HYPERKALEMIA

APPROACH
AND
MANAGEMENT
Dr. RENUKA RAYANA
1st year Med PG
MIMS
HYPERKALEMIA
■ Defined as a plasma potassium level of >5.5 mEq/L

Causes:

I. Pseudohyperkalemia

■ Artificial increase in K+ after Venipuncture, fist clenching

■ Invitro efflux of k: thrombocytosis, erythrocytosis,

leukocytosis,

■ In vitro hemolysis:

Hereditary defects in red cell membrane transport

II. Intra- to extracellular shift
■ Acidosis – Uptake of H+, efflux of K+

NAGMA

■ Hyperosmolality; hypertonic dextrose, mannitol, IVIG -

Solvent Drag effect

■ β2 -Adrenergic antagonists (non cardioselective agents)

Suppresses catecholamine stimulated renin release- in

turn aldosterone synthesis

■ Digoxin and related glycosides (yellow oleander)- Inhibits

Na/K ATPase
■ Hyperkalemic periodic paralysis- Episodic muscle
weakness associated with Hyper kalemia. It is a
Na channelopathy

■ Cationic amino acids (Lysine, arginine, and ε-

aminocaproic acid)cause efflux of k

■ Succinylcholine; depolarises Muscle cells, Efflux of

K+ through AChRs

■ Rapid tumor lysis

III. Inadequate excretion

A. Inhibition of the renin-angiotensin-aldosterone axis;

(↑ risk of hyperkalemia when these drugs are used in

combination)

■ ACE inhibitors

■ Renin inhibitors; Aliskiren

■ ARBS

■ Blockade of the mineralocorticoid receptor:

- Spironolactone, Eplerenone,

■ Blockade of the epithelial sodium channel (ENaC):

Amiloride, Triamterene, Trimethoprim
B. Decreased Distal Delivery

■ CHF

■ Volume depletion

C. Hyporeninemic Hypoaldosteronism

■ Tubulointerstitial diseases:

SLE, sickle cell anemia, obstructive uropathy

■ Diabetes, diabetic nephropathy

■ Drugs: NSAIDs, COX2 inhibitors, β-blockers, cyclosporine,

tacrolimus

■ CKD, advanced age

■ Pseudo hypoaldosteronism type II

D. Renal resistance to mineralocorticoid

■ Tubulointerstitial diseases:

SLE, amyloidosis, sickle cell anemia, obstructive

uropathy, post ATN

■ Hereditary:

Pseudohypoaldosteronism type I

E. Advanced renal insufficiency

■ CKD,ESRD

■ Acute oliguric kidney injury

F. Primary Adrenal Insufficiency
■ Autoimmune: Addison’s disease, polyglandular
endocrinopathy

■ Infectious: HIV,CMV,TB, disseminated fungal infection

■ Infiltrative: amyloidosis, malignancy, metastatic cancer

■ Drug-associated: heparin, LMW heparin

■ Hereditary: adrenal hypoplasia congenita, congenital

lipoid adrenal hyperplasia, aldosterone synthase
deficiency

■ Adrenal hemorrhage or infarction, APLA syndrome

Clinical Features

■ Hyperkalemia is a medical emergency due to its effect

on heart.

■ Patients may complain of palpitations, chest pain or

syncope.

■ There may be sudden cardiac death.

■ Cardiac Arrythmias include- Sinus Bradycardia, Sinus

arrest, VT, VF, Asystole
ECG Changes

■ ECG findings generally correlate with the potassium

level,

■ Potentially life-threatening arrhythmias - occur without

warning at almost any level of hyperkalemia.

■ In patients with organic heart disease and an

abnormal baseline ECG, bradycardia may be the
only new ECG abnormality.
K+ 5.5-6.5 mEq/L

■ Early changes include tall, peaked T waves with a

narrow base, best seen in precordial leads;

K+ level of 6.5-7.5mEq/L

■ In addition to peaked T waves,

■ Decreased or disappearing P waves

K+ level of 7-8mEq/L

In addition to the above changes there will be wide QRS

K+ level higher than 8.0 mEq/L

■ The ECG shows absence of P wave,

■ progressive QRS widening, and .

■ The progressively widened QRS eventually merges with

the T wave, forming a sine wave pattern.

■ Ventricular fibrillation or asystole follows.

