1

07/03/2020
ELECTROLYTES
(SODIUM,POTASSIUM)

PRESENTED BY
MUKESH SHAH
INTERN (MBBS)
BMCTH
 2

 Total body Na+. 85-90% of total body Na+ is extracellular and constitutes the predominate
solute in the ECF.
 Changes to the body's total Na+ content typically results from a loss or gain of this Na+-rich
fluid, leading to contraction or expansion of the ECF space.
 Clinically, this manifests as volume depletion (hypotension, tachycardia) and volume
expansion (peripheral or pulmonary edema).
 Na+ concentration is distinct from Na+ content. Na+ concentration reflects the amount of
Na+ distributed in a fixed quantity of water.
 An increase in TBW can decrease the Na+ concentration even if the body's total Na+ content
remains unchanged.
 The intact kidney can respond to altered Na+ content in the ECF space by increasing or
decreasing Na+ reabsorption. This response is mediated by cardiovascular, renal, hepatic, and
central nervous system sensors of the effective circulating volume.
07/03/2020
 3
Hyponatremia

 Hyponatremia is defined as a plasma [Na+] <135 mEq/L.

 GENERAL PRINCIPLES
 To maintain a normal [Na+], the ingestion of water must be matched with an equal volume of water
excretion.
 Any process that limits the elimination of water or expands the volume around a fixed Na+ content may lead
to a decrease in Na+ concentration.
 Expansion of the space surrounding the Na+ content can occur in a variety of ways:
 Pseudohyponatremia refers to a laboratory phenomenon by which a high content of plasma proteins and
lipids expands the nonaqueous portion of the plasma sample, leading to an errant report of a low ECF [Na+].
This can be averted with Na+-sensitive electrodes, and the normal ECF [Na+] can be confirmed with a
normal serum osmolality.
 Hyperosmolar hyponatremia
 Hypovolemic hyponatremia
 Hypervolemic hyponatremia 07/03/2020
4

07/03/2020
5

07/03/2020
6

07/03/2020
 7
Clinical Presentation

 The clinical features of hyponatremia are related to the osmotic intracellular water shift leading
to cerebral edema.
 Therefore, the symptoms are primarily neurologic, and their severity is dependent on both the
magnitude and rapidity of decrease in plasma [Na+].
 Acute hyponatremia (i.e., developing in <2 days), patients may complain of nausea and
malaise with [Na+] of approximately 125 mEq/L.
 As the plasma [Na+] falls further, symptoms may progress to include headache, lethargy,
confusion, and obtundation. Stupor, seizures, and coma do not usually occur unless the plasma
[Na+] falls acutely below 115 mEq/L.
 Chronic hyponatremia (>3 days in duration), adaptive mechanisms designed to defend cell
volume occur and tend to minimize the increase in ICF volume and its symptoms

07/03/2020
 8
TREATMENT

 Management requires one to determine the rate of correction, the appropriate intervention, and
the presence of other underlying disorders.
 The rate of correction of hyponatremia depends on the acuity of its development and the presence
of neurologic dysfunction.
 Acute symptomatic hyponatremia. Severe symptomatic hyponatremia, with evidence of
neurologic dysfunction, should generally be treated promptly with hypertonic saline;
 however, any saline solution that is hypertonic to the urine (if the urine osmolality is known at the
start of therapy) can increase the [Na+] when oral water intake is restricted.

07/03/2020
 9

 The risks of correcting hyponatremia too rapidly are volume overload and the development of
central pontine myelinolysis (CPM). CPM results from damage to neurons due to rapid
osmotic shifts. In its most overt form, it is characterized by flaccid paralysis, dysarthria, and
dysphagia, and in more subtle presentations, it can be confirmed by CT scan or MRI of the
brain.
 The risk of precipitating CPM is increased with correction of the [Na+] by >12 mEq/L in a
24-hour period .
 In addition to overaggressive correction, other risk factors for developing CPM include
preexisting hypokalemia, malnutrition, and alcoholism.
 In patients with severe hyponatremia, in whom an immediate rise in [Na+] is necessary,
[Na+] should be corrected 1-2 mEq/L/h for 3-4 hours.
 However, this initial rate of correction should be tapered off once the patient is safe, such that
the rise in [Na+] does not exceed 10-12 mEq/L over the 24-hour period
07/03/2020
 10

 Chronic asymptomatic hyponatremia. The risk of iatrogenic injury is actually increased

in patients with chronic hyponatremia.
 Because cells gradually adapt to the hypo-osmolar state, an abrupt normalization presents
a dramatic change from the accommodated osmotic milieu. As such, we suggest a more
modest rate of correction on the order of 5-8 mEq/L over a 24-hour period.

