Fluid and Electrolyte and Acid-base Imbalance New Recovered]

8/6/2019 Fluid and Electrolyte and Acid-base Imbalance New Recovered]

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By Dr Lee June Lyng


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Fluid Volume

Electrolyte Imbalance- Sodium, K,Ca

Acid-Base Disturbance Metabolic Acidosis,

Resp Acidosis, Metabolic Alkalosis


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Total body waterWater constitutes

approximately 50 to60% of total body

weightdivided into two

functional fluidcompartments, the

extracellular andintracellular

% of TBW

Plasma 5%

Interstitial fluid15%

Intracellularvolume 40%

ECF(1/3)

ICF(2/3)


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Intake

Output

LiquidWater in foodMetabolism

1,200 -1,500 ml700 - 1,000 ml200 - 400 ml

UrineFecesInsensible Loses:

SkinLungs

1,200 -1,500 ml100 - 250 ml

350 - 400 ml350 - 400 ml

TOTAL 2,100 2,900 ml TOTAL 2,100 2,900 ml


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Fluid Movement by Diffusion and Osmosis

Diffusion- means by which substances such asnutrients and wastes produces move between bloodand interstitial spaces


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Osmolality refers to the concentration ofsolutes in 1 liter of solution

OSMOSIS: diffusion of H2O across a selectivelypermeable membrane from an area of lower soluteconcentration to an area of higher soluteconcentration.


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ATPNa-Kpump

ECF ICF

Cellmembra

ne

Na, Cl, and HCO3 K, Mg/Phosphateand proteinNa has osmotic and

electrical properties andit is a/w water

Any Na containing fluidsare distributedthroughout the ECF

Adds volume atintravascular and

interstitial

Expand theintravascular volume

#Na in ECF high , H2o

will be high!!


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ECF volumeRegulate to help BP

by salt balance2 mech:Short termBaroreceptorsFluid shifts btw

plasma andinterstitial fluid

Long termBy kidneys and thirst

mechanism

ECF osmolarityRegulate to prevent

swelling/shrinking ofcells by H2O blance


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Short term control measures to maintain BPBaroreceptors reflex


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Fluid shifts between plasma and interstitial fluidBarrier - blood vesselsAccording to HP and COPEg: decreased in plasma volume compensated by

shifting fluid from interstitial fluid and vice versa.


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Long termBy kidney and thirst mechanism.


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Decreased Na load inthe body

Decreased arterial BP

DecreasedGFR

Decreased Na

filteration

Increasedaldosterone

Increased Na

reabsorption

Decreased Naexcretion

Increased Na retention

Increased plasmavolume

Increased ECF volume


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ThirstHypothalamus- thirst

center of the brainActivated by an

increase in ECFOsmolality due to:

Hypotension

PolyuriaFluid volume

depletion


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REGULATION OF FLUID VOLUME

HYPERVOLEMIA HYPOVOLEMIA

stimulatesinhibits

ADH

INCREASED

URINATION

of

Dilute urine

NORMAL FLUID VOLUME RESTORED

DECREASED

URINATION

of

Concentrated urine

Aldosterone Thirst Thirst ADH Aldosterone


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Types of Intravenous Fluids:

ISOTONIC a solution that has the same osmotic pressure externallyas that found across a semi-permeable membrane

--0.9% NaCl, D5W, 5% Dextrose in 0.225% Saline and LRS

HYPOTONIC a solution that has a lower osmotic press than that of

the blood causing the cell to expand and swell.(They contain lowerconcentration of salt/ solute than other solution)

--0.3 % NaCl, D in water, 0.45 % NaCl and distilled water.

HYPERTONIC a solution that has a higher osmotic pressure thanthat of the blood causing the cell to shrink. ( It has higherconcentration of solutes.)

