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Page 1: F&E Lecture (new 2010)

WELCOMEWELCOME

Page 2: F&E Lecture (new 2010)

FLUIDS and FLUIDS and ELECTROLYTESELECTROLYTES

Ronald Joseph J. Rebollido, R.N.

Page 3: F&E Lecture (new 2010)

ObjectivesObjectivesOn the completion of this concept On the completion of this concept

the students will be able to:the students will be able to:

• Differentiate fluid regulation Differentiate fluid regulation processes: osmosis, diffusion, processes: osmosis, diffusion, filtration and active transport.filtration and active transport.

• Differentiate the various Differentiate the various laboratory tests for evaluating laboratory tests for evaluating fluid status according to their use.fluid status according to their use.

Page 4: F&E Lecture (new 2010)

ObjectivesObjectives

• Describe the role of other Describe the role of other homeostatic mechanism in regulating homeostatic mechanism in regulating fluid composition and volume.fluid composition and volume.

• Describe the etiology, clinical Describe the etiology, clinical manifestations, management and manifestations, management and plan effective nursing care for clients plan effective nursing care for clients with fluid and electrolyte imbalances.with fluid and electrolyte imbalances.

Page 5: F&E Lecture (new 2010)

ObjectivesObjectives• Describe the pathophysiologic, clinical Describe the pathophysiologic, clinical

manifestations, medical and nursing manifestations, medical and nursing management of patients with acid-base management of patients with acid-base disturbances.disturbances.

• State the purpose of intravenous therapy State the purpose of intravenous therapy and different types of intravenous and different types of intravenous solutions.solutions.

• Plan effective nursing care of clients with Plan effective nursing care of clients with burns.burns.

Page 6: F&E Lecture (new 2010)

COURSE COURSE OUTLINEOUTLINE

Page 7: F&E Lecture (new 2010)

I. Physiology of Fluids & I. Physiology of Fluids & ElectrolytesElectrolytes

a.a. Amount & Composition of Body FluidsAmount & Composition of Body Fluids

b.b. ElectrolytesElectrolytes

c.c. Regulation of Body Fluids CompartmentsRegulation of Body Fluids Compartments

1. Osmosis 1. Osmosis

2. Diffusion 2. Diffusion

3. Filtration3. Filtration

4. Active Transport (Sodium-Potassium 4. Active Transport (Sodium-Potassium pump)pump)

Page 8: F&E Lecture (new 2010)

I. Physiology of Fluids & I. Physiology of Fluids & ElectrolytesElectrolytes

d. Routes of Gains & Lossesd. Routes of Gains & Losses1. Kidneys1. Kidneys2. Skin2. Skin3. Lungs3. Lungs4. GI Tract4. GI Tract

e. Laboratory Tests for Evaluating Fluid Statuse. Laboratory Tests for Evaluating Fluid Status1. Osmolality / Osmolarity1. Osmolality / Osmolarity2. Urine Specific Gravity2. Urine Specific Gravity3. Blood Urea Nitrogen3. Blood Urea Nitrogen4. Creatinine4. Creatinine

Page 9: F&E Lecture (new 2010)

I. Physiology of Fluids & I. Physiology of Fluids & ElectrolytesElectrolytes

5. Hematocrit5. Hematocrit6. Urine Sodium6. Urine Sodium

f. Homeostatic Mechanismsf. Homeostatic Mechanisms1. kidney Functions1. kidney Functions2. Heart & Blood Vessel Functions2. Heart & Blood Vessel Functions3. Lung Functions3. Lung Functions4. Pituitary Functions4. Pituitary Functions

Page 10: F&E Lecture (new 2010)

I. Physiology of Fluids & I. Physiology of Fluids & ElectrolytesElectrolytes

5. Adrenal Functions5. Adrenal Functions

6. Parathyroid Functions6. Parathyroid Functions

7. Other Mechanisms7. Other Mechanisms

a. Baroreceptorsa. Baroreceptors

b. Renin-Angiotensin-Aldosterone b. Renin-Angiotensin-Aldosterone systemsystem

c. ADH & Thirstc. ADH & Thirst

d. Osmoreceptorsd. Osmoreceptors

e. Release of Atrial Natriuretic Peptidee. Release of Atrial Natriuretic Peptide

Page 11: F&E Lecture (new 2010)

II. Fluid Volume & Electrolyte II. Fluid Volume & Electrolyte DisturbancesDisturbances

a.a. Fluid Volume Deficit (Hypovolemia)Fluid Volume Deficit (Hypovolemia)

b.b. Fluid Volume Excess (Hypervolemia)Fluid Volume Excess (Hypervolemia)

c.c. Electrolyte ImbalancesElectrolyte Imbalances

1. Significance of Sodium1. Significance of Sodium

a. Sodium Deficit (Hyponatremia)a. Sodium Deficit (Hyponatremia)

a1. Dilutional Hyponatremiaa1. Dilutional Hyponatremia

Page 12: F&E Lecture (new 2010)

II. Fluid Volume & Electrolyte II. Fluid Volume & Electrolyte DisturbancesDisturbances

b1. Sodium Excess (Hypernatremia)b1. Sodium Excess (Hypernatremia)

2. Significance of Potassium2. Significance of Potassiuma. Potassium Deficit (Hypokalemia)a. Potassium Deficit (Hypokalemia)b. Potassium Excess (Hyperkalemia)b. Potassium Excess (Hyperkalemia)

3. Significance of Calcium3. Significance of Calciuma. Calcium Deficit (Hypocalcemia)a. Calcium Deficit (Hypocalcemia)b. Calcium Excess (Hypercalcemia)b. Calcium Excess (Hypercalcemia)

Page 13: F&E Lecture (new 2010)

II. Fluid Volume & Electrolyte II. Fluid Volume & Electrolyte DisturbancesDisturbances

4. Significance of Magnesium4. Significance of Magnesium

a. Magnesium Deficit (Hypomagnesemia)a. Magnesium Deficit (Hypomagnesemia)

b. Magnesium Excess (Hypermagnesemia)b. Magnesium Excess (Hypermagnesemia)

5. Significance Of Phosphorus5. Significance Of Phosphorus

a. Phosphorus Deficit a. Phosphorus Deficit (Hypophosphatemia)(Hypophosphatemia)

b. Phosphorus Excess b. Phosphorus Excess (Hyperphosphatemia)(Hyperphosphatemia)

Page 14: F&E Lecture (new 2010)

II. Fluid Volume & Electrolyte II. Fluid Volume & Electrolyte DisturbancesDisturbances

6. Significance of Chloride6. Significance of Chloride

a. Chloride Deficit a. Chloride Deficit (Hypochloremia)(Hypochloremia)

b. Chloride Excess b. Chloride Excess (Hyperchloremia)(Hyperchloremia)

Page 15: F&E Lecture (new 2010)

III. Acid-Base DisturbancesIII. Acid-Base Disturbances

a. Acid-Base Balancea. Acid-Base Balance

1. Chemical buffer System1. Chemical buffer System

2. Kidneys2. Kidneys

3. Lungs3. Lungs

b. Acid-Base Disturbancesb. Acid-Base Disturbances

1. Acute & Chronic Metabolic 1. Acute & Chronic Metabolic Acidosis Acidosis (Base Bicarbonate (Base Bicarbonate Deficit)Deficit)

Page 16: F&E Lecture (new 2010)

III. Acid-Base DisturbancesIII. Acid-Base Disturbances

2. Acute & Chronic Metabolic 2. Acute & Chronic Metabolic Alkalosis Alkalosis (Base Bicarbonate (Base Bicarbonate Excess)Excess)

3. Acute & Chronic Respiratory 3. Acute & Chronic Respiratory Acidosis Acidosis (Carbonic Acid Excess)(Carbonic Acid Excess)

4. Acute And Chronic Respiratory 4. Acute And Chronic Respiratory Alkalosis Alkalosis (Carbonic Acid Deficit)(Carbonic Acid Deficit)

Page 17: F&E Lecture (new 2010)

IV. Parenteral Fluid TherapyIV. Parenteral Fluid Therapy

a.a. Purpose of Parenteral Fluid TherapyPurpose of Parenteral Fluid Therapy

b.b. Types Of SolutionTypes Of Solution

1. Isotonic Fluids1. Isotonic Fluids

2. Hypotonic Fluids2. Hypotonic Fluids

3. Hypertonic Fluids3. Hypertonic Fluids

V. BurnsV. Burns

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General General Composition of Composition of

Body FluidsBody Fluids

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GeneralGeneral CompositionComposition

•WaterWater

•ElectrolytesElectrolytes

•ProteinsProteins

•Other Other substancessubstances

Page 20: F&E Lecture (new 2010)

Factors affecting amount of body Factors affecting amount of body fluidsfluids

•AgeAge

•Sex / GenderSex / Gender

•Body fatBody fat

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Total Volume of Total Volume of Body WaterBody Water

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Volume body of waterVolume body of water

•The body consist The body consist 60-70%60-70% of of waterwater

Adult male : Adult male : 60 - 70% of body wt.60 - 70% of body wt.

Female : Female : 50 - 55% of body wt.50 - 55% of body wt.

Elderly : Elderly : 45 % of body wt.45 % of body wt.

Infants : Infants : 75 – 80% of body wt.75 – 80% of body wt.

Page 23: F&E Lecture (new 2010)

DistributionDistribution

Page 24: F&E Lecture (new 2010)

IntracellularIntracellular

•Found within the cells, it Found within the cells, it consists of around, consists of around, 60%60% or or 2/32/3 portion of the portion of the body weight. body weight.

Page 25: F&E Lecture (new 2010)

ExtracellularExtracellular

•Found outside the cells, Found outside the cells, it consist of around, it consist of around, 40%40% or or 1/3 1/3 portion of body portion of body weight.weight.

Page 26: F&E Lecture (new 2010)

Divisions of ECFDivisions of ECF

•Intravascular fluidIntravascular fluid – found in – found in the circulatory system (fluid the circulatory system (fluid within blood vessels), 10% within blood vessels), 10% body water.body water.

•Interstitial fluidInterstitial fluid – found – found between the cells, 25% between the cells, 25% body water (e.g. lymph) body water (e.g. lymph)

Page 27: F&E Lecture (new 2010)

Divisions of ECFDivisions of ECF

•Transcellular fluidTranscellular fluid – similar to – similar to interstitial fluid, they are product interstitial fluid, they are product of secretions and diffusion from of secretions and diffusion from cells, 5% body water ( e.g. cells, 5% body water ( e.g. CSFCSF, , salivasaliva, , gastric juicesgastric juices, , pericardialpericardial, , pleuralpleural, , intraocularintraocular and and sweatsweat))

Page 28: F&E Lecture (new 2010)

Other Way to Describe Other Way to Describe DistributionDistribution

Intravascular Intravascular vs.vs. InterstitialInterstitial

Inside blood vessels

Outside blood vessels

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Principles of Principles of MovementMovement

Water movesWater moves

intracellular intracellular interstitialinterstitial

intravascularintravascular

Page 30: F&E Lecture (new 2010)

ElectrolytesElectrolytes

•is a substance that is a substance that dissociates and forms ions dissociates and forms ions that able to conduct that able to conduct electric current when electric current when mixed with water.mixed with water.

•unit of measurement: unit of measurement: mEq/LmEq/L

Page 31: F&E Lecture (new 2010)

Types of IonsTypes of Ions

•Cation Cation – positively charge (+) – positively charge (+) e.g. e.g. Na+Na+,, K+ K+, , Ca++Ca++,, Mg++ Mg++

•Anion Anion – negatively charge (-) – negatively charge (-) e.g. e.g. Cl-Cl-, , HCO3-HCO3-, , PO4-PO4-, , SO4-SO4-,, Organic acids Organic acids andand Proteinate Proteinate..

Page 32: F&E Lecture (new 2010)

Electrochemical Electrochemical PropertiesProperties

• Like charges repelLike charges repel• Opposite charges Opposite charges

attractattract

Page 33: F&E Lecture (new 2010)

Major electrolytes in Major electrolytes in ECFECF

•Na+ and Cl-Na+ and Cl- –Sodium level is the primary Sodium level is the primary determinant of ECF determinant of ECF concentration.concentration.

Page 34: F&E Lecture (new 2010)

Major electrolytes in Major electrolytes in ICFICF

•K+ and PO4-K+ and PO4-–98% K+ of the body is 98% K+ of the body is inside the cells, 2% is in the inside the cells, 2% is in the ECF.ECF.

Page 35: F&E Lecture (new 2010)

Regulation of body Regulation of body fluidsfluids

•Osmosis Osmosis – fluid shifting from – fluid shifting from low solute concentration to low solute concentration to high solute concentration.high solute concentration. Osmolality Osmolality – determines the – determines the number of dissolved particles number of dissolved particles contain in a unit of fluid.contain in a unit of fluid.

Page 36: F&E Lecture (new 2010)

OsmosisOsmosis

semi-permeablemembrane

before after

Page 37: F&E Lecture (new 2010)

Regulation of body fluidsRegulation of body fluids

•Diffusion Diffusion – particle movement – particle movement from an area of high solute from an area of high solute concentration to low solute concentration to low solute concentration concentration (e.g. exchange (e.g. exchange of O2 and CO2 in capillaries of O2 and CO2 in capillaries and alveoli)and alveoli)..

Page 38: F&E Lecture (new 2010)

Regulation of body fluidsRegulation of body fluids

•Filtration Filtration – removal of particles – removal of particles from a solution through the from a solution through the movement of fluid across a movement of fluid across a membranemembrane (e.g. passage of (e.g. passage of water and electrolytes from water and electrolytes from arterial capillary bed to the arterial capillary bed to the interstitial fluid)interstitial fluid). .

Page 39: F&E Lecture (new 2010)

Regulation of body fluidsRegulation of body fluids

•Active transportActive transport – is an energy – is an energy requiring process that requiring process that transport ion from an area of transport ion from an area of lower concentration to one of lower concentration to one of higher concentration. (higher concentration. (e.g.e.g. process ofprocess of sodium – potassium sodium – potassium pumppump) ) ATPATP is required for is required for energy energy

Page 40: F&E Lecture (new 2010)

Forces Involved in Forces Involved in Movement of Fluid Movement of Fluid Between Capillaries Between Capillaries

and Interstitial and Interstitial SpacesSpaces

Page 41: F&E Lecture (new 2010)

Colloid Osmotic Colloid Osmotic PressurePressure

•Osmotic pull inside capillaries Osmotic pull inside capillaries exerted by large plasma proteins.exerted by large plasma proteins.

e.g.e.g.– albuminalbumin– globulinsglobulins– FibrinogenFibrinogen

Page 42: F&E Lecture (new 2010)

Colloid Osmotic Colloid Osmotic PressurePressure

•pulls fluid from interstitial space to pulls fluid from interstitial space to intravascular spaceintravascular space

• limits movement of fluid from limits movement of fluid from intravascular space to interstitial intravascular space to interstitial spacespace

Page 43: F&E Lecture (new 2010)

Colloid Osmotic Colloid Osmotic PressurePressure

Page 44: F&E Lecture (new 2010)

Colloid Osmotic Colloid Osmotic PressurePressure

Page 45: F&E Lecture (new 2010)

Colloid Osmotic Colloid Osmotic PressurePressure

Page 46: F&E Lecture (new 2010)

Hydrostatic PressureHydrostatic Pressure

•The pressure created by the The pressure created by the weight of fluid against the wall weight of fluid against the wall that contains it.that contains it.

• hydrostatic pressure in blood hydrostatic pressure in blood vessels results from the weight of vessels results from the weight of fluid itself and the force resulting fluid itself and the force resulting from cardiac contractionfrom cardiac contraction

Page 47: F&E Lecture (new 2010)

hydrostaticHydrostatic pressure = 37 mmHg

Colloid osmotic press= 25 mm Hg

12

Net filtration pressure is +12 mm Hg in favor of pushing fluid out of capillary

Hydrostatic pressure = 18 mmHg

Colloid osmotic press= 25 mm Hg

-7

Net pressure is now in favor of pulling fluid back into capillary

Page 48: F&E Lecture (new 2010)
Page 49: F&E Lecture (new 2010)

Third – Space Fluid Third – Space Fluid ShiftShift

Page 50: F&E Lecture (new 2010)

Third – Space Fluid ShiftThird – Space Fluid ShiftDefinition:Definition: Loss of extracellular fluid into Loss of extracellular fluid into

a space that does not contribute to a space that does not contribute to ICF and ECF equilibrium, “ICF and ECF equilibrium, “Third Third SpacingSpacing”.”.

