S – Skeletal muscle weaknessU – U Wave (on EKG) – specific to hypokalemiaC – Constipation or illiusT – Toxicity of DigoxinI – Irregular, weak pulseO – Orthostatic hypotensionN - Numbness

Fluid & Electrolytes: K, Ca, Mg, Phosphorus, Cl

Potassium• Major electrolyte in intracellular fluid (98% of k in the body is inside the cell. The 2% in the ECF and that 2% is important for neuromuscular function)• Normal serum K+ is 3.5 to 5.0 mEq/L• Influences both skeletal and cardiac muscle activity• Minor variations are significant• Renal system important in keeping balanced potassium – kidneys adjust the amt of K to be excreted in the urine and as K levels rise, this creates movement of K into the renal tubules with the loss of K in the urine. Renal failure is the #1 cause of Hyperkalemia.• Body does not conserve potassium. Needs to be adjusted daily. Bananas are the best source

Hypokalemia• K+ < 3.5 mEq/L• Cause

– GI suction, vomiting, diarrhea– TPN or IVF without K+ replacement– Trauma – K leaves the cells when injured– Diabetes – uncontrolled – Low oral intake of K+– Sweat loss– Medications – diuretics (could use aldactone for K sparing), laxatives, insulin

Renal Loss of K+• Diuretics• Hyperaldosteronism (causes increased retention or Na & H2O then increases excretion of K)• High dose Na+ PCNs• Large dose corticosteroids

S/S Hypokalemia• Fatigue• Anorexia, N/V, Decrease bowel motility• Muscle weakness & leg cramps• Impaired glucose tolerance• Paresthesias (numbness & tingling)• Impaired renal concentrating ability• Diminished deep tendon reflexes• Flaccid paralysis – late sign• Increased sensitivity to digitalis• Dysrhythmias• Severe hypokelemia – death by cardiac arrestHypokalemia commonly accompanies alkalosis

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Hypokalemia & Cardiac Changes• ↓ strength of contraction• Myocardium irritability• ST segment depression• K+ < 2.7 mEq/L may result in PACs, PVC's, Vfib or cardiac arrest• K+ < 3.5 assoc. with metabolic alkalosis, high pH & high HCO3• Digoxin toxicity – Hypokalemia potentiates the action of digoxin

Works by inhibiting the myocardial cell Na/K pump thereby increasing the cellular K

Hypokalemia: Lab Results• K+ deficit < 3.5 mEq/L• K+ < 3.5mEq/L often assoc. with metabolic alkalosis, high pH, & high HCO3• K+ < 2.7 may result in dangerous dysrhythmias - Danger signs: arrhythmias, cardiac arrest, dig toxicity, muscle paralysis, resp arrest• pH & HCO3

Medical Treatment Hypokalemia• K+ replacement (PO or IV)• Increase on a daily basis

– 40-80 mEq/day• At risk patient

– 50-100 mEq/day• K+ rich foods• Treat the underlying cause

Oral K+ Supplements• Minimize GI irritation

– Dilute liquid & effervescent supplement– Give tabs & capsules w/ 8 oz. H2O– Give K+ with food

• Adverse reaction – N/V, diarrhea, GI bleed

Oral Potassium Supplements• Avoid overdose (hyperkalemia)• ↓ K+ dose if using K+ salt substitute• Not used with K+ sparing diuretics

Intravenous K+ Supplement• Must be diluted• Do NOT give by direct IVP – causes cardiac arrest!• Max. dose is 60 mEq at a time• Must use IV pump• Monitor renal output• CHS policy – pt on heart monitor• Monitor IV site for extravasation

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Nursing Interventions: Hypokalemia• Identify pt at risk – esp. if on Digoxin• Monitor ECG & BP• Monitor serum K+• Pt education – diuretics & laxatives• Administer K+ supplements PO or IV• ↑ dietary K+• Monitor urine output

Hyperkalemia• Serum K+ > 5.5 mEq/L• Causes

– Renal failure is the #1 cause– Release of K+ from damaged cells – ex: chemo kills cells and causes the release– Acidosis– Addison’s Disease– K+ sparing diuretics– High K+ intake– Medications– If you’re giving blood, the longer the blood sits there the higher the K gets

S/S Hyperkalemia• Main effects cardiac function• Muscle weakness and paralysis• Ventricular conduction is slowed• Paresthesias & irritability

