Published Dec 24, 2012
jep039
10 Posts
Anyone have a great study tool that helped them absorb all this boring fluid and electrolyte materials!? I am finding it hard to fully comprehend everything by just reading the book over and over!... I want to ace the exam on it and actually know it so that I can understand everything in clinicals as well! I know it is a very important topic, just so boring to learn!
Thanks guys!
"We're all in this together!"
ala2ch
21 Posts
Fluid and Electrolytes:
Balance and Disturbance
Fluid and Electrolyte Balance
Ø Necessary for life and homeostasis
Ø Nursing role is to help prevent and treat fluid and electrolyte disturbances
l Understand the physiology
l Identify imbalance
l Effective teaching for prevention
Fluid
Ø Approximately 60% of the typical adult is fluid
Ø Varies with age, body size, and gender
Ø Intracellular fluid (contains 2/3 of total fluid)
Ø Extracellular fluid (ECF)
l Intravascular (plasma)
l Interstitial (Lymph)
l Transcellular (CSF, intraocular…)
Ø “Third spacing”: loss of ECF into a space that does not contribute to equilibrium (other than ICF or ECF spaces). Symptoms are decreased urinary output, increased heart rate, deceased blood pressure and edema. Occurs in ascites, peritonitis, bowel obstruction, massive bleeding into a cavity and burn.
Electrolytes
Ø Active chemicals that carry positive (cations) and negative (anions) electrical charges expressed as milliequivalents per liter.
• Major cations:
l Sodium
l Potassium
l Calcium
l Magnesium
l Hydrogen ions
• Major anions:
l Chloride
l Bicarbonate
l Phosphate
l Sulfate
Ø Electrolyte concentrations differ in the fluid compartments
Ø Major cation in ECF
l Sodium: it affects the overall concentration of ECF and is important in regulating the volume of body fluid.
Ø Major cation in ICF
l Potassium: release of large quantity of potassium from ICF can be extremely dangerous.
Regulation of Fluid
Ø Movement of fluid through capillary walls depends on:
l Hydrostatic pressure
Pressure exerted on the walls of blood vessels
l Osmotic pressure
Pressure exerted by the protein in the plasma
Ø The direction of fluid movement depends on the differences of hydrostatic and osmotic pressure
Osmosis
Ø Movement of fluid from an area of lower solute concentration to an area of higher solute concentration
Diffusion
Ø Movement of molecules and ions from an area of higher concentration to an area of lower concentration
Active Transport
Ø Movement against the concentration gradient
Ø Sodium-potassium pump maintains the higher
Ø Concentration of extracellular sodium and intracellular potassium
Ø Requires adenosine (ATP) for energy
Routes of Gains and Losses
Ø Gain
l Dietary intake of fluid and food or enteral feeding
l Parenteral fluids
Ø Loss
l Kidney: urine output approximately is 1 mL of urine per kilogram of body weight per hour (1 mL/kg/h) in all age groups.
l Skin loss: sensible and insensible losses. The chief solutes in sweat are sodium, chloride, and potassium.
l Lungs: eliminate water vapor (insensible loss) at a rate of approximately 400 mL every day
l GI tract: The usual loss through the gastrointestinal (GI) tract is only 100 to 200 mL daily
Homeostatic Mechanisms
Major functions of the kidneys in maintaining normal fluid balance include the following:
Ø Regulation of ECF volume and by selective retention and excretion of body fluids
Ø Regulation of electrolyte levels in the ECF by selective retention of needed substances and excretion of unneeded substances
Ø Regulation of pH of the ECF by retention of hydrogen ions
Ø Excretion of metabolic wastes and toxic substances
The normal BUN is 10 to 20 mg/dL
Creatinine is the end product of muscle metabolism. It is a better indicator of renal function than BUN
Normal serum creatinine is approximately 0.7 to 1.4 mg/dL
Gerontologic Considerations
Ø Reduced homeostatic mechanisms: cardiac, renal, and respiratory function
Ø Decreased body fluid percentage
Ø Medication use
Ø Presence of concomitant conditions
Fluid Volume Imbalances
Ø Fluid volume deficit (FVD): hypovolemia
Ø Fluid volume excess (FVE): hypervolemia
Fluid Volume Deficit
Ø Loss of extracellular fluid exceeds intake of water, and electrolytes are lost in the same proportion as they exist in normal body fluids
Ø Dehydration refers to loss of water alone with increased serum sodium level
Ø May occur in combination with other imbalances
Ø Causes: fluid loss from vomiting, diarrhea, GI suctioning, sweating, decreased intake, and inability to gain access to fluid
Ø Risk factors: diabetes insipidus, adrenal insufficiency, hemorrhage, and third space shifts
Ø Manifestations: rapid weight loss, decreased skin turgor, oliguria, concentrated urine, postural hypotension, rapid and weak pulse, increased temperature, cool and clammy skin due to vasoconstriction, lassitude, thirst, muscle weakness, and cramps
Ø Laboratory data: elevated BUN in relation to serum creatinine, increased hematocrit, and possible serum electrolyte changes
Ø Medical management: provide fluids to meet body needs
l Oral fluids
l IV solutions
Isotonic Solutions
0.9% NaCl (isotonic, also called normal saline [NS])
Na+ 154 mEq/L
Cl- 154 mEq/L
(308 mOsm/L)
Also available with varying concentrations of dextrose(the most frequently used is a 5% dextrose concentration)
- An isotonic solution that expands the extracellular fluid (ECF) volume, used in hypovolemic states, resuscitative efforts, mild Na+ deficit
- Supplies an excess of Na+ and Cl-; can cause fluid volume excess if used in excessive volumes, particularly in patients with compromised renal function, heart failure, or edema
- Not desirable as a routine maintenance solution, as it provides only Na+ and Cl- (and these are provided in excessive amounts)
- When mixed with 5% dextrose, the resulting solution becomes hypertonic in relation to plasma and, in addition to the above described electrolytes, provides 170 cal/L
Lactated Ringer's solution (Hartmann's solution)
Na+ 130 mEq/L
K+ 4 mEq/L
Ca++ 3 mEq/L
Cl- 109 mEq/L
Lactate (metabolized to bicarbonate)
28 mEq/L (274 mOsm/L)
Also available with varying concentrations of dextrose (the most common is 5% dextrose)
- An isotonic solution that contains multiple electrolytes in roughly the same concentration as found in plasma (note that solution is lacking in Mg++): provides 9 cal/L
- Used in the treatment of hypovolemia, burns, fluid lost as diarrhea, and for acute blood loss replacement
- Lactate is rapidly metabolized into HCO3- in the body.
