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SODIUM
Function Maintains tonicity of ECF Regulates acid-base balance Facilitates nerve conduction and neuromuscular function Facilitates glandular secretion Maintain H2O balance.
Renal absorption on excretion Aldosterone sodium reabsorption in collecting duct of nephrons Where sodium goes, water follows
HYPONATREMIA (SODIUM DEFICIT) Causes Manifestation Sodium loss Due to ECF volume and ICF volume GI fluid loss, sweating, dieresis Muscle twitching, weakness Osmotic swelling of the cell Water excess Hypotonic tube feeding, drinking water, Lethargy, confusion, seizures Excess IV D5W Altered neurotransmitter Conditions SIADH, head injury, AIDS, malignant tumor Hypotension, Tachycardia
extracellular circulatory volume
Nursing Responsibilities Monitor I&O. Sodium-rich foods in diet, juice, bouillon Use NSS (not distilled water) for irrigation o Give Isotonic fluid solution first before shifting to hypertonic solution. o Saline has Na components Avoid tap water enemas. Safety precautions. (side rails, ambulation supervision) Administer IVF (NaCl 0.9% IV, plasma expanders)
o To prevent shock and electrolyte replacement
Limit water intake as indicated. HYPERNATREMIA (SODIUM EXCESS) Causes Manifestation Loss of fluids Due to ECF volume and ICF volume Insensible (hyperventilation, fever), Agitation, restlessness, fever, ALOC diarrhea
Altered cellular metabolism
Water deprivation Excess salt intake (IV, hypertonic tube feedings, table salt) Conditions (e.g. Diabetes insipidus, heat stroke)
Nursing Responsibilities Monitor I&O. Restrict sodium in diet and IV fluids. o E.g. Administer D5W (not NSS) as prescribed oral fluids Administer diuretics as prescribed. Dialysis as indicated. Observe safety precautions. Monitor for changes in behaviour. Major cause of hypernatremia: FVD
POTASSIUM
Normal Serum level: Regulation 3.5- 5mEq/ L Function Maintains cell electrical neutrality. Facilitate cardiac muscle transmission of nerve impulses. Facilitates neuromuscular transmission of nerve impulse. Maintains acid-base balance.
Renal excretion or conservation Aldosterone K secretion. Movement in and out of the cell. Insulin moves K into the cell. Tissue damage moves K out of the cell.
HYPOKALEMIA (POTASSIUM DEFICIT) Causes Manifestation Loss of potassium Characterized by neuromuscular Vomiting, gastric suction, diarrhea, irritability heavy perspiration, potassium wastig Dizziness, hypotension, ECG changes, drugs, diuretics, hyperaldosteronism cardiac arrest Changes in membrane excitability Poor intake of potassium Debilitated clients, alcoholics Nausea, vomiting, anorexia, diarrhea, peristalsis, abdominal distension Cellular potassium dumping bowel motility Alkalosis, treatment of acidosis Muscle weakness, fatigue, leg cramps
neuromuscular excitability
Nursing Responsibilities Monitor ECG, HR and rhythm. Teach client regarding potassium-rich foods. o Fruits in general, except apple Teach client how to prevent excessive loss of potassium. o E.g. laxatives, diuretics Monitor client receiving digitalis.
Toxicity: BANDAM (Bradycardia, Anorexia, N&V, Diarrhea, Altered Vision: Halos, Male: Gynecomastia) Potassium-sparing diuretics o E.g. spinorolactone, aldactone Administer oral K supplements as ordered with food or fluid. Kalium Durule- potassium oral supplement Potassium may cause GI bleeding/ lesions in stomach Administer IV potassium replacement therapy. Nursing responsibilities for K-replacement therapy o Never administer IV potassium per bolus. o Check renal function before administration. No pee.. No K! o Administer IV potassium solution at a rate no faster than 10-20mEq/L o Monitor for pain and inflammation on the injection site. o Usually combined to plain NSS. o Mix well the solution because K may settle in the bottom of the bottle. o If UO > 20ml for 2hrs do not give the solution. May cause cardiac arrest. o HYPERKALEMIA (POTASSIUM EXCESS) Causes Manifestation Decreased potassium excretion Characterized by neuromuscular Renal failure, hyperaldosteronism, irritability potassium-sparing diuretics Tachycardia to bradycardia, ECG changes, cardiac arrest High potassium intake Hypopolarization and alteration in repolarization Excessive salt substitutes, excessive or rapid IV potassium therapy Nausea, diarrhea, abdominal cramps Cellular potassium shifting Tissue damage (e.g. burns, infection), acidosis
GI motility
Calcium Gluconcate
o
o
o
Kayexalate (Polyterene sulfonate) per orem/ enema o Potassium exchange resin Sodium bicarbonate o To counteract acidosis/ metabolic acidosis Dialysis as indicated o Peritoneal/ hemodialysis
Foods to eat Butter, cranberry juice, hard candy, root beer, sugar, honey, ginger
8.6- 10.2 mg/dL 4.5-5.5 mEq/dL Function Bone and teeth formation Nerve impulse transmission Muscle contraction regulation Cardiac pacemaker (automaticity) maintenance. Blood clotting factor Enzyme activation (e.g. pancreatic lipase & phospholipase)
CALCIUM
Redistribution between bones. Parathyroid hormone and calcitriol serum calcium levels Calcitonin calcium level Vitamin D for better Ca absorption
HYPOCALCEMIA (CALCIUM DEFICIT) Causes Manifestation Specific conditions Characterized by neuromuscular Hyperthyroidism, surgical removal of irritability the parathyroids, acute pancreatitis, CNS: Tingling, convulsions hyperphophatemia, thyroid calcium, draining fistula GI: peristalsis, nausea, vomiting, diarrhea Low Vit.D diet Malabsorption, hypomagnesia, alkalosis, sepsis, alcohol abuse MS: Muscle spasms, tetany, Chvosteks and trousseau sign, fractures CV: dysrhythmia
Colaborative Management Calcium diet Oral Calcium salts as prescribed Vit.D and Parathormone supplement (e.g. Biphosphate) as prescribed, Estrogen, replacement (post menopause) Amphogel (Al hydroxide) as prescribed o Phosphate-binder lowers phosphate, Calcium Ca gluconate per IV if severe Promote safety, seizures and fractures precautions Monitor breathing: Laryngospasms Postural hypotension may develop. Ventilator may be prescribed.
