MANAGEMENT OF

HYPOKALAEMIA AND
HYPERKALAEMIA IN
SURGICAL PATIENT
DR. Osemwota F O
Introduction
Potassium ion is cation, it’s a positively charged
electrolyte, which is important physiologically due to their
important function in nerve conduction and muscle
contraction. In most cells, the dominant conductance on
the plasma membrane is potassium, so this gradient
actually sets the cell voltage. The resting membrane
potentials of these tissues are directly related to the
relative intracellular and extracellular Potassium
concentrations.
RENAL HANDLING OF
POTASSIUM
Renal Regulation of Potassium
Potassium is freely filtered in the glomerulus.
It is reabsorbed in the proximal tubule almost in
proportion to the amount of water that is
reabsorbed, and this is not regulated.
It is also reabsorbed in the thick ascending limb,
driven by the lumen positive voltage there, and it is
passively reabsorbed.
So at beginning of the cortical collecting duct, the
luminal fluid has almost no potassium in it.
It is really irrelevant how much K+ that is filtered,
because none of it makes it to the urine.
Renal Regulation of Potassium ctd
•Then what happens is K+ is secreted in the
cortical collecting duct, and the amount of K +
secretion in the cortical collecting duct determines
the amount of K+ in the urine.

•There is a little bit of K+ reabsorption in the

medullary collecting duct.

•In fact almost all of the regulation and almost all

of the renal disorders of potassium homeostasis
can be ascribed to the cortical collecting duct.
Principal Cell

•The principal cell in the Cortical

Collecting Duct regulates
Potassium secretion.

•It has an epithelial sodium channel

on the luminal side, and an apically
located potassium channel.

•There is a basolateral
sodium/potassium ATPase, and also
a basolaterally located potassium
channel.

•In kidney cells, the Na/K ATPase is

located on only one side of the cell.

•It pumps sodium out of the cell and

pumps potassium into the cell.
 
•Disturbances in potassium homoeostasis are
common, especially among hospitalised
patients.
•Given the fact that untreated hypokalaemia
or hyperkalaemia is associated with high
morbidity and mortality, it is critical to
recognise and treat these disorders promptly
Intake of Potassium
Diets are relatively rich in potassium with the
average western diet containing 50 - 100
mmol of potassium a day.
Food and fruits high in potassium include : -
Banana, oranges, tomato, avocado, green
beans, carrot, yam, guava etc.
HYPOKALAEMIA
HYPOKALAEMIA
 Hypokalaemia, defined as plasma [K
+] less than 3.5 mEq/L.
 A decrease in plasma [K +] from 4
mEq/L to 3 mEq/L usually represents
a 100- to 200-mEq deficit,
 whereas plasma [K +] below 3 mEq/L
can represent a deficit anywhere
between 200 mEq and 400 mEq.
CAUSES
EXCESS RENAL LOSS

Mineralocorticoid excess
Primary hyperaldosteronism (Conn’s syndrome)
Renin excess
Renovascular
hypertension Diuresis
Chronic metabolic alkalosis
G.I LOSS
Renal tubular acidosis
Vomiting
Diarrhea,
ECF → ICF shifts
Acute alkalosis
Hypokalemic periodic paralysis
Barium ingestion
Insulin therapy
CLINICAL MANIFESTATION
 Most patients are asymptomatic until
plasma [K +] falls below 3 mEq/L.

 Cardiovascular effects are most

prominent and include an abnormal
ECG , arrhythmias, decreased cardiac
contractility, and a labile arterial blood
pressure due to autonomic
dysfunction.
 Chronic hypokalemia has also been
reported to cause myocardial fibrosis.
 ECG manifestations are primarily due
to delayed ventricular repolarization
and include T-wave flattening and
inversion,
 an increasingly prominent U wave, ST-
segment depression, increased P-
wave amplitude, and prolongation of
the P–R interval .
CLINICAL MANIFESTATION

 Neuromuscular effect: weakness +/-

respiratory failure

TREATMENT
 Hypokalaemia is corrected by
administration of IV KCL

 Kdeficit(in mmol)=(Knormal lower

limit – Kmeasured) x kg body weight
x 0.6
TREATMENT
 Intravenous replacement usually be reserved for patients
with, or at risk for, significant cardiac manifestations or
severe muscle weakness.

