Your SlideShare is downloading. ×
0
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Fluid and Electrolytes
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×
Saving this for later? Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime – even offline.
Text the download link to your phone
Standard text messaging rates apply

Fluid and Electrolytes

14,580

Published on

Fuids, Types and Fluids, Types of Solutions, Hypo/hypervolemia, Burns, Electrolytes (Sodium, Potassium, Calcium, Phosphate) and Imbalances

Fuids, Types and Fluids, Types of Solutions, Hypo/hypervolemia, Burns, Electrolytes (Sodium, Potassium, Calcium, Phosphate) and Imbalances

Published in: Education
5 Comments
28 Likes
Statistics
Notes
  • I am going back to bedside nsg after 24 years; this PowerPoint is beyond wonderful. I would so much like to pay you for a copy of this presentation. Would you consider allowing me to pull off a copy if I paid you $25.00? It would be such a bargain for me. I am going to try to contact you (I don't want to put out my email in public (no offense, commenters).
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
  • nice. I would love a copy of it.E-mail is funmiolukiran78@yahoo.com
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
  • very nice ppt thanks alot
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
  • I would love a copy of this Ppt presentation. Thank you. Fran
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
  • WONDERFUL PPTS....
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
No Downloads
Views
Total Views
14,580
On Slideshare
0
From Embeds
0
Number of Embeds
5
Actions
Shares
0
Downloads
0
Comments
5
Likes
28
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
No notes for slide

Transcript

  • 1. Fluids andElectrolytes<br />Ma. Tosca Cybil A. Torres, RN, MAN <br />
  • 2. OBJECTIVES<br />After this lecture/discussion, the learner should be able to:<br /> 1. Describe the mechanisms that maintain fluid, electrolyte and acid-base balance.<br /> 2. Compare the mechanisms and effects of fluid deficit and excess.<br /> 3. Discuss the mechanisms and effects of deficits and excess.<br /> 4. Describe the mechanisms that maintain acid-base balance.<br /> 5. Differentiate between metabolic and respiratory acidosis and alkalosis.<br /> 6. Apply the pathophysiologic principles of acid-base balance to the interpretation of ABG measurements.<br /> 7. Analyze the components of ABGs to identify the type of acid-base balance.<br /> 8. Describe the causes and effects of each type of acid-base balance.<br /> 9. Use ABG findings in formulating the care of the patient with an acid-base imbalance.<br /> 10. Describe the management of patients with a fluid, electrolyte, or acid-base imbalance.<br />
  • 3. Fluids <br />
  • 4. HOW IMPORTANT IS WATER?<br /><ul><li> Between 50% and 60% of the human body by weight is water
  • 5. 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
  • 6. Water facilitates cellular metabolism and proper cellular chemical functioning
  • 7. Water acts as a solvent for electrolytes and nonelectrolytes
  • 8. Helps maintain normal body temperature
  • 9. Facilitates digestion and promotes elimination
  • 10. Acts as a tissue lubricant</li></li></ul><li>VARIATIONS IN FLUID CONTENT<br />BODY FAT<br />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.<br />This is also true between sexes because females tend to have proportionally more body fat than males.<br />There is also an increase in fat cells in older people<br />
  • 11. VARIATIONS IN FLUID CONTENT<br />50%<br />Adult Female<br />60%<br />Adult Male<br />45%<br />Elderly <br />77% <br />Infants<br />AGE<br />
  • 12.
  • 13.
  • 14. AVENUES BY WHICH WATER ENTERS AND LEAVES THE BODY<br />
  • 15. ANTIDIURETIC HORMONE REGULATION MECHANISMS<br />Osmoreceptors in hypothalamus<br />↑Osmolarity<br />Hypothalamus<br />↓<br />Posterior pituitary gland<br />↓Blood volume or ↓BP<br />Volume receptor <br />Atria and great veins<br />Kidney tubules<br />↑ADH<br />↑H2O reabsorption<br />Narcotics, Stress, Anesthetic agents, Heat, Nicotine, Antineoplastic agents, Surgery<br />↑vascular volume and ↓osmolarity<br />
  • 16. ALDOSTERONE-RENIN-ANGIOTENSIN SYSTEM<br />RENIN<br />Juxtaglomerular cells-kidney<br />Angiotensinogen in plasma<br />↓Serum Sodium ↓Blood volume<br />Angiotensin I<br />Angiotensin-converting enzyme<br />Via vasoconstriction of arterial smooth muscle<br />↑Sodium resorption (H2O resorbed with sodium); ↑ Blood volume<br />Angiotensin II<br />Kidney tubules<br />ALDOSTERONE<br />Adrenal Cortex<br />Intestine, sweat glands, Salivary glands<br />
  • 17. Fluid Types<br />Fluids in the body generally aren’t found in pure forms<br />Isotonic, hypotonic, and hypertonic types<br />Defined in terms of the amount of solute or dissolve substances in the solution<br />Balancing these fluids involves the shifting of fluid not the solute involved <br />
  • 18. Isotonic Solutions<br />No net fluid shifts occur between isotonic solutions because the solution are equally concentrated<br />Ex. NSS or 0.9SS<br />
  • 19. Hypotonic Solutions<br />Has a lower solute concentration than another solution<br />Fluid from the hypotonic solution would shift into the second solution until the two solutions had equal concentrations<br />Ex. Half normal or 0.45%SS<br />
  • 20. Hypertonic Solutions<br />Has a higher solute concentration than another solution<br />Fluid from the second solution would shift into the hypertonic solution until the two solutions had equal concentrations<br />Ex. D5NSS<br />
  • 21. Fluid Movements<br />Fluids and solutes constantly move within the body, which allows the body to maintain homeostasis<br />Fluids along with nutrients and waste products constantly shift within the body’s compartments from the cell to the interstitial spaces, to the blood vessels and back again<br />
  • 22. Fluid Movements<br />Types of Transport<br />A. Active transport <br />B. Passive transport<br />Diffusion<br />Osmosis<br />Filtration<br />
  • 23. Assessment<br />CLINICAL MEASUREMENT<br />Daily weights<br />Each kg = 1 L of fluid<br />To gain accuracy:<br />Balance the scale before each use and weigh the client;<br />At same time each day before breakfast after the first void<br />Wear the same or similar clothing<br />On the same scale<br /> Vital signs<br />Tachycardia – first sign of hypovolemia<br />Fluid I & O<br />Oral fluids<br />Ice chips<br />Foods that tend to become fluid at room temperature<br />Tube feedings<br />Parenteral fluids<br />IV meds<br />Catheter or tube irrigant<br />Urinary output – if with diaper, 1 g = 1 mL<br />Vomitus or liquid feces<br />Diaphoresis<br />Tube drainage<br />Wound dressing or wound fistula<br />
  • 24. LABORATORY TESTS FOR EVALUATING FLUID STATUS<br />Osmolality – measures the solute concentration per kilogram in blood and urine.<br />Osmolarity – concentration of solution per liter.<br />BUN – (10-20 mg/dL)made up of urea, an end product of protein metabolism by the liver.<br />Creatinine (0.7 to 1.5 mg/dL)- end product of muscle metabolism<br />Serum electrolytes<br />CBC<br />
  • 25. Diagnosis<br />Fluid volume deficit<br />High risk for Fluid volume deficit<br />Fluid volume excess<br />Altered oral mucous membrane<br />
  • 26. FLUID BALANCE<br /> The desirable amount of fluid intake and loss in adults ranges from 1500 to 3500 mL each 24 hours. Ave= 2500 mL<br /> Normally INTAKE = OUTPUT<br />FLUID IMBALANCE<br /><ul><li>Changes in ECF volume = alterations in sodium balance
  • 27. Change in sodium/water ratio = either hypoosmolarity or hyperosmolarity
  • 28. Fluid excess or deficit = loss of fluid balance
  • 29. As with all clinical problems, the same pathophysiologic change is not of equal significance to all people
  • 30. For example, consider two persons who have the same viral syndrome with associated nausea and vomiting</li></ul>Man with renal failure<br />Life threatening E+ disturbances<br />ECF Volume Depletion<br />No Significant E+ disturbances<br />
  • 31. FLUID DEFICIT/HYPOVOLEMIA<br />May occur as a result of:<br />Reduced fluid intake<br />Loss of body fluids<br />Sequestration (compartmentalizing) of body fluids<br />Pathophysiology and Clinical Manifestations<br />DECREASED FLUID VOLUME<br />Stimulation of thirst center in hypothalamus<br />↑ ADH Secretion<br />Renin-Angiotensin-Aldosterone System Activation<br />↑ Water resorption<br />Person complains of thirst<br />↑ Sodium and Water Resorption<br />↓ Urine Output<br />↑ Urine specific gravity <br />
  • 32. Pathophysiology and Clinical Manifestations<br />UNTREATED FLUID VOLUME DEFICIT<br />Depletion of fluids available<br />↑ BODY TEMPERATURE<br />Cells become unable to continue providing water to replace ECF losses<br />Dry mucous membranes<br />Signs of circulatory collapse <br />↓ blood pressure<br />↑ heart rate<br />↑ respiratory rate<br />Difficulty with speech<br />Restlessness and Apprehension<br />
  • 33. Hypovolemia<br />Nursing Intervention<br />Monitor fluid intake and output<br />Checked daily weight (a 1lb(0.45kg) weight loss equals a 500 ml fluid loss)<br />Monitor hemodynamic values such as CVP<br />Monitor results of laboratory studies<br />Assess level of consciousness<br />Administer and monitor I.V. fluids<br />Apply and adjust oxygen therapy as ordered<br />If patient is bleeding, apply direct continuous pressure to the area and elevate it if possible<br />Assess skin turgor<br />Assess oral mucous membranes<br />Turn the patient at least every 2 hours to prevent skin breakdown <br />Encourage oral fluids<br />
