Chapter 11 Assessment and Care of Patients With Problems of Fluid and Electrolyte Balance Flashcards
FLUID AND ELECTROLYTE BALANCE
Keeping this balance within normal ranges is part of homeostasis.
homeostatic mechanisms
many control actions to prevent dangerous changes
(extracellular fluid [ECF]
the fluid outside the cells
(intracellular fluid [ICF]
the fluid inside the cells
The ECF includes
interstitial fluid (fluid between cells, “third space”); blood, lymph, bone, and connective tissue water; and the transcellular fluids
Transcellular fluids include
cerebrospinal fluid, synovial fluid, peritoneal fluid, and pleural fluid
Water delivers
dissolved nutrients and electrolytes to all organs, tissues, and cells
Changes in either the amount of water or the amount of electrolytes in body fluids:
can reduce the function of all cells, tissues, and organs.
solvent
is the water portion of fluids.
Solutes
are the particles dissolved or suspended in the water.
electrolytes
When solutes express an overall electrical charge
Filtration
is the movement of fluid (water) through a cell or blood vessel membrane because of water pressure (hydrostatic pressure) differences on both sides of the membrane.
hydrostatic pressure
“water-pushing” pressure, because it forces water outward from a confined space through a membrane
Permeable
porous membrane separates the two spaces.
equilibrium
hydrostatic pressure is the same in both fluid spaces
disequilibrium
If the hydrostatic pressure is not the same in both spaces
(gradient)
graded difference
one space has a higher hydrostatic pressure than the other.
filtration
When a gradient exists, water movement until they are at equilibrium again
filters
water moving across gradient from high to low pressure
Blood pressure
moves whole blood from the heart to capillaries where filtration can occur to exchange water, nutrients, and waste products between the blood and the tissues.
hydrostatic pressure difference: blood
between the capillary blood and the interstitial fluid determines whether water leaves the blood vessels and enters the tissue spaces.
pores
Large spaces in the capillary membrane
water filters freely when a hydrostatic pressure gradient is present
Edema
(excess tissue fluid)
when does edema form
changes in hydrostatic pressure differences between the blood and the interstitial fluid such as in right-sided heart failure
right-sided heart failure
the volume of blood in the right side of the heart increases because the right ventricle is too weak to pump blood well into lung blood vessels. As blood backs up into the venous and capillary systems, the capillary hydrostatic pressure rises until it is higher than the pressure in the interstitial space. Excess filtration from the capillaries into the interstitial tissue space then forms visible edema.
Diffusion
is the movement of particles (solute) across a permeable membrane from an area of higher particle concentration to an area of lower particle concentration
concentration gradient
when two fluid spaces have different concentrations of the same type of particles.
Diffusion- how
Any membrane that separates two spaces is struck repeatedly by particles. When the particle strikes a pore in the membrane that is large enough for it to pass through, diffusion occurs
steepness
degree of difference
larger the concentration difference between the two sides, the steeper the gradient
selective
permit diffusion of some particles but not others.
impermeable
closed
glucose
cannot cross some cell membranes without the help of insulin. Insulin binds to insulin receptors on cell membranes, which then makes the membranes much more permeable to glucose.
facilitated diffusion
Diffusion across a cell membrane that requires a membrane-altering system
Osmosis
is the movement of water only through a selectively permeable (semipermeable) membrane.
Osmolarity
is the number of milliosmoles in a liter of solution
osmolality
is the number of milliosmoles in a kilogram of solution.
normal osmolarity value for plasma and other body fluids
270 to about 300 mOsm/L
isosmotic /isotonic
Having the same osmotic pressures.
hyperosmotic, or hypertonic
Fluids with osmolarities greater than 300 mOsm/L
tend to pull water from the isosmotic fluid space into the hyperosmotic fluid space until an osmotic balance occurs
hypo-osmotic, or hypotonic
Fluids with osmolarities of less than 270 mOsm/L are
water is pulled from the hypo-osmotic fluid space into the isosmotic fluid spaces of the interstitial and ICF fluids.
thirst mechanism
The feeling of thirst is caused by the activation of cells in the brain that respond to changes in ECF osmolarity.
thirst mechanism steps
- loses body water but most of the particles remain
- ECF volume is decreased, and its osmolarity is increased (is hypertonic)
- cells in the thirst center shrink as water moves from the cells into the hypertonic ECF.
- shrinking of these cells triggers an adult’s awareness of thirst and increases the urge to drink
- Drinking replaces the amount of water lost through sweating and dilutes the ECF osmolarity, restoring it to normal.