07/03/2020
 11
Severe, symptomatic hyponatremia.

 In patients with symptomatic hyponatremia, hypertonic saline provides an immediate and titratable intervention
necessary to acutely raise serum Na+ levels while avoiding the disastrous complications of overcorrection.
 The most accurate way to correct hyponatremia entails a detailed registry matching total solute and water output
with desired input.
 In clinical practice, this is often impractical. In lieu of this, the following equation is often used to approximate
the change in [Na+] in mEq/L from the infusion of 1 L of fluid:
 Δ[Na+] = ([Na+i] + [K+i] − [Na+s]) ÷ {TBW + 1}
 [Na+i] and [K+i] are the sodium and potassium concentrations in the infused fluid, and [Na+s] is the starting
serum sodium . Recall that TBW is estimated by multiplying the lean weight (in kilograms) by 0.6 in men (and
0.5 in women). This formula does not account for ongoing electrolyte or water losses and is only a rough guide.

07/03/2020
 12
Asymptomatic hyponatremia

 Hypovolemic hyponatremia. In patients with asymptomatic hypovolemic hyponatremia, isotonic saline can be used to restore the
intravascular volume. Restoration of a euvolemic state will reduce the impetus toward renal water retention, leading to normalization of
[Na+].
 If the duration of hyponatremia is unknown, the process described earlier can be used to calculate the expected change from 1 L of 0.9% NS,
the rate of administration, and the maximal amount that can be given to avoid overcorrection.
 Hypervolemic hyponatremia. Hyponatremia in CHF and cirrhosis often reflects the severity of the
 underlying disease. However, the hyponatremia itself is typically asymptomatic. Although effective
 circulating volume is decreased, the administration of fluid may worsen the volume-overloaded state. Definitive treatment requires
management of the underlying condition, although restriction of water intake and increasing water diuresis may help to attenuate the degree of
hyponatremia.
 Oral fluid intake should be less than daily urine output.Urinary excretion of water can be promoted through the use of loop diuretics, which
reduce the concentration gradient necessary to reabsorb water in the distal nephron.
 Vasopressin antagonists may also be helpful in both euvolemic (SIADH) and hypervolemic hyponatremia (particularly CHF). When using
medications to promote water loss, laboratory data and volume status must be followed extremely closely, because the effect on water and
electrolyte loss cannot be accurately predicted.
07/03/2020
 13

 SIADH should first be distinguished from the previously listed conditions that stimulate
vasopressin secretion. The standard first-line therapy is water restriction and correction of
any contributing factors (nausea, pneumonia, drugs, etc.). If this fails or if the patient is
symptomatic, the following can be attempted to promote water excretion.
 Water restriction. The amount of fluid restriction necessary depends on the extent of
water elimination. A useful guide to the necessary degree of fluid restriction is as follows:
 If (Urine Na+ + Urine K+)/Serum Na+ <0.5, restrict to 1 L/d.
 If (Urine Na+ + Urine K+)/Serum Na+ is 0.5-1.0, restrict to 500 mL/d.
 If (Urine Na+ + Urine K+)/Serum Na+ is >1, the patient has a negative renal free water
clearance and is actively reabsorbing water. Any amount of water given may be retained,
and clinicians should consider the following options to enhance free water excretion.