  • 34. Hypovolemia<br />Warning Signs<br />Cool pale skin over the arms and legs<br />Decreased central venous pressure<br />Delayed capillary refill<br />Deterioration in mental status flat jugular veins<br />Orthostatic hypotension<br />Tachycardia<br />Urine output initially more than 30ml/min, then dropping below 10ml/hour<br />Weak or absent peripheral pulses<br />Weight loss<br />
  • 35. Collaborative Care Management<br />Identification of vulnerable patients and risk factors:<br />* Compromised mental state * Physical limitations * Disease states * Limited access to adequate food and fluids<br />Development of a plan of care<br />Family members should be educated about the importance of fluid and nutrition intake<br />Collaboration with the nurse, patient, family members, and other health care providers for continued assessment and treatment of problems<br />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<br />
  • 36. Collaborative Care Key Points<br />1 Liter of water = 1 kg of water by weight<br />Fluid replacement are calculated according to this ratio plus 1.5 L to fulfill the current daily needs<br />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.<br />Oral fluid resuscitation is preferable but if the patient is unable to tolerate fluids, IV Therapy may be ordered<br />Vital signs should be assessed regularly<br />Postural hypotension is common for postural persons with fluid volume deficit. How do we assess this?<br />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.<br />Daily weighing is also useful to monitor fluid and electrolyte balance<br />Laboratory results should be reviewed for various fluid and electrolyte disturbances so that appropriate adjustments to therapy can be initiated<br />
  • 37. Fluid Replacement Therapy<br />Aimed at restoring and maintaining homeostasis<br />Methods:<br />Oral and gastric feeding<br />Parenteral therapy<br />Choice of therapy affected by several factors<br />Type and severity of imbalance<br />Patient’s overall health status, age, renal and cardiovascular status<br />Usual maintenance requirements<br />
  • 38. Fluid Replacement Therapy<br />Advantages<br />Provides the patient with life-sustaining fluids, electrolytes, and drugs<br />Immediate and predictable therapeutic effects<br />Preferred for administering fluids, electrolytes, and drugs in emergency situations<br />Allows fluid intake when a patient has GI malabsorption<br />Permits accurate dosage titration for analgesics and other drugs<br />
  • 39. Fluid Replacement Therapy<br />Disadvantages<br />Solution incompatibility<br />Adverse reactions<br />Infection<br />
  • 40. Fluid Replacement Therapy<br />Administration routes<br />Oral route : oral ingestion of fluids and electrolytes as liquids or solids administered directly into the GI tract<br />Nasogastric route: instillation of fluids and electrolytes through feeding tubes, such as NG, gastrostomy and jejunostomy tubes<br />I.V. route: administration of fluids and electrolytes directly into the bloodstream using continuous infusion, bolus, or I.V. push injection through peripheral or central venous site<br />
  • 41. Which among the following IV solutions contains the highest potassium content?A. D5 IMBB. Lactated Ringer's SolutionC. D5 LRSD. D5 0.3 NaCl<br />
  • 42. Composition of Different Intravenous Solution<br />
  • 43. Fluid Replacement TherapyISOTONIC SOLUTION<br />
  • 44. Fluid Replacement TherapyHYPOTONIC SOLUTION<br />
  • 45. Fluid Replacement TherapyHYPERTONIC SOLUTION<br />
  • 46. FLUID EXCESS/HYPERVOLEMIA<br />Renal and endocrine disturbances, malignancies, adenomas<br />Psychiatric Disorders, SIADH, Certain head injuries<br />Dietary Sodium Indiscretion<br />Failure of renal or hormonal regulatory functions<br />Excessive Sodium Intake<br />Overhydration<br />FLUID VOLUME EXCESS/HYPERVOLEMIA<br />Sodium <br />ADH<br />Extracellular volume expands<br />Fluid becomes progressively hyponatremic<br />Normal Extracellular fluid<br />Normal sodium concentration<br />Renal Tubules<br />
  • 47. <ul><li>Since ECF becomes hypoosmolar, fluid moves into the cells to equalize the concentration on both sides of the cell membrane
  • 48. Thus there, is an increase in intracellular fluid
  • 49. The brain cells are particularly sensitive to the increase of intracellular water, the most common signs of hypoosmolaroverhydration are changes in mental status. Confusion, ataxia, and convulsions may also occur.
  • 50. 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</li></li></ul><li>Hypervolemia<br />Evaluating pitting edema<br />Press your fingertip firmly into the patients skin over a bony surface for a few seconds. Then note the depth of the imprint your finger leaves on the skin<br />A slight imprint indicates +1 pitting edema<br />A deep imprint, with the skin slow to return to its original contour, indicates a +4 pitting edema<br />When the skin resists pressure and appears distended, the condition is called brawny edema, which causes the skin to swell so much that fluid cant be displaced<br />
  • 51. Hypervolemia<br />Diagnostic Findings:<br />Decreased hematocrit resulting from hemodilution<br />Normal serum Na level<br />Low serum K and BUN levels <br />either due to hemodilution or higher levels may indicate renal failure<br />Low oxygen level<br />Abnormal chest x-ray<br />Indicates fluid accumulation<br />May reveal pulmonary edema or pleural effusions<br />
  • 52. Hypervolemia<br />Treatment<br />Na and fluid intake restriction<br />Diuretics to promote excess fluid excretion<br />Morphine and nitroglycerin (Nitro-Dur) for pulmonary edema<br />Dilate blood vessels<br />Reduce pulmonary congestion and amount of blood returning to the heart<br />Digoxin for heart failure<br />Strengthens cardiac contractions<br />
  • 53. Hypervolemia<br />Treatment<br />Supportive measures<br />Oxygen administration<br />Bed rest<br />Hemodialysis or continuous renal replacement therapy for renal dysfunction<br />
  • 54. Hypervolemia<br />Nursing Interventions<br />Monitor fluid intake and output<br />Monitor daily weight<br />Monitor cardiopulmonary status<br />Auscultate breathe sounds<br />Assess for complaints of dyspnea<br />Monitor chest x-ray results<br />Monitor arterial blood gas values<br />Assess for peripheral edema<br />Inspect the patient for sacral edema<br />Monitor infusion of I.V. solutions<br />Monitor the effects of prescribed medications<br />
  • 55. BURN<br />
  • 56. General Information<br />Involve destruction of the epidermis, dermis, or subcutaneous layers of the skin<br />Can be permanently disfiguring and incapacitating and possibly life-threatening<br />
  • 57. General Information<br />Associated imbalances result from alterations in skin integrity and internal body membranes, and from effect of heat on body water and solute loss that may result from cellular destruction<br />
  • 58. General Information<br />Type and severity of imbalance depends on burn type and depth, percentage body surface area involved and burn phase<br />
  • 59. Pathophysiology<br />Burn phase<br />Fluid- accumulation phase<br />Fluid-remobilization phase<br />Convalescent phase<br />Burn Phase:<br />Refer to stages that describe physiologic changes occurring after a burn <br />
  • 60. Pathophysiology<br />Burn phase<br />Fluid- accumulation phase<br />Fluid-remobilization phase<br />Convalescent phase<br /><ul><li>Fluid-accumulation phase:
  • 61. Last fro 36 to 48 hours after a burn injury
  • 62. Fluid shifts from vascular compartment to interstitial space – third-space shift
  • 63. Edema caused by shifted fluid, which typically reaches maximum within 8 hours after injury
  • 64. Circulation possibly compromised and pulses diminished from severe edema</li></li></ul><li>Pathophysiology<br />Burn phase<br />Fluid- accumulation phase<br />Fluid-remobilization phase<br />Convalescent phase<br />Several reasons for fluid imbalances during fluid-accumulation phase<br />Damage to capillaries causing altered vessel permeability<br />Diminished kidney perfusion<br />Production and release of stress hormones such as aldosterone and ADH<br />
  • 65. Pathophysiology<br />Burn phase<br />Fluid- accumulation phase<br />Fluid-remobilization phase<br />Convalescent phase<br /><ul><li>Respiratory problems
  • 66. Muscle and tissue injuries
  • 67. GI problems
  • 68. Electrolyte imbalances:
  • 69. Common during fluid accumulation phase due to body’s hypermetabolic needs and priority that fluid replacement takes over nutritional needs during emergency phase</li></li></ul><li>Pathophysiology<br />Burn phase<br />Fluid- accumulation phase<br />Fluid-remobilization phase<br />Convalescent phase<br /><ul><li>Fluid- remobilization phase :
  • 70. Also known as diuresis stage
  • 71. Starts about 48 hours after initial burn
  • 72. Fluid shifted back to vascular compartment
  • 73. Edema at burn site decreased, blood flow to kidneys increased, increased urine output
  • 74. Fluid and electrolyte imbalances can still occur</li></li></ul><li>Pathophysiology<br />Burn phase<br />Fluid- accumulation phase<br />Fluid-remobilization phase<br />Convalescent phase<br /><ul><li>Convalescent phase:
