours to the fluid
output of the body.
However, in cases of increased respiratory
rate, as may occur with fever or
respiratory problems, such as pneumonia,
the amount of fluid lost during respiration
can increase significantly, potentially
leading to fluid deficits.
The lungs also play a role in acid-base
balance by regulating excretion of carbon
dioxide (CO2). (Daniels, 2007)
RESPIRATORY SYSTEM

RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM

RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
https://www.youtube.com/watch?v=PDE2qdS2ZvY&t=1
85s

Antidiuretic hormone (ADH), released by the posterior
pituitary gland, regulates water excretion from the
kidneys.
Osmoreceptors in the hypothalamus respond to
increases in serum osmolality and decreases in blood
volume, stimulating ADH production and release.
ADH acts on the distal tubules of the kidney, making them
more permeable to water and thus increasing water
reabsorption.
With increased water reabsorption, urine output falls,
blood volume is restored, and serum osmolality drops as
the water dilutes body fluids.
Increased amounts of ADH are also released in response
to stress situations such as nausea, pain, surgery and
anesthesia, narcotics, and nicotine.
Its release is inhibited by alcohol and medications such
as phenytoin, as well as by increased blood volume and
decreased serum osmolality.
ANTI DIURETIC HORMONE(vasopressin)

ANTI DIURETIC HORMONE(vasopressin)

• Atrial natriuretic peptide (ANP) is a
hormone released by atrial muscle
cells in response to distention from
fluid overload.
• ANP affects several body systems,
including the cardiovascular, renal,
neural, GI, and endocrine systems,
but it primarily opposes the renin–
angiotensin–aldosterone system by
inhibiting renin secretion and
blocking the secretion and sodium-
retaining effects of aldosterone.
• As a result, ANP promotes sodium
wasting and increased urine output.
ATRIAL NATRIURETIC PEPTIDE

ATRIAL NATRIURETIC PEPTIDE MECHANISM
https://www.youtube.com/watch?v=bWZqN1my5sQ

Cortisol increases glomerular
filtration rate, and renal plasma flow
from the kidneys thus increasing
phosphate excretion, as well as
increasing sodium and water
retention and potassium excretion in
high amounts acting as aldosterone (in
high amounts cortisol is converted to
cortisone which acts on mineral
corticoid receptor mimicking the
effect of aldosterone).
It also increases sodium and water
absorption and potassium excretion in
the intestines.[27]
CORTISOL

Parathyroid hormone is the
most important endocrine
regulator of calcium and
phosphorus concentration in
extracellular fluid.
This hormone is secreted
from cells of the parathyroid
glands and finds its major
target cells in bone and
kidney.
PARATHYROID
HORMONE

OSMOTIC FORCES are the principal determinant f water
distribution in the body. Water accounts for the osmotic
pressure in the tissues and cells of the body. Osmotic
pressure is actually determined by the movement or draw
of water through a selectively permeable membrane
toward an area of greater solute concentration. To
determine the osmotic pressure of a solute, the
osmolality of the solution must be determine.
Osmolality- number of osmoles (Osm) of a substance
contained within a kilogram of water
Osmole- number of molecules in 1g molecular weight of
undissociated solute
A solution with 1 Osm in each kg of water has an
osmolality of 1 Osm/kg, and a solution with an osmolality
of 1 milliosmole (mOsm) per kilogram contains 0.001
Osm/kg solute.
Normal serum osmolality is 285-295 mOsm/kg.
OSMOTIC FORCES IN WATER DISTRIBUTION

Capillaries are formed of endothelium
MOVEMENT OF FLUIDS AT THE CAPILLARY MEMBRANE
Substances move through the gaps or spaces of the endothelium
The process occurs by diffusion, so that equilibrium exist at the capillary
line
Starling’s law – dynamic equilibrium- achieved between the hydrostatic
pressure of the blood and the colloid osmotic pressure within the
capillaries

Blood enters the capillary in a hydrostatic pressure that is generated by the heart.
As fluid filters out of the capillary into the tissue spaces, the hydrostatic pressure
decreases.
The high pressure exerted at the arteriolar end of the capillary is a simple outward
force, or pushing force, which moves fluid from the vessel to the interstitial spaces
The hydrostatic pressure exerted at the arteriolar end of the capillary averages 30-
40 mm Hg, but drops to approximately 10-15 mm Hg at the venous end
The hydrostatic pressure provides an outward force, enhanced by a negative
interstitial pressure and the interstitial fluid colloid osmotic pressure (ISCOP)

The pressure exerted by the plasma proteins in the vessels, the colloid osmotic or oncotic
pressure (COP), is an osmotic pulling or inward force that draws water toward it.
Plasma proteins primarily exert their colloidal effect by drawing water back into the vessel
The average COP is 28 mm Hg, a pressure that remains constant across the capillary.
The small amounts of protein that escape into the tissue spaces during the process of fluid
movement cannot be reabsorbed by the blood vessels.
These excesses of fluid and protein are absorbed by the lymphatic system and returned through
lymphatic channels to the blood.
The lymphatic system carries away proteins and large matter from the tissue spaces directly into
the blood capillaries.
https://www.youtube.com/watch?v=ZJVUTkgYhhg&t=99s

EDEMA
• palpable swelling produced by
expansion of the interstitial fluid
volume may be localized or
generalized, pitting or nonpitting,
depending on its cause
• The mechanism causing skin edema
also can cause fluid shifts in other
vulnerable areas of the body. These
fluid shifts are sometimes termed
third-space shifts
PLASMA TO INSTERTITIAL
https://www.youtube.com/watch?v=6ecmOuCIoNc

• Third spacing is a shift of fluid from the
vascular space into an area where it is not
available to support normal physiologic
processes.
• Fluid may be sequestered in the abdomen or
bowel, or in other actual or potential body
spaces as the pleural or peritoneal space.
• Fluid may also become trapped within soft
tissues following trauma or burns.
• The trapped fluid represents a volume loss
and is unavailable for normal physiologic
processes.
• In many cases, fluid is sequestered in
interstitial tissues and is unavailable to
support cardiovascular function.
PLASMA TO INSTERTITIAL

Decreased colloid osmotic pressure in the
capillary
e.g. Burns, Liver failure
Increased capillary hydrostatic pressure
e.g. Congestive Heart Failure
Increased capillary permeability
e.g. Burns, Allergic Reactions
Lymphatic obstruction or increased
interstitial colloid osmotic pressure
e.g. Surgical removal of lymph structures
MAJOR CAUSES OF EDEMATOUS STATE

Diuretic therapy
Elevating the
affected extremity
Elastic support
stockings in the
morning
Albumin IV
MANAGEMENT OF EDEMA

INSTERTITIAL TO PLASMA
Movement back
of edema to
circulatory
volume
e.g. excessive
administration
of hypertonic
solution

NCM 212 Concept Lecture on Fluids and Electrolyte
FLUID VOLUME
IMPAIRMENT
BY AMIE PEREZ DE JESUS

OBJECTIVES
At the end of the lecture, you will be able to:
• Differentiate fluid volume deficit and fluid
volume excess in terms of the following:
• Etiology
• Pathophysiology
• Manifestation
• Diagnostics
• Medical management
• Nursing management
• Nursing diagnosis
• Understand and demonstrate IV therapy.

There are primarily two types of fluid imbalances
(a) Fluid volume deficit and (b) Fluid volume excess.
Both type of imbalances can be life-threatening and are
often seen in acute care settings.
Patients with many underlying pathologies develop one of
these fluid imbalances and without careful management,
serious and critical conditions may develop
FLUID VOLUME IMPAIRMENT

Fluid volume deficit (FVD) is a decrease in intravascular,
interstitial, and/or intracellular fluid in the body.
Fluid volume deficits may be the result of excessive fluid
losses, insufficient fluid intake, or failure of regulatory
mechanisms and fluid shifts within the body.
FVD is a relatively common problem that may exist alone or
in combination with other electrolyte or acid–base
imbalances. (Lemone)
FLUID VOLUME DEFICIT

ISOOSMOLAR FLUID VOLUME DEFICIT
Occurs when sodium and water are lost in equal amounts.
HYPEROSMOLAR FLUID VOLUME DEFICIT
Occurs when more fluid is lost than sodium, resulting in
higher serum osmolality than normal ( > 295 mOsm/kg)
HYPOOSMOLAR FLUID VOLUME DEFICIT
Occurs when electrolyte loss is greater than fluid (rare).

excessive loss of GI fluids from vomiting, diarrhea,
GI suctioning, intestinal fistulas, and intestinal
drainage.
diuretics, renal disorders, endocrine disorders,
excessive exercise, hot environment, hemorrhage,
and chronic abuse of laxatives and/or enemas.
inability to access fluids, inability to request or to
swallow fluids, oral trauma, or altered thirst
mechanisms.
Older adults are at particular risk for fluid volume
deficit.
ETIOLOGY

PATHOPHYSIOLOGY
Fluid volume deficit can develop slowly or rapidly, depending on the type of fluid loss.
Loss of extracellular fluid volume can lead to hypovolemia, decreased circulating blood
volume.
Electrolytes often are lost along with fluid, resulting in an isotonic fluid volume deficit.

PATHOPHYSIOLOGY
When both water and electrolytes are lost, the serum sodium level remains normal,
although levels of other electrolytes such as potassium may fall.
Fluid is drawn into the vascular compartment from the interstitial spaces as the body
attempts to maintain tissue perfusion.
This eventually depletes fluid in the intracellular compartment as well.

PATHOPHYSIOLOGY
Hypovolemia stimulates regulatory mechanisms to maintain circulation.
The sympathetic nervous system is stimulated, as is the thirst mechanism.
ADH and aldosterone are released, prompting sodium and water retention by the kidneys.
Severe fluid loss, as in hemorrhage, can lead to shock and cardiovascular collapse.

MANIFESTATION
● Rapid weight loss is a good indicator of fluid volume deficit.
○ Each liter of body fluid weighs about 1 kg (2.2 lb).
○ The severity of the fluid volume deficit can be estimated by the
percentage of rapid weight loss:
○ A loss of 2% of body weight represents a mild FVD; 5%, moderate FVD;
and 8% or greater, severe FVD (Metheny, 2000).
● Loss of interstitial fluid causes skin turgor to diminish. When pinched, the skin
of a patient with FVD remains elevated.
● Postural or orthostatic hypotension is a sign of hypovolemia. A drop of more
than 15 mmHg in systolic blood pressure when changing from a lying to
standing position often indicates loss of intravascular volume.

