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B. FLUID VOLUME EXCESS: HYPERVOLEMIA 4. Teach patient about edema, ascites, and fluid therapy.
Definition : Refers to the isotonic expansion of Advise elevation of the extremities, restriction of
the ECF caused by the abnormal retention of fluids, necessity of paracentesis, dialysis and diuretic
water and sodium therapy.
There is excessive retention of water and 5. Instruct patient to avoid over-the-counter medications
electrolytes in equal proportion. Serum sodium without first checking with the health care provider
concentration remains NORMAL because they may contain sodium
NURSING MANAGEMENT
The Nursing Process in HYPONATREMIA
1. Provide continuous assessment by doing an accurate
ASSESSMENT intake and output, daily weights, mental status
Sodium Deficit (Hyponatremia) examination, urinary sodium levels and GI
manifestations. Maintain seizure precaution
Clinical Manifestations 2. Detect and control Hyponatremia by encouraging food
Clinical manifestations of hyponatremia depend on the intake with high sodium content, monitoring patients
cause, magnitude, and rapidity of onset. on lithium therapy, monitoring input of fluids like IVF,
Although nausea and abdominal cramping occur, most parenteral medication and feedings.
of the symptoms are neuropsychiatric and are probably 3. Return the Sodium level to Normal by restricting water
related to the cellular swelling and cerebral edema intake if the primary problem is water retention.
associated with hyponatremia. Administer sodium to normovolemic patient and
As the extracellular sodium level decreases, the elevate the sodium slowly by using sodium chloride
cellular fluid becomes relatively more concentrated and solution
„pulls” water into the cells.
In general, those patients having acute decline in serum
sodium levels have more severe symptoms and higher SODIUM EXCESS: HYPERNATREMIA
mortality rates than do those with more slowly
developing hyponatremia. Serum Sodium level is higher than 145 mEq/L
Features of hyponatremia associated with sodium loss There is a gain of sodium in excess of water or a
and water gain include anorexia, muscle cramps, and a loss of water in excess of sodium.
feeling of exhaustion.
When the serum sodium level drops below 115 mEq/L Pathophysiology:
(SI: 115 mmol/L), thee ff signs of increasing
intracranial pressure occurs: Etiologic factors
lethargy a. Fluid deprivation
Confusion b. Water loss from Watery diarrhea, fever, and
muscular twitching hyperventilation
focal weakness c. Administration of hypertonic solution
hemiparesis d. Increased insensible water loss
papilledema e. Inadequate water replacement, inability to swallow
convulsions f. Seawater ingestion or excessive oral ingestion of salts
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
Decreased potassium in the body impaired nerve
excitation and transmission signs/symptoms such as ASSIST IN THE MEDICAL INTERVENTION
weakness, cardiac dysrhythmias etc.. 1. Provide oral or IV replacement of potassium
2. Infuse parenteral potassium supplement. Always dilute
the K in the IVF solution and administer with a pump.
The Nursing Process in Hypokalemia
IVF with potassium should be given no faster than 10-
20-mEq/ hour!
3. NEVER administer K by IV bolus or IM
Clinical Manifestations
Potassium deficiency can result in widespread NURSING MANAGEMENT
derangements in physiologic functions and especially
nerve conduction. 1. Continuously monitor the patient by assessing the
Most important, severe hypokalemia can result in death cardiac status, ECG monitoring, and digitalis
through cardiac or respiratory arrest. precaution
Clinical signs rarely develop before the serum 2. Prevent hypokalemia by encouraging the patient to eat
potassium level has fallen below 3 mEq/L (51: 3 potassium rich foods like orange juice, bananas,
mmol/L) unless the rate of fall has been rapid. cantaloupe, peaches, potatoes, dates and apricots.
Manifestations of hypokalemia include fatigue, 3. Correct hypokalemia by administering prescribed IV
anorexia, nausea, vomiting, muscle weakness, potassium replacement. The nurse must ensure that the
decreased bowel motility, paresthesias, dysrhythmias, kidney is functioning properly!
and increased sensitivity to digitalis. 4. Administer IV potassium no faster than 20 mEq/hour
If prolonged, hypokalemia can lead to impaired renal and hook the patient on a cardiac monitor. To
concentrating ability, causing dilute urine, polyuria, EMPHASIZE: Potassium should NEVER be given IV
nocturia, and polydipsia bolus or IM!!