  • 75. Begins after first two phases has been resolved
  • 76. Characterized by healing or reconstruction of burn wound
  • 77. Major fluid shifts now resolved but possible further fluid and electrolyte imbalances exist as a result of inadequate dietary intake
  • 78. Anemia is common – severe burns typically destroy red blood cells</li></li></ul><li>Characteristics<br />1. Minor Burns<br />Partial thickness burns are no greater than 15% of the TBSA in the adult<br />Full thickness burns are < 2% of the TBSA in the adult<br />Burn areas do not involve the eyes, ears, hands, face, feet, or perineum<br />There are no electrical burns or inhalation injuries<br />The client is an adult younger than 60 y.o.<br />The client has no preexisting medical condition at the time of the burn injury<br />No other injury occurred with the burn<br />
  • 79. Characteristics<br />2. Moderate Burns<br />Partial thickness burns are deep and are 15% to 25% of the TBSA in the adult<br />Full thickness burns are 2% to 10% of the TBSA in the adult<br />Burn areas do not involve the eyes, ears, hands, face, feet, or perineum<br />There are no electrical burns or inhalation injuries<br />The client is an adult younger than 60 y.o.<br />The client has no chronic cardiac, pulmonary, or endocrine disorder at the time of the burn injury<br />No other complicated injury occurred with the burn<br />
  • 80. Characteristics<br />3. Major Burns<br />Partial thickness burns are > 25% of the TBSA in the adult<br />Full thickness burns are > 10% of the TBSA <br />Burn areas involve the eyes, ears, hands, face, feet, or perineum<br />The burn injury was an electrical or inhalation injury<br />The client is older than 60 y.o.<br />The client has a chronic cardiac, pulmonary, or metabolic disorder at the time of the burn injury<br />Burns are accompanied by other injuries<br />
  • 81. Reparative Process<br />Assessment of Extent<br />Extent / Degree<br />In about 5 days, epidermis peels, heals spontaneously.<br />Itching and pink skin persist for about a week.<br />No scarring.<br />Heals spont. If it does not become infected w/in 10 days - 2 weeks.<br />Pink to red: slight edema, which subsides quickly.<br />Pain may last up to 48 hours.<br />Relieved by cooling.<br />Sunburn is a typical example.<br />First Degree<br />Takes several weeks to heal.<br />Scarring may occur.<br />Takes several weeks to heal.<br />Scarring may occur.<br />Superficial:<br />Pink or red; blisters form (vesicles); weeping, edematous, elastic.<br />Superficial layers of skin are destroyed; wound moist and painful.<br />Deep dermal:<br />Mottled white and red: edematous reddened areas blanch on pressure.<br />May be yellowish but soft and elastic – may or may not be sensitive to touch; sensitive to cold air.<br />Hair does not pull out easily<br />Second degree<br />Assessment of Burn Injury<br />
  • 82. Reparative Process<br />Assessment of Extent<br />Extent / Degree<br />Eschar must be removed. Granulation tissue forms to nearest epithelium from wound margins or support graft.<br />For areas larger than 3-5 cm, grafting is required.<br />Expect scarring and loss of skin function.<br />Area requires debridement, formation of granulation tissue, and grafting.<br />Destruction of epithelial cells – epidermis and dermis destroyed<br />Reddened areas do not blanch with pressure.<br />Not painful; inelastic; coloration varies from waxy white to brown; leathery devitalized tissue is called eschar.<br />Destruction of epithelium, fat, muscles, and bone.<br />Third degree<br />Assessment of Burn Injury<br />
  • 83. Burn:Classification<br />Superficial (1° burns)<br />Involve only the epidermal layer of the skin.<br />sunburns are commonly first-degree burns.<br />59<br />
  • 84. 1° burn<br />2° burn<br />60<br />
  • 85. 61<br />Superficial burn (1° burn)<br />
  • 86. 62<br />Present of blisters indicates superficial partial-thickness injury.<br />Blister may ↑size because continuous exudation and collection of tissue fluid.<br />Healing phase of partial thickness, itching and dryness because ↑vascularization of sebaceous glands, ↓reduction of secretions and ↑perspiration.<br />Partial thickness (2°burn)<br />
  • 87. 2° burn<br />63<br />
  • 88. 64<br />Partial thickness (2°burn)<br />
  • 89. Burn:Classification<br />3.Full thickness (third-degree burn)<br />Destruction of the epidermis and the entire dermis, subcutaneous layer, muscle and bone.<br />Nerve ending are destroyed-painless wound.<br />Eschar may be formed due to surface dehydration.<br />Black networks of coagulate capillaries may be seen.<br />Need skin grafting because the destroyed tissue is unable to epithelialize.<br />Deep partial-thickness burn may convert to a full-thickness burn because of infection, trauma or ↓blood supply.<br />65<br />
  • 90. 3° burn<br />66<br />
  • 91. Eschar:composed of denatured protein<br />67<br />
  • 92. 68<br />Full thickness (3°burn)<br />
  • 93. Extent of surface area burned<br />Rule ofnines-An estimated of the TBSA involved as a result of a burn.<br />The rule of nines measures the percentage of the body burned by dividing the body into multiples of nine.<br />The initial evaluation is made upon arrival at the hospital.<br />69<br />
  • 94. Lund and Browder<br />More precise method of estimating <br />Recognizes that the percentage of BSA of various anatomic parts.<br />By dividing the body into very small areas and providing an estimate of proportion of BSA accounted for by such body parts<br />Includes, a table indicating the adjustment for different ages<br />Head and trunk represent larger proportions of body surface in children. <br />70<br />
  • 95. 71<br />
  • 96. Lund and Browder chart<br />72<br />
  • 97. TYPES OF BURNS<br />Thermal Burns:<br /> caused by exposure to flames, hot liquids, steam or hot objects<br />Chemical Burns:<br />Caused by tissue contact with strong alkali, or organic compounds<br /> Systemic toxicity from cutaneous absorption can occur<br />Radiation Burns: <br />caused by exposure to UV light, x-rays, or radioactive source<br />
  • 98. TYPES OF BURNS<br />Electrical Burns:<br />Caused by heat generated by electrical energy as it passes through the body<br /> Results in internal tissue damage<br />Cutaneous burns cause muscle and soft tissue damage that may be extensive, particularly in high voltage electrical injuries<br /> Alternating current is more dangerous than direct current because it is associated with CP arrest, ventricular fibrillation, tetanic muscle contractions, and long bone or vertebral fractures<br />
  • 99. Potential Imbalance<br /><ul><li>Hypovolemia
  • 100. Approximately 10% of plasma volume lost into tissue soon after a severe burn
  • 101. Occurs because of the third space shift causes multiple effects:
  • 102. With burn’s damage to the skin surface, decrease in skins ability to prevent water loss; patient can lose up to 8L of fluid per day (400ml/hour)
  • 103. Potential for blood loss, adding to fluid volume losses</li></li></ul><li>Potential Imbalance<br />Hypervolemia<br />Usually develops 3 to 5 days after a major burn injury<br />Occurs during the fluid remobilization phase, as fluid shifts from the interstitial space back to the vascular compartment<br />May be exacerbated by excessive administration of I.V. fluids<br />
  • 104. Potential Imbalance<br />Hyperkalemia / Hypokalemia<br />Hypocalcemia<br />Hyponatremia / Hypernatremia<br />Metabolic acidosis<br />Respiratory acidosis<br />
  • 105. Burns<br />NURSING PRIORITY:<br /> The client with burn injury is often awake, mentally alert, and cooperative at first. The level of consciousness may change as respiratory status change or as the fluid shift occurs, precipitating hypovolemia. If the client is unconscious or confused, assess him or her for the possibility of a head injury.<br />
  • 106. Burns<br />Assess for<br />Patent airway<br />Presence of adequate breath sounds<br />Symptoms of hypoxia<br />Pulmonary damage<br />Burns around the face, neck, mouth or in the oral mucosal area<br />Circulatory status<br />Tachycardia and hypotension occur early<br />Elevate UO<br />
  • 107. Burns<br />Assess for<br />GI function – check last time client ate<br />Fluid status<br />UO (30 ml/hr)<br />Hypotension (< 90/60)<br />Confusion / disorientation<br />Circulatory status of the extremities<br />
  • 108. Burns<br /><ul><li>Treatment
  • 109. Respiratory status takes priority over the treatment of the burn injury
  • 110. If burn area is small  cold compress or immerse in cool water (not ice) to ↓ heat
  • 111. May have ointment on the burn area
  • 112. Analgesics IV, IM, SQ. oral forms may not be absorbed effectively</li></li></ul><li>Burns<br />Nursing intervention<br />Maintain patent airway; prevent hypoxia<br />Evaluate fluid status; determine circulatory status<br />Prevent of decrease infection<br />Maintain nutrition<br />Prevent contractures and scarring<br />Promote acceptance and adaptation to alterations in body image<br />
  • 113. Burns<br />First 24 hours<br />
  • 114. Burns<br />Second 24 hours<br />
  • 115. Considerations<br /><ul><li>AGE AND GENERAL HEALTH
  • 116. Mortality rates are higher for children < 4 y.o, particularly those < 1 y.o., and for clients over the age of 60 years.
