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

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

3.  Definition
 Brief review of potassium regulation
processes
 Causes
 Clinical Manifestations
 Therapy

4.  Hyperkalemia = plasma K+ concentration >
5.1mmol/L
 Critical hyperkalemia = plama K+
concentration > 6.5 mmol/L

5. -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

6.  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

7. 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

8. I. Potassium release from cells
II. Excessive Intake
III. Decreased renal loss
IV. Iatrogenic
(Consider pseudohyperkalemia)

9.  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

10. 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 for renal potassium
excretion

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

12. Causes
Shift from (ICF to
ECF)
Excessive intake Decreased renal excretion
Hyperosmolality
rhabdomyolysis
tumor lysis
Succinylcholin
insulin deficiency
acute acidosis.
Diabetes mellitus (esp diabetic
nephropathy
Renal failure
Congestive heart failure
SLE
Sickle cell anemia
NSAID
ACE Inhibitor
Potassium sparing Diuretics
Multiple Myeloma
chronic partial urinary tract obstruction
Oral or IV
Potassium
Supplementatio
n
Salt substitute
Blood
transfusion

13. 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),

14.  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

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

16. Physical
-Vital signs generally are normal
Except
bradycardia due to heart block
or tachypnea due to respiratory muscle
weakness.

17. 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)

18. 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

22. Measure complete metabolic profile
-Low bicarbonate may suggest hyperkalemia due
to metabolic acidosis.
-Hyperglycemia suggests diabetes mellitus.

23. 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

24. The second step
-Is to identify and remove sources of potassium
intake
-Change the diet to a low-potassium diet.

25. 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

26. 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.

27. -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.
-In patients with hyporeninemia or hypoaldosteronism
Renal excretion can be enhanced by administration of
an aldosterone analogue, such as 9-alpha
fluorohydrocortisone acetate (Florinef).

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

29.  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.

31.  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.

32.  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.

33. 1st Line option

34.  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 life-threatening
arrhythmias related to hyperkalemia, but its effect
is brief and additional agents must be used