5. A concentration greater than 60 mEq/L is not advisable
ASSESSMENT for peripheral veins.
Physical examination
Muscle weakness
Decreased bowel motility and abdominal distention
Paresthesias
POTASSIUM EXCESS: HYPERKALEMIA
Dysrhythmias
Increased sensitivity to digitalis Serum potassium greater than 5.5 mEq/L
Pathophysiology
Subjective cues
Nausea , anorexia and vomiting Etiologic factors
Fatigue, muscles cramps a. Iatrogenic, excessive intake of potassium
Excessive thirst, if severe b. Renal failure- decreased renal excretion of
potassium
Laboratory findings c. Hypoaldosteronism and Addison‟s disease
1. Serum potassium is less than 3.5 mEq/L d. Improper use of potassium supplements
2. ECG: FLAT “T” waves, or inverted T waves,
depressed ST segment and presence of the “U” wave Other factors
and prolonged PR interval. 1. Pseudohyperkalemia- tight tourniquet and
3. Metabolic alkalosis hemolysis of blood sample, marked leukocytosis
MS: Fluids and Electrolyte Abejo
Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN
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. IMPLEMENTATION
The earliest changes, often occurring at a serum
potassium level greater than 6 mEq/ L (SI: 6 ASSIST IN MEDICAL INTERVENTION
mmol/L), are peaked narrow T waves and a shortened 1. Monitor the patient‟s cardiac status with cardiac
QT interval. machine
If the serum potassium level continues to rise, the PR 2. Institute emergency therapy to lower potassium level
interval becomes prolonged and is followed by by:
disappearance of the P waves. a. Administering IV calcium gluconate-
Finally, there is decomposition and prolongation of antagonizes action of K on cardiac conduction
the QRS complex. Ventricular dysrhythmias and b. Administering Insulin with dextrose-causes
cardiac arrest may occur at any point in this temporary shift of K into cells
progression. c. Administering sodium bicarbonate-alkalinizes
Note that in Severe hyperkalemia causes muscle plasma to cause temporary shift
weakness and even paralysis, related to a d. Administering Beta-agonists
depolarization block in muscle. e. Administering Kayexalate (cation-exchange
Similarly, ventricular conduction is slowed. resin)-draws K+ into the bowel
Although hyperkalemia has marked effects on the NURSING MANAGEMENT
peripheral neuromuscular system, it has little effect on
the central nervous system. 1. Provide continuous monitoring of cardiac status,
Rapidly ascending muscular weakness leading to dysrhythmias, and potassium levels.
flaccid quadriplegia has been reported in patients with 2. Assess for signs of muscular weakness, paresthesias,
very high serum potassium levels. nausea
Paralysis of respiratory muscles and those required for 3. Evaluate and verify all HIGH serum K levels
phonation can also occur. 4. Prevent hyperkalemia by encouraging high risk patient
Gastrointestinal manifestations, such as nausea, to adhere to proper potassium restriction
intermit tent intestinal colic, and diarrhea, may occur 5. Correct hyperkalemia by administering carefully
in hyperkalemic patients. prescribed drugs. Nurses must ensure that clients
receiving IVF with potassium must be always
monitored and that the potassium supplement is given
ASSESSMENT correctly
Physical Examination 6. Assist in hemodialysis if hyperkalemia cannot be
Diarrhea corrected.
Skeletal muscle weakness 7. Provide client teaching. Advise patients at risk to avoid
Abnormal cardiac rate eating potassium rich foods, and to use potassium salts
Subjective Cues sparingly.