  • 117. Debilitating disorders, such as cardiac, respiratory, endocrine, and renal d/o, negatively influence the client’s response to injury and treatment.
  • 118. Mortality rate is higher when the client has a pre-existing disorder at the time of the burn injury</li></li></ul><li>Electrolytes <br />
  • 119. Which one is not a cation?A. Calcium B. Magnesium C. Phosphorous D. Sodium<br />
  • 120. Anions and Cations<br />Anions<br />Cations<br />Calcium<br />Magnesium<br />Potassium<br />Sodium<br />Bicarbonate<br />Chloride<br />Phosphorous<br />
  • 121.
  • 122. WHAT DO ELECTROLYTES DO?<br />Promote neuromuscular irritability<br />Maintain body fluid volume and osmolarity<br />Distribute body water between fluid compartments<br />Regulate acid-base balance<br />
  • 123. Sodium (Na+)<br /><ul><li> Controls and regulates volume of body fluids
  • 124. Its concentration is the major determinant of ECF volume
  • 125. Is the chief electrolyte of ECF
  • 126. Influence ICF Volume
  • 127. Participates in the generation and transmission of nerve impulses
  • 128. Is an essential electrolyte in the sodium-potassium pump
  • 129. RDA: not known precisely. 500 mg
  • 130. Eliminated primarily by the kidneys, smaller in feces and perspiration
  • 131. Salt intake affects sodium concentrations
  • 132. Sodium is conserved through reabsorption in the kidneys, a process stimulated by aldosterone
  • 133. Normal value: 135-145 mEq/L</li></li></ul><li>HYPONATREMIA<br />Refers to the serum sodium concentration less than 135 mEq/L<br />Common with thiazide diuretic use, but may also be seen with loop and potassium-sparing diuretics as well<br />Occurs with marked sodium restriction, vomiting and diarrhea, SIADH, etc. The etiology may be mulfactorial<br />May also occur postop due to temporary alteration in hypothalamic function, loss of GI fluids by vomiting or suction, or hydration with nonelectrolyte solutions<br />Postoperative hyponatremia is a more serious complication in premenopausal women. The reasons behind this is unknown<br />Therefore monitoring serum levels is critical and careful assessment for symptoms of hyponatremia is important for all postoperative patients<br />
  • 134. PATHOPHYSIOLOGY OF HYPONATREMIA<br />Sodium loss from the intravascular compartment<br />Diffusion of water into the interstitial spaces<br />Sodium in the interstitial space is diluted<br />Decreased osmolarity of ECF<br />Water moves into the cell as a result of sodium loss<br />Extracellular compartment is depleted of water<br />CLINICAL SYMPTOMS<br />
  • 135. CLINICAL MANIFESTATIONS OF HYPONATREMIA<br />Muscle Weakness<br />APATHY<br />Postural hypotension<br />Nausea and<br />Abdominal Cramps<br />Weight Loss<br />In severe hyponatremia: mental confusion, delirium, shock and coma<br />
  • 136. COLLABORATIVE CARE MANAGEMENT<br />General goal: correct sodium imbalance and restore normal fluid and electrolyte homeostasis<br />Recognition of people at risk for hyponatremia is essential for its prevention: athletes, persons working in hot environments<br />Salt is always replaced along with water<br />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<br />Generally, an increased sodium and water intake provides adequate treatment<br />Education as the importance of sodium and fluid balance and the rationale for prescription medications to ensure compliance<br />Daily weight. MIO<br />Monitoring of sodium levels to determine extent of replacement<br />Generally, PNSS or PLRS is prescribed<br />Too rapid restoration of sodium balance, hypertonic sodium solutions may provoke brain injury <br />
  • 137. HYPERNATREMIA<br />A serum sodium level above 145 mEq/L is termed hypernatremia<br />May occur as a result of fluid deficit or sodium excess<br />Frequently occurs with fluid imbalance<br />Develops when an excess of sodium occurs without a proportional increase in body fluid or when water loss occurs without proportional loss of sodium<br />Risk Factors: excess dietary or parenteral sodium intake, watery diarrhea, diabetes insipidus, damage to thirst center, those with physical or mental status compromise, and people with hypothalamic dysfunction<br />
  • 138. PATHOPHYSIOLOGY OF HYPERNATREMIA<br />Increased Sodium concentration in ECF<br />Osmolarity rises<br />Water leaves the cell by osmosis and enters the the extracellular compartments<br />Dilution of fluids in ECF<br />Cells are water depleted<br />CLINICAL SYMPTOMS<br />Suppression of aldosterone secretion<br />Sodium is exreted in the urine<br />
  • 139. CLINICAL MANIFESTATIONS<br />Dry, sticky mucous membranes<br />Firm, rubbery tissue turgor<br />DEATH<br />Tachycardia<br />Manic excitement<br />
  • 140. COLLABORATIVE CARE MANAGEMENT<br />Recognition of risk factors: bedridden and debilitated patients, diabetes insipidus, fluid deprivation, the elderly and the very young<br />A careful and accurate record of MIO permits quick recognition of negative fluid balance<br />People with kidney failure, CHF, or increased aldosterone production may require dietary sodium intake restriction<br />Usually, osmolar balance can be restored with oral fluids. If not, the parenteral route may be necessary<br />Fluid resuscitation must be undertaken with particular caution in patients with compromised cardiac or renal function<br />The nurse should closely monitor the patient’s response to fluids and be alert to symptoms of fluid overload<br />
  • 141. Potassium (K+)<br /><ul><li> Major cation of the ICF. Chief regulator of cellular enzyme activity and cellular water content
  • 142. The more K, the less Na. The less K, the more Na
  • 143. 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
  • 144. Assists in regulation of acid-base balance by cellular exchange with H
  • 145. RDA: not known precisely. 50-100 mEq
  • 146. Sources: bananas, peaches, kiwi, figs, dates, apricots, oranges, prunes, melons, raisins, broccoli, and potatoes, meat, dairy products
  • 147. Excreted primarily by the kidneys. No effective conserving mechanism
  • 148. Conserved by sodium pump and kidneys when levels are low
  • 149. Aldosterone triggers K excretion in urine
  • 150. Normal value: 3.5 – 5 mEq/L</li></li></ul><li>CAUSES AND EFFECTS OF HYPOKALEMIA<br />Known as a low level of serum potassium, less than 3.5 mEq/L <br />Decreased Intake<br />↓ Food and Fluids as in starvation<br />Failure to replace GI losses<br />Increased Loss<br />↑ Aldosterone<br />Gastrointestinal losses<br />Potassium-losing diuretics<br />Loss from cells as in trauma, burns<br />Shift of Potassium into Cells<br />(No change in total body potassium)<br />HYPOKALEMIA<br />CNS<br />Lethargy, Diminished deep-tendon reflexes, Confusion, Mental depression<br />CV System<br />Decrease in standing BP, Dysrhythmias, ECG changes, Myocardial damage, Cardiac arrest<br />Muscles<br />Weakness, Flaccid paralysis, Weakness of respiratory muscles, Respiratory arrest<br />GI Tract<br />Anorexia N&V Abdominal distention<br />Kidneys<br />↓Capacity to concentrate waste, water loss, thirst, kidney damage<br />
  • 151. PATHOPHYSIOLOGY OF HYPOKALEMIA<br />= Action Potential<br />Nerve and Muscle Activity<br />The cell becomes less excitable<br />Low Extracellular K+<br />Increase in resting membrane potential<br />
  • 152. Aldosterone is secreted<br />Sodium is retained in the body through resorption by the kidney tubules<br />Potassium is excreted<br />Use of certain diuretics such as thiazides and furosemide, and corticosteroids<br />Increased urinary output<br />Loss of potassium in urine<br />
  • 153. COLLABORATIVE CARE MANAGEMENT<br />Being alert to the conditions that cause potassium depletion such as vomiting, diarrhea and diuretics, by monitoring the patient for early warning signs<br />No more than 3 enemas without consulting a physician<br />Education about the importance of adequate dietary intake of potassium <br />In severe hypokalemia, a patient may die unless potassium is administered promptly<br />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<br />If PO, taken with at least ½ glass of water<br />Cardiac monitoring is useful<br />Potassium sparing diuretics such as triamterene, spironolactone, etc<br />Symptoms of K depletion: muscle weakness, anorexia, nausea and vomiting = appropriate referral<br />
