NR 324 Exam 1 Study Guide Chapters 17, 26, 27, 28, 29, and ABG interpretation.
NR 324 Exam 1 Study Guide
Chapters 17, 26, 27, 28, 29, and ABG
... [Show More] interpretation.
Fluid & Electrolyte
1. Potassium Chloride intravenous- care of patient, how much (meq/hr) is the infusion rate?(p.316)
Potassium Chloride intravenous can be administered to treat a patient with hypokalemia.
Except in severe deficiencies, KCL is never given unless there is urine output of at least 0.5ml/kg of body weight per hour
Safety Alert:
• KCL given intravenously must always be diluted.
• Never give KCL via IV push or in concentrated amounts.
• IV bags containing KCL should be inverted several times to ensure even distribution in the bag.
• Never add KCL to a hanging IV bag to prevent giving a bolus dose.
How much (meq/hr) is the infusion rate?
The preferred maximum concentration is 40 mEq/L; however, stronger concentrations may be given
for severe hypokalemia (up to 80mEq/L) with continuous cardiac monitoring.
The rate of IV administration of KCL should not exceed 10 to 20mEq per hour and should be administered by infusion pump to ensure correct administration rate. Because KCL is irritating to the vein, assess IV sites at least hourly for phlebitis and infiltration
o Infiltration can cause necrosis and sloughing of the surrounding tissue.
Central IV lines should be used when rapid correction of hypokalemia is necessary
2. ABG interpretation( do the practice questions that teacher gave& p324 & hesi 43,44)
An acid-base balance must be maintained in the body because alterations can result in alkalosis or acidosis.
Maintain the acid –base balance involves 3 systems
• Chemical buffer
o The chemical buffer act immediately to prevent major change in the body fluid pH by removing or releasing hydrogen ions.
The main chemical buffer is the Bicarbonate-Carbonic acid (HCO3-
H2CO30system.
• Normally there are 20parts of bicarbonate to 1 part of carbonic acid. If the 20:1 ratio is altered, the pH is changed( ratio is important not absolute values)
• Carbonic acid (H2CO3) is form when carbon dioxide (CO2) combines with water (H2O).
• Excess CO2 in the body alters the ratio and creates an imbalance. Other buffer system involve:
o Monohydrogen-dihydrogen phosphate
o Intracellular and plasma protein
o Hemoglobin
• Respiratory system (lungs)
o The respiratory system responds in minutes and reaches maximum effectiveness in hours
Control CO2 content through respirations (carbonic acid content)
Control, to a small extent, water balance (CO2+H2O=H2CO3)
Release excess CO2 by increasing respiratory rate.
Retain CO2 by decreasing respiratory rate.
The rate of the CO2 is control by the respiratory center in the medulla in the brainstem.
If the respiratory problem is the cause of an acid –base imbalance (e.g., respiratory failure), the respiratory system loses its ability to correct a pH alteration.
• Renal system (kidney)
o The renal response takes 2 to 3 days to respond maximally, but the kidneys can maintain balance indefinitely in chronic imbalance.
Regulate bicarbonate levels by retaining and reabsorbing bicarbonate as needed.
a very slow compensatory mechanism ( can require hour or days).
Cannot help with compensation when metabolic acidosis is created by renal failure
If the renal system is the cause of and acid-base imbalance (e.g., renal failure), it loses its ability to correct a pH alteration.
Arterial Blood Gas (ABG) values provide valuable information about a patient’s acid-base status, the underlying cause of the imbalance, the body’s ability to regulate pH, and the patient’s overall oxygen status. (p. 324, shows the steps on how to diagnose acid disturbances and identification of compensatory processes).