07/03/2020
 14

 High dietary solute load. The volume of water excreted as urine is governed by a
relatively fixed urine osmolality. Thus, increasing solute intake with a high-salt, high-
protein diet or administration of oral urea (30-60 g) may increase the capacity for water
excretion and improve the hyponatremia.
 Loop diuretics impair the urinary concentrating mechanism and can enhance free water
excretion.
 Vasopressin antagonists promote a water diuresis and may be useful in the therapy of
SIADH. Both IV (conivaptan) and oral (tolvaptan) preparations are approved for the
treatment of euvolemic hyponatremia.
 However, given the risks of overcorrection, these agents should be initiated in a closely
monitored inpatient setting.
 Lithium and demeclocycline interfere with the collecting tubule's ability to respond to ADH
but are rarely used because of significant side effects. They should only be considered in
07/03/2020
severe hyponatremia that is unresponsive to more conservative measures
 15
Hypernatremia

 GENERAL PRINCIPLES
 Hypernatremia is defined as a plasma [Na+] >145 mEq/L and represents a state of
hyperosmolality
 Hypernatremia may be caused by a primary Na+ gain or a water deficit, the latter being
much more common.
 Normally, this hyperosmolar state stimulates thirst and the excretion of a maximally
concentrated urine.
 For hypernatremia to persist, one or both of these compensatory mechanisms must be
impaired.

07/03/2020
 16
Clinical Presentation

 Hypernatremia results in contraction of brain cells as water shifts to attenuate the rising ECF
osmolality.
 Thus, the most severe symptoms of hypernatremia are neurologic, including
 altered mental status, weakness, neuromuscular irritability, focal neurologic deficits, and,
occasionally, coma or seizures.
 As with hyponatremia, the severity of the clinical manifestations is related to the acuity and
magnitude of the rise in plasma [Na+].
 Chronic hypernatremia is generally less symptomatic as a result of adaptive mechanisms designed
to defend cell volume.
 CDI and NDI generally present with complaints of polyuria and thirst. Signs of volume depletion or
neurologic dysfunction are generally absent unless the patient has an associated thirst abnormality.

07/03/2020
17

07/03/2020
18

07/03/2020
19

07/03/2020
 20
POTASSIUM

 Potassium is the major intracellular cation

 ECF [K+] is normally 3.5-5.0 mEq/L (the intracellular concentration is
roughly 150 mEq/L , difference is maintained by the Na+/K+ adenosine
triphosphatase pump
 90% of orally taken potassium is absorbed by GI tract
 The elimination of potassium occurs predominately through renal
excretion at the distal nephron

07/03/2020
 21
HYPOKALEMIA

 Hypokalemia is defined as a plasma [K+] <3.5 mEq/L

 CAUSES
 Diminished intake
 Transcellular shift (result from alkalemia, insulin, and catecholamine release)
 Non-renal K+ loss ( vomiting ,diarrhea )
 Renal K+ loss accounts for most cases of chronic hypokalemia
[use of diuretics and osmotic diuresis (e.g., glycosuria)]

07/03/2020
22

07/03/2020
23

07/03/2020
 24
Clinical Presentation

 Symptoms seldom occur unless the plasma [K+] is <3.0 mEq/L

 Fatigue, myalgias, and muscular weakness or cramps of the lower extremities are
common
 May manifest with complaints of constipation or frank paralytic ileus (smooth
muscle weakness)
 Severe hypokalemia may lead to complete paralysis, hypoventilation, or
rhabdomyolysis

07/03/2020
 25
DIAGNOSIS

 Urine K+ ( The appropriate response to hypokalemia is to excrete <25mEq/d of

K+ in the urine)
 Acid-base status (generally associated with metabolic alkalosis)
 ECG
 flattening or inversion of the T wave, a prominent U wave, ST-segment
depression, and a prolonged QU interval.
 Severe K+ depletion may result in a prolonged PR interval, widening of the QRS
complex.

07/03/2020
 26
TREATMENT

 Correction of the K+ deficit can be accomplished with either oral or IV therapy

 IV therapy :
 Maximum concentration for administration through central venous catheter = 40
mmol/100ml @20 mmol/hr ( max. of 40 mmol/hr under cardiac monitoring )
 Maximum concentration for administration through peripheral vein through IV
canula = 10 mmol/100ml ( 10 mmol/hr )

