Electrolytes are an integral component of human physiology and homeostasis.
Management of hypo and hyperkalemia is difficult in most of the hospital settings
In this ppt we have explained it in a simplified manner
2. Hypokalemia
• PREVENT OR TREAT LIFE-
THREATENING COMPLICATIONS
(ARRHYTHMIAS, PARALYSIS,
RHABDOMYOLYSIS, AND
DIAPHRAGMATIC WEAKNESS)
• REPLACE THE POTASSIUM
DEFICIT
• TO DIAGNOSE AND CORRECT
THE UNDERLYING CAUSE
3. Causes
Decreased Intake
Anorexia Nervosa
Alcoholism
Intracellular Shift
Insulin (e.g. during DKA resuscitation).
Beta-agonists (albuterol, terbutaline, epinephrine – including endogenous epinephrine surges from
stress).
Hypothermia.
Alkalemia (small effect).
Hypokalemic periodic paralysis.
Familial form with onset <20 years old.
#2) Acquired form associated with hyperthyroidism, typically in Asian and Mexican men.
4. Extra Renal Potassium Loss
Diarrhea.
Vomiting or large-volume gastric suction.
Profound sweating.
5. Renal Potassium Loss
Secondary to another electrolyte abnormality:
Hypomagnesemia.
Metabolic alkalosis.
Polyuria with increased distal delivery of sodium and water to the tubule:
Potassium wasting diuretics (e.g. thiazides, loop diuretics, acetazolamide, mannitol).
Sodium-wasting nephropathy (e.g. post-ATN or post-obstructive).
High-dose penicillins.
Mineralocorticoid excess:
Cushing's syndrome.
Primary hyperaldosteronism.
Exogenous steroid.
Licorice ingestion.
Renal tubular acidosis types I or II
6.
7.
8. Redistributive hypokalemia
Redistribution occurs due to increase cellular uptake through Na K ATPase
pump. following:
Hypokalemia
Alkalosis
Acute digoxin
intoxication
Succinylcholine
Beta agonists
9. rebound hyperkalemia
can develop fatal hyperkalemic arrhythmias
The risk of rebound hyperkalemia is particularly high in patients with hypokalemic or
thyrotoxic periodic paralysis in whom rebound hyperkalemia has been described in 40 to
60 percent of treated attacks
10. Potassium deficit
The potassium deficit varies directly with the severity of hypokalemia
Acute
• the serum potassium concentration fell by approximately 0.27 mEq/L for
every 100 mEq reduction in total body potassium stores
Chronic
• a potassium deficit of 200 to 400 mEq is required to lower the serum
potassium concentration by 1 mEq/L
11. 0.27 mEq/l = 100 mEq
If K is 2.48 mEq/l then there is decrease in Potssium of 1.08 mEq/l from lower
normal limit of 3.5 mEq/l. so there is a deficit of 400 mEq.
12.
13. Total potassium deficit = Potassium deficit + daily requirement of potassium
Kdeficit (in mEq) = (Knormal lower limit − Kmeasured) × kg body weight × 0.4
Daily requirement of potassium = Weight of patient in Kg x 1
14. Kdeficit (in mEq) = (Knormal lower limit − Kmeasured) × kg body weight × 0.4
For example Potassium Deficit for a 60 kg person with a Potassium
level of 2.5 mEq/L will be
Kdeficit (in mEq/l) = (3.5−2.5) × 60× 0.4
=1 × 60× 0.4
=24 mEq
15. Daily requirement of potassium = Weight of patient in Kg x 1
Daily requirement = 60x1= 60 mEq
Total potassium deficit = Potassium deficit + daily requirement of
potassium
Total Potassium deficit= 24+60=84mEq
16. Potassium preparations
Potassium can be administered as
Potassium chloride
Potassium phosphate
Potassium bicarbonate or its precursors (potassium citrate, potassium acetate)
Potassium gluconate
17. Potassium bicarbonate or its precursors are preferred in patients with
hypokalemia and metabolic acidosis (Renal tubular acidosis or diarrhea).
Only Potassium acetate is available for intravenous use.
18. Potassium phosphate should be considered only in the rarely seen patients
with hypokalemia and hypophosphatemia,
This occurs with proximal (type 2) renal tubular acidosis associated with
Fanconi syndrome and phosphate wasting
19. Potassium chloride is preferred in all other patients for two major reasons
Patients with hypokalemia and metabolic alkalosis are often chloride depleted due, for example,
to diuretic therapy or vomiting.