• Uncompensated respiratory Alkalosis with hypoxemia(Kidney clearance)
• Uncompensated Respiratory Acidosis with Hypoxemia
• Partially compensated Respiratory Acidosis
• Partially compensated Metabollic Alkalosis(Kidney and lungs are helping each other)
• Fully compensated Respiratory Alkalosis(Good prognosis)
Page44 hesi
Acid-base condition pH Pco2
(mm Hg) HCO3
(mEq/L)
Normal 7.34-7.45 35-45 22-26
Respiratory
Acidosis ↓ ↑
Normal
Respiratory
Alkalosis ↑ ↓ Normal
Metabolic
Acidosis ↓ Normal ↓
Metabolic
Alkalosis ↑ Normal ↑
• Respiratory
• Opposite
• Metabolic
• Equal
A. pH 7.50, pco2 30,HC03 26
B. PH 7.30, Pco2 42,HC03 20
C. pH 7.48, Pco2 42, HCO3 32
D. pH 7.29, Pco2, 55, HCO3 26 (Refer to Hesi page 46 for Answers)
3. Fluid volume deficit- assessment findings- which is most important?(p. 309 & hesi p.39)
Fluid deficit occurs when the body loses water and electrolytes isotonically, that is in the same proportion as exists in the normal body fluid
Causes:
• Vomiting
• Diarrhea
• GI suctioning
• Sweating
• Inadequate fluid intake
• Massive Edema, as in initial stage of major burns
• Ascites
• Elderly forgetting to drink
• Diabetic insipidus
Assessment findings:
• Weight loss (1 pint of fluid loss=1pound of weight loss)
• Decreased skin turgor
• Oliguria (concentrated Urine)
• Dry and sticky mucous membranes
• Postural hypotension or weak, rapid pulse
Labs findings:
• Elevated BUN and creatinine
• Increased serum osmolarity
• Elevated hemoglobin and hematocrit
Treatment
• Strict I&O
• Replacement of fluids isotonically, preferably orally
Page 309 for mor info
4. Fluid Deficit- post burn- greatest concern
After airway, the most urgent need is preventing irreversible shock by replacing fluids and electrolytes (success p.420)
5. Low serum protein level- implications
( I think of the Edema because you won’t have enough albumin to pull that water from the interstitial space)
6. Hyponatremia- signs and symptoms, most important assessment findings and monitoring, care of patient (p. 313hesi p.40)
• The normal sodium is 135-145
• Sodium is the main cation of the ECF
• Play a major role in maintaining the concentration and volume of the ECF.
o Therefore, sodium is the primary determinant of ECF osmolality. Sodium affects the water distribution between ECF and ICF.
• Sodium is also important in the generation and transmission of nerve impulse and the regulation of acid-base balance.
• The GI tract absorbs sodium from food.
• Sodium leaves the body through urine, sweat, and feces.
• The Kidneys are the primary regulator of sodium balance.
o The kidney regulates the ECF concentration of sodium by excreting or retaining water under the influence of ADH.
• Aldosterone also plays a big role in sodium regulation by promoting sodium reabsorption from the renal tubules.
o Aldosterone (p.1206): is a potent mineralocorticoid that maintains extracellular fluid volume. It acts at the renal tubules to promote renal reabsorption of sodium (Na+) and excretion of potassium (K+) and hydrogen ions (H+).
• Changes in the serum of sodium level may reflect a primary water imbalance, a primary sodium imbalance, or a combination of the two. Sodium imbalances are typically associated with imbalances in ECF volume.
Hyponatremia
• Patho:
• Causes:
o may result from loss of sodium-containing fluids
o from water excess(dilutional hyponatremia)
o or combination of both
• Nursing implementation or treatment:
o Restrict fluid
o Hypertonic saline solution(3%NaC) can be given to restore the serum sodium level( if severe symptoms like seizures develop)
o
Hesi p. 40
Abnormality and common causes Signs and symptoms or assessment findings Treatment or intervention
Hyponatremia(↓Na)
Diuretics
GI fluid loss
Hypotonic tube feeding
D5W or hypotonic IV fluids
Diaphoresis
Anorexia, nausea, vomiting
Weakness
Lethargy
Confusion
Muscle cramps, twitching
Seizures
Na<135mEq/L
Restrict fluid(safer)
If IV saline solution prescribed administer very slow.
7. Diuretic therapy- hypokalemia- interaction with what other drug?(p.315)
Patient taking Digoxin, Digitalis experience increased digoxin toxicity if their serum potassium level is low. Skeletal muscle weakness and paralysis may occur with hypokalemia.
*Severe hypokalemia can cause weakness and paralysis of respiratory muscles, leading to shallow respirations and respiratory arrest.
8. Hypercalcemia- plan of care(p.317)
Two thirds of hypercalemia cases are caused by hyperparathyroidism and one third are caused by malignancy, especially from breast cancer, lung cancer, and multiple myeloma.
Hypercalcemia is also associated with vitamin D overdose.
Excess calcium leads to reduced excitability of both muscles and nerves.
Plan of care for hypercalcemia:
• The basic treatment of hypercalcemia is promotion of excretion of calcium in urine by administration of a loop diuretic (ex. Furosemide [Lasix]), and hydration of the patient with isotonic saline infusions.
• In hypercalcemia, the patient must drink 3000 to 4000ml of fluid daily to promote the renal excretion of calcium and to decrease the possibility of kidney stone formation.
• Synthetic calcitonin can also be administered to lower serum calcium levels. A diet low in calcium may be prescribed.
• Mobilization with weight-bearing activity is encouraged to enhance bone mineralization. Plicamycin (Mithrancin), a cytotoxic antibiotic, inhibits bone resorption and thus lowers the serum level. In hypercalcemia related to malignancy the drug of choice is paramidronate (Aredia), which inhibits the activity of osteoclasts(cells that break down bone and result in calcium release)
o Paramidronate is preferred over plimacamycin because it does not have cytotoxic side effects and it inhibits bone resorption without inhibit bone formation and mineralization. [Show Less]