F&E cards for final

Question 1

Fluid overload common causes

Answer 1

• 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

Question 2

Dehydration common causes

Answer 2

• 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

Question 3

Relative dehydration

Answer 3

Dehydration may be an actual decrease in total body water caused by either too little intake of fluid or too great a loss of fluid. It also can occur without an actual loss of total body water such as when water shifts from the plasma into the interstitial space. This condition is called relative dehydration.

Question 4

Isotonic dehydration

Answer 4

Isotonic dehydration
Dehydration may occur with just water (fluid) loss or with water and electrolyte loss (isotonic dehydration).
Isotonic dehydration is the most common type of fluid loss problem. Fluid is lost only from the extracellular fluid (ECF) space, including both the plasma and the interstitial spaces. There is no shift of fluids between spaces, so the intracellular fluid (ICF) volume remains normal
Circulating blood volume is decreased (hypovolemia) and leads to reduced perfusion.
The body’s defenses compensate during dehydration to maintain PERFUSION to vital organs in spite of hypovolemia. The main defense is increasing vasoconstriction and peripheral resistance to maintain blood pressure and circulation.

Question 5

signs and symptoms of dehydration

Answer 5

Heart rate increases
peripheral pulses weak,
blood pressure decreases
hypotension more severein standing position (orthostatic hypotension
neck and hand veins flat
increased HR
skin turgor poor
skin dry scaly
oral mucous membranes dry, cracks fissures, tongue furrowed
cognition changes in older adult may be first sign-
sometimes low grade fever which can also cause dehydration
urine concentrated with speciofic gracity over 1.030 dark color strong odor
concern-patient without kidney disease urine output below 500ml/day

Question 6

goals for dehydration

Answer 6

The patient with dehydration is expected to have sufficient fluid volume for adequate perfusion. Indicators include that the patient has:
• 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

Question 7

treating dehydration

Answer 7

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).

Question 8

Crystalloids

Answer 8

Crystalloids are IV fluids that contain water, minerals (electrolytes), and sometimes other water-soluble substances such as glucose. These fluids rapidly disperse to all body fluid compartments and are most useful when dehydration includes both the intracellular and extracellular compartments.

Question 9

colloids-blood products

Answer 9

Colloids are IV fluids that contain larger non–water-soluble molecules that increase the osmotic pressure in the plasma volume. These fluids are most useful in helping to maintain plasma volume with a lower infused volume

Question 10

Indications that the patient’s underlying cause of dehydration is well managed and that the imbalance is corrected include that the patient:

Answer 10

• 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

Question 11

fluid overload

Answer 11

The most common type of fluid overload is hypervolemia (Fig. 11-9) because the problems result from excessive fluid in the extracellular fluid (ECF) space (Vascular and interstitial) Most problems caused by fluid overload are related to excessive fluid in the vascular space or to dilution of specific electrolytes and blood components. The conditions leading to fluid overload are related to excessive intake or inadequate excretion of fluids.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.

Question 12

s/s of fluid overload

Answer 12

Fluid Overload-signs and symptoms
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
Respiratory Changes
• Increased respiratory rate
• Shallow respirations
• Shortness of breath
• Moist crackles present on auscultation
Skin and Mucous Membrane Changes
• Pitting edema in dependent areas
• Skin pale and cool to touch
Neuromuscular Changes
• Altered level of consciousness
• Headache
• Visual disturbances
• Skeletal muscle weakness
• Paresthesias
Gastrointestinal Changes
• Increased motility
• Enlarged liver

Usually serum electrolyte values are normal; but decreased hemoglobin, hematocrit, and serum protein levels may result from excessive water in the vascular space (hemodilution).

Question 13

compensatory mechanisms for fluid overload

Answer 13

increased ECF volume=circulatory overload=Increased MAP=fluid shift plasma to interstitial space(edema) also decreased secretion of ADH from post.pituitary and aldosterone from adrenal gland ng with increased secretion of natriuetic peptide (right atrium) all =increased renal excretion of sodium and water=normal plasma volume

also from circulatory overload=increased venous return =increased cardiac contractility =Increased MAP

Question 14

isotonic IV sol

Answer 14

NS, 5% dextrose in water D5W, 5%dextrose in 0.225%saline, LR,

Question 15

Hypertonic IV sol

Answer 15

10% Dextrose in water D10W, 5% dextrose in 0.9% saline(NS), 5%dextrose in 0.45% saline, 5%dextrose in LR

Question 16

hypotonic IV sol

Answer 16

0.45% saline

Question 17

Drug therapy for fluid overload

Answer 17

Drug therapy focuses on removing excess fluid. Diuretics are used for fluid overload if kidney function is normal. Drugs may include high-ceiling (loop) diuretics such as furosemide (Lasix, Furoside ).
If there is concern that too much sodium and other electrolytes would be lost using loop diuretics or if the patient has syndrome of inappropriate antidiuretic hormone (SIADH), conivaptan (Vaprisol) or tolvaptan (Samsca) may be prescribed.
monitor ECG with electrolyte imbalances

Question 18

Each pound (0.5 kg) of weight gained (after the first half pound) equates to abou

Answer 18

500 mL of retained fluid.

Question 19

osmolarity of fluid spaces in body

Answer 19

270-300mOsm

Question 20

foods high in potassium

Answer 20

The high potassium level in foods such as meat and citrus fruit could increase the ECF potassium level and lead to major problem

Question 21

Three processes control FLUID AND ELECTROLYTE BALANCE to keep the internal environment stable even when the external environment changes.

Answer 21

These processes (filtration, diffusion, and osmosis) determine whether fluids and particles move across cell membranes.