  • 154. CAUSES AND EFFECTS OF HYPERKALEMIA<br /><ul><li>Serum potassium level greater than 5.5 mEq/L</li></ul>Excess Intake<br />Dietary intake of excess of kidney’s ability to excrete; Excess parenteral administration<br />Decreased Loss<br />Potassium-sparing diuretics; Renal failure; Adrenal insufficiency<br />Shift of Potassium out of the Cells<br />Extensive injuries, crushing injuries, metabolic acidosis<br />HYPERKALEMIA<br />CNS<br />Numbness, paresthesias<br />CV System<br />Conduction disturbance, ventricular fibrillation, Cardiac Arrest<br />GI Tract<br />N&V Diarrhea, Colic<br />Muscles<br />Early: irritability<br />Late: weakness leading to flaccid paralysis<br />Kidneys<br />Oliguria leading to anuria<br />
  • 155. COLLABORATIVE CARE MANAGEMENT<br />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<br />Severity guides therapy<br />Mild: Withholding provoking agent (i.e., K supp)<br />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<br /><ul><li>Bowel function must be maintained if Kayexelate therapy is to be effective
  • 156. Potassium-wasting diuretics may be prescribed to promote further potassium loss. Dialysis for patients with renal failure to eliminate excess potassium
  • 157. Intravenous Ca Gluconate may be prescribed to counteract the cardiac effects of hyperkalemia
  • 158. Insulin infusions and IV NaCO3 may be used to promote intracellular uptake of K</li></li></ul><li>Calcium (Ca2+)<br /><ul><li> Most abundant electrolyte in the body. 99% in bones and teeth
  • 159. Close link between calcium and phosphorus. High PO4, Low Ca
  • 160. Necessary for nerve impulse transmission and blood clotting and is also a catalyst for muscle contraction and other cellular activities
  • 161. Needed for Vitamin B12 absorption and use
  • 162. Necessary for strong bones and teeth and thickness and strength of cell membranes
  • 163. RDA: 1g for adults. Higher for children and pregnant and lactating women according to body weight, older people, esp. post-menopausal
  • 164. Found in milk, cheese, and dried beans; some in meat and vegetables
  • 165. Use is stimulated by Vitamin D. Excreted in urine, feces, bile, digestive secretions, and perspiration
  • 166. Normal value 8.5 – 10.5 mg/dl</li></li></ul><li>CAUSES AND EFFECTS OF HYPOCALCEMIA<br />Decreased Ionized Ca<br />Large tranfusion with citrated blood<br />Excess Loss<br />Kidney Disease<br />Decrease in GI Tract and Bone Absorption<br />↑Magnesium<br />↑Calcitonin<br />↓Vitamin D<br />↓Parathyroid Hormone<br />Inadequate Intake<br />Dietary Deficit<br />HYPOCALCEMIA<br />CNS<br />Tingling <br />↓ convulsions<br />Bones<br />Osteoporosis leading to Fractures<br />Other<br />Abnormal deposits of calcium in body tissues<br />Muscles<br />Muscle spasm <br />↓ <br />Tetany<br />Cardiovascular System<br />Dysrhythmias<br />↓<br />Cardiac arrest<br />
  • 167. PATHOPHYSIOLOGY OF HYPOCALCEMIA<br /><ul><li>Calcium ions are thought to line the pores of cell membranes, especially neurons
  • 168. Calcium and Sodium repel each other
  • 169. When serum calcium levels are low, this blocking effect is minimized
  • 170. When Sodium moves more easily into the cell, depolarization takes place more easily
  • 171. This results in increased excitability of the nervous system leading to muscle spasm, tingling sensations, and if severe, convulsions and tetany
  • 172. Skeletal, smooth, and cardiac muscle functions are all affected by overstimulation</li></ul>CELL<br />Calcium<br />Sodium<br />
  • 173. CLINICAL MANIFESTATIONS OF HYPOCALCEMIA<br />PAINFUL MUSCULAR SPASMS (TETANY) ESPECIALLY OF FEET AND HANDS (CARPOPEDAL SPASMS), MUSCLE TWITCHING AND CONVULSIONS MAY FOLLOW<br />TREATMENT<br />COMPLAINT OF NUMBNESS AND TINGLING OF EARS, NOSE, FINGERTIPS OR TOES<br />
  • 174. TESTS USED TO ELICIT SIGNS OF CALCIUM DEFICIENCY<br />TROUSSEAU'S SIGN<br />CHVOSTEK'S SIGN<br />
  • 175. COLLABORATIVE CARE MANAGEMENT<br />Identify risk factors: Inadequate calcium intake, excess calcium loss, Vitamin D deficiency, patients with poor diets<br />Education about the importance of adequate calcium and Vitamin D intake<br />Patients undergoing thyroid, parathyroid, and radical neck surgery are particularly vulnerable to hypocalcemia secondary to parathyroid hormone deficit<br />Monitoring of serum calcium levels and correction of deficits<br />Citrate is added to store blood to prevent coagulation. <br />Citrate + Transfusion = Citrate+Calcium<br />Normally, Liver + Citrate = Quick metabolism<br />Preexisting calcium deficit/hepatic dysfunction/large amounts of BT very rapidly = hypocalcemia<br />With acute hypocalcemia, Ca Gluconate is used + Continuous cardiac monitoring<br />Mild Hypocalcemia: High calcium diet or oral calcium salts<br />If PTH or Vit D Deficiency is the cause: aluminum hydroxide gel is used because when serum phosphate level rises, calcium level falls<br />Complication: Bone demineralization<br />Therefore, careful ambulation should be encouraged to minimize bone resorption<br />
  • 176. HYPERCALCEMIA: Serum concentration > 10mg/dLCauses and Effects<br />Loss from bones<br />Immobilization, Carcinoma with bone metastases, Multiple myeloma<br />Excess Intake<br />↑ Calcium diet (esp. milk)<br />Antacids containing calcium<br />Increase in factors Causing Mobilization from bone<br />↑PTH, ↑ Vitamin D, steroid therapy<br />HYPERCALCEMIA<br />CNS<br />↓Deep-tendon reflexes<br />↓<br />Lethargy<br />↓<br />Coma<br />Muscles<br />Muscle fatigue, hypotonia<br />↓<br />↓ GI motility<br />Kidneys<br />Stones<br />↓<br />Kidney Damage<br />Bones<br />Bone pain<br />↓<br />Osteoporosis<br />↓<br />Fractures<br />CV System<br />Depressed activity<br />↓<br />Dysrhythmias<br />↓<br />Cardiac Arrest<br />
  • 177. HOW IT HAPPENS<br />HYPERCALCEMIA<br />DEPRESSED NERVE AND MUSCLE ACTIVITY<br />DEEP TENDON REFLEXES MAY BE DECREASED OR ABSENT<br />MYOCARDIAL FUNCTION IS ALTERED<br />
  • 178. CLINICAL MANIFESTATIONS OF HYPERCALCEMIA<br />Constipation<br />Cardiac Dysrhythmias<br />Nausea<br />Decreased GI Motility<br />Mental status changes: lethargy, confusion, memory loss<br />
  • 179. CLINICAL MANIFESTATIONS OF HYPERCALCEMIA<br />Calcium accumulates in the ECF and passes through the kidneys<br />Immobilization<br />Bone Demineralization<br />Calcium Stones<br />Ca Precipitation<br />
  • 180. COLLABORATIVE CARE MANAGEMENT<br />Mild hypercalcemia: hydration and education about avoiding foods high in calcium or medications that promote calcium elevation<br />Ambulation as appropriate; weight-bearing exercises as tolerated<br />Trapeze, resistance devices<br />Marked hypercalcemia: prevention of pathologic fractures, individualized plan of care<br />Prevention of renal calculi: encourage oral fluids to prevent concentrated urine: 3000 to 4000 mL/day unless contraindicated<br />Acid-ash fruit juices: cranberry juice and prune juice<br />Severe hypercalcemia: medical emergency: continuous cardiac monitoring, hydration, IV furosemide, Calcitonin and/or plicamycin (mithramycin), q2 serum and urinary electrolytes<br />
  • 181. Magnesium (Mg2+)<br /><ul><li> Mostly found within body cells: heart, bone, nerve, and muscle tissues
  • 182. Second most important cation in the ICF, 2nd to K+
  • 183. 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
  • 184. RDA: about 18-30 mEq; children require larger amounts
  • 185. Sources: vegetables, nuts, fish, whole grains, peas, and beans
  • 186. Absorbed in the intestines and excreted by the kidneys
  • 187. Plasma concentrations of magnesium range from 1.5 – 2.5 mEq/L, with about one third of that amount bound to plasma proteins</li></li></ul><li>HYPOMAGNESEMIA: Serum level < 1.5 mEq/L<br />Usually coexists with hypokalemia and less often with hypocalcemia<br />Decreased Intake<br />Prolonged malnutrition, Starvation<br />Impaired absorption from GI Tract<br />Malabsorption syndrome, Alcohol Withdrawal Syndrome, Hypercalcemia, Diarrhea, Draining gastrointestinal fistula<br />Excessive Excretion<br />↑Aldosterone, Conditions causing large losses of urine<br />HYPOMAGNESEMIA<br />Mental Changes<br />Agitation, Depression, Confusion<br />Muscles<br />Cramps, Spasticity, Tetany<br />CV System<br />Tachycardia, Hypotension, Dysrhythmias<br />CNS<br />Convulsions, Paresthesias, Tremor, Ataxia<br />HYPOKALEMIA<br />
  • 188. PATHOPHYSIOLOGY OF HYPOMAGNESEMIA<br />Low serum magnesium level<br />Increased acetylcholine release<br />Increased neuromuscular irritability<br />Increased sensitivity to acetylcholine at the myoneural junction<br />Diminished threshold of excitation for the motor nerve<br />Enhancement of myofibril contraction<br />
  • 189. PATHOPHYSIOLOGY OF HYPOMAGNESEMIA<br />High Serum Calcium<br />Increased acetylcholine release<br />Increased neuromuscular irritability<br />Increased sensitivity to acetylcholine at the myoneural junction<br />Diminished threshold of excitation for the motor nerve<br />Enhancement of myofibril contraction<br />Excretion of Magnesium<br />By the GI tract<br />High Serum Calcium<br />
