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
• The presence of potassium in
the blood

• Normal range: 3.5 – 5 mEq/L

= low levels of
potassium, deficient potassium

= 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
HYPERKALEMIA

Potassium level
more than 5.5
mEq/L
• 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

• 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

• 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

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
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
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
 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
• 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.

• 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
• Hypophosphatemia
• Hyperchloremia
• 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 [HCO3-]
0.03 PCO2
 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