ala2ch

Does this diagnosis looks ok ? About the yissue perfusion i really cant tell if the patient have the same signs and symptoms of renal tissue perfusion ??[TABLE] [TR] [TD] Impaired Gas Exchange related to altered alveolar-capillary membrane changes (collapse of the alveoli due to pneumonia) and altered LOC manifested by hypoxia, inability to move secretions, and semi-comatosed state, CPOT is zero. [/TD] [/TR] [/TABLE] [TABLE] [TR] [TD] Impaired Gas Exchange related to altered alveolar-capillary membrane changes (collapse of the alveoli due to pneumonia) and altered LOC manifested by hypoxia, inability to move secretions, and semi-comatosed state, CPOT is zero. [/TD] [/TR] [/TABLE]

cr 4.3 and BUN 59

426 people viewed my post and still no response ???????? please anyone help meeeeee the deadline of my online careplan is midnight and now it's 8:15 p.m please anyone

he was intbated on mechanical ventilator the a new trach was planned for him no ICP was present

I listed all the findings i got from the patient's chart and cardix that's why u feel its a fake patient

This is a real patient ! I really cant tell what is his priority ND ! I really appreciate your response after 274 people viewed my post only u responded please help me ! He has petechiae on his upper extremeties, his IV site and ashsplit is dry and clean, his lungs are clear, he responds only to painful stimuli. Thank YOu !

Hi Guys, I want to develop a nursing care plan for my patient but I can't really tell which two nursing diagnosis to develop as a priority. A case of a 59 year old male known to have End stage renal disease, hypertension, diabetes type II, parkinsonism (on Madopar), vascular dementia,history of cerebrovascular accidents, who was presented to the ER with decreased level of consciousness, respiratory distress, and decreased PO intake. The patient inserted a tracheostomy on my clinical day, he is semi-comatosed, has diarrhea, acintobacter and lactose-fermenting bacilli as hospital-acquired infections. Chest X-ray showed congestion with a ? evidence of underlying pneumonia. He was admitted with uremic encephalopathy and dyspnea. Creatinine 20 , BUN 225. He has sacral stage II and bilateral hells stage II pressure ulcers. Activity: CBR , Diet: Fresubin Fiber 87 ml/hr has right internal jugular ash split for hemodialysis, foley catheter. His current medications are: Flagyl5600 mg per OG Q 8 hrs Caltrate 600 mg per OG Q hrs Madopar 250 per OG TID Colistin inhaled 80 mg by nebulizer Q 12 hrs Eprex 10000 units subcutaneously once per week Nexium 40 mg IVD Q 12 hrs Atrovent 6 puffs + Ventoline 4 puffs by aerochamber Q 8 hrs Colistin 80 mg IVD daily to be given after dialysis Please anyone can help respond as soon as possible :) Thank You !

I understand what u mean but my instructor told me one related factor and defining characteristic is not enough so i really did what u said i put everything that is related top a copd patient in order to convince my instructor im aware of what u are talking about but i didn't find any other convincing diagnosis thanks for the comment but its too late for now because i submitted the care plan already :)

Thank You everyone for your help I really appreciate it Sadala dear thanx for the emphasis I asked this questuion because I am studying for my final exam of medsurg It was helpful to know when to have normocytic and normochromic anemia Thanks Again :)

I can't figure what exactly is the difference between Normocytic and Normochromic Anemia ! Can Anyone help me please :) Thank You !!

this is my lecture that i took for fluid and electrolytes i hope i covered everything !

