Professional Documents
Culture Documents
Locations of ECF:
1. Interstitial: fluid between most cells
2. Intravascular: fluid within blood
vessels; also called plasma
3. Transcellular: fluids of body
including urine, digestive secretion,
cerebrospinal, pleural, synovial,
intraocular, gonadal, pericardial
C.
D.
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V.
C.
D.
E.
Output:
1,000 mls
300 mls
1,200 mls
TOTAL
2,500 mls
Skin
Lungs
Feces
Kidneys
TOTAL
500 mls
300 mls
150 mls
1,500 mls
2,500 mls
Renin-Angiotensin
1. drop in blood volume in kidneys = renin released
2. renin = acts on plasma protein angiotensin
(released by the liver) to form angiotensin I
3. ACE = converts Angiotensin I to Angiotensin II in
the lungs
4. Angiotensin II = vasoconstriction & aldosterone
release
MS: Fluids and Electrolyte
Abejo
IV Fluids
Isotonic
Hypotonic
Hypertonic
LR
PNSS (0.9%NSS)
NM
D5W
- isotonic in bag
- dextrose=quickly
metabolized=hypotonic
D2.5W
0.45% NSS
0.3% NSS
0.2% NSS
D50W
D10W
D5NSS
D5LR
3%NSS
PATHOPHYSIOLOGY:
Risk Factors --- inadequate fluids in the body ---- decreased
blood volume ----- decreased cellular hydration ---- cellular
shrinkage ---- weight loss, decreased turgor, oliguria,
hypotension, weak pulse, etc.
ASSESSMENT:
Physical examination
Subjective cues
Thirst
Nausea, anorexia
Muscle weakness and cramps
Change in mental state
Laboratory findings
1.
2.
3.
4.
NURSING MANAGEMENT
1.
2.
3.
4.
5.
6.
7.
8.
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B.
4.
5.
PATHOPHYSIOLOGY
Excessive fluid --- expansion of blood volume ----- edema,
increased neck vein distention, tachycardia, hypertension.
ELECTROLYTES
Sources of electrolytes
IMPLEMENTATION
ASSIST IN MEDICAL INTERVENTION
1.
2.
3.
NURSING MANAGEMENT
1.
2.
3.
Functions of Electrolytes
Maintains fluid balance
Regulates acid-base balance
Needed for enzymatic secretion and activation
Needed for proper metabolism and effective
processes of muscular contraction, nerve
transmission
Types of Electrolytes
CATIONS- positively charged ions; examples are
sodium, potassium, calcium
ANIONS- negatively charged ions; examples are
chloride and phosphates]
The major ICF cation is potassium (K+); the
major ICF anion is Phosphates
The major ECF cation is Sodium (Na+); the major
ECF anion is Chloride (Cl-)
ELECTROLYTE IMBALANCES
Subjective cue/s
Shortness of breath
Change in mental state
Laboratory findings
1. BUN and Creatinine levels are LOW because of
dilution
2. Urine sodium and osmolality decreased (urine
becomes diluted)
3. CXR may show pulmonary congestion
SODIUM
8.
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In summary:
Physical Examination
Altered mental status
Vomiting
Lethargy
Muscle twitching and convulsions (if sodium level is
below 115 mEq/L)
Focal weakness
Pathophysiology
Etiologic Factors
a. Fluid loss such as from Vomiting and nasogastric
suctioning
b. Diarrhea
c. Sweating
d. Use of diuretics
e. Fistula
Other factors
a. Dilutional hyponatremia
Water intoxication, compulsive water
drinking where sodium level is diluted
with increased water intake
b. SIADH
Excessive secretion of ADH causing
water retention and dilutional
hyponatremia
PATHOPHYSIOLOGY
Decrease sodium concentration --- hypotonicity of plasma -- water from the intravascular space will move out and go to
the intracellular compartment with a higher concentration --cell swelling --Water is pulled INTO the cell because of
decreased extracellular sodium level and increased
intracellular concentration
The Nursing Process in HYPONATREMIA
Subjective Cues
Nausea
Cramps
Anorexia
Headache
Laboratory findings
1. Serum sodium level is less than 135 mEq/L
2. Decreased serum osmolality
3. Urine specific gravity is LOW if caused by sodium loss
4. In SIADH, urine sodium is high and specific gravity is
HIGH
IMPLEMENTATION
ASSIST IN MEDICAL INTERVENTION
1. Provide sodium replacement as ordered. Isotonic saline
is usually ordered.. Infuse the solution very cautiously.