MANIFESTATION
● Venous pressure falls as well, causing flat neck
veins, even when the patient is recumbent.
● Compensatory mechanisms to conserve water and
sodium and maintain circulation account for many of
the manifestations of fluid volume deficit, such as
tachycardia; pale, cool skin (vasoconstriction); and
decreased urine output.
● The specific gravity of urine increases as water is
reabsorbed in the tubules.

MULTISYSTEM EFFECTS OF FLUID VOLUME DEFICIT
● Mucuos Membranes
● Dry; may be sticky
● Decrease tongue size,
longitudinal furrows increase
Urinary
● Decrease urine output
● Oliguria (severe FVD)
● Increase in urine specific gravity

Neurologic
● Altered mental status
● Anxiety, restlessness
● Diminished alertness/condition
● Possible coma (severe FVD)
Integumentary
● Diminished skin turgor
● Dry skin
● Pale, cool extremities

Cardiovascular
● Tachycardia
● Orthostatic hypotension (moderate
FVD)
● Falling systolic/diastolic pressure
(severe FVD)
● Flat neck veins
● Decrease venous filling
● Decrease pulse volume
● Decrease capillary refill
● Increase hematocrit

Metabolic Processes
● Decrease body temperature
(isotonic FVD)
● Increase body temperature
(dehydration)
● Thirst
● Weight loss
○ 2-5% mild FVD
○ 6-9% moderate FVD
○ >10% severe FVD
Potential Complication
● Hypovolemic shock
Musculoskeletal
● Fatigue

DIAGNOSTICS
Serum electrolytes.
● In an isotonic fluid deficit,
sodium levels are within normal
limits; when the loss is water
only, sodium levels are high.
Decreases in potassium are
common.
Laboratory and diagnostic tests may be ordered when fluid volume deficit is suspected.
Such tests measure the following:
Serum osmolality.
● Measurement of serum
osmolality helps to differentiate
isotonic fluid loss from water
loss. With water loss, osmolality
is high; it may be within normal
limits with an isotonic fluid loss.

DIAGNOSTICS
Hemoglobin and hematocrit.
● The hematocrit often is elevated
due to loss of intravascular
volume and hemoconcentration.
Urine specific gravity and
osmolality.
● As the kidneys conserve water,
both the specific gravity and
osmolality of urine increase.

DIAGNOSTICS
Central venous pressure (CVP).
● The CVP measures the mean
pressure in the superior vena
cava or right atrium, providing an
accurate assessment of fluid
volume status.

● is the blood pressure in the venae cavae, near the
right atrium of the heart.
● CVP reflects the amount of blood returning to the
heart and the ability of the heart to pump the blood
back into the arterial system.
● It is acquired by threading a central venous
catheter (subclavian double lumen central line
shown) into any of several large veins. It is
threaded so that the tip of the catheter rests in
the lower third of the superior vena cava.
● The pressure monitoring assembly is attached to
the distal port of a multilumen central vein
catheter.
Central venous pressure (CVP)

The CVP catheter is an important tool used to assess right
ventricular function and systemic fluid status.
● Normal CVP is 2-6 mm Hg.
● CVP is elevated by :
○ overhydration which increases venous return
○ heart failure or PA stenosis which limit venous
outflow and lead to venous congestion
○ positive pressure breathing, straining,
● CVP decreases with:
○ hypovolemic shock from hemorrhage, fluid shift,
dehydration
○ negative pressure breathing which occurs when
the patient demonstrates retractions or
mechanical negative pressure which is
sometimes used for high spinal cord injuries.
Central venous pressure (CVP)

MEDICAL MANAGEMENT:
Correction of fluid loss depends on the acuteness and
severity of the fluid deficit. Goals are to replace F/E (Na
primarily) that have been loss.
FLUID RESTORATION
ORAL REHYDRATION
● The safest and most effective
● For mild fluid deficits in which a loss of electrolytes has
been minimal (e.g., moderate exercise in warm weather),
water alone may be used for fluid replacement.
● *When the fluid deficit is more severe and when electrolytes
have also been lost, a carbohydrate/electrolyte solution
such as a sports drink, ginger ale, or a rehydrating solution
(e.g., Pedialyte or Rehydralyte) is more appropriate. These
solutions provide sodium, potassium, chloride, and calories
to help meet metabolic needs.

MEDICAL MANAGEMENT: FLUID RESTORATION
IV REHYDRATION
● When the fluid deficit is severe or the
patient is unable to ingest fluids, the IV
route is used to administer replacement
fluids.

MEDICAL MANAGEMENT:
● Client with severe ECFVD accompanied by severe heart, liver and
kidney disease can’t tolerate large volumes of fluid or sodium
without the risk of development of heart failure
● Unstable clients needs to be monitored to detect ↑ pressure from
fluids
1) Fluid volume status by CVP insertion
2) Lab values (Na, K, BUN, Osmolarity)
3) Body Weight
4) Urine output
MONITOR FOR COMPLICATIONS OF FLUID RESTORATION

MEDICAL MANAGEMENT:
CORRECTION OF UNDERLYING PROBLEM
Medication
● Antiemetic
● Antidiarrheal
● Antibiotics
● Antidiuretics

NURSING MANAGEMENT
Nurses are responsible for
(1) identifying patients at risk for
fluid volume deficit,
(2) initiating and carrying out
interventions to prevent and treat
fluid volume deficit,
(3) monitoring the effects of
therapy.

NURSING MANAGEMENT
● I & O every 8o or hourly (Record all output accurately)
● VS every 2-4 o, report changes from baseline VS; Assess CVP every
4hrs (if patient has cvp access)
● Weight patient daily and record
● Peripheral vein filling (Capillary refill 3-5 sec)
● Renal client / relatives to report urine output ‹ than 30 m/L x 2
consecutive hours or ‹ 240 ml x 80 period

NURSING MANAGEMENT
● Assess for dryness of mucous membrane and skin turgor (check should be
done)
● Oral care to ↓ discomfort related to mucous membrane dryness
● Monitor plasma sodium, BUN, Glucose, HCT to determine osmolality
● Assess the client for confusion, easy indication of ICF involvement.
● Keep fluids easily accessible
● Administer and monitor intake of oral fluids as prescribed.
● Administer IV fluids as prescribed using an infusion pump. Monitor for indicators
of fluid overload if rapid fluid replacement is ordered: dyspnea, tachypnea,
tachycardia, increased CVP, jugular vein distention, and edema.
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INTRAVENOUS THERAPY
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ALTERNATIVE ACCESS ROUTES
CENTRAL VENOUS CATHETERS
● Central venous catheters terminate in the superior
vena cava near the heart.
● They are used when peripheral sites are inadequate
or when large amounts of fluid or irritating
medication must be given.
● Central catheter devices include a percutaneous
catheter, peripherally inserted central catheter
(PICC), tunneled catheter, and implanted port.

● These devices can have one, two, or three
lumens in the catheter or one or more port
chambers.
● Each lumen exits the site in a separate
line, called a tail. Multilumen catheters
allow for the administration of
incompatible solutions at the same time.
● Be careful not to confuse a central
catheter with a dialysis catheter.
● Dialysis catheters should be used only for
dialysis and not for IV therapy, and should
be accessed only by physicians or
specially trained dialysis nurses.

PERCUTANEOUS CENTRAL CATHETER
● A percutaneous central catheter is inserted
by a physician into the jugular or subclavian
vein. After insertion, correct placement is
determined by x-ray before the catheter is
used.
● These short-term central venous catheters
may remain in place up to several weeks, but
usual placement time is 7 days. These
catheters are inserted at the bedside and are
cost effective for short-term central venous
access in the acute care setting.

PERIPHERALLY INSERTED
CENTRAL CATHETER (PICC)
● A PICC line is a long catheter that is
inserted in the arm and terminates in
the central circulation. This device is
used when therapy will last more than
2 weeks or the medication is too
caustic for peripheral administration.

TUNNELED CATHETERS
● Central venous tunneled catheters
(CVTCs) are intended for use for
months to years to provide long-term
venous access. CVTCs are composed
of polymeric silicone with a Dacron
polyester cuff that anchors the
catheter in place subcutaneously. The
catheter tip is placed in the superior
vena cava.

● Ports
● A port is a reservoir that is surgically implanted into a
pocket created under the skin, usually in the upper
chest. An attached catheter is tunneled under the skin
into a central vein. An advantage of a port is that, when
not in use, it can be flushed and left unused for long
periods.
● Ports can be used to administer chemotherapeutic
agents and antibiotics that are toxic to tissues and
are suitable for long-term therapy. Ports should be
accessed only by specially trained RNs. Most ports
require the use of special noncoring needles that are
specifically designed for this purpose.

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Fluids and Electrolytes Compiled Notes.pdf

AMIE PEREZ DE JESUS
Clinical Instructor
FLUID
VOLUME
EXCESS

OBJECTIVES
At the end of the lesson, you will be able to:
1. Define fluid volume excess.
2. Identify different etiologic factors that could lead to fluid volume excess.
3. Discuss the pathophysiology of fluid volume excess and including it’s clinical
manifestation.
4. Differentiate extracellular and intracellular fluid volume excess according to
their causes and manifestations.
5. Enumerate the different diagnostics used to confirm fluid volume excess.
6. Enumerate the medical management along the nursing intervention for
patient suffering fluid volume excess.
7. Identify common nursing diagnosis used for fluid volume excess.

FLUID VOLUME EXCESS
Fluid volume excess results when both water and sodium are retained in
the body.
Fluid volume excess may be caused by fluid overload (excess water and
sodium intake) or by impairment of the mechanisms that maintain
homeostasis.
The excess fluid can lead to excess (1) intravascular fluid (hypervolemia)
and (2) excess interstitial fluid (edema).

TABLE OF CONTENTS
Here you could describe
the topic of the section.
01
ABOUT THE DISEASE
03
02 Here you could describe
DIAGNOSIS
04 Here you could describe
TREATMENT
RECOMMENDATIONS
Here you could describe

ETIOLOGY
• Fluid volume excess usually results from conditions
that cause retention of both sodium and water.
• Excessive intake of sodium-containing foods
• Drugs that cause sodium retention
• The administration of excess amounts of sodium-
containing IV fluids (such as 0.9% NaCl or Ringer’s
solution).