It has been estimated that administration of non-chloride-containing potassium salts in the
presence of metabolic alkalosis results in the retention of only 40 percent as much potassium
as the administration of potassium chloride
Potassium chloride raises the serum potassium concentration at a faster rate than potassium
bicarbonate.
20. Mild to moderate hypokalemia
A serum potassium concentration of 3.0 to 3.4 mEq/L.
This degree of potassium depletion usually produces no symptoms.
Exceptions include
Patients with heart disease (particularly if they are taking digitalis or certain other
antiarrhythmic drugs or are undergoing cardiac surgery)
Patients with cirrhosis, in whom hypokalemia can increase ammonia generation
and promote the development of hepatic encephalopathy.
Treatment of mild to moderate hypokalemia depends upon the cause of
the hypokalemia and acid-base status
23. Renal Potassium Wasting
Chronic diuretic therapy, Primary aldosteronism
Potassium supplements at usual doses produce only modest elevations in
serum potassium
A potassium-sparing diuretic is likely to be more effective.
Amiloride is usually preferred to a mineralocorticoid receptor antagonist
because it is better tolerated.
Primary aldosteronism is an important exception
since spironolactone or eplerenone is preferred to block apparent adverse
effects of excess aldosterone on the heart and vascular system
24. Heart Failure
In patients with moderately severe to severe heart failure, there is increased risk of
hyperkalemia with potassium replacement.
Several factors may act together to markedly reduce urinary potassium excretion
Decreased renal perfusion due to the fall in cardiac output,
Therapy with an angiotensin inhibitor
Therapy with spironolactone or eplerenone.
Among patients with heart failure, mineralocorticoid receptor antagonists should
be given only if the serum creatinine is less than or equal to 2.5 mg/dL (221
micromol/L) in men and 2.0 mg/dL (177 micromol/L) in women and the serum
potassium is less than 5.0 mEq/L.
25. Patients with mild to moderate hypokalemia who are treated with potassium
supplements are typically treated with oral therapy.
Patients who cannot take oral therapy require intravenous repletion.
Sequential monitoring of the serum potassium is essential to determine the
response.
26. Severe or symptomatic hypokalemia
serum potassium less than 2.5 to 3.0 mEq/L
Potassium must be given more rapidly to patients with hypokalemia that is severe
or symptomatic (arrhythmias, marked muscle weakness, or rhabdomyolysis).
Potassium repletion is most easily accomplished orally but can be given
intravenously.
Oral dose Rise in K
40 to 60 mEq 1 to 1.5 mEq/L
135 to 160 mEq 2.5 to 3.5 mEq/L
27. The serum potassium concentration will then fall back toward baseline over a few hours, as most
of the exogenous potassium is taken up by the cells
A patient with a serum potassium concentration of 2.0 mEq/L, for example, may have a 400 to
800 mEq potassium deficit.
In patients with severe hypokalemia, potassium chloride can be given
orally in doses of 40 mEq, three to four times per day
particularly in patients also treated with intravenous potassium, 20 mEq every two to three hours.
28. Monitoring
the serum potassium should initially be measured every two to four hours to ascertain the
response to therapy.
If tolerated, this regimen should be continued until the serum potassium concentration is
persistently above 3.0 to 3.5 mEq/L and symptoms or signs attributable to hypokalemia have
resolved.
Thereafter, the dose and frequency of administration can be reduced to that used in mild to
moderate hypokalemia since aggressive repletion is no longer required and gastric irritation can
be avoided.
29. Intravenous potassium repletion
Potassium chloride can be given intravenously as an adjunct to oral
replacement in patients
Who have severe symptomatic hypokalemia
In patients with less severe hypokalemia who are unable to take oral medications.
Potential constraints to intravenous therapy for severe hypokalemia include
a risk of volume overload in susceptible subjects and hyperkalemia due to
excessive repletion.
30. Choice of fluid
A saline rather than a dextrose solution should be used for initial therapy
Since the administration of dextrose stimulates the release of insulin
which drives extracellular potassium into the cells.
This can lead to a transient 0.2 to 1.4 mEq/L reduction in the serum
potassium concentration, particularly if the solution contains only 20
mEq/L of potassium.
The transient reduction in serum potassium can induce arrhythmias in
susceptible patients, such as those taking digitalis
31. Potassium replacement in DKA
These patients typically have a substantial reduction in potassium
stores due to urinary losses, but usually present with normal or even
high serum potassium levels due to transcellular potassium shifts.
Patients who present with hypokalemia have an even larger potassium
deficit .