Clinical Manifestation:Clinical Manifestation:

1. 1. urine output (early sign)urine output (early sign)

2. heart rate2. heart rate

3. body weight3. body weight

4. Edema 4. Edema

Page 51: F&E Lecture (new 2010)

Third – Space Fluid ShiftThird – Space Fluid Shift

Etiology:Etiology:

1. Liver cirrhosis1. Liver cirrhosis

2. Burns2. Burns

3. Peritonitis3. Peritonitis

4. Bowel Obstruction4. Bowel Obstruction

5. Massive bleeding into a joint or 5. Massive bleeding into a joint or cavitycavity

Page 52: F&E Lecture (new 2010)

Third – Space Fluid ShiftThird – Space Fluid Shift

Examples:Examples:

PeritonitisPeritonitis - - inflammatory inflammatory process process causing the causing the fluid to build up fluid to build up in the in the peritoneum.peritoneum.

Page 53: F&E Lecture (new 2010)

Third – Space Fluid ShiftThird – Space Fluid Shift

AscitesAscites – large – large accumulation accumulation of fluid in the of fluid in the peritoneal peritoneal cavity.cavity.

Page 54: F&E Lecture (new 2010)

Third – Space Fluid ShiftThird – Space Fluid Shift

Pleural effusionPleural effusion – – accumulation of accumulation of fluid in the fluid in the pleural space.pleural space.

Page 55: F&E Lecture (new 2010)

Routes of Gains and Routes of Gains and LossesLosses

• GainsGains

• Water and electrolytes are gained Water and electrolytes are gained in various waysin various ways

a. Drinking and eating (a. Drinking and eating (healthyhealthy persons persons))

b. Parenteral, NGT, Gastric feeding and b. Parenteral, NGT, Gastric feeding and IV therapy (IV therapy (sick patientssick patients))

Page 56: F&E Lecture (new 2010)

Routes of Gains and Routes of Gains and LossesLosses

• Losses Losses a. a. KidneysKidneys – urine production about 1 to 2 – urine production about 1 to 2

liters per day (liters per day (min. 400ml urge to urinate & min. 400ml urge to urinate & worry if <800 ml/day or <30 ml/hrworry if <800 ml/day or <30 ml/hr))

b. b. G.I. tractG.I. tract – feces about 100 – 200 ml per – feces about 100 – 200 ml per dayday

c. c. Insensible lossesInsensible losses – Skin: sweat 600ml/day – Skin: sweat 600ml/day Lungs: 400 Lungs: 400

ml/dayml/day

Page 57: F&E Lecture (new 2010)

Laboratory test for fluid Laboratory test for fluid statusstatus• OsmolalityOsmolality - reflects the concentration of - reflects the concentration of

fluid that affects the movement of between fluid that affects the movement of between the fluid compartment by osmosis.the fluid compartment by osmosis.

• Osmolarity Osmolarity – another term that describes the – another term that describes the concentration of a solution which is concentration of a solution which is measured in mOsm/liter.measured in mOsm/liter.

Normal serum value: Normal serum value: 280-300 mOsm/kg280-300 mOsm/kgUrine: Urine: 250-900 mOsm/kg250-900 mOsm/kg

Page 58: F&E Lecture (new 2010)

Laboratory test for fluid Laboratory test for fluid statusstatus

•Urine specific gravityUrine specific gravity – – determines the urine determines the urine concentration.concentration.

Normal urine value: Normal urine value: 1.010 to 1.0251.010 to 1.025

Page 59: F&E Lecture (new 2010)

Laboratory test for fluid Laboratory test for fluid statusstatus

•Blood Urea Nitrogen (BUN) Blood Urea Nitrogen (BUN) – – measures urea, which is end measures urea, which is end product of protein metabolism.product of protein metabolism.

Normal serum value: Normal serum value: 10 to 20 10 to 20 mg/dl or 3.5 to 7 mmol/Lmg/dl or 3.5 to 7 mmol/L

Page 60: F&E Lecture (new 2010)

Laboratory test for fluid Laboratory test for fluid statusstatus

•CreatinineCreatinine – is the end product of – is the end product of muscle metabolism, indicator of muscle metabolism, indicator of renal function.renal function.

Normal serum value: Normal serum value: 0.7 - 1.5 0.7 - 1.5 mg/dl or 60 – 130 mmol/Lmg/dl or 60 – 130 mmol/L

Page 61: F&E Lecture (new 2010)

Laboratory test for fluid Laboratory test for fluid statusstatus

•Hematocrit Hematocrit – measures the – measures the volume percentage of RBC volume percentage of RBC (erythrocytes) in whole blood.(erythrocytes) in whole blood.

Normal serum value: Normal serum value:

•Male: Male: 44 – 52%44 – 52%

•Female: Female: 39 – 47%39 – 47%

Page 62: F&E Lecture (new 2010)

Laboratory test for fluid Laboratory test for fluid statusstatus

•Urine sodiumUrine sodium – determines the Na+ – determines the Na+ concentration in the urine (asses concentration in the urine (asses volume status), useful in the volume status), useful in the diagnosis of hyponatremia & acute diagnosis of hyponatremia & acute renal failurerenal failure

Normal value: Normal value: 50 – 220 mEq/24 hrs.50 – 220 mEq/24 hrs.

Page 63: F&E Lecture (new 2010)

Homeostatic Homeostatic MechanismMechanism

Page 64: F&E Lecture (new 2010)

Homeostatic Homeostatic MechanismMechanism

a. a. Renal System (Kidneys) Renal System (Kidneys) – Filter about 170 liters plasma/day Filter about 170 liters plasma/day

and excrete 1.5 L urine/day and excrete 1.5 L urine/day – Regulation of pH of the ECF Regulation of pH of the ECF

retention/excretion of hydrogen retention/excretion of hydrogen ions.ions.

– Excretion of metabolic waste and Excretion of metabolic waste and toxic substances.toxic substances.

– Regulation of ECF volume and Regulation of ECF volume and electrolytes level.electrolytes level.

Page 65: F&E Lecture (new 2010)

Homeostatic Homeostatic MechanismMechanism

b. b. Cardiovascular sytem (heart & Cardiovascular sytem (heart & blood vessels)blood vessels)

– circulates blood through the circulates blood through the kidneys to maintain adequate kidneys to maintain adequate renal function thus urine renal function thus urine formationformation

Page 66: F&E Lecture (new 2010)

Homeostatic Homeostatic MechanismMechanism

c.c. Pulmonary system (Lungs)Pulmonary system (Lungs)

- remove approximately 300 ml. - remove approximately 300 ml. fluid/dayfluid/day

- Maintain acid-base balance by - Maintain acid-base balance by controlling controlling Carbon dioxideCarbon dioxide (CO2) and (CO2) and Carbonic acidCarbonic acid (H2CO3) excretion. (H2CO3) excretion. PCO2 PCO2 most powerful respiratory stimulant.most powerful respiratory stimulant.

Page 67: F&E Lecture (new 2010)

Homeostatic Homeostatic MechanismMechanism

d.d. Pituitary glandPituitary gland-secretes -secretes Antidiuretic hormoneAntidiuretic hormone (ADH) from posterior pituitary gland (ADH) from posterior pituitary gland that promote water retention. that promote water retention.

e. e. Adrenal glandsAdrenal glands-secretes -secretes AldosteroneAldosterone causes causes sodium retention (thus water sodium retention (thus water retention) and potassium loss at retention) and potassium loss at the kidneys.the kidneys.-secretes -secretes CortisolCortisol..

Page 68: F&E Lecture (new 2010)

Homeostatic Homeostatic MechanismMechanism

f. f. Parathyroid glandsParathyroid glands

- secrete - secrete Parathyroid hormoneParathyroid hormone (PTH) which regulates calcium (PTH) which regulates calcium and phosphate balance.and phosphate balance.

Page 69: F&E Lecture (new 2010)

Homeostatic Homeostatic MechanismMechanism

•Other MechanismsOther Mechanisms

a.a. Baroreceptors Baroreceptors– Small nerve receptors that detect Small nerve receptors that detect

changes in pressure within blood changes in pressure within blood vessel and transmit this vessel and transmit this information to the CNS.information to the CNS.

Page 70: F&E Lecture (new 2010)

Homeostatic Homeostatic MechanismMechanismb. renin-angiotensin-aldosterone b. renin-angiotensin-aldosterone

systemsystem

c. ADH and Thirstc. ADH and Thirst

d. Osmoreceptorsd. Osmoreceptors

e. Release of Atrial Natriuretic Peptidee. Release of Atrial Natriuretic Peptide

Page 71: F&E Lecture (new 2010)

Physiology Physiology (Atrial Natriuretic Peptide)(Atrial Natriuretic Peptide)

Page 72: F&E Lecture (new 2010)

ATRIAL NATRIURETIC PEPTIDEATRIAL NATRIURETIC PEPTIDE

Blood volumeBlood volume

Blood pressureBlood pressure

Stretch of atriaStretch of atria

ANP release from cardiac cells in atriaANP release from cardiac cells in atria

Vascular resistance byVascular resistance by ADH release by PPGADH release by PPG Glomerular filtrationGlomerular filtration

causing vasodilationcausing vasodilation rate w/c urinaryrate w/c urinary

excretion of Naexcretion of Na

Blood pressureBlood pressure

Suppression of reninSuppression of renin Vascular volumeVascular volume

Inhibits action angiotensinInhibits action angiotensin Blood pressureBlood pressure

aldosteronealdosterone Preload / AfterloadPreload / Afterload

Page 73: F&E Lecture (new 2010)

Physiology / Physiology / PathophysiologyPathophysiology

(Fluid Regulation Cycle)(Fluid Regulation Cycle)

Page 74: F&E Lecture (new 2010)

Blood volume / Serum osmolality Blood volume / Serum osmolality

( Thirst & water intake)( Thirst & water intake)ECF volume deficit ECF volume deficit stimulatesstimulates

ADH production hypothalamusADH production hypothalamus (osmoreceptors)(osmoreceptors) Arterial B/P (stimulates Baroreceptors) Arterial B/P (stimulates Baroreceptors)

Symphathetic dischargeSymphathetic discharge inhibits / diuresis resultsinhibits / diuresis results

Renal perfusionRenal perfusion

Water & Na+Water & Na+ Renin release ( GFR) Renin release ( GFR) ADH release into ADH release into bloodstreambloodstream filtered by kidneyfiltered by kidney peripheral vasoconstriction peripheral vasoconstriction from posterior pituitary gland from posterior pituitary gland

Angiotensin I & IIAngiotensin I & II

Blood volume Blood volume Aldosterone by adrenal cortex Aldosterone by adrenal cortex Reabsorption of water Reabsorption of water by distal by distal

Serum osmolalitySerum osmolality tubules tubules

Na+ and water excretion by kidneysNa+ and water excretion by kidneys

Blood pressureBlood pressure Urine excretion Urine excretion

Circulating volume of water & Na+ Circulating volume of water & Na+ (Loss of K+)(Loss of K+)

Page 75: F&E Lecture (new 2010)

Fluid Volume Fluid Volume DisturbancesDisturbances

Page 76: F&E Lecture (new 2010)

FLUID VOLUME DEFICITFLUID VOLUME DEFICIT(Hypovolemia)(Hypovolemia)

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Fluid Volume Deficit Fluid Volume Deficit (hypovolemia)(hypovolemia)

Definition:Definition: is an excessive loss of water is an excessive loss of water and electrolytes in equal proportion; and electrolytes in equal proportion; vascular and intracellular dehydration.vascular and intracellular dehydration.

Etiology:Etiology: 1. Vomiting & Diarrhea1. Vomiting & Diarrhea

2. GI suctioning & Sweating 2. GI suctioning & Sweating

3. Decreased intake 3. Decreased intake

Risk Factors:Risk Factors: Diabetes insipidus, Diabetes insipidus, Hemorrhage, adrenal insufficiency, Hemorrhage, adrenal insufficiency, Third-spacing, coma.Third-spacing, coma.

Page 78: F&E Lecture (new 2010)

Clinical Manifestation:Clinical Manifestation:

1. Acute weight loss1. Acute weight loss

2. Decreased skin turgor2. Decreased skin turgor

3. Oliguria & concentrated urine3. Oliguria & concentrated urine

4. Postural hypotension & increased temp.4. Postural hypotension & increased temp.

5. Flattened neck veins and decreased CVP5. Flattened neck veins and decreased CVP

6. Cool & clammy skin, thirst & cramps6. Cool & clammy skin, thirst & cramps

7. Nausea & muscle weakness7. Nausea & muscle weakness

Fluid Volume Deficit Fluid Volume Deficit (hypovolemia)(hypovolemia)

Page 79: F&E Lecture (new 2010)

Laboratory and Diagnostic study findings:Laboratory and Diagnostic study findings:

1. Urine specific gravity is >1.0201. Urine specific gravity is >1.020

2. Elevated BUN 2. Elevated BUN ((Blood Urea NitrogenBlood Urea Nitrogen))

3. Elevated Hematocrit3. Elevated Hematocrit

Fluid Volume Deficit Fluid Volume Deficit (hypovolemia)(hypovolemia)

Page 80: F&E Lecture (new 2010)

Medical Management:Medical Management:

1. Increased Oral fluid intake1. Increased Oral fluid intake

2. IV therapy (Lactated Ringer’s, 2. IV therapy (Lactated Ringer’s,

0.9% NaCl or NSS)0.9% NaCl or NSS)

Fluid Volume Deficit Fluid Volume Deficit (hypovolemia)(hypovolemia)

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Nursing Problem/s:Nursing Problem/s:

1. Fluid Volume Deficit: Actual or1. Fluid Volume Deficit: Actual or

PotentialPotential

Nursing Management:Nursing Management:

1. Maintain normal fluid balance.1. Maintain normal fluid balance.

- Monitor I&O- Monitor I&O

- Monitor urine specific gravity- Monitor urine specific gravity

- Weigh client daily- Weigh client daily

- Administer Oral & IV fluids- Administer Oral & IV fluids

Fluid Volume Deficit Fluid Volume Deficit (hypovolemia)(hypovolemia)

Page 82: F&E Lecture (new 2010)

2.2. Provide ongoing assessment.Provide ongoing assessment.

- Check vital signs, LOC, CVP, breath - Check vital signs, LOC, CVP, breath

sounds & skin color (to avoid volumesounds & skin color (to avoid volume

overload)overload)

3. Maintain skin integrity.3. Maintain skin integrity.

4. Provide frequent oral care. 4. Provide frequent oral care.

5. Teach client to change position slowly.5. Teach client to change position slowly.

Fluid Volume Deficit Fluid Volume Deficit (hypovolemia)(hypovolemia)

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Fluid Volume ExcessFluid Volume Excess(Hypervolemia)(Hypervolemia)

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Definition:Definition: is an excessive retention of water and is an excessive retention of water and electrolytes in equal proportion; increased electrolytes in equal proportion; increased local or total body fluid volume.local or total body fluid volume.

Etiology:Etiology:

1. Excessive fluid intake1. Excessive fluid intake

2. Renal diseases2. Renal diseases

3. Congestive Heart Failure3. Congestive Heart Failure

4. Cirrhosis of the Liver4. Cirrhosis of the Liver

Risk Factors:Risk Factors: Increased Na+ consumption, Increased Na+ consumption, excessive administration of Na+ containing IVFexcessive administration of Na+ containing IVF

Fluid Volume Excess Fluid Volume Excess (hypervolemia)(hypervolemia)

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Clinical Manifestation:Clinical Manifestation:

1. Edema (1. Edema (feetfeet, , ankles ankles and and sacrumsacrum))

2. Distended neck veins2. Distended neck veins

3. Crackles, shortness of breath & 3. Crackles, shortness of breath & wheezingwheezing

4. Weight and urine output4. Weight and urine output

5. CVP, Heart Rate and Blood Pressure5. CVP, Heart Rate and Blood Pressure

Fluid Volume Excess Fluid Volume Excess (hypervolemia)(hypervolemia)

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Laboratory and Diagnostic study:Laboratory and Diagnostic study:1. Decreased BUN and Hematocrit1. Decreased BUN and Hematocrit

Medical Management:Medical Management:1. Administering diuretics1. Administering diuretics

- - Thiazides diureticsThiazides diuretics; ; hydrochlorothiazidehydrochlorothiazide(HydroDIURIL), trichlormethiazide (HydroDIURIL), trichlormethiazide

(Diurese), drug of choice to mild to moderate FVE.(Diurese), drug of choice to mild to moderate FVE.- - Loop diureticsLoop diuretics; ; Furosemide Furosemide (Lasix), (Lasix), Torsemide (Demadex) drug of choice to severe Torsemide (Demadex) drug of choice to severe

FVE.FVE.

