NURS 2140 Fluid and Electrolytes Acid Base and IV Therapy

NURS 2140

Fluid and Electrolytes Acid Base and IV TherapyTeresa Champion, RN MSNMetropolitan Community CollegeWinter 20121BODY COMPOSITION AND FUNCTIONPRIMARY FLUID = Water60% total body weight (1 L = 2.2 lbs)2 2.5 L of water per dayTWO PRIMARY FLUID COMPARTMENTSIntracellular (ICF)Extracellular (ECF)FUNCTIONS:TransportingRemovingRegulationLubricatingFood Digestion

ICF: Intracellular fluid (in the cell) most abundant 2/3sECF: Extracellular fluid (lymph system, interstitial fluid, intravascular fluid or plasma) TCF: Transcellular fluid (ECF) (cerebral spinal fluid, fluid in joints, GI tract, and peritoneal fluid)

Water in the body is used to or for: Transporting nutrients & oxygen to cells carry immune cells to injury site for bodys defense Removing waste from cells Provides medium in which electrolyte chemical reactions can occur facilitates the movement of electrolytes Regulation of body temperature Lubricates joints and membranes Provides medium for food digestion enzymes in saliva and mucus assist in passage and provide mechanisms for hydrolyzing foods into elements the body can absorb

liter of water weighs 2.2 lbs

Body Fluid Intracellular 40%- Extracellular 20% - Intravascular 5%Interstitial (15%) - Transcellular

2

3Intake = Output

4Regulation of Body FluidOsmosis movement of water from lower particle concentration to higher particle concentrationDiffusion movement of molecules from higher to lower concentration (simple or facilitated)Filtration movement of molecules through a semi-permeable membrane from higher concentration to lower concentration as a result of hydrostatic pressure Hydrostatic pressure pressure exerted on the surrounding tissues due to the presence of water. 5

There are two ways in which substances can enter or leave a cell: 1) Passive a) Simple Diffusion b) Facilitated Diffusion (carrier)c) Osmosis (water only) 2) Active a) Molecules b) Particles Diffusion filtration done by the kidneys an elevated pressure gradient resists the transfer of elements into the high-pressure area (renal Capillaries) and filters ions from the high pressure area (renal capillaries) into the low pressure area (renal collecting tubules)

Facilitated uses a carrier protein (glucose, sodium ions, chloride ions) lipids

Active transport require energy moves large molecules like sodium, potassium, calcium, iron, hydrogen and some of the sugars and the amino acids6

7Oncotic vs Hydrostatic Pressure Filtration is directly opposed by the oncotic pressure of plasma proteins, especially Albumin in the blood stream. Arteriole high hydrostatic pressure - (~32mmHg)Venus low hydrostatic pressure (~15 mmHg)Plasma oncotic pressure (~22mmHg)

http://www.youtube.com/watch?v=VMvD29-Agtghttp://www.youtube.com/watch?v=mpg7ON2CfFEhttp://www.youtube.com/watch?v=dAO8igIysaA

Homeostasis - thus in a steady state ECF = ICF 8OSMOLALITY Number of molecules of solute per kg of waterNORMAL OSMOLALITY of blood is 275 295 milliosmoles per kg (mOsm/kg) of body weightIsotonic Fluids - same osmolality as blood plasma)Hypotonic Fluids - less concentration than blood plasma (< 275 mOsm/kg)Hypertonic Fluids - greater concentration than blood plasma (>295 mOsm/kg)

Isotonic no osmotic pull keeps fluids in place (0.9% NS, D5W, D5% 1/4NS - D5 0.2% NS)

Hypotonic causes a fluid shift out of the vascular space (blood vessels) into the cells and interstitial space these solutions hydrate cells while reducing fluid in the vascular space. (1/2 Normal Saline 0.45% NS)

Hypertonic causes a fluid shift into the vascular space (blood vessels) pulls fluid out of the cells and the interstitial spaces into the intravascular space. (reduces risk for edema, regulates BP, helps regulate Urine output (D5NS, D5% NS, D5% LR, 10% Dextrose) 9Homeostatic MechanismsFluid Balance - regulated by:Osmoreceptors of the hypothalamus - stimulates release of ADH and stimulates thirst. Baroreceptors (pressure sensitive cells) in carotids and aorta also stimulate the release of ADHBaroreceptors in glomerular arterioles in kidney will secrete Renin and start the Renin-Angiotension (RAA) cascade thus resulting in release of aldosterone from the adrenal glands and cause sodium retention = fluid retention (water follows sodium)RAA (Renin-angiotensin-aldosterone): cascade initiated by decrease in renal perfusion or low Na+ If extracellular volume is decreased renal perfusion decreases renin secreted by kidneys renin acts to produce angiotensin I which then converts to angiotensin II results in massive vasoconstriction increases renal arterial perfusion and causes increased thirst, a release of aldosterone (causes the retention of Na and Water)

