DYSELECTROLYTEMIA

DR PRASAD LDV
SENIOR RESIDENT
 HYPERKALEMIA
Hyperkalemia is defined as measured serum [K+]
of >5.5 mEq/L.

CLASSICATION :

MILD 5.5 -6 mEq/L

MODERATE 6.1 – 6.9 mEq/L
SEVERE > 7 mEq/L
 ETIOLOGY
Pseudohyperkalemia
Tourniquet use
Hemolysis (in vitro)
Leukocytosis
Thrombocytosis

Intra- to extracellular potassium shift

Acidosis
Heavy exercise
β-Blockade
Insulin deficiency
Digitalis intoxication
Hyperkalemic periodic paralysis
Potassium load:
•Potassium supplements
•Potassium-rich foods
•IV potassium
Potassium-containing drugs
Transfusion of aged blood
Hemolysis (in vivo)
GI bleeding
Cell destruction after chemotherapy
Rhabdomyolysis/crush injury*
Extensive tissue necrosis
Decreased potassium excretion:
•Renal failure*
•Drugs—potassium-sparing diuretics,* β-blockade, NSAIDs, angiotensin-
converting enzyme inhibitors
•Aldosterone deficiency*
•Selective defect in renal potassium excretion
•Pseudohypoaldosteronism, systemic lupus erythematosus, sickle cell disease,
obstructive uropathy, renal transplantation, type IV renal tubular acidosis.
•Frequent or important ED diagnostic
considerations.
Cardiovascular and neurologic dysfunction is the
primary manifestation of hyperkalemia dysrhythmias,
including second- and third-degree heart block, wide-
complex tachycardia, ventricular fibrillation, and
even asystole.

Neuromuscular signs and symptoms of hyperkalemia

include muscle cramps, weakness, paralysis, paresthesias,
tetany, and focal neurologic deficits,….
 ECG CHANGES…

6.5–7.5meq Prolonged PR interval( AV

DISSOCIATION), tall peaked T waves (common),
short QT interval.

7.5–8.0 meq Flattening of the P wave, QRS widening.

10–12meq QRS complex degradation into a sinusoidal

pattern ,arrhythmias ,asytole.
Emergency Therapy of Hyperkalemia

Therapy Dose and Route Onset of Action Duration of Effect Mechanism.

1. Albuterol (nebulized) 2.5 milligrams in 4 mL normal saline,
nebulized over 20 min ,action in 15–30 min upto 2–4 h Up regulates cyclic adenosine
monophosphate, shifts [K+] into cell.(4 times the dose of broncho dilation).

2. Calcium chloride (10%)* 5–10 mL IV action in 1–3 min upto 30–50 min of
Membrane stabilization, mostly through central line .
Calcium gluconate (10%)* 10–20 mL slow IV over 5 – 10 min action in 1–3 min upto 30–
50 min of Membrane stabilization ,can be repeated after 5 min according to ECG
changes.
3. NaHCO3 50–100 mEq IV action in 5–10 min upto 1–2 h ,Shifts [K+] into cell (reserved
for acidotic pts ).
4. Insulin and glucose 5–10 units regular insulin IV action in 30 min upto 4–6 h Shifts
[K+] into cell 1–2 amps D50W IV..
5. Furosemide 40 milligrams IV Varies Renal [K+] excretion.

6. Sodium polystyrene sulfonate 25–50 grams PO or PR action in 1–2 h upto 4–6 h GI

[K+] excretion.

7.Hemodialysis — Minutes Varies Removes [K+](most effective option .)

 CAUTION………
If calcium is to be given to a patient on digitalis,
great caution must be exercised, because
hypercalcemia potentiates the toxic effects of
digitalis.
Calcium Chloride- Complication: severe
thrombophlebitis.
Potential Complications of Calcium administration

•Bradycardia, hypotension and peripheral vasodilatation.

• Generally these occur if administered too quickly

Avoid in digoxin toxicity (use magnesium 1-2 gm iv as
alternative)
 HYPOKALEMIA

Hypokalaemia is defined as a potassium level < 3.5mmol/L

Moderate hypokalaemia is a serum level of < 3.0 mmol/L

Severe hypokalaemia is defined as a level < 2.5 mmol/L

•Causes of Hypokalemia….
•Extracellular to intracellular potassium shifts:

•Alkalosis.
•Increased plasma insulin (treatment of diabetic ketoacidosis).
•β-Adrenergic.
•Hypokalemic periodic paralysis.

•Decreased intake:

•Poor dietary intake, geophagia.