- Not to be given with a pH > 7.5 because bicarbonate is formed as lactate breaks down, causing alkalosis
- Should not be used in renal failure because it contains potassium and can cause hyperkalemia
- Similar to plasma
5% dextrose in water (D5W)
No electrolytes
50 g of dextrose
- An isotonic solution that supplies 170 cal/L and free water to aid in renal excretion of solutes
- Used in treatment of hypernatremia, fluid loss, and dehydration
- Should not be used in excessive volumes in the early postoperative period (when antidiuretic hormone secretion is increased due to stress reaction)
- Should not be used solely in treatment of fluid volume deficit, because it dilutes plasma electrolyte concentrations
- Should be used with caution in patients with renal or cardiac disease because of risk of fluid overload
Hypotonic solutions
0.45% NaCl (half-strength saline)
Na+ 77 mEq/L
Cl- 77 mEq/L
(154 mOsm/L)
Also available with varying concentrations of dextrose (the most common is a 5% concentration)
- Provides Na+, Cl-, and free water
- Free water is desirable to aid the kidneys in elimination of solute.
- Lacking in electrolytes other than Na+ and Cl-
- When mixed with 5% dextrose, the solution becomes slightly hypertonic to plasma and in addition to the above-described electrolytes provides 170 cal/L.
- Used to treat Na+ and Cl- depletion
Hypertonic Solutions
3% NaCl (hypertonic saline)
Na+ 513 mEq/L
Cl- 513 mEq/L
(1026 mOsm/L)
- Used to increase ECF volume, decrease cellular swelling
- Highly hypertonic solution used only in critical situations to treat hyponatremia
- Must be administered slowly and cautiously, because it can cause intravascular volume overload and pulmonary edema
- Supplies no calories
- Assists in removing intracellular fluid excess
5% NaCL (hypertonic solution)
Na+ 855 mEq/L
Cl- 855 mEq/L
(1710 mOsm/L)
- Highly hypertonic solution used to treat symptomatic hyponatremia
- Administered slowly and cautiously, because it can cause intravascular volume overload and pulmonary edema
Fluid Volume Deficit—Nursing Management
Ø Monitor intake and output (I&O)
Ø Monitor for symptoms: skin and tongue turgor, mucosa, urinary output (UO), and mental status
Ø Initiate measures to minimize fluid loss
Ø Provide oral care
Ø Administer oral fluids
Ø Administer parenteral fluids
Fluid Volume Excess
Ø Due to fluid overload or diminished homeostatic mechanisms
Ø Risk factors: heart failure, renal failure, and cirrhosis of the liver
Ø Contributing factors: excessive dietary sodium or sodium-containing IV solutions
Ø Manifestations: edema; distended neck veins; abnormal lung sounds (crackles); tachycardia; increased BP, and CVP; increased weight; increased UO; shortness of breath;
Ø Medical management is directed at the cause, restriction of fluids and sodium, and the administration of diuretics .
Ø If renal function is so severely impaired that pharmacologic agents cannot act efficiently, other modalities are considered to remove sodium and fluid from the body. Hemodialysis or peritoneal dialysis may be used to remove nitrogenous wastes and control potassium and acid–base balance, and to remove sodium and fluid.
Fluid Volume Excess—Nursing Management
Ø Take I&O and daily weights; assess for lung sounds, edema, and other symptoms; monitor responses to medications such as diuretics
Ø Promote adherence to fluid restrictions and patient teaching related to sodium and fluid restrictions
Ø Monitor and avoid sources of excessive sodium;
Ø Promote rest, favors diuresis of edema fluid
Ø Use semi-Fowler’s position for orthopnea to promote lung expansion
Ø Provide skin care and positioning/turning
Ø Patient education about symptoms of edema
Electrolyte Imbalances
Ø Sodium: hyponatremia and hypernatremia
Ø Potassium: hypokalemia and hyperkalemia
Ø Calcium: hypocalcemia and hypercalcemia
Sodium Imbalances
Ø Sodium is the primary determinant of ECF osmolality.
Ø Decreased sodium is associated with parallel changes in osmolality.
Ø Sodium has a major role in controlling water distribution throughout the body.
Ø Sodium is regulated by ADH, thirst, and the renin–angiotensin–aldosterone system.
Effect of extracellular sodium level on cell size
Hyponatremia
Ø Serum sodium less than 135 mEq/L
Ø dilutional hyponatremia (water intoxication), the patient's serum sodium level is diluted by an increase in the ratio of water to sodium.
Ø Causes: adrenal insufficiency, water intoxication, SIADH (sustained secretion of ADH by the hypothalamus or production of an ADH-like substance from a tumor), and losses by vomiting.
Ø Manifestations: poor skin turgor, dry mucosa, headache, decreased BP, and neurologic changes. When the serum sodium level decreases to less than 115, signs of increasing ICP, such as lethargy, confusion, muscle twitching, hemiparesis and seizures may occur.
Ø Medical management: water restriction (800 mL in 24 hours) and sodium replacement (sodium by mouth, nasogastric tube, or a parenteral route). Serum sodium must not be increased by more than 12 mEq/L in 24 hours to avoid neurologic damage.
Ø Nursing management: assessment and prevention, monitoring of dietary sodium and fluid intake.
Ø Nursing alert: When administering fluids to patients with cardiovascular disease, the nurse assesses for signs of circulatory overload. Highly hypertonic sodium solutions (3% and 5% sodium chloride) should be administered only in intensive care settings under close observation.
Hypernatremia
Ø Serum sodium greater than 145mEq/L
Ø Causes: excess water loss, excess sodium administration, diabetes insipidus, and hypertonic IV solutions
Ø Manifestations: primarily neurologic and are the consequence of increased plasma osmolality. Water moves out of the cell into the ECF, resulting in cellular dehydration. thirst; elevated temperature; dry, swollen tongue; sticky mucosa; neurologic symptoms; restlessness; disorientation; hallucinations in severe hypernatremia. Permanent brain damage can occur.
l Thirst may be impaired in the elderly or ill.
Ø Medical management: hypotonic electrolyte solution or D5W. Treatment of hypernatremia consists of a gradual lowering of the serum sodium level by the infusion of an isotonic nonsaline solution ( dextrose 5%) to avoid cerebral edema.
Ø Nursing management: assessment and prevention, assess for over-the-counter (OTC) sources of sodium, offer and encourage fluids to meet patient needs, and provide sufficient water with tube feedings.
Potassium Imbalances
Ø Potassium influences both skeletal and cardiac muscle activity.
Ø Alterations in its concentration change myocardial irritability and rhythm.