Question 22

Osmolarity

Answer 22

Osmolarity is the number of milliosmoles in a liter of solution;
Because 1 L of water weighs 1 kg, in human physiology osmolarity and osmolality are considered the same, although osmolarity is the actual concentration measured most often. The normal osmolarity value for plasma and other body fluids ranges from 270 to about 300 mOsm/L. The body functions best when the osmolarity of all body fluid spaces is close to 300 mOsm/L.

Question 23

Osmolality

Answer 23

; osmolality is the number of milliosmoles in a kilogram of solution. Because 1 L of water weighs 1 kg, in human physiology osmolarity and osmolality are considered the same, although osmolarity is the actual concentration measured most often.

Question 24

isosmotic or isotonic

Answer 24

The body functions best when the osmolarity of all body fluid spaces is close to 300 mOsm/L. When all fluids have this particle concentration, the fluids are isosmotic or isotonic (also called normotonic) to each other.

Question 25

hyperosmotic, or hypertonic,

Answer 25

Fluids with osmolarities greater than 300 mOsm/L are hyperosmotic, or hypertonic, compared with isosmotic fluids. These fluids have a greater osmotic pressure than do isosmotic fluids and tend to pull water from the isosmotic fluid space into the hyperosmotic fluid space until an osmotic balance occurs. If a hyperosmotic (hypertonic) IV solution (e.g., 3% or 5% saline) were infused into a patient with normal extracellular fluid (ECF) osmolarity, the infusing fluid would make the adult’s blood hyperosmotic. To balance this situation, the interstitial fluid would be pulled into the circulation in an attempt to dilute the blood osmolarity back to normal. In addition, fluid would also be drawn from the intracellular fluid (ICF) compartment. As a result, the interstitial and ICF volumes would shrink, and the plasma volume would expand.

Question 26

hypo-osmotic, or hypotonic,

Answer 26

Fluids with osmolarities of less than 270 mOsm/L are hypo-osmotic, or hypotonic, compared with isosmotic fluids. Hypo-osmolar fluids have a lower osmotic pressure than isosmotic fluids, and water is pulled from the hypo-osmotic fluid space into the isosmotic fluid spaces of the interstitial and ICF fluids. As a result, the interstitial and ICF fluid volumes would expand, and the plasma volume would shrink. An example of a hypotonic IV fluid is 0.45% saline.

Question 27

Insensible water loss–

Answer 27

Water losses also can result from salivation, drainage from fistulas and drains, and GI suction. This loss is called insensible water loss because no mechanisms control it. In a healthy adult insensible water loss is about 500 to 1000 mL/day. This loss increases greatly during thyroid crisis, trauma, burns, states of extreme stress, and fever.

Risks for insensible water loss
being mechanically ventilated, those with rapid respirations, and those undergoing continuous GI suctioning. If not balanced by intake, insensible loss can lead to severe dehydration and electrolyte imbalances.
Water loss through stool
Water loss through stool increases greatly with severe diarrhea or excessive fistula drainage.

Question 28

obligatory urine output

Answer 28

The minimum amount of urine per day needed to excrete toxic waste products is 400 to 600 mL. This minimum volume is called the obligatory urine output. If the 24-hour urine output falls below the obligatory output amount, wastes are retained and can cause lethal electrolyte imbalances, acidosis, and a toxic buildup of nitrogen.

Question 29

aldosterone,

Answer 29

Aldosterone is secreted by the adrenal cortex whenever sodium levels in the extracellular fluid (ECF) are low. Aldosterone prevents both water and sodium loss. When aldosterone is secreted, it acts on the kidney nephrons, triggering them to reabsorb sodium and water from the urine back into the blood. This action increases blood osmolarity and blood volume. Aldosterone also promotes kidney potassium excretion.

Question 30

antidiuretic hormone (ADH),

Answer 30

Antidiuretic hormone (ADH), or vasopressin, is released from the posterior pituitary gland in response to changes in blood osmolarity. The hypothalamus contains the osmoreceptors that are sensitive to changes in blood osmolarity. Increased blood osmolarity, especially an increase in the level of plasma sodium, results in a slight shrinkage of these cells and triggers ADH release from the posterior pituitary gland. Because the action of ADH retains just water, it only indirectly regulates electrolyte retention or excretion.

Question 31

natriuretic peptide (NP).

Answer 31

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. (The peptide secreted by the heart ventricular cells is known as brain natriuretic peptide [BNP].) These peptides are 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. Kidney reabsorption of sodium is inhibited at the same time that urine output is increased. The outcome is decreased circulating blood volume and decreased blood osmolarity.

Question 32

A major regulator of fluid balance, also known as the renin-angiotensin system (RAS).

Answer 32

most important body fluids to keep in balance for optimal function are the blood volume (plasma volume) and the fluid inside the cells (intracellular fluid).
Maintaining blood volume at a sufficient level for blood pressure to remain high enough to ensure adequate PERFUSION is critical for life.
the kidney is a major regulator of water and sodium balance to maintain blood pressure and perfusion to all tissues and organs, the kidneys monitor blood pressure, blood volume, blood oxygen levels, and blood osmolarity (related to sodium concentration).
When kidneys sense that any one of these parameters is getting low, they 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.

triggering event for renin secretion is any change in the blood indicating that PERFUSION is at risk. Low blood pressure is a triggering event- it reduces perfusion to tissues and organs.
Anything that reduces blood volume (e.g., dehydration, hemorrhage) below a critical level always lowers blood pressure.
Low blood oxygen levels also are triggering events because with too little oxygen in the blood it cannot supply the needed oxygen and the tissues and organs could die.
A low blood sodium level also is a triggering event because sodium and water are closely linked. Where sodium goes, water follows.
So anything that causes the blood to have too little sodium prevents water from staying in the blood. The result is low blood volume with low blood pressure and poor tissue perfusion.