Furthermore, treatment with insulin and intravenous fluids will exacerbate
the hypokalemia and minimize the efficacy of potassium repletion.
Thus, insulin therapy should be delayed until the serum potassium is
above 3.3 mEq/L to avoid possible complications of hypokalemia such as
cardiac arrhythmias, cardiac arrest, and respiratory muscle weakness.
32. Potassium replacement in DKA
Although isotonic saline is often the initial replacement fluid used in
treating diabetic ketoacidosis or nonketotic hyperglycemia.
The addition of potassium will make this a hypertonic fluid (since
potassium is as osmotically active as sodium), thereby delaying
reversal of the hyperosmolality.
Thus, 40 to 60 mEq of potassium per liter in one-half isotonic saline
is preferred.
33. Adverse effects of intravenous
potassium
Pain and phlebitis can occur during parenteral infusion of potassium
into a peripheral vein.
This primarily occurs at rates above 10 mEq/hour, but can be seen at
lower rates.
If pain occurs, either the infusion rate or, preferably, the potassium
concentration should be reduced.
34. Another potential problem with administering high potassium
concentrations in a single infusion container is inadvertent
administration of a large amount of potassium in a short
period of time, which is more likely to occur when an
infusion pump is not used.
Since the total extracellular potassium is normally 50 to 70
mEq, rapid infusion of 40 to 60 mEq of potassium can result
in severe hyperkalemia.
35. Recommended approach
Rate of administration
The recommended maximum rate of potassium administration is 10 to 20
mEq/hour in most patients. However, initial rates as high as 40 mEq/hour
have been used for life-threatening hypokalemia
In any 1000 mL-sized container of appropriate non-dextrose fluid, a
maximum of 60 mEq of potassium is suggested.
In a small-volume mini-bag of 100 to 200 mL of water that is to be infused
into a peripheral vein, 10 mEq of potassium is suggested.
In a small-volume mini-bag of 100 mL of water that is to be infused into a
large central vein, maximum of 40 mEq of potassium is suggested.
41. Calcium
Calcium directly antagonizes the membrane actions of hyperkalemia,
while hypocalcemia increases the cardiotoxicity of hyperkalemia.
Calcium can be given as either calcium gluconate or calcium chloride.
Calcium chloride contains three times the concentration of elemental
calcium compared with calcium gluconate (13.6 versus 4.6 mEq in 10
mL of a 10 percent solution).
However, calcium gluconate is generally preferred because calcium
chloride may cause local irritation at the injection site.
42. The usual dose of calcium gluconate is 1000 mg (10 mL of a 10 percent
solution) infused over two to three minutes, with constant cardiac monitoring.
The usual dose of calcium chloride is 500 to 1000 mg (5 to 10 mL of a 10
percent solution), also infused over two to three minutes, with constant
cardiac monitoring.
The dose of either formulation can be repeated after five minutes if the ECG
changes persist or recur.
43. Concentrated calcium infusions (particularly calcium chloride) are irritating to
veins, and extravasation can cause tissue necrosis.
As a result, a central or deep vein is preferred for administration of calcium
chloride.
Calcium gluconate can be given peripherally, ideally through a small needle or
catheter in a large vein.
Calcium should not be given in bicarbonate-containing solutions, which can
lead to the precipitation of calcium carbonate.
44. Insulin with glucose
Insulin administration lowers the serum potassium concentration by driving
potassium into the cells, primarily by enhancing the activity of the Na-K-
ATPase pump in skeletal muscle.
Glucose is usually given with insulin to prevent the development of
hypoglycemia.
However, insulin should be given alone if the serum glucose is ≥250 mg/dL
(13.9 mmol/L).
The serum glucose should be measured every hour for five to six hours after
the administration of insulin, given the risk of hypoglycemia.
45. Regimens
One commonly used regimen for administering insulin and glucose is
10 to 20 units of regular insulin in 500 mL of 10 percent dextrose,
given intravenously over 60 minutes.
Another regimen consists of a bolus injection of 10 units of regular
insulin, followed immediately by 50 mL of 50 percent dextrose (25 g
of glucose).
The effect of insulin begins in 10 to 20 minutes, peaks at 30 to 60
minutes, and lasts for four to six hours.
In almost all patients, the serum potassium concentration drops by 0.5
to 1.2 mEq/L.
46. Repeated dosing
Removal of excess potassium from the body (eg, with hemodialysis or
a gastrointestinal cation exchanger) is sometimes not feasible or must
be delayed.