Ø To maintain potassium balance, the renal system must function, because 80% of the potassium excreted daily leaves the body by way of the kidneys.
Ø Aldosterone also increases the excretion of potassium by the kidney.
Hypokalemia
Ø Below-normal serum potassium (
Ø Causes: GI losses, medications, alterations of acid–base balance (when alkalosis is present, a temporary shift of serum potassium into the cells occurs), hyperaldosteronism, and poor dietary intake.
l potassium deficit occurs frequently with diarrhea
l patients with persistent insulin hypersecretion may experience hypokalemia, because insulin promotes the entry of potassium into skeletal muscle and hepatic cells.
Manifestations:
Ø Fatigue, anorexia, nausea, vomiting, dysrhythmias, muscle weakness, cramps, paresthesias.
Ø Hypokalemia increases sensitivity to digitalis, predisposing the patient to digitalis toxicity at lower digitalis levels.
Ø Metabolic alkalosis is commonly associated with hypokalemia. Hydrogen ions move out of the cells in alkalotic states to help correct the high pH, and potassium ions move in to maintain an electrically neutral state.
Ø Medical management: increased dietary potassium, potassium replacement, and IV for severe deficit.
Ø Nursing management: assessment (severe hypokalemia is life-threatening), monitoring of electrocardiogram (ECG), arterial blood gases (ABGs), and dietary potassium, and providing nursing care related to IV potassium administration
Ø Nursing Alert:
l Potassium is never administered by IV push or intramuscularly to avoid replacing potassium too quickly. IV potassium must be administered using an infusion pump.
Hyperkalemia
Ø Serum potassium greater than 5.0 mEq/L
Ø Although hyperkalemia is less common than hypokalemia, it is usually more dangerous, because cardiac arrest is more frequently associated with high serum potassium levels.
Ø Causes: usually treatment-related, impaired renal function, and acidosis.
Ø Manifestations: cardiac changes and dysrhythmias.
Ø Medical management: monitor ECG, cation exchange resin (Kayexalate), IV sodium bicarbonate, IV calcium gluconate (calcium antagonizes the action of hyperkalemia on the heart), regular insulin and hypertonic dextrose, limit dietary potassium; and perform dialysis
Ø Nursing alert: Potassium supplements are extremely dangerous for patients who have impaired renal function and thus decreased ability to excrete potassium.
Effect of Potassium on ECG
Flat T waves or inverted T waves or both, suggesting ischemia, and depressed ST segments an elevated U wave is specific to hypokalemia
Peaked, narrow T waves; ST-segment depression; and a shortened QT interval.
The PR interval becomes prolonged and is followed by disappearance of the P waves
Ø Potassium-sparing diuretics may cause elevation of potassium and should not be used in patients with renal dysfunction
Calcium Imbalances
Ø More than 99% of the body's calcium is located in the skeletal system
Ø Calcium is a major component of bones and teeth.
Ø Calcium plays a major role in transmitting nerve impulses and helps regulate muscle contraction and relaxation, including cardiac muscle.
Ø Calcium also plays a role in blood coagulation
Hypocalcemia
Ø Serum level less than 8.5 mg/dL
Ø Causes: hypoparathyroidism, malabsorption, renal failure (because these pts. Have elevated serum phosphate levels). Hyperphosphatemia usually causes a reciprocal drop in the serum calcium level, inadequate vitamin D consumption.
Ø Manifestations: Tetany (the most characteristic manifestation of hypocalcemia), hyperactive DTRs, Trousseau’s sign (carpal spasm upon inflating a blood pressure cuff on the upper arm).
Trousseau’s Sign
Hypocalcemia (continue)
Ø Acute symptomatic hypocalcemia is life-threatening and requires prompt treatment with IV administration of calcium
Ø Medical management: IV of calcium gluconate; calcium and vitamin D supplements; diet
Ø Nursing management: assessment as severe hypocalcemia is life-threatening, exercise to decrease bone calcium loss, patient teaching related to diet and medications, and nursing care related to IV calcium administration.
Ø Too-rapid IV administration of calcium can cause cardiac arrest, preceded by bradycardia. IV administration of calcium is particularly dangerous in patients receiving digitalis-derived medications
Hypercalcemia
Ø Serum level above 10.5 mg/dL
Ø hypercalcemic crisis (serum calcium level to 17 mg/dL (4.3 mmol/L) or higher) has a mortality rate as high as 50% if not treated promptly.
Ø Causes: hyperparathyroidism, bone loss related to immobility. Vitamin D intoxication can cause calcium excess. Calcium levels are inversely related to phosphorous levels.
Ø Manifestations: Hypercalcemia reduces neuromuscular excitability because it suppresses activity at the myoneural junction. Therefore, muscle weakness, incoordination, ECG changes, and dysrhythmias. Cardiac standstill can occur when the serum calcium level is about 18mg/dL.
Ø Medical management: treat underlying cause, administer phosphates and calcitonin. Calcitonin reduces bone resorption, increases the depositing of calcium and phosphorus in the bones, and increases urinary excretion of calcium. Inorganic phosphate salts can be administered orally, by NG, or intravenously.
Ø Nursing management: assessment as hypercalcemic crisis has high mortality, encourage ambulation, IV phosphate therapy is used with extreme caution in the treatment of hypercalcemia, because it can cause severe calcification in various tissues, hypotension, tetany.
➢ Necessary for life and homeostasis
➢ Nursing role is to help prevent and treat fluid and electrolyte disturbances
Understand the physiology
Identify imbalance
Effective teaching for prevention
➢ Approximately 60% of the typical adult is fluid
➢ Varies with age, body size, and gender
➢ Intracellular fluid (contains 2/3 of total fluid)
➢ Extracellular fluid (ECF)
Intravascular (plasma)
Interstitial (Lymph)
Transcellular (CSF, intraocular…)
➢ “Third spacing”: loss of ECF into a space that does not contribute to equilibrium (other than ICF or ECF spaces). Symptoms are decreased urinary output, increased heart rate, deceased blood pressure and edema. Occurs in ascites, peritonitis, bowel obstruction, massive bleeding into a cavity and burn.
➢ Active chemicals that carry positive (cations) and negative (anions) electrical charges expressed as milliequivalents per liter.
Sodium
Potassium
Calcium
Magnesium
Hydrogen ions
Chloride
Bicarbonate
Phosphate
Sulfate
➢ Electrolyte concentrations differ in the fluid compartments
➢ Major cation in ECF
Sodium: it affects the overall concentration of ECF and is important in regulating the volume of body fluid.
