kuliolektrolit Dan Keseimbangan Asam Basa

7/28/2019 kuliolektrolit Dan Keseimbangan Asam Basa

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Keseimbangan cairan, asam danbasa dan elektrolit


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Fungsi Air dalam Fisiologi

Manusia1. Media semua reaksi kimia tubuh

2. Berperan dalam pengaturan distribusi kimia &biolistrik dalam sel

3. Alat transport hormon & nutrien4. Membawa O2 dari paru-paru ke sel tubuh

5. Membawa CO2 dari sel ke paru-paru

6. Mengencerkan zat toksik dan waste productsertamembawanya ke ginjal dan hati

7. Distribusi panas ke seluruh tubuh


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Distribusi Cairan Tubuh

Volume cairan tubuh- wanita (17-39 th) : 50% BB- pria (17-39 th): 60% BB

Distribusi cairan tubuh- cairan intrasel (CIS) = 2/3 cairan tubuh- cairan ekstrasel (CES) = 1/3 cairan tubuh

* intravaskular (plasma) = 25% CES* intersisial = 75% CES


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Komposisi Ion pd Cairan Tubuh


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Perpindahan Cairan &

Elektrolit1. Difusiperpindahan molekul dari tekanan/konsentrasi tinggi ketekanan/konsentrasi rendah

2. Osmosis

perpindahan air dari konsentrasi zat terlarut rendah kekonsentrasi zat terlarut tinggiosmolaritas: ukuran konsentrasi suatu larutan- isotonus konsentrasi larutan = plasma darah

3. Transport aktifperpindahan molekul dari tekanan/konsentrasi rendah kekonsntrasi tinggi dgn menggunakan energi


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Tekanan Cairan

1. Tekanan osmotik & onkotikTekanan osmotik: tekanan untuk mencegah aliranosmotik cairan

Tekanan onkotik: gaya tarik s/ koloid agar air tetapberada dalam plasma darah di intravaskular

2. Tekanan hidrostatik (filtration force)tekanan yang digunakan oleh air dalam sistemtertutup


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Perpindahan cairan di

kapiler


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Selektivitas Permeabilitas

Membran Membran sel

lipid bilayer

Permeabilitas membran sel bersifat selektifterhadap: ion (kanal ion), air (aquaporin)


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PENGATURAN VOLUME CAIRAN

EKSTRASEL


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Peranan ginjal


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Filtrasi, Reabsorpsi, Sekresi &

Ekskresi di Nefron


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Respons thd Peningkatan Tekanan Darah


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Respons thd Penurunan Tekanan Darah


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Peranan Atriopeptin


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Peranan Renin-Angiotensin-Aldosteron


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Respons thd Asupan Garam


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PENGATURAN OSMOLARITAS CAIRANEKSTRASEL


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Perubahan osmolaritas di

Nefron


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Peranan Vasopresin


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Mekanisme Kerja Vasopresin/ADH


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Perubahan Volume & Osmolaritas Cairan


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Faktor-faktor yang mempengaruhi

Keseimbangan Cairan &

Elektrolit

Umur

Suhu lingkungan Diet

Stres

Penyakit


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Keseimbangan Asam & Basa

Keseimbangan asam-basa pengaturankonsentrasi ion H+ dalam cairan tubuh

Ion H

+

sbg hasil dari metabolisme:C6H12O6 + O2CO2 + H2OH2CO3H+ + HCO3-

[H+] dlm plasma pH plasma darah = 7,4

Sistem dapar (buffer) menghambatperubahan pH yang besar jika adapenambahan asam atau basa


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Sistem Dapar

1. Asam karbonat:Bikarbonat

sistem dapar di CES untuk asam non-karbonat

2. Protein

sistem dapar di CIS & CES

3. Hemoglobin

sistem dapar di eritrosit untuk asam karbonat

4. Phosphat

sistem dapar di ginjal dan CIS


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Keseimbangan ion H+


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Mekanisme Regulasi Keseimbangan

Asam-Basa

Sistem dapar hanya mengatasi ketidakseimbanganasam-basa sementara

Ginjal: meregulasi keseimbangan ion H+

denganmenghilangkan ketidakseimbangan kadar H+ secaralambat; terdapat sistem dapar fosfat & amonia