The serum sodium must NOT be increased by greater
than 12 mEq/L because of the danger of pontine
osmotic demyelination
2. Administer lithium and demeclocycline in SIADH
3. Provide water restriction if with excess volume
NURSING MANAGEMENT
1.
ASSESSMENT
Sodium Deficit (Hyponatremia)
Clinical Manifestations
Clinical manifestations of hyponatremia depend on the
cause, magnitude, and rapidity of onset.
Although nausea and abdominal cramping occur, most
of the symptoms are neuropsychiatric and are probably
related to the cellular swelling and cerebral edema
associated with hyponatremia.
As the extracellular sodium level decreases, the
cellular fluid becomes relatively more concentrated and
pulls water into the cells.
In general, those patients having acute decline in serum
sodium levels have more severe symptoms and higher
mortality rates than do those with more slowly
developing hyponatremia.
Features of hyponatremia associated with sodium loss
and water gain include anorexia, muscle cramps, and a
feeling of exhaustion.
When the serum sodium level drops below 115 mEq/L
(SI: 115 mmol/L), thee ff signs of increasing
intracranial pressure occurs:
lethargy
Confusion
muscular twitching
focal weakness
hemiparesis
papilledema
convulsions
2.
3.
Pathophysiology:
Etiologic factors
a. Fluid deprivation
b. Water loss from Watery diarrhea, fever, and
hyperventilation
c. Administration of hypertonic solution
d. Increased insensible water loss
e. Inadequate water replacement, inability to swallow
f. Seawater ingestion or excessive oral ingestion of salts
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Other factors
a. Diabetes insipidus
b. Heat stroke
c. Near drowning in ocean
d. Malfunction of dialysis
IMPLEMENTATION
ASSIST IN THE MEDICAL INTERVENTION
1.
2.
PATHOPHYSIOLOGY
Increased sodium concentration --- hypertonic plasma ---water will move out form the cell outside to the interstitial
space ----- CELLULAR SHRINKAGE ----- then to the
blood ---- Water pulled from cells because of increased
extracellular sodium level and decreased cellular fluid
concentration
3.
NURSING MANAGEMENT
1.
2.
3.
4.
5.
6.
Laboratory findings
1. Serum sodium level exceeds 145 mEq/L
2. Serum osmolality exceeds 295 mOsm/kg
3. Urine specific gravity and osmolality INCREASED
or elevated
MS: Fluids and Electrolyte
POTASSIUM
Functions:
1.
2.
3.
4.
5.
Subjective Cues
Delusions and hallucinations
Extreme thirst
Behavioral changes
6.
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Pathophysiology
Etiologic Factors
a. Gastro-intestinal loss of potassium such as
diarrhea and fistula
b. Vomiting and gastric suctioning
c. Metabolic alkalosis
d. Diaphoresis and renal disorders
e. Ileostomy
Other factor/s
a. Hyperaldosteronism
b. Heart failure
c. Nephrotic syndrome
d. Use of potassium-losing diuretics
e. Insulin therapy
f. Starvation
g. Alcoholics and elderly
PATHOPHYSIOLOGY
IMPLEMENTATION
ASSIST IN THE MEDICAL INTERVENTION
1.
2.
Clinical Manifestations
Potassium deficiency can result in widespread
derangements in physiologic functions and especially
nerve conduction.
Most important, severe hypokalemia can result in death
through cardiac or respiratory arrest.
Clinical signs rarely develop before the serum
potassium level has fallen below 3 mEq/L (51: 3
mmol/L) unless the rate of fall has been rapid.
