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    Keseimbangan Elektrolit Dan Asam Basa: Dr. Satriawan Abadi, SP - Pd-Kic

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    This document discusses electrolyte imbalances, specifically focusing on potassium (kalium) levels. It defines hypokalemia as a potassium level below 3.5 mEq/L and hyperkalemia as above 5 mEq/L. Symptoms of hypokalemia include ECG changes and muscle weakness, while hyperkalemia symptoms include peaked T waves on ECG and potentially fatal arrhythmias. The document provides guidelines for treating electrolyte imbalances and restoring normal potassium levels.

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    Keseimbangan Elektrolit Dan Asam Basa: Dr. Satriawan Abadi, SP - Pd-Kic

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    drroytambunan
    48 views79 pages
    This document discusses electrolyte imbalances, specifically focusing on potassium (kalium) levels. It defines hypokalemia as a potassium level below 3.5 mEq/L and hyperkalemia as above 5 mEq/L. Symptoms of hypokalemia include ECG changes and muscle weakness, while hyperkalemia symptoms include peaked T waves on ECG and potentially fatal arrhythmias. The document provides guidelines for treating electrolyte imbalances and restoring normal potassium levels.

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    This document discusses electrolyte imbalances, specifically focusing on potassium (kalium) levels. It defines hypokalemia as a potassium level below 3.5 mEq/L and hyperkalemia as above 5 mEq/L. Symptoms of hypokalemia include ECG changes and muscle weakness, while hyperkalemia symptoms include peaked T waves on ECG and potentially fatal arrhythmias. The document provides guidelines for treating electrolyte imbalances and restoring normal potassium levels.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    48 views79 pages

    Keseimbangan Elektrolit Dan Asam Basa: Dr. Satriawan Abadi, SP - Pd-Kic

    Uploaded by

    drroytambunan
    This document discusses electrolyte imbalances, specifically focusing on potassium (kalium) levels. It defines hypokalemia as a potassium level below 3.5 mEq/L and hyperkalemia as above 5 mEq/L. Symptoms of hypokalemia include ECG changes and muscle weakness, while hyperkalemia symptoms include peaked T waves on ECG and potentially fatal arrhythmias. The document provides guidelines for treating electrolyte imbalances and restoring normal potassium levels.

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    © All Rights Reserved
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    of 79

    KESEIMBANGAN ELEKTROLIT

    DAN ASAM BASA

    Dr. SATRIAWAN ABADI, Sp.PD-KIC


    Regulating Electrolytes
    • Sodium
    • Potassium
    • Calcium
    • Magnesium
    • Chloride
    • Phosphate
    • Bicarbonate
    Composition of Body Fluids
    Electrolyte Imbalances
    • Hyponatremia
    • Hypomagnesemia
    • Hypernatremia
    • Hypermagnesemia
    • Hypokalemia
    • Hypochloremia
    • Hyperkalemia
    • Hyperchloremia
    • Hypocalcemia
    • Hypophosphatemia
    • Hypercalcemia
    • Hyperphosphatemia
    S S IU M
    POTA
    What is kalemia?

    • The presence of potassium in the


    blood

    • Normal range: 3.5 – 5 mEq/L

    • Hypokalemia = low levels of


    potassium, deficient potassium

    • Hyperkalemia = high levels of


    potassium, excess potassium
    functions
    Regulates neuromuscular excitability and muscle contraction

    Needed for glycogen formation and protein sunthesis

    Correction of acid base imbalances. Potassium ion can be


    exchanged with hydrogen ion (H+)
    Acid Base Status
    Alkalemia promotes K+ uptake by cells
    Acidemia diminishes K+ uptake by cells

    H+ K+

    K+ H+

    ACIDOSIS ALKALOSIS
    An oversimplification in acidosis
    Hypokalemia

    Hyperkalemia
    HYPERKALEMIA

    Potassium level more


    than 5.5 mEq/L
    Hyperkalemia
    Serum Potassium
    concentration > 5 mEq/L
    Results from

    • Mnemonic = AIDS

    • Acidosis – Metabolic acidosis: bicarbonate is low, pH become acidic

    low blood pH causes H+ to go into the cell and cause lysis so that it releases its potassium
    content into the blood stream

    K+ leaking out to ECF -> hyperkalemia

    • Insulin Deficiency – normally insulin binds to the Na+ / K+ pump that causes K+ to flow into
    the cell and Na+ out of the cell.