Sine Wave appearance
 APPROACH
■ The cause of hyperkalemia is usually evident from
History
Physical examination
Basic laboratory tests

■ The history should focus

Medications
Diet and dietary habits
Reduction of urine output
BP, volume status

Symptoms that suggest a particular cause (e.g.,

periodic weakness).
 APPROACH
Clear evidence of transcellular shift:

■ Hypertonicity

■ Beta blockers

■ Succinylcholine

■ Metabolic acidosis

■ Decreased insulin
 APPROACH
Lab tests
■ RFT

■ Serum osmolality,Electrolytes- including Mg, Ca

■ Urine PH, creatinine, potassium, sodium, and

osmolality

■ Complete blood count (CBC)

■ Metabolic profile

■ ECG

■ TTKG
If urinary Na<20 indicates distal Na delivery is the
limiting factor

Volume replacement or with furosemide may

effectively decrease the serum K
■ The serum-to-tubular fluid ratio of potassium at the
TRANSTUBULAR POTASSIUM
level of the cortical collecting tubule, where
GRADIENT(TTKG)
potassium is secreted.

■ TTKG = Uk x Posm
Sk x Uosm
■ TTKG <7 – Impaired renal K excretion may be due
to hypoaldosterone ,aldosterone resistance,
hyporenemic hypoaldosteronism

■ TTKG>10–indicates intact renal mechanism of K

excretion.

■ With intact renal function if hyperkalemia persists

its due to decreased circulating volume
APPROACH TO HYPERKALEMIA
 TREATMENT
Three main approaches to the treatment of
hyperkalemia :

■ ●Antagonizing the membrane effects of potassium

with calcium

■ ●Driving extracellular potassium into the cells

■ ●Removing excess potassium from the body

■ ECG manifestations of hyperkalemia- medical
emergency and treated urgently.

■ Patients with significant hyperkalemia (K+≥6.5 mM) in

the absence of ECG changes should also be
aggressively managed

.
 Immediate antagonism of the cardiac
effects of hyperkalemia
■ IV calcium serves to protect the heart by increasing the
action potential threshold

■ Recommended dose is 10 mL of 10% calcium

gluconate(or 3-4ml of calcium chloride) infused
intravenously over 2–3 min with cardiac monitoring

■ Effect starts in 1-3min ,lasts for 30-60min

■ Dose can be repeated if no change in ecg or reoccurs

■ Should be given carefully in patients on digoxin

■ 10ml calcium gluconate +100ml of 5% dextrose is

infused over 20-30 min to avoid acute
hypercalcemia
 Redistribution into cells
1. Insulin
■ lowers plasma K+ concentration by shifting K+ into cells

■ 10U IV Regular insulin followed immediately by 50ml of 50%

dextrose

■ Effect begins in 10-20 min,peaks at 30-60min,lasts for 4-6hrs

■ Followed by 10%dextrose @50;75ml/hr

■ If glucose >200-250mg/dl then insulin is administered alone

with glucose monitoring
 Redistribution into cells
2. β2-agonists
■ Most commonly albuterol, are effective but
underused agents for the acute management of
hyperkalemia.

■ Dose:10-20mg albuterol+4ml NS inhaled over 10min

■ Effect starts in 30min peaks in 90 min lasts for 2-6hrs

■ Side effects: hyperglycemia and tachycardia

■ ~20% ESRD pateints are resisitant to beta2 agonists

IV Bicarbonate: used in metabolic acidosis

■ NO ROLE in acute treatment of hyper kalemia

■ Slowly attenuates hyperkalemia

■ Should not be given repeatedly as hypertonic IV bolus

because its associated with hyper natremia

■ Infused as 150mEq + 1litre of D5

Removal of Potassium:

Cation exchange resins, Diuretics, and Hemodialysis.

1. Cation Exchange Resins:

■ Sodium polystyrene sulfonate (SPS) exchanges Na+

for K+in the GI tract and increases the fecal excretion
of K+

■ Dose of SPS is 15–30 g of powder, almost always given

in a premade suspension with 33% sorbitol.

■ The effect of SPS on plasma K+ concentration is slow;

■ The full effect may take up to 24 h and usually
requires repeated doses every 4–6 h.

■ Side effect: intestinal necrosis of colon or ileum is

rare but fatal complication with SPS alone or along
with sorbitol

■ So when ever possible alternative therapies are

used for acute management

■ Alternatively calcium based resins may be more

appropriate in patients with increased ECFV
■ Therapy with iv saline may be beneficial in hypovolemic patients
with oliguria and decreased distal delivery of Na+, reduced renal K+
excretion.

2.Loop and Thiazide diuretics:

Can be used to reduce plasma K+ concentration in volume-replete or

hypervolemic patients with sufficient renal function

3.Hemodialysis :

It is the most effective and reliable method to reduce plasma K+ .

■ Hemodialysis is the most effective and reliable
method to reduce plasma K+ .

■ The amount of K+ removed during hemodialysis

depends on
■ The relative distribution of K+ between ICF and ECF

■ The type and surface area of the dialyzer used,

■ dialysate and blood flow rates,

■ dialysate flow rate, dialysis duration, and the plasma-

to- dialysate K+ gradient.