2. Restricting fluids and sodium intake2. Restricting fluids and sodium intake

Fluid Volume Excess Fluid Volume Excess (hypervolemia)(hypervolemia)

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3. Hemodialysis3. Hemodialysis

Nursing Problem/s:Nursing Problem/s:1. Fluid Volume Excess: Actual or 1. Fluid Volume Excess: Actual or PotentialPotential

Nursing Management:Nursing Management:1. Maintain normal fluid balance.1. Maintain normal fluid balance.

- Monitor I&O- Monitor I&O

Fluid Volume Excess Fluid Volume Excess (hypervolemia)(hypervolemia)

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Fluid Volume Excess Fluid Volume Excess (hypervolemia)(hypervolemia)

- Weigh client daily- Weigh client daily- Assess V/S, for peripheral and sacral- Assess V/S, for peripheral and sacraledemaedema- Monitor rate of IVF- Monitor rate of IVF

2. Prevent or minimize edema.2. Prevent or minimize edema.- - Assess lung sounds Assess lung sounds (monitor(monitorpulmonary edema)pulmonary edema)- Turn to sides every 2 hours- Turn to sides every 2 hours- Bed Rest- Bed Rest

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Fluid Volume Excess Fluid Volume Excess (hypervolemia)(hypervolemia)

- administer diuretics as prescribed.- administer diuretics as prescribed.

3. Provide client and family Hx teaching.3. Provide client and family Hx teaching.-Teach client the fundamentals of a-Teach client the fundamentals of aNa-restricted diet.Na-restricted diet.-Restrict Na+ and water as ordered.-Restrict Na+ and water as ordered.- Avoid OTC drugs.- Avoid OTC drugs.

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Electrolyte Electrolyte DisturbancesDisturbances

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Significance of SodiumSignificance of Sodium• The most abundant cation electrolyte in ECF.The most abundant cation electrolyte in ECF.

• Primary determinant of ECF osmolality and Primary determinant of ECF osmolality and regulator of ECF volume.regulator of ECF volume.

• Helps regulate acid-base balance.Helps regulate acid-base balance.

• Responsible for the action potential of Responsible for the action potential of nervous and muscle fibers, the basic factor nervous and muscle fibers, the basic factor to communication between nerves and to communication between nerves and muscles.muscles.

• Food high in Na+: Food high in Na+: celerycelery, , processed foodsprocessed foods, , snack foodssnack foods, , smoked meatssmoked meats and and cheesecheese. .

Normal serum value: Normal serum value: 135-145 mEq/L135-145 mEq/L

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HyponatremiaHyponatremia

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HyponatremiaHyponatremia

Definition:Definition: is a serum sodium level is a serum sodium level <135 mEq/L resulting from excessive <135 mEq/L resulting from excessive sodium loss or excessive water gain.sodium loss or excessive water gain.

Etiology: Etiology:

1. Fluid loss (1. Fluid loss (vomitingvomiting,, diarrhea diarrhea,, fistulafistula, , diaphoresisdiaphoresis, , NGT suctioningNGT suctioning & & diureticsdiuretics))

2. Adrenal insufficiency2. Adrenal insufficiency

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HyponatremiaHyponatremia

3. Syndrome of inappropriate 3. Syndrome of inappropriate antidiuretic hormone excretion antidiuretic hormone excretion (SIADH)(SIADH)

4. Compulsive water drinking 4. Compulsive water drinking (psychogenic polydipsia)(psychogenic polydipsia)

5. Excessive water gain from intake 5. Excessive water gain from intake of Na+ deficient IV fluids.of Na+ deficient IV fluids.

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Dilutional HyponatremiaDilutional Hyponatremia – also called – also called ““water intoxicationwater intoxication”, sodium level is ”, sodium level is diluted by an increased in the ratio of diluted by an increased in the ratio of water to sodium.water to sodium.

SIADHSIADH – result of excessive ADH – result of excessive ADH activity, with water retention and activity, with water retention and dilutional hyponatremia.dilutional hyponatremia.

HyponatremiaHyponatremia

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Clinical manifestation:Clinical manifestation:

1. Anorexia, nausea, and vomiting1. Anorexia, nausea, and vomiting

2. Muscle cramps2. Muscle cramps

3. Altered LOC (3. Altered LOC (lethargylethargy, , disorientationdisorientation, , headacheheadache, , confusion confusion & & convulsionconvulsion//seizureseizure with Na+ with Na+ level <115 mEq/Llevel <115 mEq/L))

HyponatremiaHyponatremia

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Laboratory and Diagnostic study:Laboratory and Diagnostic study:

1. Sodium level <135 mEq/L1. Sodium level <135 mEq/L

2. Urinalysis: Na+ & specific gravity level 2. Urinalysis: Na+ & specific gravity level low if caused by Na+ loss and high if caused low if caused by Na+ loss and high if caused by SIADH.by SIADH.

Medical Management:Medical Management:

1. Sodium replacement (1. Sodium replacement (oraloral, , NGT NGT && parenteralparenteral))

2. Water restriction2. Water restriction

HyponatremiaHyponatremia

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HyponatremiaHyponatremia

Nursing Problems:Nursing Problems:

1. Altered level of consciousness1. Altered level of consciousness

2. Altered thought processes2. Altered thought processes

3. Altered bowel elimination3. Altered bowel elimination

4. Fluid volume deficit/excess4. Fluid volume deficit/excess

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Nursing Management:Nursing Management:

1. Maintain fluid balance.1. Maintain fluid balance.

- Monitor I&O accurately- Monitor I&O accurately

- Weigh the client daily- Weigh the client daily

- Assess for signs of fluid volume excess- Assess for signs of fluid volume excess

2. Prevent injury.2. Prevent injury.

- Assess neurologic (e.g. - Assess neurologic (e.g. lethargylethargy, , seizureseizure

confusionconfusion & & muscle twitchingmuscle twitching))

HyponatremiaHyponatremia

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3. 3. Maintain seizure precautionsMaintain seizure precautions

4. Monitor serum Na+ level4. Monitor serum Na+ level

5. Maintain strict water restriction 5. Maintain strict water restriction when when hyponatremia is present hyponatremia is present with normal or with normal or fluid volume fluid volume excess.excess.

HyponatremiaHyponatremia

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HypernatremiHypernatremiaa

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HypernatremiaHypernatremia

Definition:Definition: is a serum Na+ level >145 is a serum Na+ level >145 mEq/L caused by gain of sodium in mEq/L caused by gain of sodium in excess of water or loss of water in excess of water or loss of water in excess of sodium.excess of sodium.

Etiology:Etiology:

1.Water loss (1.Water loss (diarrheadiarrhea, , feverfever, , hyperventilationhyperventilation & & diabetes diabetes insipidusinsipidus))

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HypernatremiaHypernatremia

2. Inadequate water replacement2. Inadequate water replacement

3. Excessive oral and parenteral Na+ 3. Excessive oral and parenteral Na+ intakeintake

4. Seawater ingestion (4. Seawater ingestion (rarelyrarely))

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HypernatremiaHypernatremia

Clinical Manifestation:Clinical Manifestation:

1. Thirst1. Thirst

2. Tented skin turgor2. Tented skin turgor

3. Elevated body temperature3. Elevated body temperature

4. Lethargy and restlessness4. Lethargy and restlessness

5. Peripheral and pulmonary edema5. Peripheral and pulmonary edema

6. Edematous dry tongue, sticky 6. Edematous dry tongue, sticky mucousmucous

membranes membranes

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HypernatremiaHypernatremia

Laboratory and Diagnostic study:Laboratory and Diagnostic study:

1. Serum Na+ level >145 mEq/L1. Serum Na+ level >145 mEq/L

2. Serum Osmolality >300 mOsm/kg2. Serum Osmolality >300 mOsm/kg

3. Increase urine specific gravity and 3. Increase urine specific gravity and osmolalityosmolality

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HypernatremiaHypernatremia

Medical Management:Medical Management:

1. Hypotonic IVF therapy (1. Hypotonic IVF therapy (Dextrose 5% inDextrose 5% in WaterWater: : D5WD5W, , 0.3 NaCl0.3 NaCl))

2. Diuretics2. Diuretics

Nursing Problems:Nursing Problems:

1. Altered Level of consciousness1. Altered Level of consciousness

2. Altered thought processes2. Altered thought processes

3. Fluid volume: deficit or excess 3. Fluid volume: deficit or excess

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HypernatremiaHypernatremia

Nursing Management:Nursing Management:

1. Maintain normal fluid balance.1. Maintain normal fluid balance.

- Monitor I&O- Monitor I&O

- Weigh client daily- Weigh client daily

- Increased fluid intake- Increased fluid intake

- Infuse hypotonic solutions - Infuse hypotonic solutions cautiouslycautiously

2. Protect client from injury2. Protect client from injury

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- Assess vital signs, skin condition, - Assess vital signs, skin condition, neurologic status and for thirst.neurologic status and for thirst.- Monitor serum Na+ level- Monitor serum Na+ level- Reposition the client frequently- Reposition the client frequently- Secure all invasive lines- Secure all invasive lines- Keep the bed sides rails up, bed in - Keep the bed sides rails up, bed in low low position, call light within reachposition, call light within reach- Obtain a medication history- Obtain a medication history

HypernatremiaHypernatremia

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HypokalemiaHypokalemia

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Significance of PotassiumSignificance of Potassium• The major cation electrolyte in ICF.The major cation electrolyte in ICF.• 98% of K+ inside the cell and 2% 98% of K+ inside the cell and 2%

outside the cell.outside the cell.• Influences both skeletal and cardiac Influences both skeletal and cardiac

muscle activity.muscle activity.• Potassium pump brings K+ into the cellsPotassium pump brings K+ into the cells• Foods high in K+: Foods high in K+: BananasBananas, , AvocadosAvocados, ,

OrangesOranges, , DatesDates, , PotatoesPotatoes, , RaisinsRaisins, , MilkMilk, , LegumesLegumes, , ApricotApricot, , MeatMeat and and Whole Whole grainsgrains..

Normal serum value: Normal serum value: 3.5 – 5.5 mEq/L3.5 – 5.5 mEq/L

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HypokalemiaHypokalemia

Definition:Definition: is a serum potassium level <3.5 is a serum potassium level <3.5 mEq/L.mEq/L.

Etiology:Etiology:

1. Inadequate dietary K+ intake.1. Inadequate dietary K+ intake.

2. Excessive loss from; Diuretics, antibiotics, 2. Excessive loss from; Diuretics, antibiotics, gastric gastric suctioning, ileostomy, colostomy, IV suctioning, ileostomy, colostomy, IV therapy therapy w/out K+ replacement and w/out K+ replacement and corticosteroids.corticosteroids.

3. Renal disorders3. Renal disorders

4. GI disorders (diarrhea & vomiting)4. GI disorders (diarrhea & vomiting)

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HypokalemiaHypokalemia

5. Metabolic alkalosis5. Metabolic alkalosis

6. Hyperaldosteronism6. Hyperaldosteronism

Clinical Manifestation: Clinical Manifestation:

1. Anorexia, nausea & vomiting1. Anorexia, nausea & vomiting

2. Fatigue2. Fatigue

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HypokalemiaHypokalemia

3. Muscle weakness, leg cramps or 3. Muscle weakness, leg cramps or paresthesiaparesthesia

4. Cardiac arrythmias4. Cardiac arrythmias

5. Decreased bowel motility, ileus or 5. Decreased bowel motility, ileus or abdominal distentionabdominal distention

Laboratory and Diagnostic study:Laboratory and Diagnostic study:

1. Serum K+ <3.5 mEq/L1. Serum K+ <3.5 mEq/L

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HypokalemiaHypokalemia2. ECG (2. ECG (flattened T waveflattened T wave, , prominent prominent U waveU wave, , depressed ST segmentdepressed ST segment and and prolonged PR intervalprolonged PR interval))

Medical Management:Medical Management:

1. Oral & IV K+ replacement therapy.1. Oral & IV K+ replacement therapy.

2. Increased K+ dietary intake.2. Increased K+ dietary intake.

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HypokalemiaHypokalemia

Nursing Problems:Nursing Problems:

1. Decreased Cardiac Output1. Decreased Cardiac Output

2. Altered Tissue Perfusion 2. Altered Tissue Perfusion

3. Altered Urinary Elimination3. Altered Urinary Elimination

4. Ineffective Breathing Pattern 4. Ineffective Breathing Pattern

5. Altered Bowel Elimination5. Altered Bowel Elimination

6. Self Care Deficits6. Self Care Deficits

7. Altered Level of Consciousness7. Altered Level of Consciousness

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HypokalemiaHypokalemia

Nursing Management:Nursing Management:

1. Prepare for and assist with 1. Prepare for and assist with therapies as prescribed.therapies as prescribed.

- Administer oral K+ daily; assess - Administer oral K+ daily; assess abdominal distention, pain or GI abdominal distention, pain or GI bleeding.bleeding.

- Infuse parenteral K+ - Infuse parenteral K+ supplement; dilute 100 ml. of solution, supplement; dilute 100 ml. of solution, use infusion pump, monitor ECG use infusion pump, monitor ECG during administration. during administration.

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HypokalemiaHypokalemia

- - Never administer potassium by Never administer potassium by IV push or intramuscularlyIV push or intramuscularly..

- Monitor serum K+ level- Monitor serum K+ level

- Monitor I&O- Monitor I&O

2. Provide client and family teaching.2. Provide client and family teaching.

3. Prevent client injury.3. Prevent client injury.

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HyperkalemiaHyperkalemia

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HyperkalemiaHyperkalemiaDefinition:Definition: is a serum potassium level is a serum potassium level

>5.5 mEq/L.>5.5 mEq/L.

Etiology:Etiology:

1. Renal failure 1. Renal failure

2. Hypoaldosteronism2. Hypoaldosteronism

3. Severe tissue trauma (3. Severe tissue trauma (burnsburns & & infectioninfection))

4. Metabolic Acidosis4. Metabolic Acidosis

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HyperkalemiaHyperkalemia5. Excessive use of K+ supplement5. Excessive use of K+ supplement

Pseudohyperkalemia:Pseudohyperkalemia: A laboratory artifact A laboratory artifact indicating an elevated blood K+ level caused indicating an elevated blood K+ level caused K+ released in vitro from cells in the blood K+ released in vitro from cells in the blood sample. sample.

Etiology:Etiology: 1. Tight tourniquet while drawing blood.1. Tight tourniquet while drawing blood.2. Hemolysis of blood sample. 2. Hemolysis of blood sample. 3. Administration of expired blood products.3. Administration of expired blood products.4. Drawing blood above site where K+ is 4. Drawing blood above site where K+ is being being infused.infused.