Fluid and Electrolytes: Balance and Disturbance Fluid and Electrolyte Balance Ø Necessary for life and homeostasis Ø Nursing role is to help prevent and treat fluid and electrolyte disturbances l Understand the physiology l Identify imbalance l Effective teaching for prevention Fluid Ø Approximately 60% of the typical adult is fluid Ø Varies with age, body size, and gender Ø Intracellular fluid (contains 2/3 of total fluid) Ø Extracellular fluid (ECF) l Intravascular (plasma) l Interstitial (Lymph) l Transcellular (CSF, intraocular…) Ø “Third spacing”: loss of ECF into a space that does not contribute to equilibrium (other than ICF or ECF spaces). Symptoms are decreased urinary output, increased heart rate, deceased blood pressure and edema. Occurs in ascites, peritonitis, bowel obstruction, massive bleeding into a cavity and burn. Electrolytes Ø Active chemicals that carry positive (cations) and negative (anions) electrical charges expressed as milliequivalents per liter. • Major cations: l Sodium l Potassium l Calcium l Magnesium l Hydrogen ions • Major anions: l Chloride l Bicarbonate l Phosphate l Sulfate Ø Electrolyte concentrations differ in the fluid compartments Ø Major cation in ECF l Sodium: it affects the overall concentration of ECF and is important in regulating the volume of body fluid. Ø Major cation in ICF l Potassium: release of large quantity of potassium from ICF can be extremely dangerous. Regulation of Fluid Ø Movement of fluid through capillary walls depends on: l Hydrostatic pressure Pressure exerted on the walls of blood vessels l Osmotic pressure Pressure exerted by the protein in the plasma Ø The direction of fluid movement depends on the differences of hydrostatic and osmotic pressure Osmosis Ø Movement of fluid from an area of lower solute concentration to an area of higher solute concentration Diffusion Ø Movement of molecules and ions from an area of higher concentration to an area of lower concentration Active Transport Ø Movement against the concentration gradient Ø Sodium-potassium pump maintains the higher Ø Concentration of extracellular sodium and intracellular potassium Ø Requires adenosine (ATP) for energy Routes of Gains and Losses Ø Gain l Dietary intake of fluid and food or enteral feeding l Parenteral fluids Ø Loss l Kidney: urine output approximately is 1 mL of urine per kilogram of body weight per hour (1 mL/kg/h) in all age groups. l Skin loss: sensible and insensible losses. The chief solutes in sweat are sodium, chloride, and potassium. l Lungs: eliminate water vapor (insensible loss) at a rate of approximately 400 mL every day l GI tract: The usual loss through the gastrointestinal (GI) tract is only 100 to 200 mL daily Homeostatic Mechanisms Major functions of the kidneys in maintaining normal fluid balance include the following: Ø Regulation of ECF volume and by selective retention and excretion of body fluids Ø Regulation of electrolyte levels in the ECF by selective retention of needed substances and excretion of unneeded substances Ø Regulation of pH of the ECF by retention of hydrogen ions Ø Excretion of metabolic wastes and toxic substances The normal BUN is 10 to 20 mg/dL Creatinine is the end product of muscle metabolism. It is a better indicator of renal function than BUN Normal serum creatinine is approximately 0.7 to 1.4 mg/dL Gerontologic Considerations Ø Reduced homeostatic mechanisms: cardiac, renal, and respiratory function Ø Decreased body fluid percentage Ø Medication use Ø Presence of concomitant conditions Fluid Volume Imbalances Ø Fluid volume deficit (FVD): hypovolemia Ø Fluid volume excess (FVE): hypervolemia Fluid Volume Deficit Ø Loss of extracellular fluid exceeds intake of water, and electrolytes are lost in the same proportion as they exist in normal body fluids Ø Dehydration refers to loss of water alone with increased serum sodium level Ø May occur in combination with other imbalances Ø Causes: fluid loss from vomiting, diarrhea, GI suctioning, sweating, decreased intake, and inability to gain access to fluid Ø Risk factors: diabetes insipidus, adrenal insufficiency, hemorrhage, and third space shifts Ø Manifestations: rapid weight loss, decreased skin turgor, oliguria, concentrated urine, postural hypotension, rapid and weak pulse, increased temperature, cool and clammy skin due to vasoconstriction, lassitude, thirst, muscle weakness, and cramps Ø Laboratory data: elevated BUN in relation to serum creatinine, increased hematocrit, and possible serum electrolyte changes Ø Medical management: provide fluids to meet body needs l Oral fluids l IV solutions Isotonic Solutions 0.9% NaCl (isotonic, also called normal saline [NS]) Na+ 154 mEq/L Cl- 154 mEq/L (308 mOsm/L) Also available with varying concentrations of dextrose(the most frequently used is a 5% dextrose concentration) - An isotonic solution that expands the extracellular fluid (ECF) volume, used in hypovolemic states, resuscitative efforts, mild Na+ deficit - Supplies an excess of Na+ and Cl-; can cause fluid volume excess if used in excessive volumes, particularly in patients with compromised renal function, heart failure, or edema - Not desirable as a routine maintenance solution, as it provides only Na+ and Cl- (and these are provided in excessive amounts) - When mixed with 5% dextrose, the resulting solution becomes hypertonic in relation to plasma and, in addition to the above described electrolytes, provides 170 cal/L Lactated Ringer's solution (Hartmann's solution) Na+ 130 mEq/L K+ 4 mEq/L Ca++ 3 mEq/L Cl- 109 mEq/L Lactate (metabolized to bicarbonate) 28 mEq/L (274 mOsm/L) Also available with varying concentrations of dextrose (the most common is 5% dextrose) - An isotonic solution that contains multiple electrolytes in roughly the same concentration as found in plasma (note that solution is lacking in Mg++): provides 9 cal/L - Used in the treatment of hypovolemia, burns, fluid lost as diarrhea, and for acute blood loss replacement - Lactate is rapidly metabolized into HCO3- in the body. - Not to be given with a pH > 