PATHOPHYSIOLOGY
01 02 03 04
Extracellular
compartment is
expanded and
increases the pressure
in the vasculature
Baroreceptors sense the
increase in pressure and
increase in their firing to
the central nervous
system (CNS)
Baroreceptors sense
the increase in
pressure and increase
in their firing to the
central nervous
system (CNS)
CNS)Reabsorption of
sodium in the renal
tubules is reduced, and
more urine is excreted.

MANIFESTATIONS
Peripheral edema,
or if severe,
anasarca (severe
generalized
edema)
Increased central
venous pressure
Tachycardia and
hypertension
Increased urine
output (polyuria)
Altered mental
status and anxiety
Full bounding
pulse
Cough and
dyspnea at rest
Reduced oxygen
saturation
Ascites (excess
fluid in the
peritoneal cavity)
Distended neck
and peripheral
veins
Orthopnea
(difficult breathing
when supine)
Moist crackles on
auscultation of the
lungs
Pulmonary edema
Decreased
hematocrit and
BUN

EXTRACELLULAR
FLUID OVERLOAD
04

EXTRACELLULAR FLUID
OVERLOAD
Occurs in either the intravascular compartment or in the interstitial area
EDEMA- most common term associated with fluid overload found in the
interstitial or lung tissue
HYPERVOLEMIA- when an overabundance of fluid occurs in the
intravascular compartment
ISOTONIC FLUID VOLUME EXCESS- type of fluid overload wherein
sodium and water remain in equal proportions with each other. Also
results from a decreased elimination of sodium and water.
ANASARCA- generalized edema

CAUSES ECF OVERLOAD
Excessive sodium intake
through diet
Administration of
hypertonic fluids
Congestive heart failure Cirrhosis
Hyperaldosteronism
Diabetes insipidus
Renal failure
Cushing’s syndrome

MANIFESTATIONS ECF OVERLOAD
PITTING PERIPHERAL EDEMA
PERIORBITAL EDEMA
SHORTNESS OF BREATH
SHIFT OF INTERSTITIAL FLUID
TO PLASMA
BOUNDING PULSE
JUGULAR VENOUS DISTENTION
ANASARCA
RAPID WEIGHT GAIN
MOIST CRACKLES
TACHYCARDIA
HYPERTENSION

INTRACELLULAR
FLUID OVERLOAD
05

INTRACELLULAR FLUID
OVERLOAD
• also known as water intoxication
• Hypotonic fluid from the intravascular space moves
by osmosis to an area of higher solute concentration
inside the cell.
• Cells run the risk of rupturing if they become too
overloaded with fluid.

CAUSES ICF OVERLOAD
Hypotonic intravenous
administration
Excessive nasogastric
tube irrigation with
free water
Syndrome of inappropriate
antidiuretic hormone
( SIADH)
Psychogenic polydipsia
Excessive administration of
free water via enteral
tube feedings

MANIFESTATIONS ICF OVERLOAD
NEUROLOGICAL (Cerebral edema)
HEADACHE
IRRITABILITY
CONFUSION
ANXIETY (Muscle weakness, Twitching)
RESPIRATORY (Dyspnea on exertion,
Increased respirations)
GASTROINTESTINAL (Nausea and
vomiting)
INCREASED THIRST
CARDIAC (Elevated blood pressure,
Decreased pulse)

DIAGNOSTICS
SERUM ELECTROLYTES
AND SERUM
OSMOLALITY are
measured, but usually
remain within normal
limits.
SERUM HEMATOCRIT
AND HEMOGLOBIN often
are decreased due to
plasma dilution from
excess extracellular
fluid.
Additional tests of renal
and liver function (such as
SERUM CREATININE, BUN,
and LIVER ENZYMES) may
be ordered to help
determine the cause of
fluid volume excess

DIAGNOSTICS
CHEST RADIOGRAPH- to
check for presence of
pulmonary congestion
ABG- fluid in the alveoli
impairs gas exchange
resulting in hypoxia as
evidenced by a low PO2

MANAGEMENT
Managing fluid volume excess focuses on
prevention in patients at risk, treating its
manifestations, and correcting the underlying
cause.

DIURETICS
Inhibit sodium and
chloride reabsorption in
the ascending loop of
Henle.
LOOP DIURETICS
Promote the excretion of
sodium, chloride,
potassium and water by
decreasing absorption in
the distal tubule
THIAZIDE-TYPE DIURETICS
Promote excretion of
sodium and water by
inhibiting sodium-
potassium exchange in
the distal tubule
POTASSIUM-SPARING
DIURETICS
Commonly used to treat fluid volume excess. They inhibit
sodium and water reabsorption, increasing urine output.
The three major classes of diuretics, each of which acts on a
different part of the kidney tubule, are as follows:

● Because sodium retention is
a primary cause of fluid
volume excess, a sodium-
restricted diet often is
prescribed.
● The primary dietary sources
of sodium are the salt
shaker, processed foods, and
foods themselves.
MANAGEMENT
● Fluid intake may be
restricted in patients who
have fluid volume excess.
● The amount of fluid allowed
per day is prescribed by the
primary care provider.
● All fluid intake must be
calculated, including meals
and that used to administer
medications orally or IV.
FLUID MANAGEMENT DIETARY MANAGEMENT

NURSING INTERVENTIONS
Nursing care focuses on preventing fluid volume excess in patients at risk and on
managing problems resulting from its effects.
• Assess vital signs, heart sounds, and volume of peripheral arteries.
• Auscultate lungs for presence or worsening of crackles and wheezes;
auscultate heart for extra heart sounds.
• Place in Fowler’s position if dyspnea or orthopnea is present.
• Monitor oxygen saturation levels and arterial blood gases(ABGs) for
evidence of impaired gas exchange (SaO2 < 92% to 95%; PaO2 < 80
mmHg). Administer oxygen as indicated.

• Assess for the presence and extent of edema, particularly in the
lower extremities and the back, sacral, and periorbital areas.
• Obtain daily weights at the same time of day, using approximately
the same clothing and a balanced scale.
• Administer oral fluids cautiously, adhering to any prescribed fluid
restriction.
• Discuss the restriction with the patient and significant others,
including the total volume allowed, the rationale, and the
importance of reporting all fluid taken.

• Provide oral hygiene at least every 2 hours. Oral hygiene contributes
to patient comfort and keeps mucous membranes intact; it also
helps relieve thirst if fluids are restricted.
• Teach patient and significant others about the sodium-restricted
diet.
• Administer prescribed diuretics as ordered, monitoring the patient’s
response to therapy.
• Promptly report significant changes in serum electrolytes or
osmolality or abnormal results of tests done to determine
contributing factors to the fluid volume excess.

NURSING DIAGNOSIS
Nursing care for the patient with excess fluid volume
includes collaborative interventions such as administering
diuretics and maintaining a fluid restriction, as well as
monitoring the status and effects of the excess fluid
volume.
FLUID VOLUME EXCESS
Tissue edema decreases oxygen and nutrient
delivery to the skin and subcutaneous tissues,
increasing the risk of injury.
RISK FOR IMPAIRED SKIN INTEGRITY
IMPAIRED GAS EXCHANGE
With fluid volume excess, gas exchange may be
impaired by edema of pulmonary interstitial tissues.
Acute pulmonary edema is a serious and potentially
life-threatening complication of pulmonary congestion.

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INTRAVENOUS
THERAPHY
AMIE PEREZ DE JESUS, RN
Clinical Instructor

INTRAVENOUS THERAPHY
Intravenous (IV) therapy is the administration of fluids or
medication via a needle or catheter (sometimes called a
cannula) directly into the bloodstream.

Patients can receive life-sustaining
fluids, electrolytes, and nutrition when
they are unable to eat or drink
adequate amounts.
The IV route also allows rapid delivery
of medication in an emergency. Many
medications are faster acting and
more effective when given via the IV
route. Other medications can be
administered continuously via IV to
maintain a therapeutic blood level.
INDICATIONS FOR INTRAVENOUS
THERAPY
Patients receive a variety of substances via IV therapy,
including fluids, electrolytes, nutrients, blood products,
and medications.

Patients with anemia or blood loss
can receive lifesaving IV
transfusions.
Patients who are unable to eat for
an extended period can have their
nutritional needs met with total
parenteral nutrition (TPN).
INDICATIONS FOR INTRAVENOUS
THERAPY

Types of Infusion
Continuous
Infusion
Intermittent
Infusion
Bolus Piggy
Back/Second
ary Infusion

Gravity Drip Electronic
Control Devices
METHODS OF INFUSION

CHANGE IN CATHETER
POSITION.
HEIGHT OF THE
SOLUTION.
PATENCY OF THE
CATHETER
Factors Affecting Flow Rates

TYPES OF IVF SOLUTIONS
CRYSTALLOIDS
Work much like colloids
but do not stay in the
intravascular circulation
as well as colloids do, so
more of them need to be
used.
COLLOIDS
Fluids that expand
the circulatory
volume due to
particles that
cannot cross a
semipermeable
membrane

IVF CLASSIFICATION
TONICITY
Isotonic
Have the same
concentration of
solutes to water as
body fluids.
Hypotonic
Have more solutes
(i.e., are more
concentrated)
than body fluids.
Hypertonic
Have fewer solutes
(i.e., are less
concentrated)
than body fluids

IVF CLASSIFICATION
TONICITY
Isotonic
When administered to a
patient requiring water, it
neither enters cells nor
pulls water from cells; it
therefore expands the
extracellular fluid volume
Hypotonic
Used when fluid is needed to
enter the cells, as in the
patient with cellular
dehydration. They are also
used as fluid maintenance
therapy.
Hypertonic
Hypertonic solutions are used
to expand the plasma
volume, as in the
hypovolemic patient. They are
also used to replace
electrolytes.