➢ Major cation in ICF
Potassium: release of large quantity of potassium from ICF can be extremely dangerous.
➢ Movement of fluid through capillary walls depends on:
Hydrostatic pressure
• Pressure exerted on the walls of blood vessels
Osmotic pressure
• Pressure exerted by the protein in the plasma
➢ The direction of fluid movement depends on the differences of hydrostatic and osmotic pressure
➢ Movement of fluid from an area of lower solute concentration to an area of higher solute concentration
➢ Movement of molecules and ions from an area of higher concentration to an area of lower concentration
➢ Movement against the concentration gradient
➢ Sodium-potassium pump maintains the higher
➢ Concentration of extracellular sodium and intracellular potassium
➢ Requires adenosine (ATP) for energy
➢ Gain
Dietary intake of fluid and food or enteral feeding
Parenteral fluids
➢ Loss
Kidney: urine output approximately is 1 mL of urine per kilogram of body weight per hour (1 mL/kg/h) in all age groups.
Skin loss: sensible and insensible losses. The chief solutes in sweat are sodium, chloride, and potassium.
Lungs: eliminate water vapor (insensible loss) at a rate of approximately 400 mL every day
GI tract: The usual loss through the gastrointestinal (GI) tract is only 100 to 200 mL daily
➢ Regulation of ECF volume and 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
➢ Regulation of pH of the ECF by retention of hydrogen ions
➢ Excretion of metabolic wastes and toxic substances
➢ Reduced homeostatic mechanisms: cardiac, renal, and respiratory function
➢ Decreased body fluid percentage
➢ Medication use
➢ Presence of concomitant conditions
➢ Fluid volume deficit (FVD): hypovolemia
➢ Fluid volume excess (FVE): hypervolemia
➢ Loss of extracellular fluid exceeds intake of water, and electrolytes are lost in the same proportion as they exist in normal body fluids
➢ Dehydration refers to loss of water alone with increased serum sodium level
➢ May occur in combination with other imbalances
➢ Causes: fluid loss from vomiting, diarrhea, GI suctioning, sweating, decreased intake, and inability to gain access to fluid
➢ Risk factors: diabetes insipidus, adrenal insufficiency, hemorrhage, and third space shifts
➢ Manifestations: rapid weight loss, decreased skin turgor, oliguria, concentrated urine, postural hypotension, rapid and weak pulse, increased temperature, cool and clammy skin due to vasoconstriction, lassitude, thirst, muscle weakness, and cramps
➢ Laboratory data: elevated BUN in relation to serum creatinine, increased hematocrit, and possible serum electrolyte changes
➢ Medical management: provide fluids to meet body needs
Oral fluids
IV solutions
• An isotonic solution that expands the extracellular fluid (ECF) volume, used in hypovolemic states, resuscitative efforts, mild Na+ deficit
• Supplies an excess of Na+ and Cl-; can cause fluid volume excess if used in excessive volumes, particularly in patients with compromised renal function, heart failure, or edema
• Not desirable as a routine maintenance solution, as it provides only Na+ and Cl- (and these are provided in excessive amounts)
• When mixed with 5% dextrose, the resulting solution becomes hypertonic in relation to plasma and, in addition to the above described electrolytes, provides 170 cal/L
• An isotonic solution that contains multiple electrolytes in roughly the same concentration as found in plasma (note that solution is lacking in Mg++): provides 9 cal/L
• Used in the treatment of hypovolemia, burns, fluid lost as diarrhea, and for acute blood loss replacement
• Lactate is rapidly metabolized into HCO3- in the body.
• Not to be given with a pH > 7.5 because bicarbonate is formed as lactate breaks down, causing alkalosis
• Should not be used in renal failure because it contains potassium and can cause hyperkalemia
• Similar to plasma
• An isotonic solution that supplies 170 cal/L and free water to aid in renal excretion of solutes
• Used in treatment of hypernatremia, fluid loss, and dehydration
• Should not be used in excessive volumes in the early postoperative period (when antidiuretic hormone secretion is increased due to stress reaction)
• Should not be used solely in treatment of fluid volume deficit, because it dilutes plasma electrolyte concentrations
• Should be used with caution in patients with renal or cardiac disease because of risk of fluid overload
• Provides Na+, Cl-, and free water
• Free water is desirable to aid the kidneys in elimination of solute.
• Lacking in electrolytes other than Na+ and Cl-
• When mixed with 5% dextrose, the solution becomes slightly hypertonic to plasma and in addition to the above-described electrolytes provides 170 cal/L.
• Used to treat Na+ and Cl- depletion
• Used to increase ECF volume, decrease cellular swelling
• Highly hypertonic solution used only in critical situations to treat hyponatremia
• Must be administered slowly and cautiously, because it can cause intravascular volume overload and pulmonary edema
• Supplies no calories
• Assists in removing intracellular fluid excess
• Highly hypertonic solution used to treat symptomatic hyponatremia
• Administered slowly and cautiously, because it can cause intravascular volume overload and pulmonary edema
➢ Monitor intake and output (I&O)
➢ Monitor for symptoms: skin and tongue turgor, mucosa, urinary output (UO), and mental status
➢ Initiate measures to minimize fluid loss
➢ Provide oral care
➢ Administer oral fluids
➢ Administer parenteral fluids
➢ Due to fluid overload or diminished homeostatic mechanisms
➢ Risk factors: heart failure, renal failure, and cirrhosis of the liver
➢ Contributing factors: excessive dietary sodium or sodium-containing IV solutions
➢ Manifestations: edema; distended neck veins; abnormal lung sounds (crackles); tachycardia; increased BP, and CVP; increased weight; increased UO; shortness of breath;
➢ Medical management is directed at the cause, restriction of fluids and sodium, and the administration of diuretics .
➢ If renal function is so severely impaired that pharmacologic agents cannot act efficiently, other modalities are considered to remove sodium and fluid from the body. Hemodialysis or peritoneal dialysis may be used to remove nitrogenous wastes and control potassium and acid–base balance, and to remove sodium and fluid.
➢ Take I&O and daily weights; assess for lung sounds, edema, and other symptoms; monitor responses to medications such as diuretics
➢ Promote adherence to fluid restrictions and patient teaching related to sodium and fluid restrictions
➢ Monitor and avoid sources of excessive sodium;
➢ Promote rest, favors diuresis of edema fluid
➢ Use semi-Fowler’s position for orthopnea to promote lung expansion
➢ Provide skin care and positioning/turning
➢ Patient education about symptoms of edema
➢ Sodium: hyponatremia and hypernatremia
➢ Potassium: hypokalemia and hyperkalemia
➢ Calcium: hypocalcemia and hypercalcemia
➢ Sodium is the primary determinant of ECF osmolality.