7.5 because bicarbonate is formed as lactate breaks down, causing alkalosis - Should not be used in renal failure because it contains potassium and can cause hyperkalemia - Similar to plasma 5% dextrose in water (D5W) No electrolytes 50 g of dextrose - An isotonic solution that supplies 170 cal/L and free water to aid in renal excretion of solutes - Used in treatment of hypernatremia, fluid loss, and dehydration - Should not be used in excessive volumes in the early postoperative period (when antidiuretic hormone secretion is increased due to stress reaction) - Should not be used solely in treatment of fluid volume deficit, because it dilutes plasma electrolyte concentrations - Should be used with caution in patients with renal or cardiac disease because of risk of fluid overload Hypotonic solutions 0.45% NaCl (half-strength saline) Na+ 77 mEq/L Cl- 77 mEq/L (154 mOsm/L) Also available with varying concentrations of dextrose (the most common is a 5% concentration) - Provides Na+, Cl-, and free water - Free water is desirable to aid the kidneys in elimination of solute. - Lacking in electrolytes other than Na+ and Cl- - When mixed with 5% dextrose, the solution becomes slightly hypertonic to plasma and in addition to the above-described electrolytes provides 170 cal/L. - Used to treat Na+ and Cl- depletion Hypertonic Solutions 3% NaCl (hypertonic saline) Na+ 513 mEq/L Cl- 513 mEq/L (1026 mOsm/L) - Used to increase ECF volume, decrease cellular swelling - Highly hypertonic solution used only in critical situations to treat hyponatremia - Must be administered slowly and cautiously, because it can cause intravascular volume overload and pulmonary edema - Supplies no calories - Assists in removing intracellular fluid excess 5% NaCL (hypertonic solution) Na+ 855 mEq/L Cl- 855 mEq/L (1710 mOsm/L) - Highly hypertonic solution used to treat symptomatic hyponatremia - Administered slowly and cautiously, because it can cause intravascular volume overload and pulmonary edema - Supplies no calories Fluid Volume Deficit—Nursing Management Ø Monitor intake and output (I&O) Ø Monitor for symptoms: skin and tongue turgor, mucosa, urinary output (UO), and mental status Ø Initiate measures to minimize fluid loss Ø Provide oral care Ø Administer oral fluids Ø Administer parenteral fluids Fluid Volume Excess Ø Due to fluid overload or diminished homeostatic mechanisms Ø Risk factors: heart failure, renal failure, and cirrhosis of the liver Ø Contributing factors: excessive dietary sodium or sodium-containing IV solutions Ø Manifestations: edema; distended neck veins; abnormal lung sounds (crackles); tachycardia; increased BP, and CVP; increased weight; increased UO; shortness of breath; Ø Medical management is directed at the cause, restriction of fluids and sodium, and the administration of diuretics . Ø If renal function is so severely impaired that pharmacologic agents cannot act efficiently, other modalities are considered to remove sodium and fluid from the body. Hemodialysis or peritoneal dialysis may be used to remove nitrogenous wastes and control potassium and acid–base balance, and to remove sodium and fluid. Fluid Volume Excess—Nursing Management Ø Take I&O and daily weights; assess for lung sounds, edema, and other symptoms; monitor responses to medications such as diuretics Ø Promote adherence to fluid restrictions and patient teaching related to sodium and fluid restrictions Ø Monitor and avoid sources of excessive sodium; Ø Promote rest, favors diuresis of edema fluid Ø Use semi-Fowler’s position for orthopnea to promote lung expansion Ø Provide skin care and positioning/turning Ø Patient education about symptoms of edema Electrolyte Imbalances Ø Sodium: hyponatremia and hypernatremia Ø Potassium: hypokalemia and hyperkalemia Ø Calcium: hypocalcemia and hypercalcemia Sodium Imbalances Ø Sodium is the primary determinant of ECF osmolality. Ø Decreased sodium is associated with parallel changes in osmolality. Ø Sodium has a major role in controlling water distribution throughout the body. Ø Sodium is regulated by ADH, thirst, and the renin–angiotensin–aldosterone system. Effect of extracellular sodium level on cell size Hyponatremia Ø Serum sodium less than 135 mEq/L Ø dilutional hyponatremia (water intoxication), the patient's serum sodium level is diluted by an increase in the ratio of water to sodium. Ø Causes: adrenal insufficiency, water intoxication, SIADH (sustained secretion of ADH by the hypothalamus or production of an ADH-like substance from a tumor), and losses by vomiting. Ø Manifestations: poor skin turgor, dry mucosa, headache, decreased BP, and neurologic changes. When the serum sodium level decreases to less than 115, signs of increasing ICP, such as lethargy, confusion, muscle twitching, hemiparesis and seizures may occur. Ø Medical management: water restriction (800 mL in 24 hours) and sodium replacement (sodium by mouth, nasogastric tube, or a parenteral route). Serum sodium must not be increased by more than 12 mEq/L in 24 hours to avoid neurologic damage. Ø Nursing management: assessment and prevention, monitoring of dietary sodium and fluid intake. Ø Nursing alert: When administering fluids to patients with cardiovascular disease, the nurse assesses for signs of circulatory overload. Highly hypertonic sodium solutions (3% and 5% sodium chloride) should be administered only in intensive care settings under close observation. Hypernatremia Ø Serum sodium greater than 145mEq/L Ø Causes: excess water loss, excess sodium administration, diabetes insipidus, and hypertonic IV solutions Ø Manifestations: primarily neurologic and are the consequence of increased plasma osmolality. Water moves out of the cell into the ECF, resulting in cellular dehydration. thirst; elevated temperature; dry, swollen tongue; sticky mucosa; neurologic symptoms; restlessness; disorientation; hallucinations in severe hypernatremia. Permanent brain damage can occur. l Thirst may be impaired in the elderly or ill. Ø Medical management: hypotonic electrolyte solution or D5W. Treatment