Commonly Administered IV Fluids
With Nursing Implications
ISOTONIC
SOLUTIONS
0.9% Saline
Lactated Ringer’s
solution
• Monitor for fluid overload; discontinue fluids
and notify the healthcare provider
• Do not administer lactated ringer’s solution to
patients with severe liver disease as the liver
may be unable to convert the lactate to
bicarbonate and the patient may become
acidotic. Do not administer if the patient has
a blood pH of >7.50
• If administering lactated ringer’s solution,
monitor potassium levels and cardiac rhythm;
if abnormals are present, notify the health
care provider

HYPOTONIC
SOLUTIONS
0.45% Saline or
0.25% Saline
D5W
• Monitor for inflammation and infiltration at IV
insertion site as hypotonic solutions may
cause cells to swell and burst, including
those at the insertions site; this narrows the
lumen of the vein
• Monitor blood sodium levels
• Do not administer to patients at risk for
increased intracranial pressure (e.g head
trauma, stroke, neurosurgery)
• Do not administer to patients at risk for third-
space shifts (burns, trauma, liver disease,
malnutrition)

HYPERTONIC
SOLUTIONS
Hypertonic fluids have
a tonicity >350 mEq/L
and include the ff:
Fluids containing
medications
D5W sodium chloride
D5W in lactated
ringer’s solution
Total parenteral
solutions
• Monitor for inflammation and
infiltration at IV insertion site as
hypertonic solutions cause cells to
shrink, exposing the basement
membrane of the vein
• Monitor blood sodium levels
• Monitor for circulatory overload
• Do not administer to patients with
diabetic ketoacidosis or impaired
cardiac or kidney function.

• Replace water loss
• Dilute meds
• Keep veins open
IVF CLASSIFICATION
ACCORDING TO PURPOSE
• Replace electrolyte loss at
ECF level
• Maintenance in patients
with no oral intake
• Replace fluid loss
• Treatment for dehydration
Promotes faster
recuperation
Increase osmotic
pressure thus
maintain
circulatory
volume
Maintenance
Hydrating Nutritional
Volume expander

1) Peripheral veins lie beneath the epidermis,
dermis, and subcutaneous tissue of the skin.
They usually provide easy access to the venous
system.
2) Central veins are located close to the heart.
Special catheters that end in a large vessel near the
heart are called central lines.
INTRAVENOUS ACCESS
Intravenous therapy can be administered into the systemic circulation via the
(1) peripheral or (2) central veins.

INTRAVENOUS ACCESS
Peripheral Vein Central vein

ADMINISTERING PERIPHERAL
INTRAVENOUS THERAPY
Check Physician’s
Order
Wash Hands Gather Equipment
Assess and
Prepare Patient
Select Site and
Dilate Vein

Age of patient
Availability of sites
Size of catheter to be used
Purpose of infusion therapy
Osmolarity of solution to be infused
Volume, rate, and length of infusion
Degree of mobility desired
Considerations for Vein Selection

● When multiple sticks are anticipated,
make the first venipuncture distally and
work proximal with subsequent
punctures.
● If therapy will be prescribed for longer
than 3 weeks, a long-term access device
should be considered.
● Avoid using venipunctures in affected
arms of patients with radical
mastectomies or a dialysis access site.
General Considerations When Initiating
Intravenous Therapy

● If possible, avoid taking a blood pressure on
the arm receiving an infusion because the
cuff interferes with blood flow and forces
blood back into the catheter. This may cause
a clot or cause the vein or catheter to rupture.
● No more than two attempts should be made
at venipuncture before getting help.
● Immobilizers should not be placed on or
above an infusion site.
General Considerations When Initiating
Intravenous Therapy

NOTE
Hand veins are used first if long-term
intravenous therapy is expected.
Hand veins can be used successfully
for most hydrating solutions, but they
are best avoided when irritating
solutions of potassium or antibiotics
are anticipated.
Vein size must also be
considered. Small veins do
not tolerate large volumes of
fluid, high infusion rates, or
irritating solutions. Large
veins should be used for
these purposes.

Peripheral
veins used
for IV
Therapy

Select the needle
(catheter)
• Needles have been largely replaced with flexible plastic
catheters that are inserted over a needle. The needle (or stylet)
is removed after the catheter is in place.
• These are available in a variety of sizes (gauges) and lengths.
• For patient comfort, choose the smallest gauge catheter that
will work for the intended purpose.
• Use smaller gauge catheters (20 to 24 gauge) for fluids and slow
infusion rates.
• Use larger catheters (18 gauge) for rapid fluid administration
and viscous solutions such as blood.
• Also consider vein size when choosing a catheter gauge.

INTRAVENOUS THERAPY
Put on gloves
Prepare the site
Insert the catheter

INTRAVENOUS THERAPY
Stabilize the Catheter
and Dress the Site
Label the Site
Dispose of Equipment

INTRAVENOUS THERAPY
Educate the Patient
Calculate Drip Rate
Document

Complications Of Peripheral Iv Therapy
Local
Complications
of IV Therapy
Signs and Symptoms Nursing Interventions
Hematoma Ecchymoses
Swelling
Inability to advance catheter
Resistance during flushing
Remove catheter
Apply pressure with 2x2
Elevate extremity
Thrombosis Slowed or stopped infusion
Fever/malaise
Inability to flush catheter
Discontinue catheter
Apply cold compress to site
Assess for circulatory impairment
Phlebitis Redness at site
Site warm to touch
Local swelling
Pain
Palpable cord
Sluggish infusion rate
Apply cold compress initially;
then warm
Consult physician if severe

Complications Of Peripheral Iv Therapy
Local
Complications
of IV Therapy
Signs and Symptoms Nursing Interventions
Infiltration
(Extravasation)
Coolness of skin at site
Taut skin
Dependent edema
Backflow of blood absent
Infusion rate slowing
Apply cool compress
Elevate extremity slightly
Follow extravasation guidelines
Have antidote available
Local Infection Redness and swelling at site
Possible exudate
Increase WBC count
Elevated T lymphocytes
Discontinue catheter and culture
site and catheter
Apply sterile dressing
over site
Administer antibiotics if ordered
Venous Spasm Sharp pain at site
Slowing of infusion
Apply warm compress to site
Restart infusion in new site if
spasm continues

Systemic Complication of Peripheral IV Therapy
Complication Signs and
Symptoms
Nursing
Interventions
Septicemia Fluctuating
temperature
Profuse sweating
Nausea/vomiting
Diarrhea
Abdominal pain
Tachycardia
Hypotension
Altered mental status
Restart new IV
system
Obtain cultures
Notify physician
Initiate antimicrobial
therapy as
ordered
Monitor patient
closely

Symptoms
Nursing
Interventions
Fluid Overload Weight gain
Puffy eyelids
Edema
Hypertension
Changes in input and
output (I&O)
Rise in central venous
pressure (CVP)
Shortness of breath
Crackles in lungs
Distended neck veins
Decrease IV flow rate
Place patient in high
Fowler’s position
Keep patient warm
Monitor vital signs
Administer oxygen
Use micro drip set or
controller

Symptoms
Nursing
Interventions
Air Embolism Lightheadedness
Dyspnea, cyanosis,
tachypnea, expiratory
wheezes, cough
chest pain, hypotension
Changes in mental
status
Coma
Call for help!
Place patient in
Trendelenburg’s
position
Administer oxygen
Monitor vital signs
Notify physician

● https://www.youtube.com/watch?v=JfLncYX190E&t=
878s&fbclid=IwAR2EztdUGsojNupBPHZFWMyI5rx_A
lPEUKZJeCBweKt1EE6bjRPg6pOnQTQ
● https://www.youtube.com/watch?v=4ntqS_R1r70&t
=269s
● https://www.youtube.com/watch?v=vE99rZ7JT3Q
● https://www.youtube.com/watch?v=JJBsqcdWdqQ
Supplementary Video

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TOPIC 3 ELECTROLYTE IMBALANCE
Electrolytes are substances that dissociate in solution to form charged particles called ions.
Cations are positively charged electrolytes; anions are negatively charged electrolytes.
Electrolytes have many functions, including assisting with the regulation of water balance,
regulating and maintaining acid–base balance, and contributing to enzyme reactions. They
are also essential for neuromuscular activity (Lemone, 2011). Electrolyte imbalances can
develop by consuming too little or too much electrolyte as well as excreting too little or too
much electrolyte. Electrolyte disturbances are involved.
Major Roles of Electrolytes:
1. Maintain body fluid osmolality - regulate water distribution
2. Nervous System - Propagation of Action Potential
3. Cardiovascular System - Cardiac conduction & contraction
SODIUM (135 to 145 mEq/L)
Sodium is one of the most important elements in the body. It accounts for 90% of extracellular
fluid cations (positively charged ions) and is the most abundant solute in extracellular fluid.
The normal serum sodium levels range from 135 to 145 mEq/L.
The body needs sodium to maintain proper extracellular fluid osmolality (concentration).
Sodium attracts fluids and helps preserve the extracellular fluid volume and fluid distribution
in the body.
It also helps transmits impulses in nerve and muscle fibers (Lippincott, 2016).
Sodium imbalances affect the osmolality of ECF and water distribution between the fluid
compartments. When sodium levels are low (hyponatremia), water is drawn into the cells of
the body, causing them to swell. In contrast, high levels of sodium in ECF (hypernatremia)
draw water out of body cells, causing them to shrink (Lemone, 2011).
The kidney is the primary regulator of sodium balance in the body. The kidney excretes or
conserves sodium in response to changes in vascular volume. A fall in blood volume prompts
several mechanisms that lead to sodium and water retention:
HYPONATREMIA
Hyponatremia, a common electrolyte imbalance, refers to sodium deficiency
in relation to the amount of water in the body. It usually results from a loss of
sodium from the body, but it may also be caused by water gains that dilute
extracellular fluid (ECF).
Classifications:
(1)Hypovolemic both sodium and water levels decrease in the extracellular area, but sodium
loss is greater than water loss.
Causes: vomiting, diarrhea, fistulas, gastric suctioning, excessive sweating, cystic fibrosis,
burns, wound drainage, osmotic diuresis,adrenal insudfficiency, diuretic use
(2)Hypervolemic both water and sodium levels increase in the extracellular area, but the
water gain is more impressive. Serum sodium levels are diluted and edema also occurs.
Causes: heart failure, liver failure, nephrotic syndrome, excessive administration of hypotonic
IV fluids, hyperaldosteronism
(3)Isovolemic sodium levels may appear low because too much fluid is in the body. Patients
may not exhibit signs of fluid volume excess, and total body sodium remains stable. Causes:
glucocorticoid deficiency, hypothyroidism, renal failure