Manifestations of hypokalemia include fatigue,
anorexia, nausea, vomiting, muscle weakness,
decreased bowel motility, paresthesias, dysrhythmias,
and increased sensitivity to digitalis.
If prolonged, hypokalemia can lead to impaired renal
concentrating ability, causing dilute urine, polyuria,
nocturia, and polydipsia
ASSESSMENT
Physical examination
Muscle weakness
Decreased bowel motility and abdominal distention
Paresthesias
Dysrhythmias
Increased sensitivity to digitalis
Subjective cues
Nausea , anorexia and vomiting
Fatigue, muscles cramps
Excessive thirst, if severe
Laboratory findings
1. Serum potassium is less than 3.5 mEq/L
2. ECG: FLAT T waves, or inverted T waves,
depressed ST segment and presence of the U wave
and prolonged PR interval.
3. Metabolic alkalosis
MS: Fluids and Electrolyte
3.
NURSING MANAGEMENT
1.
2.
3.
4.
5.
Etiologic factors
a. Iatrogenic, excessive intake of potassium
b. Renal failure- decreased renal excretion of
potassium
c. Hypoaldosteronism and Addisons disease
d. Improper use of potassium supplements
Other factors
1. Pseudohyperkalemia- tight tourniquet and
hemolysis of blood sample, marked leukocytosis
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2.
3.
4.
PATHOPHYSIOLOGY
Increased potassium in the body ---- Causing irritability of
the cardiac cells --- Possible arrhythmias!!
Clinical Manifestations
By far the most clinically important effect of
hyperkalemia is its effect on the myocardium.
Cardiac effects of an elevated serum potassium level
are usually not significant below a concentration of 7
mEq/L (SI: 7 mmol/L), but they are almost always
present when the level is 8 mEq/L (SI: 8 mmol/L) or
greater.
As the plasma potassium concentration is increased,
disturbances in cardiac conduction occur.
The earliest changes, often occurring at a serum
potassium level greater than 6 mEq/ L (SI: 6
mmol/L), are peaked narrow T waves and a shortened
QT interval.
If the serum potassium level continues to rise, the PR
interval becomes prolonged and is followed by
disappearance of the P waves.
Finally, there is decomposition and prolongation of
the QRS complex. Ventricular dysrhythmias and
cardiac arrest may occur at any point in this
progression.
Note that in Severe hyperkalemia causes muscle
weakness and even paralysis, related to a
depolarization block in muscle.
Similarly, ventricular conduction is slowed.
Although hyperkalemia has marked effects on the
peripheral neuromuscular system, it has little effect on
the central nervous system.
Rapidly ascending muscular weakness leading to
flaccid quadriplegia has been reported in patients with
very high serum potassium levels.
Paralysis of respiratory muscles and those required for
phonation can also occur.
Gastrointestinal manifestations, such as nausea,
intermit tent intestinal colic, and diarrhea, may occur
in hyperkalemic patients.
ASSESSMENT
Physical Examination
Diarrhea
Skeletal muscle weakness
Abnormal cardiac rate
Subjective Cues
Nausea
Intestinal pain/colic
Palpitations
Laboratory Findings
1. Peaked and narrow T waves
2. ST segment depression and shortened QT interval
3. Prolonged PR interval
4. Prolonged QRS complex
5. Disappearance of P wave
6. Serum potassium is higher than 5.5 mEq/L
7. Acidosis
MS: Fluids and Electrolyte
IMPLEMENTATION
ASSIST IN MEDICAL INTERVENTION
1. Monitor the patients cardiac status with cardiac
machine
2. Institute emergency therapy to lower potassium level
by:
a. Administering IV calcium gluconateantagonizes action of K on cardiac conduction
b. Administering Insulin with dextrose-causes
temporary shift of K into cells
c. Administering sodium bicarbonate-alkalinizes
plasma to cause temporary shift
d. Administering Beta-agonists
e. Administering Kayexalate (cation-exchange
resin)-draws K+ into the bowel
NURSING MANAGEMENT
1.