of hypernatremia consists of a gradual lowering of the serum sodium level by the infusion of an isotonic nonsaline solution ( dextrose 5%) to avoid cerebral edema. Ø Nursing management: assessment and prevention, assess for over-the-counter (OTC) sources of sodium, offer and encourage fluids to meet patient needs, and provide sufficient water with tube feedings. Potassium Imbalances Ø Potassium influences both skeletal and cardiac muscle activity. Ø Alterations in its concentration change myocardial irritability and rhythm. Ø To maintain potassium balance, the renal system must function, because 80% of the potassium excreted daily leaves the body by way of the kidneys. Ø Aldosterone also increases the excretion of potassium by the kidney. Hypokalemia Ø Below-normal serum potassium ( Ø Causes: GI losses, medications, alterations of acid–base balance (when alkalosis is present, a temporary shift of serum potassium into the cells occurs), hyperaldosteronism, and poor dietary intake. l potassium deficit occurs frequently with diarrhea l patients with persistent insulin hypersecretion may experience hypokalemia, because insulin promotes the entry of potassium into skeletal muscle and hepatic cells. Manifestations: Ø Fatigue, anorexia, nausea, vomiting, dysrhythmias, muscle weakness, cramps, paresthesias. Ø Hypokalemia increases sensitivity to digitalis, predisposing the patient to digitalis toxicity at lower digitalis levels. Ø Metabolic alkalosis is commonly associated with hypokalemia. Hydrogen ions move out of the cells in alkalotic states to help correct the high pH, and potassium ions move in to maintain an electrically neutral state. Ø Medical management: increased dietary potassium, potassium replacement, and IV for severe deficit. Ø Nursing management: assessment (severe hypokalemia is life-threatening), monitoring of electrocardiogram (ECG), arterial blood gases (ABGs), and dietary potassium, and providing nursing care related to IV potassium administration Ø Nursing Alert: l Potassium is never administered by IV push or intramuscularly to avoid replacing potassium too quickly. IV potassium must be administered using an infusion pump. Hyperkalemia Ø Serum potassium greater than 5.0 mEq/L Ø Although hyperkalemia is less common than hypokalemia, it is usually more dangerous, because cardiac arrest is more frequently associated with high serum potassium levels. Ø Causes: usually treatment-related, impaired renal function, and acidosis. Ø Manifestations: cardiac changes and dysrhythmias. Ø Medical management: monitor ECG, cation exchange resin (Kayexalate), IV sodium bicarbonate, IV calcium gluconate (calcium antagonizes the action of hyperkalemia on the heart), regular insulin and hypertonic dextrose, limit dietary potassium; and perform dialysis Ø Nursing alert: Potassium supplements are extremely dangerous for patients who have impaired renal function and thus decreased ability to excrete potassium. Effect of Potassium on ECG Flat T waves or inverted T waves or both, suggesting ischemia, and depressed ST segments an elevated U wave is specific to hypokalemia Peaked, narrow T waves; ST-segment depression; and a shortened QT interval. The PR interval becomes prolonged and is followed by disappearance of the P waves Hyperkalemia Ø Potassium-sparing diuretics may cause elevation of potassium and should not be used in patients with renal dysfunction Calcium Imbalances Ø More than 99% of the body's calcium is located in the skeletal system Ø Calcium is a major component of bones and teeth. Ø Calcium plays a major role in transmitting nerve impulses and helps regulate muscle contraction and relaxation, including cardiac muscle. Ø Calcium also plays a role in blood coagulation Hypocalcemia Ø Serum level less than 8.5 mg/dL Ø Causes: hypoparathyroidism, malabsorption, renal failure (because these pts. Have elevated serum phosphate levels). Hyperphosphatemia usually causes a reciprocal drop in the serum calcium level, inadequate vitamin D consumption. Ø Manifestations: Tetany (the most characteristic manifestation of hypocalcemia), hyperactive DTRs, Trousseau’s sign (carpal spasm upon inflating a blood pressure cuff on the upper arm). Trousseau’s Sign Hypocalcemia (continue) Ø Acute symptomatic hypocalcemia is life-threatening and requires prompt treatment with IV administration of calcium Ø Medical management: IV of calcium gluconate; calcium and vitamin D supplements; diet Ø Nursing management: assessment as severe hypocalcemia is life-threatening, exercise to decrease bone calcium loss, patient teaching related to diet and medications, and nursing care related to IV calcium administration. Ø Too-rapid IV administration of calcium can cause cardiac arrest, preceded by bradycardia. IV administration of calcium is particularly dangerous in patients receiving digitalis-derived medications Hypercalcemia Ø Serum level above 10.5 mg/dL Ø hypercalcemic crisis (serum calcium level to 17 mg/dL (4.3 mmol/L) or higher) has a mortality rate as high as 50% if not treated promptly. Ø Causes: hyperparathyroidism, bone loss related to immobility. Vitamin D intoxication can cause calcium excess. Calcium levels are inversely related to phosphorous levels. Ø Manifestations: Hypercalcemia reduces neuromuscular excitability because it suppresses activity at the myoneural junction. Therefore, muscle weakness, incoordination, ECG changes, and dysrhythmias. Cardiac standstill can occur when the serum calcium level is about 18mg/dL. Ø Medical management: treat underlying cause, administer phosphates and calcitonin. Calcitonin reduces bone resorption, increases the depositing of calcium and phosphorus in the bones, and increases urinary excretion of calcium. Inorganic phosphate salts can be administered orally, by NG, or intravenously. Ø Nursing management: assessment as hypercalcemic crisis has high mortality, encourage ambulation, IV phosphate therapy is used with extreme caution in the treatment of hypercalcemia, because it can cause severe calcification in various