Paru-paru: berespons scr cepat thd perubahan kadarH+ dalam darah & mempertahankan kadarnya

sampai ginjal menhilangkan ketidakseimbangantersebut


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Regulasi Pernapasan dlm

Keseimbangan Asam-Basa

Kadar CO2 meningkat pH menurun

Kadar CO2 menurun pH meningkat

Kadar CO2 & pH merangsang kemoreseptoryg kemudian akan mempengaruhi pusatpernapasan hipoventilasi meningkatkan kadar CO2

dlm darah hiperventilasi menurunkan kadar CO2dlm darah


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Regulasi Pernapasan dlm



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Regulasi Ginjal dlm


Sekresi H+ ke dalam filtrat & reabsorpsiHCO3- ke CES menyebabkan pH ekstraselmeningkat

HCO3- di dlm filtrat diabsorbsi

Laju sekresi H+ meningkat akibat penurunanpH cairan tubuh atau peningkatan kadar

aldosteron

Sekresi H+ dihambat jika pH urin < 4,5


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Gangguan Keseimbangan

Asam-Basa1. Asidosis respiratori

hipoventilasi retensi CO2H2CO3H+

2. Alkalosis respiratori

hiperventilasiCO2 banyak yg hilangH2CO3H+

3. Asidosis metabolik

Diare, DMHCO3-PCO2H

+

4. Alkalosis metabolik

muntahH+HCO3-PCO2


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Kompensasi Sistem Pernafasan

terhadap Asidosis Metabolik


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Kompensasi Ginjal terhadap

Asidosis Respiratorik


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Nomogram Davenport


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INTERPRETASI AGD

Lihat pH darah

pH < 7,35 pH > 7,45

ASIDOSISALKALOSIS

Lihat pCO2 Lihat HCO3-

< 40mmHg > 40 mmHg < 24 mM > 24 mM

METABOLIKRESPIRATORIKRESPIRATORIKMETABOLIK


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TERKOMPENSASI atau TIDAK?

Lihat pH kembali- jika mendekati kadar normal (7,35-7,45) terkompensasi

- jika belum mendekati normal tidak terkompensasi atau terkompensasi

sebagian

Jika asidosis respiratorik dgn HCO3-

< 24 mM

terkompensasi sebagian

Jika asidosis metabolik dgn pCO2 < 40 mmHg


Jika alkalosis respiratorik dgn HCO3- > 24 mM

terkompensasi sebagian Jika alkalosis metabolik dgn pCO2 > 40 mmHg



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GANGGUAN ELEKTROLIT

Dr. SUHAEMI, SpPD, Finasim


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Electrolyte and protein anion concentrations in plasma,


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Electrolyte and protein anion concentrations in plasma,

interstitial fluid, & intercellular fluid


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Electrolytes

sodium (Na+

) potassium (K+)

chloride (Cl-)

calcium (Ca2+)

magnesium (Mg2+)

bicarbonate (HCO3-

) phosphate (PO4

2-)

sulfate (SO42-)


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Korey Stringer

1974 - 2001

Korey Stringer was a professional football player forthe Minnesota Vikings. He collapsed during practicefrom excessive heat and died the following day.


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Electrolytes

Charged particles in solution

Cations (+)

Anions (-)

Integral part of metabolic and cellularprocesses


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Positive or Negative?

Cations (+)

Sodium Potassium

Calcium

Magnesium

Anions (-)

Chloride Bicarbonate

Phosphate

Sulfate


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Major Cations

EXTRACELLULAR

SODIUM (Na+)

INTRACELLULAR

POTASSIUM (K+)


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Electrolyte Imbalances

Hyponatremia/

hypernatremia

Hypokalemia/

Hyperkalemia

Hypomagnesemia/

Hypermagnesemia

Hypocalcemia/

Hypercalcemia Hypophosphatemia/

Hyperphosphatemia

Hypochloremia/

Hyperchloremia


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Sodium

Major extracellular cation

Attracts fluid and helps preserve fluid volume

Combines with chloride and bicarbonate to help

regulate acid-base balance

Normal range of serum sodium 135 - 145 mEq/L


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Sodium and Water

If sodium intake suddenly increases,extracellular fluid concentration also rises

Increased serum Na+ increases thirst and therelease of ADH, which triggers kidneys toretain water

Aldosterone also has a function in water andsodium conservation when serum Na+ levelsare low


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Sodium-Potassium Pump

Sodium (abundantoutside cells) tries to

get into cells

Potassium (abundant

inside cells) tries to get

out of cells

Sodium-potassiumpump maintains

normal concentrations

Pump uses ATP,magnesium and anenzyme to maintain

sodium-potassiumconcentrations

Pump prevents cellswelling and creates

an electrical chargeallowingneuromuscularimpulse transmission

k l i


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Hypokalemia

Usually secondary to: GI loss (vomiting, diarrhea) Urinary losses (diuretics, RTA)