Renin causes conversion of angiotensinogen to angiotension I.Angiotensin I is then converted by Angiotensin converting enzyme to Angiotensin II (lungs)Angiotensin II then stimulates the release of aldosterone by the adrenal glands. Aldosterone causes the kidneys to retain Na+ and water-Volume regulator.released if Na+ is low and K+ is high; increases reabsorption of Na+ (where salt goes, water follows) and the excretion of K+

10

11Role of the HeartAtrial Natriuretic Peptide: (ANP): secreted from atrial cells of heart (in response to too much volume in the blood) acts as diureticinhibits thirst mechanismsuppresses the RAA cascade

12Role of the KidneysFilter approx 180 Liters of blood per day; GFR (glomerular filtration rate)Produces urine between 1-2 Liters/dayIf loss of 1% to 2% of body water, will conserve water by reabsorbing more water from filtrate; urine will be more concentrated If gain of excess body water, will excrete more water from filtrate; urine will be more diluted

13Lab Tests for Evaluating Fluid BalanceSERUMNormal LevelsOsmolality275-295 mOsm/kg of waterHematocrit40-50%*BUN5-20 mg/dlSodium135 145 mEq/LPotassium3.5 5.0 mEq/LChloride95-108 mEq/LBicarbonate(CO2)22-28 mEq/L -Arteriole24-30 mEq/L -VenousURINENormal LevelsSpecific Gravity1.005 1.030Osmolality50-1200 mOsm/kg of waterSodium40-220 mEq/dayPotassium25-100 mEq/day*Males are slightly higher than females Males 42% to 52%Females 37% to 47%14Evaluation of Fluid StatusNormal serum hematocrit40 50%Dilute serumLow hematocrit and electrolyte levelsConcentrated serumElevated hematocrit and electrolyte levels

15Clinical Manifestations of Overhydration and DehydrationOVERHYDRATIONDEHYDRATIONCrackles in lungsDry mouth and tongue, mucous membranesS3 Heart SoundTachycardiaDyspneaSevere thirst (maybe not in elderly)Reduced blood oxygen levels and increased CO2 levels respiratory acidosisIncreased temperature (may rise 1 or 2 degrees)Bounding pulsesWeak pulsesIncreased blood pressureOrthostatic Hypotension, systemic hypotensionIncreased edema, ascites

tenting skin

Increased neck swelling jugular vein distensionFlat neck veinsDecreases in HCT, Serum Osmolality, Serum Sodium, Potassium, Chloride, Bicarbonate, BUN; Urine Specific Gravity < 1.005; Urine Osmolality >1,200 mOsm/kgIncreases in HCT, Serum Osmolality, Serum Sodium, Potassium, Chloride, Bicarbonate, BUN, Creatinine; Urine specific Gravity >1.030; Urine Osmolality < 50 mOsm/kg16Nursing ConsiderationsAssess for headache, dizziness, syncopeCHF-SOB, dyspnea, activity intoleranceMaintaining accurate I & ODaily weightsMonitoring Lab valuesFrequency and consistency of stoolsMeals include adequate fluid intakeDehydration in the ElderlyIncreased risks for dehydration:Decrease in thirstLack of fluid replacementUse of diuretic medications for high BPSusceptibility to contagious diseasesNursing Care PlanDehydrationRisk for imbalanced Fluid Volume Related to excessive fluid loss/inability to take in fluids AEB .OverhydrationRisk for Imbalanced Fluid Volume Related to excessive fluid intake/decreased urination AEB .Dehydration Overhydration

AEB :AEB:

Low Blood PressureHigh BPRapid pulseWeak pulseIncreased body temperatureDyspnea, increased respirationsDizziness on standing orthostatic hypotensionEdema, Weight gain of >2 lbs per day

Interventions:Interventions:

Provide source of fluids pt can retainRestrict fluids and sodiumN/V provide anti-emenics and parental fluidsProvide diuretics as orderedMonitor IV flow ratesMonitor K levels with diureticsOutcome: Adequate fluid balanceOutcome:Adequate Fluid Balance19ElectrolytesSubstance that develops an electrical charge when dissolved in water Cation - positive chargedAnion - negative chargedExamples of cations: Sodium, Potassium, Magnesium, CalciumExamples of anions: Chloride, Bicarbonate, Phosphorous

20SodiumNormal serum values135-145 mEq/LMost abundant cation in ECFFunctionsECF volume water balanceAcid-base balanceNerve impulse control sodium potassium pumpLevels below 115 mEq/L brain damage, seizuresSodium is primarily excreted through the kidneys, but other avenues are GI Secretions and sweat.

Sodium is the most abundant cation in the extracellular fluid.Sodium is regulated by the Kidneys and is influenced by the hormone aldosteroneSodium is mainly responsible for water retention and the serum osmolality level.

Doubling sodium can give you a rough estimate of serum osmolality. example: Na level of 142 x2 = 284 osmolality of serum. A more accurate serum osmolality level 2 x serum NA + BUN/3 + glucose/18 = serum osmolality (mOsm/kg) example 2 x 142 + 15/3 + 115/18 = 2 x 142 + 5 + 6.4 = 295.4 or 295 mOsm/kg.