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HyperkalemiaHyperkalemia

Clinical Manifestation:Clinical Manifestation:

1. Cardiac Arrythmias1. Cardiac Arrythmias

2. Muscle weakness, paresthesia and 2. Muscle weakness, paresthesia and paralysisparalysis

3. Irritability and anxiety3. Irritability and anxiety

4. Abdominal cramps with diarrhea4. Abdominal cramps with diarrhea

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HyperkalemiaHyperkalemia

Laboratory and Diagnostic study:Laboratory and Diagnostic study:

1. Serum K+ level >5.5 mEq/L1. Serum K+ level >5.5 mEq/L

2. ECG (2. ECG (Peaked T wavesPeaked T waves, , prolonged prolonged PR PR interval interval andand QRS duration QRS duration, , absent P absent P waveswaves and and ST ST depressiondepression))

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HyperkalemiaHyperkalemia

Medical Management:Medical Management:1. 1. Kayaxelate: Kayaxelate: cation exchange resin cation exchange resin (oral or (oral or retention Enema)retention Enema)2. Ca gluconate (2. Ca gluconate (emergency casesemergency cases))3. Decreased K+ dietary intake3. Decreased K+ dietary intake4. NaCHO3 IV administration4. NaCHO3 IV administration5. Regular insulin and hypertonic 5. Regular insulin and hypertonic dextrose IV dextrose IV administrationadministration6. Hemodialysis6. Hemodialysis

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HyperkalemiaHyperkalemia

Nursing Problems:Nursing Problems:

1. Decreased Cardiac Output1. Decreased Cardiac Output

2. Altered Urinary Elimination Pattern2. Altered Urinary Elimination Pattern

3. Activity Intolerance3. Activity Intolerance

4. Ineffective breathing pattern4. Ineffective breathing pattern

5. Altered Bowel Elimination5. Altered Bowel Elimination

6. Self-care Deficits6. Self-care Deficits

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HyperkalemiaHyperkalemia

Nursing Management:Nursing Management:

1. Prepare for and assist with 1. Prepare for and assist with aggressive therapy as prescribed.aggressive therapy as prescribed.

- Cation-exchange resins - Cation-exchange resins ((kayaxelatekayaxelate))

- Calcium gluconate- Calcium gluconate

- IV NaCHO3- IV NaCHO3

- IV regular insulin and glucose- IV regular insulin and glucose

- Hemodialysis - Hemodialysis

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HyperkalemiaHyperkalemia

2. Prevent client injury.2. Prevent client injury.

- Asses muscular weakness, - Asses muscular weakness, cardiac arrythmias, paresthesia, cardiac arrythmias, paresthesia, nausea and intestinal colic.nausea and intestinal colic.

- - Evaluate and verify all serum Evaluate and verify all serum potassium levels.potassium levels.

- Monitor ECG for abnormalities.- Monitor ECG for abnormalities.

- Monitor serum K+ level. - Monitor serum K+ level.

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HyperkalemiaHyperkalemia

- When administering K+ intravenously, - When administering K+ intravenously, always administer it with an infusion pump.always administer it with an infusion pump.

3. Provide client and family teaching.3. Provide client and family teaching.

- Advise clients at increased risk for - Advise clients at increased risk for hyperkalemia (hyperkalemia (e.g. those with renal failuree.g. those with renal failure) to ) to avoid K+ rich foods.avoid K+ rich foods.

- K+ low foods:- K+ low foods: butter butter,, margarine margarine, , cranberry juicecranberry juice, , ginger aleginger ale, , jelly beansjelly beans, , hard hard candy candy andand honey honey..

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HyperkalemiaHyperkalemia

- Caution the client to use salts - Caution the client to use salts substitute sparingly (substitute sparingly (contains contains approximately 60 mEq/tsp. of K+approximately 60 mEq/tsp. of K+))

- Assess for hyperkalemia who is - Assess for hyperkalemia who is receiving receiving K+ sparing diureticsK+ sparing diuretics..

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HypocalcemiaHypocalcemia

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Significance of CalciumSignificance of Calcium

• Is a major component of bones and teeth.Is a major component of bones and teeth.• 99%99% of the body’s Ca++ is located in the skeletal of the body’s Ca++ is located in the skeletal

system, system, 1%1% in the blood circulation. in the blood circulation.• Plays a major role in transmitting nerve impulses Plays a major role in transmitting nerve impulses

and blood coagulation.and blood coagulation.• Helps to regulate muscle contraction and relaxation Helps to regulate muscle contraction and relaxation

including cardiac muscle.including cardiac muscle.• PTH & calcitonin controls the serum calcium level.PTH & calcitonin controls the serum calcium level.• Plays a major role in blood coagulation. Plays a major role in blood coagulation. • Food rich in Ca++: Food rich in Ca++: MilkMilk, , Green Leafy VegetablesGreen Leafy Vegetables,,

Canned SalmonCanned Salmon, , SardinesSardines and and Fresh OysterFresh Oyster..

Normal serum value: Normal serum value: 8.5 to 10.5 mg/dL.8.5 to 10.5 mg/dL.

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HypocalcemiaHypocalcemia

Definition:Definition: is a serum calcium level <8.5 is a serum calcium level <8.5 mg/dl.mg/dl.

Etiology:Etiology:

1.1. Primary or surgical Primary or surgical hypoparathyroidism due to hypoparathyroidism due to thyroidectomy.thyroidectomy.

2.2. PancreatitisPancreatitis

3.3. Inadequate vitamin D intake or Inadequate vitamin D intake or synthesissynthesis

4.4. Renal failure (Renal failure (HyperphosphatemiaHyperphosphatemia))

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HypocalcemiaHypocalcemia5. Drug Therapy (aminoglycosides, 5. Drug Therapy (aminoglycosides, corticosteroids & caffeine)corticosteroids & caffeine)6. Insufficient calcium intake6. Insufficient calcium intake

Clinical Manifestations:Clinical Manifestations:1. Tetany (e.g. tingling in fingers & 1. Tetany (e.g. tingling in fingers & circumoral area and muscle spasm circumoral area and muscle spasm associated with pain in extremities and face)associated with pain in extremities and face)

- Positive - Positive Trousseau’s signTrousseau’s sign and and Chvostek’s signChvostek’s sign3. Mental changes (depression, impaired 3. Mental changes (depression, impaired memory, confusion and delirium)memory, confusion and delirium)4. Seizures ( irritability CNS & peripheral 4. Seizures ( irritability CNS & peripheral nerves)nerves)

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TROUSSEAU’S SIGNTROUSSEAU’S SIGN

• A TEST FOR MUSCLE CRAMPS IN WHICH A WRIST SPASM IS A TEST FOR MUSCLE CRAMPS IN WHICH A WRIST SPASM IS BROUGHT ABOUT BY INFLATING A BLOOD PRESSURE CUFF ON THE BROUGHT ABOUT BY INFLATING A BLOOD PRESSURE CUFF ON THE UPPER ARM TO A HIGHER THAN NORMAL SYSTOLIC BLOOD FOR 3 UPPER ARM TO A HIGHER THAN NORMAL SYSTOLIC BLOOD FOR 3 MINS. A POSITIVE TEST MAY BE SEEN IN RESULTS THAT SHOW MINS. A POSITIVE TEST MAY BE SEEN IN RESULTS THAT SHOW ABNORMALLY LOW CALCIUM & MAGNESIUM IN THE BLOOD.ABNORMALLY LOW CALCIUM & MAGNESIUM IN THE BLOOD.

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HypocalcemiaHypocalcemiaLaboratory and Diagnostic study:Laboratory and Diagnostic study:

1. Serum calcium level is <8.5 mg/dL.1. Serum calcium level is <8.5 mg/dL.2. ECG reveals a prolonged QT interval.2. ECG reveals a prolonged QT interval.3. Ventricular tachycardia (torsades de 3. Ventricular tachycardia (torsades de pointes)pointes)

Medical Management:Medical Management: 1. IV therapy of Ca++ gluconate and 1. IV therapy of Ca++ gluconate and Ca++ chloride and Ca gluceptate.Ca++ chloride and Ca gluceptate. 2. Vitamin D therapy may be instituted 2. Vitamin D therapy may be instituted to increase Ca++ absorption in the GI to increase Ca++ absorption in the GI tract.tract.

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HypocalcemiaHypocalcemia

3. Increase dietary intake of Ca++ 3. Increase dietary intake of Ca++ 1000 to 1,500 mg/day.1000 to 1,500 mg/day.

Nursing Problems:Nursing Problems:

1. Alteration in Comfort1. Alteration in Comfort

2. Altered thought processes2. Altered thought processes

3. Altered Level of Consciousness3. Altered Level of Consciousness

4. Altered Bowel Elimination4. Altered Bowel Elimination

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HypocalcemiaHypocalcemia

Nursing Management:Nursing Management:

1. Prepare for and assist with therapy.1. Prepare for and assist with therapy.

- Institute and maintain seizure - Institute and maintain seizure precautions.precautions.

- Administer parenteral Ca++- Administer parenteral Ca++ ((take precautions to prevent tissue take precautions to prevent tissue infiltration, w/c can lead to tissue infiltration, w/c can lead to tissue necrosis & sloughingnecrosis & sloughing))

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- Do not add Ca++ to parenteral - Do not add Ca++ to parenteral solutions bicarbonate or phosphorus. solutions bicarbonate or phosphorus. ((precipitate willprecipitate will formform))

- Administer Ca++ cautiously to a - Administer Ca++ cautiously to a client receiving digitalis.client receiving digitalis.

- Maintain a relaxed, quiet - Maintain a relaxed, quiet environment, and promote adequate environment, and promote adequate rest.rest.

2. Administer Vitamin D (2. Administer Vitamin D (increases Ca++ increases Ca++ absorption from the GI tractabsorption from the GI tract) )

HypocalcemiaHypocalcemia

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HypocalcemiaHypocalcemia

3. Provide client and family teaching.3. Provide client and family teaching.

- Instruct to increase dietary Ca++ - Instruct to increase dietary Ca++ intake.intake.

- Instruct persons at risk for - Instruct persons at risk for osteoporosis to maintain dietary intake osteoporosis to maintain dietary intake of Ca++ supplements.of Ca++ supplements.

- Instruct on value of regular - Instruct on value of regular exercise.exercise.

4. Monitor serum calcium level.4. Monitor serum calcium level.

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HypercalcemiHypercalcemiaa

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HypercalcemiaHypercalcemia

Definition:Definition: is serum calcium level >10.5 is serum calcium level >10.5 mg/dL.mg/dL.

Etiology: Etiology:

1. Excessive Ca++ administration or 1. Excessive Ca++ administration or intake.intake.

2. Movement of Ca++ from bones to 2. Movement of Ca++ from bones to serum, as occurs in prolonged serum, as occurs in prolonged immobilization. immobilization.

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HypercalcemiaHypercalcemia

4. Drug therapy with thiazides diuretics4. Drug therapy with thiazides diuretics5. Hyperparathyroidism (neoplastic 5. Hyperparathyroidism (neoplastic diseases)diseases)

Clinical Manifestations:Clinical Manifestations:1. Anorexia, nausea and vomiting.1. Anorexia, nausea and vomiting.2. Constipation2. Constipation3. Muscular weakness, incoordination3. Muscular weakness, incoordination4. Altered level of consciousness (slurred 4. Altered level of consciousness (slurred speech, confusion, lethargy & coma).speech, confusion, lethargy & coma).

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HypercalcemiaHypercalcemia

5. Polyuria and polydipsia5. Polyuria and polydipsia6. Cardiac arrhythmias6. Cardiac arrhythmias

Laboratory and diagnostic study: Laboratory and diagnostic study: 1. Serum Ca level is >10.5 mg/dL.1. Serum Ca level is >10.5 mg/dL.2. ECG reveals a shortened QT interval, 2. ECG reveals a shortened QT interval, bradycardia and heart blocks.bradycardia and heart blocks.

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HypercalcemiaHypercalcemia

Medical Management:Medical Management:

1. Chemotheraphy.1. Chemotheraphy.

2. Partial Parathyroidectomy2. Partial Parathyroidectomy

3. IV administration of 0.9% NaCl.3. IV administration of 0.9% NaCl.

4. Administration of Furosemide (Lasix) 4. Administration of Furosemide (Lasix) and IV Phosphate.and IV Phosphate.

5. Calcitonin5. Calcitonin

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HypercalcemiaHypercalcemia

Nursing Problems:Nursing Problems:

1. Altered Level of Consciousness1. Altered Level of Consciousness

2. Altered Bowel Elimination2. Altered Bowel Elimination

3. Decreased Cardiac Output3. Decreased Cardiac Output

4. Activity Intolerance4. Activity Intolerance

5. Altered Pattern of Urinary 5. Altered Pattern of Urinary EliminationElimination

6. Alteration in Comfort: Pain6. Alteration in Comfort: Pain

Page 145: F&E Lecture (new 2010)

HypercalcemiaHypercalcemia

Nursing Management:Nursing Management:

1. Prepare for and assist with therapy:1. Prepare for and assist with therapy:

- Administer parenteral saline - Administer parenteral saline solution to dilute serum Ca++ and solution to dilute serum Ca++ and inhibit tubular reabsorption of Ca++.inhibit tubular reabsorption of Ca++.

- Administer parental phosphate to - Administer parental phosphate to enhance deposition of Ca++.enhance deposition of Ca++.

- Administer furosemide (- Administer furosemide (LasixLasix) to ) to increase Ca++ excretion.increase Ca++ excretion.

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HypercalcemiaHypercalcemia

- Monitor serum Ca++.- Monitor serum Ca++.

- Treat the underlying cause, w/c - Treat the underlying cause, w/c may include calcitonin for may include calcitonin for hyperparthyroidism & mythramycin hyperparthyroidism & mythramycin and corticosteroids for cancers.and corticosteroids for cancers.

2. Maintain normal bowel elimination.2. Maintain normal bowel elimination.

-Asses for dehydration, mental -Asses for dehydration, mental confusion & psychotic behavior. confusion & psychotic behavior.

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HypercalcemiaHypercalcemia

- Encourage 3 to 4 quarts of fluid - Encourage 3 to 4 quarts of fluid daily & dietary fiber intake to help with daily & dietary fiber intake to help with constipation.constipation.

3. Institute injury prevention measures 3. Institute injury prevention measures for mental confusion:for mental confusion:

- Keep bed side rails up, keep bed - Keep bed side rails up, keep bed brakes locked, reposition the client brakes locked, reposition the client often & secure all invasive lines.often & secure all invasive lines.

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HypercalcemiaHypercalcemia

4. Provide client and family teaching on 4. Provide client and family teaching on the causes & treatment of the causes & treatment of hypercalcemia:hypercalcemia:

- Teach the client about importance - Teach the client about importance of early ambulation to reduce Ca++ loss of early ambulation to reduce Ca++ loss from bones during hospitalization.from bones during hospitalization.

- Encourage the client to participate - Encourage the client to participate in daily weight-bearing activities.in daily weight-bearing activities.

Page 149: F&E Lecture (new 2010)

HypomagneseHypomagnesemiamia

Page 150: F&E Lecture (new 2010)

Significance of MagnesiumSignificance of Magnesium

• Plays a major role in neuromuscular Plays a major role in neuromuscular irritability and contractility.irritability and contractility.

• Next to K+, Mg++ most abundant Next to K+, Mg++ most abundant intracellular cation.intracellular cation.

• Exerts effect on cardiovascular sytem, acting Exerts effect on cardiovascular sytem, acting peripherally to produce vasodilation.peripherally to produce vasodilation.

• Plays a major role in carbohydrate and Plays a major role in carbohydrate and protein metabolism.protein metabolism.

• Food rich in Mg++: Food rich in Mg++: Green leafy vegetablesGreen leafy vegetables, , NutsNuts, , LegumesLegumes, , Whole GrainsWhole Grains, , SeafoodSeafood, , Peanut ButterPeanut Butter & & ChocolateChocolate. . Normal serum value: Normal serum value: 1.5 to 2.5 mEq/L.1.5 to 2.5 mEq/L.

Page 151: F&E Lecture (new 2010)

HypomagnesemiaHypomagnesemia

Definition: Definition: is a serum magnesium level is a serum magnesium level <1.5 mEq/L.<1.5 mEq/L.

Etiology: Etiology:

1. Poor nutrition1. Poor nutrition

2. Alcoholism2. Alcoholism

3. GI and renal losses without 3. GI and renal losses without replacementreplacement

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HypomagnesemiaHypomagnesemia

Clinical Manifestations:Clinical Manifestations:

1. 1. Positive Trousseau’sPositive Trousseau’s & & Chvostek’s Chvostek’s signssigns

2. Neuromuscular irritability2. Neuromuscular irritability

3. Insomnia3. Insomnia

4. Mood changes4. Mood changes

5. Cardiac arrhythmias5. Cardiac arrhythmias

Page 153: F&E Lecture (new 2010)

HypomagnesemiaHypomagnesemia

Laboratory and Diagnostic study:Laboratory and Diagnostic study:

1. Serum Mg level is <1.5 mEq/L.1. Serum Mg level is <1.5 mEq/L.

2. ECG reveals a flattened T wave, 2. ECG reveals a flattened T wave, prominent U wave & depressed ST prominent U wave & depressed ST segment.segment.

