Prepared by:Dr. Muhammad Asim FazalMEEQAT GENERAL HOSPITALALMADINAH ALMUNAWARAH

Definition

Brief review of potassium regulation processes

Causes

Clinical Manifestations

Therapy

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

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 aldosteroneand plasma K+ concentration

Potassium homeostasis

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

-Gastrointestinal absorption is complete, resulting in daily excess intake of about 1 mmol/kg/d

I. Potassium release from cells

II. Excessive Intake

III. Decreased renal loss

IV. Iatrogenic

(Consider pseudohyperkalemia)

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

- 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

Excessive intake

-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)

CausesShift from (ICF to ECF)

Decreased renal excretion Excessive intake

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 Supplementation

Salt substitute

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 withred cell hemolysis during the blood draw

(tourniquet too tight or the blood left sitting too long),

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 wavesProlonged PR interval and QRS durationAV conduction delayLoss of P wavesProgression of QRS duration leading to sine wave patternVentricular fibrillation or asystole

Weakness and fatigue(most common)

fFank muscle paralysis

Shortness of breath

Palpitations

Symptoms

-Vital signs generally are normal

Exceptbradycardia due to heart block

or tachypnea due to respiratory muscle weakness.

Physical

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.

-Measure glucose and potassium every 2 hours

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

-Ventolin Nebulization

The third step

-Potassium shift from intravascular to intracellular

-Glucose and Insulin InfusionInsulin Regular 10 units IV 50 ml 50% of dextrose

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.

-In patients with hyporeninemia or hypoaldosteronismRenal 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.

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 and asystole.

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.

1st Line option

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