--D5LRS, Mannitol, 10% D in water, and 5% D in 0.45% NaCl


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Electrolyte Solutions for Parenteral Administration

Electrolyte Composition (mEq/L)solution Na Cl K HCO3 Ca Mg mOsm

Extracellular fluid 142 103 4 27 5 3 280-310

Lactated Ringer's 130 109 4 28 3 2730.9% Sodiumchloride

154 154 308

D5 0.45% Sodiumchloride

77 77 407

D5 W(isotonic and itbecomes hypotoniconce dextrosemetabolized)

253

3% Sodiumchloride 513 513 1026


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Alternative Resuscitative Fluids

Solution Molecular Weight Osmolality(mOsm/L)

Sodium (mEq/L

Hypertonic saline(7.5%)

2565 1283

Albumin 5% 70,000 300 130-160

Albumin 25% 70,000 1500 130-160

Dextran 40 40000 308 154

Dextran 70 70,000 308 154

Hetastarch 450000 310 154

Hextend 670000 307 143

Gelofusine 30000 n/a 154


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Hypertonic saline (7.5%) -treatment modalityin patients with closed head injuries. It hasbeen shown to increase cerebral perfusionand decrease intracranial pressure, thusdecreasing brain edemahypertonic saline is an arteriolar vasodilator,

thus,it may cause bleeding


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Colloids are also used in surgical patients and

have long been debated as effective volumeexpanders compared to isotonic crystalloidsDue to their molecular weight, they are

confined to the intravascular space and their

infusion results in more efficient plasma volumeexpansion.However, in severe hemorrhagic shock,

capillary membrane permeability increases,permitting colloids to enter the interstitialspace, which can worsen edema and impairtissue oxygenation


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four major types of colloids availablealbumin, dextrans, hetastarch, and gelatins

Colloid solutions with smaller size particlesand lower molecular weights exert a greateroncotic effect, but are retained within thecirculation for a shorter period of time thanlarger and higher molecular weight colloids


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Disadvantage of colloidsd/t high molecular weight, kidneys unable to

filter and it may cause plug at the glomerulusfilter, thus, may cause kidney failure.


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Surgical patients needMaintenance volume requirements

On going lossesVolume excess/deficitsMaintenance electrolyte requirementsElectrolyte excess/deficits


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Body weight Fluid required

0-10Kg 100ml/kg/d

next 10-20Kg 50 ml/kg/d

subsequent Kg 20ml/kg/d

15ml/Kg/d for elderly


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1st 10kg x 100mls = 1000mls

2nd 10kg x 50mls = 500mls

Next 50kg x 20mls= 1000mls

TOTAL 2500 mls /d


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NG

drains

fistulae

third space losses

Concentration is similar to plasma

Replace with isotonic fluids


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Acute

vital signs changes Blood pressure

Heart rate CVP

tissue changes not obvious

urine output low


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Chronic

Decreased skin turgor

Sunken eyes

OliguriaOrthostatic hypotension

High BUN/Creatine ratio


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Nil per oral deficit=no. of hours of NPO xmaintainence fluidrequirement (ml/h)

Bowel prep 1LSuperficial surgical

trauma 1-2ml/kg/hr

Minimal surgicaltrauma 3-4ml/kg/hr( hernia, head, necksurgery)

Mod surgical trauma5-6ml/kg/hr(hysterectomy,chestsurgery)

Severe surgicaltrauma 8 -10ml/kg/hr(or more) in AAArepair,nephrectomy


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Fluid deficit = 120ml/h (x) 10h = 1200ml (+)1000ml (bowel prep) = 2200mlReplace 1st hour, at 2nd half, at 3rd hour

Maintainence 120ml/h (x) 3h= 360ml

3rd space loss 6ml/kg/hr (X) 3 h=1440ml

Bl loss = 500ml (x) 3= 1500ml

Total fluid replacement= 5500ml


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Na 1-2mEq/Kg/d

K 0.5 - 1 mEq/Kg/d


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Usually correct over 24 hours

For ill patients calculate over shorter periodand reassess e.g. 1, 2 hours or 3 hours for e opcases

Deficits - correct half the amount over theperiod and reassess

By fluid challenge

Normally, 10 20ml/kg

In elderly or co-morbid, 5ml/kg


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Mildly hypertonic Balanced with Chloride

ECF Replacement Fluid

contains no protein so the oncotic pressure in the bloodis slightly lowered following the saline infusion. This has2 effects: Movement of fluid into the ISF is favoured (Starlings

Hypothesis) Glomerulo-tubular imbalance occurs: the lowered oncotic

pressure immediately leads to an increase in GFR and less

reabsorption of water in the proximal tubuleUrine flow increases. ADH is not affected.