tissues, hypotension, tetany. Fluid and Electrolytes: Balance and Disturbance Fluid and Electrolyte Balance ➢ Necessary for life and homeostasis ➢ Nursing role is to help prevent and treat fluid and electrolyte disturbances  Understand the physiology  Identify imbalance  Effective teaching for prevention Fluid ➢ Approximately 60% of the typical adult is fluid ➢ Varies with age, body size, and gender ➢ Intracellular fluid (contains 2/3 of total fluid) ➢ Extracellular fluid (ECF)  Intravascular (plasma)  Interstitial (Lymph)  Transcellular (CSF, intraocular…) ➢ “Third spacing”: loss of ECF into a space that does not contribute to equilibrium (other than ICF or ECF spaces). Symptoms are decreased urinary output, increased heart rate, deceased blood pressure and edema. Occurs in ascites, peritonitis, bowel obstruction, massive bleeding into a cavity and burn. Electrolytes ➢ Active chemicals that carry positive (cations) and negative (anions) electrical charges expressed as milliequivalents per liter. • Major cations:  Sodium  Potassium  Calcium  Magnesium  Hydrogen ions • Major anions:  Chloride  Bicarbonate  Phosphate  Sulfate ➢ Electrolyte concentrations differ in the fluid compartments ➢ Major cation in ECF  Sodium: it affects the overall concentration of ECF and is important in regulating the volume of body fluid. ➢ Major cation in ICF  Potassium: release of large quantity of potassium from ICF can be extremely dangerous. Regulation of Fluid ➢ Movement of fluid through capillary walls depends on:  Hydrostatic pressure • Pressure exerted on the walls of blood vessels  Osmotic pressure • Pressure exerted by the protein in the plasma ➢ The direction of fluid movement depends on the differences of hydrostatic and osmotic pressure Osmosis ➢ Movement of fluid from an area of lower solute concentration to an area of higher solute concentration Diffusion ➢ Movement of molecules and ions from an area of higher concentration to an area of lower concentration Active Transport ➢ Movement against the concentration gradient ➢ Sodium-potassium pump maintains the higher ➢ Concentration of extracellular sodium and intracellular potassium ➢ Requires adenosine (ATP) for energy Routes of Gains and Losses ➢ Gain  Dietary intake of fluid and food or enteral feeding  Parenteral fluids ➢ Loss  Kidney: urine output approximately is 1 mL of urine per kilogram of body weight per hour (1 mL/kg/h) in all age groups.  Skin loss: sensible and insensible losses. The chief solutes in sweat are sodium, chloride, and potassium.  Lungs: eliminate water vapor (insensible loss) at a rate of approximately 400 mL every day  GI tract: The usual loss through the gastrointestinal (GI) tract is only 100 to 200 mL daily Homeostatic Mechanisms Major functions of the kidneys in maintaining normal fluid balance include the following: ➢ Regulation of ECF volume and by selective retention and excretion of body fluids ➢ Regulation of electrolyte levels in the ECF by selective retention of needed substances and excretion of unneeded substances ➢ Regulation of pH of the ECF by retention of hydrogen ions ➢ Excretion of metabolic wastes and toxic substances The normal BUN is 10 to 20 mg/dL Creatinine is the end product of muscle metabolism. It is a better indicator of renal function than BUN Normal serum creatinine is approximately 0.7 to 1.4 mg/dL Gerontologic Considerations ➢ Reduced homeostatic mechanisms: cardiac, renal, and respiratory function ➢ Decreased body fluid percentage ➢ Medication use ➢ Presence of concomitant conditions Fluid Volume Imbalances ➢ Fluid volume deficit (FVD): hypovolemia ➢ Fluid volume excess (FVE): hypervolemia Fluid Volume Deficit ➢ Loss of extracellular fluid exceeds intake of water, and electrolytes are lost in the same proportion as they exist in normal body fluids ➢ Dehydration refers to loss of water alone with increased serum sodium level ➢ May occur in combination with other imbalances ➢ Causes: fluid loss from vomiting, diarrhea, GI suctioning, sweating, decreased intake, and inability to gain access to fluid ➢ Risk factors: diabetes insipidus, adrenal insufficiency, hemorrhage, and third space shifts ➢ Manifestations: rapid weight loss, decreased skin turgor, oliguria, concentrated urine, postural hypotension, rapid and weak pulse, increased temperature, cool and clammy skin due to vasoconstriction, lassitude, thirst, muscle weakness, and cramps ➢ Laboratory data: elevated BUN in relation to serum creatinine, increased hematocrit, and possible serum electrolyte changes ➢ Medical management: provide fluids to meet body needs  Oral fluids  IV solutions Isotonic Solutions 0.9% NaCl (isotonic, also called normal saline [NS]) Na+ 154 mEq/L Cl- 154 mEq/L (308 mOsm/L) Also available with varying concentrations of dextrose(the most frequently used is a 5% dextrose concentration) • An isotonic solution that expands the extracellular fluid (ECF) volume, used in hypovolemic states, resuscitative efforts, mild Na+ deficit • Supplies an excess of Na+ and Cl-; can cause fluid volume excess if used in excessive volumes, particularly in patients with compromised renal function, heart failure, or edema • Not desirable as a routine maintenance solution, as it provides only Na+ and Cl- (and these are provided in excessive amounts) • When mixed with 5% dextrose, the resulting solution becomes hypertonic in relation to plasma and, in addition to the above described electrolytes, provides 170 cal/L Lactated Ringer's solution (Hartmann's solution) Na+ 130 mEq/L K+ 4 mEq/L Ca++ 3 mEq/L Cl- 109 mEq/L Lactate (metabolized to bicarbonate) 28 mEq/L (274 mOsm/L) Also available with varying concentrations of dextrose (the most common is 5% dextrose) • An isotonic solution that contains multiple electrolytes in roughly the same concentration as found in plasma (note that solution is lacking in Mg++): provides 9 cal/L • Used in the treatment of hypovolemia, burns, fluid lost as diarrhea, and for acute blood loss replacement • Lactate is rapidly metabolized into HCO3- in the body. • Not to be given with a pH > 7.5 because