•GI loss :

•Vomiting, nasogastric suction, diarrhea (laxative, enema abuse), malabsorption,

•ureterosigmoidostomy, enteric fistula, villous adenoma
•Renal loss:
•Diuretic therapy*
•Primary aldosteronism
•Secondary aldosteronism
•Licorice ingestion
•Excessive use of chewing tobacco
•Renal tubular acidosis
•Postobstructive diuresis
•Osmotic diuresis

Drugs and toxins:

•Carbenicillin, penicillin, amphotericin B, l-dopa, lithium, thallium,
theophylline,dopamine.
•Sweat loss
•Heavy exercise, heat stroke, febrile illness

•Other:
Hypomagnesemia, acute leukemia, IV hyperalimentation, recovery from
megaloblastic anemia.
Symptoms and Signs of Hypokalemia
Cardiovascular:

• Hypertension
• Orthostatic hypotension
• Potentiating of digitalis toxicity
• Dysrhythmias (usually tachydysrhythmias)
• T-wave flattening, U waves, ST depression.

Neuromuscular:

• Malaise, weakness, fatigue

• Hyporeflexia
• Cramps
• Paresthesias
• Paralysis
• Rhabdomyolysis.

GI:
• Ileus
Renal :

•Increased ammonia production.

•Urinary concentrating defects.

•Metabolic alkalemia, paradoxical

aciduria.

•Nephrogenic diabetes insipidus.

•Endocrine.

•Glucose intolerance.
 ECG changes……

•Increased amplitude and width of the P wave

•Prolongation of the PR interval
•T wave flattening and inversion
•ST depression
•Prominent U waves (best seen in the precordial leads)
•Apparent long QT interval due to fusion of the T and U waves
(= long QU interval)
•With worsening hypokalaemia:
•Frequent supraventricular and ventricular ectopic
•Supraventricular tachyarrhythmia's: AF, atria flutter, atria
tachycardia
•Potential to develop life-threatening ventricular arrhythmias,
e.g. VT, VF and Torsades de Pointes
MANAGEMENT……
The treatment of hypokalemia is replacement of [K+].
This can be done orally in stable patients who are able
to tolerate oral intake.

 Foods rich in [K+] (baked potatoes, spinach, lima

beans, dried prunes,tomatoes, and bananas), salt
substitutes.
 IV replacement is appropriate for patients with severe
hypokalemia.

 To prevent sudden or excessive elevations in [K+], IV KCl should be

administered in 10-mEq increments over 30 to 60 minutes, via a well-
running peripheral IV line.

A cumulative dose of 20 mEq will raise serum [K+] by about 0.25 mEq/L.

CHOICE OF FLUID TO ADMINISTER K+ ??????????

No more than 40mEq should be added to each liter of IV fluid, and
infusion rates should be no greater than 40 mEq/h.

 Cardiac monitoring is recommended for infusion rates >20 mEq/h.

 HYPONATREMIA
Hyponatremia is strictly defined as a measured serum
[Na+] <135 mEq/L.

CLASSIFICATION :
Hypertonic Hyponatremia (Osmotic Pressure
>295.
Isotonic Hyponatremia (Osmotic Pressure 275 to
295)
Hypotonic Hyponatremia (Osmotic Pressure
<275).
Hypotonic Hyponatremia
(Osmotic Pressure <275

•Hypovolemic hyponatremia

• Euvolemic hyponatremia

•Hypervolemic hyponatremia
 ETIOLOGY
Hypertonic hyponatremia (Posm >295)
Hyperglycemia
Mannitol excess
Glycerol therapy
Isotonic (pseudo) hyponatremia (Posm 275–295)
Hyperlipidemia
Hyperproteinemia (e.g., multiple myeloma,
Waldenström macroglobulinemia
 HyponatremiaHypotonic (Posm <275)
Hypovolemic…..

Renal:

•Diuretic use
•Salt-wasting nephropathy (renal tubular acidosis, chronic renal failure,
•interstitial nephritis)
•Osmotic diuresis (glucose, urea, mannitol, hyperproteinemia)
•Mineralocorticoid (aldosterone) deficiency

Extrarenal:

•Volume replacement with hypotonic fluids

•GI loss (vomiting, diarrhea, fistula, tube suction)
•Third-space loss (e.g., burns, hemorrhagic pancreatitis, peritonitis)
•Sweating (e.g., cystic fibrosis)
HYPERVOLEMIA

•Urinary [Na+] >20 mEq/L

•Renal failure (inability to excrete free water)

•Urinary [Na+] <20 mEq/L

•Congestive heart failure (perceived as low-flow state by kidneys, stimulates

ADH)

•Nephrotic syndrome (low serum protein secondary to urinary loss)

•Cirrhosis (low intravascular oncotic pressure secondary to decreased

protein production)
 Euvolemic (urine [Na+] usually >20 mEq/L)
•Syndrome of inappropriate secretion of antidiuretic hormone.
•Hypothyroidism (possible increased ADH or deceased glomerular
filtration rate)
•Pain, stress, nausea, psychosis (stimulates ADH)

•Drugs: ADH, nicotine, sulfonylureas, morphine, barbiturates, NSAIDs,

acetaminophen, carbamazepine, phenothiazines, tricyclic antidepressants,
colchicine, clofibrate, cyclophosphamide, isoproterenol, tolbutamide,
vincristine, monoamine oxidase inhibitor.