Nausea 8. Monitor patients for hypokalemia who are receiving
Intestinal pain/colic potassium-sparing diuretic
Palpitations
Laboratory Findings CALCIUM
1. Peaked and narrow T waves
2. ST segment depression and shortened QT interval Majority of calcium is in the bones and teeth
3. Prolonged PR interval Small amount may be found in the ECF and ICF
4. Prolonged QRS complex Normal serum range is 8.5 – 10.5 mg/dL
5. Disappearance of P wave Sources: milk and milk products; diet; IVF and
6. Serum potassium is higher than 5.5 mEq/L medications
7. Acidosis
MS: Fluids and Electrolyte Abejo
Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN
Functions: HYPOCALCEMIA
Low levels of calcium in the blood
1. Needed for formation of bones and teeth
2. For muscular contraction and relaxation Risk Factors
3. For neuronal and cardiac function a. Hypoparathyroidism (idiopathic or postsurgical)
4. For enzymatic activation b. Alkalosis (Ca binds to albumin)
5. For normal blood clotting c. Corticosteroids (antagonize Vit D)
d. Hyperphosphatemia
Regulations: e. Vit D deficiency
f. Renal failure (vit D deficiency)
1. GIT- absorbs Ca+ in the intestine; Vitamin D helps to
increase absorption Clinical Manifestation
2. Renal regulation- Ca+ is filtered in the glomerulus Decreased cardiac contractility
and reabsorbed in the tubules: Arrhythmia
3. Endocrine regulation: ECG: prolonged QT interval, lengthened ST
segment
Parathyroid hormone from the parathyroid glands Trousseau’s sign (inflate BP cuff 20mm above
is released when Ca+ level is low. PTH causes systole for 3 min = carpopedal spasm)
release of calcium from bones and increased
retention of calcium by the kidney but PO4 is
excreted
Calcitonin from the thyroid gland is released when
the calcium level is high. This causes excretion of
both calcium and PO4 in the kidney and promoted
deposition of calcium in the bones.
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
HYPERCALCEMIA HYPOMAGNESEMIA
Collaborative ManagementM
PHOSPHORUS 1. Aluminum antacids as phosphate binders: Al
carbonate (Basaljel), Al hydroxide (Amphojel)
primary intracellular anion 2. Ca carbonate for hypocalcemia
part of ATP – energy 3. Avoid phosphate laxatives/enemas
85% bound with Ca in teeth/bones, skeletal muscle 4. Increase fluid intake
reciprocal balance with Ca 5. Diet: low Phos, no carbonated drinks
absorption affected by Vit D, regulation affected by
PTH (lowers P level)
Normal value : 2.5-4.5 mg/dL CHLORIDE
HYPOPHOSPHATEMIA Sources:
salt, canned food, cheese, milk, eggs, crab, olives
Risk Factors
a. Decreased Vit D absorption, sunlight exposure
b. Hyperparathyroidism (increased PTH) HYPOCHLOREMIA
c. Aluminum & Mg-containing antacids (bind P)
d. Severe vomiting & diarrhea Risk Factors
a. Diuresis
Clinical Manifestation b. Metabolic alkalosis
Anemia, bruising (weak blood cell membrane) c. Hyponatremia, prolonged D5W IV
Seizures, coma d. Addison‟s
Muscle weakness, paresthesias
Constipation, hypoactive bowel sounds Clinical Manifestation
Slow, shallow respirations (met. Alkalosis)
*Like hypercalcemia Hypotension (Na & water loss)
Step 2
Look at the PCO2
Is it up or down?
Acid-Base Balance Mechanisms If it reflects an opposite response as the pH,
then you know that the condition is a
respiratory imbalance
If it does not reflect an opposite response as the
Buffer - prevents major changes in ECF by releasing or
pH - move to step III
accepting H ions
Step 3
Buffer mechanism: first line (takes seconds)
Look at the HCO3
1. combine with very strong acids or bases to
Does the HCO3 reflect a corresponding
convert them into weaker acids or bases
response with the pH
2. Bicarbonate Buffer System
If it does then the condition is a metabolic
- most important
imbalance
- uses HCO3 & carbonic acid/H2CO3 - (20:1)
- closely linked with respiratory & renal
mechanisms
3. Phosphate Buffer System FACTORS AFFECTING BODY FLUIDS,
- more important in intracellular fluids, where ELECTROLYTES AND ACID-BASE BALANCE
concentration is higher
- similar to bicarbonate buffer system, only uses AGE
phosphate Infants have higher proportion of body water than
4. Protein Buffer System adults
- hemoglobin, a protein buffer, promotes Water content of the body decreases with age
movement of chloride across RBC membrane in Infants have higher fluid turn-over due to immature
exchange for HCO3 kidney and rapid respiratory rate
Respiratory: tries to compensate by hyperventilation: 1. Correcting underlying cause will often improve
deep and rapid respirations known as Kussmaul‟s alkalosis
respirations 2. Restore fluid volume and correct electrolyte
imbalances (usually IV NaCl with KCL).