bicarbonate is formed as lactate breaks down, causing alkalosis • Should not be used in renal failure because it contains potassium and can cause hyperkalemia • Similar to plasma 5% dextrose in water (D5W) No electrolytes 50 g of dextrose • An isotonic solution that supplies 170 cal/L and free water to aid in renal excretion of solutes • Used in treatment of hypernatremia, fluid loss, and dehydration • Should not be used in excessive volumes in the early postoperative period (when antidiuretic hormone secretion is increased due to stress reaction) • Should not be used solely in treatment of fluid volume deficit, because it dilutes plasma electrolyte concentrations • Should be used with caution in patients with renal or cardiac disease because of risk of fluid overload Hypotonic solutions 0.45% NaCl (half-strength saline) Na+ 77 mEq/L Cl- 77 mEq/L (154 mOsm/L) Also available with varying concentrations of dextrose (the most common is a 5% concentration) • Provides Na+, Cl-, and free water • Free water is desirable to aid the kidneys in elimination of solute. • Lacking in electrolytes other than Na+ and Cl- • When mixed with 5% dextrose, the solution becomes slightly hypertonic to plasma and in addition to the above-described electrolytes provides 170 cal/L. • Used to treat Na+ and Cl- depletion Hypertonic Solutions 3% NaCl (hypertonic saline) Na+ 513 mEq/L Cl- 513 mEq/L (1026 mOsm/L) • Used to increase ECF volume, decrease cellular swelling • Highly hypertonic solution used only in critical situations to treat hyponatremia • Must be administered slowly and cautiously, because it can cause intravascular volume overload and pulmonary edema • Supplies no calories • Assists in removing intracellular fluid excess 5% NaCL (hypertonic solution) Na+ 855 mEq/L Cl- 855 mEq/L (1710 mOsm/L) • Highly hypertonic solution used to treat symptomatic hyponatremia • Administered slowly and cautiously, because it can cause intravascular volume overload and pulmonary edema • Supplies no calories Fluid Volume Deficit—Nursing Management ➢ Monitor intake and output (I&O) ➢ Monitor for symptoms: skin and tongue turgor, mucosa, urinary output (UO), and mental status ➢ Initiate measures to minimize fluid loss ➢ Provide oral care ➢ Administer oral fluids ➢ Administer parenteral fluids Fluid Volume Excess ➢ Due to fluid overload or diminished homeostatic mechanisms ➢ Risk factors: heart failure, renal failure, and cirrhosis of the liver ➢ Contributing factors: excessive dietary sodium or sodium-containing IV solutions ➢ Manifestations: edema; distended neck veins; abnormal lung sounds (crackles); tachycardia; increased BP, and CVP; increased weight; increased UO; shortness of breath; ➢ Medical management is directed at the cause, restriction of fluids and sodium, and the administration of diuretics . ➢ If renal function is so severely impaired that pharmacologic agents cannot act efficiently, other modalities are considered to remove sodium and fluid from the body. Hemodialysis or peritoneal dialysis may be used to remove nitrogenous wastes and control potassium and acid–base balance, and to remove sodium and fluid. Fluid Volume Excess—Nursing Management ➢ Take I&O and daily weights; assess for lung sounds, edema, and other symptoms; monitor responses to medications such as diuretics ➢ Promote adherence to fluid restrictions and patient teaching related to sodium and fluid restrictions ➢ Monitor and avoid sources of excessive sodium; ➢ Promote rest, favors diuresis of edema fluid ➢ Use semi-Fowler’s position for orthopnea to promote lung expansion ➢ Provide skin care and positioning/turning ➢ Patient education about symptoms of edema Electrolyte Imbalances ➢ Sodium: hyponatremia and hypernatremia ➢ Potassium: hypokalemia and hyperkalemia ➢ Calcium: hypocalcemia and hypercalcemia Sodium Imbalances ➢ Sodium is the primary determinant of ECF osmolality. ➢ Decreased sodium is associated with parallel changes in osmolality. ➢ Sodium has a major role in controlling water distribution throughout the body. ➢ Sodium is regulated by ADH, thirst, and the renin–angiotensin–aldosterone system. Effect of extracellular sodium level on cell size Hyponatremia ➢ Serum sodium less than 135 mEq/L ➢ dilutional hyponatremia (water intoxication), the patient's serum sodium level is diluted by an increase in the ratio of water to sodium. ➢ Causes: adrenal insufficiency, water intoxication, SIADH (sustained secretion of ADH by the hypothalamus or production of an ADH-like substance from a tumor), and losses by vomiting. ➢ Manifestations: poor skin turgor, dry mucosa, headache, decreased BP, and neurologic changes. When the serum sodium level decreases to less than 115, signs of increasing ICP, such as lethargy, confusion, muscle twitching, hemiparesis and seizures may occur. ➢ Medical management: water restriction (800 mL in 24 hours) and sodium replacement (sodium by mouth, nasogastric tube, or a parenteral route). Serum sodium must not be increased by more than 12 mEq/L in 24 hours to avoid neurologic damage. ➢ Nursing management: assessment and prevention, monitoring of dietary sodium and fluid intake. ➢ Nursing alert: When administering fluids to patients with cardiovascular disease, the nurse assesses for signs of circulatory overload. Highly hypertonic sodium solutions (3% and 5% sodium chloride) should be administered only in intensive care settings under close observation. Hypernatremia ➢ Serum sodium greater than 145mEq/L ➢ Causes: excess water loss, excess sodium administration, diabetes insipidus, and hypertonic IV solutions ➢ Manifestations: primarily neurologic and are the consequence of increased plasma osmolality. Water moves out of the cell into the ECF, resulting in cellular dehydration. thirst; elevated temperature; dry, swollen tongue; sticky mucosa; neurologic symptoms; restlessness; disorientation; hallucinations in severe hypernatremia. Permanent brain damage can occur.  