– Respiratory and speech muscles• Flaccid muscular paralysis

– Legstrunkarms (including respiratory)• GI hyperactivity

– N/V, colic, & diarrheaAs the K level increases, symptoms changes from irritability to weakness

Hyperkalemia & Cardiac Changes• Slows heart rate• ECG changes

– Tall, peaked T wave, short QT interval– Longer PR interval, widening QRS complex– Risk for Heart Block, A-fib, or, V-fib

• Severe K+– Decreased heart contraction strength– Dilated & flaccid heart (when K is greater than 7)

ECG & Potassium Hyperkalemia: Lab Data• Serum potassium > 5.5 mEq/L• ECG abnormalities• Arterial blood gases – low pH indicating acidosisMetabolic acidosis is usually accompanied by hyperkalemia

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Hyperkalemia Medical Treatment• K+ restricted diet• Stop K containing medications• Monitor for “Digitalis toxicity”• Cation-exchange resins

– Kayexalate – PO or PR – substitutes Na for K and gets it out of the system– 1Gm of resin removes 1 mEq K+

• Dialysis - If conservative methods not suffice

Emergency Medical Treatment: Hyperkalemia• Ca Gluconate – IV

– Does NOT K+– Antagonizes K+ action on heart– Always has to be on ECG

• Hypertonic Glucose & Insulin– Insulin - facilitates K+ movement into cells– Glucose - insulin release from pancreas

• NaHCO3– K+ shifts into cells

Nursing Interventions: Hyperkalemia• Be aware of pt at risk• Monitor for:

– Generalized weakness & dysrhythmias– Irritability & GI symptoms– Nausea & intestinal colic– ECG or lab abnormalities

• Prevention of hyperkalemia• Educate pt: medication & diet• Do NOT draw blood above K+ infusion site

Calcium4

• Serum Ca++ level 8.6 – 10.2 mg/dl (total)• 99% stored in bones (bones & teeth)• Found in three forms:

- bound: to proteins (less than 50%)- ionized: found in serum (50% of calcium and is most important)- complexed: combined with nonprotein anions: phosphate, citrate, and carbonate

Ionized Calcium• Activate body chemical rxn• Muscle contractions and relaxation• Promote transmission of nerve impulse• Cardiac contractility & automaticity• Formation of prothrombinCalcium and Phosphorus have a reciprocal relationshipCa low=Phos highCa high=Phos low

Calcium Regulators• Parathyroid Hormone (PTH) pulls

– Releases Ca from the bone– Increases Ca absorption from GI

Increases Ca absorption from renal tubules

• Calcitonin – secreted by thyroid (keeps)– Antagonist of PTH– Secretion stimulated by high serum Ca++– Inhibits Ca reabsorption from bone

• Phosphate– Reciprocal relationship with Ca– ↑Ca = ↓ Phos

• Vitamin D– Necessary for absorption & utilization of Ca

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Hypocalcemia• Serum Ca++ < 8.5 mg/dl• Causes include:

- hypoparathyroidism & surgical hypoparathyroidism- malabsorption syndrome- vitamin D deficiency- prolonged admin. of Ca free IVF- acute pancreatitis

Causes- Excessive admin. of citrated blood- Alkalosis- Hyperphosphatemia- Hypomagnesemia- Thyroid cancer- Low serum albumin- Cimetidine (Tagamet)- Alcohol Abuse- Medications

S/Sx• Tetany (# 1 sign)• Vary with severity, duration & rate of development• Numbness & tingling• Spasms of muscles of extremities & face• Pain• Hyperactive deep tendon reflexes• Abdominal muscle spasms• Respiratory effects• Altered mood & memory• Convulsion/Seizures• Laryngeal spasm• + Trousseau’s• + Chvostek’s

+ Trousseau’s Sign• Carpopedal spasm of hand when

o Blood supply ↓o Pressure on nerve

• Occurs several minutes after BP cuff inflated > systolic BP

+ Chvostek’s Sign• Spasm of muscles innervated by facial nerve• Tap facial nerve anterior to ear lobe below zygomatic process

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Cardiac Effects• Prolonged QT interval• Prolonged ST segment• ↓ cardiac contractility• ↓sensitivity to Digoxin

Lab Data• Serum calcium levels < 8.5 mg/dl• Albumin/protein levels can give incorrect levels of Ca• Ionized (serum) levels of Ca should be obtained for accurate results• PTH levels rise in response to hypocalcemia• Magnesium and phosphorus levels should also be obtainedLow Magnesium=Low CalciumHigh Phosphorus=Low CalciumHigh pH=Low Calcium

Hypocalcemia Medical Treatment• Acute symptomatic ↓ Ca is emergency.