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ProblemsToo much chloride may cause hyperchloraemic

metabolic acidosis due to tendency of H+reabsorption in kidney tubules

Hypertonicity retention


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How much?Provide normal requirement (1-2 mmol/kg/day)A 50kg person = 50 100 mmol/kg/dayMeans 1 to 2 pints of 0.9% saline is enough


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Isotonic, ECF replacement fluidlactate as a bicarbonate precursor

metabolism of lactate occurs in the liver

does not contribute to development of anacidosis as they are administered with Na+rather than H+ as the cation

Also contains Ca++ and K+


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Problems:Gluconeogenic propertiesPro-inflammatory responseCalcium precipitates with citrate (anticoagulant

present in blood causes clotting of blood inthe infusion tubing)

Potassium load, especially in hyperkalaemiaMetabolic alkalosis


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Good for:ECF deficit associated withAcidosisHypokalaemia (except for existing alkalosis)


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ProblemsCellular edemaHyperglycaemiaVessel irritant (20% concentration and higher)


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Less sodium contentAny solution of < 0.45% sodium will require

dextrose in combination prevents cell lysis

Limited use


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Examples: 3% saline, Mannitol, SodiumBicarbonate

Good in very few situations. Usage must bespecific3% saline: life threatening severe

hyponatraemiaMannitol: Cerebral edema, renal protectionSodium Bicarbonate: severe metabolic acidosis


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ProblemsIntracellular dehydration manifested by

CNS symptomsCVS instability


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CATIONS ANIONS

Na- 135-145 m Eq/L

K- 3.5 5.0 m Eq/L

Ca- 2.1-2.65 mEq/L

Mg -1.5 2.5 mEq/L

HCO3- 22-26 mEq/L

Cl- 96-106 mEq/L

PO4 1.2 -3.0 mEq/L


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Derminant of serum osmolality

Chloride is the anion that usuallyaccompanies Na

Sodium balance is regulated by theinteraction among neural, hormonal, andvascular mechanisms

Renal glomerulus filters 1000 mEq of

sodium/hr and 99% is reabsorbed in the loopof Henle


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Primary regulator of ECF volume

Establishing electrochemical state necessaryfor muscle contraction and nerve impulse

transmissionWHERE SODIUM GOES WATER FOLLOWS


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Serum Sodium < 135 mEq/LRF: Excessive perspiration

Altered thirst mech.

w/o access to fluids rapid rehydration after excessive fluid loss

altered percentage of total body water

decreased intake of sodium: fruits, vegetables, oatmeal, rice,wheat, fresh meat, chicken, fish

excessive administration of diuretic and laxatives

NGT irrigation with plain water

Vomiting, diarrhea


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Types:Hypovolemic: Na loss > H2O lossEuvolemic: TBW is mod. increased & total body

Na is normal

Hypervolemic: Greater increased in TBW than intotal Na


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Volume status

high Normal low

increased intakePost op ADH

scretionDrugs eg: ACE-I,

tricyclicantidepressants

(Dilutionalhyponatremia)

HyperglycemiaSIADH

Water intoxicationdiuretics

Decreased sodiumintake

GI loss(urine Na islow 20mEq/l)

a/w dehydration


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Sign and symptoms of hyponatremia

Central nervous system Headache, confusion,hyper- or hypoactive deeptendon reflexes, seizures,coma, increasedintracranial pressure

Musculoskeletal Weakness, fatigue,muscle cramps/twitching

Gastrointestinal Anorexia, nausea,vomiting, watery diarrhea

Cardiovascular Hypertension andbradycardia if significantincreases in intracranialpressure

Tissue Lacrimation, salivation

Renal Oli uria

Shows < 125


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Na < 135 mEq/LCl < 96 mEq/L

Serum Osmolality


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If Na> 120, aggressive treatment not requiredIf Na < 110,and symptomatic, for rapid

correction BUT can correct 10-12 mmol/l perday.