Thirst may be impaired in the elderly or ill. ➢ Medical management: hypotonic electrolyte solution or D5W. Treatment of hypernatremia consists of a gradual lowering of the serum sodium level by the infusion of an isotonic nonsaline solution ( dextrose 5%) to avoid cerebral edema. ➢ Nursing management: assessment and prevention, assess for over-the-counter (OTC) sources of sodium, offer and encourage fluids to meet patient needs, and provide sufficient water with tube feedings. Potassium Imbalances ➢ Potassium influences both skeletal and cardiac muscle activity. ➢ Alterations in its concentration change myocardial irritability and rhythm. ➢ To maintain potassium balance, the renal system must function, because 80% of the potassium excreted daily leaves the body by way of the kidneys. ➢ Aldosterone also increases the excretion of potassium by the kidney. Hypokalemia ➢ Below-normal serum potassium ( ➢ Causes: GI losses, medications, alterations of acid–base balance (when alkalosis is present, a temporary shift of serum potassium into the cells occurs), hyperaldosteronism, and poor dietary intake.  potassium deficit occurs frequently with diarrhea  patients with persistent insulin hypersecretion may experience hypokalemia, because insulin promotes the entry of potassium into skeletal muscle and hepatic cells. Manifestations: ➢ Fatigue, anorexia, nausea, vomiting, dysrhythmias, muscle weakness, cramps, paresthesias. ➢ Hypokalemia increases sensitivity to digitalis, predisposing the patient to digitalis toxicity at lower digitalis levels. ➢ Metabolic alkalosis is commonly associated with hypokalemia. Hydrogen ions move out of the cells in alkalotic states to help correct the high pH, and potassium ions move in to maintain an electrically neutral state. ➢ Medical management: increased dietary potassium, potassium replacement, and IV for severe deficit. ➢ Nursing management: assessment (severe hypokalemia is life-threatening), monitoring of electrocardiogram (ECG), arterial blood gases (ABGs), and dietary potassium, and providing nursing care related to IV potassium administration ➢ Nursing Alert:  Potassium is never administered by IV push or intramuscularly to avoid replacing potassium too quickly. IV potassium must be administered using an infusion pump. Hyperkalemia ➢ Serum potassium greater than 5.0 mEq/L ➢ Although hyperkalemia is less common than hypokalemia, it is usually more dangerous, because cardiac arrest is more frequently associated with high serum potassium levels. ➢ Causes: usually treatment-related, impaired renal function, and acidosis. ➢ Manifestations: cardiac changes and dysrhythmias. ➢ Medical management: monitor ECG, cation exchange resin (Kayexalate), IV sodium bicarbonate, IV calcium gluconate (calcium antagonizes the action of hyperkalemia on the heart), regular insulin and hypertonic dextrose, limit dietary potassium; and perform dialysis ➢ Nursing alert: Potassium supplements are extremely dangerous for patients who have impaired renal function and thus decreased ability to excrete potassium. Effect of Potassium on ECG Flat T waves or inverted T waves or both, suggesting ischemia, and depressed ST segments an elevated U wave is specific to hypokalemia Peaked, narrow T waves; ST-segment depression; and a shortened QT interval. The PR interval becomes prolonged and is followed by disappearance of the P waves Hyperkalemia ➢ Potassium-sparing diuretics may cause elevation of potassium and should not be used in patients with renal dysfunction Calcium Imbalances ➢ More than 99% of the body's calcium is located in the skeletal system ➢ Calcium is a major component of bones and teeth. ➢ Calcium plays a major role in transmitting nerve impulses and helps regulate muscle contraction and relaxation, including cardiac muscle. ➢ Calcium also plays a role in blood coagulation Hypocalcemia ➢ Serum level less than 8.5 mg/dL ➢ Causes: hypoparathyroidism, malabsorption, renal failure (because these pts. Have elevated serum phosphate levels). Hyperphosphatemia usually causes a reciprocal drop in the serum calcium level, inadequate vitamin D consumption. ➢ Manifestations: Tetany (the most characteristic manifestation of hypocalcemia), hyperactive DTRs, Trousseau’s sign (carpal spasm upon inflating a blood pressure cuff on the upper arm). Trousseau’s Sign Hypocalcemia (continue) ➢ Acute symptomatic hypocalcemia is life-threatening and requires prompt treatment with IV administration of calcium ➢ Medical management: IV of calcium gluconate; calcium and vitamin D supplements; diet ➢ Nursing management: assessment as severe hypocalcemia is life-threatening, exercise to decrease bone calcium loss, patient teaching related to diet and medications, and nursing care related to IV calcium administration. ➢ Too-rapid IV administration of calcium can cause cardiac arrest, preceded by bradycardia. IV administration of calcium is particularly dangerous in patients receiving digitalis-derived medications Hypercalcemia ➢ Serum level above 10.5 mg/dL ➢ hypercalcemic crisis (serum calcium level to 17 mg/dL (4.3 mmol/L) or higher) has a mortality rate as high as 50% if not treated promptly. ➢ Causes: hyperparathyroidism, bone loss related to immobility. Vitamin D intoxication can cause calcium excess. Calcium levels are inversely related to phosphorous levels. ➢ Manifestations: Hypercalcemia reduces neuromuscular excitability because it suppresses activity at the myoneural junction. Therefore, muscle weakness, incoordination, ECG changes, and dysrhythmias. Cardiac standstill can occur when the serum calcium level is about 18mg/dL. ➢ Medical management: treat underlying cause, administer phosphates and calcitonin. Calcitonin reduces bone resorption, increases the depositing of calcium and phosphorus in the bones, and increases urinary excretion of calcium. Inorganic phosphate salts can be administered orally, by NG, or intravenously. ➢ Nursing management: assessment as hypercalcemic crisis has high mortality, encourage ambulation, IV phosphate therapy is used with extreme caution in the treatment of hypercalcemia, because it can cause severe calcification in various tissues, hypotension, tetany.

