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FCC fluids and Electrolytes from Shenell D.

FCC fluids and Electrolytes from Shenell D.

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  • Ca +2 does not require B12 for absorption as stated ibn this slide. Calcium request Vitamin D not B12.
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  • nice presentation. Please send me a copy to my email drcclwin@gmail.com. Thanks a lot. Best wishes.
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  • WOW THIS IS so enlightening pls can you email this to me brisibeseri@yahoo.com
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  • Hello Maam Shenell. Very nice presentation... Please send me a copy of this to my email malunapone@yahoo.com. It will help me a lot in my lecture. Thanks a lot. Regards and God bless...
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  • Dear Madame, your slide is very nice & informative, could you send me a copy to my email please? my email is lfitri@yahoo.com. Thank you.
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Fluidsandelectrolytes Fluidsandelectrolytes Presentation Transcript

  • FLUIDS AND ELECTROLYTES
  • OBJECTIVES
    • After this lecture/discussion, the learner should be able to:
    • 1. Describe the mechanisms that maintain fluid, electrolyte and acid-base balance.
    • 2. Compare the mechanisms and effects of fluid deficit and excess.
    • 3. Discuss the mechanisms and effects of deficits and excess.
    • 4. Describe the mechanisms that maintain acid-base balance.
    • 5. Differentiate between metabolic and respiratory acidosis and alkalosis.
    • 6. Apply the pathophysiologic principles of acid-base balance to the interpretation of ABG measurements.
    • 7. Analyze the components of ABGs to identify the type of acid-base balance.
    • 8. Describe the causes and effects of each type of acid-base balance.
    • 9. Use ABG findings in formulating the care of the patient with an acid-base imbalance.
    • 10. Describe the management of patients with a fluid, electrolyte, or acid-base imbalance.
    • HOW IMPORTANT IS WATER?
    • Between 50% and 60% of the human body by weight is water
    • Water provides a medium for transporting nutrients to cells and wastes from cells and for transporting substances such as hormones, enzymes, blood platelets, and red and white blood cells
    • Water facilitates cellular metabolism and proper cellular chemical functioning
    • Water acts as a solvent for electrolytes and nonelectrolytes
    • Helps maintain normal body temperature
    • Facilitates digestion and promotes elimination
    • Acts as a tissue lubricant
  • VARIATIONS IN FLUID CONTENT BODY FAT Because fat cells contain little water and lean tissue is rich in water, the more obese the person, the smaller the percentage of total body water compared with body weight. This is also true between sexes because females tend to have proportionally more body fat than males. There is also an increase in fat cells in older people
  • VARIATIONS IN FLUID CONTENT AGE 77% Infants 60% Adult Male 50% Adult Female 45% Elderly
  •  
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  • AVENUES BY WHICH WATER ENTERS AND LEAVES THE BODY
  • ANTIDIURETIC HORMONE REGULATION MECHANISMS ↓ Blood volume or ↓BP Volume receptor Atria and great veins Hypothalamus ↓ Posterior pituitary gland Osmoreceptors in hypothalamus ↑ Osmolarity ↑ ADH Kidney tubules ↑ H2O reabsorption ↑ vascular volume and ↓osmolarity Narcotics, Stress, Anesthetic agents, Heat, Nicotine, Antineoplastic agents, Surgery
  • ALDOSTERONE-RENIN-ANGIOTENSIN SYSTEM Juxtaglomerular cells-kidney ↓Serum Sodium ↓Blood volume Angiotensin I Kidney tubules Angiotensin II Adrenal Cortex ↑ Sodium resorption (H2O resorbed with sodium); ↑ Blood volume Angiotensinogen in plasma RENIN Angiotensin-converting enzyme ALDOSTERONE Intestine, sweat glands, Salivary glands Via vasoconstriction of arterial smooth muscle
  • FLUID BALANCE
    • The desirable amount of fluid intake and loss in adults ranges from 1500 to 3500 mL each 24 hours. Ave= 2500 mL
    • Normally INTAKE = OUTPUT
    FLUID IMBALANCE
    • Changes in ECF volume = alterations in sodium balance
    • Change in sodium/water ratio = either hypoosmolarity or hyperosmolarity
    • Fluid excess or deficit = loss of fluid balance
    • As with all clinical problems, the same pathophysiologic change is not of equal significance to all people
    • For example, consider two persons who have the same viral syndrome with associated nausea and vomiting
    ECF Volume Depletion No Significant E+ disturbances Man with renal failure Life threatening E+ disturbances
  • FLUID DEFICIT/HYPOVOLEMIA
    • May occur as a result of:
      • Reduced fluid intake
      • Loss of body fluids
      • Sequestration (compartmentalizing) of body fluids
    Pathophysiology and Clinical Manifestations DECREASED FLUID VOLUME Stimulation of thirst center in hypothalamus Person complains of thirst ↑ ADH Secretion ↑ Water resorption ↓ Urine Output Renin-Angiotensin-Aldosterone System Activation ↑ Sodium and Water Resorption ↑ Urine specific gravity except with osmotic diuresis
  • Pathophysiology and Clinical Manifestations UNTREATED FLUID VOLUME DEFICIT Depletion of fluids available ↑ BODY TEMPERATURE Dry mucous membranes Difficulty with speech Cells become unable to continue providing water to replace ECF losses Signs of circulatory collapse ↓ blood pressure ↑ heart rate ↑ respiratory rate Restlessness and Apprehension
  • Collaborative Care Management Identification of vulnerable patients and risk factors: * Compromised mental state * Physical limitations * Disease states * Limited access to adequate food and fluids Development of a plan of care Family members should be educated about the importance of fluid and nutrition intake Collaboration with the nurse, patient, family members, and other health care providers for continued assessment and treatment of problems Ongoing assessment and detailed action plan of fluid and serum electrolyte balance. Factors such as medications (particularly diuretics), hyperventilation, fever, burns, diarrhea, and diabetes with appropriate referral
  • Collaborative Care Key Points
    • 1 Liter of water = 1 kg of water by weight
    • Fluid replacement are calculated according to this ratio plus 1.5 L to fulfill the current daily needs
    • For example, JUAN, a one-year-old, lost 1 kg of water from diarrhea as weighed from his diaper over the last 24 hours. Therefore, since 1 kg=1 L, fluid replacement therapy for him will involve 1 L of fluids + 1500 L.
    • Oral fluid resuscitation is preferable but if the patient is unable to tolerate fluids, IV Therapy may be ordered
    • Vital signs should be assessed regularly
    • Postural hypotension is common for postural persons with fluid volume deficit. How do we assess this?