Page 154: F&E Lecture (new 2010)

HypomagnesemiaHypomagnesemia

Medical Management:Medical Management:

1. IV MgSO4 administration1. IV MgSO4 administration

2. Oral Mg++ salts therapy2. Oral Mg++ salts therapy

3. Increased dietary Mg++ intake3. Increased dietary Mg++ intake

Page 155: F&E Lecture (new 2010)

HypomagnesemiaHypomagnesemia

Nursing ProblemsNursing Problems::

1. Potential for Injury: Seizures1. Potential for Injury: Seizures

2. Altered Level of Consciousness2. Altered Level of Consciousness

3. Decreased Cardiac Output3. Decreased Cardiac Output

Page 156: F&E Lecture (new 2010)

HypomagnesemiaHypomagnesemia

Nursing Management:Nursing Management:

1. Prepare for assist with therapy:1. Prepare for assist with therapy:

- Administer parenteral Mg++ - Administer parenteral Mg++ replacement therapy on an infusion replacement therapy on an infusion pump to prevent rapid administration pump to prevent rapid administration & to prevent cardiac arrest.& to prevent cardiac arrest.

- Monitor for signs of Mg++ - Monitor for signs of Mg++ toxicity; (toxicity; (Respiratory distressRespiratory distress, , diaphoresisdiaphoresis, , anxietyanxiety, , hypotensionhypotension, , decreased urinary outputdecreased urinary output) )

Page 157: F&E Lecture (new 2010)

HypomagnesemiaHypomagnesemia

- Monitor ECG & pulse for - Monitor ECG & pulse for abnormalitiesabnormalities

- Monitor serum Mg++- Monitor serum Mg++2. Prevent injury:2. Prevent injury:

- Institute and maintain seizure - Institute and maintain seizure precautions.precautions.

- Institute safety measures for - Institute safety measures for mental confusion.mental confusion.

- Asses client’s ability to swallow - Asses client’s ability to swallow before administering oral medications or before administering oral medications or feeding client.feeding client.

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HypomagnesemiaHypomagnesemia

- Monitor client’s digitalis closely - Monitor client’s digitalis closely because a deficit of Mg++ predisposes because a deficit of Mg++ predisposes to digitalis toxicity.to digitalis toxicity.

3. Provide client and family teaching:3. Provide client and family teaching:

- Discuss the misuse of diuretics - Discuss the misuse of diuretics and laxatives.and laxatives.

- Identify dietary sources of Mg++- Identify dietary sources of Mg++

Page 159: F&E Lecture (new 2010)

HypermagnesemiaHypermagnesemia

Page 160: F&E Lecture (new 2010)

HypermagnesemiaHypermagnesemia

Definition:Definition: is a serum Mg level >2.5 is a serum Mg level >2.5 mEq/L.mEq/L.

Etiology:Etiology:1. Renal Failure1. Renal Failure2. Overuse of Mg++ containing antacids 2. Overuse of Mg++ containing antacids

((MylantaMylanta, , Maalox & RiopanMaalox & Riopan))3. Overuse of enema or laxative with 3. Overuse of enema or laxative with Mg++ Mg++ ((Milk of MagnesiaMilk of Magnesia))4. Diabetic Ketoacidososis (4. Diabetic Ketoacidososis (severe severe dehydrationdehydration))

Page 161: F&E Lecture (new 2010)

HypermagnesemiaHypermagnesemia

Clinical Manifestations:Clinical Manifestations:

1. Nausea & Vomiting1. Nausea & Vomiting

2. Facial flushing2. Facial flushing

3. Sensation of warmth3. Sensation of warmth

4. Lethargy, Disarthria & drowsiness4. Lethargy, Disarthria & drowsiness

5 Lost deep tendon reflex & muscle 5 Lost deep tendon reflex & muscle weakness / paralysisweakness / paralysis

6. Cardiac arrhythmias / cardiac arrest 6. Cardiac arrhythmias / cardiac arrest

Page 162: F&E Lecture (new 2010)

HypermagnesemiaHypermagnesemia

Laboratory and diagnostic study:Laboratory and diagnostic study:

1. Serum Mg level is >2.5 mEq/L.1. Serum Mg level is >2.5 mEq/L.

2. ECG reveals prolonged QT interval 2. ECG reveals prolonged QT interval and AV blocks.and AV blocks.

Page 163: F&E Lecture (new 2010)

HypermagnesemiaHypermagnesemia

Medical Management:Medical Management:

1. IV Ca Gluconate administration1. IV Ca Gluconate administration

2. Hemodialysis with a Mg++ free 2. Hemodialysis with a Mg++ free dialysatedialysate

3. Loop Diuretics and 0.45% NaCl.3. Loop Diuretics and 0.45% NaCl.

Page 164: F&E Lecture (new 2010)

HypermagnesemiaHypermagnesemia

Nursing Problems:Nursing Problems:

1. Ineffective Breathing Pattern1. Ineffective Breathing Pattern

2. Decreased Cardiac Output2. Decreased Cardiac Output

3. Fluid Volume: Deficit or Excess3. Fluid Volume: Deficit or Excess

4. Altered Tissue Perfusion4. Altered Tissue Perfusion

Page 165: F&E Lecture (new 2010)

HypermagnesemiaHypermagnesemia

Nursing Management:Nursing Management:

1. Prepare for assist and therapy:1. Prepare for assist and therapy:

- Discontinue all parenteral & oral - Discontinue all parenteral & oral Mg++Mg++

- - During respiratory or cardiac During respiratory or cardiac emergencies, collaborate w/ the emergencies, collaborate w/ the respiratory therapist providing respiratory therapist providing ventilatory ventilatory support.support.

- Administer Ca++ gluconate - Administer Ca++ gluconate

Page 166: F&E Lecture (new 2010)

HypermagnesemiaHypermagnesemia

- Prepare client for hemodialysis- Prepare client for hemodialysis

- Administer diuretics and 0.45% - Administer diuretics and 0.45% normal normal saline (causes excretion of Mg+saline (causes excretion of Mg++)+)

- Monitor serum Mg++- Monitor serum Mg++

2. Prevent Injury2. Prevent Injury

- Monitor vital signs (- Monitor vital signs (cardiovascularcardiovascular & & respiratory statusrespiratory status, , patellar reflexespatellar reflexes & & changes in level of consciousness changes in level of consciousness

closelyclosely) )

Page 167: F&E Lecture (new 2010)

HypermagnesemiaHypermagnesemia

- Institute safety precautions, - Institute safety precautions, including keeping bed side rails up, including keeping bed side rails up, keeping bed brakes locked & keeping bed brakes locked & repositioning the client often.repositioning the client often.

3. Provide client and family teaching.3. Provide client and family teaching.

- Teach the client about the - Teach the client about the adverse effects associated with adverse effects associated with overuse of Mg++ containing antacids overuse of Mg++ containing antacids and cathartics. and cathartics.

Page 168: F&E Lecture (new 2010)

HypermagnesemiaHypermagnesemia

- Instruct the client to read all - Instruct the client to read all over-the-counter drug labels over-the-counter drug labels carefully for Mg++ content.carefully for Mg++ content.

Page 169: F&E Lecture (new 2010)

HypophosphateHypophosphatemiamia

Page 170: F&E Lecture (new 2010)

Significance of PhosphateSignificance of Phosphate• The primary anion in the ICF.The primary anion in the ICF.• 85% in bones & teeth, 14% in soft tissues & 85% in bones & teeth, 14% in soft tissues &

less 1% in the ECF.less 1% in the ECF.• Plays a major role in the formation of ATP & Plays a major role in the formation of ATP &

2,3 diphosphoglycerate.2,3 diphosphoglycerate.• Essential to the function of muscles, nerves Essential to the function of muscles, nerves

and RBC.and RBC.• Maintenance of acid-base balance and the Maintenance of acid-base balance and the

nervous system. nervous system. • Food rich in phosphorus: Food rich in phosphorus: hard cheesehard cheese, , cream cream , ,

nutsnuts, , dried fruitsdried fruits, , vegetablesvegetables & & whole grainwhole grain..

Normal serum value: Normal serum value: 2.5 to 4.5 mg/dL.2.5 to 4.5 mg/dL.

Page 171: F&E Lecture (new 2010)

HypophosphatemiaHypophosphatemia

Definition:Definition: is a serum phosphorus level is a serum phosphorus level <2.5 mg/dL.<2.5 mg/dL.

Etiology :Etiology :

1. Overzealous intake or administration 1. Overzealous intake or administration of carbohydrates.of carbohydrates.

2. Prolonged intense hyperventilation, 2. Prolonged intense hyperventilation, alcohol withdrawal and diabetic alcohol withdrawal and diabetic ketoacidosis.ketoacidosis.

Page 172: F&E Lecture (new 2010)

HypophosphatemiaHypophosphatemia

3. Excess phosphorus binding by 3. Excess phosphorus binding by antacids containing Mg++, Ca++ or antacids containing Mg++, Ca++ or albumin.albumin.

4. Vitamin D deficiency (4. Vitamin D deficiency (osteomalaciaosteomalacia))

Clinical Manifestation:Clinical Manifestation:

1. Irritability, apprehension, weakness, 1. Irritability, apprehension, weakness, numbness, confusion, seizure and numbness, confusion, seizure and coma. coma.

Page 173: F&E Lecture (new 2010)

HypophosphatemiaHypophosphatemia

2. Hypoxia leading to an increase in 2. Hypoxia leading to an increase in respiratory rate and alkalosis.respiratory rate and alkalosis.

3. Muscle weakness and pain.3. Muscle weakness and pain.

4. Platelet dysfunction (bleeding).4. Platelet dysfunction (bleeding).

5. Increased susceptibility to infection. 5. Increased susceptibility to infection.

Page 174: F&E Lecture (new 2010)

Laboratory and Diagnostic study:Laboratory and Diagnostic study:

1. Serum phosphorus level <2.5 mg/dl.1. Serum phosphorus level <2.5 mg/dl.

2. Serum Mg++ level may be 2. Serum Mg++ level may be decreased decreased (increased excretion in (increased excretion in urine)urine)

Medical Management:Medical Management:

1. Oral and IV phosphorus therapy1. Oral and IV phosphorus therapy

HypophosphatemiaHypophosphatemia

Page 175: F&E Lecture (new 2010)

Nursing Problems:Nursing Problems:

1. Altered Level of Consciousness1. Altered Level of Consciousness

2. Decreased Cardiac Output2. Decreased Cardiac Output

3. Activity Intolerance3. Activity Intolerance

4. Alteration in Comfort4. Alteration in Comfort

5. Potential for Infection5. Potential for Infection

6. Decreased Tissue Perfusion 6. Decreased Tissue Perfusion

HypophosphatemiaHypophosphatemia

Page 176: F&E Lecture (new 2010)

Nursing Management:Nursing Management:

1. Prepare for and assist with therapy.1. Prepare for and assist with therapy.

- Slow TPN administration to - Slow TPN administration to malnourished clients.malnourished clients.

- Monitor serum phosphorus level- Monitor serum phosphorus level

- Monitor for possible complication - Monitor for possible complication of IV phosphorus which may include of IV phosphorus which may include HypocalcemiaHypocalcemia

2. Prevent Injury. 2. Prevent Injury.

HypophosphatemiaHypophosphatemia

Page 177: F&E Lecture (new 2010)

- Assess V/S , signs of - Assess V/S , signs of apprehension, apprehension, confusion and mental confusion and mental status.status.

- Institute safety precautions.- Institute safety precautions.

3. Provide client and family teachings.3. Provide client and family teachings.

-Discuss the importance of -Discuss the importance of preventing preventing infection. infection.

HypophosphatemiaHypophosphatemia

Page 178: F&E Lecture (new 2010)

HyperphosphatemiHyperphosphatemiaa

Page 179: F&E Lecture (new 2010)

HyperphosphatemiaHyperphosphatemia

Definition:Definition: is a serum phosphorus level is a serum phosphorus level >4.5 mg/dl.>4.5 mg/dl.

Etiology:Etiology:

1. Renal Failure1. Renal Failure

2. Chemotherapy 2. Chemotherapy

3. High phosphorus intake3. High phosphorus intake

4. Profound muscle necrosis4. Profound muscle necrosis

Page 180: F&E Lecture (new 2010)

HyperphosphatemiaHyperphosphatemia

Clinical Manifestation:Clinical Manifestation:

1. Soft tissue calcifications1. Soft tissue calcifications

2. Tetany2. Tetany

3. Anorexia, Nausea and Vomiting3. Anorexia, Nausea and Vomiting

4. Muscle weakness, hyperreflexia and 4. Muscle weakness, hyperreflexia and tachycardia.tachycardia.

Page 181: F&E Lecture (new 2010)

HyperphosphatemiaHyperphosphatemiaLaboratory and Diagnostic study:Laboratory and Diagnostic study:

1. Serum phosphorus level is >4.5 mg/dl.1. Serum phosphorus level is >4.5 mg/dl.2. X-ray studies may show skeletal 2. X-ray studies may show skeletal changes changes with abnormal bone with abnormal bone development.development.

Medical Management:Medical Management:1. Restrictions of dietary phosphate.1. Restrictions of dietary phosphate.2. Administration of Vit. D (oral: 2. Administration of Vit. D (oral: Rocatrol), Rocatrol), (I.V. Calcijex)(I.V. Calcijex)3. Dialysis 3. Dialysis

Page 182: F&E Lecture (new 2010)

HyperphosphatemiaHyperphosphatemia

Nursing Problems: Nursing Problems:

1. Alteration in Comfort1. Alteration in Comfort

2. Altered Thought Processes2. Altered Thought Processes

3. Altered Level of Consciousness3. Altered Level of Consciousness

4. Altered Bowel Elimination4. Altered Bowel Elimination

Page 183: F&E Lecture (new 2010)

HyperphosphatemiaHyperphosphatemia

Nursing Management:Nursing Management:

1. Prevent injury.1. Prevent injury.

- - Institute and monitor for seizure Institute and monitor for seizure precautions.precautions.

- Monitor serum phosphorus level- Monitor serum phosphorus level

2. Provide client and family teaching.2. Provide client and family teaching.

- Instruct client to avoid foods high - Instruct client to avoid foods high in in phosphorus.phosphorus.

Page 184: F&E Lecture (new 2010)

HyperphosphatemiaHyperphosphatemia

- Instruct the client to avoid - Instruct the client to avoid phosphate-containing substances phosphate-containing substances such such as laxatives and enemas as laxatives and enemas that contain that contain phosphate.phosphate.

Page 185: F&E Lecture (new 2010)

HypochloremiHypochloremiaa

Page 186: F&E Lecture (new 2010)

SignificanceSignificance ofof ChlorideChloride

• The major anion of the ECF is found more in The major anion of the ECF is found more in interstitial and fluid compartments than in interstitial and fluid compartments than in blood.blood.

• Serum level of chloride reflects a change in Serum level of chloride reflects a change in dilution or concentration of the ECF.dilution or concentration of the ECF.

• Plays a major role in the CSF formation in the Plays a major role in the CSF formation in the brain.brain.

• Chloride is produced in the stomach Chloride is produced in the stomach ((hydrochlorichydrochloric acidacid))

• Food rich in chloride: Food rich in chloride: Tomato juiceTomato juice, , salty brothsalty broth, , canned vegetablescanned vegetables, , processed meatsprocessed meats & & fruitsfruits..

Normal serum level: Normal serum level: 96 to 106 mEq/L.96 to 106 mEq/L.

Page 187: F&E Lecture (new 2010)

HypochloremiaHypochloremia

Definition:Definition: is a serum chloride level <96 is a serum chloride level <96 mEq/L.mEq/L.