Responsible for the sodium potassium pump sodium shifts into cells as potassium shifts out of cells repeatedly to maintain water balance and Neuromuscular activity. When sodium shifts in potassium shifts out depolarization occurs and when sodium shifts out and potassium shifts back in repolarization occurs. Cellular activity.

Regulation of acid base sodium combines readily with chloride (Cl) or bicarbonate (HCO3) to regulate acid base balance.

21Sodium Deficit - Levels < 135 mEq/LHyponatremiaLoss through GI tract, skin or kidneysAn increased amount of sodium shift into the cells when there is a potassium deficitAn excessive ADH release (SIADH) causing Water retention and sodium deficitInadequate sodium intake, increased water intakeExcessive use of 5% dextrose solutionLevels below 115 mEq/L brain damage

Most common causes of sodium loss (hyponatremia) is through the GI tract. Altered cellular functionRenal lossesElectrolyte free fluids (dextrose) - Dextrose breaks down in the body to form free water and causes an increase in water in the body.Hormonal influences

22Pathophysiology of decreased sodium imbalancesCNS excess water moves into the cerebral tissues increased intracranial pressureGI loss causes acid base imbalancesKidneys renal dysfunction promotes sodium and water retention resulting in diluted sodium level (fluid overload)Cellular activity - decrease in Na-K pump

The Central Nervous system is the most sensitive to sodium losses.

23Causes of HyponatremiaDietary changes low sodium intake, excessive water intake, fad diets/fasting, anorexia nervosa, prolonged use of IV D5WGI Losses vomiting, diarrhea, GI Suctioning, Tap water enemas, GI surgery, Bulimia. Renal Loses Salt wasting kidney disease, diuretics.Hormonal Influences - ADH, SIADH.Decreased adrenocortical hormone: Addisons disease.Altered Cellular Function Hypervolemic state: heart failure, cirrhosis BurnsSkinDietary changes low sodium intake over several months can lead to hyponatremia. Water in excessive amounts dilutes Extracellular fluid in addition, IV D5W will also dilute the ECF and cause water intoxication.

GI Sodium and chloride are high in concentration in gastric juices and intestinal mucosa.

Kidney in advanced renal disorders, the tubules do not respond to ADH, therefore, there is a loss of sodium, chloride and water. The excessive use of diuretics or excessive potent diuretics will decrease sodium and chloride levels.

Hormonal ADH promotes water reabsorption from the distal tubules. Surgical pain, increased use of narcotics, head trauma cause more water to be reabsorbed and dilutes ECF

Altered Cellular function heart failure, cirrhosis and nephrosis causes hypervolemic states and increases ECF, thus diluting the serum sodium and chloride levels.

BURNS great quantities of sodium are lost from burns, oozing wounds

Skin Large amounts of sodium are lost from skin when there is an increase in environmental temperature, fever, large skin wounds.24Sodium Excess - Levels > 145 mEq/LHypernatremiaExcessive secretion of aldosterone or cortisolExcessive sodium intakeDecreased water intakeGI disordersDecreased renal function

Dietary changes - 25Pathophysiology of increased sodium imbalancesOverproduction of adrenal hormones excessive secretions of aldosterone and cotrisol promote an increase in the sodium levelCellular activity increases the sodium pump action, causes cellular irritability. 26Causes of HypernatremiaDietary Changes Increased sodium intake, decreased water intake, Administration of 3% saline solutionsGI Disorders severe vomiting, DiarrheaDecreased Renal Function reduced glomerular filtrationEnvironmental Changes Increased temperature and humidity, water lossHormonal Influence Increased adrenocortical hormone production: oral or IV cortisone or Cushing's syndrome. Altered Cellular Function Heart Failure, Renal DiseasesTrauma Head injuryDietary inadequate fluid intake and increased use of table salt, canned vegetables, soups, and processed foods can increase serum sodium. Administration of concentrated 3% saline solutions can cause hypernatremia.

GI With severe vomiting, water loss can be greater than sodium loss, causing a dangerously high sodium level.

Environmental Increased environmental and body temperature can cause profuse perspiration and water loss can be greater than sodium loss.

Hormonal excessive adrenocortical hormone can cause sodium excess. Cortisone ingestion or hyperfunction of the adrenal gland (Cushings Syndrome).