– Requires prompt adm. of IV Calcium• 10% Ca-Gluconate

– For severe symptoms• Ca-Chloride

– Never give IM – faster than Ca-Gluconate• Oral Ca or Vitamin D

Nursing Interventions Hypocalcemia• Identify pt at risk• Seizure precautions if severe ↓Ca• Monitor airway• Monitor ECG• Educate pt: Ca loss & risks & Ca rich foods (green leafy veggies, canned salmon, sardines, fresh oysters, dairy products)

Hypercalcemia• Calcium > 10.5 mg/dl• If severe – dangerous with mortality• Causes include:

– Hyperparathyroidism – most common cause– malignant neoplastic disease and chemotherapies – second most common– prolonged immobilization– large doses Vit. D & Vit. A

S/S• Decreased neuromuscular excitability:Muscle weakness and incoordination• GI motility: anorexia, N/V, constipation – leads to dehydration• Altered memory, confusion, slurred speech, lethargy, acute psychotic behavior, & coma• Depressed deep tendon reflexes• Bone pain & abdominal pain• Hypercalcemic crisis: severe polyuria & polydipsia, intractable nausea, abdominal cramps, lethargy,

coma and cardiac arrest7

• Can cause kidney stones

Cardiac Changes – focus on cardiac changes inn Na & K – not so much these• Calcium: inotropic effect on heart & reduces heart rate (decreases the contractility)• Shorten ST segment & QT interval• Prolonged PR interval• Potentiate digoxin toxicity

Lab Data• Serum calcium > 10.2 mg/dl• ECG-dysrythmias• PTH- increased• X-ray-reveal osteoporosis• Urine

Medical Treatment• Treat underlying cause• Dilute serum Ca++ with NS – encourages dieresis to get Ca out• Lasix/furosemide• IV phosphate• Calcitonin• Glucocorticoids – inhibit the intestinal absorption of Ca• Hemodialysis or CAPD

Nursing Interventions• Monitor for pt risk• ↑activity & fluids if possible• Ca++ intake• Safety measures for confusion• Monitor ECG, I&O, breath sounds• Monitor for Digoxin toxicity• Prevent Ca++ renal stones

Magnesium• Normal 1.3 – 2.3 mEq/L

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• Mg is important for neuromuscular function• Activator for enzymes• Carbohydrate & protein metabolism• Vasodilation in peripheral arteries• Found in bone and tissue• Eliminated by kidneysMagnesium is the 2nd most abundant cation in the intracellular compartment, next to K

Hypomagnesemia• Mg < 1.3 mEq/L• 1/3 Mg is bound to protein, 2/3 remains as free cation• Causes include:• GI loss

-Alcoholism: decrease dietary intake, impairs renal conservation, intestinal malabsorption, intermittent diarrhea and vomiting

The kidney is the primary route of magnesium excretionChronic alcoholism is the most common cause – because of poor dietary intake

Causes• Intestinal malabsorption syndromes• Diarrhea• Diuretics• Prolonged admin. Mg free IVF/TPN• NG Suction• Renal or liver disease• Diabetic ketoacidosis• Lower GI tract has the highest magnesium concentration

S/Sx• Usually occur Mg < 1.0 mEq/L• Most are neuromuscular: hyperexcitability with muscle weakness, tremors & athetoid movements (slow,

involuntary movement)• Tetany• + Trouseau’s and Chvostek’s• Seizures• Laryngeal stridor• Signs of low hypocalcemia r/t low PTH• Alterations in mood: apathy, depression, agitation, dizziness, insomnia, audio or visual hallucinations,

psychoses• Digoxin Toxicity

Cardiac Changes• Predisposes to dysrhythmias

– PVC or V-fib• ↑risk for digoxin toxicity• ECG:

– Prolonged PR & QT intervals– Widening QRS complex– depressed ST segment– Flattened T waves– Prominent U waves

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TremorsTwitchingTetanyHyperDTR

SeizuresTetanyAnorexiaRapid HRVomitingEmotionalDeep tendon reflexes increased

Lab Data• Mg < 1.3 mEq/L• Potassium• Calcium• ECG• Urine Mg. level

Medical Treatment• Diet

– Can be used alone for mild _ Mg– Green vegetables, meat, seafood, nuts, seeds, legumes, whole grains,peanut butter, cocoa– Spinach is the best source