    • For example, in the care of LOIDA, a 31 year old with severe DHN, you take her blood pressure (130/80) and pulse (75) while she’s lying down. Then you ask her to sit at the edge of bed. When you take her blood pressure again, you get 115/80 and when you take her pulse, you get 80. This is consistent with intravascular volume depletion.
    • Daily weighing is also useful to monitor fluid and electrolyte balance
    • Laboratory results should be reviewed for various fluid and electrolyte disturbances so that appropriate adjustments to therapy can be initiated
  • FLUID EXCESS/HYPERVOLEMIA Psychiatric Disorders, SIADH, Certain head injuries Dietary Sodium Indiscretion Renal and endocrine disturbances, malignancies, adenomas Overhydration Excessive Sodium Intake Failure of renal or hormonal regulatory functions FLUID VOLUME EXCESS/HYPERVOLEMIA Sodium Normal Extracellular fluid Normal sodium concentration ADH Renal Tubules ADH ADH ADH ADH ADH Extracellular volume expands Fluid becomes progressively hyponatremic
    • Since ECF becomes hypoosmolar, fluid moves into the cells to equalize the concentration on both sides of the cell membrane
    • Thus there, is an increase in intracellular fluid
    • The brain cells are particularly sensitive to the increase of intracellular water, the most common signs of hypoosmolar overhydration are changes in mental status. Confusion, ataxia, and convulsions may also occur.
    • Other clinical manifestations include: hyperventilation, sudden weight gain, warm, moist skin, increased ICP: slow bounding pulse with an increase in systolic and decrease in diastolic pressue and peripheral edema, usually not marked
  •  
  • WHAT DO ELECTROLYTES DO? Promote neuromuscular irritability Maintain body fluid volume and osmolarity Distribute body water between fluid compartments Regulate acid-base balance
  • Sodium (Na+)
    • Controls and regulates volume of body fluids
    • Its concentration is the major determinant of ECF volume
    • Is the chief electrolyte of ECF
    • Influence ICF Volume
    • Participates in the generation and transmission of nerve impulses
    • Is an essential electrolyte in the sodium-potassium pump
    • RDA: not known precisely. 500 mg
    • Eliminated primarily by the kidneys, smaller in feces and perspiration
    • Salt intake affects sodium concentrations
    • Sodium is conserved through reabsorption in the kidneys, a process stimulated by aldosterone
    • Normal value: 135-145 mEq/L
  • HYPONATREMIA
    • Refers to the serum sodium concentration less than 135 mEq/L
    • Common with thiazide diuretic use, but may also be seen with loop and potassium-sparing diuretics as well
    • Occurs with marked sodium restriction, vomiting and diarrhea, SIADH, etc. The etiology may be mulfactorial
    • May also occur postop due to temporary alteration in hypothalamic function, loss of GI fluids by vomiting or suction, or hydration with nonelectrolyte solutions
    • Postoperative hyponatremia is a more serious complication in premenopausal women. The reasons behind this is unknown
    • Therefore monitoring serum levels is critical and careful assessment for symptoms of hyponatremia is important for all postoperative patients
  • PATHOPHYSIOLOGY OF HYPONATREMIA
    • Sodium loss from the intravascular compartment
    Diffusion of water into the interstitial spaces Sodium in the interstitial space is diluted Decreased osmolarity of ECF Water moves into the cell as a result of sodium loss Water moves into the cell as a result of sodium loss Extracellular compartment is depleted of water CLINICAL SYMPTOMS
  • CLINICAL MANIFESTATIONS OF HYPONATREMIA Muscle Weakness APATHY Postural hypotension Nausea and Abdominal Cramps Weight Loss In severe hyponatremia: mental confusion, delirium, shock and coma
  • COLLABORATIVE CARE MANAGEMENT
    • General goal: correct sodium imbalance and restore normal fluid and electrolyte homeostasis
    • Recognition of people at risk for hyponatremia is essential for its prevention: athletes, persons working in hot environments
    • Salt is always replaced along with water
    • Management includes educating vulnerable people to recognize signs and symptoms of sodium depletion and maintaining sufficient sodium and water intake to replace skin and insensible fluid loss
    • Generally, an increased sodium and water intake provides adequate treatment
    • Education as the importance of sodium and fluid balance and the rationale for prescription medications to ensure compliance
    • Daily weight. MIO
    • Monitoring of sodium levels to determine extent of replacement
    • Generally, PNSS or PLRS is prescribed
    • Too rapid restoration of sodium balance, hypertonic sodium solutions may provoke brain injury
  • HYPERNATREMIA
    • A serum sodium level above 145 mEq/L is termed hypernatremia
    • May occur as a result of fluid deficit or sodium excess
    • Frequently occurs with fluid imbalance
    • Develops when an excess of sodium occurs without a proportional increase in body fluid or when water loss occurs without proportional loss of sodium
    • Risk Factors: excess dietary or parenteral sodium intake, watery diarrhea, diabetes insipidus, damage to thirst center, too young, too old, those with physical or mental status compromise, and people with hypothalamic dysfunction
  • PATHOPHYSIOLOGY OF HYPERNATREMIA
    • Increased Sodium concentration in ECF
    Osmolarity rises Water leaves the cell by osmosis and enters the the extracellular compartments Dilution of fluids in ECF Cells are water depleted Suppression of aldosterone secretion Sodium is exreted in the urine CLINICAL SYMPTOMS
  • CLINICAL MANIFESTATIONS Dry, sticky mucous membranes Firm, rubbery tissue turgor Manic excitement Tachycardia DEATH
  • COLLABORATIVE CARE MANAGEMENT
    • Recognition of risk factors: bedridden and debilitated patients, diabetes insipidus, fluid deprivation, the elderly and the very young
    • A careful and accurate record of MIO permits quick recognition of negative fluid balance
    • People with kidney failure, CHF, or increased aldosterone production may require dietary sodium intake restriction
    • Usually, osmolar balance can be restored with oral fluids. If not, the parenteral route may be necessary
    • Fluid resuscitation must be undertaken with particular caution in patients with compromised cardiac or renal function
    • The nurse should closely monitor the patient’s response to fluids and be alert to symptoms of fluid overload
  • Potassium (K+)
    • Major cation of the ICF. Chief regulator of cellular enzyme activity and cellular water content
    • The more K, the less Na. The less K, the more Na
    • Plays a vital role in such processes such as transmission of electrical impulses, particularly in nerve, heart, skeletal, intestinal and lung tissue; CHON and CHO metabolism; and cellular building; and maintenance of cellular metabolism and excitation