Altered Cellular Function usually with hear failure and renal disease27Clinical Manifestations of Sodium ImbalancesHyponatremiaNausea, vomiting, diarrhea, abdominal crampsTachycardia, hypotensionHeadaches, apprehension, lethargy, confusion, depression, seizuresMuscle weaknessDry skin, pale dry mucus membranesSerum Na 145 mEq/LSerum osmolality > 295 mOsm/kgUrine Specific Gravity >1.030Urine Sodium < 40 mEq/day

28Chloride Normal Levels95-108 mEq/LPrimary extracellular anionCreates electrical neutrality when combined with sodiumBody Water BalanceHydrochloric acidBuffers carbonic acidAnion gap - calculated AG = (Na + K) (Cl + HC03 (metabolic acidosis)

Hypochloremia 108 mEq/LCausesHyperparathyroidism, dehydrationRespiratory acidosisManifestationsLethargy, disorientationIncreased rate and depth of respirations

ChloridePrimary extracellular anionCreates electrical neutrality when combined with sodiumHydrochloric acidBuffers carbonic acidAnion gap - calculated AG = (Na + K) (Cl + HC03 (metabolic acidosis)PotassiumNormal serum values3.5- 5.0 mEq/LMost abundant cation in ICFFunctionsTransmission and conduction of nerve impulses and the contraction of skeletal, cardiac and smooth muscles (na-K pump)Assists with regulation intracellular osmolalityEnzyme production for cellular metabolismMaintains Acid-base BalanceLevels less than 2.5 mEq/L and greater than 7.0 mEq/L can cause cardiac arrestPotassium is excreted through the kidneys (80-90%) and feces (10-20%)A potassium deficit is associated with alkalosis and a potassium excess is associated with acidosis. 33Potassium Deficit - Levels < 3.5 mEq/LHypokalemia causesDietary changes decrease in dietary intakeCellular Potassium Loss Tissue Injury, Muscle contractionGI losses vomiting, diarrhea, GI suctioning, intestinal fistula, laxative abuse, bulimia, enemasHormonal Influences Aldosterone (Cushing syndrome), licorice, StressDrugs adrenergic, epinephrine, decongestants, amphotericin B, beta2 adrenergic agonist, aminoglycosides, large doses of penicillins, potassium wasting diruetics, steroids Redistribution - Insulin, alkalotic statesElectrolyte loss - Magnesium

Dietary malnutrition, starvation, unbalanced diets, anorexia nervosa, alcoholism, crash diets.

Cellular cellular and tissue damage cause potassium to be released into intravascular fluid and then lost through the kidneys from trauma, tissue injury, surgery, burns etc. Potassium will be needed to repair injured tissue.

GI lots of K in the GI tract with GI losses (loss of secretions) large amounts of K ions are lost.

Hormonal Steroids, especially cortisone and aldosterone promote potassium excretion and sodium retention. Stress increases the production of steroids in the body. In Cushings Syndrome there is an excess production of adrenocortical hormones (corticol and aldosterone). Licorice contains glyceric acid, which has an aldosterone effect.

Drugs these drugs promote renal excretion of potassium\Cellular redistribution of potassium - Insulin moves glucose and potassium into cells. Metabolic alkalosis promotes the movement of potassium into cells

Drugs promote potassium excretion

Magnesium deficiency (hypomagnesemia) can cause renal excretion of potassium. Potassium deficit is not corrected until the magnesium deficit is corrected.

34Potassium Excess - Levels > 5.0 mEq/LHyperkalemia causesDietary excessive intake, supplements, salt substitutes, herbal juicesIV Potassium replacements with poor renal functionDecreased renal function acute and chronic renal failureAltered Cellular Function injury, metabolic acidosis, stored blood >1-3 weeks oldHormonal Deficiency Addisons diseaseDrugs K-sparing diuretics, ACE inhibitors, beta blockersPseudohyperkalemia poor blood samplesDietary consumption greater than excretion rate, many salt substitutes have high potassium content, Nutritional supplements and herbal juices have high K content.

IV Potassium adequate urine output must be determined when giving k supplements, especially IV routes.

Decreased renal function Potassium is mostly excreted in urine via kidneys, anuria and oliguria cause potassium retention in the plasma

Cellular injury increased potassium increase due to cell breakdown. If potassium levels released from cells are not excreted by kidneys it could cause a build up of potassium levels in the plasma. In acidotic states, the hydrogen ion moves into the cells and potassium moves out of the cells, increasing the potassium levels in the plasma (serum). Stored blood that is greater then 1-3 weeks old causes some RBC breakdown (hemolysis) and then potassium is released into the serum (ECF).

Addisons disease reduced secretion of the adrenocortical hormones causes a retention of potassium and a loss of sodium

Drugs potassium sparing diuretics cause an aldosterone deficiency promoting potassium retention. ACE inhibitors increase the state hypoaldosteronism (decrease aldosterone) thus decrease sodium and increase potassium) and impair renal potassium excretion. Beta blockers decrease reuptake of potassium and decrease the Na-K-ATPase function. (neuro-cellular transmission)

Pseudohyperkalemia hemolysis of blood, tourniquet too tight, rapidly drawing blood, using small needles (small gauges) clenching of fist during blood draw can all cause a falsely elevated k level. 35Clinical Manifestations of Potassium ImbalancesHypokalemiaGI anorexia, N/V, diarrhea, abdominal distention, decreased peristalsis or ileusCardiac dysrhythmias, vertigo (dizziness), cardiac arrestECG Flat or inverted T waves, depressed STRenal polyuriaNeuromuscular malaise, drowsiness, muscular weakness, confusion, mental depression, diminished deep tendon reflexes, respiratory paralysisLab Values - 5.0 mEq/LAcidosisIn acid states when there is an increase in hydrogen ions in acidotic states K leaves the cell and Hydrogen ions enter the cell in order to maintain blood pH.