•Water intoxication (psychogenic polydipsia, lesion in thirst center).

•Glucocorticoid deficiency (glucocorticoids required to suppress ADH).
•Positive pressure ventilation.
•Porphyria.
•Essential (reset osmostat or sick cell syndrome—usually in the elderly).
 CNS MANIFESTATIONS :

•altered consciousness, agitation, headache,

seizures, and even coma.

•The severity of symptoms is dependent on not only the rapidity

but also the magnitude of the decrease in the serum[Na+].

•Acute hyponatremia occurring in 24 hours or less and

resulting in a serum [Na+] of <120 mEq/L, or declining at a
rate of 0.5 mEq/L or more per hour, can cause neurologic
manifestations such as muscular twitching, seizures, and
coma.
 Cardiovascular System
•shock occurs at lesser degrees of TBW depletion in hyponatremia than similar
fluid deficits when the plasma is hypertonic or isotonic.

Musculoskeletal System
•muscle cramps and weakness can occur during strenuous exercise, especially if
excess sweating is replaced with water.

Renal System

•A urine [Na+] <10 mEq/L usually indicates that the renal handling of
[Na+] is intact and that the effective arterial blood volume is contracted.

•In contrast, a urine [Na+] >20 mEq/L often indicates intrinsic renal tubular
damage or a natriuretic response to hypervolemia
 Investigations….

Plasma osmolality

Urine sodium and osmality

Uric acid levels

Fractional sodium
 Diagnosis…

Therefore, the first step in the evaluation of a

patient with a low measured [Na+] should include
a clinical evaluation of ECF volume status and
measured and calculated plasma osmolalities.

Urine osmolilty and specific gravity.

 Treatment ………
Issues to be addressed.
Symptomatic VS asymptomatic.
Acute vs chronic .
Volume status .
Osmolarity (mOsm/l) 2 x(Na )+Glucose + B U N
18 2.8
 Sodium administration
IV saline vs oral salt tablets
If iv saline 3% or 0.9%.
Rate ?
How long ?
How often to recheck Na.
NA DEFECIT= TBW* (DesiredNa -
SerumNa)

sodium infusion rate:

3% NS =wt * desired rate of Na in
meq/lit/hr .

If NS wt *1.5 .

Duration of therapy : rate of

correction * Na goal – Na initial .

 Recheck Na every 2 hrs .

• ADH receptors antagonist
tolvaptan , conivaptan
;
MECHANISM BLOCK ADH LEAD TO PURE WATER DIURESIS
LIMITATION; OVER RAPID CORRECTION
LIVER FAILURE

• Fluid restriction
•50-70% of dialy requirement ie 1-1.5 l/day

•Cosider in hypervolemic patients .

 HYPERNATREMIA….

Hypernatremia is defined as serum [Na+] >150

mEq/L

Osmolality (mOsm/kg) Manifestations

350–375 Restlessness, irritability

375–400 Tremulousness, ataxia
400–430 Hyperreflexia, twitching, Spasticity.

>430 Seizures and death

TREATMENT……
•The cornerstone of treatment is volume repletion.

•Volumeshould be replaced first with NS or lactated Ringer’s solution.

Either will have, by definition, a lower [Na+] than the patient’s serum.

 Most hypernatremic states, there is a total body [Na+] deficit, and the use of
NS allows a more gradual decrease in serum [Na+

Plasma-expanding fluids should continue until tissue perfusion is restored.

Once perfusion hasbeen established, the solution should be converted to 0.45%
saline or anotherhypotonic solution until the urine output is at least 0.5
mL/kg/h
•The reduction in [Na+] should not exceed 10 to 15 mEq/L per day .

•As a general rule, each liter of water deficit results in serum [Na+] rise
of 3 to 5 mEq/L

•water deficit (L) =measured [Na+]/normal [Na+]– 1

•Unless the hypernatremia is of short duration, idiogenic osmoles are

presumably present in brain cells.