➢ Decreased sodium is associated with parallel changes in osmolality.
➢ Sodium has a major role in controlling water distribution throughout the body.
➢ Sodium is regulated by ADH, thirst, and the renin–angiotensin–aldosterone system.
➢ Serum sodium less than 135 mEq/L
➢ dilutional hyponatremia (water intoxication), the patient's serum sodium level is diluted by an increase in the ratio of water to sodium.
➢ Causes: adrenal insufficiency, water intoxication, SIADH (sustained secretion of ADH by the hypothalamus or production of an ADH-like substance from a tumor), and losses by vomiting.
➢ Manifestations: poor skin turgor, dry mucosa, headache, decreased BP, and neurologic changes. When the serum sodium level decreases to less than 115, signs of increasing ICP, such as lethargy, confusion, muscle twitching, hemiparesis and seizures may occur.
➢ Medical management: water restriction (800 mL in 24 hours) and sodium replacement (sodium by mouth, nasogastric tube, or a parenteral route). Serum sodium must not be increased by more than 12 mEq/L in 24 hours to avoid neurologic damage.
➢ Nursing management: assessment and prevention, monitoring of dietary sodium and fluid intake.
➢ Nursing alert: When administering fluids to patients with cardiovascular disease, the nurse assesses for signs of circulatory overload. Highly hypertonic sodium solutions (3% and 5% sodium chloride) should be administered only in intensive care settings under close observation.
➢ Serum sodium greater than 145mEq/L
➢ Causes: excess water loss, excess sodium administration, diabetes insipidus, and hypertonic IV solutions
➢ Manifestations: primarily neurologic and are the consequence of increased plasma osmolality. Water moves out of the cell into the ECF, resulting in cellular dehydration. thirst; elevated temperature; dry, swollen tongue; sticky mucosa; neurologic symptoms; restlessness; disorientation; hallucinations in severe hypernatremia. Permanent brain damage can occur.
Thirst may be impaired in the elderly or ill.
➢ Medical management: hypotonic electrolyte solution or D5W. Treatment of hypernatremia consists of a gradual lowering of the serum sodium level by the infusion of an isotonic nonsaline solution ( dextrose 5%) to avoid cerebral edema.
➢ Nursing management: assessment and prevention, assess for over-the-counter (OTC) sources of sodium, offer and encourage fluids to meet patient needs, and provide sufficient water with tube feedings.
➢ Potassium influences both skeletal and cardiac muscle activity.
➢ Alterations in its concentration change myocardial irritability and rhythm.
➢ To maintain potassium balance, the renal system must function, because 80% of the potassium excreted daily leaves the body by way of the kidneys.
➢ Aldosterone also increases the excretion of potassium by the kidney.
➢ Below-normal serum potassium (
➢ Causes: GI losses, medications, alterations of acid–base balance (when alkalosis is present, a temporary shift of serum potassium into the cells occurs), hyperaldosteronism, and poor dietary intake.
potassium deficit occurs frequently with diarrhea
patients with persistent insulin hypersecretion may experience hypokalemia, because insulin promotes the entry of potassium into skeletal muscle and hepatic cells.
➢ Fatigue, anorexia, nausea, vomiting, dysrhythmias, muscle weakness, cramps, paresthesias.
➢ Hypokalemia increases sensitivity to digitalis, predisposing the patient to digitalis toxicity at lower digitalis levels.
➢ Metabolic alkalosis is commonly associated with hypokalemia. Hydrogen ions move out of the cells in alkalotic states to help correct the high pH, and potassium ions move in to maintain an electrically neutral state.
➢ Medical management: increased dietary potassium, potassium replacement, and IV for severe deficit.
➢ Nursing management: assessment (severe hypokalemia is life-threatening), monitoring of electrocardiogram (ECG), arterial blood gases (ABGs), and dietary potassium, and providing nursing care related to IV potassium administration
➢ Nursing Alert:
Potassium is never administered by IV push or intramuscularly to avoid replacing potassium too quickly. IV potassium must be administered using an infusion pump.
➢ Serum potassium greater than 5.0 mEq/L
➢ Although hyperkalemia is less common than hypokalemia, it is usually more dangerous, because cardiac arrest is more frequently associated with high serum potassium levels.
➢ Causes: usually treatment-related, impaired renal function, and acidosis.
➢ Manifestations: cardiac changes and dysrhythmias.
➢ Medical management: monitor ECG, cation exchange resin (Kayexalate), IV sodium bicarbonate, IV calcium gluconate (calcium antagonizes the action of hyperkalemia on the heart), regular insulin and hypertonic dextrose, limit dietary potassium; and perform dialysis
➢ Nursing alert: Potassium supplements are extremely dangerous for patients who have impaired renal function and thus decreased ability to excrete potassium.
➢ Potassium-sparing diuretics may cause elevation of potassium and should not be used in patients with renal dysfunction
➢ More than 99% of the body's calcium is located in the skeletal system
➢ Calcium is a major component of bones and teeth.
➢ Calcium plays a major role in transmitting nerve impulses and helps regulate muscle contraction and relaxation, including cardiac muscle.
➢ Calcium also plays a role in blood coagulation
➢ Serum level less than 8.5 mg/dL
➢ Causes: hypoparathyroidism, malabsorption, renal failure (because these pts. Have elevated serum phosphate levels). Hyperphosphatemia usually causes a reciprocal drop in the serum calcium level, inadequate vitamin D consumption.
➢ Manifestations: Tetany (the most characteristic manifestation of hypocalcemia), hyperactive DTRs, Trousseau’s sign (carpal spasm upon inflating a blood pressure cuff on the upper arm).
➢ Acute symptomatic hypocalcemia is life-threatening and requires prompt treatment with IV administration of calcium
➢ Medical management: IV of calcium gluconate; calcium and vitamin D supplements; diet
➢ Nursing management: assessment as severe hypocalcemia is life-threatening, exercise to decrease bone calcium loss, patient teaching related to diet and medications, and nursing care related to IV calcium administration.
➢ Too-rapid IV administration of calcium can cause cardiac arrest, preceded by bradycardia. IV administration of calcium is particularly dangerous in patients receiving digitalis-derived medications
➢ Serum level above 10.5 mg/dL
➢ hypercalcemic crisis (serum calcium level to 17 mg/dL (4.3 mmol/L) or higher) has a mortality rate as high as 50% if not treated promptly.
➢ Causes: hyperparathyroidism, bone loss related to immobility. Vitamin D intoxication can cause calcium excess. Calcium levels are inversely related to phosphorous levels.