• Mg replacement– Assess renal function – route of Mg elimination– PO Slow-Mag

• Diarrhea possible side effect– IV or IM– MOM helps for constipation– Because the kidneys are the main route of excretion, u have to watch the BUN, creatinine

Admin. Of Mg Sulfate IV• Monitor rate closely

– Too rapid: risk cardiac arrest– Dose: based on severity– Rate not to exceed 150 mg/min or 67 mEq over 8 hours (severe)

• Contraindicated in heart blockBefore u start the med, check DTR FIRST• Monitor urinary output

– 100 ml q 4 hr• Assess patellar reflexes• Monitor respiratory status

– Risk respiratory arrest

Nursing Interventions• Identify & monitor pt at risk• Asses of digoxin toxicity• Seizure precautions• Monitor airway• Safety for confusion / psychosis• Pt education: diuretics & laxative use• Pt education: diet

Hypermagnesemia• Mg > 2.5 mEq/L• Causes

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– Hemolyzed blood samples – can get a false high level– Renal failure – most common cause– Addison’s Disease– Excessive use antacids and laxatives– Untreated ketoacidosis– Excessive infusion– Hypothermia– Lithium toxicity

S/S• Acute elevations: peripheral and CNS depression• Mild increases:

-low blood pressure-N/V-facial flushing-sensations warmth

• Higher increases:-lethargy-dysarthria – difficulty articulating; damage to a central or peripheral motor nerve-drowsiness-loss of deep tendon reflexes-muscle weakness and paralysis-depressed respirations-coma

Cardiac Changes• Sinus Bradycardia• Prolonged PR, & QT intervals• Tall T waves• Widened QRS• Heart Block• Cardiac arrest in diastole

Lab Data• Mg > 2.5 mEq/L• ECG• K+ increased• Ca- increased• Creatinine clearance decreases to less than 3.0 ml/min.

Medical Treatment• Prevention is key• Avoid administration of Mg in renal failure• Hemodialysis• Emergency treatment if respiratory or cardiac problems develop– Ventilator support– Calcium Gluconate• Direct antagonist to Magnesium• 5 – 10 mEq may reverse cardiac or respiratory problems• Lasix• NaCL or LR

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Nursing Interventions• Monitor pt at risk• Monitor vital signs

– Low BP– Shallow resp. with apnea

• Assess patellar reflexes– Absent reflexes implies Mg > 7.0

• Monitor LOC– Drowsy, lethargy, coma

• Monitor pt at risk• Monitor vital signs

– Low BP– Shallow resp. with apnea

• Assess patellar reflexes– Absent reflexes implies Mg > 7.0

• Monitor LOC– Drowsy, lethargy, coma

Phosphorus• Normal 2.5-4.5 mg/dl (adult)• Essential for fxn of muscle & RBCs

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• Essential to nervous system• Essential to metabolism of:

– Carbohydrate– Protein– Fats

• Aids in the formation of ATP and 2,3 diphosphoglycerate• Maintenance in acid-base balance• 85% is located in bones and teeth• 14% located in soft tissue• 1% in ECF• Critical to nerve and muscle functionImportant for WBC Phagocytosis & platelet function

Hypophosphatemia• Phosphorus < 2.5 mg/dl• Causes–Severe protein –

• calorie malnutrition• Anorexia• Alcoholism

• Overfeeding with simple carbohydrates• Elderly debilated & unable to eat• Hepatic encelopathy• Prolonged intense hyperventilation

– Alcohol withdrawal– Diabetic ketoacidosis– Major thermal burns

Total phosphorus in the body is related to dietary intake, hormonal regulation, kidney excretion, and transcellular shifts

S/S • Most signs & symptoms 2nd to deficiency

– Impaired cellular energy resources (ATP)– Impaired oxygen delivery to tissues (2,3Diph) DPG

• Neurological– Irritability, Apprehension, weakness,– Numbness, confusion– Seizure, fatigue, parasthesia, coma

• Hyperglycemia– 2nd to predisposed insulin resistance

• Muscle damage– 2nd to _ ATP level in muscle tissue– Muscle weakness & pain– Acute rhabdomyolysis• Disintegration of striated muscle– Impaired ventilation

o 2nd to weakened respiratory muscles

Lab Data• Phos < 2.5 mg/dl• Glucose/insulin administration causes a decrease in phosphorus

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• PTH• Alkaline phosphatase• X-ray