Diagnostic test findings: 3. With severe cases, acidifying solution may be
1. ABG: pH < 7.35, HCO3 < 22 administered.
2. Electrolytes: Serum K+ >5.0 mEq/L 4. Assessment
3. Serum Ca+2 > 10.0 mg/dL Vital signs
4. Serum Mg+2 < 1.6 mg/dL Neuro, cardiac, respiratory assessment
Repeat arterial blood gases and electrolytes
Collaborative Management
1. Medications: Correcting underlying cause will
often improve acidosis
2. Restore fluid balance, prevent dehydration with
IV fluids
Selected Water and Electrolyte
3. Correct electrolyte imbalances Solutions
4. Administer Sodium Bicarbonate IV, if acidosis is
severe and does not respond rapidly enough to
treatment of primary cause. (Oral bicarbonate is
sometimes given to clients with chronic metabolic Isotonic Solutions
acidosis) Be careful not to overtreat and put client
into alkalosis A. 0.9% NaCl (isotonic, also called NSS)
5. As acidosis improves, hydrogen ions shift out of Na+ 154 mEq/L
cells and potassium moves intracellularly. Cl- 154 mEq/L
Hyperkalemia may become hypokalemia and (308 mOsm/L)
potassium replacement will be needed. Also available with varying concentrations of dextrose (the
6. Assessment most frequent used is a 5% dextrose concentration
Vital signs
Intake and output An isotonic solution that expands the ECF
Neuro, GI, and respiratory status; volume, used in hypovolemic states, resuscitative
Cardiac monitoring efforts, shock, diabetic ketoacidosis, metabolic
Reassess repeated arterial blood gases and alkalosis, hypercalcemia, mild Na deficit
electrolytes Supplies an excess of Na and Cl; can cause fluid
volume excess and hyperchloremic acidosis if
used in excessive volumes, particularly in patients
METABOLIC ALKALOSIS with compromised renal function, heart failure or
pH >7.45 edema
HCO3 > 26 mEq/L Not desirable as a routine maintenance solution,
Caused by a bicarbonate excess, due to loss of as it provides only Na and Cl (and these are
acid, or a bicarbonate excess in the body provided in excessive amounts)
When mixed with 5% dextrose, the resulting
Common Stimuli solution becomes hypertonic in relation to plasma,
a. Loss of hydrogen and chloride ions through and in addition to the above described
excessive vomiting, gastric suctioning, or electrolytes, provides 170cal/L
excessive diuretic therapy Response to Only solution that may be administered with
hypokalemia blood products
b. Excess ingestion of bicarbonate rich antacids or
excessive treatment of acidosis with Sodium
Bicarbonate B. Lactated Ringer’s solution (Hartmann’s solution)
Na+ 130 mEq/L
Signs and Symptoms K+ 4 mEq/L
Compensation: Lungs respond by decreasing the Ca++ 3 mEq/L
depth and rate of respiration in effort to retain carbon Cl- 109 mEq/L
dioxide and lower pH Lactate (metabolized to bicarbonate) 28 mEq/L (274
Neuro: altered mental status, numbness and tingling mOsm/L)
around mouth, fingers, toes, dizziness, muscle spasms Also available with varying concentration of dextrose (the
(similar to hypocalcemia due to less ionized calcium most common is 5% dextrose)
levels)
Respiratory: shallow, slow breathing An isotonic solution that contains multiple
electrolytes in roughly the same concentration as
Diagnostic test findings found in plasma (note that solution is lacking in
1. ABG‟s: pH> 7.45, HCO3 >26 Mg++) provides 9 cal/L
2. Electrolytes: Serum K+ < 3.5 mEq/L Used in the tx of hypovolemia, burns, fluid lost as
3. Electrocardiogram: as with hypokalemia bile or diarrhea, and for acute blood loss
replacement
Lactate is rapidly metabolized into HCO3- in the
body. Lactated Ringer‟s solution should not be
used in lactic acidosis because the ability to
convert lactate into HCO3- is impaired in this
Collaborative Management disorder.
MS: Fluids and Electrolyte Abejo
Lecture Notes on Fluids and Electrolytes
Prepared By: Mark Fredderick R Abejo R.N, MAN