Sodium (Na+)
Elevated:
Hypernatremia; dehydration; kidney disease; hypercortisolism
Sodium (Na+) Low:
Hyponatremia; fluid overload; liver disease; adrenal insufficiency
Potassium (K+) high
Hyperkalemia; dehydration; kidney disease; acidosis; adrenal insufficiency; crush injuries
Potassium (K+) low
Hypokalemia; fluid overload; diuretic therapy; alkalosis; insulin administration; hyperaldosteronism
Calcium (Ca2+) high
Hypercalcemia; hyperthyroidism; hyperparathyroidism
Calcium (Ca2+) low
Hypocalcemia; vitamin D deficiency; hypothyroidism; hypoparathyroidism; kidney disease; excessive intake of phosphorus-containing foods and drinks
Chloride (Cl−) high
Hyperchloremia; metabolic acidosis; respiratory alkalosis; hypercortisolism
Chloride (Cl−) low
Hypochloremia; fluid overload; excessive vomiting or diarrhea; adrenal insufficiency; diuretic therapy
Magnesium (Mg2+) high
Hypermagnesemia; kidney disease; hypothyroidism; adrenal insufficiency
Magnesium (Mg2+) low
Hypomagnesemia; malnutrition; alcoholism; ketoacidosis
Skin change
Loss of elasticity
Decreased turgor
Decreased oil production
Results in:
Skin becomes an unreliable indicator of fluid status, especially the back of the hand
Dry, easily damaged skin
kidney change
Decreased glomerular filtration
Decreased concentrating capacity
Results in:
Poor excretion of waste products
Increased water loss, increasing the risk for dehydration
muscle change
Decreased muscle mass
Results in:
Decreased total body water
Greater risk for dehydration
Neurologic change
Diminished thirst reflex
Results in:
Decreased fluid intake, increasing the risk for dehydration
endocrine change
Adrenal atrophy
Results in:
Poor regulation of sodium and potassium, increasing the risk for hyponatremia and hyperkalemia
muscle vs fat cells
Muscle cells contain mostly water, and fat cells have little water
sensation of thirst
A rising blood osmolarity or a decreasing blood volume triggers
fluid daily
2300 mL
obligatory urine output
The minimum amount of urine per day needed to excrete toxic waste products
400 to 600 mL
if obligatory urine output is not met
lethal electrolyte imbalances, acidosis, and a toxic buildup of nitrogen.
insensible water loss
no mechanisms control it
about 500 to 1000 mL/day.
Aldosterone
is secreted by the adrenal cortex whenever sodium levels in the extracellular fluid (ECF) are low.
Aldosterone prevents both water and sodium loss.
acts on the kidney nephrons, triggering them to reabsorb sodium and water from the urine back into the blood
Antidiuretic hormone (ADH),
or vasopressin, is released from the posterior pituitary gland in response to changes in blood osmolarity.
retains just water
acts on kidney nephrons, making them more permeable to water.
Natriuretic peptides (NPs)
are hormones secreted by special cells that line the atria of the heart (atrial natriuretic peptide [ANP]) and the ventricles of the heart
secreted in response to increased blood volume and blood pressure, which stretch the heart tissue. NP binds to receptors in the nephrons, creating effects that are opposite of aldosterone.
The Renin-Angiotensin II Pathway
kidneys monitor blood pressure, blood volume, blood oxygen levels, and blood osmolarity
When the kidneys sense that any one of these parameters is getting low, they begin to secrete a substance called renin that sets into motion a group of hormonal and blood vessel responses to ensure that blood pressure is raised back up to normal
Anything that reduces blood volume (e.g., dehydration, hemorrhage) below a critical level:
always lowers blood pressure.
Renin
activates angiotensinogen 1 to 2
Angiotensin II``
starts several actions to increase blood volume and blood pressure
- decrease urine output
- aldosterone secretion
- increases peripheral resistance and reduces the size of the vascular bed
low sodium for hypertension
high sodium intake raises the blood level of sodium, causing more water to be retained in the blood volume and raising blood pressure.