Pathophysiology
Normally, the body gets rid of excess water by secreting less Antidiuretic Hormone (ADH);
less ADH causes diuresis. For that to happen, the nephrons must be functioning normally,
receiving and excreting excess water and reabsorbing sodium.
Hyponatremia develops when this regulatory function goes haywire. Serum sodium levels
decrease, and fluid shifts occur. When the blood vessels contain more water and less sodium,
fluid moves by osmosis from the extracellular area into the more concentrated intracellular
area.
With more fluid in the cells and less in the blood vessels, cerebral edema and hypovolemia
(fluid volume deficit) can occur.
Manifestations
The manifestations of hyponatremia depend on the rapidity of onset, the severity, and the
cause of the imbalance. If the condition develops slowly, manifestations are usually not
experienced until the serum sodium levels reach 125 mEq/L. In addition, the manifestations
of hyponatremia vary, depending on extracellular fluid volume.
a. Poor skin turgor
b. Dry mucosa
c. Decrease saliva production
d. Orthostatic hypotension
e. Nausea, abdominal cramping
f. Neurologic changes such as: lethargy, confusion, signs of increase ICP, muscle twitch,
seizure
Laboratory Findings
• Serum osmolality less than 280 mOsm/kg (dilute blood)
• Serum sodium level less than 135 mEq/L (low sodium level in blood)
• Urine specific gravity less than 1.010
• Elevated hematocrit and plasma protein levels
Medical Management
• Generally, treatment varies with the cause and severity of hyponatremia.
Hypervolemia/isovolemia
a. Fluid restrictions
b. Oral sodium supplements
Hyponatremia
a. Give isotonic IV fluids (e.g. normal saline)
b. Offer High sodium foods
In SEVERE cases:
a. Infusion of hypertonic saline solution (3% or 5% saline)

Nursing Management
Watch patients at risk for hyponatremia, including those with heart failure, cancer, or GI
disorders with fluid losses. Review patient’s medications, noting those that are associated with
hyponatremia. For patients who develop hyponatremia, take the following actions:
• Monitor and record vital signs, especially blood pressure and pulse, and watch for
orthostatic hypotension and tachycardia
• Monitor neurologic status frequently
Report any deterioration in level of consciousness.
• Accurately measure and record intake and output.
• Assess skin turgor at least every 8 hours for signs of dehydration.
• Restrict fluid intake as ordered (fluid restriction is the primary treatment for dilutional
hyponatremia).
• Administer oral sodium supplements as ordered.
• Provide a safe environment for patients with altered thought processes
• Seizure precautions
HYPERNATREMIA
Hypernatremia, a less common problem than hyponatremia, refers to
excess of sodium relative to the amount of water in the body.
Pathophysiology
The cells play a role in maintaining sodium balance. When serum osmolality increases
because of hypernatremia, fluid moves by osmosis from inside the cell to outside the cell. As
fluid leaves the cells, they become dehydrated and shrink.
Manifestations
Thirst is the first manifestation of hypernatremia. If thirst is not relieved, the primary
manifestations relate to altered neurologic function. Initial lethargy, weakness, and irritability
can progress to seizures, coma, and death in severe hypernatremia. Both the severity of the
sodium excess and the rapidity of its onset affect the manifestations of hypernatremia. You
may also observe the following: a. Low grade fever
b. Flushed skin
c. Dry mucous membranes
d. Oliguria
e. Orthostatic hypotension
Laboratory Findings
The following laboratory and diagnostic tests may be ordered with the following findings:
• Serum sodium levels are greater than 145 mEq/L
• Serum osmolality is greater than 295 mOsm/kg
Medical Management
Treatment for hypernatremia varies with the cause. The underlying disorder must be
corrected, and serum sodium levels and related diagnostic tests must be monitored. Note
that the fluids should be given gradually over 48 hours to avoid shifting water into brain
cells.

Nursing Management
•Intravenous fluid replacement (dextrose 5% in water)
to return serum sodium levels to normal
• Sodium intake restrictions
• Administer diuretics to increase sodium loss
Nursing Management
If patient develop hypernatremia, take the following measures:
• Monitor and record vital signs, especially blood pressure and pulse
• Check neurologic status frequently.
• Report any deterioration in the level of consciousness
• Carefully measure and record intake and output.
• Assess skin and mucous membranes for signs of breakdown and infection
• Monitor serum sodium level and report any increase. • Assist with oral hygiene. Lubricate
the patient’s lips frequently.
• Provide a safe environment for confused or agitated patients
POTASSIUM (3.5 to 5.0 mEq/L)
A major cation (ion with a positive charge) in intracellular fluid, potassium plays a critical role
in many metabolic cell functions. Only 2% fluid; 98% of the body’s potassium is found in
extracellular fluid. That significant difference affects nerve impulse transmission. The normal
serum (ECF) potassium level is 3.5 to 5.0 mEq/L. To maintain balance, potassium must be
replaced daily through diet. Virtually all foods contain potassium, although some foods and
fluids are richer sources of this element than others.
Aldosterone helps regulate potassium elimination by the kidneys. An increased potassium
concentration in ECF stimulates aldosterone production by the adrenal gland. The kidneys
respond to aldosterone by increasing potassium excretion. Changes in aldosterone secretion
can profoundly affect the serum potassium level.
Potassium directly affects how well the body cells, nerves, and muscles function by:
• Maintaining cells’ electrical neutrality and osmolality
• Aiding neuromuscular transmission of nerve impulses
• Assisting skeletal and cardiac muscle contraction and electrical conductivity
• Affecting acid-base balance in relationship to the hydrogen ion.
HYPOKALEMIA
Hypokalemia is an abnormally low serum potassium level. It usually results
from excess potassium loss, although hospitalized patients may be at risk
for hypokalemia because of inadequate potassium intake.
Pathophysiology
Inadequate intake and excessive output of potassium can cause a moderate drop in its level,
upsetting the balance and causing a potassium deficiency. Potassium shifts from the
extracellular space to the intracellular space and hides in the cells. Because the cells contain
more potassium than usual, less can be measured in the blood.

Causes:
a. Inadequate potassium intake
b. Severe GI losses, e.g. suction, lavage, prolonged vomiting can deplete the body’s
potassium supply as a result potassium levels drop
c. Drug associated, e.g. diuretics, (esp. thiazides and furosemides), corticosteroids, insulin d.
Decrease bowel motility
Manifestations
The signs and symptoms of a low potassium level reflect how important the electrolyte is to
normal body functions.
a. Skeletal muscle weakness, especially in the legs
a sign of a moderate loss of potassium.
This also includes paresthesia and leg cramps
b. Decreased bowel sounds, constipation, paralytic ileus
c. Weak and irregular pulse
d. Orthostatic hypotension and palpitations
e. ECG changes, flattened or inverted T wave, prominent U wave
Figure 3-1 (Left) Normal ECG wave ; (Right) Inverted T wave
Laboratory Findings
The following test results may develop to confirm the diagnosis of hypokalemia:
a. Serum potassium level less than 3.5 mEQ/L
b. Increased 24-hour urine level
Medical Management
a. Identify and treat the cause
treatment for hypokalemia focuses on restoring a normal potassium balance, preventing
serious complications, and removing or treating the underlying causes.
b. Oral and IV replacements (40-80 meq/day – Kalium durule or K IV), it can be safely given
at the same time

Nursing Management
Careful monitoring and skilled interventions can help prevent hypokalemia and spare your
patient from its associated complications. The following actions are considered.
a. Monitor vital signs, especially blood pressure
hypokalemia is commonly associated with hypovolemia, which can cause orthostatic
hypotension
b. Check heart rate and rhythm and ECG tracings in patients with serum potassium level less
than 3 meQ/L
hypovolemia causes tachyarrthymias
c. Assess respiratory rate, depth and pattern
hypokalemia may weaken or paralyze respiratory muscles. Notify the doctor immediately
if respirations become shallow and rapid.
d. Monitor serum potassium levels
changes in serum potassium level can lead to serious cardiac complications.
e. Administer potassium infusions cautiously.
HYPERKALEMIA
Hyperkalemia can result from inadequate excretion of potassium,
excessively high intake of potassium, or a shift of potassium from the ICF
to the ECF. Hyperkalemia affects neuromuscular and cardiac function.
Causes:
a. Increased dietary intake
b. Blood transfusion (stored blood)
serum potassium level increases longer the blood is stored.
c. Rapid IV potassium administration
d. Renal insufficiency
e. Metabolic acidosis, potassium shift to ECF in exchange of H ions
Pathophysiology
Potassium move from the extracellular to the intracellular compartment and increases cell
excitability, so that cells respond to stimuli of less intensity and may actually discharge
independently without a stimulus.
Manifestations
Signs and symptoms of hyperkalemia reflect its effects on neuromuscular and cardiac
functioning in the body.
a. Nausea, abdominal cramping and diarrhea
the early signs of hyperkalemia due to smooth - muscle hyperactivity
b. Muscle weakness that in turn lead to flaccid paralysis
c. Decreased heart rate, irregular pulse, decreased cardiac output, hypotension
d. ECG changes, elevated T wave
Figure 3-2 Elevated T wave