Once the kidneys sense that PERFUSION is at risk, special cells in the kidney tubule begin to secrete renin into the blood. Renin then activates angiotensinogen. Activated angiotensinogen is angiotensin I, which is activated by the enzyme angiotensin-converting enzyme or ACE to its most active form, angiotensin II

Angiotensin II starts several actions to increase blood volume and blood pressure. First it constricts arteries and veins throughout the body which increases peripheral resistance and reduces the size of the vascular bed, which raises blood pressure as a compensatory mechanism without adding more blood volume.
Angiotensin II constricts the size of the arterioles that feed the kidney nephrons which results in a lower glomerular filtration rate and a huge reduction of urine output. Decreasing urine output prevents further water loss so more is retained in the blood to help raise blood pressure.
Angiotensin II also causes the adrenal glands to secrete the hormone aldosterone.
Aldosterone is nicknamed the “water-and-sodium-saving hormone” because it causes the kidneys to reabsorb water and sodium, preventing them from being excreted into the urine.
This response allows more water and sodium to be returned to the blood, increasing blood pressure, blood volume, and PERFUSION.

Question 33

Sodium

Answer 33

135-145
vital for muscle contraction, cardiac contraction, nerve impulse transmission
where sodium goes water follows
changes in plasmasodium change distribution of other electrolytes

regulated by kidneys under e influences of aldosterone, antidiuretic hormone (ADH), and natriuretic peptide (NP)

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. Together these hormones increase kidney sodium excretion and water reabsorption.

Question 34

Hyponatremia

Answer 34

below 135-136
The problems caused by hyponatremiaa occur from two changes—reduced excitable membrane depolarization and cellular swelling.

Hyponatremia makes depolarization slower so excitable membranes are less excitable.
With hyponatremia the osmolarity of the ECF is lower than that of the intracellular fluid (ICF). As a result, water moves into the cell, causing swelling. Even a small amount of swelling can reduce cell function. Larger amounts of swelling can make the cell burst (lysis) and die.

common cause of low sodium levels is the prolonged use and overuse of diuretics, especially in older adults. When these drugs are used to manage fluid overload, sodium is lost along with water. 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.

Question 35

S/S of hyponatremia

Answer 35

caused by its effects on excitable cellular activity. The cells especially affected are those involved in cerebral, neuromuscular, and intestinal smooth muscle and cardiovascular functions.

Cerebral changes are the most obvious problems of hyponatremia. Behavioral changes result from cerebral edema and increased intracranial pressure. note patient’s behavior, level of consciousness, and cognition.
A sudden onset of acute confusion or increased confusion is often seen in older adults who have low serum sodium levels
When severe seizures coma or death may occur
Neuromuscular-muscle weakness -assess patients neuromuscular status each shift-DTR diminish, weakness worse in arms and legs
If muscle weakness is present, mimmediately check respiratory effectiveness because ventilation depends on adequate strength and function of respiratory muscles.
Intestinal changes-increased motility-nausea, diarrhea, abdominal cramping-assess for bowel sounds
Cardiovascular changes-seen as changes in cardiac output-
The cardiac responses to hyponatremia with hypovolemia (decreased plasma volume) include a rapid, weak, thready pulse.
Peripheral pulses difficult to palpate-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.
When hyponatremia occurs with hypervolemia (fluid overload), cardiac changes include a full or bounding pulse with normal or high blood pressure. Peripheral pulses are full and difficult to block; however, they may not be palpable if edema is present.

Can occur with fluid overload or fluid volume deficit

Question 36

When hyponatremia occurs with fluid deficit

Answer 36

Severe hyponatremia may be treated with small-volume infusions of hypertonic saline, most often 3% saline (Schreiber, 2013b), although 5% saline can be used for extreme hyponatremia.

Question 37

When hyponatremia occurs with fluid excess

Answer 37

drug therapy includes drugs that promote the excretion of water rather than sodium such as conivaptan (Vaprisol) or tolvaptan (Samsca)

Question 38

Drug therapy for hyponatremia caused by inappropriate secretion of antidiuretic hormone (ADH)

Answer 38

may include lithium (Carbolith, Lithane ) and demeclocycline (Declomycin). Assess hourly for signs of excessive fluid loss, potassium loss, and increased sodium levels.

Question 39

Mild cases

Answer 39

Nutrition- can help in mild cases-increasing oral sodium intake and restricting oral fluid intake.

Question 40

Hypernatremia

Answer 40

over 145 It can be caused by or can cause changes in fluid volume.

Common Causes of Hypernatremia
Actual Sodium Excesses
• Hyperaldosteronism
• Kidney failure
• Corticosteroids
• Cushing's syndrome or disease
• Excessive oral sodium ingestion
• Excessive administration of sodium-containing IV fluids
Relative Sodium Excesses
• Nothing by mouth
• Increased rate of metabolism
• Fever
• Hyperventilation
• Infection
• Excessive diaphoresis
• Watery diarrhea
• Dehydration

As serum sodium level rises, a larger difference in sodium levels occurs between the extracellular fluid (ECF) and the intracellular fluid (ICF). More sodium is present to move rapidly across cell membranes during depolarization, making excitable tissues more easily excited. This condition is called irritability, and excitable tissues over-respond to stimuli.
In addition, water moves from the cells into the ECF to dilute the hyperosmolar ECF. Thus, when serum sodium levels are high, severe cellular dehydration with cellular shrinkage occurs. Eventually the dehydrated excitable tissues may no longer be able to respond to stimuli.

Question 41

s/s of hypernatremia

Answer 41

Changes are first seen in excitable membrane activity, especially nerve, skeletal muscle, and cardiac function.