Etiology:Etiology:

1. Chloride-deficient formulas1. Chloride-deficient formulas

2. Salt-restricted diet2. Salt-restricted diet

3. GI tube drainage3. GI tube drainage

4. Severe vomiting and diarrhea4. Severe vomiting and diarrhea

Page 188: F&E Lecture (new 2010)

HypochloremiaHypochloremia

Clinical Manifestation:Clinical Manifestation:

1. Seizures1. Seizures

2. Hyperexcitability of muscles2. Hyperexcitability of muscles

3. Tetany3. Tetany

4. Muscle cramps and weakness4. Muscle cramps and weakness

5. Coma5. Coma

Page 189: F&E Lecture (new 2010)

HypochloremiaHypochloremia

Laboratory and Diagnostic study:Laboratory and Diagnostic study:

1. Serum chloride level is <96 mEq/L.1. Serum chloride level is <96 mEq/L.

Medical Management:Medical Management:

1. IV administration of 0.9% & 0.45% 1. IV administration of 0.9% & 0.45% NaCl.NaCl.

2. Increase dietary intake of Cl rich 2. Increase dietary intake of Cl rich foods. foods.

Page 190: F&E Lecture (new 2010)

HypochloremiaHypochloremia

Nursing Problems:Nursing Problems:

1. Altered Level of Consciousness1. Altered Level of Consciousness

2. Altered Bowel Elimination2. Altered Bowel Elimination

3. Self-care deficits3. Self-care deficits

4. Altered Urinary Elimination4. Altered Urinary Elimination

Page 191: F&E Lecture (new 2010)

HypochloremiaHypochloremia

Nursing Management:Nursing Management:

1. Monitor I&O & V/S1. Monitor I&O & V/S

2. Monitor Arterial Blood Gas (ABG) and 2. Monitor Arterial Blood Gas (ABG) and serum electrolytesserum electrolytes

3. Assess LOC of the client3. Assess LOC of the client

4. Check for muscle strength and 4. Check for muscle strength and movementmovement

5. Changes are reported to the 5. Changes are reported to the physician.physician.

Page 192: F&E Lecture (new 2010)

HyperchloremiaHyperchloremia

Definition:Definition: is serum chloride level >106 is serum chloride level >106 mEq/L.mEq/L.

Etiology:Etiology:

1. Metabolic Acidosis1. Metabolic Acidosis

2. Bicarbonate ions loss via kidney or 2. Bicarbonate ions loss via kidney or the GI the GI tract. tract.

Page 193: F&E Lecture (new 2010)

HyperchloremiaHyperchloremia

Clinical Manifestation:Clinical Manifestation:

1. Tachypnea & weakness1. Tachypnea & weakness

2. Lethargy and diminished cognitive 2. Lethargy and diminished cognitive abilityability

3. Rapid and deep respiration3. Rapid and deep respiration

4. Dysrhythmias and coma4. Dysrhythmias and coma

Laboratory and Diagnostic study:Laboratory and Diagnostic study:

1. Serum chloride level is >106 mEq/L.1. Serum chloride level is >106 mEq/L.

Page 194: F&E Lecture (new 2010)

HyperchloremiaHyperchloremia

2. Serum Na+ level >145 mEq/L.2. Serum Na+ level >145 mEq/L.

3. Serum pH is <7.35, 3. Serum pH is <7.35,

4. Serum bicarbonate is <22 mEq/L.4. Serum bicarbonate is <22 mEq/L.

Medical Management:Medical Management:

1. IV administration of Lactated Ringers1. IV administration of Lactated Ringers

2. IV administration of Na+ bicarbonate2. IV administration of Na+ bicarbonate

Page 195: F&E Lecture (new 2010)

HyperchloremiaHyperchloremia

Nursing Problems:Nursing Problems:

1. Ineffective Breathing Pattern1. Ineffective Breathing Pattern

2. Altered Tissue Perfusion2. Altered Tissue Perfusion

3. Self-Care Deficits3. Self-Care Deficits

4. Altered Level of Consciousness4. Altered Level of Consciousness

Nursing Management:Nursing Management:

1. Monitor I&O1. Monitor I&O

2. Monitor V/S, Arterial Blood Gas (ABG)2. Monitor V/S, Arterial Blood Gas (ABG)

3. Prevent Injury3. Prevent Injury

Page 196: F&E Lecture (new 2010)

Acid-BaseAcid-Base DisturbancesDisturbances

Page 197: F&E Lecture (new 2010)

Basic Concepts of Acid-Base Basic Concepts of Acid-Base

• Acid Acid – is any substance that ionizes in – is any substance that ionizes in water and forms hydrogen ions (H+) and water and forms hydrogen ions (H+) and anions. anions. An acid is a hydrogen donor.An acid is a hydrogen donor.

• BaseBase – is any substance that can bind to – is any substance that can bind to hydrogen ions. hydrogen ions. A base is a hydrogen A base is a hydrogen acceptor.acceptor.

• pHpH – hydrogen ion concentration in the – hydrogen ion concentration in the blood, is a measure of acid-base balance.blood, is a measure of acid-base balance.

Normal serum value: Normal serum value: 7.35 to 7.457.35 to 7.45

Page 198: F&E Lecture (new 2010)

Basic Concepts of Acid-BaseBasic Concepts of Acid-Base

• AcidityAcidity – a decrease in pH which denotes an – a decrease in pH which denotes an increase in hydrogen ions, <7.35increase in hydrogen ions, <7.35

• AlkalinityAlkalinity – an increase in the pH which – an increase in the pH which denotes a decrease in hydrogen ions, >7.45denotes a decrease in hydrogen ions, >7.45

• Salts Salts – the compound (besides water formed – the compound (besides water formed when an acid is neutralized by a base)when an acid is neutralized by a base)

Page 199: F&E Lecture (new 2010)

Basic Concepts of Acid-BaseBasic Concepts of Acid-Base

Common Acids:Common Acids:1. Hydrochloric Acid1. Hydrochloric Acid2. Carbonic Acid2. Carbonic Acid3. Acetic Acid3. Acetic Acid4. Lactic Acid4. Lactic Acid

Common Bases:Common Bases:1. Magnesium hydroxide1. Magnesium hydroxide

2. Aluminum hydroxide 2. Aluminum hydroxide

Page 200: F&E Lecture (new 2010)

Basic Concepts of Acid-BaseBasic Concepts of Acid-Base

Common Salts:Common Salts:

1. Sodium Chloride1. Sodium Chloride

2. Potassium Chloride2. Potassium Chloride

3. Calcium Phosphate3. Calcium Phosphate

4. Silver Nitrate, Ferrous SO4, NaCHO3 4. Silver Nitrate, Ferrous SO4, NaCHO3

Page 201: F&E Lecture (new 2010)

Basic Concepts of Acid-BaseBasic Concepts of Acid-Base

Two By-products of metabolic processes:Two By-products of metabolic processes:

1. 1. Respiratory acidsRespiratory acids – volatile carbonic – volatile carbonic acid resulting from the breakdown of acid resulting from the breakdown of carbon dioxide eliminated thru the lungs.carbon dioxide eliminated thru the lungs.

2. 2. Metabolic acidsMetabolic acids – non-volatile – non-volatile hydrogen ions formed in the body or that hydrogen ions formed in the body or that enters the body thru GI tract or enters the body thru GI tract or parenteral route eliminated the kidneys.parenteral route eliminated the kidneys.

Page 202: F&E Lecture (new 2010)

Regulation of Acid-Base Regulation of Acid-Base BalanceBalance1.1. Chemical Buffer sytem:Chemical Buffer sytem:

- - First line of defenseFirst line of defense, it is any , it is any substance that can neutralize excess substance that can neutralize excess acids or bases to keep the pH within acids or bases to keep the pH within normal limits.normal limits.- - Bicarbonate (HCO3)Bicarbonate (HCO3) and and carbonic acid carbonic acid

(H2CO3)(H2CO3)- - Ratio Ratio 20 HCO3 : 1 H2CO320 HCO3 : 1 H2CO3- - Phosphate buffer systemPhosphate buffer system; intracellular; intracellular- - Protein buffer systemProtein buffer system; blood Hgb.; blood Hgb.

Page 203: F&E Lecture (new 2010)

Regulation of Acid-Base Regulation of Acid-Base BalanceBalance2. 2. Respiratory regulation:Respiratory regulation:

- The lungs work to maintain acid-base - The lungs work to maintain acid-base balance by controlling carbon dioxide balance by controlling carbon dioxide (CO2) and carbonic acid (H2CO3) (CO2) and carbonic acid (H2CO3) excretion.excretion.

- - second line of defensesecond line of defense ( takes minutes) ( takes minutes)

3. 3. Renal system: Renal system:

- The kidneys reabsorb bicarbonate - The kidneys reabsorb bicarbonate (HCO3), secrete hydrogen ions in proximal (HCO3), secrete hydrogen ions in proximal and distal tubules. and distal tubules.

Page 204: F&E Lecture (new 2010)

Regulation of Acid-Base Regulation of Acid-Base BalanceBalance

- - third line of defensethird line of defense (takes hours to (takes hours to days)days)

Normal arterial blood gas (ABG) values:Normal arterial blood gas (ABG) values:

pH – 7.35 to 7.45pH – 7.35 to 7.45

PO2 – 80 to 100 mmHgPO2 – 80 to 100 mmHg

PCO2 – 35 to 45 mmHgPCO2 – 35 to 45 mmHg

HCO3 – 22 to 26 mEq/LHCO3 – 22 to 26 mEq/L

Page 205: F&E Lecture (new 2010)

Metabolic Metabolic AcidosisAcidosis

Page 206: F&E Lecture (new 2010)

Metabolic AcidosisMetabolic Acidosis

Definition:Definition: is an acid-base imbalance resulting is an acid-base imbalance resulting from excessive absorption or retention of from excessive absorption or retention of acid or excessive excretion of HCO3.acid or excessive excretion of HCO3.

Anion Gap:Anion Gap: reflects normally unmeasured reflects normally unmeasured several anions in the plasma. It is based several anions in the plasma. It is based primarily on three electrolytes ( primarily on three electrolytes ( Na+Na+,, Cl & Cl & HCO3 or CO2HCO3 or CO2))

Normal serum value: Normal serum value: 8 to 12 mEq/L8 to 12 mEq/L 8 to 12 mmol/L8 to 12 mmol/L

Page 207: F&E Lecture (new 2010)

Metabolic AcidosisMetabolic Acidosis

Formula:Formula: Anion gap= Na - (Cl + HCO3)Anion gap= Na - (Cl + HCO3)

Clinical Classification:Clinical Classification:

a.a. Normal anion gap Normal anion gap acidosis acidosis – anion gap is 8-– anion gap is 8-12 mEq/L and is referred to 12 mEq/L and is referred to Hyperchloremic Hyperchloremic acidosisacidosis..

Causes:Causes:

1. Direct loss of HCO3 (1. Direct loss of HCO3 (diarrheadiarrhea, , lower lower intestinal fistula intestinal fistula & & ureterotomiesureterotomies))

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Metabolic AcidosisMetabolic Acidosis

2. Excessive use of diuretics2. Excessive use of diuretics

3. Early renal insufficiency3. Early renal insufficiency

4. Excessive administration of chloride4. Excessive administration of chloride

5. Administration of TPN without HCO3 5. Administration of TPN without HCO3

b. b. High anion gap acidosisHigh anion gap acidosis – anion gap 30 – anion gap 30 mEq/L or more.mEq/L or more.

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Metabolic AcidosisMetabolic Acidosis

Causes:Causes:1. Ketoacidosis (with starvation)1. Ketoacidosis (with starvation)2. Lactic Acidosis2. Lactic Acidosis3. Late phase of salicylate poisoning3. Late phase of salicylate poisoning4. Uremia4. Uremia5. Methanol or ethylene glycol toxicity5. Methanol or ethylene glycol toxicity

c. c. Negative anion gap acidosisNegative anion gap acidosis – anion – anion gap below 8 mEq/Lgap below 8 mEq/L

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Metabolic AcidosisMetabolic Acidosis

Cause:Cause:

1. Hypoproteneimia1. Hypoproteneimia

Clinical Manifestation:Clinical Manifestation:

1. Headache1. Headache

2. Drowsiness and confusion2. Drowsiness and confusion

3. Weakness3. Weakness

4. Increased respiratory rate and depth4. Increased respiratory rate and depth

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Metabolic AcidosisMetabolic Acidosis

Laboratory and Diagnostic study:Laboratory and Diagnostic study:

1. ABG: pH <7.35 and bicarbonate <22 1. ABG: pH <7.35 and bicarbonate <22 mEq/L.mEq/L.

Medical management:Medical management:

1. Hemodialysis and Peritoneal dialysis1. Hemodialysis and Peritoneal dialysis

2. Administration of bicarbonate2. Administration of bicarbonate

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Metabolic AcidosisMetabolic Acidosis

Nursing Problems:Nursing Problems:

1. Altered Level of Consciousness1. Altered Level of Consciousness

2. Ineffective breathing pattern2. Ineffective breathing pattern

3. Altered Tissue Perfusion 3. Altered Tissue Perfusion

Nursing Management:Nursing Management:

1. Restore normal metabolism1. Restore normal metabolism

- Sodium Bicarbonate P.O. / I.V.- Sodium Bicarbonate P.O. / I.V.

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Metabolic AcidosisMetabolic Acidosis

- Fluid replacement; Lactated - Fluid replacement; Lactated Ringer’s Ringer’s solution solution

- High calorie diet- High calorie diet

- Correct the underlying problems- Correct the underlying problems

- Prepare for dialysis in kidney - Prepare for dialysis in kidney failurefailure

- Hourly Intake & Output- Hourly Intake & Output

- Regular insulin for ketoacidosis - Regular insulin for ketoacidosis

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Metabolic AlkalosisMetabolic Alkalosis

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Metabolic AlkalosisMetabolic Alkalosis

Definition:Definition: is an acid-base imbalance is an acid-base imbalance characterized by excessive loss of acid or characterized by excessive loss of acid or excessive gain of bicarbonate.excessive gain of bicarbonate.

Etiology: Etiology:

1. Prolonged vomiting or gastric suctioning.1. Prolonged vomiting or gastric suctioning.

(the most common cause)(the most common cause)

2. Excessive intake of antacid or baking 2. Excessive intake of antacid or baking soda soda

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Metabolic AlkalosisMetabolic Alkalosis

Clinical Manifestation:Clinical Manifestation:1. Tingling of fingers and toes1. Tingling of fingers and toes2. Dizziness, belligerence or confusion2. Dizziness, belligerence or confusion3. Tetany3. Tetany4. Slow, shallow respirations & possibly 4. Slow, shallow respirations & possibly apneaapnea

Laboratory and Diagnostic study:Laboratory and Diagnostic study:1. ABG; pH 7.45 and HCO3 above 26 1. ABG; pH 7.45 and HCO3 above 26 mEq/LmEq/L

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Metabolic AlkalosisMetabolic Alkalosis

Medical Management:Medical Management:

1. Treatment of the underlying 1. Treatment of the underlying disorder.disorder.

2. IV administration of NSS2. IV administration of NSS

3. KCl administration 3. KCl administration

4. Administration of H2 antagonist 4. Administration of H2 antagonist (cimetidine, ranitidine & famotidine)(cimetidine, ranitidine & famotidine)

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Metabolic AlkalosisMetabolic Alkalosis

Nursing Problems:Nursing Problems:

1. Altered Level of Consciousness1. Altered Level of Consciousness

2. Ineffective Breathing Pattern2. Ineffective Breathing Pattern

3. Altered Tissue Perfusion3. Altered Tissue Perfusion

Nursing Management:Nursing Management:

1. Irrigate NGT with saline.1. Irrigate NGT with saline.

2. Monitor I&O, ABG results2. Monitor I&O, ABG results

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Metabolic AlkalosisMetabolic Alkalosis

3. IV saline with K+ added.3. IV saline with K+ added.

4. Monitor vital signs4. Monitor vital signs

5. Institute safety precautions5. Institute safety precautions

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Respiratory Respiratory AcidosisAcidosis

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Respiratory AcidosisRespiratory Acidosis

Definition:Definition: is an acid-base imbalance is an acid-base imbalance characterized by increased arterial characterized by increased arterial PCO2 and decreased blood pH.PCO2 and decreased blood pH.