Medical Treatment• Prevention• TPN & TF should have adequate Phos.• Phosphorus – PO

– Aluminum Phosphate (Phosphojel)• Phosphorus < 1.0 mg/dl (severe)

– K-Phosphate or Na-Phosphate• 0.2 mMol /kg/hr is max. rate• Risk of hypocalcemia & tetanyGiving a high phosphate=risk for low calcium due to inverse relationship

Nursing Interventions• Identify & monitor pt at risk• Gradual introduction of TPN & TF

– Avoid rapid shift of phosphorus• Prevent infection• Monitor serum phosphate levels• Administer meds safely• Teach about diet

Hyperphosphatemia• Phosphorus > 4.5 mg/dl• Causes

– Renal failure = most common cause due to the kidney’s inability to excrete phosphoruso ↓Excretion of phosphorus

– Chemotherapy for neoplastic disease – due to significant cell destruction– ↑Phosphorus intake– Profound muscle necrosis– Hypoparathyroidism

S/S• Similar to S/S of hypocalcemia• Tetany

– Mild to moderate: Tingling then numbness – fingertips & around mouth– Severe: Spreads proximally to limbs & face severity

• Muscle spasm & pain• Progressive renal impairment

Lab Data• Phos > 4.5 mg/dl• Calcium will be low• X-ray• PTH • Bun and creatinine Medical Treatment• Treat underlying disorder• If 2nd to tumor cell lysis

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– Allopurinol – prevent urate nephropathy• If 2nd to renal failure

– Phosphate binding gels – take it out of the circulatory system by binding to it– phosphate diet– Dialysis

• Acute hyperphosphatemia– NS – IVF

o Promotes renal excretion– Hypertonic dextrose & regular insulin

o Drive phosphorus into cells– Hemodialysis or Peritoneal dialysis– Surgery

Nursing Interventions• Identify & monitor pt at risk• Monitor lab results• Pt education: Avoid meds with Phos.

– Laxatives & enemas• Change in urine output

Nursing Interventions• Pt education: Avoid ↑Phos. Foods

– Dried fruit & vegetables– sardines– Hard cheeses,– Whole grain cereal– Nuts

Chloride• Normal: 97 – 107 mEq/L

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• Major anion in ECF along with Na• Chloride in ISF & lymph > in IVF• Assists in maintaining serum osmolality & osmotic pressure• Component in gastric fluid , pancreatic fluid, & in sweat• Inverse relationship to bicarbonate ↑Cl = ↓HCO3

Hypochloremia• Cl < 96 mEq/L• Causes– Prolonged vomiting– Prolonged NG suctioning– Prolonged diarrhea– GI drainage– Salt restricted diet– Diuretics

S/S• Bicarbonate level• Na level• Hyperexcitability of muscles

– Tetany, twitching, weakness• Hyperactive deep tendon reflexes• Cardiac dysrhythmia• Water excess

Lab Data• Cl < 96 mEq/L• Sodium• Potassium• Arterial Blood Gases: metabolic alkalosis• Urine chloride level

Medical Treatment• Correct the cause• IV therapy: NS or ½NS• Ammonium chloride– Dose calculated on chloride deficit– 100mEq / 500ml NS – give slowly– Treat metabolic alkalosis– Foods high in chloride

Nursing Interventions• Monitor I&O• Monitor bicarbonate & sodium level• Assess LOC, muscle strength & movementAvoid bottled water• Pt education: food in chloride

– Tomato juice = best source of chloride

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– canned vegetables– broth, fruit, processed meat

Hyperchloremia• Cl > 107 mEq/L• Causes:

– Loss of bicarbonateo Kidneyo GI tract

S/S - rarely produces s/sx on its on major symptoms are usually due to metabolic acidosis• S/S same as those of metabolic acidosis, hypervolemia and hypernatremia.• ↑Na level• Fluid retention• Tachypnea• Weakness• Lethargy• ↓Cognitive ability• HTN• If Untreated

– ↓Cardiac output– Dysrhythmias– Coma

Medical Treatment• IV fluid – Lactated Ringer’s - slowly• Diuretics• Restrict –

– Sodium– Chloride– Fluids other than LR until Cl level ↓

Lab Data• Cl > 108 mEq/L• Sodium >145• pH <7.35• Serum bicarbonate <22• Urine chloride increased

Nursing Interventions• Monitor for those pt at risk• Monitor vital signs• Monitor I&O• Fluid restriction other than LR• Monitor ABG• Pt education: diet restrictions

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