Laboratory Findings
The following test results help confirm the diagnosis and determine the severity of
hyperkalemia:
a. Serum potassium level greater than 5 mEq/L
b. Decreased arterial pH, indicating acidosis
c. ECG abnormalities
Medical Management
Treatment for hyperkalemia is aimed at lowering the potassium level, treating its cause,
stabilizing the myocardium, and promoting renal and gastrointestinal excretion of potassium.
The severity of hyperkalemia dictates how it should be treated.
a. Diet restrictions
b. May administer loop diuretics for mild hyperkalemia
to increase potassium loss from the body or to resolve any acidosis present
c. Sodium polystyrene sulfonate (Kayexalate)
a cation-exchange resin (common treatment for hyperkalemia)
d. Hemodialysis, if patient has renal failure
Patients at risk for hyperkalemia require frequent monitoring of serum potassium and other
electrolyte levels. Take these actions.
a. Assess vital signs.
b. Monitor the patient’s intake and output
Report an output of less than 30 mL/hour.
c. Prepare to administer a slow calcium chloride or gluconate IV infusion to counteract the
myocardial depressant effects of hyperkalemia
d. Keep in mind when giving Kayexalate that serum sodium levels may rise. Watch for signs
of heart failure.
e. Monitor ECG changes
CALCIUM (4.5-5.5 meq/L)
Calcium is a positively charged ion, or cation, found in both extracellular and intracellular fluid.
About 99% of the body’s calcium is found in the bones and the teethOnly 1% is found in serum
and in soft tissue.
Functions:
a. Skeletal and heart muscle relaxation, activation, excitation and contraction
b. Maintains cellular permeability
c. Promotes blood coagulation
d. Nerve impulse transmission
Three (3) Forms of calcium exist in the body:
1. 45% is bound to protein, mostly albumin; part of the total serum calcium concentration
2. 40% is ionized calcium, it is the calcium that is physiologically active and clinically
important for neuromuscular transmission.
3. 15% is bound to other substances such as phosphate, citrate, or carbonate

System Interactions:
a. Parathyroid Hormone (PTH) , raises the plasma calcium level by promoting the transfer of
calcium from the bone to plasma
b. Calcium is dependent upon calcitriol, the most active from of vitamin D
c. Calcitonin, a calcium-lowering hormone produced by the thyroid gland , acts against PTH
by transferring calcium from the plasma to the skeletal system
HYPOCALCEMIA
Hypocalcemia can result from decreased total body calcium stores or low
levels of extracellular calcium with normal amounts of calcium stored in
bone. The systemic effects of hypocalcemia are caused by decreased
levels of ionized calcium in extracellular fluid.
Causes:
a. Inadequate intake
b. Hypoparathyroidism, resulting from surgery (parathyroidectomy, thyroidectomy, radical
neck dissection)
c. Electrolyte imbalances
Low serum albumin (most common cause)
d. Malabsorption
can result from increased intestinal motility
e. Vitamin D deficiency
due to lack sun exposure or malabsorption)
f. Massive blood transfusion, liver unable to metabolize citrate (added to prevent clotting) g.
Chronic diarrhea
h. Diuretic phase of ARF
i. Severe burns
Pathophysiology
Extracellular calcium acts to stabilize neuromuscular cell membranes. This effect is reduced
in hypocalcemia, increasing neuromuscular irritability. Thus, electrical activity occurs
spontaneously and continuously.
Manifestations
Signs and symptoms of hypocalcemia reflect calcium’s effects on nerve transmission and
muscle and heart functions; therefore, neuromuscular and cardiovascular findings are most
evident.
a. Anxiety, confusion and irritability that can progress to seizures
b. Paresthesia, muscle twitching, cramps or tremors
c. Diarrhea
d. Hyperactive tendon reflexes
e. Fractures may occur
f. Brittle nails, dry skin and hair
g. Positive Chvostek’s (contraction of facial muscles produced by tapping the facial nerve in
front of the ear), Trousseau’s sign (carpal spasm induced by inflating a blood pressure
cuff on the upper arm to above systolic blood pressure for 2 to 5 minutes); due to increase
nerve excitability h. Decreased cardiac output and subsequent arrhythmias
i. Prolonged QT segment on electrocardiogram (ECG)

Figure 3-3 Trousseau’s sign / Chvostek’s Sign
Laboratory Findings
These test results can help diagnose hypocalcemia and determine the severity of the
deficiency:
a. Elevated total serum calcium level
b. Low Ionized calcium level (ionized calcium measurement is the definitive method to
diagnose hypocalcemia)
c. Low albumin level
d. Characteristic ECG changes, prolonged ST segment
Figure 3-4 ECG changes in Hypercalcemia, Hypocalcemia
Medical Management
Treatment for hypocalcemia focuses on correcting the imbalance as quickly and safely as
possible.
The underlying cause should be addressed to prevent recurrence.
a. Dietary supplement, e.g milk, cheese, cereal
b. Oral/IV calcium, e.g. Calcium carbonate/gluconate
c. Vitamin D supplements, facilitates GI absorption of calcium
Nursing Management
Here’s what you can do if the patient develops hypocalcemia:
b. Place patient on a cardiac monitor, and evaluate for changes in heart rate and rhythm
c. Check for Chvostek’s and Trousseau’s sign
d. Serum levels monitoring

HYPERCALCEMIA
Hypercalcemia is a common metabolic emergency that occurs when
serum calcium level rises, or the rate of calcium entry into extracellular
fluid exceeds the rate of calcium excretion by the kidneys.
Causes:
a. Hyperparathyroidism (most common cause) the body excretes more PTH than normal,
which greatly strengthens the effects of the hormone
b. Metastatic malignancy
causes bone destruction as malignant cells invade the bones and cause the release of a
hormone similar to PTH
c. Thiazide diuretics
potentiates PTH and decrease excretion in kidneys
d. Increase Vitamin D (can prompt an increase in serum calcium levels) & prolong use of
alkaline antacid (calcium carbonate) e. Prolong immobility
Manifestations
Signs and symptoms of hypercalcemia are intensified if the condition develops acutely.
Symptoms are also more severe if calcium levels are greater than 5.5 mEq/L
a. Muscle weakness
b. Bradycardia
c. Shortened QT interval
d. Decreased gastrointestinal motility (anorexia, n/v)
e. Stone formation
Laboratory Findings
The laboratory and diagnostic tests that may be ordered are
as follows:
a. Elevated serum calcium level
b. Elevated Ionized calcium level
c. Digoxin toxicity if patient is taking digoxin)
d. Characteristic ECG changes (Shortened QT interval)
Figure 3-5 Normal QT wave; Shortened QT wave

Medical Management
The management of hypercalcemia focuses on correcting the underlying cause and reducing
the serum calcium level.
a. ECG monitoring
b. Treat with IV saline
the sodium in the solution is typically used for hydration in these cases
c. Loop diuretics (Lasix)
promotes calcium excretion
d. Administer Calcitonin (IM/SC)
Nursing Management
Be sure to monitor the calcium levels of patients who are at risk for hypercalcemia, such as
those who have cancer or parathyroid disorders, are immobile, or are receiving a calcium
supplement. For a patient who develops hypercalcemia, you can take the following actions:
b. Watch the patient for arrhythmias
c. ECG monitoring
d. Calcium levels monitoring
e. Encourage Mobilization
f. Dietary limits of vitamin D/Calcium
MAGNESIUM
(1.5-2.5 meq/L)
Function:
a. Promotes enzyme reactions within the cell during carbohydrate metabolism
b. Influences vasodilation and irritability and contractility of the cardiac muscles, thereby
helping the cardiovascular system function normally
c. Aids in neurotransmission and hormone-receptor binding
d. Makes production of parathyroid hormone possible
HYPOMAGNESEMIA
Hypomagnesemia is a common problem in critically ill patients. It is may
be caused by deficient magnesium intake, excessive losses, or a shift
between the intracellular and extracellular compartment
Causes:
Any condition that impairs either of the body’s magnesium regulators – the GI system or the
urinary system – can lead to a magnesium shortage. These conditions fall into four (4) main
categories:
a. Poor dietary intake of magnesium
b. Poor magnesium absorption by the GI tract
c. Excessive magnesium loss from the GI tract
d. Excessive magnesium loss from the urinary tract
Pathophysiology
Hypomagnesemia causes increased neuromuscular excitability which commonly occurs with
hypokalemia and hypocalcemia

Manifestations
Signs and symptoms of hypomagnesemia can range from mild to life-threatening
Generally speaking, your patient’s signs and symptoms may resemble those you
would see with a potassium or calcium imbalance. However, you can’t always count
on detecting hypomagnesemia from clinical findings alone. a. Altered level of
consciousness, tetany, seizures
b. Emotional lability
c. vomiting
d. Tremors, twitching, tetany, hyperactive deep tendon reflexes
e. Rapid heart rate
f. Chvostek’s and Trousseau’s sign
Laboratory Findings
Diagnostic test results that point to hypomagnesemia include:
a. Serum magnesium level below 1.5 mEq/L (possibly with a below normal serum albumin
level)
b. Low potassium and calcium level
d. Elevated serum levels of digoxin in a patient receiving the drug
Medical Management
Treatment for hypomagnesemia depends on the underlying cause of the condition and the
patient’s clinical findings:
a. Dietary management, (green leaf vegetables, nuts, legumes, seafood, wholegrain,
chocolates)
b. Intravenous infusion/ intramuscular injection, before magnesium administration, renal
function should be assessed
Nursing Management
The best treatment for hypomagnesemia is prevention, so keep a watchful eye on patients at
risk for this imbalance such as those who can’t tolerate oral intake. For patients who have
already been diagnosed with hypomagnesemia, take the following actions:
a. Assess the patient’s mental status and report changes
b. Evaluate the patient’s neuromuscular status regularly by checking for hyperactive Deep
Tendon Reflexes, tremors, and tetany.
c. Check for Chvostek’s and Trousseau’s sign
d. Monitor patients who have lost an excessive amount of fluid, they are at risk for magnesium
deficiency
e. Urine output should be monitored at least every 4 hours. Magnesium generally isn’t
administered if urine output is less than 100 mL in 4 hours.
f. If patient id receiving digoxin, monitor him closely for signs and symptoms of digoxin toxicity
(such as nausea, vomiting and bradycardia
g. During magnesium replacement, check the cardiac monitor frequently and assess the
patient closely for signs of magnesium excess, such as hypotension and respiratory
distress. Keep calcium gluconate at the bedside in case signs occur