ACE inhibitors”
disrupt the renin-angiotensin II pathway by reducing the amount of angiotensin-converting enzyme (ACE) made so less angiotensin II is present. With less angiotensin II, there is less vasoconstriction and reduced peripheral resistance, less aldosterone production, and greater excretion of water and sodium in the urine
Dehydration cause
- Hemorrhage
- Vomiting
- Diarrhea
- Profuse salivation
- Fistulas
- Ileostomy
- Profuse diaphoresis
- Burns
- Severe wounds
- Long-term NPO status
- Diuretic therapy
- GI suction
- Hyperventilation
- Diabetes insipidus
- Difficulty swallowing
- Impaired thirst
- Unconsciousness
- Fever
- Impaired motor function
Fluid Overload cause
- Excessive fluid replacement
- Kidney failure (late phase)
- Heart failure
- Long-term corticosteroid therapy
- Syndrome of inappropriate antidiuretic hormone (SIADH)
- Psychiatric disorders with polydipsia
- Water intoxication
dehydration
fluid intake or retention is less than what is needed to meet the body’s fluid needs, resulting in a deficit of fluid volume, especially plasma volume.
older adult dehydration risks
decreased thirst sensation
difficulty moving
less total body water
drugs that increase fluid excretion
hypovolemia
Circulating blood volume is decreased leads to reduced perfusion
Isotonic dehydration
Fluid is lost only from the extracellular fluid (ECF) space
Mild dehydration
corrected or prevented easily by matching fluid intake with fluid output
history questions
Ask specific questions about food and liquid intake.
Collect specific information about exact intake and output volumes and obtain serial daily weight measurements.
Ask specific questions about prescribed and over-the-counter drugs
Ask about the presence of kidney or endocrine diseases.
Cardiovascular changes
- Heart rate increases
- Peripheral pulses are weak, difficult to find, and easily blocked
- Blood pressure also decreases
- Hypotension is more severe with the patient in the standing position than in the sitting or lying position
- neck and hand veins are flat, even when the neck and hands are not raised above the level of the heart.
Respiratory changes
increased respiratory rate is a compensatory mechanism that attempts to maintain oxygen delivery when perfusion is decreased.
Skin changes
- dehydration skin turgor is poor
- The skin is dry and scaly.
- The tongue surface may have deep furrows.
- oral mucous membranes may be dry and covered with a thick, sticky coating and may have cracks and fissures
Neurologic changes
changes in mental status and temperature with reduced PERFUSION in the brain.
Kidney changes
affect urine volume and concentration
Urine output below 500 mL/day for a patient without kidney disease is cause for concern.
laboratory findings with dehydration show
elevated levels of hemoglobin, hematocrit, serum osmolarity, glucose, protein, blood urea nitrogen, and electrolytes because more water is lost and other substances remain, increasing blood concentration
hemoconcentration
increasing blood concentration
The priority problems for the patient who has dehydration are:
- Dehydration due to excess fluid loss or inadequate fluid intake
- Potential for injury due to blood pressure changes and muscle weakness
Indicators patient is not dehydrated anymore
- Blood pressure at or near his or her normal range
- Daily urine output within 500 mL of total daily fluid intake (or at least 30 mL per hour)
- Moist mucous membranes
- Normal skin turgor
focus of management for the patient with dehydration
prevent further fluid loss, to increase fluid volumes to normal, and to prevent injury.
The Patient With Dehydration interventions
- When possible, provide oral fluids that meet the patient’s dietary restrictions (e.g., sugar-free, low-sodium, thickened).
- Collaborate with other members of the interprofessional team to determine the amount of fluids needed during a 24-hour period.
- Ensure that fluids are offered and ingested on an even schedule at least every 2 hours throughout 24 hours.
- Teach unlicensed assistive personnel to actively participate in the hydration therapy and not to withhold fluids to prevent incontinence.
- Infuse prescribed IV fluids at a rate consistent with hydration needs and any known cardiac, pulmonary, or kidney problems.
- Monitor the patient’s response to fluid therapy at least every 2 hours for indicators of adequate rehydration or the need for continuing therapy, especially:
- Pulse quality
- Urine output
- Pulse pressure
- Weight (every 8 hours)
- Monitor for and report indicators of fluid overload, including:
- Bounding pulse
- Difficulty breathing
- Neck vein distention in the upright position
- Presence of dependent edema
- Assess the IV line and the infusion site at least hourly for indications of infiltration, extravasation, or phlebitis (e.g., swelling around the site, pain, cordlike veins, reduced drip rate).
- Administer drugs prescribed to correct the underlying cause of the dehydration (e.g., antiemetics, antidiarrheals, antibiotics, antipyretics).
