KESEIMBANGAN ELEKTROLIT

DAN A S A M 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
• Hyperphos phatemi a
Kalemia

• The presence of potassium in the

blood

• Normal range: 3.5 – 5 mEq/L

• Hypokalemia = low levels of
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

+ +

+ +

An oversimplification in acidosis
Hypokalemia

Hyperkalemia
HYPERKALEM IA

Potassium level more

than 5.5 mEq/L
 Hyperkalemia
Serum Potassium concentration > 5 mEq/L
•Mnemonic = AIDS

•Acidosis – Metabolic acidosis: bicarbonate is low, pH becomeacidic

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
•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
•Drugs Results from
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

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)
 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
Decreased intake Redistribution
into cells
Renal Extra renal
 PATHOPHYSIOLOGY OF HYPOKALEMIA

= Action Potential

Nerve and Muscle Activity

Increase in
Low
resting
Extracellular
membrane excitable
K+
potential
 Hypokalemia
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
 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 DON’T GIVE MORE THAN
• Never add KCl to Iso M  10-20mEq/hr
 40 mEq/L
 240 mEq/L/day

REMEMBER – THAT HYPOKALEMIA IS

SAFER THAN HYPERKALEMIA
AVOID OVERENTHUSIASM in Rx
 K RICH FOOD
• Fruit juices • Dry fruits
• 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
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.
Adrogue: NEJM, Volume 342(21).May 25,
 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 referred as respiratory
acidosis (high PCO2) and respiratory alkalosis (low PCO2)

• HCO3 is regulated by renal process, abnormalities that

primarily alter the referred as metabolic acidosis (low
HCO3) and metabolic alkalosis (high HCO3)
Handerson Hasselbach Equation
RANGKUMAN GANGGUAN
KESEIMBANGAN ASAM BASA

DISORDER pH PRIM ER RESPON

KOM PENS AS I
ASIDOSIS pCO2
HCO3-
M ETABOLIK
ALKALOSIS HCO3- pCO2
M ETABOLIK
ASIDOSIS pCO2 HCO3-
RES PIRATORI
ALKALOSIS pCO2 HCO3-
RES PIRATORI
THANKYOU