Rapid correction may cause pontinemyelinolysis.

Hypervolemic hyponatremia

Restrict H2O and Na intakeDiuretics


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Hypovolemic hyponatremiaRehydration usually with normal salineAmount depleted: mild 5%, mod 5-8%, severe

8-12%

[% x BW(kg) x 1000] ml


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Isovolemic hyponatremiaNo and mild symptomsFluid restriction (eg: 800 1000ml) till serum Na

rises

Severe symptoms:Seizure and coma require rapid increase of patients

ECF tonicity. Eg: 3 mmol in 3 hrSevere confusion requires mod increased of ECF

tonicity. Eg: 3-6 mmol in 12 hr

3 % saline(hypertonic) + IV frusemide


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Eg : 60 kg male with level Na is 111 andseizure.

Calculation:TBW = 60 x 0.6 = 36LTo correct 3 mmol/l in 1st 3 hoursChange in serum Na= [infusate Na serum Na]/

(TBW + 1)So 1 L of 3%NaCl will elevate [Na] by (513 111)/

(36 +1)= 10.9mmol/l


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To aim for 3 mmol/l [Na] elevation, 3/10.9 =0.275L of 3%NaCl needs to be infused over 3hour which is 92ml/hr for 3 hr

Frusemide given with itration t ensure that

urine output is similar to fluid inputIf Na is 114 after 3 hrs, pt has no more

seizures but GCS is not full, thus, 3%Naclinfusion can be halved which is 46ml/hr foranother 6 hr


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Serum Sodium > 146 mEq/LTypes:

Hypovolemic hypernatremia: TBW is greatly decreasedcompared to Na

Euvolemic hypernatremia: TBW is decrease relative tonormal total body Na

Hypervolemic hypernatremia: TBW is increased but Na gainis > H2O gain


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Volume status

High Normal Low

Iatrogenic Naadministration

Mineralcorticoidsexcess such asAldosteronism,

Cushings disease,

congenital adrenalhyperplasiaUrine Na is typically

> 20 mEq/L andurine osmolarity is

> 300 mOsm/L

Non-renal water lossthru skin and GI loss

Renal water loss

such as DI, renaldisease , diuretics

Non renal waterloss thru skin and

GI lossRenal water loss

such as renaltubular disease,DI,

osmotic diureticsurine Na is lessthan 20 mEq/L andurine osmolarity isless than 300 to

400 mOsm/L


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Signs and symptoms of hypernatremia

Central nervous system Restlessness, lethargy,ataxia, irritability, tonicspasms, delirium,seizures, coma, SAH(d/tshift of fluid fr ICF to ECF,

thus causes traction tothe cerebral vessels)

Musculoskeletal Weakness

Cardiovascular Tachycardia, hypotension,syncope

Tissue Dry sticky mucousmembranes, red swollentongue, decreased salivaand tears, thirst

Renal Oliguria

Shows > 155


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Hypernatremia Target fall in serum [Na] is 10 mmol/L/day

1.Water depletion1. Should be given water orally if tolerated

2. If not, set up an IV infusion of D5% or 0.45%NaCL3. Daily fluid requirement: 40ml/kg/day

4. Change in serum Na = (infusate Na serum Na)/(total body water + 1)

5. Correction of deficit:

1. Desired TBW =[ TBW(current) x measuredNa(mmol/l)]/desired Na

2. Water deficit = Desired TBW(normal) TBW (curent)


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Functions:

Regulates ICF osmolality

Promotes transmission and conduction of nerveimpulses

Muscle contraction

Enzyme action for cellular metabolism and glycogen

storage in the liveracid-base balance

Alkalosis


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can cause hypokalemia

Acidosis

can cause hyperkalemiaSubstance that can alter K+ levels: InsulinGlucagon Adrenocortical hormones

cortisol and aldosteroneStress

Catecholamines & beta- adrenergic agonists Alpha-adrenergic agonists

Epinephrine has alpha & beta adrenergic properties


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Serum Potassium < 3.5 mEq/LEtiology and RF:

A. Inadequate K+ intake body does not conserve K+Debilitated, confused, restrained, lacking access

to K+ sources, malnourished, anorexic, bulimicPotassium- restricted diets or some wt.

reduction diets

( corn, potato, apple, blueberry, cranberry,

coffee, cola, gingerale, soda)Those receiving K+ free IV solns


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B. K+ excretion exceeds K+ intakeVomiting, diarrhea, suctioning, intestinal fistulae,

ileostomyOsmotic diuresis that occurs with DKASurgical clientsAlcoholic clients

Certain drugs (loop, osmotic, thiazide diuretics,cathartics, steroids)Clients who are in the healing phase after a severe

tissue injury or burnCushings syndromeDiuretic Phase of RFHyperaldosteronism


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serum K

K gradient

resting membrane potential

neuromuscular irritabilityand excitability


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GIIleus, constipation

NeuromuscularDecreased reflexes,

fatigue, weakness,paralysis

CVSCardiac arrest

ECGU wave


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Oral therapyOral KCL 1-2 g every 2-4 hrly till K is around 3.5mmol/l

Slow release K(1 tab=8mmol)

Effervescent K( 1tab = 14mmol)

IV therapyOnly for symptomatic pt and severe hypok

Around 40 mmol/l(


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serum K


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Altered resting membrane potential

Cell membrane becomes easily excitable

Increased depolarization or action potential

Repeated irritation of cell membrane

Excitation threshold of membrane

Cells become less excitable

Weak, flaccid paralysis of muscles


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GINausea/vomiting,

colic, diarrhea

Neuromuscular

Weakness, paralysis,respiratory failure

CVSArrhymthia

Cardiac arrest

ECGPeaked T waves

(early change) Flattened P wave

Prolonged PRinterval (first-degreeblock)

Widened QRScomplex

Sine wave formation Ventricular

fibrillation


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COCKTAIL regimeCation exchange

resinKalimate and

resonium AOrally

Beta agonist therapy

HD or PD


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FUNCTIONS:

catalyst (nerve impulses)stimulates muscle contractionnormal cellular permeability

blood coagulationabsorption of Vitamin B12Bones and teeth99% of the bodys Ca# is in the bones & teeth

1 % is in the tses. And IV space


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Serum Calcium < 8.4mg/dl or < 2.1 mmol/l

Etiologypancreatitis,

massive soft tissueinfections such asnecrotizing fasciitis

renal failure pancreatic and small

bowel fistulasHypoparathyroidism

abnormalities inmagnesium

tumor lysissyndrome

Hungry bonesyndrome

MalignancyProstate Ca- d/t

increasedosteoclastic activity

Clinical Manifestations:

h i


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paresthesia

ed CO

ed peristalsis and drh

Prolonged bleeding times and hemorrhage

Bones become brittle and results in pathologicfractures

Facial Twitching (Chvosteks sign)

Carpopedal spasm (Trousseaus sign)ECG changes: prolonged QT interval

Severe: seizure, tetany, hemorrhage, cardiac collapse

True level of free Ca: ionized Ca level


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Acute symptomatic10 20 ml of 10% calcium gluconate (90mg of

elemental calcium/10 ml) IV over 10 minfollowed by infusion at 0.5 2mg/kg/hr

Ca mustbe diluted in D5% or salineMaintain serum Ca between 2-2.25 mmol/l


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Long term Mx:Oral calcium supplementsDosage is 1-2 g elemental calcium daily in divided

dose

Calcium lactate 300 mg contains 39 mg ofelemental calciumCalcium carbonate contains 400mg elemental Ca