Also think about : co-existing electrolyte abnormality

(hypomagnesemia), hyperaldosteronism, insulin therapy,albuterol, alkalosis)

Indications for replacement: Evidence of potassium loss

Significant deficit in body potassium

Acute therapy in redistributive disorders (periodicparalysis, thyrotoxicosis)

k l i


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Hypokalemia

Symptoms: usually manifest when serum K


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Therapy

Calculate potassium deficit (if normal distribution is present-

do NOT use in DKA or HONK)

Acute: .27meq/L decrease in serum K+ for every 100meq reduction in totalpotassium stores

Chronic: 1meq/L decrease in serum K+ for every 200-400meq reduction in

total potassium stores

Simplified:

Goal K Serum K x 100 = total meq K required

serum Cr

10meq of KCL will raise the serum K by ~.1meq/L

Formulations


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Formulations

Potassium Chloride : PREFERRED AGENT

Most patients with hypokalemia and acidosis are also chloridedepleted

Raises serum potassium at a faster rate

Available as salt substitute, liquid, slow release tablet or capsule, andIV

Oral: 40meq tid-qid; IV: Peripheral line 10meq/hr

Central line 20meq/hr

Potassium Bicarbonate/Citrate/Acetate: can be used in patients with hypokalemia and metabolic acidosis

Potassium Phosphate: Rarely used (Fanconi syndrome with phosphate wasting)

Example


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Example 72 year old female admitted for weakness and dehydration

due to acute gastroenteritis. She is having up to 6 BM/day.

Her serum K on admission is 2.5 meq and serum Cr is 2.0. EKGreveals u-waves.

1. How much potassium do you order?4-2.5 x 100 = 75meq

2

2. What formulation do you choose?

KCL; if bicarb is low then consider potassium bicarb or acetate

3. What route should the potassium be administered? 40meq(initial) oral and 40meq IV; (re-assess 2-4 hours later and give more

orally if needed and tolerating po)4. Serum potassium remains low, what else could be

contributing?

Low magnesium, ongoing diarrhea

H i


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Hypomagnesemia

Average daily intake: 360mg

Presence of low magnesium (nearly 12% of hospitalizedpatients) suspected in following cases: Chronic diarrhea

Hypocalcemia

Refractory hypokalemia

Ventricular arrhythmias

Symptoms/Signs : Tetany (seizures in children/neonates)

Hypokalemia

Hypoparathyroidism hypocalcemia (


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What Do You See?

CNS

Altered LOC

Confusion

Hallucinations


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What Do You See?

Neuromuscular

Muscle weakness

Leg/foot cramps

Hyper DTRs

Tetany

Chvosteks & Trousseaus signs


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What Do You See?

Cardiovascular

Tachycardia

Hypertension

EKG changes


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What Do You See?

Gastrointestinal

Dysphagia

Anorexia

Nausea/vomiting

Therapy


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Therapy IV if symptomatic (magnesium sulfate)

1.5-1.9mg/dL 2g magnesium sulfate IV

1.2-1.4mg/dL4g .8-1.1mg/dL 6g


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Therapy

Goal of therapy: maintain plasma magnesium concentration over 1.0mg/dL acutely in

symptomatic patients

In cardiac patients, maintain Mg >1.7 (usually goal 2.0mg/dL) to avoidarrhythmias

Serum levels are poor reflection of actual body stores (mostlyintracellular) so aim for high-normal serum level

Adverse effects: Abrupt elevation of plasma Mg can remove the stimulus for Mg

retention and lead to increased excretion

Diarrhea

Drug interactions

Magnesium intoxication, Aluminum intoxication


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Mag Sulfate Infusion

Use infusion pump - no faster than 150mg/min

Monitor vital signs for hypotension and

respiratory distress

Monitor serum Mg++ level q6h

Cardiac monitoring

Calcium gluconate as an antidote foroverdosage

Hypocalcemia


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Hypocalcemia

Clinical Manifestations: Acute: serum Ca


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Therapy Correct for albumin

Ca lower by .8mg/dL for every 1g/dL reduction in serum albumin

or check ionized calcium Level can be altered by acid/base disturbance

Symptomatic or acute serum Ca 7.5mg/dL or chronic: Oral therapy: calcium carbonate or citrate 1-2g/day (500mg bid-

qid)