  • 190. PATHOPHYSIOLOGY OF HYPOMAGNESEMIA<br />MAGNESIUM<br />INHIBITS TRANSPORT OF PTH<br />DECREASE IN THE AMOUNT OF CALCIUM BEING RELEASED FROM THE BONE<br />POSSIBLE CALCIUM DEFICIT<br />
  • 191. CLINICAL MANIFESTATIONS OF HYPOMAGNESEMIA<br />DEPRESSION<br />CONFUSION<br />CRAMPS<br />TETANY<br />CONVULSIONS<br />
  • 192. COLLABORATIVE CARE MANAGEMENT<br />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<br />Recognition of signs and symptoms of magnesium deficiency<br />Magnesium is essential for potassium resorption, so if hypokalemia does not respond to potassium replacement, hypomagnesemia should be suspected<br />Treatment of the underlying cause is the first consideration in hypomagnesemia<br />Severe: parenteral magnesium replacement is indicated<br />IV therapy: continuous cardiac monitoring<br />Safety measures for patients with mental status changes<br />
  • 193. HYPERMAGNESEMIA: Serum Mg level 2.5 mEq/L<br />Seldom develops in the presence of normal renal function<br />May occur as a result of Mg replacement<br />May occur when MgSO4 is administered to prevent seizures resulting from eclampsia<br />Careful monitoring is imperative<br />
  • 194. PATHOPHYSIOLOGY<br />Renal failure, Excessive IV infusion of magnesium, Decreased GI elimination and/or absorption, etc.<br />Accummulation of Mg in the body<br />Mg Level Rises<br />Altered Electrical Conduction<br />Slowed heart rate and AV Block<br />Diminishing of reflexes, drowsiness, lethargy<br />Severe Respiratory Depression<br />Peripheral vasodilation<br />RESPIRATORY ARREST may occur<br />Hypotension, flushing, and increased skin warmth<br />
  • 195. COLLABORATIVE CARE MANAGEMENT<br />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<br />Any patient receiving parenteral magnesium therapy should be assessed frequently for signs of hypermagnesemia<br />Mild hypermagnesemia: withholding magnesium-containing medications may suffice<br />Renal failure: dialysis<br />Severe: may require treatment with calcium gluconate (10-20 mL of 10% Ca Gluconate administered over 10 minutes)<br />If cardiorespiratory collapse is imminent, the patient may require temporary pacemaker and ventilator support<br />
  • 196. NURSING MANAGEMENT OF PATIENT WITH FLUID AND ELECTROLYTE IMBALANCES<br />
  • 197. Parameter_____Fluid Excess___ Fluid Loss/Electrolyte Imbalance____<br />Behavior Tires easily; Change in behavior, confusion, apathy<br />Head, neck Facial edema, distended neck Headache, thirst, dry mucous membranes veins<br />Upper GI Anorexia, nausea, vomiting <br /> Skin Warm, moist, taut, cool feeling Dry, decreased turgor where edematous<br />Respiration Dyspnea, orthopnea, productive Changes in rate and depth of respiration cough, moist breath sounds<br />Circulation Loss of sensation in edematous Pulse rate changes, dysrhythmia, posturalareas, pallor, bounding pulse, increased blood pressure hypotension <br />Abdomen Increased girth, fluid wave Distention, abdominal cramps<br />Elimination Constipation Diarrhea, constipation<br />Extremities Dependent edema, “pitting” Muscle weakness, tingling, tetany , discomfort from weight of bedclothes <br />A<br />
  • 198. Refractory Edema<br />Pitting edema<br />Dependent edema<br />
  • 199. A<br />LABORATORY VALUES<br />FLUID DEFICITFLUID EXCESS<br /> Hemoconcentration Hemodilution<br />↑ Hct, BUN, E+ levels↓ Hct, BUN, E+ levels<br />↑ Urine Specific Gravity ↓ Urine Specific Gravity<br />
  • 200. Determined from analysis of patient data<br />Diagnostic TitlePossible Etiologic Factors<br /> 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<br /> 2 Excess Fluid Volume Excess fluid intake, excess sodium intake, compromised regulatory processes<br />D<br />
  • 201. P<br />EXPECTED PATIENT OUTCOMES<br />1. 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<br />2. Will verbalize understanding of treatment plan and causative factors that led to the imbalance<br />
  • 202. 1,2 Intake and Output Monitoring<br /> - Type and amount of fluid the patient has received and the route by which they were administered<br /> - Record of solid food intake. Gelatin or Popsicles are recorded as fluids<br /> - Ice chips are recorded by dividing the amount of chips by ½ (60 mL of chips = 30 mL water)<br /> - 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)<br /> - With acid-base balance upset, gastric secretions may have a fruity odor because of ketone bodies<br /> - Bile: thicker than gastric juice, dark green to brown, acrid odor, bitter taste when vomiting<br /> - NGT irrigation added to intake<br /> - Stools: difficult to estimate amount; consistency, color, and number of stools provide a reasonable estimate<br /> - Peritoneal or pleural fluid drainage is recorded as output as with its amount, color, and clarity <br /> - Character and volume of urine. Place signs and materials so that an accurate record of UO is maintained<br />I<br />
  • 203. 1,2 Intake and Output Monitoring<br /> - Evaluate and refer urine specific gravity as appropriate (normal value is 1.003 – 1.030). The implications are:<br /> High Dehydration<br /> Low SIADH, overhydration<br /> - 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<br /> - Accurate recording of the temperature to help the physician determine how much fluid should be replaced <br />1,2 Daily Weight<br /> - Evaluate trends in weight (An increase in 1kg in weight is equal to the retention of 1L of fluid in an edematous patient)<br /> Considerations: <br /> - Daily weights early in the morning after voiding but before he or she has eaten or defecated<br />I<br />
  • 204. 1 Replacement of Fluid and Electrolytes<br /> General Principles:<br /> - Either by oral intake (healthiest way), tube feeding, intravenous infusion, and/or total parenteral nutrition<br /> - Normal saline solution and plain water should also be given by slow drip to replace daily fluid loss<br /> - IV administration per doctor’s orders<br /> - Fluid replacement considerations:<br /> * 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 <br /> shifts)<br /> * Administer concentrated solutions of Na, Glucose or protein because they require body fluids for dilution<br /> * Consider the size of the patient (small adult has less fluid in each compartment, especially in the intravascular compartment)<br /> - Promote oral intake as appropriate<br /> * Caution with coffee, tea, and some colas<br />I<br />
  • 205. * small amount at frequent intervals is more useful than a large amount presented less often<br /> * Always give consideration to cultural and aesthetic aspects of eating<br /> - 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)<br /> - Avoid irritating foods<br /> - Stimulation of saliva may be aided by hard candy or chewing gum or carboxymethylcellulose (artificial saliva)<br /> - Keep lips moist and well lubricated<br /> - 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.<br /> - 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)<br /> - Increase usual daily requirement of foods when losses must be restored, as tolerated<br />I<br />
  • 206. * Patients with cardiac and renal impairments are instructed to avoid foods containing high levels of sodium, potassium and bicarbonate<br /> - Administer replacement solutions through tube feeding as is<br /> * Either water, physiologic solution of NaCl, high protein liquids, or a regular diet can be blended, diluted and given by gavage<br /> * The water content in the tube feeding needs to be increased if:<br /> 1 the patient complains of thirst<br /> 2 the protein or electrolyte content of the tube feeding is high<br /> 3 the patient has fever or disease causing an increased metabolic rate<br /> 4 UO is concentrated<br /> 5 signs of water deficit develop<br /> - Administer parenteral fluids as necessary<br />I<br />
  • 207. * Types of solutions<br /> - D5W (hypotonic) is given short-term for hyponatremia<br /> - 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<br /> - Dextrose 5% in 0.2% normal saline is generally used as a maintenance fluid<br /> - Dextrose 5% in ½ normal saline is generally used as a replacement solution for losses caused by gastrointestinal drainage<br /> - PNSS is given primarily when large amounts of sodium have been lost and for patients with hyponatremia<br /> - LRS is also isotonic because it remains in the extracellular space<br /> - Fructose or 10-20% glucose in distilled water are hypertonic solutions and may partially meet body needs for CHOs<br /> - 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<br />I<br />