➢ Manifestations: Hypercalcemia reduces neuromuscular excitability because it suppresses activity at the myoneural junction. Therefore, muscle weakness, incoordination, ECG changes, and dysrhythmias. Cardiac standstill can occur when the serum calcium level is about 18mg/dL.
➢ Medical management: treat underlying cause, administer phosphates and calcitonin. Calcitonin reduces bone resorption, increases the depositing of calcium and phosphorus in the bones, and increases urinary excretion of calcium. Inorganic phosphate salts can be administered orally, by NG, or intravenously.
➢ Nursing management: assessment as hypercalcemic crisis has high mortality, encourage ambulation, IV phosphate therapy is used with extreme caution in the treatment of hypercalcemia, because it can cause severe calcification in various tissues, hypotension, tetany.
this is my lecture that i took for fluid and electrolytes i hope i covered everything !
nurseprnRN, BSN, RN
1 Article; 5,116 Posts
A quickie on fluids and Na+ balance, the most common condition you will encounter.
Na+ and Water Balance, or why you have to remember that serum sodium doesn't tell you anything at all about sodium :) , and that saline is not water and salt.(Now, don't overthink this. Of course if you want to make a bottle of saline, you will mix plain water with sodium chloride. But read this without thinking about that, because .... well, it works better if you think of saline as an entity for purposes of this discussion. Read it and then ask me if you still have questions.)
OK, thought experiment time: Draw pictures with little molecules or such if you like, it will help. You have a beaker full of salt water, with a Na+ level of, say, 140 (hmmmm, what a coincidence). You pour half of it out. What is the Na+ level in the remainder? Right, 140, because that measurement is a measurement of CONCENTRATION, not a count of the absolute number of sodium molecules. Got that? If not, work on it, because you have to "get" it.
Now you refill the beaker to its previous level, full up, with plain water... or, say, D5W, which is the same thing, physiologically. Now what's your sodium level? Right, 70, because you have twice as much water per amt of sodium.
Go back to the half-full beaker again, the one with a serum (oooh, a Freudian slip! I think I'll leave it. Serum counts as saline.) sodium of 140. Fill it up with an equal volume of....normal saline, which for purposes of this discussion has a sodium level about the same as blood serum. What's the serum sodium now? Right, still 140. As a matter of fact, you can pour quite a bit of NS into a body and not really influence the serum sodium that much at all. The way you change the serum sodium is by changing the amt of WATER.
Repeat to yourself: "Serum sodium tells you about water balance." and "Saline is not sodium and water." (I used to have a poster of this and have my classes chant it three times before going on :) ....I wanted to be sure they would remember it for later)
OK, deep breath. Now we look at water balance from the other side.
Saline pretty much stays in its vascular place (unless you cut a blood vessel and spill some out). But water....ah, water travels. As a matter of fact, that's the other poster. Repeat three times: "Saline stays, water travels." (think: rivers flow from place to place, but the ocean pretty much stays where it is.) What the heck importance is that?
Back to your original beaker.... the one full of stuff with a serum Na+ of 140. Evaporate half of the water. What is the serum sodium now? Right, 280 (whooee, bigtime dehydration) As a matter of fact, if you lose enough water from your body to get your serum sodium up to 170 or so (("Serum sodium tells you about water balance")), you'll probably die, especially if you do it rapidly. Why? Because water travels in and out of all your cells. If you lose water from your intravascular space, sweat it out, or pee it out because your kidneys are unable to concentrate urine for some reason, thus making your bloodstream more concentrated, water molecules on the other side of the cell walls all over town say, "Whoops! Gotta go!"...because water travels across cell membranes from an area of more water per volume (lower salt concentration) to the area of less water per volume (higher salt concentration). So if you are de-hydrated, meaning water-poor, all your cells shrink. Most importantly, if your brain cells shrink enough from water loss, they pull away from your pia mater/meninges and you have an intracerebral bleed. Bummer.
(Interestingly, this is why you have a headache with your hangover after an alcohol binge. Alcohol temporarily disables your kidneys from retaining water, so they let too much out. You pee a lot, and your brain shrinks just enough to put a little tension on your pia mater/meninges. Bingo, headache.) (Ahhh, digressed again....)
OK, now put this all together and tell me why your hematocrit is a lousy indicator of water balance (as a matter of fact, a nigh-on USELESS indicator of dehydration), but a good indication of saline balance.
OK. You are walking down the street with a perfectly good crit of 40 and a serum sodium of 140 (and normal other lytes). You are accosted by someone with a sharp thing and before you know it, a whole lot of your circulating volume is running into the storm drain. Fortunately, you are whisked into a nearby ER immediately, having had your bleeding stopped by a nearby Boy Scout with good First Aid Merit Badge training (ummmm, I teach that too). The ER nurse draws a baseline crit and lytes. What are they?
OK, crit is still 40...because hct is a *percentage of the blood that is red cells*, not a count of the absolute number of red cells you have. So even if you lose a lot of your blood, your crit is unchanged. Until they start fluid-resuscitating you with.... normal (not half-normal) saline (or RL, which acts like it for purposes of this discussion).
Na+ is still 140, because you have lost saline (serum counts as saline) but not water.
Thought experiment time again. Take two tubes of whole blood, that is, serum and red cells. They both have a Hct ( which is often spoken as “crit”) of 40, that is, 40% of the volume of each tube is taken up solely by RBC's. We already know what happens if you add saline to one of them: the crit drops, right? But what happens to the crit of a tube of blood if you add water-- like D5W? Answer: Nothing. Why? Because the crit is a % of volume....and when you add water, the water travels into the cells too. So they swell up, and their %age size change means no change in the crit of the tube. They still take up (in this example) 40% of the volume. What happens if, instead of adding water to your original tube of hct=40 blood, you evaporate half of the water out of it? (The answer is NOT, "Make gravy." Shame on you.) No, the hct stays the same, because the cells lose water too, and they shrink as much as the liquidy part did. Same percentage of red cells in the resulting volume = no change in hematocrit.
So. When you have someone dehyrated (as evidenced by their elevated serum Na+), you give him water (or D5W). This dilutes his serum Na+ back towards normal and allows his shrunken dehydrated cells to regain their girlish plumpness. Normal saline will not help, as it will not change the serum sodium level ("Saline is not sodium and water") and will not move into cells to restore their lost water content ("Saline stays, water travels.")