•Consequently, overly rapid rehydration and lowering of serum [Na+]

can cause brain cells to swell, resulting in cerebral edema and an
increased likelihood of seizures, permanent neurologic sequelae, or
even death.

•In acute hypernatremia, serum[Na+] levels can be corrected rather

rapidly with little fear of cerebral edema, because idiogenic osmoles
will not yet be present in brain cells.
HYPOCALEMIA….

•The measured serum [Ca2+] ranges from 8.5 to 10.5 milligrams/dL

and is maintained by the function of parathyroid hormone
(parathormone,PTH), vitamin D metabolites (1,25-dihydroxyvitamin D3, or
calcitriol),and calcitonin.

•Alkalosis produces a decrease in ionized fraction with no change in

the total serum [Ca2+]. Each 0.1 rise in pH lowers ionized [Ca2+] by
about 3% to 8%.

• Acidosis produces an increase in ionized fraction with no change in

the total serum [Ca2+]

•Hypocalcemia is defined by an ionized [Ca2+] level

<2.0 mEq/L. Normal ionized [Ca2+] is 2.1 to 2.6 mEq/L (1.05 to 1.3
mmol/L)
 •If a patient is asymptomatic or if the hypocalcemia is not severe or prolonged
for >10 to 14 days,treatment may not be required. Oral [Ca2+] therapy with or
without vitaminD may be sufficient.

•IV calcium is recommended only in cases of symptomatic or severe

hypocalcemia (ionized [Ca2+] <1.3 mEq/L or <0.65 mmol/L), because IV
[Ca2+] administration causes vasoconstriction and possible ischemia, especially
in patients with low cardiac output who already have significant
peripheral vasoconstriction. With severe acute hypocalcemia, 10 mL of
10% CaCl2 (or 10 to 30 mL of 10% [Ca2+] gluconate) may be given IV
over 10 to 20 minutes followed by a continuous IV infusion of 10% CaCl2
at 0.02 to 0.08 mL/kg/h (1.4 to 5.6 mL/h in a 70-kg patient). The serum
[Ca2+] should then be rechecked before continuing parenteral [Ca2

•During massive transfusions, if the blood is being given faster than 1

unit every 5 minutes, 10 mL of 10% CaCl2 can be given after every 4 to 6
units of blood if a patient is in shock or has heart failure despite adequate
volume replacement therapy

•Hypocalcemia is difficult to correct if hypomagnesaemia is also

present. Hypomagnesaemia states reduce PTH and [Ca2+] releases from
bone. Therefore, magnesium should be replaced before, or in conjunction
with, [Ca2+] replacement
 Hypercalcemia
Defined as a total [Ca2+] >10.5 milligrams/dL or an ionized
calcium level >2.7 mEqI.
conduction of the heart is slowed and automaticity is decreased
with a shortening of the refractory period
On ECG:
depressed ST segments,
widened T waves, and shortened ST segments and QT intervals.
Brady arrhythmias may occur, with bundle branch patterns that
may progress to second-degree block or complete heart block.
Levels above20 milligrams/dL may cause cardiac arrest
Up to one third of patients with hypercalcemia have associated
hypokalemia. Hypomagnesemia also is common.
 Hypomagnesemia
ECG changes

prolonged PR and QT intervals, widened QRS complexes, depression of ST

segments, and inversion of T waves, especially in the precordial leads.

similar to those caused by hypokalemia and/or hypocalcemia, and many of

these changes may be related to[Mg2+] deficiency altering cardiac intracellular
potassium content.

Hypokalemia, hypocalcemia, and hypophosphatemia are

often present with severe hypomagnesaemia and must be monitored
carefully

The first 10 to 15 mEq(1.5 to 2.0 grams) of IV [MgSO4] can be given over 1 to 2

hours. This may be followed by up to 4 to 6 grams per day thereafter.
Approximately half of the administered [Mg2+] will be lost in the urine.
 
 Hypermagnesemia

The possibility of hypermagnesemia should be considered in patients

with hyperkalemia or hypercalcemia.
Hypermagnesemia also should be suspected in patients with renal
failure, particularly in those who are taking magnesium-containing
antacids.
Calcium directly antagonizes the effects of magnesium; severe
symptomatic hypermagnesemia can be treated with 5 mL 10% CaCl2 IV
over 5 minutes.
Patients with renal failure may benefit from dialysis using a decreased
[Mg2+] bath that lowers serum [Mg2+].
• REFERENCE
TITINALLIS EMERGENCY MEDICINE
ROSENS EMERGENCY MEDICINE
OHEM
OHAM
HARRISON INTERNAL MEDICINE
LIFE IN FASTLANE