Add Vitamin D in following cases: Hypoparathyroidism: Vitamin D (Calcitriol .25-.5mcg bid)

Vitamin D deficiency: 50,000IU/week for 6-8 weeks then 800-1000IUdaily

Erogcalciferol (D3)

Cholecalciferol (D2)

Therapy


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Therapy

Goals of therapy:

Treat and prevent manifestations of hypocalcemia In hypoparathyroidism: to raise serum Ca to low-normal range (8.0-

8.5mg/dL)

Adverse Effects: Rapid infusion- bradycardia, hypotension

Extravasation- tissue necrosis

Hypercalcemia

Hypercalciuria Constipation

Hypophosphatemia

Milk-alkali syndrome

Example


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Example

35 y/o male with hypoparathyroidism secondary to DiGeorges

presents with serum Ca of 6.2, albumin of 3.8, ionized Ca .77. Hassome mild muscle cramps, otherwise asymptomatic.

1. How do you initially treat his hypocalcemia?

- IV Calcium Gluconate 1g IV over 10-20min2. Repeat serum Ca is 6.6, how do you proceed with treatment?

-start Calcium gluconate 1mg/mL in D5W 50mL/hr infusion

2. After initial treatment, what maintenance regimen should you

initiate?-Calcitriol (.5mcg bid, titrated up in this patient)

-Calcium carbonate (1950mg po tid in this patient)

Preferred Route PreferredFormulation

Dosage Response


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Formulation

Potassium Oral PotassiumChloride

10meq tabs .1 increaseserum K for

10meq given

Magnesium Oral

IV- arrhythmia

MagnesiumOxide

Magnesium

Sulfate

2-4 tabs/day(420mg; 20meq/tab)

2g IVP or slow

infusion

.5 increase for2g (50meq) IV

Calcium IV- acute

Oral- maintenance

CalciumGluconate

CalciumCarbonate

1-2amp (rapid)

1mg/mL in D5W,50mL/hr Infusion

1-2g/day

.5mg/dLincrease serumCa for 1g given

Phosphate Oral SodiumPhosphate(neutra-phos)

1-2 packet tid-qid1packet=250mg or

8mmol

(weight based)

1.2mg/dLincrease serumPO4


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Electrolyte Imbalances

Electrolyte Normal range

(mmol / L)

Excess Defiency

Sodium

Na+

135 - 145 Hypernatremia(increased urine excretion;

excess water loss)

Hyponatremia

(dehydration; diabetes-

related low blood pH;

vomiting, diarrhea)

Potassium

K+3.5 5.0 Hyperkalemia

(renal failure, low blood pH)

Hypokalemia

(gastointestinal conditions)

Hydrogen carbonate

HCO3-

24 - 30 Hypercapina(high blood pH;

hypoventilation)

Hypocapnia

(low blood pH; hyper-

ventilation; dehydration)

Chloride

Cl-100 - 106 Hyperchloremia

(anemia, heart conditions,

dehydration)

Hypochloremia

(acute infections; burns;

hypoventilation)


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Regulation of Sodium

Renal tubule reabsorption affected byhormones:

Aldosterone

Renin/angiotensin

Atrial Natriuretic Peptide (ANP)

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Electrolyte imbalances:

Sodium

Hypernatremia (high levels of sodium)

Plasma Na+ > 145 mEq / L

Due to Na + or water Water moves from ICF ECF

Cells dehydrate

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77

Hypernatremia Due to:


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Hypernatremia Due to:

Hypertonic IV soln.

Oversecretion of aldosterone Loss of pure water

Long term sweating with chronic fever

Respiratory infection water vapor loss

Diabetes polyuria

Insufficient intake of water (hypodipsia)

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Clinical manifestations

of Hypernatremia

Thirst

Lethargy

Neurological dysfunction due to dehydrationof brain cells

Decreased vascular volume

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Treatment of Hypernatremia

Lower serum Na+

Isotonic salt-free IV fluid

Oral solutions preferable

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Hyponatremia


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Overall decrease in Na+ in ECF

Two types: depletional and dilutional Depletional Hyponatremia

Na+ loss:

diuretics, chronic vomiting Chronic diarrhea

Decreased aldosterone

Decreased Na+ intake

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Dilutional Hyponatremia:


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Dilutional Hyponatremia:

Renal dysfunction with intake of hypotonic fluids

Excessive sweating increased thirst intake ofexcessive amounts of pure water

Syndrome of Inappropriate ADH (SIADH) or oliguricrenal failure, severe congestive heart failure, cirrhosis

all lead to: Impaired renal excretion of water

Hyperglycemia attracts water

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Cli i l if t ti f


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Clinical manifestations of

Hyponatremia Neurological symptoms

Lethargy, headache, confusion, apprehension, depressedreflexes, seizures and coma

Muscle symptoms Cramps, weakness, fatigue

Gastrointestinal symptoms

Nausea, vomiting, abdominal cramps, and diarrhea

Tx limit water intake or discontinue meds

83

h ?