36Hypokalemia flattened, inverted T wave with a U wave sometimes present

37Hyperkalemia peaked T Wave

A- normalB t wave starting to elevateC peaked T wave early signD PR interval prolonged and continuation of peaked T waveE P wave disappears, QRS prolonged idioventricular cardiac arrest38CLINICAL MANAGEMENT OF POTASSIUM IMBALANCESHypokalemiaOral supplements (tablets, capsules, liquid)Oral potassium is very irritating to the gastric mucosa and should be given diluted and not on an empty stomachIV Potassium DILUTED in an IV SolutionNever more than 10mEq of KCL per hourNever given undiluted as a bolus injectionFor life threatening hypokalemia (10,000 units/d and low molecular heparin (lovenox) inhibits aldosterone production

ACE increase the state of hypoaldosteronism (decrease Na and increase K) and impair renal exertion of potassium

Beta Blockers decrease cellular uptake of K

NSAIDS clock cellular potassium uptake40CalciumNormal serum values 8.5- 10.5 mg/dL Ionized Calcium 4.0 5.0 mg/dLCation found in both ECF and ICF, but greater concentration in ECFMaintains cellular membrane stability 98% in bones and teeth, 2% in the serumOf the 2% in serum - 45% is bound to albumin and 50% is ionized calcium physiologically activeSerum pH greatly affects calcium levels metabolic acidosis increases ionized calcium levels, alkalosis opposite effectNormal ionized Ca levels are 4.0 to 5.0 mg/dLSerum Ca levels are regulated by Vitamin D, calcitonin (thyroid glad) and parathyroid hormone (PTH) from parathyroid glandThere is a direct relationship between Ca and Phosphorous, when Ca is low Phosphorous is high and vise versa.

Vitamin D is necessary for the body to absorb calcium in the intestinesPhosphorous Is an anion that inhibits calcium absorption

Phosphorous and Calcium combine in the GI tract under the influence of Vitamin D and are exchanged for one another in the kidney

41Calcium RegulationWhen serum Calcium is low:When serum Calcium is High:PARATHYROID GLAND releases PTH. PTH mobilizes calcium from the bone, increases renal reabsorption of calcium and promotes calcium absorption in the intestines in the presence of Vitamin D to increase serum Calcium levelsTHYROID GLAND releases Calcitonin. Calcitonin increases calcium return to the bone and decreases serum Calcium levelsVitamin DCalcium absorption42Functions of CalciumNeuromuscularnormal nerve and muscle activity, causes transmission of nerve impulses and contraction of skeletal muscles. Cardiaccontraction of the myocardium (heart muscle)Cellular and Bloodmaintenance of normal cellular permeability - decreased calcium increases cellular permeabilityCoagulation of blood. Promotes clotting by converting prothrombin into thrombinBone and teeth constructionCalcium along with phosphorous forms bones and teeth make them strong and durable43Calcium Deficit - Levels < 8.5 mg/dL and Ionized Ca is 10.5 mg/dL and Ionized Ca is >5.0 mg/dLHypercalemia causesPrimary hyperparathyroidism Bone malignancy, fractures and immobilityDrug toxicity (lithium carbonate, vitamin a and d, thiazides)Excessive use of calcium supplements, anti-acids and calcium saltsRenal Impairment and diuretics (thiazides)Steroid therapyDecreased serum phosphorousHyperparathyroidism increases the production of PTH-releases Ca from the bone

Bone malignancy, fractures and immobility will promote calcium loss from the bones. Some other malignancies (lung, breast, ovaries, prostrate and bladder) will cause an ectopic PTH production.

Renal impairment and thiazides decrease renal excretion of calcium Thiazides in addition, increase the action of PTH on the kidneys, promoting calcium reabsorption. BUT Loop diuretics will decrease serum calcium.

Steroids mobilize calcium release from the bones

Decreased phosphorous levels increase serum calcium levels to the extent the kidneys are unable to excrete the excess calcium.

45Clinical Manifestations of Calcium ImbalancesHYPOCALCEMIACNS and MuscularAnxiety, irritabilityTetany, muscle twitching (Chvosteks sign)Numbness and tinglingCarpopedal spasm (Trousseaus sign)ConvulsionsAbdominal and muscle crampsCardiac Weak contractionsECG/EKG lengthened ST segment and prolonged QT intervalBlood reduction in prothrombin (reduced clotting)BoneWith prolonged deficiency fractures occur easily

HYPERCALCEMIACNS and MuscularDepression/apathyWeak, flabby musclesCardiac Signs of heart blockCardiac arrest in systoleDecreased or diminished ST segment and shortened QT intervalBonePathologic fractureDeep pain over bony areasThinning of bonesRenalFlank painCalcium stones in kidney Eyes conjunctival calcificationsSkin caliphylaxis lesions on the skin (mostly lower extremities) irregular violet plaques or nodules 46Important Clinical tests for HypocalemiaChvotseks Signhttps://www.youtube.com/watch?v=ep6IEqnyxJU