    • Assists in regulation of acid-base balance by cellular exchange with H
    • RDA: not known precisely. 50-100 mEq
    • Sources: bananas, peaches, kiwi, figs, dates, apricots, oranges, prunes, melons, raisins, broccoli, and potatoes, meat, dairy products
    • Excreted primarily by the kidneys. No effective conserving mechanism
    • Conserved by sodium pump and kidneys when levels are low
    • Aldosterone triggers K excretion in urine
    • Normal value: 3.5 – 5 mEq/L
  • CAUSES AND EFFECTS OF HYPOKALEMIA
    • Known as a low level of serum potassium, less than 3.5 mEq/L
    Decreased Intake ↓ Food and Fluids as in starvation Failure to replace GI losses Increased Loss ↑ Aldosterone Gastrointestinal losses Potassium-losing diuretics Loss from cells as in trauma, burns Shift of Potassium into Cells (No change in total body potassium) HYPOKALEMIA GI Tract Anorexia N&V Abdominal distention CNS Lethargy, Diminished deep-tendon reflexes, Confusion, Mental depression Muscles Weakness, Flaccid paralysis, Weakness of respiratory muscles, Respiratory arrest CV System Decrease in standing BP, Dysrhythmias, ECG changes, Myocardial damage, Cardiac arrest Kidneys ↓ Capacity to concentrate waste, water loss, thirst, kidney damage
  • PATHOPHYSIOLOGY OF HYPOKALEMIA = Action Potential Nerve and Muscle Activity Low Extracellular K+ Increase in resting membrane potential The cell becomes less excitable
  • Sodium is retained in the body through resorption by the kidney tubules Potassium is excreted Aldosterone is secreted Use of certain diuretics such as thiazides and furosemide, and corticosteroids Increased urinary output Loss of potassium in urine
  • COLLABORATIVE CARE MANAGEMENT
    • Being alert to the conditions that cause potassium depletion such as vomiting, diarrhea and diuretics, by monitoring the patient for early warning signs
    • No more than 3 enemas without consulting a physician
    • Education about the importance of adequate dietary intake of potassium
    • In severe hypokalemia, a patient may die unless potassium is administered promptly
    • The safest way to administer K is orally. When K is given IV, the rate of flow must be monitored closely and should be diluted. Should not exceed 20 mEq/hr
    • If PO, taken with at least ½ glass of water
    • Cardiac monitoring is useful
    • Potassium sparing diuretics such as triamterene, spironolactone, etc
    • Symptoms of K depletion: muscle weakness, anorexia, nausea and vomiting = appropriate referral
    • Serum potassium level greater than 5.5 mEq/L
    CAUSES AND EFFECTS OF HYPERKALEMIA Excess Intake Dietary intake of excess of kidney’s ability to excrete; Excess parenteral administration Decreased Loss Potassium-sparing diuretics; Renal failure; Adrenal insufficiency Shift of Potassium out of the Cells Extensive injuries, crushing injuries, metabolic acidosis HYPERKALEMIA GI Tract N&V Diarrhea, Colic CNS Numbness, paresthesias Muscles Early: irritability Late: weakness leading to flaccid paralysis CV System Conduction disturbance, ventricular fibrillation, Cardiac Arrest Kidneys Oliguria leading to anuria
  • COLLABORATIVE CARE MANAGEMENT
    • Patients at risk should be identified: impaired renal function to avoid OTC, esp. NSAIDS which provoke hyperkalemia; and salt substitutes that are high in potassium
    • Severity guides therapy
      • Mild: Withholding provoking agent (i.e., K supp)
      • Severe (>6 mEq/L: cation-exchange resin such as Kayexalate (act by exchanging the cations in the resin for the potassium in the intestine  potassium is then excreted in the stool; Continuous cardiac monitoring
    • Bowel function must be maintained if Kayexelate therapy is to be effective
    • Potassium-wasting diuretics may be prescribed to promote further potassium loss. Dialysis for patients with renal failure to eliminate excess potassium
    • Intravenous Ca Gluconate may be prescribed to counteract the cardiac effects of hyperkalemia
    • Insulin infusions and IV NaCO3 may be used to promote intracellular uptake of K
  • Calcium (Ca2+)
    • Most abundant electrolyte in the body. 99% in bones and teeth
    • Close link between calcium and phosphorus. High PO4, Low Ca
    • Necessary for nerve impulse transmission and blood clotting and is also a catalyst for muscle contraction and other cellular activities
    • Needed for Vitamin B12 absorption and use
    • Necessary for strong bones and teeth and thickness and strength of cell membranes
    • RDA: 1g for adults. Higher for children and pregnant and lactating women according to body weight, older people, esp. post-menopausal
    • Found in milk, cheese, and dried beans; some in meat and vegetables
    • Use is stimulated by Vitamin D. Excreted in urine, feces, bile, digestive secretions, and perspiration
    • Dec. serum calcium = PTH hormone release = calcium reabsorption
    • Normal value 8.5 – 10.5 mg/dl
  • CAUSES AND EFFECTS OF HYPOCALCEMIA Decreased Ionized Ca Large tranfusion with citrated blood Excess Loss Kidney Disease Draining fistula Decrease in GI Tract and Bone Absorption ↑ Magnesium ↑ Calcitonin ↓ Vitamin D ↓ Parathyroid Hormone HYPOCALCEMIA Bones Osteoporosis leading to Fractures CNS Tingling ↓ convulsions Other Abnormal deposits of calcium in body tissues Muscles Muscle spasm ↓ Tetany Cardiovascular System Dysrhythmias ↓ Cardiac arrest Inadequate Intake Dietary Deficit
  • PATHOPHYSIOLOGY OF HYPOCALCEMIA
    • Calcium ions are thought to line the pores of cell membranes, especially neurons
    • Calcium and Sodium repel each other
    • When serum calcium levels are low, this blocking effect is minimized
    • When Sodium moves more easily into the cell, depolarization takes place more easily
    • This results in increased excitability of the nervous system leading to muscle spasm, tingling sensations, and if severe, convulsions and tetany
    • Skeletal, smooth, and cardiac muscle functions are all affected by overstimulation
    CELL Sodium Calcium
  • CLINICAL MANIFESTATIONS OF HYPOCALCEMIA COMPLAINT OF NUMBNESS AND TINGLING OF EARS, NOSE, FINGERTIPS OR TOES TREATMENT PAINFUL MUSCULAR SPASMS (TETANY) ESPECIALLY OF FEET AND HANDS (CARPOPEDAL SPASMS), MUSCLE TWITCHING AND CONVULSIONS MAY FOLLOW
  • TESTS USED TO ELICIT SIGNS OF CALCIUM DEFICIENCY TROUSSEAU'S SIGN CHVOSTEK'S SIGN
  • COLLABORATIVE CARE MANAGEMENT
    • Identify risk factors: Inadequate calcium intake, excess calcium loss, Vitamin D deficiency, patients with poor diets
    • Education about the importance of adequate calcium and Vitamin D intake
    • Patients undergoing thyroid, parathyroid, and radical neck surgery are particularly vulnerable to hypocalcemia secondary to parathyroid hormone deficit
    • Monitoring of serum calcium levels and correction of deficits
    • Citrate is added to store blood to prevent coagulation.