07/03/2020
 27
TREATMENT

Serum potassium Administration through Administration through

central venous catheter peripheral vein

<2.6 mmol/L 100 mmol of KCl KCl 10 mmol X 10 dose

2.6 – 2.9 mmol/L 80 mmol of KCl KCl 10 mmol X 8 dose

3 – 3.2 mmol/L 60 mmol of KCl KCl 10 mmol X 6 dose

</= 3.2 mmol/L 40 mmol of KCl KCl 10 mmol X 4 dose

>3.2 and <3.5 mmol/L 20 mmol of KCl KCl 10 mmol X 2 dose

07/03/2020
 28
ORAL REPLACEMENT

Serum potassium Oral KCl replacement

 Oral therapy

3.2 – 3.5 mmol/L 20 mEq X 1 dose

3.0 – 3.1 mmol/L 40 mEq X 1 dose then an additional 20 mEq in

2hr X 1 dose
2.6 – 2.9 mmol/L 40 mEq X 1 dose then an additional 40 mEq in
2hrs
<2.6 mmol/L 40 mEq X 1 dose then 20 mEq in every 2 hrs X
3 dose

07/03/2020
 29
Hyperkalemia

 GENERAL PRINCIPLES
 Hyperkalemia is defined as a plasma [K+] >5.0 mEq/L.
 Pseudohyperkalemia represents an artificially elevated plasma [K+] due to K+ movement
out of cells immediately before or following vein puncture
 True hyperkalemia occurs as a result of
 Transcellular shift
 Increased exposure to K+
 Decreased renal K+ excretion(most commonly )

07/03/2020
30

07/03/2020
31

07/03/2020
 32
DIAGNOSIS

 Clinical Presentation
 Cardiac arrhythmogenesis
 May present with palpitations, syncope, or even sudden cardiac death
 Severe hyperkalemia causes partial depolarization of the skeletal muscle cell
membrane
 (manifest as weakness, potentially progressing to flaccid paralysis and
hypoventilation if the respiratory muscles are involved )

07/03/2020
33

07/03/2020
34

07/03/2020
 35
Diagnostic Testing

 Renal [K+] excretion and the renin-angiotensin-aldosterone axis

 ECG changes include increased T-wave amplitude or peaked T waves.
 More severe degrees of hyperkalemia result in :
 a prolonged PR interval , loss of P waves. Progressive widening of the QRS
complex

07/03/2020
 36
TREATMENT

 Severe hyperkalemia with ECG changes is a medical emergency and requires immediate treatment
directed at minimizing membrane depolarization and acutely reducing the ECF [K+].
 Acute therapy may consist of some or all of the following (the hypokalemic effect is additive).
 Calcium gluconate : 10 mL of a 10% solution infused over 2-3 minutes , the dose can be repeated
if no improvement in the ECG is seen after 5-10 minutes.
 Insulin : A commonly used combination is 10-20 units of regular insulin and 25-50 g of glucose
administered IV
 Hyperglycemic patients should be given the insulin alone

07/03/2020
 37
TREATMENT

 NaHCO3 : In severe hyperkalemia associated with metabolic acidosis. In the acute

setting, it can be given as an IV isotonic solution (three ampules of NaHCO3 in 1 L
of 5% dextrose).
 β2-Adrenergic agonists : lowering the plasma [K+] by 0.5-1.5 mEq/L, and the
effect lasts for 2-4 hours. Albuterol can be administered in a dose of 10-20 mg as a
continuous nebulized treatment over 30-60 minutes.

07/03/2020
 38
TREATMENT

1. Longer term means for [K+] removal.

 Increasing distal Na+ delivery in the kidney enhances renal K+ clearance. This can be achieved with the
administration of saline in patients who appear volume depleted. Otherwise, diuretics can be used if renal
function is adequate.
 Cation exchange resins, such as sodium polystyrene sulfonate (Kayexalate), promote the exchange of Na+
for K+ in the GI tract. When given by mouth, the usual dose is 25-50 g mixed with 100 mL 20% sorbitol to
prevent constipation.
 This generally lowers the plasma [K+] by 0.5-1.0 mEq/L within 1-2 hours and lasts for 4-6 hours. Sodium
polystyrene sulfonate can also be administered as a retention enema consisting of 50 g resin in 150 mL tap
water.
 Newer agents such as sodium zirconium cyclosilicate are being studied and have shown improved safety
profiles in preliminary studies.
07/03/2020
 39

THANK YOU

07/03/2020