  • 208. * Administration<br /> - The rate should be regulated according to the patient’s needs and condition per doctor’s orders<br /> - Monitor UO carefully. Refer marked decreases!<br /> - Verify orders for potassium administration in patients with renal failure and untreated adrenal insufficiency<br /> - Usual rate for fluid loss replacement: 3ml/min<br /> - Recognize signs of pulmonary edema (bounding pulse, engorged peripheral veins, hoarseness, dyspnea, cough, and rales) that can result from ↑IV rate<br />- If infiltration occurs, the infusion should be stopped immediately and relocated. Peripheral IV sites are generally rotated every 72 hours<br /> - 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<br /> - Pronounced and continued thirst despite administration of fluids is not normal and should be reported (may indicate DM or hypercalcemia)<br />I<br />
  • 209. I<br /> * Patient/Family Education<br /> - Include the signs and symptoms of water excess in discharge instructions<br /> - With drug therapy, instruct patient and family regarding correct method of administration, correct dose, and therapeutic and adverse effects<br /> - Instruct to read labels for nutritional content<br /> * For K restriction: avoid organ meats, fresh and dried fruits, and salt substitutes<br /> - Skin assessment and care, positioning techniques for patients with mobility restrictions<br />
  • 210. E<br /> * Achievement of outcomes is successful in disturbances in fluid and electrolyte balance:<br /> 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<br /> 2 States possible causes of imbalance and plan to prevent recurrence of imbalances<br /> 3 Reports a decrease or absence of symptoms causing discomfort<br />
  • 211. Fluids and Electrolytes<br />Acid-base balance<br />
  • 212. DRAWING ARTERIAL BLOOD GASES<br />ALLEN’S TEST<br />ARTERIAL PUNCTURE<br />
  • 213. NORMAL ACID-BASE BALANCE<br />Definition and Implications<br />Normal Value<br />Parameter<br />Partial pressure of oxygen in arterial blood (decreases with age)<br />In adults < 60 years:<br /> 60-80 mmHg = mild hypoxemia<br /> 40-60 mmHg = moderate hypoxemia<br /> < 40 mmHg = severe hypoxemia<br />80-100 Hg<br />PaO2<br />Identifies whether there is acidemia or alkalemia:<br />pH<7.35 = acidosis; pH>7.45 = alkalosis<br />7.35-7.45<br />pH<br />Partial pressure of CO2 in the arterial blood:<br />PCO2<35 mmHg = respiratory alkalosis<br />PCO2>45 mmHg = respiratory acidosis<br />35-45 mmHg<br />PaCO2<br />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<br />22-26 mEq/L<br />Standard HCO3<br />
  • 214.
  • 215. BASIC REGULATION OF ACID-BASE BALANCE<br /> CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3<br />Kidney<br />Lungs<br />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<br />
  • 216. TYPES OF ACID-BASE DISTURBANCES<br />Depression of the central nervous system, as evidenced by disorientation followed by coma<br />ACIDOSIS<br />Overexcitability of the nervous system; muscles may go into a state of tetany and convulsioons<br />ALKALOSIS<br />
  • 217.
  • 218. EXPECTED DIRECTIONAL CHANGES WITH ACID-BASE IMBALANCES<br />HCO3<br />PCO2<br />pH<br />CONDITION<br />Normal<br />↑<br />↑<br />↑<br />↑<br />↑<br />↓<br />↓<br />Normal<br />Respiratory Acidosis<br />Uncompensated<br />Partly Compensated<br />Compensated<br />Normal<br />↓<br />↓<br />↓<br />↓<br />↓<br />↑<br />↑<br />Normal<br />Respiratory Alkalosis<br />Uncompensated<br />Partly Compensated<br />Compensated<br />↓<br />↓<br />↓<br />Normal<br />↓<br />↓<br />↓<br />↓<br />Normal<br />Metabolic Acidosis<br />Uncompensated<br />Partly Compensated<br />Compensated<br />↑<br />↑<br />↑<br />Normal<br />↑<br />↑<br />↑<br />↑<br />Normal<br />Metabolic Alkalosis<br />Uncompensated<br />Partly Compensated<br />Compensated<br />
  • 219.
  • 220. Compensation<br />
  • 221. RESPIRATORY ACIDOSIS: CARBONIC ACID EXCESS<br />Damage to the respiratory center in the medulla, drug or narcotic use, obstruction of respiratory passages, respiratory and respiratory muscle disorders<br />Decrease in the rate of pulmonary ventilation<br />Increase in the concentration of CO2, carbonic acid, and hydrogen ions<br />RESPIRATORY ACIDOSIS<br />Potassium moves out of the cells<br />HYPERKALEMIA<br />VENTRICULAR FIBRILLATION<br />
  • 222.
  • 223. NURSING MANAGEMENT OF RESPIRATORY ACIDOSIS<br />ASSESSMENT<br /> * Health Hx: complaints of headache, confusion, lethargy, nausea, irritability, nausea, irritability, anxiety, dyspnea, and blurred vision, preexisting conditions<br /> * Physical Examination: lethargy to stupor to coma, tachycardia, hypertension, cardiac dysrhythmias, airway patency<br />NURSING DIAGNOSES include but are not limited to:<br />Diagnostic TitlePossible Etiologic Factors<br />1 Impaired gas exchange Hypoventilation<br />2 Disturbed thought processes Central nervous system depression<br />3 Anxiety Hypoxia, hospitalization<br />4 Risk for ineffective family Illness of a family member coping<br />5 Ineffective airway clearance Hypoventilation, secretions<br />6 Ineffective breathing pattern Hypoventilation, dyspnea<br />
  • 224. NURSING MANAGEMENT OF RESPIRATORY ACIDOSIS<br />EXPECTED PATIENT OUTCOMES include but are not limited to:<br /> 1 Will maintain airway patency and adequate breathing rate and rhythm will return of ABGs to patient’s normal level<br /> 2 Will be alert and oriented to time, place, and person, or to his or her normal baseline level of consciousness<br /> 3 Will cope with anxiety<br /> 4 Will exhibit effective coping and awareness of effective support systems<br /> 5 Will have secretions that are normal for self in amount and can be raised<br /> 6 Will maintain adequate rate and depth of respirations using pursed lip and other breathing techniques when necessary (as in the patient with COPD)<br />
  • 225. NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS<br />INTERVENTIONS<br /> 1 Supporting effective gas exchange<br /> - Provide a position of comfort to allow ease of respiration<br /> - Obtain and monitor ABG results and VS. Refer accordingly<br /> - Provide and monitor supplemental oxygen as ordered<br /> - Turn the patient q2 and PRN<br /> - Provide pulmonary hygiene PRN<br /> - Maintain adequate hydration<br /> - Provide comfort measures such as mouth care<br /> - Assist with ADLs<br /> - Instruct patient regarding coughing and deep breathing and management of disease condition, especially COPD<br /> 2 Coping with disturbed thought processes<br /> - Do frequent neurologic assessments<br /> - Monitor and document person’s baseline LOC frequently<br />
  • 226. NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS<br /> - Reorient as necessary by providing calendars, clocks, etc.<br /> 3 Relieving anxiety<br /> - Provide a calm, relaxed environment<br /> - Give clear, concise explanations of treatment plans<br /> - Encourage expression of feelings<br /> - Provide support and information to patient and family<br /> - Teach relaxation techniques<br /> - Assist the patient to identify coping mechanisms to deal with anxiety and stress<br /> 4 Enhancing coping mechanisms<br /> - Provide support and information to family members about the patient’s ongoing condition<br /> - Reassure them that there is a physiologic cause for the patient’s behavior<br />
  • 227. NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS<br /> - Encourage questions and open communication<br /> 5 Promote airway clearance<br /> - Implement regular breathing and coughing exercises<br /> - Do suctioning as necessary<br /> - Maintain good hydration<br /> - Do chest physiotherapy as appropriate<br /> 6 Promoting an effective breathing pattern<br /> - Maintain alveolar ventilation<br /> - Teach the patient proper breathing techniques as well as panic control breathing <br />
  • 228. NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS<br />EVALUATION. Achievement of outcomes is successful when the patient:<br /> 1a. Demonstrates improved ventilation and oxygenation<br /> 1b Has vital signs, ABGs, and cardiac rhythm within own normal range<br /> 2 Returns to baseline LOC<br /> 3 Reports reduced anxiety<br /> 4 Family uses adequate coping mechanisms<br /> 5 Is able to raise secretions on own<br /> 6 Demonstrate effective breathing techniques<br />
  • 229. RESPIRATORY ALKALOSIS: CARBONIC ACID DEFICIT<br />Anxiety, hysteria, fever, hypoxia, pain, pulmonary disorders, lesions affecting the respiratory center in the medulla, brain tumor, encephalitis, meningitis, hyperthyroidism, gram-negative sepsis<br />Hyperventilation: Excessive pulmonary ventilation<br />Decrease in hydrogen ion concentration<br />RESPIRATORY ALKALOSIS<br />
  • 230.