    • Citrate + Transfusion = Citrate+Calcium
    • Normally, Liver + Citrate = Quick metabolism
    • Preexisting calcium deficit/hepatic dysfunction/large amounts of BT very rapidly = hypocalcemia
    • With acute hypocalcemia, Ca Gluconate is used + Continuous cardiac monitoring
    • Mild Hypocalcemia: High calcium diet or oral calcium salts
    • If PTH or Vit D Deficiency is the cause: aluminum hydroxide gel is used because when serum phosphate level rises, calcium level falls
    • Complication: Bone demineralization
    • Therefore, careful ambulation should be encouraged to minimize bone resorption
  • HYPERCALCEMIA: Serum concentration > 10mg/dL Causes and Effects Loss from bones Immobilization, Carcinoma with bone metastases, Multiple myeloma Excess Intake ↑ Calcium diet (esp. milk) Antacids containing calcium Increase in factors Causing Mobilization from bone ↑ PTH, ↑ Vitamin D, steroid therapy HYPERCALCEMIA Kidneys Stones ↓ Kidney Damage CNS ↓Deep-tendon reflexes ↓ Lethargy ↓ Coma Bones Bone pain ↓ Osteoporosis ↓ Fractures Muscles Muscle fatigue, hypotonia ↓ ↓ GI motility CV System Depressed activity ↓ Dysrhythmias ↓ Cardiac Arrest
  • HOW IT HAPPENS HYPERCALCEMIA DEPRESSED NERVE AND MUSCLE ACTIVITY DEEP TENDON REFLEXES MAY BE DECREASED OR ABSENT MYOCARDIAL FUNCTION IS ALTERED
  • CLINICAL MANIFESTATIONS OF HYPERCALCEMIA Decreased GI Motility Cardiac Dysrhythmias Constipation Nausea Mental status changes: lethargy, confusion, memory loss
  • CLINICAL MANIFESTATIONS OF HYPERCALCEMIA Immobilization Bone Demineralization Calcium accumulates in the ECF and passes through the kidneys Ca Precipitation Calcium Stones
  • COLLABORATIVE CARE MANAGEMENT
    • Mild hypercalcemia : hydration and education about avoiding foods high in calcium or medications that promote calcium elevation
    • Ambulation as appropriate; weight-bearing exercises as tolerated
    • Trapeze, resistance devices
    • Marked hypercalcemia : prevention of pathologic fractures, individualized plan of care
    • Prevention of renal calculi: encourage oral fluids to prevent concentrated urine: 3000 to 4000 mL/day unless contraindicated
    • Acid-ash fruit juices: cranberry juice and prune juice
    • Severe hypercalcemia : medical emergency: continuous cardiac monitoring, hydration, IV furosemide, Calcitonin and/or plicamycin (mithramycin), q2 serum and urinary electrolytes
  • Magnesium (Mg2+)
    • Mostly found within body cells: heart, bone, nerve, and muscle tissues
    • Second most important cation in the ICF, 2 nd to K+
    • Functions: Metabolism of CHO and CHON, protein and DNA synthesis, DNA and RNA transcription, and translation of RNA, maintains normal intracellular levels of potassium, helps maintain electric activity in nervous tissue membranes and muscle membranes
    • RDA: about 18-30 mEq; children require larger amounts
    • Sources: vegetables, nuts, fish, whole grains, peas, and beans
    • Absorbed in the intestines and excreted by the kidneys
    • Plasma concentrations of magnesium range from 1.5 – 2.5 mEq/L, with about one third of that amount bound to plasma proteins
  • HYPOMAGNESEMIA: Serum level < 1.5 mEq/L
    • Usually coexists with hypokalemia and les often with hypocalcemia
    Decreased Intake Prolonged malnutrition, Starvation Impaired absorption from GI Tract Malabsorption syndrome, Alcohol Withdrawal Syndrome, Hypercalcemia, Diarrhea, Draining gastrointestinal fistula Excessive Excretion ↑ Aldosterone, Conditions causing large losses of urine HYPOMAGNESEMIA Mental Changes Agitation, Depression, Confusion CNS Convulsions, Paresthesias, Tremor, Ataxia Muscles Cramps, Spasticity, Tetany CV System Tachycardia, Hypotension, Dysrhythmias HYPOKALEMIA
  • PATHOPHYSIOLOGY OF HYPOMAGNESEMIA Low serum magnesium level Increased acetylcholine release Increased neuromuscular irritability Increased sensitivity to acetylcholine at the myoneural junction Diminished threshold of excitation for the motor nerve Enhancement of myofibril contraction
  • PATHOPHYSIOLOGY OF HYPOMAGNESEMIA High Serum Calcium Increased acetylcholine release Increased neuromuscular irritability Increased sensitivity to acetylcholine at the myoneural junction Diminished threshold of excitation for the motor nerve Enhancement of myofibril contraction High Serum Calcium Excretion of Magnesium By the GI tract
  • PATHOPHYSIOLOGY OF HYPOMAGNESEMIA MAGNESIUM INHIBITS TRANSPORT OF PTH DECREASE IN THE AMOUNT OF CALCIUM BEING RELEASED FROM THE BONE POSSIBLE CALCIUM DEFICIT
  • CLINICAL MANIFESTATIONS OF HYPOMAGNESEMIA CONFUSION DEPRESSION CRAMPS TETANY CONVULSIONS
  • COLLABORATIVE CARE MANAGEMENT
    • Recognition of people at risk: people taking loop diuretics and digoxin should be encouraged to eat foods rich in magnesium, such as fruits, vegetables, cereals, and milk
    • Recognition of signs and symptoms of magnesium deficiency
    • Magnesium is essential for potassium resorption, so if hypokalemia does not respond to potassium replacement, hypomagnesemia should be suspected
    • Treatment of the underlying cause is the first consideration in hypomagnesemia
    • Severe: parenteral magnesium replacement is indicated
    • IV therapy: continuous cardiac monitoring
    • Safety measures for patients with mental status changes
  • HYPERMAGNESEMIA: Serum Mg level 2.5 mEq/L
    • Seldom develops in the presence of normal renal function
    • May occur as a result of Mg replacement
    • May occur when MgSO4 is administered to prevent seizures resulting from eclampsia
    • Careful monitoring is imperative
  • PATHOPHYSIOLOGY Renal failure, Excessive IV infusion of magnesium, Decreased GI elimination and/or absorption, etc. Accummulation of Mg in the body Diminishing of reflexes, drowsiness, lethargy Mg Level Rises Severe Respiratory Depression RESPIRATORY ARREST may occur Altered Electrical Conduction Slowed heart rate and AV Block Peripheral vasodilation Hypotension, flushing, and increased skin warmth
  • COLLABORATIVE CARE MANAGEMENT
    • Identification of patients at risk: those with impaired renal function to avoid OTC that contain magnesium such as Milk of Magnesia and some Mg-containing antacids