If you have someone who is hypovolemic, as evidenced by (hmmm? what? how do you assess hypovolemia? How about BP, CVP, JVD, PAd, LVEDP, etc? You pick 'em), you give him saline, which goes into his vascular space where you want it for circulating volume but doesn't go anywhere else. D5W will not do the job, as it will travel into cells (not just RBC's, but all cells, and most of it will thus not be available in the vascular space to make blood pressure).
So why do dehydrated old ladies have high crits AND high serum Na+'s? Well, as I was fond of telling my students, it's perfectly possible to have two things wrong at once.
Let's look at a couple of people and see if that helps.
1) Serum Na+ 140, Hct 25, BP 110/60. OK, so this guy is relatively anemic, but his circulating volume is OK (as evidenced by an adequate BP) and his water balance is fine (as evidenced by his normal Na+). Who does this? Well, anemia can have many causes, but if he comes in with a hx of a recent bleed with fluid resuscitation, you could guess that he had a perfectly good crit until he lost some red cells out his GI bleed or stab wound or bloody ortho surgery or something, and we were stingy and just gave him NS back. His crit is called "dilutional," as in, "His red cells are floating in saline."
2) Serum Na+ 118, Hct 40, BP 110/60. This guy has 'way too much water on board, as evidenced by his Na+ that's 'way low ("dilutional" too). We call him hyponatremic, but it's not that he has lost sodium (in most cases), it's that he retained too much water. He hasn't lost saline, as evidenced by his decent BP ("Saline is not sodium and water"). Who does this? Well, remember the dread "SIADH"? "Syndrome of inappropriate antidiuretic hormone"? Lessee.... inappropriate, ummm, too much. Antidiuretic, ummmm, doesn't allow diuresis, holds onto water.... Bingo. He's retaining water, and his Na+ is called "dilutional" because all those little Na+s are floating around in too much water. Some degree of SIAHD is actually pretty common--- you can do it with anesthesia, mechanical ventilation (there's stretch receptors in the lungs, see, and....oh, later), and a host of common meds. Of course, you can also get a low serum sodium in a hurry if some fool tanks you rapidly with a liter or two of D5W, or , like that poor woman in a SoCal radio contest, you drink a ton of plain water over a short period of time. She died of acute cerebral edema when her brain swelled up faster than her skull would stretch to accommodate it.
Hope this makes some level of sense. Ask if it doesn't.
Last, get a copy of the Physiology Coloring Book, not a joke but a really good resource that helps you learn by engaging multiple parts of your brain. Free 2-day shipping for students from Amazon and I think they have a downloadable version too, but you want the hard copy for max benefit. (no financial interest in this book, Amazon, or much else)
blt99
30 Posts
What type of learner are you?
I ask because I am highly kinetic and visual (on the VARK test) and the last thing I am is read/write. I can't look at black letters on a white paper and absorb it. Doesn't work for me. For me, I act stuff out or make silly body movements (think YMCA dance) or draw simple pictures that tell a story.
One set of books I have found helpful are the "made incredibly easy!" books, and there is one for fluids and electrolytes.
Also Mosby's memory card book for fluids and electrolytes has cute cartoony pictures. I used the ones for pharm and they helped to inspire creativity.
phuretrotr
292 Posts
Before I pour my heart and soul into teaching you about ABG's, do you need help with them as well?
Let them start another thread on that. It seems to be a big source of anxiety-- and misunderstanding-- for a lot of students and new grads. :)
I KNOW! It use to be for me too for the longest time, but THEN I learned the tic-tac-toe or X & O method with the table/chart... Will never forget it again.
hlj123
31 Posts
A quickie on fluids and Na+ balance, the most common condition you will encounter. Na+ and Water Balance, or why you have to remember that serum sodium doesn't tell you anything at all about sodium :) , and that saline is not water and salt.(Now, don't overthink this. Of course if you want to make a bottle of saline, you will mix plain water with sodium chloride. But read this without thinking about that, because .... well, it works better if you think of saline as an entity for purposes of this discussion. Read it and then ask me if you still have questions.)OK, thought experiment time: Draw pictures with little molecules or such if you like, it will help. You have a beaker full of salt water, with a Na+ level of, say, 140 (hmmmm, what a coincidence). You pour half of it out. What is the Na+ level in the remainder? Right, 140, because that measurement is a measurement of CONCENTRATION, not a count of the absolute number of sodium molecules. Got that? If not, work on it, because you have to "get" it. Now you refill the beaker to its previous level, full up, with plain water... or, say, D5W, which is the same thing, physiologically. Now what's your sodium level? Right, 70, because you have twice as much water per amt of sodium. Go back to the half-full beaker again, the one with a serum (oooh, a Freudian slip! I think I'll leave it. Serum counts as saline.) sodium of 140. Fill it up with an equal volume of....normal saline, which for purposes of this discussion has a sodium level about the same as blood serum. What's the serum sodium now? Right, still 140. As a matter of fact, you can pour quite a bit of NS into a body and not really influence the serum sodium that much at all. The way you change the serum sodium is by changing the amt of WATER. Repeat to yourself: "Serum sodium tells you about water balance." and "Saline is not sodium and water." (I used to have a poster of this and have my classes chant it three times before going on :) ....I wanted to be sure they would remember it for later)OK, deep breath. Now we look at water balance from the other side. Saline pretty much stays in its vascular place (unless you cut a blood vessel and spill some out). But water....ah, water travels. As a matter of fact, that's the other poster. Repeat three times: "Saline stays, water travels." (think: rivers flow from place to place, but the ocean pretty much stays where it is.) What the heck importance is that?Back to your original beaker.... the one full of stuff with a serum Na+ of 140. Evaporate half of the water. What is the serum sodium now? Right, 280 (whooee, bigtime dehydration) As a matter of fact, if you lose enough water from your body to get your serum sodium up to 170 or so (("Serum sodium tells you about water balance")), you'll probably die, especially if you do it rapidly. Why? Because water travels in and out of all your cells. If you lose water from your intravascular space, sweat it out, or pee it out because your kidneys are unable to concentrate urine for some reason, thus making your bloodstream more concentrated, water molecules on the other side of the cell walls all over town say, "Whoops! Gotta go!"