5. CLINICAL MANIFESTATIONS
Neurological manifestations predominate and
are generally thought to result from cellular
dehydration.
Restlessness,
lethargy,
Hyperreflexia
seizures,
coma, and ultimately death may occur
Rapid decreases in brain volume can rupture
cerebral veins and result in focal intracerebral or
subarachnoid hemorrhage.
6. TREATMENT
The treatment of hypernatremia is
aimed at restoring plasma osmolality
to normal as well as correcting the
underlying cause.
Water deficit is calculated by
Free H2O deficit = {(plasma Na+/
140) – 1} × TBW
correction should be done over 48 h
with a hypotonic solution such as 5%
dextrose in water
7. Rapid correction of hypernatremia can
result in seizures, brain
edema, permanent neurological
damage, and even death.
In general, decreases in plasma
sodium concentration should not
proceed at a rate faster than 0.5
mEq/L/h.
The goal of treatment is Na+ less
8. ANESTHETIC
CONSIDERATION
Hypernatremia has been demonstrated
to increase the MAC for inhalation
anesthetics
Elective surgery should be postponed in
patients with significant hypernatremia
(>150 mEq/L)
Both water and isotonic fluid deficits
should be corrected prior to elective
surgery.
10. HYPONATREMIA
Na+ less than 135 mEq/L.
Most common electrolyte disorder
Hyponatremia is commonly caused by
cellular edema with the presence of
hypotonicity.
12. CLINICAL MANIFESTATION
Patients with ([Na +] > 125 mEq/L)
are frequently asymptomatic.
Serious manifestation occur below
120
Early symptoms are typically
nonspecific and may include
anorexia, nausea, and weakness.
Progressive cerebral edema, however,
results in lethargy, confusion,
seizures, coma, and finally death.
13. TREATMENT
• The treatment of hyponatremia is
directed at correcting both the
underlying disorder as well as the
plasma [Na+].
• Correction of plasma [Na+] to greater
than 125 mEq/L is usually suffi cient to
alleviate symptoms.
14. Desired value, the Na+ deficit, can be estimated by the
following formula:
Na+ deficit =TBW ×(desired [Na+]−present [Na+]
Excessively rapid correction of hyponatremia has
been associated with demyelinating lesions in the pons
( central pontine myelinolysis),
Th e following correction rates have been suggested:
for
mild symptoms, 0.5 mEq/L/h or less; for
moderate symptoms, 1 mEq/L/h or less; and for
severe symptoms, 1.5 mEq/L/h or less.
15. ANESTHETIC
CONSIDERATION
A plasma sodium concentration greater than 130
mEq/L is usually considered safe for patients
undergoing general anesthesia.
In most circumstances, plasma [Na+] should be
corrected to greater than 130 mEq/L for elective
procedures, even in the absence of neurological
symptoms.
Lower concentrations may result in significant
cerebral edema that can be manifested
intraoperatively as a decrease in MAC or
postoperatively as agitation, confusion, or
somnolence.
17. HYPOKALEMIA
Hypokalemia, 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.
19. 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.
20. 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 .
21.
22. 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
23. ANESTHETIC
CONSIDERATION
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.
24. 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
26. HYPERKALEMIA
Hyperkalemia exists when plasma [K
+] exceeds 5.5 mEq/L.
kidneys can excrete as much as 500
mEq of K +per day.
So hyperkalemia rarely occurs in
normal individuals
27. 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.
28. 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.
29.
30. TREATMENT
Hyperkalemia exceeding 6 mEq/L
should always be corrected.
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
31. 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
32. 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
33. ANESTHETIC
CONSIDERATION
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.
34. The avoidance of metabolic or
respiratory acidosis is critical
Ventilation should be controlled under
general anesthesia, and mild
hyperventilation may be desirable.