    • Any patient receiving parenteral magnesium therapy should be assessed frequently for signs of hypermagnesemia
    • Mild hypermagnesemia: withholding magnesium-containing medications may suffice
    • Renal failure: dialysis
    • Severe: may require treatment with calcium gluconate (10-20 mL of 10% Ca Gluconate administered over 10 minutes)
    • If cardiorespiratory collapse is imminent, the patient may require temporary pacemaker and ventilator support
  • NURSING MANAGEMENT OF PATIENT WITH FLUID AND ELECTROLYTE IMBALANCES
  • A Parameter_____Fluid Excess___ Fluid Loss/Electrolyte Imbalance____ Behavior Tires easily; Change in behavior, confusion, apathy Head, neck Facial edema, distended neck Headache, thirst, dry mucous membranes veins Upper GI Anorexia, nausea, vomiting Skin Warm, moist, taut, cool feeling Dry, decreased turgor where edematous Respiration Dyspnea, orthopnea, productive Changes in rate and depth of respiration cough, moist breath sounds Circulation Loss of sensation in edematous Pulse rate changes, dysrhythmia, postural areas, pallor, bounding pulse, hypotension increased blood pressure Abdomen Increased girth, fluid wave Distention, abdominal cramps Elimination Constipation Diarrhea, constipation Extremities Dependent edema, “pitting” Muscle weakness, tingling, tetany , discomfort from weight of bedclothes
  • Pitting edema Dependent edema Refractory Edema
  • A LABORATORY VALUES FLUID DEFICIT FLUID EXCESS Hemoconcentration Hemodilution ↑ Hct, BUN, E+ levels ↓ Hct, BUN, E+ levels ↑ Urine Specific Gravity ↓ Urine Specific Gravity
  • D Determined from analysis of patient data Diagnostic Title Possible Etiologic Factors 1 Deficient fluid volume Active fluid volume loss (hemorrhage, diarrhea, gastric intubation, wounds, diaphoresis), inadequate fluid intake, failure of regulatory mechanisms, sequestration of body fluids 2 Excess Fluid Volume Excess fluid intake, excess sodium intake, compromised regulatory processes
  • P EXPECTED PATIENT OUTCOMES 1,2. Will maintain functional fluid volume as evidenced by adequate urinary output, stable weight, normal vital signs, normal urine specific gravity, moist mucus membranes, balanced intake and output, elastic skin turgor, prompt capillary refill, and absence of edema 2 Will verbalize understanding of treatment plan and causative factors that led to the imbalance
    • 1,2 Intake and Output Monitoring
    • - Type and amount of fluid the patient has received and the route by which they were administered
    • - Record of solid food intake. Gelatin or Popsicles are recorded as fluids
    • - Ice chips are recorded by dividing the amount of chips by ½ (60 mL of chips = 30 mL water)
    • - Accurate output record and described by color, content, and odor (Normally, gastric contents are watery and pale yellow-green; they usually have a sour odor)
    • - With acid-base balance upset, gastric secretions may have a fruity odor because of ketone bodies
    • - Bile: thicker than gastric juice, dark green to brown, acrid odor, bitter taste when vomiting
    • - NGT irrigation added to intake
    • - Stools: difficult to estimate amount; consistency, color, and number of stools provide a reasonable estimate
    • - Peritoneal or pleural fluid drainage is recorded as output as with its amount, color, and clarity
    • - Character and volume of urine. Place signs and materials so that an accurate record of UO is maintained
    I
    • 1,2 Intake and Output Monitoring
    • - Evaluate and refer urine specific gravity as appropriate (normal value is 1.003 – 1.030). The implications are:
    • High Dehydration
    • Low SIADH, overhydration
    • - Drainage, fluid aspirated from any body cavity must be measured. With dressings, fluid loss is the difference between the wet dressings and the dry weight of the dressing
    • - Accurate recording of the temperature to help the physician determine how much fluid should be replaced
    • 1,2 Daily Weight
    • - Evaluate trends in weight (An increase in 1kg in weight is equal to the retention of 1L of fluid in an edematous patient)
    • Considerations:
    • - Daily weights early in the morning after voiding but before he or she has eaten or defecated
    I
    • 1 Replacement of Fluid and Electrolytes
    • General Principles:
    • - Either by oral intake (healthiest way), tube feeding, intravenous infusion, and/or total parenteral nutrition
    • - Normal saline solution and plain water should also be given by slow drip to replace daily fluid loss
    • - IV administration per doctor’s orders
    • - Fluid replacement considerations:
    • * Most effective when apportioned over 24 hr period (Better regulation, ↓potential for calculi formation and subsequent renal damage, ↓potential for circulatory overload which may cause in fluid and electrolyte
    • shifts)
    • * Administer concentrated solutions of Na, Glucose or protein because they require body fluids for dilution
    • * Consider the size of the patient (small adult has less fluid in each compartment, especially in the intravascular compartment)
    • - Promote oral intake as appropriate
    • * Caution with coffee, tea, and some colas
    I
    • * small amount at frequent intervals is more useful than a large amount presented less often
    • * Always give consideration to cultural and aesthetic aspects of eating
    • - Give mouth care to a dehydrated patient before and after meals and before bedtime (Xerostomia may lead to disruption of tissues in the oral cavity)
    • - Avoid irritating foods
    • - Stimulation of saliva may be aided by hard candy or chewing gum or carboxymethylcellulose (artificial saliva)
    • - Keep lips moist and well lubricated
    • - Give salty broth or soda crackers for sodium replacement and tea or orange juice for potassium replacement as appropriate. Bananas, citrus fruits and juices, some fresh vegetables, coffee, and tea are relatively high in potassium and low in sodium. Milk, meat, eggs, and nuts are high in protein, sodium and potassium.