 Because of potassium’s irritative effect on peripheral

veins, peripheral intravenous replacement should not exceed
8 mEq/h.

 Dextrose-containing solutions should generally be avoided

because the resulting hyperglycemia and secondary
insulin secretion may actually worsen the low plasma [K
+].

 More rapid intravenous potassium replacement (10–20

mEq/h) requires central venous administration and
close monitoring of the ECG.

 Intravenous replacement should generally not exceed

240 mEq/d
ANESTHETIC
CONSIDERATIO
N
 The decision to proceed with elective
surgery is often based on lower
plasma [K +] limits somewhere
between 3 and 3.5 mEq/L.
 In general, chronic mild hypokalemia
(3–3.5 mEq/L) without ECG changes
does not substantially increase
anesthetic risk.
 The intraoperativelypotassium should be
given if atrial or ventricular arrhythmias
develop.

 Glucose-free intravenous solutions should be

used and hyperventilation avoided to prevent
further decreases in plasma [K +].

 Increased sensitivity to neuromuscular

blockers (NMBs) may be seen; therefore
dosages of NMBs should be reduced 25–
50%, and a nerve stimulator should be used
to follow both the degree of paralysis and the
adequacy of reversal
HYPERKALAEMIA
HYPERKALEMIA
 Hyperkalaemia exists when plasma
[K
+] exceeds 5.5 mEq/L.

 kidneys can excrete as much as 500

mEq of K +per day.

 So hyperkalaemia rarely occurs

in normal individuals
CLINICAL MANIFESTATION
 Th e most important effects of
hyperkalemia are on skeletal and cardiac
muscle.

 Skeletal muscle weakness is generally

not seen until plasma [K +] is greater
than 8 mEq/L,

 Cardiac manifestations are primarily

due to delayed depolarization, and are
consistently present when plasma [K +]
is greater than 7 mEq/L.
 ECG changes characteristically progress
sequentially from symmetrically peaked
T waves →widening of the QRS
complex →prolongation of the P–R
interval →loss of the P wave →loss of R-
wave amplitude →ST-segment
depression →an ECG that resembles a
sine wave, before progression to
ventricular fibrillation and asystole.

 Hypocalcemia, hyponatremia, and

acidosis accentuate the cardiac effects
of hyperkalemia.
 TREATMENT
Hyperkalaemia exceeding 6mEq/L should
always be corrected.

In clinical practice, parenteral administration

of potassium through:- IV fluids,
hyperalimentation and red blood cell
transfusion should be considered when
evaluating patients with hyperkalaemia.
TREATMENT
Treatment is directed to reversal of
cardiac manifestations and skeletal
muscle weakness, and to restoration of
normal plasma [K+]

Calcium (5–10 mL of 10% calcium

gluconate or 3–5 mL of 10% calcium
chloride) partially antagonizes the
cardiac effects of hyperkalemia and is
useful in patients with marked
hyperkalemia
 When metabolic acidosis is present,
intravenous sodium bicarbonate
(usually 45 mEq) will promote cellular
uptake of potassium and can
decrease plasma [K+] within 15 min

 Β Agonists promote cellular uptake of

potassium and may be useful in acute
hyperkalemia associated with
massive transfusions
 An intravenous infusion of glucose
and insulin (30–50 g of glucose with
10 units of insulin) is also eff ective in
promoting cellular uptake of potassium
and lowering plasma [K+], but may
take up to 1 h for peak effect.

 Dialysis is indicated in symptomatic

patients with severe or refractory
hyperkalemia
ANESTHETIC
CONSIDERATIO
N
Elective surgery should not be
undertaken in patients with significant
hyperkalemia.
 Succinylcholine is contraindicated, as
is the use of any potassium containing
intravenous solutions such as
lactated Ringer’s injection.
 The avoidance of metabolic or
respiratory acidosis is critical

 Ventilation should be controlled under

general anesthesia, and mild
hyperventilation may be desirable.
 CONCLUSION
Disturbances in potassium homoestasis
manifested as either hypokalaemia or hyperkaemia
result in cardiac and muscular abnormalities which
if left untreated are associated with high morbidity
and mortality.

Therefore Hypokalaemia and Hyperkalaemia must

be recognised early and prompt treatment
instituted.
.