Trousseaus Signhttps://www.youtube.com/watch?v=H13yn9AwtPY&feature=relmfu

47ECG changes with Calcium Imbalances

Normal ST segment and QT IntervalHypocalcemia ST segment is lengthened, QT interval is prolongedHypercalcemia ST segment is shortened, QT interval is shortened PR interval is normally 0.12 to 0.20QRS is 0.04 to 0.12*QT interval is 0.28 to 0.4048Clinical Management of Calcium ImbalancesHypocalcemiaOral supplements and IV calcium diluted in D5W (not normal saline)IV calcium should be given slowly at 1-3ml/minVitamin D supplements

HypercalcemiaTreat underlying causeIV Normal Saline Loop DiureticsCalcitonin SQIV phosphatesOthers:CorticosteroidsAntitumor antibioticsNormal saline should not be used because sodium encourages calcium loss.

IV Calcium given slowly to prevent hypotension, bradycardia and other dysrhymias.

IV fluids like normal saline expand blood volume and decreases calcium reabsorption by renal tubules plus normal saline enhances calcium loss.

Loop diuretics (lasix) prevents fluid overload and promotes calcium excretion.

Sodium or potassium phosphates

Anti-tumor antibiotics plicamycin, (Mithracin, Mithramycin)49MAGNESIUMNormal serum values 1.4- 2.1 mg/dLIntracellular Cation (2nd most)Only 1% of body magnesium is in the blood serum the rest is stored in muscle and boneOf the 1% - 2/3 is ionized (free) and 1/3 is bound to plasma proteinsWhen calcium absorption goes up magnesium absorption goes downAlcohol decreases magnesium absorptionMany of the same foods rich in potassium and also rich in magnesium (green vegetable, whole grains, fish, seafood and nuts). Mg deficiency is usually asymptomatic until 2.1 mg/dLHypermagnesemia CausesDietary prolonged use/excessive use of magnesium-containing anta-acids (Maalox), laxatives (MOM) and IV magnesium sulfateRenal Dysfunction Renal insufficiency and failureSevere Dehydration Diabetic ketoacidosisThe kidneys excrete 40% of magnesium, with renal insufficiency and failure magnesium is increases.

Loss of body fluids due to diuresis from diabetic ketoacidosis causes a hemoconcentration of magnesium in the blood, which can result in and increased magnesium level. 53Clinical Manifestations of Magnesium ImbalancesHypomagnesemiaNeuromuscular hyperirritability, tetany-like symptoms, tremors, twitching of the face, spasticity, increased tendon reflexesCardiac Hypertension, cardiac dysrhythmias - PVCs, VT (Torsades), VF, and flat or inverted T wave, ST depression (like low K levels)

HypermagnesemiaNeuromuscular CNS depression, lethargy, drowsiness, weakness, paralysis, loss of deep tendon reflexesHypotension, Complete heart block (3rd degree), bradycardia, Widened QRS complex, prolonged QT intervalOthers: Flushing, respiratory depression

54Hypomagnesemia

Polymorphic VT life threatening Vfib

55Clinical Management of Magnesium ImbalancesHypomagnesemiaOral or IV replacementsDiet high in magnesium - green vegetables, whole grains, legumes, nutsHypermagnesemiaCorrect the underlying causeIV saline or calciumDialysis56Phosphorous Normal levels 2.5 4.5 mg/dLMajor Intracellular anionNeeded for metabolism, nerve and muscle functionPart of energy unitsComponent of phospholipids (cellular and organelle membranes)Regulated by calcitonin, parathyroid hormone AND Vitamin DLevels vary with acid-base balanceGlucose, insulin or sugar-containing foods temporarily shift phosphorous into the cells

PTH acts on phosphorous and calcium differently.

PTH stimulates the renal tubules to excrete phosphorous, decreasing serum phosphorous it increases serum calcium levels by pulling calcium from the bone

Both calcium and phosphorous need vitamin D for intestinal absorption57Functions of PhosphorousNeuromuscular normal nerve and muscle activityBones and teeth bone and teeth formation, strength and durabilityCellular forms high energy compounds (ATP, ADP, AMP), is the backbone of nucleic acids and stores metabolic energyFormation of red blood cell enzyme (2,3-diphosphoglycerate) that delivers oxygen to tissuesUtilization of B vitaminsMetabolism of fats, carbohydrates and proteinsMaintenance of ACID BASE balance in body fluids

58Phosphorous deficit < 2.5 mg/dLHypophosphatemia CausesDietary - Vitamin D deficiency, chronic alcoholism TPNGI malabsorption, vomiting, diarrheaHormonal Influence Hyperparathyroidism (increased PTH) Drugs aluminum containing antacids (binders), diureticsCellular Diabetic KetoacidosisAcid-Base disorders Respiratory alkalosis, metabolic alkalosis

With Chronic alcoholism dietary insufficiencies and increased diuresis

TPN is usually a phosphorous free or phosphorous poor solution. Plus the high concentration of glucose and protein given IV rapidly will cause a phosphorous shift into the cells causing a decreased serum phosphorous level

Phosphorous is absorbed in the jejunum in the presence of vitamin D

Phosphorous binders aluminum hydroxide, magnesium hydroxide, Excessive use of phosphorous binders (phosphorous binds with aluminum.