    when insulin can’t bind, K+ can’t flow into the cell, and stays outside

    K+ in the ECF -> hyperkalemia


    Hyperkalemia
    Serum Potassium concentration >
    5 mEq/L
    Results from
    • Drugs

    1. Digitalis or Digoxin: competes with K+ at the Na+ / K+ pump

    Takes the place of K+,


    decreasing cellular K+ and making it stay outside of the cell

    K+ in the ECF -> hyperkalemia


    Hyperkalemia
    Serum Potassium concentration >
    5 mEq/L
    Results from
    • Drugs

    2. Succinylcholine: causes up-regulation of nicotinic


    acetylcholine receptors on the muscle membrane

    up-regulation causes the amount of receptors to increase,


    resulting in K+ efflux into the plasma

    3. Beta blockers: take the place of beta agonists

    stop activation of cyclicAMP, then protein kinase, and then phosphorylation of the the
    sodium potassium ATPase pump

    Can’t pump out K+, so K+ stays outside of the cell

    K+ in the ECF -> hyperkalemia


    Hyperkalemia
    Serum Potassium concentration >
    5 mEq/L
    Clinical Manifestations
    1. ECG

    - Early: Increased T wave amplitude or peaked T waves. Middle: Prolonged PR interval and
    QRS duration, atrioventricular conduction delay, loss of P waves.

    - Late: Progressive widening on QRS complex and merging with T wave to produce sine wave
    pattern.
    ECG changes
    • Tall Peaked T waves (K 6.5)

    • Prolonged PR, Flat or absent P waves(K


    7.5)
    ECG CHANGES
    • Widened QRS (>0.12 Sec) ,

    • Sine wave pattern(S and T waves merging)


    (K 8.5)
    ECG CHANGES

    • Bradycardia, Ventricular Tachycardia (K


    9.0)
    Hyperkalemia
    management
    • Immediately discontinue any IV potassium
    containing fluid/any drugs that may cause
    hyperkalemia.
    HYPOKALEMIA

    Potassium level less


    than 3.5 mEq/L
    Hypokalemia

    Increased loss
    Redistribution
    Decreased intake
    into cells
    Renal Extra renal
    PATHOPHYSIOLOGY OF HYPOKALEMIA

    = Action Potential

    Nerve and Muscle Activity

    Increase in The cell


    Low becomes
    resting
    Extracellular less
    membrane
    K+ excitable
    potential
    Hypokalemia
    Clinical Manifestations Serum Potassium concentration <
    3.5 mEq/L
    1. ECG

    - Early: Flat or inverted T wave, Prominent U wave, DT segment depression, prolonged


    QU interval.

    - Late: Prolonged PR interval, decreased voltage and widening of QRS interval,


    increased risk of ventricular dysrhythmias.
    Hypokalemia

    • Defined as plasma concentration of K+ < 3.5 mEq/L

    • Mild Hypokalemia : 3.0 – 3.5 mEq/L : asymptomatic

    • Moderate Hypokalemia < 3.0 mEq/L : symptomatic

    • Severe Hypokalemia <2.5 mEq/L

    Clinical manifestations of hypokalemia vary greatly between


    individual patients &
    their severity depends on degree of hypokalemia
    Hypokalemia
    We need more Serum Potassium concentration <
    potassium!!! 3.5 mEq/L
    Treatment goals
    • Prevent hypokalemia
    • Correct hypokalemia
    • Prevent complications
    • Minimize losses
    • Correct underlying etiology
    IV KCl Therapy
     Reserved for symptomatic and severe cases

     Common Guidelines

    – Continuous ECG monitoring

    – Avoid till urine output is established

    – Don’t give > 10- 20 mEq/L/ hour (typically 0.5mEq/kg/hr)

    ( 10ml of 15% KCL – 20 mEq/L)