2.
3.
4.
5.
6.
7.
8.
Functions:
1.
2.
3.
4.
5.
HYPOCALCEMIA
Low levels of calcium in the blood
Risk Factors
a. Hypoparathyroidism (idiopathic or postsurgical)
b. Alkalosis (Ca binds to albumin)
c. Corticosteroids (antagonize Vit D)
d. Hyperphosphatemia
e. Vit D deficiency
f. Renal failure (vit D deficiency)
Clinical Manifestation
Decreased cardiac contractility
Arrhythmia
ECG: prolonged QT interval, lengthened ST
segment
Trousseaus sign (inflate BP cuff 20mm above
systole for 3 min = carpopedal spasm)
Regulations:
1.
2.
3.
Tetany
Hyperreflexia, seizures
Laryngeal spasms/stridor
Diarrhea, hyperactive bowel sounds
Bleeding
Collaborative Management
1. Calcium gluconate 10% IV
2. Calcium chloride 10% IV
3. both usually given by Dr, very slowly; venous irritant;
cardiac probs
4. Oral: calcium citrate, lactate, carbonate; Vit D
supplements
5. Diet: high calcium
6. Watch out for tetany, seizures, laryngospasm, resp &
cardiac arrest
7. Seizure precautions
Sources:
milk, yogurt, cheese, sardines, broccoli, tofu, green leafy
vegetables
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HYPERCALCEMIA
HYPOMAGNESEMIA
Clinical Manifestation
groans (constipation)
moans (psychotic noise)
bones (bone pain, especially if PTH is elevated)
stones (kidney stones)
psychiatric overtones (including depression and
confusion)
Clinical Manifestation
Weakness
muscle cramps
cardiac arrhythmia
increased irritability of the nervous system with
tremors, athetosis, jerking, nystagmus and an
extensor plantar reflex. Confusion
disorientation
hallucinations
depression
epileptic fits
hypertension, tachycardia and tetany.
Arrhythmia
ECG: shortened QT interval, decreased ST
segment
Hyporeflexia, lethargy, coma
Collaborative Management
1. If parathyroid tumor = surgery
2. Diet: low Ca, stop taking Ca Carbonate antacids,
increase fluids
3. IV flushing (usually NaCl)
4. Loop diuretics
5. Corticosteroids
6. Biphosphonates, like etidronate (Calcitonin) &
alendronate (Fosamax)
7. Plicamycin (Mithracin) inhibits bone resorption
8. Calcitonin IM or intranasal
9. Dialysis (severe case)
10. Watch out for digitalis toxicity
11. Prevent fractures, handle gently
MAGNESIUM
Functions:
1. important in maintaining intracellular activity
2. affects muscle contraction, & especially relaxation
3. maintains normal heart rhythm
4. promotes vasodilation of peripheral arterioles
Sources:
green leafy vegetables, nuts, legumes, seafood, whole
grains, bananas, oranges, cocoa, chocolate
HYPERMAGNESEMIA
Etiologic Factors
a. Magnesium treatment for pre-eclampsia
b. Renal failure
c. Diabetic Ketoacidosis
d. Excessive use of Mg antacids/laxatives
PATHOPHYSIOLOGY
Increase Mg. ----- Blocks acetylcholine release ---- decrease
excitability of muscle
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Clinical Manifestation
Hyporeflexia
Hypotension, bradycardia, arrhythmia
Flushing
Weakness, lethargy, coma
Decreased RR & respiratory paralysis
Loss of DTRs
HYPERPHOSPHATEMIA
Risk Factors
a. Acidosis (Ph moves out of cell)
b. Cytotoxic agents/chemotherapy in cancer
c. Renal failure
d. Hypocalcemia
e. Massive BT (P leaks out of cells during storage of
blood)
f. Hyperthyroidism
Clinical Manifestation
Calcification of kidney, cornea, heart
Muscle spasms, tetany, hyperreflexia
*like hypercalcemia
Collaborative Management
1. Diuretics
2. Stop Mg-containing antacids & enemas
3. IV fluids rehydration
4. Calcium gluconate (antidote, antagonizes
cardiac & respiratory effects of Mg)
5. Dialysis if RF
PHOSPHORUS
Functions:
1. bone/teeth formation & strength
2. phospholipids (make up cell membrane integrity)
3. part of ATP
4. affects metabolism, Ca levels