HYPERCALCEMIA (CALCIUM EXCESS) Causes Manifestation Loss from bones CNS: DTR, lethargy, coma Immobilization, Vit.D and steroid Severe hypercalcemia >16 mg/dL therapy GI: peristalsis, constipation, paralytic ileus Certain conditions Hyperparathyroidism, malignancy of the bones, Pagets disease, MM
Hypercalcimic crisis > 17mg/dL
MS: Muscle fatigue, hypotonia, fractures CV: dysrhythmia Renal: stones (calculi)
Colaborative Management increase clients movement and exercise fluid intake as ordered (3-4L/day) o To prevent dehydration and renal stone formation Acid-ash diet o E.g. cranberry juice, prunes Encourage ingestion of fiber o To prevent constipation Protect confused client, prevent fractures. NSS per IV o Sodium promote Calcium excretion Mithracin (Mithramycin) as prescribed o To reduce serum levels 0.9% NaCL- most prescribed IV, used to dilute Ca level in body o Together with Furosemide, which promotes Ca excretion Calcitonin substitutes- derived from salmon; excreted in urine Calcitonin- should be administered ONLY via IM Mithramycin- inhibit bone resorption - WOF its hepatotoxic and nephrotoxic effects
MAGNESIUM
Normal Serum level: 1.8- 3 mg/dL 1.3-2.3 mEq/dL 0.8- 1.2 mmol/L Regulation Conservation and excretion by kidney
Function
Na-K pump regulator Relaxing muscle contraction Nerve impulse transmission Cardiac function regulation CHON transport
HYPOMAGNESEMIA (MAGNESIUM DEFICIT) Causes Manifestation Excessive loss from GIT CNS: convulsion, paresthesia, tremors, NG suctioning, diarrhea, fistula ataxia drainage Mental changes: agitation, depression, confusion Long term drug usage Diuretics, Aminoglycosides MS: cramps, spasticity, tetany Conditions Chronic alcoholism, Pancreatitis, Burns CV: tachycardia, hypertension, dysrhythmias
Collaborative Management Seizure precautions and protective measures o Assess ability to swallow water before oral feeding. o Monitor for laryngeal stridor o Safety measures in case of seizure. Monitor for digitalis toxicity: BANDAM Administer supplemental Mg as ordered. Refer clients to alcohol treatment program as indicated Magnesium Sulfate (Mg SO4) Monitor VS May lead to asystole Used to treat pre-eclampsia <67 mEq/8hrs or <150mg/min MgSO4 toxicity: o WOF: loss of DTR o Urine output < 100ml/4hrs Then stop administration Calcium Gluconate- antidote Assess ability to swallow water before feeding because patients may experience dysphagia risking them for aspiration. Dont restrain patient when seizure develop. HYPERMAGNESEMIA (MAGNESIUM EXCESS) Causes Manifestation Abnormal retention of Magnesium CNS: DTR, lethargy, drowsiness, coma Renal failure, adrenal insufficiency CV: peripheral vasodilation, flushing,
hypotension, bradycardia Respiratory: Depression MS: muscle weakness, paralysis GI: nausea, vomiting
Collaborative Management Monitor VS and LOC Notify MD if DTR, patellar reflexes are absent. Advise client with renal disease to contact health care provider before using OTC. Ca Gluconate per IV to antagonize MgSO4 Dialysis as indicated (renal failure) Correct underlying cause
ABG ANALYSIS
Normal Values Blood ph: pO2 : pCO2 : HCO3 : BE/ BD: *ROME Interpretations: pH < 7.35 = acidosis ph > 7.45 = alkalosis *if pH is 7 & below or 7.8 and above, death occurs
pH pH
pCO2 pCO2
Compensated Compensated
Uncompensate d N or N or Uncompensate d N or
Alkalosis
N or