Coordinate with unlicensed assistive personnel (UAP) by teaching:
offer 60 to 120 mL of fluid every hour to patients who are dehydrated or who are at risk for dehydration.
withholding fluids due to incontinence is not appropriate
record amount of fluids ingested
Crystalloids
IV fluids that contain water, minerals (electrolytes), and sometimes other water-soluble substances such as glucose
most useful when dehydration includes both the intracellular and extracellular compartments
Colloids
are IV fluids that contain larger non–water-soluble molecules that increase the osmotic pressure in the plasma volume.
most useful in helping to maintain plasma volume with a lower infused volume
The two most important areas to monitor during rehydration
pulse rate and quality and urine output.
Antidiarrheal drugs
are prescribed when diarrhea causes dehydration.
Antimicrobial
therapy may be used in patients with bacterial diarrhea.
Antiemetics
may be used when vomiting causes dehydration
Antipyretics
to reduce fever are helpful when fever makes dehydration worse.
patient with dehydration is at risk for falls because
orthostatic hypotension, dysrhythmia, muscle weakness, and possible confusion.
Indications that the patient’s underlying cause of dehydration is well managed
- Maintains a daily fluid intake of at least 1500 mL (or drinks at least 500 mL more than his or her daily urine output)
- Can state the indications of dehydration
- Starts fluid replacement at the first indication of dehydration
- Correctly follows treatment plans for ongoing health problems that increase the risk for dehydration
Fluid overload, also called overhydration,
is an excess of body fluid. fluid intake or retention is greater than the body’s fluid needs.
response to mild or moderate fluid overload
especially increased urine output, and edema formation.
when overload is severe or occurs in an adult with poor cardiac or kidney function:
it can lead to heart failure and pulmonary edema.
Dilution of sodium and potassium
can lead to seizures, coma, and death.
Fluid Overload
Cardiovascular Changes
- Increased pulse rate
- Bounding pulse quality
- Elevated blood pressure
- Decreased pulse pressure
- Elevated central venous pressure
- Distended neck and hand veins
- Engorged varicose veins
- Weight gain
Fluid Overload
Respiratory Changes
- Increased respiratory rate
- Shallow respirations
- Shortness of breath
- Moist crackles present on auscultation
Fluid Overload
Skin and Mucous Membrane Changes
- Pitting edema in dependent areas
* Skin pale and cool to touch
Fluid Overload
Neuromuscular Changes
- Altered level of consciousness
- Headache
- Visual disturbances
- Skeletal muscle weakness
- Paresthesias
Fluid Overload
Gastrointestinal Changes
- Increased motility
* Enlarged liver
Fluid Overload labs
Usually serum electrolyte values are normal; but decreased hemoglobin, hematocrit, and serum protein levels
hemodilution
excessive water in the vascular space
pulmonary edema and fluid overload
Assess the patient with fluid overload at least every 2 hours to recognize pulmonary edema
If indications of worsening fluid overload are present (bounding pulse, increasing neck vein distention, presence of crackles in lungs, increasing peripheral edema, reduced urine output), respond by notifying the health care provider.
skin breakdown
turn every two hours and use pressure reducing things
Diuretics
are used for fluid overload if kidney function is normal.
drug therapy assessment
Monitor the patient for response to drug therapy, especially weight loss and increased urine output. Observe for indications of electrolyte imbalance, especially changes in electrocardiogram (ECG) patterns. Assess sodium and potassium values every 8 hours or whenever they are drawn.
Drug therapy
focuses on removing excess fluid.
Nutrition therapy for the patient with chronic fluid overload
may involve restrictions of both fluid and sodium intake.
Monitoring intake and output and weight
provides information on therapy effectiveness.
Fluid retention may not be visible, may show as:
Rapid weight gain is the best indicator of fluid retention and overload.
Each pound (0.5 kg) of weight gained (after the first half pound) equates:
to about 500 mL of retained fluid.
Electrolytes, or ions,
are substances dissolved in body fluid that carry an electrical charge.
Cations
anions
have positive charges;
have negative charges.
Sodium (Na+)
is the major cation (positively charged particle) in the extracellular fluid (ECF) and maintains ECF osmolarity.
sodium in charge of
vital for muscle contraction, cardiac contraction, and nerve impulse transmission.
Sodium levels and movement influence water balance because:
“where sodium goes, water follows.” The ECF sodium level determines whether water is retained, excreted, or moved from one fluid space to another
Low serum sodium levels
inhibit the secretion of ADH and NP and trigger aldosterone secretion.
High serum sodium levels
inhibit aldosterone secretion and stimulate secretion of ADH and NP.