Etiology:Etiology:1. COPD (1. COPD (asthmaasthma, , emphysema emphysema etc.)etc.)2. Acute disorders: 2. Acute disorders: chest wall traumachest wall trauma, , pulmonary edemapulmonary edema, , atelectasisatelectasis, , pneumothoraxpneumothorax, , pneumonia pneumonia and and Guillain-Barre syndromeGuillain-Barre syndrome

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Respiratory AcidosisRespiratory Acidosis

Clinical Manifestation:Clinical Manifestation:1. Acute respiratory acidosis 1. Acute respiratory acidosis

- Increased pulse and respiratory rate- Increased pulse and respiratory rate- Increased blood pressure- Increased blood pressure- Mental cloudiness and feeling of - Mental cloudiness and feeling of fullness in headfullness in head

2. Chronic respiratory acidosis2. Chronic respiratory acidosis- Weakness- Weakness- Dull headache- Dull headache

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Respiratory AcidosisRespiratory Acidosis

Laboratory and Diagnostic study:Laboratory and Diagnostic study:

1. ABG: blood pH below 7.35 and above 1. ABG: blood pH below 7.35 and above PCO2PCO2

Medical Management:Medical Management:

1. Mechanical ventilation1. Mechanical ventilation

2. Bronchodilators (reduce bronchial spasm)2. Bronchodilators (reduce bronchial spasm)

3. Adequate hydration3. Adequate hydration

4. Antibiotics (to treat infection)4. Antibiotics (to treat infection)

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Respiratory AcidosisRespiratory AcidosisNursing Problems:Nursing Problems:

1. Altered Level of Consciousness1. Altered Level of Consciousness2. Ineffective Breathing Pattern2. Ineffective Breathing Pattern3. Altered Tissue Perfusion3. Altered Tissue Perfusion

Nursing Management:Nursing Management:1. Monitor ABG values1. Monitor ABG values2. Improve ventilation2. Improve ventilation3. Position client on semi fowler’s 3. Position client on semi fowler’s position position

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Respiratory AcidosisRespiratory Acidosis

4. Treat chronic respiratory acidosis by 4. Treat chronic respiratory acidosis by low-flow O2.low-flow O2.

5. Maintain a quiet and relaxing 5. Maintain a quiet and relaxing environment.environment.

6. Keep needed items within the 6. Keep needed items within the client’s reach.client’s reach.

7. Monitor the V/S 7. Monitor the V/S

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Respiratory Respiratory AlkalosisAlkalosis

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Respiratory AlkalosisRespiratory Alkalosis

Definition:Definition: is an acid-base imbalance is an acid-base imbalance characterized by decreased arterial characterized by decreased arterial PCO2 and increased blood pH.PCO2 and increased blood pH.

Etiology:Etiology:

1. Hyperventillation1. Hyperventillation

2. Fever 2. Fever

3. Salicylate poisoining3. Salicylate poisoining

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Respiratory AlkalosisRespiratory Alkalosis

Clinical Manifestation:Clinical Manifestation:1. Lightheadedness1. Lightheadedness2. Inability to concentrate2. Inability to concentrate3. Convulsion3. Convulsion4. Positive Chvostek sign4. Positive Chvostek sign5. Muscle twitching5. Muscle twitching

Laboratory and Diagnostic study:Laboratory and Diagnostic study:1. ABG: pH above 7.45 and PCO2 1. ABG: pH above 7.45 and PCO2 below 38 mmHg.below 38 mmHg.

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Respiratory AlkalosisRespiratory Alkalosis

Medical Management:Medical Management:

1. Paper bag breathing1. Paper bag breathing

2. Administration of sedative2. Administration of sedative

Nursing Problems:Nursing Problems:

1. Altered Level of Consciousness1. Altered Level of Consciousness

2. Ineffective Breathing Pattern2. Ineffective Breathing Pattern

3. Altered Tissue Perfusion3. Altered Tissue Perfusion

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Respiratory AlkalosisRespiratory Alkalosis

Nursing Management:Nursing Management:

1. Monitor ABG results1. Monitor ABG results

2. Treatment is aimed at underlying cause 2. Treatment is aimed at underlying cause ((decreasing paindecreasing pain, , feverfever & & anxiety anxiety))

3. Encourage slow, deep breathing, instruct 3. Encourage slow, deep breathing, instruct to to breathe into and out of paper bag.breathe into and out of paper bag.

4. Institute and maintain seizure precautions 4. Institute and maintain seizure precautions as as necessary.necessary.

5. Assist the client with activities as 5. Assist the client with activities as necessary necessary

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Parenteral Fluid Parenteral Fluid TherapyTherapy

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Purpose of Parenteral Fluid Purpose of Parenteral Fluid TherapyTherapy

• To provide water, electrolytes and To provide water, electrolytes and nutrients to meet daily requirements.nutrients to meet daily requirements.

• To replace water and correct To replace water and correct electrolyte deficits.electrolyte deficits.

• To administer medications and blood To administer medications and blood products.products.

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Types of FluidsTypes of Fluids

1.1. Isotonic Isotonic - a solution that exerts the - a solution that exerts the same osmotic pressure as that found same osmotic pressure as that found in plasma.in plasma.

e.g. e.g. D5WaterD5Water, , 0.9% Normal saline0.9% Normal saline, , Lactated Ringer’sLactated Ringer’s, , Blood componentsBlood components

2.2. HypotonicHypotonic - a solution that exerts less - a solution that exerts less osmotic pressure than that of blood osmotic pressure than that of blood plasma.plasma.

e.g. e.g. 0.45% NSS0.45% NSS,, 0.2% NSS 0.2% NSS

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Types of FluidsTypes of Fluids

3.3. Hypertonic Hypertonic - a solution that exerts a - a solution that exerts a higher osmotic pressure than that of higher osmotic pressure than that of blood plasma.blood plasma.

e.g. e.g. Dextrose 5% NaClDextrose 5% NaCl, , Dextrose Dextrose 10% Water10% Water, , Dextrose 20% WaterDextrose 20% Water, , 3% 3% NaClNaCl, , D5% Lactated Ringer’sD5% Lactated Ringer’s, , HyperalimentationHyperalimentation

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Composition of FluidsComposition of Fluids

• Saline solutionsSaline solutions – water and electrolytes – water and electrolytes (Na+, Cl+)(Na+, Cl+)

• Dextrose solutionsDextrose solutions – water or saline and – water or saline and caloriescalories

• Lactated Ringer’sLactated Ringer’s – water and – water and electrolytes (Na+, K+, Mg++, Ca++, electrolytes (Na+, K+, Mg++, Ca++, lactate)lactate)

• Balanced isotonicBalanced isotonic – varies water, – varies water, electrolyte, some calories (Na+, K+, electrolyte, some calories (Na+, K+, mg++, Cl-, HCO3-, gluconate)mg++, Cl-, HCO3-, gluconate)

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Composition of FluidsComposition of Fluids

• Whole blood and blood components Whole blood and blood components – – PRBC, Platelet Concentrate, Fresh PRBC, Platelet Concentrate, Fresh Frozen Plasma & CryoprecipitateFrozen Plasma & Cryoprecipitate

• Plasma expandersPlasma expanders – Albumin, Dextran, – Albumin, Dextran, Plasma protein, Plasma protein,

• Parenteral hyperalimentationParenteral hyperalimentation – Fluids, – Fluids, Electrolytes, Amino acids and Calories Electrolytes, Amino acids and Calories

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IVF Regulation FormulaIVF Regulation Formula

gtts/min.gtts/min. = Total amount x Drop Factor = Total amount x Drop Factor (gtts/ml)(gtts/ml)

No. of hours x 60 minutesNo. of hours x 60 minutes

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Factors to considerFactors to consider

Factors to consider of selecting a site of Factors to consider of selecting a site of venipuncture:venipuncture:

1. Condition of the vein1. Condition of the vein

2. Type of fluid or medication to be infused2. Type of fluid or medication to be infused

3. Duration of the therapy3. Duration of the therapy

4. Patient’s age and size4. Patient’s age and size

5. Whether the patient is right or left handed5. Whether the patient is right or left handed

6. Patient’s medical history and current health status6. Patient’s medical history and current health status

7. Skill of the person performing the venipuncture7. Skill of the person performing the venipuncture

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Intravenous ComplicationsIntravenous ComplicationsSystemic complications:Systemic complications:a. Fluid Overloada. Fluid Overloadb. Air Embolismb. Air Embolismc. Septicemiac. Septicemia

Local complications:Local complications:a. Infiltration & Extravasationa. Infiltration & Extravasationb. Phlebitisb. Phlebitisc. Thrombophlebitisc. Thrombophlebitisd. Hematomad. Hematomae. Clotting & Obstructione. Clotting & Obstruction

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Nursing ManagementNursing Management

a. Choosing an I.V. sitea. Choosing an I.V. site

b. Selecting venipuncture devicesb. Selecting venipuncture devices

c. Teaching the patientc. Teaching the patient

d. Preparing the sited. Preparing the site

e. Performing venipuncturee. Performing venipuncture

f. Monitoring flowf. Monitoring flow

g. Discontinuing the I.V. infusion g. Discontinuing the I.V. infusion

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BURNSBURNS

Page 243: F&E Lecture (new 2010)

BURNSBURNSDefinition:Definition: caused by a transfer of energy from caused by a transfer of energy from

a heat source to the body. Heat may be a heat source to the body. Heat may be transferred through conduction or transferred through conduction or electromagnetic radiation.electromagnetic radiation.

Category of Burns:Category of Burns:1. Thermal (including Electrical)1. Thermal (including Electrical)2. Radiation2. Radiation3. Chemical3. Chemical

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Layers of SkinLayers of Skin

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Classification of BURNSClassification of BURNS

Classification of Burns:Classification of Burns:1. Superficial Partial-1. Superficial Partial-

thicknessthickness - The - The epidermis is epidermis is destroyed or destroyed or injured and a injured and a portion of the portion of the dermis may be dermis may be injured, skin is red, injured, skin is red, dry and it may dry and it may blister.blister.- complete - complete recovery within a recovery within a week, peeling is week, peeling is present &present & no scarring.no scarring.

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Classification of BURNSClassification of BURNS

2. 2. Deep Partial-Deep Partial-thicknessthickness – – Destruction of the Destruction of the epidermis and upper epidermis and upper layers of the dermis layers of the dermis and injury to deeper and injury to deeper portion of dermis, portion of dermis, wound is painful, red wound is painful, red and exudes fluid.and exudes fluid.- recovery 2 to 4 - recovery 2 to 4 weeks, some weeks, some scarring and scarring and depigmentation depigmentation contractures, contractures, infection may lead to infection may lead to full thickness.full thickness.

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Classification of BURNSClassification of BURNS

3. 3. Full-thicknessFull-thickness – Total – Total destruction of epidermis, destruction of epidermis, dermis and underlying dermis and underlying tissues, wound color tissues, wound color ranges widely from white ranges widely from white to red, brown or black, to red, brown or black, wound is painless and wound is painless and leathery (nerve fibers, hair leathery (nerve fibers, hair follicles and sweat glands follicles and sweat glands are destroyed).are destroyed).- eschar sloughs; grafting - eschar sloughs; grafting necessary; scarring & loss necessary; scarring & loss of contour and function; of contour and function; contractures; loss of digits contractures; loss of digits or extremity possible.or extremity possible.

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Zones of Burn InjuryZones of Burn Injury

Zones of Burn injury:Zones of Burn injury:1. 1. Zone of coagulationZone of coagulation – –

The inner area where The inner area where cellular death occurs cellular death occurs and sustains the most and sustains the most damage. damage.

2. 2. Zone of StasisZone of Stasis – The – The middle area has a middle area has a compromised blood compromised blood supply, inflammation supply, inflammation and tissue injury.and tissue injury.

3. 3. Zone of HyperemiaZone of Hyperemia – The – The outer area that outer area that sustains the least sustains the least damage.damage.

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Factors in Burn DepthFactors in Burn Depth

Factors in Determining the depth of the Factors in Determining the depth of the burn:burn:

1. How the injury occurred1. How the injury occurred

2. Causative agent2. Causative agent

3. Temperature of the burning agent3. Temperature of the burning agent

4. Duration of contact with the agent4. Duration of contact with the agent

5. Thickness of the skin5. Thickness of the skin

Page 250: F&E Lecture (new 2010)

Methods to Estimate BurnMethods to Estimate Burn

Methods to estimate Methods to estimate Total Body Surface Total Body Surface Area Burned:Area Burned:

1. 1. Rule of Nines – Rule of Nines – A quick A quick way to calculate the way to calculate the extent of burns, it is extent of burns, it is an estimation of the an estimation of the TBSA involved in a TBSA involved in a burn. burn.

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Methods to Estimate BurnMethods to Estimate Burn

2. 2. Lund and Browder Lund and Browder Method – Method – A more A more precise method of precise method of estimating the estimating the extent of a burn extent of a burn which recognizes which recognizes that the percentage that the percentage of TBSA of various of TBSA of various anatomic parts, anatomic parts, especially the head, especially the head, legs and changes legs and changes with growth.with growth.

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Methods to Estimate BurnMethods to Estimate Burn

3. 3. Palm Method –Palm Method – In patients with In patients with scattered burns, scattered burns, a method to a method to estimate the estimate the percentage of percentage of burn is the palm burn is the palm of the patient of the patient which is which is approximately approximately equivalent to equivalent to 1% TBSA.1% TBSA.

Page 253: F&E Lecture (new 2010)

Local and Systemic Local and Systemic ResponsesResponses

Local and Systemic Responses to burns:Local and Systemic Responses to burns:

1. Cardiovascular1. Cardiovascular2. Burn Edema2. Burn Edema3. Effects on Fluids, Electrolytes and Blood 3. Effects on Fluids, Electrolytes and Blood

VolumeVolume4. Pulmonary Response4. Pulmonary Response5. Other Systemic Responses5. Other Systemic Responses

- Renal Function- Renal Function- Immune System- Immune System- Skin- Skin- GIT (Paralytic Ileus and Curling’s Ulcer)- GIT (Paralytic Ileus and Curling’s Ulcer)

Page 254: F&E Lecture (new 2010)

Phases of BurnsPhases of Burns

Phases of Burn Care:Phases of Burn Care:1. Emergent / Resuscitative Phase: 1. Emergent / Resuscitative Phase: From onset From onset

of injury to completion of fluid resuscitation. of injury to completion of fluid resuscitation. Management Priorities:Management Priorities:a. First Aida. First Aidb. Prevention of shockb. Prevention of shockc. Prevention of respiratory distressc. Prevention of respiratory distressd. Detection and treatment of concomitant d. Detection and treatment of concomitant

injuriesinjuriese. Wound assessment and initial caree. Wound assessment and initial care

Page 255: F&E Lecture (new 2010)

Emergent / Resuscitative Emergent / Resuscitative PhasePhase

Emergency Procedure at the Burn Emergency Procedure at the Burn Scene:Scene:

1. Extinguish the fire1. Extinguish the fire

2. Cool the Burn2. Cool the Burn

3. Remove restrictive objects3. Remove restrictive objects

4. Cover the wound4. Cover the wound

5. Irrigate chemical burns5. Irrigate chemical burns

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Emergent / Resuscitative Emergent / Resuscitative PhasePhase

On-the-scene Care:On-the-scene Care:

1. Prevent injury to the rescuer1. Prevent injury to the rescuer

2. ABC’s assessment2. ABC’s assessment

3. Assess the V/S (Apical Pulse, HR & B/P)3. Assess the V/S (Apical Pulse, HR & B/P)

4. Neurologic status assessment4. Neurologic status assessment

5. Cool the wound5. Cool the wound

6. Establish an airway & supply O26. Establish an airway & supply O2

7. Insert Large-Bore intravenous line.7. Insert Large-Bore intravenous line.

Page 257: F&E Lecture (new 2010)

Fluid & Electrolytes ChangesFluid & Electrolytes ChangesFluids and Electrolytes Changes in the Fluids and Electrolytes Changes in the

Emergent/Resuscitative Phase:Emergent/Resuscitative Phase:

Shock Phase / Edema at Burn Site:Shock Phase / Edema at Burn Site:

1. 1. Generalized dehydrationGeneralized dehydration – due to plasma leaks – due to plasma leaks through damaged capillaries.through damaged capillaries.

2. 2. Reduction of blood volumeReduction of blood volume – due to plasma – due to plasma loss, fall of blood pressure and diminished loss, fall of blood pressure and diminished cardiac output.cardiac output.

3. 3. Decreased urinary outputDecreased urinary output – due to fluid loss, – due to fluid loss, decreased renal blood flow, Na+ & water decreased renal blood flow, Na+ & water retention.retention.

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Fluid & Electrolytes ChangesFluid & Electrolytes Changes

4. 4. Potassium excessPotassium excess – due to massive – due to massive cellular trauma.cellular trauma.

