HYPERKALEMIA AND

ITS MANAGEMENT
Prepared by:
Dr. Muhammad Asim Fazal
MEEQAT GENERAL HOSPITAL
ALMADINAH ALMUNAWARAH

Objectives
Definition
Brief review of potassium regulation
processes
Causes
Clinical Manifestations
Therapy

Definition

Hyperkalemia = plasma K+ concentration >

5.1mmol/L

Critical hyperkalemia = plama K+

concentration > 6.5 mmol/L

-The normal serum level of potassium is 3.5 to 5

mmol/L
-Daily Requirements 1-1.5 mmol/kg

-Dietary sources include dried fruits; legumes; meats;

poultry; fish; soy; bananas; citrus fruits; potatoes;
tomatoes; broccoli; mushrooms; dark, leafy green
vegetables

Potassium Regulation Review

Intracellular concentration about 150
mmol/L
The passive outward diffusion of K+ is the
most important factor that generates the
resting membrane potential.
Maintenance of steady state requires K+
ingestion = K+ excretion
Nearly all regulation of renal K+ excretion
and total body K+ balance occurs in the
distal nephron, via principal cells
Potassium secretion regulated by
aldosterone and plasma K+ concentration

Potassium
homeostasis
-Gastrointestinal absorption is complete, resulting in
daily excess intake of about 1 mmol/kg/d
This excess is
(10%) excreted through the gut
(90%) excreted through the kidneys
- The most important site of regulation is the
distal nephron, including the distal convoluted
tubule, the connecting tubule, and the cortical
collecting tubule

Causes of Hyperkalemia
I.

Potassium release from cells

II.

Excessive Intake

III.

Decreased renal loss

IV.

Iatrogenic

(Consider pseudohyperkalemia)

Potassium release from cells

Intravascular hemolysis
Tumor Lysis Syndrome
Rhabdomyolysis
Metabolic acidosis
Hyperglycemia
Severe Digitalis toxicity
Hyperkalemic periodic paralysis
Beta-blockers
Succinylcholine; especially in case massive
trauma, burns or neuromuscular disease

Excessive intake
-Uncommon cause of hyperkalemia.

-The mechanisms for shifting potassium intracellularly

and for renal excretion allow a person with normal
potassium homeostatic mechanisms to ingest
virtually unlimited quantities of potassium in healthy
individuals.

-Most often, it is caused in a patient with impaired

mechanisms for the intracellular shift of potassium or
forrenal potassium excretion

Decreased excretion
Is the most common cause- -The causes of decreased renal potassium
excretion include:
- renal failure
diabetes mellitus
sickle cell disease
Medications (eg, potassium-sparing diuretics,
NSAID,angiotensin-convening enzyme inhibitors)

Causes
Shift from (ICF
to ECF)

Decreased renal excretion

Hyperosmolality

Diabetes mellitus (esp diabetic

nephropathy

rhabdomyolysis
Renal failure

Excessive intake
Oral or IV
Potassium
Supplementati
on

tumor lysis
Congestive heart failure
Succinylcholin

Salt substitute
SLE

insulin deficiency
Sickle cell anemia
acute acidosis.
NSAID
ACE Inhibitor
Potassium sparing Diuretics
Multiple Myeloma
chronic partial urinary tract

Blood
transfusion

Pseudohyperkalemia
-It is the term applied to the clinical situation in
which in vitro lysis of cellular contents leads to the
measurement of a high serum potassium level not
reflective of the true in vivo level.

-Condition occurs most commonly with

red cell hemolysis during the blood draw
(tourniquet too tight or the blood left sitting too
long),

Clinical Manifestations
Weakness,

which can progress to flaccid paralysis and

hypoventilation.
Secondary to prolonged partial depolarization from the elevated K+ ,
which impairs membrane excitability.

Metabolic

acidosis, which further increases K+

Secondary to hyperkalemia impairing renal ammoniagenesis and

absorption, and thus net acid excretion.
Altered

electrical activity of heart, cardiac arrhythmias .

ECG changes in order of appearance:

Tall, narrow-based, peaked T waves
Prolonged PR interval and QRS duration
AV conduction delay
Loss of P waves
Progression of QRS duration leading to sine wave pattern
Ventricular fibrillation or asystole

Symptoms
Weakness and fatigue(most common)
fFank muscle paralysis
Shortness of breath
Palpitations

Physical
-Vital signs generally are normal

Except
bradycardia due to heart block
or tachypnea due to respiratory muscle
weakness.