Hyponatremia
LOW SODIUM
is an electrolyte imbalance in which the serum sodium (Na+) level is below 136 mEq/L (mmol/L).
hyponatremia what happens and whats the result
SODIUM FOLLOWS WATER LOW SODIUM IN ECF CAUSES WATER TO GO INTO CELLS
osmolarity of the ECF is lower than that of the intracellular fluid (ICF). As a result, water moves into the cell, causing swelling.
can reduce cell function or cause cell to burst
Hyponatremia can result from
the loss of total body sodium, the movement of sodium from the blood to other fluid spaces, or the dilution of serum sodium from excessive water in the plasma.
problems of hyponatremia
- Cerebral changes CONFUSION CAN BE SUDDEN
- Neuromuscular changes are seen as general muscle weakness.
- Intestinal changes include increased motility, causing nausea, diarrhea, and abdominal cramping.
- Cardiovascular changes are seen as changes in cardiac output.
cardiac responses to hyponatremia with hypovolemia (decreased plasma volume)
- rapid, weak, thready pulse.
- Peripheral pulses are difficult to palpate and are easily blocked.
- Blood pressure is decreased, and the patient may have severe orthostatic hypotension, leading to light-headedness or dizziness. -The central venous pressure is low.
cardiac responses to hyponatremia occurs with hypervolemia (fluid overload)
-full or bounding pulse with normal or high blood pressure. -Peripheral pulses are full and difficult to block
sometimes hard to palpate due to edema
priorities for nursing care of the patient with hyponatremia
monitoring the patient’s response to therapy and preventing hypernatremia and fluid overload.
Drug therapy hyponatremia fluid deficit
- reducing the doses of any drugs that increase sodium loss such as most diuretics
- IV saline infusions for fluid deficit
- small-volume infusions of hypertonic saline in severe cases (3%)
Drug therapy hyponatremia- fluid excess
-drugs that promote the excretion of water rather than sodium (such as conivaptan (Vaprisol) or tolvaptan (Samsca)
mild hyponatremia
nutrition therapy
increasing oral sodium intake and restricting oral fluid intake
Drug therapy for hyponatremia caused by inappropriate secretion of antidiuretic hormone (ADH)
may include lithium (Carbolith, Lithane image) and demeclocycline (Declomycin).
Hypernatremia
HIGH SODIUM
is a serum sodium level over 145 mEq/L (mmol/L).
irritability
More sodium is present to move rapidly across cell membranes during depolarization, making excitable tissues more easily excited.
Hypernatremia LEADS TO:
cell shrinkage more water in ECF than ICF
Eventually the dehydrated excitable tissues may no longer be able to respond to stimuli.
Symptoms of hypernatremia first
excitable membrane activity, especially nerve, skeletal muscle, and cardiac function.
Nervous system changes In hypernatremia with normal or decreased fluid volumes
the patient may have a short attention span and be agitated or confused.
Nervous system changes in hypernatremia with fluid overload
the patient may be lethargic, stuporous, or comatose.
Skeletal muscle changes Mild
hypernatremia
cause muscle twitching and irregular muscle contractions
Skeletal muscle changes moderate
hypernatremia
muscles and nerves are less able to respond to a stimulus, and muscles become progressively weaker
Skeletal muscle changes late
hypernatremia
deep tendon reflexes are reduced or absent.
Cardiovascular changes
hypernatremia
include decreased contractility because high sodium levels slow the movement of calcium into the heart cells.
Nursing care priorities for the patient with hypernatremia
include monitoring his or her response to therapy and ensuring patient safety by preventing hyponatremia and dehydration.
Hypernatremia caused by reduced kidney sodium excretion drug therapy
diuretics that promote sodium loss
Drug therapy is used to restore fluid balance when hypernatremia is caused by fluid loss
Isotonic saline (0.9%) and dextrose 5% in 0.45% sodium chloride are most often prescribed
Nutrition therapy to prevent or correct mild hypernatremia involves :
ensuring adequate water intake, especially among older adults
Potassium (K+)
is the major cation of the intracellular fluid (ICF). The normal plasma potassium level ranges from 3.5 to 5.0 mEq/L (mmol/L)
The normal ICF potassium level is
about 140 mEq/L (mmol/L)
large difference in potassium concentration between the ICF and the extracellular fluid (ECF) is critical for:
excitable tissues to depolarize and generate action potentials.
sodium-potassium pump
in all body cells
moves extra sodium ions from the ICF and moves extra potassium ions from the ECF back into the cell. In this way the serum potassium level remains low, and the cellular potassium remains high
Hypokalemia
is a serum potassium level below 3.5 mEq/L (mmol/L)
It can be life threatening because every body system is affected.