5. 5. Sodium deficitSodium deficit – due to trapped Na+ in – due to trapped Na+ in fluid and exudate edema, shift of Na+ fluid and exudate edema, shift of Na+ into the cell.into the cell.

6. 6. Metabolic acidosisMetabolic acidosis – due to loss of – due to loss of bicarbonate ions accompanies Na+ bicarbonate ions accompanies Na+ loss.loss.

7. 7. Hemoconcentration Hemoconcentration (elevated Hct)(elevated Hct) – – due to liquid blood component is lost due to liquid blood component is lost into extravascular space.into extravascular space.

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Emergent / Resuscitative Emergent / Resuscitative PhasePhase

Guidelines and Formulas for Fluid Guidelines and Formulas for Fluid Replacement in Burn Patients:Replacement in Burn Patients:

1. 1. Consensus formula: Consensus formula:

LR or other balanced saline solution:LR or other balanced saline solution: 2 2 to 4 ml. X kg. body wt. X % TBSAto 4 ml. X kg. body wt. X % TBSA

- Half to be given in 1- Half to be given in 1stst 8 hours; 8 hours; remaining half to be given over next 16 remaining half to be given over next 16 hours.hours.

Page 260: F&E Lecture (new 2010)

Emergent / Resuscitative Emergent / Resuscitative PhasePhase2.2. Evans Formula: Evans Formula:

a. a. Colloids:Colloids: 1 ml. X kg. body wt. X % TBSA 1 ml. X kg. body wt. X % TBSAb. b. Electrolytes (saline):Electrolytes (saline): 1 ml. X kg. body wt. X % 1 ml. X kg. body wt. X % TBSATBSAc. c. Glucose (5% in water):Glucose (5% in water): 2,000 ml. for 2,000 ml. for insensible lossinsensible lossDay 1: half to be given in 1Day 1: half to be given in 1stst 8 hours & 8 hours & remaining half over next 16 hours.remaining half over next 16 hours.Day 2: half of the previous day’s colloids and Day 2: half of the previous day’s colloids and electrolytes, all of insensible fluid replacement.electrolytes, all of insensible fluid replacement.Maximum of 10,000 ml. over 24 hours. Deep-Maximum of 10,000 ml. over 24 hours. Deep-partial and Full-Thickness burns exceeding 50% partial and Full-Thickness burns exceeding 50% TBSA are calculated on the basis of 50% TBSA.TBSA are calculated on the basis of 50% TBSA.

Page 261: F&E Lecture (new 2010)

Emergent / Resuscitative Emergent / Resuscitative PhasePhase

3. 3. Brooke Army Formula:Brooke Army Formula:a. a. Colloids:Colloids: 0.5 ml. X kg. body wt. X % TBSA 0.5 ml. X kg. body wt. X % TBSAb. b. Electrolytes (LR solution):Electrolytes (LR solution): 1.5 ml. X kg. body 1.5 ml. X kg. body wt. X wt. X % TBSA% TBSAc. c. Glucose (5% in water):Glucose (5% in water): 2,000 ml. for 2,000 ml. forinsensible loss insensible loss Day 1: half to be given in the 1Day 1: half to be given in the 1stst 8 hours, 8 hours, remaining remaining half over next 16 hours.half over next 16 hours.Day 2: half of colloids, half of electrolytes, all of Day 2: half of colloids, half of electrolytes, all of

insensible fluid replacement.insensible fluid replacement.Deep-Partial and Full-Thickness burns exceeding Deep-Partial and Full-Thickness burns exceeding 50% 50% TBSA are calculated on the basis of 50% TBSA are calculated on the basis of 50% TBSA. TBSA.

Page 262: F&E Lecture (new 2010)

Emergent / Resuscitative Emergent / Resuscitative PhasePhase

4. 4. Parkland/Baxter Formula:Parkland/Baxter Formula:

LR solution:LR solution: 4 ml. X kg. body wt. X TBSA 4 ml. X kg. body wt. X TBSA

Day 1: half to be given in 1Day 1: half to be given in 1stst 8 hours, 8 hours, half to be given over next 16 hours.half to be given over next 16 hours.

Day 2: Varies, colloid is added.Day 2: Varies, colloid is added.

5. 5. Hypertonic Saline Solution:Hypertonic Saline Solution: administration of concentrated NaCl & administration of concentrated NaCl & Lactate, do not increase rate for the 1Lactate, do not increase rate for the 1stst 8 8 hours, serum Na+ must be monitored.hours, serum Na+ must be monitored.

Page 263: F&E Lecture (new 2010)

Emergent / Resuscitative Emergent / Resuscitative PhasePhase

Nursing Problems:Nursing Problems:1. 1. Impaired gas exchangeImpaired gas exchange

Goal:Goal: Maintenance of adequate tissue oxygenation Maintenance of adequate tissue oxygenation2. 2. Ineffective airway clearanceIneffective airway clearance

Goal:Goal: Maintain patent airway and adequate airway Maintain patent airway and adequate airway clearanceclearance

3. 3. Fluid volume deficitFluid volume deficitGoal:Goal: Restoration of optimal fluid and electrolyte Restoration of optimal fluid and electrolyte balance and perfusion of vital organsbalance and perfusion of vital organs

4. 4. HypothermiaHypothermiaGoal:Goal: Maintenance of adequate body temperature Maintenance of adequate body temperature

5. 5. PainPainGoal:Goal: Control of pain Control of pain

6. 6. AnxietyAnxietyGoal:Goal: Minimization of client’s and family’s anxiety Minimization of client’s and family’s anxiety

Page 264: F&E Lecture (new 2010)

Emergent / Resuscitative Emergent / Resuscitative PhasePhase

7. 7. Acute respiratory failure, distributive shock, acute Acute respiratory failure, distributive shock, acute renal failure, compartment syndrome, paralytic Ileus renal failure, compartment syndrome, paralytic Ileus and Curling’s ulcerand Curling’s ulcerGoal:Goal: Absence of complications Absence of complications

8. 8. Fluid volume excessFluid volume excessGoal:Goal: Maintenance of optimal fluid balance Maintenance of optimal fluid balance

9. 9. Risk for infectionRisk for infectionGoal:Goal: Absence of localized or systemic infection Absence of localized or systemic infection

10. 10. Altered nutrition (less than body requirements)Altered nutrition (less than body requirements)Goal: Attainment of anabolic nutritional statusGoal: Attainment of anabolic nutritional status

11. 11. Impaired skin integrityImpaired skin integrityGoal:Goal: Demonstration of improved skin integrity Demonstration of improved skin integrity

12. 12. Impaired physical mobilityImpaired physical mobilityGoal:Goal: Achievement of optimal physical mobility Achievement of optimal physical mobility

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Emergent / Resuscitative Emergent / Resuscitative PhasePhase

13. 13. Ineffective individual copingIneffective individual copingGoal:Goal: Use of appropriate coping strategies to deal with Use of appropriate coping strategies to deal with postburn problems postburn problems

14. 14. Altered family processesAltered family processesGoal:Goal: Achievement of appropriate patient/family Achievement of appropriate patient/family processesprocesses

15. 15. Knowledge deficitKnowledge deficitGoal:Goal: Verbalization of understanding of the course of Verbalization of understanding of the course of burn treatment by patient and familyburn treatment by patient and family

16. 16. Congestive heart failure, pulmonary edema, sepsis, Congestive heart failure, pulmonary edema, sepsis, acuteacute respiratory failure, ARDS, visceral damage respiratory failure, ARDS, visceral damage (electrical burns)(electrical burns)Goals:Goals: Absence of complication Absence of complication

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Emergent / Resuscitative Emergent / Resuscitative PhasePhase

Nursing Management:Nursing Management: Emergent / Emergent / ResuscitativeResuscitative

1. Aseptic management of the burn wounds 1. Aseptic management of the burn wounds and invasive lines must be observed.and invasive lines must be observed.

2. Monitor V/S frequently.2. Monitor V/S frequently.3. Monitor I&O accurately3. Monitor I&O accurately4. Assist in I.V. therapy.4. Assist in I.V. therapy.5. Assess LOC, psychological, pain and anxiety 5. Assess LOC, psychological, pain and anxiety

level and behavior.level and behavior.6. Assess the client’s and family’s 6. Assess the client’s and family’s

understanding of the injury and treatment.understanding of the injury and treatment.

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Acute or Intermediate PhaseAcute or Intermediate Phase

2. 2. Acute or Intermediate Phase:Acute or Intermediate Phase: From the From the beginning of diuresis to near completion beginning of diuresis to near completion of wound closure.of wound closure.Management Priorities:Management Priorities:a. Wound care and closurea. Wound care and closureb. Prevention or treatment of b. Prevention or treatment of complications, complications, including infectionincluding infectionc. Nutritional supportc. Nutritional support

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Acute or Intermediate PhaseAcute or Intermediate Phase

Fluid and Electrolyte Changes in the Acute Fluid and Electrolyte Changes in the Acute Phase:Phase:

State of Diuresis:State of Diuresis:

1. Hemodilution1. Hemodilution – due to blood cell concentration – due to blood cell concentration diluted as fluid enters the intravascular diluted as fluid enters the intravascular compartment; loss of red blood cells destroyed compartment; loss of red blood cells destroyed at burn site.at burn site.

2. 2. Increased urinary outputIncreased urinary output – due to fluid shift – due to fluid shift into intravascular compartment increases into intravascular compartment increases renal blood flow and causes increased urine renal blood flow and causes increased urine formation.formation.

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Acute or Intermediate PhaseAcute or Intermediate Phase

3. 3. Sodium deficitSodium deficit – due to diuresis, Na+ – due to diuresis, Na+ is lost with water existing serum is lost with water existing serum sodium is diluted by water influx.sodium is diluted by water influx.

4. 4. Potassium deficitPotassium deficit – beginning on the – beginning on the 44thth or 5 or 5thth postburn day, K+ shifts from postburn day, K+ shifts from extracellular fluid into cells.extracellular fluid into cells.

5. 5. Metabolic acidosisMetabolic acidosis – due to loss – due to loss sodium depletes fixed base, relative sodium depletes fixed base, relative CO2 content increasesCO2 content increases

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Acute or Intermediate PhaseAcute or Intermediate Phase

Medical Management:Medical Management:

1. Infection Prevention1. Infection Prevention

2. Wound cleaning2. Wound cleaning

- - HydrotherapyHydrotherapy

3. Topical Antibacterial Therapy3. Topical Antibacterial Therapy

- - Silver Sulfadiazine 1% (Silvadene)Silver Sulfadiazine 1% (Silvadene)

- Mafenide acetate 5% to 10% (Sulfamylon)- Mafenide acetate 5% to 10% (Sulfamylon)

- Silver Nitrate 0.5%- Silver Nitrate 0.5%

- Acticoat- Acticoat

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Acute or Intermediate PhaseAcute or Intermediate Phase

4. Wound Dressing4. Wound Dressing- Occlusive Method- Occlusive Method

5. Dressing Changes5. Dressing Changes6. Wound Debridement 6. Wound Debridement

- - Natural DebridementNatural Debridement- Mechanical Debridement- Mechanical Debridement- Surgical Debridement- Surgical Debridement

7. Grafting the Burn Wound7. Grafting the Burn Wound- - Biologic Dressings Biologic Dressings (Homografts, Heterografts)(Homografts, Heterografts)- Biosynthetic and Synthetic Dressings- Biosynthetic and Synthetic Dressings- Dermal Substitutes- Dermal Substitutes- Autografts - Autografts (CEA, cultured epithelial autograft)(CEA, cultured epithelial autograft)

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Acute or Intermediate PhaseAcute or Intermediate Phase

8. Pain Management8. Pain Management

9. Nutritional Support9. Nutritional Support

Disorders of Wound Healing:Disorders of Wound Healing:

1. 1. ScarsScars

2. 2. KeloidsKeloids

3. 3. Failure to HealFailure to Heal

4. 4. ContracturesContractures

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Acute or Intermediate PhaseAcute or Intermediate Phase

Nursing Problems:Nursing Problems:1. 1. Fluid volume excessFluid volume excess

Goal:Goal: Maintenance of optimal fluid balance Maintenance of optimal fluid balance2. 2. Risk for infectionRisk for infection

Goal:Goal: Absence of localized or systemic infection Absence of localized or systemic infection3. 3. Altered nutrition (less than body requirements)Altered nutrition (less than body requirements)

Goal: Attainment of anabolic nutritional statusGoal: Attainment of anabolic nutritional status4. 4. Impaired skin integrityImpaired skin integrity

Goal:Goal: Demonstration of improved skin integrity Demonstration of improved skin integrity5. 5. Impaired physical mobilityImpaired physical mobility

Goal:Goal: Achievement of optimal physical mobility Achievement of optimal physical mobility

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Acute or Intermediate PhaseAcute or Intermediate Phase

6. 6. Ineffective individual copingIneffective individual copingGoal:Goal: Use of appropriate coping strategies to deal Use of appropriate coping strategies to deal with postburn problems with postburn problems

7. 7. Altered family processesAltered family processesGoal:Goal: Achievement of appropriate patient/family Achievement of appropriate patient/family processesprocesses

8. 8. Knowledge deficitKnowledge deficitGoal:Goal: Verbalization of understanding of the course of Verbalization of understanding of the course of burn treatment by patient and familyburn treatment by patient and family

9. 9. Congestive heart failure, pulmonary edema, sepsis, Congestive heart failure, pulmonary edema, sepsis, acuteacute respiratory failure, ARDS, visceral damage respiratory failure, ARDS, visceral damage (electrical burns)(electrical burns)Goals:Goals: Absence of complication Absence of complication

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Acute or Intermediate PhaseAcute or Intermediate Phase

Nursing Management:Nursing Management: Acute PhaseAcute Phase1. Restoring Normal Fluid Balance1. Restoring Normal Fluid Balance2. Preventing Infection2. Preventing Infection3. Maintaining Adequate Nutrition3. Maintaining Adequate Nutrition4. Promoting Skin Integrity4. Promoting Skin Integrity5. Relieving Pain and Discomfort5. Relieving Pain and Discomfort6. Promoting Physical Mobility6. Promoting Physical Mobility7. Supporting Patient and Family Processes7. Supporting Patient and Family Processes8. Monitoring and managing Potential Complications8. Monitoring and managing Potential Complications

- Sepsis- Sepsis- Acute Respiratory Failure and Acute Respiratory - Acute Respiratory Failure and Acute Respiratory Distress Distress SyndromeSyndrome- Visceral Damage- Visceral Damage

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Rehabilitation PhaseRehabilitation Phase

3. 3. Rehabilitation Phase:Rehabilitation Phase: From major wound From major wound closure to return to individual’s optimal closure to return to individual’s optimal level of physical and psychosocial level of physical and psychosocial adjustment.adjustment.Management Priorities:Management Priorities:a. Prevention of scars and contracturesa. Prevention of scars and contracturesb. Physical, occupational and vocational b. Physical, occupational and vocational rehabilitationrehabilitationc. Functional and cosmetic reconstructionc. Functional and cosmetic reconstructiond. Psychosocial counselingd. Psychosocial counseling

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Rehabilitation PhaseRehabilitation Phase

Nursing Problems:Nursing Problems:1. Activity Intolerance1. Activity Intolerance2. Disturbed Body Image2. Disturbed Body Image3. Deficient Knowledge3. Deficient Knowledge

Planning / Goals:Planning / Goals:1. Increased participation in ADL1. Increased participation in ADL2. Increased understanding of the injury, treatment 2. Increased understanding of the injury, treatment

and planned follow-up careand planned follow-up care3. Adaptation and Adjustment to alterations in body 3. Adaptation and Adjustment to alterations in body

image, self-concept and lifestyleimage, self-concept and lifestyle4. Absence of complications4. Absence of complications

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Rehabilitation PhaseRehabilitation Phase

Nursing Management:Nursing Management:1. Promoting activity tolerance1. Promoting activity tolerance2. Improving body image and self-concept2. Improving body image and self-concept3. Monitoring and managing potential 3. Monitoring and managing potential

complications (Contractures, Impaired complications (Contractures, Impaired psychological adaptation to the burn injury)psychological adaptation to the burn injury)

4. Promoting home and community-based care4. Promoting home and community-based care- Teaching patient self-care- Teaching patient self-care- Continuing care - Continuing care

Burn Care in the Home:Burn Care in the Home:

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END of CONCEPTEND of CONCEPT