  • 231. NURSING MANAGEMENT OF RESPIRATORY ALKALOSIS<br />ASSESSMENT<br /> * Health Hx: anxiety, shortness of breath, muscle cramps or weakness, palpitations, panic, dyspnea<br /> * 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<br />NURSING DIAGNOSES include but are not limited to:<br />Diagnostic TitlePossible Etiologic Factors<br />1 Anxiety Stress, fear<br />2 Ineffective breathing pattern Hyperventilation, anxiety<br />3 Disturbed thought processes CNS excitability; irritability<br />4 Risk for injury Change in LOC, and potential for seizures<br />
  • 232. NURSING MANAGEMENT OF RESPIRATORY ALKALOSIS<br />EXPECTED PATIENT OUTCOMES include but are not limited to:<br /> 1 Will report decreased anxiety; verbalizes methods to cope with anxiety<br /> 2 Will return to normal respiratory rate and rhythm or at least decreased hyperventilation, with return to baseline ABGs<br /> 3 Will exhibit reorientation to person, place, and time as per patient’s baseline<br /> 4 Will be free from injury<br />INTERVENTIONS<br /> 1 Allay anxiety<br /> - Give antianxiety medications as ordered<br /> - Have patient breath into a paper bag<br /> - Teach relaxation techniques when initial anxiety attack is over<br />
  • 233. NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS<br />INTERVENTIONS<br /> 2 Promoting an Effective Breathing Pattern<br /> - Encourage the patient to slow his or her RR<br /> - Maintain a calm and comforting attitude<br /> - Position the patient to promote maximal ease of inspiration<br /> - Assist the patient with relaxation techniques<br /> 3 Coping with Disturbed Thought Processes<br /> - Do frequent reorientation<br /> - Encourage family to participate in patient’s care<br /> - Use simple, direct statements or directions<br /> - Allow the patient adequate time to respond<br /> 4 Preventing injuries<br /> - Perform neurologic assessment frequently and document<br /> - Institute safety and seizure precautions<br /> - Assess frequently for muscle strength and coordination<br />
  • 234. NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS<br />EVALUATION. Achievement of outcomes is successful when the patient:<br /> 1 Reports reduction in anxiety levels<br /> 2a Demonstrates effective normal breathing patterns<br /> 2b Has ABG results within patient’s normal baseline<br /> 3 Returns to normal baseline LOC and orientation level<br /> 4 Remains free from injury; no seizure activity<br />
  • 235. METABOLIC ACIDOSIS: BICARBONATE DEFICIT<br />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<br />Excess organic acids are added to body fluids or bicarbonate is lost<br />Decrease in bicarbonate concentration<br />METABOLIC ACIDOSIS<br />
  • 236.
  • 237. NURSING MANAGEMENT OF METABOLIC ACIDOSIS<br />ASSESSMENT<br /> * Health Hx: anorexia, nausea, vomiting, abdominal pain, headache, thirst if the patient is dehydrated<br /> * 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<br />NURSING DIAGNOSES include but are not limited to:<br />Diagnostic TitlePossible Etiologic Factors<br />1 Disturbed thought processes Secondary to CNS depression<br />2 Decreased cardiac output Dysrhythmias<br />3 Risk for injury Secondary to altered mental state<br />4 Risk for imbalanced fluid Diarrhea, renal failure<br /> volume<br />
  • 238. NURSING MANAGEMENT OF METABOLIC ACIDOSIS<br />EXPECTED PATIENT OUTCOMES include but are not limited to:<br /> 1 Will return to usual baseline LOC<br /> 2 Will return to normal baseline parameters for vital signs with improved CO and decreased or resolved dysrhythmias<br /> 3 Will remain in a safe, secure environment without injury<br /> 4 Will maintain fluid and electrolyte balance and stable renal status<br />INTERVENTIONS<br /> 1 Coping with disturbed thought processes<br /> - Monitor LOC and reorient as necessary<br /> - Monitor VS, esp. RRR, BP, and T<br /> - Monitor ABGs to assess the effects of treatment<br /> - Institute cardiac monitoring as ordered<br />
  • 239. NURSING MANAGEMENT OF PATIENT WITH METABOLIC ACIDOSIS<br /> 2 Supporting cardiac output <br /> - Monitor VS, MIO, and fluid and electrolyte balance<br /> - Institute cardiac monitoring to evaluate cardiac status<br /> 3 Promoting safety<br /> - Provide a safe, secure and monitored environment<br /> - Institute safety precautions<br /> 4 Promoting return of fluid and electrolyte balance<br /> - Monitor MIO<br /> - Administer medications per medical order<br />
  • 240. NURSING MANAGEMENT OF PATIENT WITH METABOLIC ACIDOSIS<br />EVALUATION. Achievement of outcomes is successful when the patient:<br /> 1 Exhibits baseline-level consciousness and orientation<br /> 2 Returns to normal baseline parameters for vital signs and Cardiac Output with cardiac dysrhythmias resolved<br /> 3 Remains free from injury<br /> 4 Maintains fluid and electrolyte balance and stable renal function<br />
  • 241. METABOLIC ALKALOSIS: BICARBONATE EXCESS<br />Loss of stomach acid, gastric suctioning, persistent vomiting, excess alkali intake, intestinal fistulas, hypokalemia, Cushing’s syndrome or aldosteronism, potassium-diuretic therapy<br />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<br />Excess of base elements<br />METABOLIC ALKALOSIS<br />
  • 242.
  • 243. NURSING MANAGEMENT OF METABOLIC ALKALOSIS<br />ASSESSMENT<br /> * 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<br /> * 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<br />NURSING DIAGNOSES include but are not limited to:<br />Diagnostic TitlePossible Etiologic Factors<br />1 Disturbed thought processes CNS excitation<br />2 Decreased cardiac output Dysrhythmias and electrolyte imbalances<br />3 Risk for injury Muscle weakness, tetany, confusion and possible seizures<br />4 Risk for imbalanced fluid Nasogastric drainage, diuretic therapy<br /> volume fistula<br />
  • 244. NURSING MANAGEMENT OF METABOLIC ALKALOSIS<br />EXPECTED PATIENT OUTCOMES include but are not limited to:<br /> 1 Will return to usual baseline LOC and orientation<br /> 2 Will return to normal baseline parameters for vital signs with improved CO with resolution of electrolyte imbalances and decreased or resolved cardiac dysrhythmias<br /> 3 Will remain in a safe, secure environment without injury<br /> 4 Will maintain fluid and electrolyte balance <br />INTERVENTIONS<br /> 1 Coping with disturbed thought processes<br /> - Monitor LOC and reorient as necessary<br /> - Monitor VS, esp. RRR, BP, and T<br /> - Monitor ABGs to assess the effects of treatment<br /> - Institute cardiac monitoring as ordered<br />
  • 245. NURSING MANAGEMENT OF PATIENT WITH METABOLIC ALKALOSIS<br /> 2 Supporting cardiac output <br /> - Monitor VS, MIO, and fluid and electrolyte balance<br /> - Institute cardiac monitoring to evaluate cardiac status<br /> 3 Promoting safety<br /> - Provide a safe, secure and monitored environment<br /> - Institute safety precautions<br /> 4 Promoting return of fluid and electrolyte balance<br /> - Monitor MIO<br /> - Administer medications per medical order<br />
  • 246. NURSING MANAGEMENT OF PATIENT WITH METABOLIC ALKALOSIS<br />EVALUATION. Achievement of outcomes is successful when the patient:<br /> 1 Manifests mental status has returned to baseline<br /> 2 Is free from cardiac dysrhythmias<br /> 3 Remains free from injury<br /> 4 Maintains fluid balance at baseline level<br />
  • 247. CRITICAL THINKING EXERCISES<br />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:<br /> pH: 7.57<br /> PaO2: 92<br /> PaCO2: 41<br /> HCO3: 36<br />Describe her acid-base status, probable cause for the imbalance and treatment<br />

×