Vit DCalcitriol 0.25 mcg od and most maintained on

0.5-2 mcg/dayAlfacalcitriol-0.25-1 mcg od and slower in onset and

longer action


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Oral therapyOral KCL 1-2 g every 2-4 hrly till serum K

reaches 3.5Slow K( 1 tab = 8 mmol)

IV therapy[ ] of less than 40 mmol/l (3 g KCl)At rate of 10mmol/hr)


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In emergency, eg in cardiac arrythmias, K canbe given at the rates up to 40mmol/h(KCl3g/hr) and in [] of 200-400mmol/l (by mixing20-40 mmol/l or 1.5 3.0 g KCl in 100 cc of

saline


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Serum Calcium > 10.5mg/dl or 2.65 mmol/l

Etiology and RF: MajorCauses

Metastatic malignancy

(Tumor Lysis Syndrome)

Hyperparathyroidism

Thiazide diuretic therapy

Other Causes:Excessive intake of

Ca supplements w/vit. D, Ca containing

antacidsProlongedimmobilization

Metabolic acidosisHypophosphatemia


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Sign and symptoms of hypercalcemia

GI Anorexia, nausea/vomiting,abdominal pain, constipation

Neuromuscular Weakness, confusion, coma, bonepain,depression,

Renal polyuria and polydipsia as kidneys

lose their ability to concentrate

CVS hypertension, cardiac arrhythmias

ECG Shortened QT interval

Prolonged PR and QRS intervalsIncreased QRS voltage T-waveflattening and widening AV block(can progress to complete heartblock, then cardiac arrest withsevere hypercalcemia)


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BiphosphonatesTreatment of choice in hypercalcemia of

malignancy

Oral phosphate(1-3g/day)

Reduces Ca absorption as long as phosphatelevel is < 1.3mmol/l

Dialysis


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Is a special group of H+ containingsubstances that dissociate/separated

When in solution can released free H+ andanions

Strong acid tends to dissociate. Eg: HCl

Weak acid not easy to get dissociate.Eg:H2Co3


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Substance that can combine with a free H+and thus, remove it from the solution

Strong base can bindbetter than H+ thanweak base.


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pH7.35 - 7.45a measurement of acidity or alkalinity, based

on the hydrogen (H+) ions present.

PaO280 to 100 mm HgThe partial pressure of oxygen that is dissolved

in arterial blood

New Born Acceptable range 40-70 mm Hg


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Base excess

2 to +2 mEq/literindicates the amount of excess or insufficient

level of bicarbonate in the system.A negative base excess indicates a base deficit

in the blood. A negative base excess isequivalent to an acid excess.The base excess is defined as the amount of H+

ions that would be required to return the pH ofthe blood to 7.35 if the pCO2 were adjusted tonormal.


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Changes in [H+] influence in K+ levelIn acidosis, there will decreased K+ secretion,

thus, leading to hyperK+In alkalosis, there will be increased in K+

secretion, thus, leading to hypoK+


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Chemical buffer systemRespiratory mechanism

Renal mechanism


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1st

line defenseIs a mixture in a solution of 2 chemical

compunds that minimize pH changes

Consists a pair of substance involved in a

reversible reactionEg: H2CO3 H+ (+) HCO3


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Body has 4 buffer systemCarbonic acid:bicarbonate buffer systemProtein buffer systemHemoglobin buffer system

Phosphate buffer system


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2nd line defense

Regulate [H+] by controlling the rate of CO2removal

Ability to alter pulmonary ventilation

Arterial [H+] increased d/t metabolic causes

Respiratory centre stimulate to increased pulventilation

Thus , decreased CO2


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In metabolic acidosis, PC detect increased [H+]

Stimulate respiratory centre to step up

ventilation

Decreased CO2

In response to decreased CO2, CC inhibitsrespiratory centre


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3rd line defense

Compensation does not begin for at least 6hours and continues for several daysH+ excretionHCO3 excretion

Increased urinary excretion of NH4+ (H++ NH

3+ =

NH4+).