Agitated/confused-with normal or decreased fluid volume, when with fludi overload may be lethargic stuporous or comatose

mild rises-muscle twitching& irregular muscle contractions
as worsens
the muscles and nerves are less able to respond to a stimulus, and muscles become progressively weaker.
Late, the deep tendon reflexes are reduced or absent. Twitching in muscle groups. Assess strength.assess DTR

decreased contractility because high sodium levels slow the movement of calcium into the heart cells
Pulse rate is increased in patients with hypernatremia and hypovolemia. Peripheral pulses are difficult to palpate and are easily blocked. Hypotension and severe orthostatic (postural) hypotension are present, and pulse pressure is reduced
e slow-to-normal bounding pulses. Peripheral pulses are full and difficult to block. Neck veins are distended, even with the patient in the upright position. Blood pressure, especially diastolic blood pressure, is increased.

Question 42

Drug therapy for Hypernatremia

Answer 42

Drug therapy-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
Although the dextrose 5% in 0.45% sodium chloride is hypertonic in the IV bag, once it is infused, the glucose is rapidly metabolized, and the fluid is really hypotonic.

caused by reduced kidney sodium excretion requires drug therapy with diuretics that promote sodium loss such as furosemide (Lasix, Furoside ) or bumetanide (Bumex, Burinex ). Assess the patient hourly for symptoms of excessive losses of fluid, sodium, or potassium.

Question 43

Potassium

Answer 43

ICF-140
plasma-3.5-5
Keeping this large difference in potassium concentration between the ICF and the extracellular fluid (ECF) is critical for excitable tissues to depolarize and generate action potentials.

It is highest in meat, fish, and many (but not all) vegetables and fruits. It is lowest in eggs, bread, and cereal grains. Typical potassium intake is about 2 to 20 g/day.

main controller of ECF potassium level is the sodium-potassium pump within the membranes of all body cells. This pump 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. At the same time, this action also helps the serum sodium level remain high and the cellular sodium level remain low.
About 80% of potassium is removed from the body by the kidney. Kidney excretion of potassium is enhanced by aldosterone.

Question 44

Hypokalemia

Answer 44

minor changes in extracellular potassium levels cause major changes in cell membrane excitability. Hypokalemia is a serum potassium level below 3.5 mEq/L (mmol/L). It can be life threatening because every body system is affected.

reduce the excitability of cells. As a result, the cell membranes of all excitable tissues such as nerve and muscle are less responsive to normal stimuli.

Causes:
Actual Potassium Deficits
• Inappropriate or excessive use of drugs:
• Diuretics
• Digitalis-like drugs
• Corticosteroids
• Increased secretion of aldosterone
• Cushing's syndrome
• Diarrhea
• Vomiting
• Wound drainage (especially GI)
• Prolonged nasogastric suction
• Heat-induced excessive diaphoresis
• Kidney disease impairing reabsorption of potassium
• Nothing by mouth
Relative Potassium Deficits
• Alkalosis
• Hyperinsulinism
• Hyperalimentation
• Total parenteral nutrition
• Water intoxication
• IV therapy with potassium-poor solutions

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 concentrating ability decreases with aging, which increases potassium loss. Older adults are more likely to use drugs that lead to potassium loss.
Drugs, especially diuretics, corticosteroids, and beta-adrenergic agonists or antagonists, can increase potassium loss through the kidneys.

hypokalemia increases the sensitivity of the cardiac muscle to the drug and may result in digoxin toxicity, even when the digoxin level is within the therapeutic range

Respiratory changes occur because of respiratory muscle weakness, resulting in shallow respirations. Assess the patient’s breath sounds, ease of respiratory effort, color of nail beds and mucous membranes, and rate and depth
of respiration.

Musculoskeletal weakness- A stronger stimulus is needed to begin muscle contraction. Patients may be too weak to stand.
DTR reduced severe can casue flaccid paralysis
thready weak pulse
palpation difficultpulse easily blockedpulse rate can be very slow to very fast. irregular heartbeat -dysrhythmias m,ay occur,
Othostatic hypotension occurs
altered mental status-short term irritability and anxiety then lethargy then acute confusion and coma

Decreased peristalsis-hypoactive tones-nausea vomiting, constipation, abdominal distension
can cause absence of peristalsis-paralytic ileus

question drugs that
cause potssium loss (thiazide and loop diuretics)

max concentration IV 1mEq/10ml of solution infusion not faster than 5-10 meq of potassium, per hour assess IV site hourly

• 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.
• 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- additional potassium and drugs to prevent potassium loss-

A potassium-sparing diuretic may be prescribed to increase urine output without increasing potassium loss. Potassium-sparing diuretics include spironolactone (Aldactone, TEVA-spironolactone image), triamterene (Dyrenium, TEVA-triamterene image), and amiloride (Midamor, Novamilor image).

Evaluate arterial blood gas values (when available) for decreased blood oxygen levels (hypoxemia) and increased arterial carbon dioxide levels (hypercapnia), which indicate inadequate gas exchange.\

Question 45

To help prevent these infections(catheter related blood stream infection), CDC recommendations include:

Answer 45

• Perform evidence-based hand hygiene before palpating the insertion site.
• Clip hair—do not shave.
• Ensure that skin is clean. If visibly soiled, cleanse with soap and water.
• Wear clean gloves for peripheral IV insertion; do not touch the access site after application of antiseptics.
• Prepare clean skin with a skin antiseptic (chlorhexidine 2% with 70% alcohol, 70% isopropyl alcohol, or povidone-iodine) with a back-and-forth motion for 30 seconds and allow the solution to dry before peripheral venous catheter insertion.
• Do not retouch the proposed insertion site. If retouching occurs, prepare the skin antiseptic again and allow to dry.

Question 46

The two most important areas to monitor during rehydration

Answer 46

are pulse rate and quality and urine output.