Actual potassium depletion
occurs when potassium loss is excessive or when potassium intake is not adequate to match normal potassium loss.
Relative hypokalemia
occurs when total body potassium levels are normal but the potassium distribution between fluid spaces is abnormal or diluted by excess water.
urine and Hypokalemia
urine concentrating ability decreases with aging, which increases potassium loss
drugs and Hypokalemia
diuretics, corticosteroids, and beta-adrenergic agonists or antagonists, can increase potassium loss through the kidneys.
disease and Hypokalemia
Disease can lead to potassium loss.
respiration changes Hypokalemia
Respiratory changes occur because of respiratory muscle weakness, resulting in shallow respirations.
CHECK RESP STATUS EVERY TWO HOURS
Musculoskeletal changes Hypokalemia
skeletal muscle weakness.
Cardiovascular changes
Hypokalemia
pulse is usually thready and weak. Palpation is difficult, and the pulse is easily blocked. Pulse rate ranges from very slow to very rapid, and an irregular heartbeat (dysrhythmia)
hypotension
Neurologic changes from hypokalemia
include altered mental status.
Intestinal changes occur with hypokalemia:
GI smooth muscle contractions are decreased, which leads to decreased peristalsis. Bowel sounds are hypoactive, and nausea, vomiting, constipation, and abdominal distention are common.
paralytic ileus
absence of peristalsis
Hypokalemia causes ECG changes in the heart including:
ST-segment depression, flat or inverted T waves, and increased U waves.
The priorities for nursing care of the patient with hypokalemia
ensuring adequate gas exchange, patient safety for falls prevention, prevention of injury from potassium administration, and monitoring the patient’s response to therapy
The Patient With Hypokalemia
- Question the continued use of drugs that increase excretion of potassium (e.g., thiazide and loop diuretics).
- Give prescribed oral potassium supplement, well diluted and with a meal or just after a meal or snack to prevent nausea and vomiting.
- Prevent accidental overdose of IV potassium by checking and re-checking the concentration of potassium in the IV solution, ensuring that the maximum concentration is no greater than 1 mEq (mmol)/10 mL of solution.
- Establish an IV access in a large vein with a high volume of flow, avoiding the hand.
- Assess the IV access for placement and an adequate blood return before administering potassium-containing solutions.
- Use a controller for solution delivery, maintaining an infusion rate not faster than 5-10 mEq (mmol) of potassium per hour.
- Assess the IV site hourly.
- Stop the infusion immediately if the patient reports pain or burning or if any sign of infiltration occurs.
- If possible, monitor electrocardiography continuously.
- Monitor patient responses every 1-2 hours to determine therapy effectiveness and the potential for hyperkalemia.
- Indications of therapy effectiveness:
- Respiratory rate is greater than 12 breaths/min.
- Oxygen saturation is at least 95% (or has returned to the patient’s normal baseline).
- The patient can cough effectively.
- Hand-grasp strength increases.
- Deep tendon reflexes are present.
- Bowel sounds are present and active.
- Pulse is easily palpated and regular.
- Systolic blood pressure when standing remains within 20 mm Hg of the systolic pressure obtained when the patient is sitting or lying down.
- ST segment returns to the isoelectric line.
- T waves increase in size and are positive.
- U waves decrease or disappear.
- Patient’s cognition resembles his or her prehypokalemic state.
- Serum potassium level is between 3.5 and 5.0 mEq/L (mmol/L).
- Indications of hyperkalemia:
- Heart rate is less than 60 beats/min.
- P waves are absent.
- T waves are tall.
- PR intervals are prolonged.
- QRS complexes are wide.
- Deep tendon reflexes are hyperactive.
- Bowel sounds are hyperactive.
- Numbness or tingling is present in the hands and feet and around the mouth.
- The patient is anxious.
- Serum potassium level is above 5.0 mEq/L (mmol/L).
- Keep patient on bedrest until hypokalemia resolves or provide assistance when out of bed to prevent falls.
Drug therapy for management and prevention of hypokalemia
includes additional potassium and drugs to prevent potassium loss
Potassium warning
Potassium is a severe tissue irritant and is never given by IM or subcutaneous injection.
Tissues damaged by potassium can become necrotic, causing loss of function and requiring surgery.