Such patients can be treated with either a continuous infusion of insulin
and glucose or bolus infusions of insulin with glucose, repeated every
two to four hours, with serial monitoring of blood glucose levels.
47. Remove potassium from the body
Diuretics,
Gastrointestinal cation exchangers
Dialysis
48. Loop diuretics in patients without
severe renal impairment
In hypervolemic patients with preserved renal function (eg, patients with
heart failure), we administer 40 mg of intravenous furosemide every 12
hours or a continuous furosemide infusion.
In euvolemic or hypovolemic patients with preserved renal function, we
administer isotonic saline at a rate that is appropriate to replete hypovolemia
and maintain euvolemia, followed by 40 mg of intravenous furosemide every
12 hours or a continuous furosemide infusion.
49. Gastrointestinal cation exchangers
Patiromer or zirconium cyclosilicate
Use patiromer (8.4 g, repeated daily as needed) or zirconium
cyclosilicate (10 g three times daily for 48 hours).
The hypokalemic effect of zirconium cyclosilicate can be appreciated
within one hour, with a mean reduction in serum potassium of 0.7
mEq/L four hours after a 10-gram dose
sodium polystyrene sulfonate [SPS]
50. SPS with or without sorbitol should not be given to the following
patients because they may be at high risk for intestinal necrosis:
Postoperative patients
Patients with an ileus or who are receiving opiates
Patients with a large or small bowel obstruction
Patients with underlying bowel disease, eg, ulcerative colitis
or Clostridioides (formerly Clostridium) difficile colitis
52. Acute metabolic acidosis
We initiate bicarbonate therapy when
Acute metabolic acidosis has generated severe acidemia (ie, pH
less than 7.1).
Patients with less severe acidemia (eg, pH 7.1 to 7.2) who have
severe acute kidney injury
(ie, a twofold or greater increase in serum creatinine or oliguria);
bicarbonate therapy in such patients can potentially prevent the need for
dialysis and may improve survival
53. The clinical impact and treatment of severe acute metabolic acidosis remain controversial.
Some studies indicate that myocardial depression, decreased catecholamine efficacy, and
arrhythmias develop when the pH falls below 7.1
Human studies of the cardiovascular effects of severe acidemia have generally not
supported these tissue or animal experimental results.
Transient decreases in pH to 6.8 in individuals with diabetic ketoacidosis are not associated
with depressed cardiac function
Thus, many clinicians initiate treatment of metabolic acidosis when the bicarbonate level is
very low (eg, <5 mEq/L) and the pH is below 7.1.
54. With acute Kidney injury
The best data come from a randomized trial of critically ill patients with severe
metabolic acidosis
Most patients had lactic acidosis, and the mean arterial pH was 7.15.
In this trial, bicarbonate therapy (to maintain a pH >7.3) had no overall effect on
mortality or organ failure.
But, among the subgroup of patients with severe acute kidney injury (defined as
a twofold or greater increase in serum creatinine or oliguria), bicarbonate
therapy reduced 28-day mortality and the need for dialysis.
55. Virtual bicarbonate distribution space
After the infusion of sodium bicarbonate into the intravascular space, it
will rapidly distribute throughout the extracellular fluid space.
Some will enter the
Intracellular fluid space
Some will be titrated by hydrogen ions released from a variety of body
acid-base buffers,
Some will be titrated by organic acids
56. HCO3 deficit = HCO3 space x HCO3 deficit per liter
HCO3 space = [0.4 + (2.6 ÷ [HCO3])] x Lean body weight (in kg)
HCO3 deficit = 0.7 x Lean body weight (in kg) x (12 - 6) = 252 mEq
57. When the decision to administer sodium bicarbonate is made for a
patient with severe acute metabolic acidosis
It is usually accomplished with 50 mL vials of hypertonic sodium
bicarbonate.
They are generally available as 8.4 percent (50 mEq/50 mL) or 7.2
percent (44.6 mEq/50 mL).
If the virtual bicarbonate space is roughly 50 percent of lean body
weight, then one vial will raise the serum HCO3 concentration by
approximately 1.3 to 1.5 mEq/L in a 70 kg patient.
58. When chronic alkali treatment is required, options include the sodium or
potassium salts of either bicarbonate or a metabolizable anion such as
citrate or lactate.
The potassium salts are indicated when hypokalemia and total body
potassium deficits exist.
In general, the initial dose is 50 to 100 mEq per day, which is then titrated
up, or down, as required.
If ongoing bicarbonate losses persist or accelerate, the dose will need to
be adjusted accordingly.
