Amount of K+ lost in stool typically 10% of dietary intake. This can increase to 60% of intake in CKD.
Pseudohyperkalemia: exit of K+ from cells at time of venipuncture; tourniquet left too long, hemolysis, marked leucocytosis or thrombocytosis (latter two secondary to release of intracellular K+ after clot formation). Mention blood transfusions with iatrogenic.
Exer. Induced proportionate to degree exertion. BB mild degree. HyperKalemic PP: autosomal dominant d/o; episodic weakness/paralysis precipitated by stimuli that cause mild hyperkalemia; mutated skeletal musc. Na+ channel. Digitalis secondary inhibition Na/K/ATPase pump.
Impaired net acid excretion occurs in the TALH.
Review: Peaked T-waves (V2-V5), widened QRS and prolonged PR interval resulting in (Sine-wave)- I, AvR, V1-V2 .
Review: ECG changes of Hyperkalemia, may review back to ECG example in slide 5
Table of Pharmacological interventions summarized
Highlight Points: Do not wait for laboratory values to initiate treatment for patient with suspected Hyperkalemia based on ECG or PE
Hyperkalemia and its management
Dr. Muhammad Asim Fazal
MEEQAT GENERAL HOSPITAL
-The normal serum level of potassium is 3.5 to 5
-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
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
-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
I. Potassium release from cells
II. Excessive Intake
III. Decreased renal loss
Tumor Lysis Syndrome
Severe Digitalis toxicity
Hyperkalemic periodic paralysis
Succinylcholine; especially in case massive
trauma, burns or neuromuscular disease
- 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
-Most often, it is caused in a patient with impaired mechanisms
for the intracellular shift of potassium or for renal potassium
-Is the most common cause
--The causes of decreased renal potassium excretion include:
sickle cell disease
Medications (eg, potassium-sparing diuretics,
NSAID,angiotensin-convening enzyme inhibitors)
Shift from (ICF to
Excessive intake Decreased renal excretion
Diabetes mellitus (esp diabetic
Congestive heart failure
Sickle cell anemia
Potassium sparing Diuretics
chronic partial urinary tract obstruction
Oral or IV
-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
Weakness, which can progress to flaccid paralysis and
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
Weakness and fatigue(most common)
fFank muscle paralysis
Shortness of breath
-Vital signs generally are normal
bradycardia due to heart block
or tachypnea due to respiratory muscle
Assess renal function.
Check serum BUN and creatinine levels to
determine whether renal insufficiency is present
Check 24-hour urine for creatinine
Estimate the glomerular filtration rate (GFR)
Changes occur when Serum Potassium >6.0 mmol
T Waves peaked or Tented
loss of P Wave
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.
The first step
-determine life-threatening toxicity.
By Perform an ECG to look for cardiotoxicity.
- if present
Administer Iv Calcium Gluconate to ameliorate
-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
Anticipate EKG improvement within 3 minutes
The second step
-Is to identify and remove sources of potassium
-Change the diet to a low-potassium diet.
The third step
-Potassium shift from intravascular to
-Glucose and Insulin Infusion
Insulin Regular 10 units IV
50 ml 50% of dextrose
-Measure glucose and potassium every 2
-Correct metabolic acidosis with sodium
bicarbonate. 50ml I/V bolus
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
Monitor volume status and aim to maintain
-In patients with hyporeninemia or hypoaldosteronism
Renal excretion can be enhanced by administration of
an aldosterone analogue, such as 9-alpha
fluorohydrocortisone acetate (Florinef).
Is a final recourse for unresponsive
hyperkalemia with renal failure.
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.
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
Patients may have severe hyperkalemia with minimal ECG
changes, and prominent ECG changes with mild hyperkalemia.
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.
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
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