If infiltration of solution containing potassium occurs
stop the IV solution immediately, remove the venous access, and notify the health care provider or Rapid Response Team.
potassium-sparing diuretic
increase urine output without increasing potassium loss
Diuretics that increase the kidney excretion of potassium:
can cause hypokalemia, especially high-ceiling (loop) diuretics
hypokalemia Nutrition therapy involves
collaboration with a dietitian to teach the patient how to increase dietary potassium intake
hypokalemia Respiratory monitoring
- performed at least hourly for severe hypokalemia.
- check oxygen saturation by pulse oximetry to determine breathing effectiveness.
- Assess respiratory muscle effectiveness by checking the patient’s ability to cough.
- Examine the face, oral mucosa, and nail beds for pallor or cyanosis
hypoxemia
decreased blood oxygen levels
hypercapnia
increased arterial carbon dioxide levels
Hyperkalemia
is a serum potassium level higher than 5.0 mEq/L (mmol/L). Even small increases above normal values can affect excitable tissues, especially the heart.
Those at greatest risk for Hyperkalemia
chronically ill patients, debilitated patients, and older adults
people with damaged kidneys
Cardiovascular changes Hyperkalemia
are the most severe problems from hyperkalemia and are the most common cause of death in patients with hyperkalemia
Hyperkalemia s/s
palpitations, skipped heartbeats, or other cardiac irregularities; and muscle twitching leg weakness, or unusual tingling or numbness in the hands, feet, or face
paresthesia
tingling and burning sensations followed by numbness in the hands and feet and around the mouth
Neuromuscular changes Hyperkalemia
skeletal muscle twitches up to muscle weakness and flaccid paralysis
Intestinal changes Hyperkalemia
include increased motility with diarrhea and hyperactive bowel sounds.
Hyperkalemia caused by kidney failure labs
occurs with elevated serum creatinine and blood urea nitrogen, decreased blood pH, and normal or low hematocrit and hemoglobin levels.
Hyperkalemia caused by dehydration labs
levels of other electrolytes, hematocrit, and hemoglobin also are elevated.
The priorities for nursing care of the patient with hyperkalemia
are assessing for cardiac complications, patient safety for falls prevention, monitoring the patient’s response to therapy, and health teaching.
Drug therapy hyperkalemia
can restore potassium balance by enhancing potassium excretion and promoting the movement of potassium from the extracellular fluid (ECF) into the cells
Cardiac monitoring hyperkalemia
allows for the early recognition of dysrhythmias and other symptoms of hyperkalemia on cardiac muscle.
Critical Rescue hyperkalemia
Assess anyone who has or is at risk for hyperkalemia to recognize cardiac changes. If the patient’s heart rate falls below 60 beats/min or if the T waves become spiked, both of which accompany hyperkalemia, respond by notifying the Rapid Response Team.
hyperkalemia teaching
includes diet, drugs, and recognition of the indicators of hyperkalemia.
Nutritional Management of Hyperkalemia
You Should Avoid
- Meats, especially organ meat and preserved meat
- Dairy products
- Dried fruit
- Fruits high in potassium:
- Bananas
- Cantaloupe
- Kiwi
- Oranges
- Vegetables high in potassium:
- Avocados
- Broccoli
- Dried beans or peas
- Lima beans
- Mushrooms
- Potatoes (white or sweet)
- Seaweed
- Soybeans
- Spinach
You May Eat
- Eggs
- Breads
- Butter
- Cereals
- Sugar
- Fruits low in potassium (fresh, frozen, or canned):
- Apples
- Apricots
- Berries
- Cherries
- Cranberries
- Grapefruit
- Peaches
- Pineapple
- Vegetables low in potassium:
- Alfalfa sprouts
- Cabbage
- Carrots
- Cauliflower
- Celery
- Eggplant
- Green beans
- Lettuce
- Onions
- Peas
- Peppers
- Squash
Calcium (Ca2+)
is an ion having two positive charges (divalent cation) that exists in the body in a bound form and an ionized (unbound or free) form.
PTH increases serum calcium levels by:
- Releasing free calcium from bone storage sites (bone resorption of calcium)
- Stimulating vitamin D activation to help increase intestinal absorption of dietary calcium
- Inhibiting kidney calcium excretion
- Stimulating kidney calcium reabsorption
Hypocalcemia
is a total serum calcium (Ca2+) level below 9.0 mg/dL or 2.25 mmol/L. Because the normal blood level of calcium is so low, any change in calcium levels has major effects on function.