    – Don’t give > 40 mEq/L

    – Don’t give more than 240mEq/ day


    Approach to Hypokalemia
    • Step 1: Redistribution or depletion?
    – Redistribution causes
    • Insulin therapy - DKA
    • Beta 2 agonists - Salbutomol
    • Metabolic alkalosis
    • Beta 2 adrenergic stimulation – AMI
    •  cell proliferation – Rx of megaloblastic anemia
    • Barium poisoining
    – Replacement of potassium in these settings may lead to
    overshoot & hyperkalemia
    Approach to Hypokalemia
    • Step 1: Redistribution or depletion?
    – Depletion causes (common)
    • GI tract losses (diarrhea, vomiting)
    • Loop/thiazide diuretic therapy
    • Other medications (e.g. amphotericin B)
    • Osmotic diuresis (DKA)
    • Refeeding syndrome (NEVER underestimate!)
    • Endocrinopathies (mineralocorticoid excess)
    • Salt wasting nephropathies/RTA’s
    • Magnesium deficiency (NEVER overlook!)
    Approach to Hypokalemia
    • Step 2: Estimate the deficit
    – For every 100 mEq below normal, serum K+ usually
    drops by 0.3 mEq/L
    • Highly variable from patient to patient, however!!
    Treatment
    • K deficit= (desired k- actual k) x 100%
    0.27

    • Estimation of K+ deficit
    – 3.0 meq/L= total body K+ deficit of 200-400
    meq/70kg
    – 2.5 meq/L = 500 meq/70kg
    – 2.0 meq/L = 700 meq/70kg
    Approach to Hypokalemia
    • Step 3: Choose route to replace K+
    – In nearly all situations, ORAL replacement is
    PREFERRED over IV replacement
    • Oral is quicker
    • Oral has less side effects (IV burns!)
    • Oral is less dangerous
    – Choose IV therapy ONLY in patients who are NPO
    (for whatever reason) or who have severe
    depletion
    Approach to Hypokalemia
    • Step 4: Choose K+ preparation
    – Oral therapy
    • Potassium Chloride is PREFERRED AGENT
    – Especially useful in Cl-responsive metabolic alkalosis
    –  in ECF K quicker with KCl compared to other salts
    • Potassium Phosphate useful when coexistant phosphorus
    deficiency
    – Often useful in DKA patients
    • Potassium bicarbonate, acetate, gluconate, or citrate
    useful in metabolic acidosis

    ORAL POTTASIUM CHLORIDE SOLUTION


    15 ML  20 mEq/L
    Approach to Hypokalemia
    • Step 4 (con’t): Choose K+ prep
    – IV therapy
    • Adjunct to maintenance fluids (10-20 mEq/L)
    – “The surgical intern’s way”
    – Try to avoid using it!!!
    » you often forget it’s there
    » hyperkalemia can then develop, especially in patients that get ARF
    in the hospital
    • IV rider/”piggyback”
    – Generally 40-60 mEq
    – KCl is PREFERRED AGENT again
    – Avoid dextrose solution (trigger insulin, shift K +)

    IV 15%POTTASIUM CHLORIDE 1ml  2 mEq/L


    10 ml  20 mEq/L
    Approach to Hypokalemia

    • Step 5: Choose dose/timing


    – Mild/moderate hypokalemia
    • 3.0 to 3.5 mEq/L
    • 60-80 mEq PO (or IV) QDay divided doses
    • Sometimes will require up to 160 mEq per day
    (refeeders, lots of diarrhea, IV diuretics)
    • Avoid too much PO at once
    – GI upset or just poor response
    • Usually divide as BID or TID dosing
    Approach to Hypokalemia
    • Step 5 (con’t): Choose dose/timing
    – Severe hypokalemia (< 3.0 mEq/L)
    • Can use combination of IV and PO, again with PO
    preferred if at all possible
    • Avoid more than 60-80 mEq PO in a single dose
    • Avoid IV infusion rates faster than 20 mEq/hour—can
    cause arrhythmia!!!
    – Most protocols won’t allow more than 10 mEq/hour rates on
    the floors (ICU’s too?)
    Approach to Hypokalemia
    • Step 6: Monitor/reassess
    – Severe hypokalemia, DKA patients
    • Reassess labs Q4-6 hours
    – Moderate hypokalemia, IV diuresis patients
    • Reassess labs BID to TID as needed
    – Mild hypokalemia
    • Reassess labs QDay or less as needed
    Approach to Hypokalemia
    • Step 7: Housekeeping/follow up
    – BE AGGRESSIVE in DKA patients & IV diuresis patients
    • May want to keep K+ over 4.0 or even 4.5 mEQ/L in
    cardiac patients, especially in those with arrhythmias
    – BE GENTLE in patients with acute or chronic renal failure
    • May wish to cut doses in half, double intervals, or not
    replace at all
    • May need to monitor very closely
    – NEVER forget to check for & treat hypomagnesemia in refractory
    hypokalemia!!!
    Hypokalemia – TAKE CARE . . .
    • Monitor IV K – ECG & S.K levels
    • Never give IV push
    • Never add KCl to Iso M
    DON’T GIVE MORE THAN
    10-20mEq/hr
    40 mEq/L
    240 mEq/L/day