HYPERMAGNESEMIA
Having too much magnesium in the serum can be just as bad as having too
little. Hypermagnesemia occurs when the body’s serum magnesium level
rises above the normal range. However, hypermagnesemia is uncommon;
typically, the kidneys can rapidly reduce the amount of excess magnesium
in the body.
Causes:
a. Impaired magnesium excretion, e.g. renal dysfunction, most common cause of
hypermagnesemia
b. Excessive magnesium intake
Pathophysiology
Elevated serum magnesium levels suppress cellular excitability, resulting to muscular
flaccidity and suppression of electrical impulses.
Laboratory Findings
a. Serum magnesium level above 2.5 mEq/L
b. ECG changes (prolonged PR interval, widened QRS complex, tall T wave.
Medical Management
a. Correct underlying cause
b. Intravenous infusion of calcium gluconate, to antagonize magnesium effect
Nursing Management
b. Checked for flushed skin and diaphoresis
c. Check for deep tendon reflexes
d. Evaluate for changes in mental status
PHOSPHOROUS (1.2 to 3.0 meq/L)
The primary anion, or negatively charged ion, found in the intracellular fluid. It’s contained in
the body as phosphate.
Functions:
a. Integral part of acid base buffer system
b. Regulate ATP use for muscle contraction, nerve transmission, electrolyte transport
c. Regulates 2,3 DPG (diphosphoglycerate) a compound in red blood cells that facilitates
oxygen delivery from the red blood cells to the tissues.
d. Regulates 2,3 DPG (diphosphoglycerate) a substance in RBC affecting oxygen affinity

HYPOPHOSPHATEMIA
Hypophosphatemia occurs when the serum phosphorous level falls
below 1.2 mEq/L. although this condition generally indicates a deficiency
of phosphorous, it can occur under various circumstances when total
body phosphorous stores are normal
Causes:
a. Respiratory alkalosis
one of the most common cause of hypophosphatemia, can stem from a number of
conditions that produce hyperventilation
b. Malabsorption syndromes
c. Diuretic use, (Thiazides, Loop diuretics, Acetazolamide)
Pathophysiology
Most effects of hypophosphatemia result from depletion of ATP and impaired oxygen delivery
to the cells due to a deficiency of the red blood cell enzyme 2,3-DPG. Severe
hypophosphatemia affects virtually every major organ system:
Manifestations
a. Muscle weakness, most common symptom
b. malaise, weakened hand grasp, myalgia (pain in the muscles)
c. rhabdomyolysis (skeletal muscle destruction), can occur with altered muscle cell activity
d. Osteomalacia/Fracture, due to loss of bone density
e. Bruising and bleeding
Laboratory Findings
Diagnostic test results may indicate hypophosphatemia or a related condition:
a. serum phosphorous level less than 1.2 mEq/L
b. elevated Creatinine Kinase level if Rhabdomyolysis is present
c. X-ray studies that reveal skeletal changes typical of osteomalacia or bone fractures
d. Abnormal electrolytes (decreased magnesium levels and increased calcium levels)
Medical Management
Treatment varies with the severity and cause of the condition:
a. Treat the underlying cause
b. Oral and intravenous supplements
Nursing care should focus on careful monitoring, safety measures and interventions to
restore normal serum phosphorous levels.
b. Assess the patient frequently for evidence of decreasing muscle strength, such as weak
hand grasps or slurred speech, and document findings regularly.
c. Assist in ambulation and activities of daily living, if needed, and keep essential objects near
the patient to prevent accidents.

HYPERPHOSPHATEMIA
Hyperphosphatemia is a serum phosphate level greater than 4.5mg/dL. As
with other electrolyte imbalances, it may be the result of impaired phosphate
excretion, excess intake, or a shift of phosphate from the intracellular space
into extracellular fluids.
Causes:
a. Renal Failure
b. Hypoparathyroidism
impairs less synthesis of parathyroid hormone(PTH), when less PTH is synthesized,
less phosphorous is excreted from the kidneys. c. Respiratory acidosis
d. Increase tissue breakdown
Pathophysiology
Effects of high phosphorous level are actually due to hypocalcemia; calcium suppresses
cellular excitability.
Manifestations
a. Hyperphosphatemia causes few symptoms (tetany, tissue calcification)
b. Symptoms occurring result from decrease calcium secondary to reciprocity
Laboratory Findings:
The following diagnostic test results may indicate hyperphosphatemia or a related condition
such as hypocalcemia:
a. Serum phosphorous above normal
b. Low serum calcium level
Medical Management:
a. Treat underlying cause
b. Restrict dietary intake
c. Administer phosphate binding antacid, this may decrease absorption of phosphorous in
the gastrointestinal system
Nursing Management
b. Monitor intake and output. (if urine output falls below 30 mL/hour, immediately notify the
doctor)
Decreased urine output can seriously affect renal clearance of excess serum
phosphorous
c. Monitor serum phosphorous and calcium levels
d. Monitor signs of tetany, such as positive Trousseau’s and Chvostek’s sign

TOPIC 4 ACID- BASE IMBALANCE
The body constantly works to maintain a balance (homeostasis) between acids and bases.
Without that balance, cells can’t function properly. As cells use nutrients to produce energy
they need to function, two-by products are formed—carbon dioxide (CO2) and hydrogen. Acid-
base balance depends on the regulation of free hydrogen ions (H+) in body fluids determines
the extent of acidity and alkalinity, both of which are measured in pH. Remember, pH levels
are inversely proportionate to H+ concentration, which means H+ concentration increases, pH
decreases (acidosis). Conversely, when H+ concentration decreases, pH increases
(alkalosis).
Key Elements:
a. Acids – are hydrogen ion donors
b. Bases – are hydrogen ion acceptors
c. pH – expression of hydrogen concentration in a solution
d. pCO2 – Partial pressure of Carbon Dioxide the measure of carbon dioxide within arterial
or venous blood.
e. HCO3 – Bicarbonate is a byproduct of the body's metabolism.
2 Categories of Metabolic Processes:
a. Volatile - can be eliminated from the body as a gas.
e.g. Carbonic acid ((H2CO3) is the only volatile acid produced in the body.
b. Nonvolatile - that must be metabolized or excreted from the body in fluid.
e.g. Lactic acid, hydrochloric acid, phosphoric acid, and sulfuric acid
Regulatory Mechanisms:
A. Chemical buffers
are substances that prevent major changes in pH by removing present in body fluid,
buffers bind with hydrogen ions to minimize the change in pH. If body fluids become too
basic or alkaline, buffers release hydrogen ions, restoring the pH.
1. Carbonic-Bicarbonate System, Bicarbonate (HCO3–)
→ a weak base; when an acid is added to the system, the hydrogen ion in the acid
combines with bicarbonate, and the pH changes only slightly. Carbonic acid (H2CO3) is
a weak acid produced when carbon dioxide dissolves in water. If a base is added to the
system, it combines with carbonic acid, and the pH remains within the normal range.
Although the amounts of bicarbonate and carbonic acid in the body vary to a certain
extent, as long as a ratio of 20 parts bicarbonate (HCO3–) to 1-part carbonic acid
(H2CO3) is maintained, the pH remains within the 7.35 to 7.45 range.
→ Acts in few seconds
2. Phosphates, important intracellular buffers, helping to maintain a stable pH within the
cells.
3.Protein Buffer, contribute to buffering of extracellular fluids. Proteins in intracellular fluid
provide extensive buffering for organic acids produced by cellular metabolism

B. Respiratory System
regulates carbonic acid in the body by eliminating or retaining carbon dioxide. Carbon
dioxide is a potential acid; when combined with water, it forms carbonic acid, a volatile
acid. Acute increases in either carbon dioxide or hydrogen ions in the blood stimulate
the respiratory center in the brain. As a result, both the rate and depth of respiration
increase. The increased rate and depth of lung ventilation eliminate carbon dioxide from
the body, and carbonic acid levels fall, bringing the pH to a more normal range. Although
this compensation for increased hydrogen ion concentration occurs. within minutes, it
becomes less effective over time. Patients with chronic lung disease may have
consistently high carbon dioxide levels in their blood. Alkalosis, by contrast, depresses
the respiratory center. Both the rate and depth of respiration decrease, and carbon
dioxide is retained. The retained carbon dioxide then combines with water to restore
carbonic acid levels and bring the pH back within the normal range.
Starts within minutes good response by 2 hours, complete by 12- 24 hours
C. Renal System
responsible for the long-term regulation of acid–base balance in the body. Excess
nonvolatile acids produced during metabolism normally are eliminated by the kidneys,
the kidneys also regulate bicarbonate levels in extracellular fluid by regenerating
bicarbonate ions as well as reabsorbing them in the renal tubules. Although the kidneys
respond more slowly to changes in pH (over hours to days), they can generate
bicarbonate and selectively excrete or retain hydrogen ions as needed. In acidosis, when
excess hydrogen ion is present and the pH falls, the kidneys excrete hydrogen ions and
retain bicarbonate. In alkalosis, the kidneys retain hydrogen ions and excrete
bicarbonate to restore acid–base balance.
Starts after few hours, complete by 5 to 7 days
Four (4) Types of Acid – Base Imbalance:
1. Respiratory Acidosis
2. Respiratory Alkalosis
3. Metabolic Acidosis
4. Metabolic Alkalosis
Note: Not a clinical diagnosis or disease, rather they are clinical syndromes associated with a
wide variety of diseases.
Acidosis
any pathologic process that cause a relative excess of acid (volatile or fixed in the body)
Alkalosis
indicates a primary condition resulting in excess in base
Table 4-1 Normal Gas Values
NORMAL GAS VALUES
pH 7.35 – 7.45
PO2 80 – 100%
PaCO2 35 – 45 mmHg
HCO3 22 – 26 mEq/L

CAUSES OF ACIDOSIS
RESPIRATORY ACIDOSIS
(Carbonic Acid Excess)
Why patient hypoventilates, carbon dioxide builds up in the bloodstream and pH drops below
normal – respiratory acidosis. The kidneys try to compensate for a drop in pH by conserving
bicarbonate (base) ions, or generating them in the kidneys, which in turn raises the pH.
>> pH 7.35; PaCO2 >42 mmHg; HCO3 normal
Causes:
a. Acute respiratory conditions (pulmonary edema, pneumonia, COPD)
less surface area decreases the amount of gas exchange that can occur, thus impending
carbon dioxide exchange.
b. Depression of respiratory center (drugs e.g narcotics; head injuries)
all metabolic acid are nonvolatile excreted to the kidneys, except carbonic acid which is
excreted as gas
c. Iatrogenic cause: inadequate mechanical ventilation
excessive oxygen administration to client with COPD which hypoventilation occurs
Manifestations
a. Hypercapnia, due to rapid rise of PaCO2 level
b. Headache, CO2 dilates cerebral blood vessels
c. Warm and flushed skin, related to the peripheral vasodilation as well as to impaired gas
exchange
d. Fine flapping tremors
e. Decreased reflexes
f. Rapid, shallow respirations; elevated pulse rate; tachycardia
g. Decreasing level of consciousness
Figure 4-1 Signs and Symptoms of Respiratory Acidosis