...because water travels across cell membranes from an area of more water per volume (lower salt concentration) to the area of less water per volume (higher salt concentration). So if you are de-hydrated, meaning water-poor, all your cells shrink. Most importantly, if your brain cells shrink enough from water loss, they pull away from your pia mater/meninges and you have an intracerebral bleed. Bummer. (Interestingly, this is why you have a headache with your hangover after an alcohol binge. Alcohol temporarily disables your kidneys from retaining water, so they let too much out. You pee a lot, and your brain shrinks just enough to put a little tension on your pia mater/meninges. Bingo, headache.) (Ahhh, digressed again....)OK, now put this all together and tell me why your hematocrit is a lousy indicator of water balance (as a matter of fact, a nigh-on USELESS indicator of dehydration), but a good indication of saline balance. OK. You are walking down the street with a perfectly good crit of 40 and a serum sodium of 140 (and normal other lytes). You are accosted by someone with a sharp thing and before you know it, a whole lot of your circulating volume is running into the storm drain. Fortunately, you are whisked into a nearby ER immediately, having had your bleeding stopped by a nearby Boy Scout with good First Aid Merit Badge training (ummmm, I teach that too). The ER nurse draws a baseline crit and lytes. What are they? OK, crit is still 40...because hct is a *percentage of the blood that is red cells*, not a count of the absolute number of red cells you have. So even if you lose a lot of your blood, your crit is unchanged. Until they start fluid-resuscitating you with.... normal (not half-normal) saline (or RL, which acts like it for purposes of this discussion).Na+ is still 140, because you have lost saline (serum counts as saline) but not water.Thought experiment time again. Take two tubes of whole blood, that is, serum and red cells. They both have a Hct ( which is often spoken as “crit”) of 40, that is, 40% of the volume of each tube is taken up solely by RBC's. We already know what happens if you add saline to one of them: the crit drops, right? But what happens to the crit of a tube of blood if you add water-- like D5W? Answer: Nothing. Why? Because the crit is a % of volume....and when you add water, the water travels into the cells too. So they swell up, and their %age size change means no change in the crit of the tube. They still take up (in this example) 40% of the volume. What happens if, instead of adding water to your original tube of hct=40 blood, you evaporate half of the water out of it? (The answer is NOT, "Make gravy." Shame on you.) No, the hct stays the same, because the cells lose water too, and they shrink as much as the liquidy part did. Same percentage of red cells in the resulting volume = no change in hematocrit.So. When you have someone dehyrated (as evidenced by their elevated serum Na+), you give him water (or D5W). This dilutes his serum Na+ back towards normal and allows his shrunken dehydrated cells to regain their girlish plumpness. Normal saline will not help, as it will not change the serum sodium level ("Saline is not sodium and water") and will not move into cells to restore their lost water content ("Saline stays, water travels.")If you have someone who is hypovolemic, as evidenced by (hmmm? what? how do you assess hypovolemia? How about BP, CVP, JVD, PAd, LVEDP, etc? You pick 'em), you give him saline, which goes into his vascular space where you want it for circulating volume but doesn't go anywhere else. D5W will not do the job, as it will travel into cells (not just RBC's, but all cells, and most of it will thus not be available in the vascular space to make blood pressure). So why do dehydrated old ladies have high crits AND high serum Na+'s? Well, as I was fond of telling my students, it's perfectly possible to have two things wrong at once. Let's look at a couple of people and see if that helps.1) Serum Na+ 140, Hct 25, BP 110/60. OK, so this guy is relatively anemic, but his circulating volume is OK (as evidenced by an adequate BP) and his water balance is fine (as evidenced by his normal Na+). Who does this? Well, anemia can have many causes, but if he comes in with a hx of a recent bleed with fluid resuscitation, you could guess that he had a perfectly good crit until he lost some red cells out his GI bleed or stab wound or bloody ortho surgery or something, and we were stingy and just gave him NS back. His crit is called "dilutional," as in, "His red cells are floating in saline."2) Serum Na+ 118, Hct 40, BP 110/60. This guy has 'way too much water on board, as evidenced by his Na+ that's 'way low ("dilutional" too). We call him hyponatremic, but it's not that he has lost sodium (in most cases), it's that he retained too much water. He hasn't lost saline, as evidenced by his decent BP ("Saline is not sodium and water"). Who does this? Well, remember the dread "SIADH"? "Syndrome of inappropriate antidiuretic hormone"? Lessee.... inappropriate, ummm, too much. Antidiuretic, ummmm, doesn't allow diuresis, holds onto water.... Bingo. He's retaining water, and his Na+ is called "dilutional" because all those little Na+s are floating around in too much water. Some degree of SIAHD is actually pretty common--- you can do it with anesthesia, mechanical ventilation (there's stretch receptors in the lungs, see, and....oh, later), and a host of common meds. Of course, you can also get a low serum sodium in a hurry if some fool tanks you rapidly with a liter or two of D5W, or , like that poor woman in a SoCal radio contest, you drink a ton of plain water over a short period of time. She died of acute cerebral edema when her brain swelled up faster than her skull would stretch to accommodate it.Hope this makes some level of sense. Ask if it doesn't. Last, get a copy of the Physiology Coloring Book, not a joke but a really good resource that helps you learn by engaging multiple parts of your brain. Free 2-day shipping for students from Amazon and I think they have a downloadable version too, but you want the hard copy for max benefit. (no financial interest in this book, Amazon, or much else)
Oh My God---I am officially bowing down to you. Do you have ANY idea how I could NEVER really grasp this???? And you make it so easy. KhadAcademy look out! Can you do videos please?? LOLLL. I'm sure if I could hear your voice and watch you draw, it would be 10x better!!!! Thank you!
OKNurse2be
167 Posts
That is actually not a bad idea to have some educators here on AN do some quick videos over some of the subjects that are harder to grasp for some students. I know I would greatly appreciate it!
Sorta impossible if we want to maintain our anonymity (can you see me working at a white board with a paper bag over my head?), but there are a number of people here (e.g., Ashley, Esme, Ruby, me, and others) who hang out on the student fora and are happy to indulge their teaching jones by helping you.
As ever, we don't do your homework for you, but if you say, "I learned this and that, but XYZ just doesn't make sense to me even though I looked up ABC, where am I going wrong?" there are people who will understand how you got to where you are and be able to help set you right. It's what we do for fun. :)
Sorta impossible if we want to maintain our anonymity (can you see me working at a white board with a paper bag over my head?), but there are a number of people here (e.g., Ashley, Esme, Ruby, me, and others) who hang out on the student fora and are happy to indulge their teaching jones by helping you. As ever, we don't do your homework for you, but if you say, "I learned this and that, but XYZ just doesn't make sense to me even though I looked up ABC, where am I going wrong?" there are people who will understand how you got to where you are and be able to help set you right. It's what we do for fun. :)
Yeah I see what you are saying. I really do appreciate all that you and the others you mentioned do to assist us students. I will be referencing back to this thread when we are doing fluid and electrolytes in a few weeks, because it's one of those things where I think I get it, and then when I get to the "how do I apply this in real life" part, I realize once again that I don't REALLY get it.