Sources:
red & organ meats (brain, liver, kidney), poultry, fish, eggs,
milk, legumes, whole grains, nuts, carbonated drinks
HYPOPHOSPHATEMIA
Risk Factors
a. Decreased Vit D absorption, sunlight exposure
b. Hyperparathyroidism (increased PTH)
c. Aluminum & Mg-containing antacids (bind P)
d. Severe vomiting & diarrhea
Clinical Manifestation
Anemia, bruising (weak blood cell membrane)
Seizures, coma
Muscle weakness, paresthesias
Constipation, hypoactive bowel sounds
*like hypocalcemia
Collaborative ManagementM
1. Aluminum antacids as phosphate binders: Al
carbonate (Basaljel), Al hydroxide (Amphojel)
2. Ca carbonate for hypocalcemia
3. Avoid phosphate laxatives/enemas
4. Increase fluid intake
5. Diet: low Phos, no carbonated drinks
CHLORIDE
Functions:
1. helps regulate BP, serum osmolarity
2. part of HCl
3. acid/base balance (exchanges with HCO3)
Sources:
salt, canned food, cheese, milk, eggs, crab, olives
HYPOCHLOREMIA
Risk Factors
a. Diuresis
b. Metabolic alkalosis
c. Hyponatremia, prolonged D5W IV
d. Addisons
Clinical Manifestation
Slow, shallow respirations (met. Alkalosis)
Hypotension (Na & water loss)
*Like hypercalcemia
Collaborative Management
1. Sodium phosphate or potassium phosphate IV
(give slowly, no faster than 10 mEq/hr)
2. Sodium & potassium phosphate orally (NeutraPhos, K-Phos) give with meals to prevent gastric
irritation
3. Avoid Phos-binding antacids
4. Diet: high Mg, milk
5. Monitor joint stiffness, arthralgia, fractures,
bleeding
Collaborative Management
1. Administer IV or Oral : KCl, NaCl
2. Diet: high Cl (& usually Na)
HYPERCHLOREMIA
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Clinical Manifestation
Deep, rapid respirations (met. Acidosis)
hyperK, hyperNa S/S
Increased Cl sweat levels in cystic fibrosis
Collaborative Management
1. Diuretics
2. Hypotonic solutions, D5W to restore balance
3. Diet: low Cl (& usually Na)
4. Treat acidosis
Step 1
Step 2
Step 3
Look at the pH
Is it up or down?
If it is up - it reflects alkalosis
If it is down - it reflects acidosis
RESPIRATORY ACIDOSIS
pH < 7.35
pCO2 > 45 mm Hg (excess carbon dioxide in the
blood)
Respiratory system impaired and retaining CO2;
causing acidosis
Common Stimuli
a. Acute respiratory failure from airway obstruction
b. Over-sedation from anesthesia or narcotics
c. Some neuromuscular diseases that affect ability to
use chest muscles
d. Chronic respiratory problems, such as Chronic
Obstructive Lung Disease
Signs and Symptoms
Compensation: kidneys respond by generating and
reabsorbing bicarbonate ions, so HCO3 >26 mm Hg
Respiratory: hypoventilation, slow or shallow
respirations
Neuro: headache, blurred vision, irritability,
confusion
Respiratory collapse leads to unconsciousness and
cardiovascular collapse
Collaborative Management
1. Early recognition of respiratory status and treat
cause
2. Restore ventilation and gas exchange; CPR for
respiratory failure with oxygen supplementation;
intubation and ventilator support if indicated
3. Treatment of respiratory infections with
bronchodilators, antibiotic therapy
4. Reverse excess anesthetics and narcotics with
medications such as naloxone (Narcan)
5. Chronic respiratory conditions
Breathe in response to low oxygen levels
Adjusted to high carbon dioxide level
through metabolic compensation (therefore,
high CO2 not a breathing trigger)
Cannot receive high levels of oxygen, or will
have no trigger to breathe; will develop
carbon dioxide narcosis
Treat with no higher than 2 liters O2 per
cannula
6. Continue respiratory assessments, monitor further
arterial blood gas results
RESPIRATORY ALKALOSIS
pH < 7.35
pCO2 < 35 mm Hg.