Hypertonic solutions are used to correct altered FLUID AND ELECTROLYTE BALANCE and acid-base imbalances by moving water out of the body’s cells and into the bloodstream. Parenteral nutrition solutions are hypertonic.
hypotonic infusates move water into cells to expand them.

Question 47

Diuretics

Answer 47

How diuretics work: Most diuretics share the same basic mechanism of action: blockade of sodium and chloride reabsorption. By blocking the reabsorption of these prominent solutes, diuretics create osmotic pressure within the nephron that prevents the passive reabsorption of water. Hence, diuretics cause water and solutes to be retained within the nephron and thereby promote the excretion of both.

Question 48

Diuretics

Answer 48

How diuretics work: Most diuretics share the same basic mechanism of action: blockade of sodium and chloride reabsorption. By blocking the reabsorption of these prominent solutes, diuretics create osmotic pressure within the nephron that prevents the passive reabsorption of water. Hence, diuretics cause water and solutes to be retained within the nephron and thereby promote the excretion of both.

The increase in urine flow that a diuretic produces is directly related to the amount of sodium and chloride reabsorption that it blocks.
drugs that act early in the nephron have the opportunity to block the greatest amount of solute reabsorption. As a result, these agents produce the greatest diuresis.

Question 49

Adverse effects of diuretics

Answer 49

Adverse effects: can cause hypovolemia (from excessive fluid loss), acid-base imbalance, and altered electrolyte levels.
***These adverse effects can be minimized by using short-acting diuretics and by timing drug administration such that the kidney is allowed to operate in a drug-free manner between periods of diuresis. Both measures will give the kidney periodic opportunities to readjust the ECF so as to compensate for any undesired alterations produced under the influence of diuretics.

Question 50

Loop Diuretics:

Furosemide

Answer 50

These drugs produce more loss of fluid and electrolytes than any other diuretics. They are known as loop diuretics because their site of action is in the loop of Henle.

Furosemide – thick segment of the ascending limb of Henle’s loop to block reabsorption of sodium and chloride–produce excessive loss-can result in dehydration-thrombosis embolism hypotension–uses for this drug–(1) pulmonary edema associated with congestive heart failure (CHF); (2) edema of hepatic, cardiac, or renal origin that has been unresponsive to less efficacious diuretics; and (3) hypertension that cannot be controlled with other diuretics.
Very useful in patients with severe renal impairment-can promote diuresis even when renal blood flow and glomerular filtration rate (GFR) are low

can produce excessive loss of sodium, chloride, and water.

Furosemide increases urinary excretion of magnesium, posing a risk of magnesium deficiency. Symptoms include muscle weakness, tremor, twitching, and dysrhythmias.

Furosemide increases urinary excretion of calcium. This action has been exploited to treat hypercalcemia.

Furosemide reduces high-density lipoprotein (HDL) cholesterol and raises low-density lipoprotein (LDL) cholesterol and triglycerides.

monitor-for dehydration-hypotension-hypokalemia-minimize by consuming potassium-rich foods (e.g., dried fruits, nuts, spinach, potatoes, bananas), taking potassium supplements, or using a potassium-sparing diuretic.
be careful with diabetics
Monitor for drsrhhythmias in older patients

not for pregnant women- breastfeeding unclear

Hypokalemia.Potassium is lost through increased secretion in the distal nephron. If serum potassium falls below 3.5 mEq/L, fatal dysrhythmias may result.
Ototoxicity.- Rarely, loop diuretics cause hearing impairment.
Hyperglycemia- Elevation of plasma glucose is a potential, albeit uncommon, complication of furosemide therapy.
Hyperuricemia- Elevation of plasma uric acid is a frequent side effect of treatment. patients predisposed to gout, elevation of uric acid may precipitate a gouty attack

Question 51

Thiazide diuretics

Answer 51

, thiazides increase renal excretion of sodium, chloride, potassium, and water. In addition, thiazides elevate plasma levels of uric acid and glucose. The principal difference between the thiazides and loop diuretics is that the maximum diuresis produced by the thiazides is considerably lower than the maximum diuresis produced by the loop diuretics. In addition, whereas loop diuretics can be effective even when urine flow is decreased, thiazides cannot.

Hydrochlorothiazide promotes urine production by blocking the reabsorption of sodium and chloride in the early segment of the distal convoluted tubule
The primary indication for hydrochlorothiazide is hypertension

Thiazides are preferred drugs for mobilizing edema associated with mild to moderate heart failure.

Thiazides promote tubular reabsorption of calcium and may thereby decrease the risk of osteoporosis in postmenopausal women. thiazides promote renal calcium retention, they may counteract the calcium loss associated with menopause and may thereby help preserve bone integrity.

Question 52

Thiazides adverse effects

Answer 52

Thiazides increase excretion of magnesium, sometimes causing magnesium deficiency. Symptoms include muscle weakness, tremor, twitching, and dysrhythmias.
Loss of sodium, chloride, and water can lead to hyponatremia, hypochloremia, and dehydration.
Hypokalemia- thiazides can cause hypokalemia from excessive potassium excretion.
Hyperglycemia-thiazides can elevate plasma levels of glucose. Significant hyperglycemia develops only in diabetic patients, who should be especially diligent about monitoring blood glucose.
Hyperuricemia-The thiazides, like the loop diuretics, can cause retention of uric acid, thereby elevating plasma uric acid.
Thiazides can increase levels of LDL cholesterol, total cholesterol, and triglycerides.

Question 53

Spironolactone [Aldactone] -Potassium-Sparing Diuretics

Answer 53

blocks the actions of aldosterone in the distal nephron. Since aldosterone acts to promote sodium uptake in exchange for potassium secretion, inhibition of aldosterone has the opposite effect: retention of potassium and increased excretion of sodium

Hypertension and edema- used most commonly in combination with a thiazide or loop diuretic.
In patients with severe heart failure, spironolactone reduces mortality and hospital admissions.
spironolactone can be used for primary hyperaldosteronism, premenstrual syndrome , polycystic ovary syndrome, and acne in young women.