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What Do You See?

Think S-A-L-T

Skin flushed

Agitation

Low grade fever

Thirst

Neurological symptoms

Signs of hypovolemia

Wh t D W D ?


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What Do We Do?

Correct underlyingdisorder

Gradual fluidreplacement

Monitor for s/s ofcerebral edema

Monitor serum Na+level

Seizure precautions

H k l i


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Hypokalemia

Serum K+ < 3.5 mEq /L

Beware if diabetic

Insulin gets K+

into cell Ketoacidosis H+ replaces K+, which is

lost in urine

adrenergic drugs or epinephrine

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C f H k l i


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Causes of Hypokalemia

Decreased intake of K+

Increased K+ loss

Chronic diuretics Acid/base imbalance

Trauma and stress

Increased aldosterone Redistribution between ICF and ECF

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Clinical manifestations of


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Hypokalemia

Neuromuscular disorders Weakness, flaccid paralysis, respiratory

arrest, constipation

Dysrhythmias, appearance of U wave

Postural hypotension

Cardiac arrest

Others table 6-5

Treatment- Increase K+ intake, but slowly, preferably by foods

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Wh t D Y S ?


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What Do You See?

Think S-U-C-T-I-O-N

Skeletal muscle weakness

U wave (EKG changes) Constipation, ileus

Toxicity of digitalis glycosides

Irregular, weak pulse

Orthostatic hypotension

Numbness (paresthesias)

Wh t D W D ?


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What Do We Do?

Increase dietary K+

Oral KCl supplements

IV K+ replacement

Change to K+-sparing diuretic

Monitor EKG changes

IV K R l t


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IV K+ Replacement

Mix well whenadding to an IVsolution bag

Concentrationsshould not exceed40-60 mEq/L

Rates usually 10-20mEq/hr

NEVER GIVE IV PUSHPOTASSIUM

Hypocalcemia


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Hyperactive neuromuscular reflexes and tetanydifferentiate it from hypercalcemia

Convulsions in severe cases

Caused by:

Renal failure

Lack of vitamin D

Suppression of parathyroid function

Hypersecretion of calcitonin

Malabsorption states Abnormal intestinal acidity and acid/ base bal.

Widespread infection or peritoneal inflammation

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Hypocalcemia


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Hypocalcemia

Diagnosis:

Chvosteks sign

Trousseaus sign

Treatment

IV calcium for acute Oral calcium and vitamin D for chronic

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Hyperkalemia


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Hyperkalemia

Serum K+ > 5 mEq/L

Less common than

hypokalemia

Caused by altered

kidney function,

increased intake (salt

substitutes), blood

transfusions, meds (K+-

sparing diuretics), cell

death (trauma)

What Do You See?


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What Do You See?

Irritability

Paresthesia

Muscle weakness (especially legs)

EKG changes (tented T wave)

Irregular pulse

Hypotension Nausea, abdominal cramps, diarrhea

What Do We Do?


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What Do We Do?

Mild

Loop diuretics (Lasix)

Dietary restriction

Moderate

Kayexalate

Emergency

10% calcium gluconate

for cardiac effects Sodium bicarbonate for

acidosis

Electrolytes


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Electrolytes

water, sucrose syrup, glucose-fructose syrup, citric acid, naturaland artificial flavors, salt, sodiumcitrate, monopotassium phosphate,ester gum, sucrose acetateisobutyrate, red 40, blue 1

Per 8 fl oz

Total fat 0gSodium 110mgPotassium 30mgTotal carbs 14g

water, dextrose, potassium citrate,sodium chloride and sodium

citrate. Nonmedicinal ingredients:FD&C Blue #1 and Red #40 (grapeflavor) and FD&C Red #40(bubblegum flavor).

Per 8 fl oz

Sodium 10.6 mgPotassium 4.7mgChloride 8.3 mgDextrose 5.9g

kuliolektrolit Dan Keseimbangan Asam Basa

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