Thank you very much Esme12 You helped me alot !! Thanks again :)

awch im sorry for that You reminded me about my first tracheostomy care I did with the help of my instructor. The patient was in coma (stupor) and when i finished everthing and was heading to go for oral care of the patient. The patient coughed and sputum went directly into my eyes. Yes this was my worst clinical experience till this day ( i am a second year nursing student ) .

I think you're 100% true about students having to do everything and I really hate it when my instructor obliges me to do those silly ridiculous thing. Once there was a patient who constantly calls for the nurse to do let's say ordinary work because the patient is all alone and obese some how. So my instructor managed to let me answer her desires : first was the charger plug then reading that newspaper then answering several silly question not even related to her disease or nursing ! I really had a bad clinical experience that day. So I hope instructors or anyone who might care for nursing students please just give us things that we are going to do when we become RNs please !!!

Hi ! I am finishing an NVD care plan. My brain is not working sufficiently anymore. I need some interventions and teaching for fluid volume deficit nursing diagnosis. Any suggestions ??? Thank You !!

Yes I will surely let you know what my grade is ! Thanks You too Merry Christmas and Happy New Year :)

Sadala well i think ur right i may want to choose an alternative diagnosis as for Esme12 thanks alot for the info it really helped me alot concerning the care plan i submited it with two diagnosis the first is ineffective breathing patterns related to immobility and stasis of secretionsand ineffective cough secondary to pneumonia manifested by the presence of diffuse expiratory wheezes and rhonchi on right lower lobe and the use of accessory muscles when breathing and increased anterioposterior chest diameter ( you may find it a little bit long because my instructor loves details and thats what i gave her ! ) the second diagnosis which was supposed to be on constipation i did it on Impaired Gas exchange related to alveolar - capillary membrane changes manifested by inability to move secretions, restlessness, and somnolence Emphasizing the first diagnosis took me three hours while the second two hours I really hope i did a good job because i really accomplished it from the buttom of my heart Thank You all again :)

Hi ! I am a second year nursing student having some difficulties accompanied with low grades in constructing care plan. so basically this is my last care plan for this semester and i want to do extremely well in it. My patient 58 year oldwas admitted to ER for COPD exacerbation with SOB and chest discomfort accompanied with dyspnea. he has edema in his feet non- productive cough constipation for 8 days and hes known to be HTN DL COPD diabetic and asthmatic so basically i came up with a nursing diagnosis which is Constipation related to decreased peristalsis secondary to pulmonary hypoxia and lack of exercise , obesity manifested by absence of bowel sounds and inability to void; is this diagnosis good enough ??? I need its pathophysiology and interventions with rationales and outcomes as soon as possible . Can u find me any good alternative but i prefer to stick to this diagnosis . Thank youuuu !!

Hi ! I am a second year nursing student having some difficulties accompanied with low grades in constructing care plan. so basically this is my last care plan for this semester and i want to do extremely well in it. My patient 58 year old was admitted to ER for COPD exacerbation with SOB and chest discomfort accompanied with dyspnea. he has edema in his feet non- productive cough constipation for 8 days and hes known to be HTN DL COPD diabetic and asthmatic so basically i came up with a nursing diagnosis which is Constipation related to decreased peristalsis secondary to pulmonary hypoxia and lack of exercise , obesity manifested by absence of bowel sounds and inability to void is this diagnosis good enough ??? I need its pathophysiology and interventions with rationales and outcomes as soon as possible . Can u find me any good alternative but i prefer to stick to this diagnosis . Thank youuuu !!