Question 54

spir. adverse effects

Answer 54

can cause a variety of endocrine effects, including gynecomastia, menstrual irregularities, impotence, hirsutism, and deepening of the voice.
The potassium-sparing effects of spironolactone can result in hyperkalemia, a condition that can produce fatal dysrhythmias- monitor heart.
If serum potassium rises above 5 mEq/L or if signs of hyperkalemia develop (e.g., abnormal heart rhythm), spironolactone should be discontinued and potassium intake restricted. Injection of insulin can help lower potassium levels by promoting potassium uptake into cells.
When given long term to rats in doses 25 to 250 times those used in humans, spironolactone has caused benign adenomas of the thyroid and testes, malignant mammary tumors, and proliferative changes in the liver.
To promote safe administration, NIOSH suggests donning a protective gown and two sets of gloves when cutting or crushing tablets.

Question 55

Hyperkalemia

Answer 55

over 5
Even small increases above normal values can affect excitable tissues, especially the heart.
A high serum potassium increases cell excitability, causing excitable tissues to respond to less intense stimuli. The heart is very sensitive to serum potassium increases; and hyperkalemia interferes with electrical conduction, leading to heart block and ventricular fibrillation.
rare in people with normal kidney function
Most cases of hyperkalemia occur in hospitalized patients and in those undergoing medical treatment). Those at greatest risk are chronically ill patients, debilitated patients, and older adults

Question 56

Common Causes of Hyperkalemia

Answer 56

• Overingestion of potassium-containing foods or medications:
• Salt substitutes
• Potassium chloride
• Rapid infusion of potassium-containing IV solution
• Bolus IV potassium injections
• Transfusions of whole blood or packed cells
• Adrenal insufficiency
• Kidney failure
• Potassium-sparing diuretics
• Angiotensin-converting enzyme inhibitors (ACEIs)
Relative Potassium Excesses
• Tissue damage
• Acidosis
• Hyperuricemia
• Uncontrolled diabetes mellitus
Age is important because kidney function decreases with aging. Ask about kidney disease; diabetes mellitus; recent medical or surgical treatment; and urine output, including frequency and amount of voidings. Ask about drug use, particularly potassium-sparing diuretics and angiotensin-converting enzyme inhibitors (ACEIs. Obtain nutrition history to determine the intake of potassium-rich foods and the use of salt substitutes (which contain potassium).

Question 57

Changes in hyperkalemia

Answer 57

Assess for-palpatations, skipped heartbeats, other cardiac irregularities. Muscle twitching, leg weakness, tingling numbness in hands feet face. Bowel changes/diarrhea

Cardivascular-Cardiovascular changes are the most severe problems from hyperkalemia and are the most common cause of death in patients with hyperkalemia. Cardiac symptoms include bradycardia; hypotension;
Ectopic beats may appear. Complete heart block, asystole, and ventricular fibrillation are life-threatening complications of severe hyperkalemia.

Neuromuscular changes with hyperkalemia have two phases. Skeletal muscles twitch in the early stages of hyperkalemia, and the patient may be aware of tingling and burning sensations followed by numbness in the hands and feet and around the mouth (paresthesia).

As hyperkalemia worsens, muscle weakness occurs, followed by flaccid paralysis.
The weakness moves up from the hands and feet and first affects the muscles of the arms and legs. Respiratory muscles are not affected until serum potassium levels reach lethal levels.

Intestinal changes include increased motility with diarrhea and hyperactive bowel sounds. Bowel movements are frequent and watery.

If it is caused by dehydration, levels of other electrolytes, hematocrit, and hemoglobin also are elevated. Hyperkalemia caused by kidney failure occurs with elevated serum creatinine and blood urea nitrogen, decreased blood pH, and normal or low hematocrit and hemoglobin levels.

Question 58

Hyperkalemia treatment

Answer 58

Drug therapy can restore potassium balance by enhancing potassium excretion and promoting the movement of potassium from the extracellular fluid (ECF) into the cells. A newly approved drug to treat hyperkalemia is patiromer (Veltassa). This oral drug binds with potassium in the GI tract and decreases its absorption

Potassium-excreting diuretics are prescribed. When kidney problems exist, more in vasive interventions may be needed
Movement of potassium from the extracellular fluid (ECF) to the intracellular fluid (ICF) can help reduce serum potassium levels temporarily. Potassium movement into the cells is enhanced by insulin. Insulin increases the activity of the sodium-potassium pumps, which move potassium from the ECF into the cell. IV fluids containing glucose and insulin are prescribed to help decrease serum potassium levels (usually 100 mL of 10% to 20% glucose with 10 to 20 units of regular insulin). These IV solutions are hypertonic and are infused through a central line or in a vein with a high blood flow to avoid local vein inflammation. Observe the patient for indications of hypokalemia and hypoglycemia during this therapy.

Cardiac monitoring allows for the early recognition of dysrhythmias and other symptoms of hyperkalemia on cardiac muscle. Compare recent ECG tracings with the tracings obtained when the patient’s serum potassium level was close to normal.
Critical rescue-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.

Question 59

Nutrition for hyperkalemia

Answer 59

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

Question 60

Calcium

Answer 60

This mineral is important for maintaining bone strength and density, activating enzymes, allowing skeletal and cardiac muscle contraction, controlling nerve impulse transmission, and allowing blood clotting.