    REMEMBER – THAT HYPOKALEMIA IS


    SAFER THAN HYPERKALEMIA
    AVOID OVERENTHUSIASM in Rx
    K RICH FOOD
    • Dry fruits
    Fruit juices
    • Tender coconut water
    Chocolate
    • Banana
    Coffee
    • Juicy fruits
    Soups
    • Salt substitutes
    PSEUDOHYPOKALEMIA
    -spurious

    • "pseudohypokalemia" occurs in acute


    myelogenous leukemia
    • large number of leucocytes in the blood
    specimen (stored at room temperature)
    • sponge-up the extracellular potassium =>
    artefactually low serum potassium reading
    s o d i u m
    Normal concentration
    of sodium

    135 to 145
    mEq/L
    Gangguan keseimb.Natrium
    - Na+: ion utama diluar sel; N: 145 meq/L
    - Intrasel 10 meq/L
    - Dipertahankan oleh sistim Na-K-ATP ase
    - Amat menentukan osmolalitas extrasel selain kadar
    glukosa dan ureum.
    osmol.=2X Na plasma+ gluc/18+ BUN/2,8
    N: osmol.efektif= 2X kadar Na plasma
    - hipoNa : akibat hilangnya Na+/ retensi cairan
    - hiperNa: hilangnya cairan/ retensi ion Na.

    48
    http://www.accessmedicine.com.proxy.westernu.edu/content.aspx?aID=10935&searchStr=hyponatremia
    GENERAL GUIDELINES
    • Na deficit = 0.6 x wt(kg) x (desired [Na] - actual [Na]) (mmol)

    • When do you need to Rx quickly?


    – Acute (<24h) severe (< 120 mEq/L) Hyponatremia
    • Prevent brain swelling or Rx brain swelling
    – Symptomatic Hyponatremia (Seizures, coma, etc.)
    • Alleviate symptoms

    • Initially treat“Quickly”: 3% NS, 1-2 mEq/L/h until:


    • Symptoms stop
    • 3-4h elapsed and/or Serum Na has reached 120 mEq/L

    • Then SLOW down correction to 0.5 mEq/L/h with 0.9% NS or simply fluid
    restriction.

    • Aim for overall 24h correction to be < 10-12 mEq/L/d to prevent myelinolysis
    Adrogue: NEJM, Volume 342(21).May 25, 2000.1581-1589
    Electrolyte Imbalances
    • Hyponatremia
    • Hypocalcemia
    • Hypernatremia
    • Hypercalcemia
    • Hypokalemia
    • Hypomagnesemia
    • Hyperkalemia
    • Hypermagnesemia
    • Hypochloremia
    • Hypochloremia • Hyperchloremia
    • Hyperchloremia • Hypophosphatemia
    • Hyperphosphatemia
    PENGENALAN TERHADAP KESEIMBANGAN
    ASAM BASA
    • PCO2 is regulated by respiration, abnormalities
    that primarily alter the PCO2 are referrred to
    as respiratory acidosis (high PCO2) and
    respiratory alkalosis (low
    PCO2)
    • [HCO3 -] is regulated primarily by renal process.
    Abnormalities that primarily alter the [HCO3-]
    are referred to as metabolic acidosis (low
    [HCO
    -
    3 ])and metabolic alkalosis
    • Henderson Hasselbach
    equation: -

    pH= 6.1 + Log [HCO 3]


    0.03 PCO 2
    RANGKUMAN GANGGUAN KESEIMBANGAN
    ASAM BASA HH

    DISORDER pH PRIMER RESPON


    KOMPENSASI
    ASIDOSIS  HCO3-  pCO2 
    METABOLIK
    ALKALOSIS  HCO3-  pCO2 
    METABOLIK
    ASIDOSIS  pCO2  HCO3- 
    RESPIRATORI
    ALKALOSIS  pCO2  HCO3- 
    RESPIRATORI
    THANK YOU

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