Medical Management
a. ABG analysis
b. Chest X-rays, can help pinpoint some cause, e.g COPD, pneumonia
c. Serum electrolytes level, in acidosis potassium leaves the cell, so expect serum level to
be elevated
d. Bronchodilators, to open constricted airways
e. Supplemental oxygen
f. Drug therapy to treat hyperkalemia
Nursing Diagnoses
• Ineffective breathing Pattern related to hypoventilation
• Impaired gas exchange related to alveolar hypoventilation
• Anxiety related to breathlessness
• Risk for injury related to decreased level of consciousness
Nursing Management
a. Maintain patent airway
b. Monitor vital signs
c. Monitor neurologic status and report significant changes
d. Administer oxygen as ordered
e. Accurate intake and output records
f. Report any variations in ABG levels
g. Coughing and deep breathing exercises
METABOLIC ACIDOSIS
(Base Bicarb Deficit)
The underlying mechanisms in metabolic acidosis are a loss of bicarbonate from extracellular
fluid, an accumulation of metabolic acids, or a combination of the two.
>> pH 7.35; pCO2 normal; HCO3 <26 mEq/L
74
Causes:
a. Diabetic ketoacidosis
decrease insulin prevents glucose uptake, thus, stored fats are oxidized (acetoacetic
acid) and is metabolize for energy
b. Renal insufficiency
decreased ability of the kidney to excrete acids
c. Prolonged vomiting, severe diarrhea
due to, loss of alkaline substances
Manifestations
Metabolic acidosis typically produces respiratory, neurologic, and cardiac sign and symptoms.
As acid builds up in the bloodstream, the lungs compensate by blowing off carbon dioxide.
a. Weakness, fatigue, general malaise
b. Anorexia, nausea, vomiting, abdominal pain
c. Decrease level of consciousness
d. Rapid, deep, labored breathing (Kussmaul’s respirations)
the first clue to metabolic acidosis
e. Decrease cardiac output and blood pressure
f. Skin is warm and dry, as a result of peripheral vasodilation
g. Diminished muscle tone and reflexes

Compensation:
- Increase respiratory rate/ depth to blow off carbon dioxide
Figure 4-2 Signs and Symptoms of Metabolic Acidosis
Medical Management
a. ABG analysis
b. Serum potassium levels
usually elevated as hydrogen ions move into the cells and potassium moves out to
maintain electroneutrality
c. Rapid acting insulin to reverse diabetic ketoacidosis and drive potassium back into the cell.
d. Intravenous Sodium bicarbonate
to neutralize blood acidity in patients with bicarbonate loss
75
e. Fluid replacement
Nursing Diagnoses
• Decreased cardiac output secondary to dysrhythmias and / or fluid volume deficits
• Risk for sensory/ perceptual alterations related to changes in neurological functioning
secondary to acidosis
• Risk for fluid volume deficit related to excessive loss from the kidneys or gastrointestinal
system
Nursing Management
Nursing care includes immediate emergency interventions and long-term treatment of the
condition and its underlying causes. Observe the following guidelines:
b. Monitor neurologic status
c. Maintain patent IV line
d. Careful administration of sodium bicarbonate
e. Proper positioning to promote chest expansion and facilitate breathing.
f. Record intake and output

RESPIRATORY ALKALOSIS
(Carbonic Acid Deficit)
In metabolic alkalosis, the underlying mechanisms include a loss of hydrogen ions (acid), a
gain in bicarbonate or booth. Above normal PaCO2 indicates that the lungs are compensating
for alkalosis. Renal compensations more effective, but slower as well.
>> pH 7.45; PaCO2 <35 mmHg; HCO3 normal
Causes
a. Vomiting
loss of hydrochloric acid from the stomach
b. Diuretic therapy (thiazides, loop diuretics)
can lead to a loss of hydrogen, potassium from the kidneys
c. Cushing’s disease
causes retention of sodium and chloride and urinary loss of potassium and hydrogen
d. Hyperventilation
most common cause of acute respiratory alkalosis
e. Severe anemia, acute hypoxia 20 high altitude
overstimulation of the respiratory system causes to breathe faster and deeper
Manifestations
a. Slow, shallow respirations
b. Nausea, vomiting
c. polyuria
d. Twitching, weakness and tetany
e. Hyperactive reflexes
f. Numbness and tingling sensation
g. Confusion or syncope
lack of carbon dioxide in the blood may lead to hyperventilation
h. Dysrhythmia: related to hypokalemia and hypocalcemia
Buffering Response: shifting of acid from intracellular fluid to blood
Movement of bicarbonate into cell in exchange of chloride
Renal compensation: increase bicarbonate excretion; decrease hydrogen ion secretion
76

Figure 4-3 Signs and Symptoms of Respiratory Alkalosis
Medical Management
a. Identify and eliminate causative factor if possible
b. Sedative or Anxiolytics agents may be given
to relieve anxiety and restore a normal breathing pattern.
c. Respiratory support, e.g. oxygen therapy to prevent hypoxemia; breathe into a paper bag
this forces the patient to breathe exhaled carbon dioxide, thereby raising the carbon
dioxide
d. ABG analysis
key diagnostic test in identifying respiratory alkalosis
e. ECG
may indicate arrhythmias or the changes associated with hypokalemia or hypocalcemia
Nursing Diagnosis
• Ineffective breathing pattern related to hyperventilation
• Altered thought processes related to altered cerebral functioning
Nursing Management
a. Allay anxiety whenever possible to prevent hyperventilation
b. Monitor vital signs, and report changes
c. Report variations in ABG and ECG
d. Maintain a calm, quiet environment

METABOLIC ALKALOSIS
(Carbonic Acid Excess)
A condition in which there is an increased pH and increased HCO3
pH > 7.45; HCO3 above 26 mEq/L; PCo2 normal
77
Causes
1. diuretic therapy
cause loss of H+, A-, k+ but precipitates ↑HCO3 level
2. ingestion of NaHCO3 or excessive NaHCO3 to correct acidosis
3. aldosterone excess
↑ Na retention, ↑ H+ and bicarbonate regeneration
4. prolonged steroid therapy
same with aldosterone effects
5. prolonged gastric suctioning or vomiting
loss or H+ ions; sengstaken, Blakemore tube (a thick catheter with triple lumen with 2
balloons; inflated at the orifice of the stomach and esophagus to apply pressure thus prevent
bleeding, the 3rd lumen is for suctioning gastric contents)
6. Massive blood transfusion (whole blood)
(citrate anticoagulant which is use for storing blood is metabolize to bicarbonate)
Manifestations
• Increased myocardial activity, palpitations
• Increased heart rate
• Rapid, shallow breathing
• Dizziness, lightheadedness
• Hyperactive reflexes
• Nausea, vomiting
Figure 4-4 Signs and Symptoms of Metabolic Alkalosis
Laboratory Findings
• ABG analysis
• Serum electrolyte levels
low potassium, calcium and chloride, HCO3 elevated
• ECG changes, low T wave
78

Medical Management
• Replacement of electrolytes
• Antiemetics may be administered to treat underlying nausea and vomiting
• Acetazolamide (Diamox)
to increase renal excretion
Nursing Diagnoses
• Ineffective breathing pattern related to hypoventilation
• Impaired gas exchange related to alveolar hypoventilation
• Anxiety related to breathlessness
Nursing Management
• Monitor vital signs
• Assess patient’s level of consciousness
• Administer oxygen
treat hypoxemia
• Monitor Intake and output

ACID BLOOD GAS (ABG) ANALYSIS
is an essential part of diagnosing, and managing a patient’s oxygenation status and
acid base balance.
the usefulness of this diagnostic tool is dependent on being able to correctly interpret
results.
NORMAL GAS VALUES
pH 7.35 – 7.45
PaO2 80 – 100%
PaCO2 35 – 45 mmHg
HCO3 22 to 26 mEq/L
Table 4-2 Evaluation of Abnormal Blood Gas Values
Identifying The Primary Process
pH
Low Normal High
Acidemia No abnormality or Alkalemia
Mixed acid disorder
High Low Low High
PCO2 HCO3 PCO2 HCO3
Respiratory Metabolic Respiratory Metabolic
Acidosis Acidosis Alkalosis Alkalosis
79
Figure 4-5 Acid Base Mnemonic

Table 4-3 Steps to ABG Analysis
STEPS TO ABG ANALYSIS
1
Look at the pH
a. if ACID-BASE BALANCE
b. Fully or completely compensated acid- base disorder
c. Mixed acid – base disorder
If pH acidosis pH alkalosis
2
Look at the PCO2, if….
Alkalosis Acidosis
3
Evaluate the pH – PCO2 relationship for possible RESPIRATORY
PROBLEM
pH Respiratory
Alkalosis
PCO2
pH Respiratory
Acidosis
PCO2
4 Look at the HCO3, Norma
Acidosis
l? , if…..
Alkalosis
5
Evaluate the pH, HCO3, and base excess for METABOLIC PROBLEM
pH
Metabolic Acidosis
HCO3
Base -2
pH
Metabolic Alkalosis
HCO3
Base +2
6
Look for Compensation
NOTE: Renal (HCO3) compensates for respiratory problem
Respiratory (PCO2) compensates for renal problem
2 Degrees of Compensation
a. Partial - compensatory component is appropriately abnormal but pH
is not yet in normal range, either acidotic or alkalotic
ex. pH PCO2 HCO3
METABOLIC ALKALOSIS PARTIALLY COMPENSATED
b. Full - Compensatory component alters
enough to return pH to normal
Ex. pH 7.45 PCO2 HCO3
METABOLIC ALKALOSIS VS RESPIRATORY ACIDOSIS FULLY
COMPENSATED
pH SHOWS THE PRIMARY PROBLEM
7.40 is absolutely normal
(7.35 – 39 = slightly acidic 7.41-45 = slightly alkaline)

7
Evaluate oxygenation
PO2 < 80 mmHg – hypoxemia; hypoventilation
60-79 Mild Hypoxemia
40-59 Moderate hypoxemia
< 40 Severe Hypoxemia
PO2 > 100 mmHg – hyperventilation

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