Bound calcium is usually attached to serum proteins, especially albumin. Ionized calcium is present in the blood and other extracellular fluid (ECF) as free calcium. Free calcium is the active form and must be kept within a narrow range in the ECF
Calcium has a steep gradient between ECF and intracellular fluid (ICF) because the amount of calcium in the ICF is very low

When more calcium is needed, parathyroid hormone (PTH) is released from the parathyroid glands. 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
When excess calcium is present in plasma, PTH secretion is inhibited, and the secretion of thyrocalcitonin (TCT), a hormone secreted by the thyroid gland, is increased. TCT causes the plasma calcium level to decrease by inhibiting bone resorption of calcium, inhibiting vitamin D–associated intestinal uptake of calcium, and increasing kidney excretion of calcium in the urine.

Question 61

Hypocalcemia

Answer 61

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.
Calcium is an excitable membrane stabilizer, regulating depolarization and the generation of action potentials. It decreases sodium movement across excitable membranes, slowing the rate of depolarization. Low serum calcium levels increase sodium movement across excitable membranes, allowing depolarization to occur more easily and at inappropriate times.

Question 62

Causes of hypocalcemia

Answer 62

Hypocalcemia is caused by many chronic and acute conditions, as well as medical or surgical treatments. 
Acute hypocalcemia results in the rapid onset of life-threatening symptoms. 
Chronic hypocalcemia occurs slowly over time, and excitable membrane symptoms may not be severe because the body has adjusted to the gradual reduction of serum calcium levels.
Common Causes of Hypocalcemia
Actual Calcium Deficits
• Inadequate oral intake of calcium
• Lactose intolerance
• Malabsorption syndromes:
• Celiac sprue
• Crohn's disease
• Inadequate intake of vitamin D
• End-stage kidney disease
• Diarrhea
• Steatorrhea
• Wound drainage (especially GI)

Relative Calcium Deficits
• Hyperproteinemia
• Alkalosis
• Calcium chelators or binders
• Citrate
• Mithramycin
• Penicillamine
• Sodium cellulose phosphate (Calcibind)
• Aredia
• Acute pancreatitis
• Hyperphosphatemia
• Immobility
• Removal or destruction of parathyroid glands

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.

Question 63

S/S hypocalcemia

Answer 63

frequent painful muscle spasms
(most s/s caused by overstimulation of nerves and muscles
Paresthesias occur at first, with sensations of tingling and numbness. If hypocalcemia continues or worsens, muscle twitching or painful cramps and spasms occur. Tingling may also affect the lips, nose, and ears. These problems may signal the onset of neuromuscular overstimulation and tetany.

Assess for hypocalcemia by testing for Trousseau’s and Chvostek’s signs. To test for Trousseau’s sign, place a blood pressure cuff around the arm, inflate the cuff to greater than the patient’s systolic pressure, and keep the cuff inflated for 1 to 4 minutes. Under these hypoxic conditions, a positive Trousseau’s sign occurs when the hand and fingers go into spasm in palmar flexion (Fig. 11-13).
To test for Chvostek’s sign, tap the face just below and in front of the ear to trigger facial twitching of one side of the mouth, nose, and cheek .

The heart rate may be slower or slightly faster than normal, with a weak, thready pulse. Severe hypocalcemia causes severe hypotension

Intestinal changes include increased peristaltic activity. Assess the abdomen for hyperactive bowel sounds. The patient may report painful abdominal cramping and diarrhea.
Skeletal changes are common with chronic hypocalcemia. Calcium leaves bone storage sites, causing a loss of bone density (osteoporosis). The 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.

Question 64

Treatment for hypocalcemia

Answer 64

focus on restoring normal calcium levels and preventing complications. These include drug therapy, nutrition therapy, reducing environmental stimuli, and preventing injury. Patient safety during restoration of serum calcium levels is a nursing care priority.
DSrug therapy direct calcium replacement (oral and IV) and drugs that enhance the absorption of calcium such as vitamin D. When neuromuscular symptoms are troublesome, drugs that decrease nerve and muscle responses also may be used.
Nutrition therapy involves a calcium-rich diet for patients with mild hypocalcemia and for those who are at continuing risk for hypocalcemia. Collaborate with the dietitian to help the patient select calcium-rich foods.
Environmental management for safety is needed because the excitable membranes of the nervous system and the skeletal system are overstimulated in hypocalcemia. Reduce stimulation by keeping the room quiet, limiting visitors, adjusting the lighting, and using a soft voice.
Injury prevention strategies are needed because the patient with long-standing calcium loss may have brittle, fragile bones that fracture easily and cause little pain.

Question 65

Hypercalcemia

Answer 65

above 10.5 mg/dL or 2.62 mmol/L. Even small increases above normal have severe effects, and all systems are affected. Hypercalcemia causes excitable tissues to be less sensitive to normal stimuli, thus requiring a stronger stimulus to function. The excitable tissues affected most by hypercalcemia are the heart, skeletal muscles, nerves, and intestinal smooth muscles.

Common Causes of Hypercalcemia
Actual Calcium Excesses
• Excessive oral intake of calcium
• Excessive oral intake of vitamin D
• Kidney failure
• Use of thiazide diuretics
Relative Calcium Excesses
• Hyperparathyroidism
• Malignancy
• Hyperthyroidism
• Immobility
• Use of glucocorticoids
• Dehydration

mild but rapidly occurring calcium excess often has more severe problems than the patient whose imbalance is severe but has developed slowly.
Cardiovascular changes are the most serious and life-threatening problems of hypercalcemia. Mild hypercalcemia at first causes increased heart rate and blood pressure. Severe or prolonged calcium imbalance depresses electrical conduction, slowing heart rate.

Hypercalcemia allows blood clots to form more easily whenever blood flow is poor. Blood clotting is more likely in the lower legs, the pelvic region, areas where blood flow is blocked by internal or external constrictions, and areas where venous obstruction occurs.