Lab
Assess renal function.
Check serum BUN and creatinine levels to
determine
whether renal insufficiency is
present
Check 24-hour urine for creatinine
clearance
Estimate the glomerular filtration rate (GFR)

ECG
Changes occur when Serum Potassium >6.0
mmol /L
A-Initial
T Waves peaked or Tented
B-Next
ST depression
loss of P Wave
QRS widening
C-Final
Biphasic wave (sine wave) QRS and T fusion

Measure complete
metabolic profile
-Low bicarbonate may suggest hyperkalemia
due to metabolic acidosis.

-Hyperglycemia suggests diabetes mellitus.

Treatment
The first step
-determine life-threatening toxicity.
By Perform an ECG to look for cardiotoxicity.
- if present
Administer Iv Calcium Gluconate to ameliorate
cardiac toxicity.
-Initial dose: 10 ml over 2-5 minutes
Second dose after 5 minutes if no response
-Effect occurs in minutes and lasts for 30-60
minutes
Anticipate EKG improvement within 3 minutes

The second step

-Is to identify and remove sources of potassium
intake

-Change the diet to a low-potassium diet.

The third step

-Potassium shift from intravascular to
intracellular
-Glucose and Insulin Infusion
Insulin Regular 10 units IV
50 ml 50% of dextrose

-Measure glucose and potassium every 2

hours
-Correct metabolic acidosis with sodium
bicarbonate. 50ml I/V bolus
-Ventolin Nebulization

The fourth step

-Is to increase potassium excretion from the body
-in normal kidney function by the administration of
parenteral saline accompanied by a loop diuretic,
such as furosemide Dose: 20-40 mg IV.

-Discontinue potassium-sparing diuretics,

angiotensin-converting enzyme inhibitors,
angiotensin receptor blockers, and other drugs that
inhibit renal potassium
excretion.
Monitor volume status and aim to maintain
euvolemia.

-Inpatients with hyporeninemia or hypoaldosteronism

Renal excretion can be enhanced by administration of
an aldosterone analogue, such as 9-alpha
fluorohydrocortisone acetate (Florinef).

Emergency dialysis
Is a final recourse for
unresponsive hyperkalemia with
renal failure.

Clinical Scenario

A 52-year-old man with hypertension and diabetes

complains of weakness, nausea, and a general sense of
illness, that has progressed slowly over 3 days. His
medications include a sulonylurea, a diuretic, and an ACE
inhibitor. On examination, he appears lethargic and ill. His
BP is 154/105 mm Hg, HR 70bpm, temperature 98.6 F, and
respiratory rate 22 breaths/min. The physical examination
reveals moderate jugular venous distension, some minor
bibasilar rales, and lower extremity edema. He is oriented
to person and place but is able to give further history. The
ECG shows a wide complex rhythm.

Laboratory studies performed are significant for potassium

7.8 mEq/L, BUN is 114 mg/dL and creatinine is 10.5.

Diagnostics/Images: ECG

ECG Changes of Hyperkalemia

Easily Distinguished ECG signs:

peaked T wave.
prolongation of the PR interval
ST changes (which may mimic myocardial
infarction)
very wide QRS, which may progress to a sine
wave pattern and asystole.

Patients may have severe hyperkalemia with

minimal ECG changes, and prominent ECG
changes with mild hyperkalemia.

Analysis

Diagnosis: Hyperkalemia- Severe

Classification of Hyperkalemia
NORMAL: 3.5 to 5.0 mEq/L.
MILD: 5.5 to 6.0 mEq/L
SEVERE: Levels of 7.0 mEq/L or greater

It is important to suspect this condition from

the history and ECG, because laboratory test
results may be delayed and the patient could
die before those test results become available.

1st Line option

Clinical Pearls
Symptoms of hyperkalemia are usually
nonspecific, so risk
factors must be used to suspect the diagnosis

ECG changes consistent with hyperkalemia should

be treated immediately as a life-threatening
emergency. Do not await laboratory confirmation.

Intravenous calcium is the antidote of choice for lifethreatening arrhythmias related to hyperkalemia,
but its effect is brief and additional agents must be
used

THANKYOU