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During alkalosis,Decreased secretion and decreased excretion

of H+ in urineIncomplete reabsorption of filtered HCO3

During acidosis, increased secretion andsubsequent increased excretion of H+ in theurineReabsorption of all filtered bicarbonate


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d/t abnormal CO2 retention(hypoventilation)

Causes

Narcotics

Pulmonary Secretions

Atelectasis

Mucus plugPneumonia

Pleural effusion

Pain from abdominal orthoracic injuries or incisions

Limited diaphragmaticexcursion from intra-abdominal pathology

Ascites

Abdominal

compartment


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Compensation :Chemical buffers take up additional H+Resp mech cant respondKidneys MOST IMPORTANT

Conserved all filtered HCO3 and add new HCO3 tothe plasma and excreting H+


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Treatment :Treat underlying causemay entail patient-initiated volume expansion

or noninvasive (bilevel positive airway pressure;

BIPAP) or invasive (endotracheal intubation)ventilation strategies.


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increased intake of acids, an increasedgeneration of acids, or an increased loss ofbicarbonate


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Increased AnionGap MetabolicAcidosisExogenous acid

ingestion SalicylateMethanol

Endogenous acidproduction

KetoacidosisLactic acidosis

Renal insufficiency

Normal Anion GapGastrointestinal

losses (diarrhea,fistulas)

Renal tubularacidosis

Potassium sparingdiuretics

Resolving DKA


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Compensation :Chemical buffer: take up H+Resp : Increasing ventilation (Kussmaul

respirations)

Kidneys: Increasing renal reabsorption and generation of

bicarbonateincrease secretion of hydrogen and thus increase

urinary excretion of NH4+ (H++ NH

3+ = NH

4+)


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administration of bicarbonate is controversial.1. The overzealous administration of

bicarbonate can lead to metabolic alkalosis,which shifts the oxyhemoglobin dissociation

curve to the left, interfering with oxygenunloading at the tissue level, and can beassociated with arrhythmias that are difficultto treat.


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2. exacerbate intracellular acidosis bicarbonate can combine with the excess H+ to

form carbonic acid, which is then converted toCO

2and water, thus raising the PCO

2.

CO2 can diffuse into cells, but bicarbonate

remains extracellular

worsening intracellular acidosis


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Causes

Increased Bicarbonate Generation


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Increased Bicarbonate Generation

1. Chloride losing (urinary chloride greater than 20mEq/L)

Mineralocorticoid excess

Profound potassium depletion

2. Chloride sparing (urinary chloride less than 20mEq/L)

Loss from gastric secretions (emesis or nasogastricsuction)

Diuretics

3. Excess administration of alkali

Acetate in parenteral nutrition

Citrate in blood transfusions

Antacids

Bicarbonate

Impaired Bicarbonate Excretion

1. Decreased GFR


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Compensation :Chemical buffer: liberates H+Resp : increased ventilationKidneys:conserve H+ and excrete excess HCO3

in urineHydrogen ion reabsorption also ensues with an

accompanied potassium ion excretionresulting hypokalemia


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Treatmentreplacement of the volume deficit with isotonic

saline and potassium once adequate urineoutput is ensured


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Decreased CO2As a result of

hyperventilation

Causes

FeverPainDrugs such as

salicylates

thyrotoxicosis

meningitis


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Acute hypocapnia can cause an uptake ofpotassium and phosphate into cells andincreased binding of calcium to albumin,leading to symptomatic hypokalemia,

hypophosphatemia, and hypocalcemia, withsubsequent arrhythmias, paresthesias, musclecramps, and seizures.

Treatment treat underlying cause


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Fluid and Electrolyte and Acid-base Imbalance New Recovered]

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