    • - Offer milk for patients with draining fistulas from any portion of the GI tract. Lactose intolerance is not necessarily a contraindication (Lactase enzyme preparations are available)
    • - Increase usual daily requirement of foods when losses must be restored, as tolerated
    I
    • * Patients with cardiac and renal impairments are instructed to avoid foods containing high levels of sodium, potassium and bicarbonate
    • - Administer replacement solutions through tube feeding as is
    • * Either water, physiologic solution of NaCl, high protein liquids, or a regular diet can be blended, diluted and given by gavage
    • * The water content in the tube feeding needs to be increased if:
    • 1 the patient complains of thirst
    • 2 the protein or electrolyte content of the tube feeding is high
    • 3 the patient has fever or disease causing an increased metabolic rate
    • 4 UO is concentrated
    • 5 signs of water deficit develop
    • - Administer parenteral fluids as necessary
    I
    • * Types of solutions
    • - D5W (hypotonic) is given short-term for hyponatremia
    • - D5NSS may be given depending on the serum levels of sodium and vascular volume + KCl to meet normal intake needs and replace losses for hyponatremia
    • - Dextrose 5% in 0.2% normal saline is generally used as a maintenance fluid
    • - Dextrose 5% in ½ normal saline is generally used as a replacement solution for losses caused by gastrointestinal drainage
    • - PNSS is given primarily when large amounts of sodium have been lost and for patients with hyponatremia
    • - LRS is also isotonic because it remains in the extracellular space
    • - Fructose or 10-20% glucose in distilled water are hypertonic solutions and may partially meet body needs for CHOs
    • - Dextran (commonly-used plasma expander) increases plasma volume by increasing oncotic pressure. May cause prolonged bleeding time and is CI in patients with renal failure, bleeding disorders, or severe CHF
    I
    • * Administration
    • - The rate should be regulated according to the patient’s needs and condition per doctor’s orders
    • - Monitor UO carefully. Refer marked decreases!
    • - Verify orders for potassium administration in patients with renal failure and untreated adrenal insufficiency
    • - Usual rate for fluid loss replacement: 3ml/min
    • - Recognize signs of pulmonary edema (bounding pulse, engorged peripheral veins, hoarseness, dyspnea, cough, and rales) that can result from ↑IV rate
    • - If infiltration occurs, the infusion should be stopped immediately and relocated. Peripheral IV sites are generally rotated every 72 hours
    • - For dextran and other plasma expanders, observe for anaphylactic reaction (apprehension, dyspnea, wheezing, tightness of chest, angioedema, itching, hives and hypotension). If this happens, switch infusion to nonprotein solution and run at KVO rate, notify physician and monitor VS
    • - Pronounced and continued thirst despite administration of fluids is not normal and should be reported (may indicate DM or hypercalcemia)
    I
    • * Patient/Family Education
    • - Include the signs and symptoms of water excess in discharge instructions
    • - With drug therapy, instruct patient and family regarding correct method of administration, correct dose, and therapeutic and adverse effects
    • - Instruct to read labels for nutritional content
    • * For K restriction: avoid organ meats, fresh and dried fruits, and salt substitutes
    • - Skin assessment and care, positioning techniques for patients with mobility restrictions
    I
    • * Achievement of outcomes is successful in disturbances in fluid and electrolyte balance:
    • 1 Maintains functional fluid volume level with adequate UO, VS within the patient’s normal limits, sp gr of urine within 1.003-1.035, moist mucous membranes, stable weight, Intake=output, elastic skin turgor, and no edema
    • 2 States possible causes of imbalance and plan to prevent recurrence of imbalances
    • 3 Reports a decrease or absence of symptoms causing discomfort
    E
  • DRAWING ARTERIAL BLOOD GASES ALLEN’S TEST ARTERIAL PUNCTURE
  • NORMAL ACID-BASE BALANCE Estimated HCO3 concentration after fully oxygenated arterial blood has been equilibrated with CO2 at a PCO2 of 40 mmHg at 38C; eliminates the influence of respiration on the plasma HCO3 concentration 22-26 mEq/L Standard HCO3 Partial pressure of CO2 in the arterial blood: PCO2<35 mmHg = respiratory alkalosis PCO2>45 mmHg = respiratory acidosis 21-30 mmHg PaCO2 Identifies whether there is acidemia or alkalemia: pH<7.35 = acidosis; pH>7.45 = alkalosis 7.35-7.45 pH Partial pressure of oxygen in arterial blood (decreases with age) In adults < 60 years: 60-80 mmHg = mild hypoxemia 40-60 mmHg = moderate hypoxemia < 40 mmHg = severe hypoxemia 80-100 Hg PaO2 Definition and Implications Normal Value Parameter
  •  
  • BASIC REGULATION OF ACID-BASE BALANCE CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3 Kidney Lungs The lungs help control acid-base balance by blowing off or retaining CO2. The kidneys help regulate acid-base balance by excreting or retaining HCO3
  • TYPES OF ACID-BASE DISTURBANCES
    • Depression of the central nervous system, as evidenced by disorientation followed by coma
    Overexcitability of the nervous system; muscles may go into a state of tetany and convulsioons ACIDOSIS ALKALOSIS
  • INTERPRETING ARTERIAL BLOOD GASES RESULTS Look at the unrelated value. Decide whether or not compensation is happening 22-26 21-30 7.35-7.45 NORMAL Decide as to what may be the direct cause of the change in pH. pCO2 or HCO3? If PCO2, it’s respiratory, if HCO3, it’s metabolic Look at the HCO3 level. Is it normal or abnormal? Look at the pCO2. Is it normal or abnormal? Is the pH acidic or alkaline? ALKALOSIS ACIDOSIS CONDITION
  • RESPIRATORY ACIDOSIS: CARBONIC ACID EXCESS Damage to the respiratory center in the medulla, drug or narcotic use, obstruction of respiratory passages, respiratory and respiratory muscle disorders Decrease in the rate of pulmonary ventilation Increase in the concentration of CO2, carbonic acid, and hydrogen ions RESPIRATORY ACIDOSIS Potassium moves out of the cells HYPERKALEMIA VENTRICULAR FIBRILLATION
  • NURSING MANAGEMENT OF RESPIRATORY ACIDOSIS
    • ASSESSMENT
    • * Health Hx: complaints of headache, confusion, lethargy, nausea, irritability, nausea, irritability, anxiety, dyspnea, and blurred vision, preexisting conditions
    • * Physical Examination: lethargy to stupor to coma, tachycardia, hypertension, cardiac dysrhythmias, airway patency
    • NURSING DIAGNOSES include but are not limited to:
    • Diagnostic Title Possible Etiologic Factors