Diabetic ketoacidosis glycosuria, polyuria increase phosphorous excretion, dextrose and insulin cause a shift of phosphorous into the cell

Respiratory and metabolic alkalosis from prolonged hyperventilation decreases serum phosphorous level by causing an intracellular shift of phosphorous. (shifts into the cells)59Phosphorous excess > 4.5 mg/dLHyperphosphatemia CausesDietary excessive administration of phosphorous containing substancesHormonal lack of PTHRenal Insufficiencies Renal Failure (ARF, CRF)Drug frequent use of phosphate laxativesCellular destruction chemo, radiation, rhabdomyolsis (breakdown of striated muscle)Acid-Base disorders Metabolic and Respiratory AcidosisAcidosis causes hyperphosphatemia moves out of cell due to buffering anion, It prevents accumulation of cellular phosphate

Cellular destruction because phosphorous is primarily intracellular damage to cells will release large amounts of Phosphorous

60Clinical Manifestations of Phosphorous ImbalancesHypophosphatemiaNeuromuscular muscle weakness, tremors, paresthesia, bone pain, hyporeflexia, seizures, delirium, hallucinations, ascending motor paralysisHematologic tissue hypoxia, possible bleeding, possible infectionCardiopulmonary weak pulse, hyperventilation, respiratory weaknessGI Anorexia, dysphagia

HyperphosphatemiaNeuromuscular Tetany (with decreased calcium), hyperreflexia, muscular weakness (more common with hypophosphatemia), flaccid paralysisCardiopulmonary tachycardiaGI- nausea, diarrhea, abdominal cramps

Bone pain weakened bones and/or fractures (pathologic) due to mobilization of phosphorous from bone matrix to replace serum losses.

Hematological tissue hypoxia (decreased oxygen-containing hemoglobin and hemolysis) causing a left shift (greater resistance for oxygen release to the tissues), bleeding platelet dysfunctionInfection leukocyte dysfunction

Tissue hypoxia can cause dysrhythmias and heart block

If phosphorous deficiency is really severe - can cause metabolic encephalopathy syndrome manifested by irritability, confusion and seizures or chest pain.

Weak pulse myocardial dysfunction

61Clinical Management of Phosphorous ImbalancesHypophosphatemiaOral phosphorous replacementsTreat underlying causes Diet high in phosphorousAvoid phosphorous binding antacidsIV phosphorous (only when levels are below 1 mg/dl) dose 12-15 mmol/L diluted in IV fluidHyperphosphatemiaPhosphorous binding antacidsCalcium based antacids are preferred in renal failure to avoid hypermagnesemia If hyperphosphatemia is accompanied by hypocalcemia correcting calcium level will reduce phosphorous levelsAdminister Insulin and glucoseInsulin and glucose will shift phosphorous back into the cells but it is temporary 62ACID BASE IMBALANCESNURS 2140Winter 2012Teresa Champion, RN, MSNACID BASE BALANCEHydrogen ions - Low concentrations but highly reactiveConcentration affects physiological functions, for example: Alters protein and enzyme functioningCan cause cardiac, renal, respiratory abnormalitiesAlters blood clotting, metabolization of meds

Acid and BasesAcids compounds that form hydrogen ion in a solutionProton donorsStrong acids give up their hydrogen ion easilyWeak acids hold on to their hydrogen ion more tightlyBases compounds that combine with hydrogen ion in a solutionProton acceptorsNeutralizes 20:1 ratio (20 parts bicarbonate to one part carbonic acid)

Acid and bases constantly react to one another to neutralize changes in the hydrogen ion concentration. The normal ratio in blood for carbonic acid to bicarbonate is 20:1 (20 parts bicarbonate to 1 part carbonic acid). A change in this ratio will result in a change of blood pH. 65The Basics explained:

pH is a measurement of the acidity or alkalinity of the blood. It is inversely proportional to the number of hydrogen ions (H+) in the blood.The more H+ present, the lower the pH will be.The fewer H+ present, the higher the pH will be.