Carbon dioxide deficit, secondary to
hyperventilation
Common Stimuli
a. Hyperventilation with anxiety from uncontrolled
fear, pain, stress (e.g. women in labor, trauma
victims)
b. High fever
c. Mechanical ventilation, during anesthesia
3.
4.
METABOLIC ACIDOSIS
pH <7.35
Deficit of bicarbonate in the blood NaHCO3 <22
mEq/L
Caused by an excess of acid, or loss of
bicarbonate from the body
Common Stimuli
a. Acute lactic acidosis from tissue hypoxia (lactic
acid produced from anaerobic metabolism with
shock, cardiac arrest)
b. Ketoacidosis (fatty acids are released and
converted to ketones when fat is used to supply
glucose needs as in uncontrolled Type 1 diabetes
or starvation)
c. Acute or chronic renal failure (kidneys unable to
regulate electrolytes)
d. Excessive bicarbonate loss (severe diarrhea,
intestinal suction, bowel fistulas)
e. Usually results from some other disease and is
often accompanied by electrolyte and fluid
imbalances
f. Hyperkalemia often occurs as the hydrogen ions
enter cells to lower the pH displacing the
intracellular potassium; hypercalcemia and
hypomagnesemia may occur
Signs and Symptoms
Compensation: respiratory system begins to
compensate by increasing the depth and rate of
respiration in an effort to lower the CO2 in the blood;
this causes a decreased level of carbon dioxide: pCO2
<35 mm HG.
Neuro changes: headache, weakness, fatigue
progressing to confusion, stupor, and coma
Cardiac: dysrhythmias and possibly cardiac arrest from
hyperkalemia
GI: anorexia, nausea, vomiting
Skin: warm and flushed
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METABOLIC ALKALOSIS
pH >7.45
HCO3 > 26 mEq/L
Caused by a bicarbonate excess, due to loss of
acid, or a bicarbonate excess in the body
1.
2.
3.
4.
Common Stimuli
a. Loss of hydrogen and chloride ions through
excessive vomiting, gastric suctioning, or
excessive diuretic therapy Response to
hypokalemia
b. Excess ingestion of bicarbonate rich antacids or
excessive treatment of acidosis with Sodium
Bicarbonate
Signs and Symptoms
Compensation: Lungs respond by decreasing the
depth and rate of respiration in effort to retain carbon
dioxide and lower pH
Neuro: altered mental status, numbness and tingling
around mouth, fingers, toes, dizziness, muscle spasms
(similar to hypocalcemia due to less ionized calcium
levels)
Respiratory: shallow, slow breathing
Diagnostic test findings
1. ABGs: pH> 7.45, HCO3 >26
2. Electrolytes: Serum K+ < 3.5 mEq/L
3. Electrocardiogram: as with hypokalemia
Collaborative Management
Hypotonic Solutions
Hypertonic Solutions
E. 3% NaCl (hypertonic saline)
Na+ 513 mEq/L
Cl- 513 mEq/L
(1026 mOsm/L)
Colloid Solutions
G. Dextran in NS or 5% D5W
Available in low-molecular-weight (Dextran 40) and highmolecular-weight (Dextran 70) forms
D. 0.45% NaCl
half-strength saline)
Na+ 77 mEq/L
Cl- 77 mEq/L
(154 mOsm/L)
Also available with varying concentration of dextrose (the
most common is 5% dextrose)
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