    • 1 Impaired gas exchange Hypoventilation
    • 2 Disturbed thought processes Central nervous system depression
    • 3 Anxiety Hypoxia, hospitalization
    • 4 Risk for ineffective family Illness of a family member coping
    • 5 Ineffective airway clearance Hypoventilation, secretions
    • 6 Ineffective breathing pattern Hypoventilation, dyspnea
  • NURSING MANAGEMENT OF RESPIRATORY ACIDOSIS
    • EXPECTED PATIENT OUTCOMES include but are not limited to:
    • 1 Will maintain airway patency and adequate breathing rate and rhythm will return of ABGs to patient’s normal level
    • 2 Will be alert and oriented to time, place, and person, or to his or her normal baseline level of consciousness
    • 3 Will cope with anxiety
    • 4 Will exhibit effective coping and awareness of effective support systems
    • 5 Will have secretions that are normal for self in amount and can be raised
    • 6 Will maintain adequate rate and depth of respirations using pursed lip and other breathing techniques when necessary (as in the patient with COPD)
    • NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS
    • INTERVENTIONS
    • 1 Supporting effective gas exchange
    • - Provide a position of comfort to allow ease of respiration
    • - Obtain and monitor ABG results and VS. Refer accordingly
    • - Provide and monitor supplemental oxygen as ordered
    • - Turn the patient q2 and PRN
    • - Provide pulmonary hygiene PRN
    • - Maintain adequate hydration
    • - Provide comfort measures such as mouth care
    • - Assist with ADLs
    • - Instruct patient regarding coughing and deep breathing and management of disease condition, especially COPD
    • 2 Coping with disturbed thought processes
    • - Do frequent neurologic assessments
    • - Monitor and document person’s baseline LOC frequently
  • NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS - Reorient as necessary by providing calendars, clocks, etc. 3 Relieving anxiety - Provide a calm, relaxed environment - Give clear, concise explanations of treatment plans - Encourage expression of feelings - Provide support and information to patient and family - Teach relaxation techniques - Assist the patient to identify coping mechanisms to deal with anxiety and stress 4 Enhancing coping mechanisms - Provide support and information to family members about the patient’s ongoing condition - Reassure them that there is a physiologic cause for the patient’s behavior
  • NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS - Encourage questions and open communication 5 Promote airway clearance - Implement regular breathing and coughing exercises - Do suctioning as necessary - Maintain good hydration - Do chest physiotherapy as appropriate 6 Promoting an effective breathing pattern - Maintain alveolar ventilation - Teach the patient proper breathing techniques as well as panic control breathing
  • NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS EVALUATION. Achievement of outcomes is successful when the patient: 1a. Demonstrates improved ventilation and oxygenation 1b Has vital signs, ABGs, and cardiac rhythm within own normal range 2 Returns to baseline LOC 3 Reports reduced anxiety 4 Family uses adequate coping mechanisms 5 Is able to raise secretions on own 6 Demonstrate effective breathing techniques
  • RESPIRATORY ALKALOSIS: CARBONIC ACID DEFICIT Anxiety, hysteria, fever, hypoxia, pain, pulmonary disorders, lesions affecting the respiratory center in the medulla, brain tumor, encephalitis, meningitis, hyperthyroidism, gram-negative sepsis Hyperventilation: Excessive pulmonary ventilation Decrease in hydrogen ion concentration RESPIRATORY ALKALOSIS
  • NURSING MANAGEMENT OF RESPIRATORY ALKALOSIS
    • ASSESSMENT
    • * Health Hx: anxiety, shortness of breath, muscle cramps or weakness, palpitations, panic, dyspnea
    • * Physical Examination: light-headedness, confusion as a result of cerebral hypoxia, hyperventilation, tachycardia or arrhythmia, muscle weakness, (+) Chvostek’s sign or Trousseau’s sign indicating a low ionized serum calcium level secondary to hyperventilation and alkalosis, hyperactive deep tendon reflexes, unsteady gait, muscle spasms to tetany, agitation, psychosis, seizures in extreme cases, decreased potassium levels
    • NURSING DIAGNOSES include but are not limited to:
    • Diagnostic Title Possible Etiologic Factors
    • 1 Anxiety Stress, fear
    • 2 Ineffective breathing pattern Hyperventilation, anxiety
    • 3 Disturbed thought processes CNS excitability; irritability
    • 4 Risk for injury Change in LOC, and potential for seizures
  • NURSING MANAGEMENT OF RESPIRATORY ALKALOSIS
    • EXPECTED PATIENT OUTCOMES include but are not limited to:
    • 1 Will report decreased anxiety; verbalizes methods to cope with anxiety
    • 2 Will return to normal respiratory rate and rhythm or at least decreased hyperventilation, with return to baseline ABGs
    • 3 Will exhibit reorientation to person, place, and time as per patient’s baseline
    • 4 Will be free from injury
    • INTERVENTIONS
    • 1 Allay anxiety
    • - Give antianxiety medications as ordered
    • - Have patient breath into a paper bag
    • - Teach relaxation techniques when initial anxiety attack is over
    • NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS
    • INTERVENTIONS
    • 2 Promoting an Effective Breathing Pattern
    • - Encourage the patient to slow his or her RR
    • - Maintain a calm and comforting attitude
    • - Position the patient to promote maximal ease of inspiration
    • - Assist the patient with relaxation techniques
    • 3 Coping with Disturbed Thought Processes
    • - Do frequent reorientation
    • - Encourage family to participate in patient’s care
    • - Use simple, direct statements or directions
    • - Allow the patient adequate time to respond
    • 4 Preventing injuries
    • - Perform neurologic assessment frequently and document
    • - Institute safety and seizure precautions
    • - Assess frequently for muscle strength and coordination
  • NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS EVALUATION. Achievement of outcomes is successful when the patient: 1 Reports reduction in anxiety levels 2a Demonstrates effective normal breathing patterns 2b Has ABG results within patient’s normal baseline 3 Returns to normal baseline LOC and orientation level 4 Remains free from injury; no seizure activity
  • METABOLIC ACIDOSIS: BICARBONATE DEFICIT Increased acid production, uncontrolled diabetes mellitus, alcoholism, starvation, renal acidosis, lactic acidosis, increased acid ingestion, ethanol, salicylates, loss of bicarbonate, severe diarrhea, intestinal fistulas, adrenal insufficiency, hypoparathyroidism Excess organic acids are added to body fluids or bicarbonate is lost Decrease in bicarbonate concentration METABOLIC ACIDOSIS