Neuromuscular changes include severe muscle weakness and decreased deep tendon reflexes without paresthesia. The patient may be confused and lethargic.
Intestinal changes are first reflected as decreased peristalsis. Constipation, anorexia, nausea, vomiting, abdominal distention, and pain are common. Bowel sounds are hypoactive or absent.

Question 66

Treating hypercalcemia

Answer 66

Drug therapy involves preventing increases in calcium and drugs to lower calcium levels. IV solutions containing calcium (e.g., Ringer’s lactate) are stopped. Oral drugs containing calcium or vitamin D (e.g., calcium-based antacids) are discontinued.
Fluid volume replacement can help restore normal serum calcium levels. IV normal saline (0.9% sodium chloride) is usually given because sodium increases kidney excretion of calcium.
Thiazide diuretics are discontinued and replaced with diuretics that enhance the excretion of calcium such as furosemide (Lasix, Furoside
Calcium chelators (calcium binders) help lower serum calcium levels. Such drugs include plicamycin (Mithracin) and penicillamine (Cuprimine).
Drugs to prevent hypercalcemia include agents that inhibit calcium resorption from bone such as phosphorus, calcitonin (Calcimar), bisphosphonates (etidronate [Didronel, Etidro­ca
NOVO-etidronatecal ]), and prostaglandin synthesis inhibitors (aspirin, NSAIDs).
Cardiac monitoring of patients with hypercalcemia is needed to identify dysrhythmias and decreased cardiac output. Compare recent ECG tracings with the patient’s baseline tracings. Especially look for changes in the T waves and the QT interval and changes in rate and rhythm.

Question 67

Magnesium

Answer 67

cation mostly stored in bones and cartilage. Little magnesium is present in the blood (see Table 11-1). The intracellular fluid (ICF) has more magnesium, and it has more functions inside the cells than in the blood. It is 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. It is most often caused by decreased absorption of dietary magnesium or increased kidney magnesium excretion. Two major causes of hypomagnesemia are inadequate intake and the use of loop or thiazide diuretics.

Common Causes of Magnesium Imbalance
Hypomagnesemia
• Malnutrition
• Starvation
• Diarrhea
• Steatorrhea
• Celiac disease
• Crohn's disease
• Drugs (diuretics, aminoglycoside antibiotics, cisplatin, amphotericin B, cyclosporine)
• Citrate (blood products)
• Ethanol ingestion

Hypermagnesemia
• Increased magnesium intake:
• Magnesium-containing antacids and laxatives
• IV magnesium replacement
• Decreased kidney excretion of magnesium resulting from kidney disease

Question 68

Hypomagnesiumia

Answer 68

The effects of hypomagnesemia are caused by increased membrane excitability and the accompanying serum calcium and potassium imbalances. Excitable membranes, especially nerve cell membranes, may depolarize spontaneously.
Cardiovascular changes associated with hypomagnesemia are serious. Low magnesium levels increase the risk for hypertension, atherosclerosis, hypertrophic left ventricle, and a variety of dysrhythmias

, when serum magnesium levels are low, intracellular potassium levels are also low. This changes the resting membrane potential in cardiac muscle cells, slowing normal conduction and triggering ectopic beats. Low magnesium levels also are associated with greater cardiac muscle cell damage after myocardial infarction.
Neuromuscular changes are caused by increased nerve impulse transmission. Normally magnesium inhibits nerve impulse transmission at synapse areas. Decreased levels 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. Positive Chvostek’s and Trousseau’s signs may be present because hypomagnesemia may occur with hypocalcemia .The patient may have tetany and seizures as hypomagnesemia worsens.
Intestinal changes are from decreased intestinal smooth muscle contraction. Reduced motility, anorexia, nausea, constipation, and abdominal distention are common. A paralytic ileus may occur when hypomagnesemia is severe.

Question 69

Treating hypomagnesimia

Answer 69

Interventions for hypomagnesemia aim to correct the imbalance and manage the specific problem that caused it. In addition, because hypocalcemia often occurs with hypomagnesemia, interventions also aim to restore normal serum calcium levels.
Drugs that promote magnesium loss such as high-ceiling (loop) diuretics, osmotic diuretics, aminoglycoside antibiotics, and drugs containing phosphorus are discontinued. Magnesium is replaced intravenously with magnesium sulfate (MgSO4) when hypomagnesemia is severe. Assess deep tendon reflexes at least hourly in the patient receiving IV magnesium to monitor effectiveness and prevent hypermagnesemia. If hypocalcemia is also present, drug therapy to increase serum calcium levels is prescribed.

Question 70

Hypermagnesemia

Answer 70

level above 2.6 mEq/L or 1.07 mmol/L.
Magnesium is a membrane stabilizer. Most symptoms of hypermagnesemia occur as a result of reduced membrane excitability. They usually are not apparent until serum magnesium levels exceed 4 mEq/L (1.6 mmol/L).

Cardiac changes include bradycardia, peripheral vasodilation, and hypotension.
ECG changes show a prolonged PR interval with a widened QRS complex. Bradycardia can be severe, and cardiac arrest is possible. Hypotension is also severe, with a diastolic pressure lower than normal. Patients with severe hypermagnesemia are in grave danger of cardiac arrest.
Central nervous system changes result from depressed nerve impulse transmission. Patients may be drowsy or lethargic. Coma may occur if the imbalance is prolonged or severe.
Neuromuscular changes include reduced or absent deep tendon reflexes. Voluntary skeletal muscle contractions become progressively weaker and finally stop.
Hypermagnesemia has no direct effect on the lungs; however, when the 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. All oral and parenteral magnesium is discontinued. When kidney failure is not present, giving magnesium-free IV fluids can reduce serum magnesium levels. High-ceiling (loop) diuretics such as furosemide (Lasix, Furoside ) can further reduce serum magnesium levels. When cardiac problems are severe, giving calcium may reverse the cardiac effects of hypermagnesemia.