Patient-Centered Care:Postmenopausal women are at risk for chronic calcium loss
This problem is related to reduced weight-bearing activities and a decrease in estrogen levels. As they age, many women decrease weight-bearing activities such as running and walking, which allows osteoporosis to occur at a more rapid rate. In addition, the estrogen secretion that protects against osteoporosis diminishes. Teach older women to continue walking and other weight-bearing activities.
indicator of hypocalcemia
report of frequent, painful muscle spasms (“charley horses”) in the calf or foot during rest or sleep
hypocalcemia Neuromuscular changes
often occur first in the hands and feet. Paresthesias occur at first, with sensations of tingling and numbness. If hypocalcemia continues or worsens, muscle twitching or painful cramps and spasms occur
hypocalcemia cardio changes
The heart rate may be slower or slightly faster than normal, with a weak, thready pulse. Severe hypocalcemia causes severe hypotension and ECG changes of a prolonged ST interval and a prolonged QT interval
hypocalcemia Intestinal changes
include increased peristaltic activity
painful abdominal cramping and diarrhea.
hypocalcemia skeletal changes
bones are less dense, more brittle, and fragile and may break easily with slight trauma. Vertebrae become more compact and may bend forward, leading to an overall loss of height.
Assess for hypocalcemia by testing for:
Trousseau’s and Chvostek’s signs.
hypocalcemia Drug therapy
includes direct calcium replacement (oral and IV) and drugs that enhance the absorption of calcium such as vitamin D.
hypocalcemia Nutrition therapy
involves a calcium-rich diet for patients with mild hypocalcemia and for those who are at continuing risk for hypocalcemia
hypocalcemia environmental management
Reduce stimulation by keeping the room quiet, limiting visitors, adjusting the lighting, and using a soft voice.
Hypercalcemia
is a total serum calcium level above 10.5 mg/dL or 2.62 mmol/L.
Hypercalcemia cardio changes
Mild hypercalcemia at first causes increased heart rate and blood pressure. Severe or prolonged calcium imbalance depresses electrical conduction, slowing heart rate.
Assess for slowed or impaired PERFUSION.
Hypercalcemia Neuromuscular changes
severe muscle weakness and decreased deep tendon reflexes without paresthesia. The patient may be confused and lethargic.
Hypercalcemia Intestinal changes
Constipation, anorexia, nausea, vomiting, abdominal distention, and pain are common. Bowel sounds are hypoactive or absent.
Hypercalcemia drug therapy
preventing increases in calcium and drugs to lower calcium levels.
Fluid volume replacement
Thiazide diuretics are discontinued and replaced with diuretics that enhance the excretion of calcium such as furosemide
Hypercalcemia Cardiac monitoring
needed to identify dysrhythmias and decreased cardiac output.
Magnesium (Mg2+) is a cation mostly stored in bones and cartilage.
important for skeletal muscle contraction, carbohydrate metabolism, generation of energy stores, vitamin activation, blood coagulation, and cell growth.
Hypomagnesemia
is a serum magnesium (Mg2+) level below 1.8 mEq/L or 0.74 mmol/L.
Hypomagnesemia cardio changes
increase the risk for hypertension, atherosclerosis, hypertrophic left ventricle, and a variety of dysrhythmias
Hypomagnesemia Neuromuscular changes
increase impulse transmission from nerve to nerve or from nerve to skeletal muscle. The patient has hyperactive deep tendon reflexes numbness and tingling, and painful muscle contractions.
patient may have tetany and seizures as hypomagnesemia worsens.
Hypomagnesemia Intestinal changes
Reduced motility, anorexia, nausea, constipation, and abdominal distention are common.
Hypermagnesemia
is a serum magnesium level above 2.6 mEq/L or 1.07 mmol/L.
membrane stabilizer
Hypermagnesemia Cardiac changes
include bradycardia, peripheral vasodilation, and hypotension.
Hypermagnesemia Central nervous system changes
Patients may be drowsy or lethargic. Coma may occur if the imbalance is prolonged or severe.
Hypermagnesemia Neuromuscular changes
include reduced or absent deep tendon reflexes. Voluntary skeletal muscle contractions become progressively weaker and finally stop.
Hypermagnesemia resp. risk
respiratory muscles are weak, respiratory insufficiency can lead to respiratory failure and death.
Interventions for hypermagnesemia
focus on reducing the serum level and correcting the underlying problem that caused the imbalance.
When cardiac problems are severe, giving calcium may reverse the cardiac effects of hypermagnesemia.