  • NURSING MANAGEMENT OF METABOLIC ACIDOSIS
    • ASSESSMENT
    • * Health Hx: anorexia, nausea, vomiting, abdominal pain, headache, thirst if the patient is dehydrated
    • * Physical Examination: confusion, hyperventilation, warm, flushed skin, bradycardia and other dysrhythmias, decreasing LOC, nausea, vomiting, diarrhea, Kussmaul respirations, and acetone breath, especially if acidosis is due to ketoacidosis. Symptoms may progress to coma if untreated
    • NURSING DIAGNOSES include but are not limited to:
    • Diagnostic Title Possible Etiologic Factors
    • 1 Disturbed thought processes Secondary to CNS depression
    • 2 Decreased cardiac output Dysrhythmias
    • 3 Risk for injury Secondary to altered mental state
    • 4 Risk for imbalanced fluid Diarrhea, renal failure
    • volume
  • NURSING MANAGEMENT OF METABOLIC ACIDOSIS
    • EXPECTED PATIENT OUTCOMES include but are not limited to:
    • 1 Will return to usual baseline LOC
    • 2 Will return to normal baseline parameters for vital signs with improved CO and decreased or resolved dysrhythmias
    • 3 Will remain in a safe, secure environment without injury
    • 4 Will maintain fluid and electrolyte balance and stable renal status
    • INTERVENTIONS
    • 1 Coping with disturbed thought processes
    • - Monitor LOC and reorient as necessary
    • - Monitor VS, esp. RRR, BP, and T
    • - Monitor ABGs to assess the effects of treatment
    • - Institute cardiac monitoring as ordered
    • NURSING MANAGEMENT OF PATIENT WITH METABOLIC ACIDOSIS
    • 2 Supporting cardiac output
    • - Monitor VS, MIO, and fluid and electrolyte balance
    • - Institute cardiac monitoring to evaluate cardiac status
    • 3 Promoting safety
    • - Provide a safe, secure and monitored environment
    • - Institute safety precautions
    • 4 Promoting return of fluid and electrolyte balance
    • - Monitor MIO
    • - Administer medications per medical order
  • NURSING MANAGEMENT OF PATIENT WITH METABOLIC ACIDOSIS EVALUATION. Achievement of outcomes is successful when the patient: 1 Exhibits baseline-level consciousness and orientation 2 Returns to normal baseline parameters for vital signs and Cardiac Output with cardiac dysrhythmias resolved 3 Remains free from injury 4 Maintains fluid and electrolyte balance and stable renal function
  • METABOLIC ALKALOSIS: BICARBONATE EXCESS Loss of stomach acid, gastric suctioning, persistent vomiting, excess alkali intake, intestinal fistulas, hypokalemia, Cushing’s syndrome or aldosteronism, potassium-diuretic therapy Excessive amounts of acid substance and hydrogen ions are lost from the body or large amounts of bicarbonate or lactate are added orally or IV Excess of base elements METABOLIC ALKALOSIS
  • NURSING MANAGEMENT OF METABOLIC ALKALOSIS
    • ASSESSMENT
    • * Health Hx : Prolonged vomiting or nasogastric suctioning, frequent self-induced vomiting, muscle weakness, light- headedness, ingestion of large amounts of licorice or antacids, use of diuretics, muscle cramping, twitching, or tingling
    • * Physical Examination : mental confusion, dizziness, changes in LOC, hyperreflexia, tetany, dysrhthmias, seizurees, respiratory failure, positive Chvostek’s or Trosseau’s sign if the patient has a low ionized serum calcium level, decreased hand grasps, generalized muscle weakness, decreased serum calcium or potassium level, impaired concentration, seizures, ECG changes consistent with hypokalemia
    • NURSING DIAGNOSES include but are not limited to:
    • Diagnostic Title Possible Etiologic Factors
    • 1 Disturbed thought processes CNS excitation
    • 2 Decreased cardiac output Dysrhythmias and electrolyte imbalances
    • 3 Risk for injury Muscle weakness, tetany, confusion and possible seizures
    • 4 Risk for imbalanced fluid Nasogastric drainage, diuretic therapy
    • volume fistula
  • NURSING MANAGEMENT OF METABOLIC ALKALOSIS
    • EXPECTED PATIENT OUTCOMES include but are not limited to:
    • 1 Will return to usual baseline LOC and orientation
    • 2 Will return to normal baseline parameters for vital signs with improved CO with resolution of electrolyte imbalances and decreased or resolved cardiac dysrhythmias
    • 3 Will remain in a safe, secure environment without injury
    • 4 Will maintain fluid and electrolyte balance
    • INTERVENTIONS
    • 1 Coping with disturbed thought processes
    • - Monitor LOC and reorient as necessary
    • - Monitor VS, esp. RRR, BP, and T
    • - Monitor ABGs to assess the effects of treatment
    • - Institute cardiac monitoring as ordered
    • NURSING MANAGEMENT OF PATIENT WITH METABOLIC ALKALOSIS
    • 2 Supporting cardiac output
    • - Monitor VS, MIO, and fluid and electrolyte balance
    • - Institute cardiac monitoring to evaluate cardiac status
    • 3 Promoting safety
    • - Provide a safe, secure and monitored environment
    • - Institute safety precautions
    • 4 Promoting return of fluid and electrolyte balance
    • - Monitor MIO
    • - Administer medications per medical order
  • NURSING MANAGEMENT OF PATIENT WITH METABOLIC ALKALOSIS EVALUATION. Achievement of outcomes is successful when the patient: 1 Manifests mental status has returned to baseline 2 Is free from cardiac dysrhythmias 3 Remains free from injury 4 Maintains fluid balance at baseline level
  • CRITICAL THINKING EXERCISES
    • A patient on your unit has a diagnosis of dehydration. The physician has ordered “force fluids”. You must make a judgment as to the type and amount since these were not specified in the order. Identify the additional patient data needed to make an appropriate nursing decision
  • CRITICAL THINKING EXERCISES
    • A 32-year-old administrative assistant comes to the urgent care center with a 72-hour history of vomiting secondary to influenza. She is lethargic and states, “My muscles are twitching.” Her RR is 18/min and HR is 110 bpm, T=100.4F. Her blood pressure is 110/68 which she states “is about normal for me.” Her ABG values are as follows:
    • pH: 7.57
    • PaO2: 92
    • PaCO2: 41
    • HCO3: 36
    • Describe her acid-base status, probable cause for the imbalance and treatment
  • EXPECTED DIRECTIONAL CHANGES WITH ACID-BASE IMBALANCES ↑ ↑ ↑ ↓ ↓ ↓ Normal ↓ ↓ Normal ↑ ↑ HCO3 Normal ↑ ↑ ↑ ↑ Normal Metabolic Alkalosis Uncompensated Partly Compensated Compensated Normal ↓ ↓ ↓ ↓ Normal Metabolic Acidosis Uncompensated Partly Compensated Compensated ↓ ↓ ↓ ↑ ↑ Normal Respiratory Alkalosis Uncompensated Partly Compensated Compensated ↑ ↑ ↑ ↓ ↓ Normal Respiratory Acidosis Uncompensated Partly Compensated Compensated PCO2 pH CONDITION