66Plasma pHInversely related to hydrogen ion concentration hydrogen ion concentration, pH hydrogen ion concentration, pH

When there is an increase in the hydrogen ion concentration in the plasma the plasma pH will decrease (acid)And vise versa67Body AcidsRespiratory Acid - CO2 eliminated by lungs (daily ~288L/day)Metabolic acids: (either excreted by kidney or metabolized in liver and Production: 0.1 mol (100 mEq)/day. Eliminated more slowly than respiratory acid Lactic acidsPyruvic acidKetoacids (DKA)Acetoatic acidsBeta-hydrobutyric acids

Normal Blood pHThe normal blood pH range is 7.35 to 7.45. Slightly alkaloticMust maintain this range for normal body functions< 7.35 Blood pH is acidotic> 7.45 blood pH is alkaloticThis is the FIRST step in interpretation of Arterial Blood Gases and plasma pH. BUFFER SYSTEMSExtracellular Buffers carbonic acid (lungs) and bicarbonate (kidneys)Intracellular BuffersPhosphate Buffer SystemDihydrogen phosphate (H2PO4) hydrogen donorHydrogen phosphate (HPO4) hydrogen acceptorProtein BuffersPlasma ProteinsHemoglobin oxyhemoglobin and deoxygenated HgbBonesCarbonate and phosphate salts in bone provide a long term supply of buffer. Excess carbon dioxide is exhaled by the lungsThe kidneys regulate (reabsorb and retain) all the bicarbonate in the body.The kidneys can excrete small amounts of acid in the tubules

In alkalosis the kidneys (respiratory or metabolic) Kidneys retain hydrogen ion and excrete bicarbonate . In respiratory acidosis and most cases of metabolic acidosis, the kidneys excrete hydrogen ion and conserve bicarbonate to correct the pH.

-----

ICF Buffers phosphorous buffers

H2PO4 and HPO4 are in equilibrium inside the cell. When there is extra hydrogen ion in the plasma, the hydrogen ions cross the cell membrane into the ICF and are consumed by HPO4. If there is extra base in plasma, then they cross cell membrane into ICF and react with H2PO4.

Protein BuffersHemoglobin is the most important because it can bind with both CO2 (carbon dioxide) and Hydrogen ions. Hemoglobin exists in two forms oxygenated hemoglobin (rich in O2 leaving left side of heart) and deoxygenated hemoglobin (O2 depleted after delivering O2 to the tissues/cells.)70Role of the lungsRegulate plasma pH minute to minute by regulating the level of Carbon Dioxide (CO2)Carbon Dioxide is measured as a partial pressure of carbon dioxide in arterial blood PaCO2 35-45mmHgLungs alter rate and depth of ventilations in order to retain or excrete CO2

Minute Volume Tidal VolumeVentilation is measured by how much air the lungs move in one minute (minute ventilation)Minute Ventilation is the product of respiratory rate and depth and is referred to as the TIDAL VOLUME (Vt)NORMAL tidal volume at rest is about 500ml. Aveolar volume = tidal volume anatomical dead spaceAveolar minute ventilation = respiratory rate x alveolar volumeMinute alveolar ventilation measures air that actually takes place in gas exchange

Normal resting respiratory rate is 12 and normal resting tidal volume is 500 that would make our minute volume of 6L/min.

12 bpm x 500mL = 6,000mL or 6L.

Anatomical Dead space is referred to as the amount of tidal volume that does not participate in the alveolar exchange. Anatomical Dead space can be estimated at 1ml/pound of body weight.

So a person that weights 150 lbs = 150 ml of anatomical dead space

Tidal volume 500ml 150 ml = 350ml of alveolar volume

Respiratory rate 12 x alveolar volume 350 ml = 4,200 ml or 4.2 L/min of alveolar ventilation

Dead SPACE is the anatomical dead space plus air that reaches the alveoli but still do not participate in gas exchange due to damage/disease like emphysema

72Terms for RespirationHypercarbic Drive increased PaCO2 levels raise the level of H+ ions, lowering pH. Central Chemorectptors (in CNS) stimulate the phrenic nerve, increasing respirationHypoxic Drive peripheral chemoreceptors in carotid arteries and arch of aorta are stimulated by low PaO2 level (45 mEq/L) with resultant drop in in pH (7.45 alkalotic)Most common cause of respiratory alkalosis is hyperventilation usually caused by pain, anxietyMedical treatmentMajor goal of therapy: treat underlying cause of condition; sedation may be ordered for the anxious patientNursing care InterventionIn addition to giving sedatives as ordered, reassure the patient to relieve anxiety Encourage patient to breathe slowly, which will retain carbon dioxide in the body

Metabolic AcidosisBody retains too many hydrogen ions or loses too many bicarbonate ions; with too much acid and too little base, blood pH falls (pH 7.45)Causes:Loss of hydrogen ions may be from prolonged nasogastric suctioning, excessive vomiting, diuretics, and electrolyte disturbancesSigns and symptoms:headache; irritability; lethargy; changes in level of consciousness; confusion; changes in heart rate; slow, shallow respirations with periods of apnea; nausea and vomiting; hyperactive reflexes; and numbness of the extremitiesMedical treatmentDepends on the underlying cause and severity of the condition

Metabolic AlkalosisNursing care AssessmentTake vital signs and daily weight; monitor heart rate, respirations, and fluid gains and losses Keep accurate intake and output records, including the amount of fluid removed by suction Assess motor function and sensation in the extremities; monitor laboratory values, especially pH and serum bicarbonate levelsInterventionTo prevent metabolic alkalosis, use isotonic saline solutions rather than water for irrigating nasogastric tubes because the use of water for irrigation can result in a loss of electrolytes