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BOX 39.1 EKG MANIFESTATIONS OFCALCIUM
ABNORMALITIES
Hypocalcemia
Increased Q- T interval
Prolonged S- T segment
T wave inversion
Ventricular dysrhythmias
Atrial tachydysrhythmias
Hypercalcemia
Decreased Q- T interval
Decreased S- T segment
Increased P- R interval
ProlongedQRS
Appearance ofJwave
Bradydysrhythmias
BOX 39.2 TREATMENT OFHYPOCALCEMIA
Immediate Treatment
INTRAVENOUS CALCIUM
Calcium gluconate 20– 30mg/ kg
Calcium chloride 10– 20 mg/ kg (central venousline)
(Note:10 mL of 10% calcium gluconate contains 94 mg
of calcium, and 10 mL of 10% calcium chloride contains
272 mg of calcium)
Long- Term Treatment
Oral calcium
VitaminD
e neuromuscular eects of hypercalcemia are nonspecic and include weakness and fatigue. Disorientation,
confusion, and hallucinations may progress to lethargy, seizures, andcoma.
cell cancers, lymphomas, and cancers of the ovaries, kidneys,
and breast are frequently associated with hypercalcemia.
7
Eects of hypercalcemia on the EKG include a shortening of the Q- T interval and the S- T segment (Figure 39.2).
Hypercalcemia tends to stabilize the cardiac cell membrane
and increases the depolarization required to initiate an
action potential.
Bradydysrhythmias are typical of hypercalcemia
(Box39.2).
ASSESSMENT OFTHE PATIENT— HYPOCALCEMIA
e history of a total thyroidectomy earlier in the day
should immediately suggest the likelihood of hypocalcemia. Dyspnea and stridor suggest hypocalcemia, but could
also be secondary to bilateral recurrent laryngeal nerve
damage. Hypotension may be a sign of decreased cardiac
output secondary to poor myocardial contractility. An
ECG should be obtained for measurement of the Q- T
interval and detection of dysrhythmias, along with a blood
sample to measure serum electrolytes and ionized calcium.
Once blood samples have been obtained, treatment can
commence.
e classic signs of hypocalcemia by physical examination
are Chovstek’s sign and Trousseau’s sign. Chovstek’s sign is
positive when twitching of the lip occurs in response to tapping the facial nerve just anterior to the ear lobe or just below
the zygomatic arch. Apositive Trousseau’s sign occurs when a
blood pressure cu inated on the upper arm provokes carpal
spasm in the hand. Apositive Trousseau’s sign is more predictive of hypocalcemia than a positive Chovstek’ssign.
Figure39.2 Short Q- T interval secondary to hypercalcemia. SOURCE:From Crawford
MH, DiMarco JP. Cardiolog y. Mosby 2001:8, 4.8., with permission.
276 SECTION C. ELECTROLYTE DISTURBANCES
ASSESSMENT OFTHE PATIENT— HYPERCALCEMIA
is patient presents with a symptom complex that is
nonspecic, and the diagnosis is not readily apparent. e
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history of chronic hypertension, renal stones, and probable osteoporosis is suggestive of chronic hypercalcemia.
iazides are known to increase ionized calcium levels, and
the administration of hydrochlorothiazide may have been
Hypercalcemia may either potentiate or decrease the
response to nondepolarizing muscle relaxants. Objective
monitoring of neuromuscular function should be employed
to guide the adequacy of relaxation and recovery of function.
the trigger for the acute increase in calcium levels. e key
to the diagnosis, however, was the signicantly elevated
serum calcium level of 4mmol/ L (16 mg/ dL). Acalcium
level of that magnitude warrants continuous monitoring of
the EKG for any evidence of intracardiac conduction delay
and bradydysrhythmias.
TREATMENT OFHYPOCALCEMIA
e treatment of signicant hypocalcemia is the intravenous administration of calcium gluconate (20– 30 mg/ kg).
Calcium chloride (10– 20 mg/ kg) can also be used, but
is very irritating to peripheral veins and should ideally be
CONSIDERATIONS FORANESTHESIA
Calcium is so vital to normal cardiac and neuromuscular
function that normocalcemia should be achieved prior
to the induction of anesthesia for any elective case. Any
changes in electrolytes or autonomic balance caused by
administered via a central venous line. Hypocalcemia that
persists aer the initial dose of calcium gluconate should be
treated with a calcium gluconate infusion.
Treatment- resistant hypocalcemia can be treated with
oral calcium preparations and vitamin D.Calcitriol is a vitamin D preparation with rapid onset of action.
anesthesia will aggravate the eects of hypocalcemia or
hypercalcemia.
Clinical Case #1 (Hypocalcemia)
Halogenated, inhaled anesthetics have been shown to prolong the Q- T interval. Although the clinical signicance
of this eect is unclear, inhaled anesthetics might increase
TREATMENT OFHYPERCALCEMIA
erapy for hypercalcemia is aimed at reducing calcium
levels, rehydration, and determining the cause of the hypercalcemia (Box 39.3). Rehydration with isotonic saline and
diuresis with loop diuretics (furosemide) aer hydration
will increase renal excretion of calcium. Calcitonin is rapid
the potential for dysrhythmias and decreased myocardial
contractility caused by hypocalcemia. Intravenous calcium
gluconate (20– 30 mg/ kg) or calcium chloride (10– 20 mg/
kg) during anesthesia should improve cardiac function.
Measurement of ionized calcium during the perioperative
period is a much better indicator of functional calcium balance than the total calciumlevel.
BOX 39.3 TREATMENT OFHYPERCALCEMIA
Fluid Therapy
Hydration with normalsaline
e eects of calcium at the neuromuscular junction are
complex. In general, it should be anticipated that hypocalcemia will potentiate the eects of nondepolarizing muscle
relaxants. Reduced doses of neuromuscular blockers should
be employed, and objective monitoring of neuromuscular
relaxation is recommended.
Clinical Case #2 (Hypercalcemia)
8
Hypercalcemia poses a greater threat during the periopera-
Diuresis with furosemide
Calcitonin
(2– 4 U/ kg sub- q or IM) every 12hours
Bisphosphanates
Pamidronate
(90 mg IV over 4hours)
tive period than hypocalcemia, as it takes longer to reduce
calcium levels than to increase levels. In most cases, treatment for hypercalcemia will have been initiated prior to the
Zoledronate
(4 mg IV over 15 minutes)
induction of anesthesia.
e cardiac eects of hypercalcemia include a decreased
Renal Dialysis
Q- T interval and delayed cardiac conduction. Fatal dysrhythmias have occurred from severe hypercalcemia.
9
If medical therapy fails or the patient has renal insufciency
HYPOCALCEMIA/HYPERCALCEMIA 277
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acting and reduces calcium levels by inhibiting the bone
resorptive eect of osteoclasts. Resistance to calcitonin, however, develops quickly. Intravenous bisphosphonates (pamidronate, zoledronate) also inhibit bone resorption and are
used more frequently than calcitonin for the treatment of
hypercalcemia.
10
Hypercalcemia is not an indication for emergent surgery and treatment allows time to determine the underlying
cause and plan denitive treatment. For the patient with
primary hyperparathyroidism, medical management provides a bridge to parathyroidectomy.
extracellular calcium into the myoplasm, and low
plasma calcium concentrations are associated with
decreased myocardial function. Normal ionized
calcium levels in the blood are 1.15mmol/ L, and
several studies show a direct correlation between the
ionized calcium level and myocardial contractility. e
eects of hypocalcemia on the electrical activity of the
heart, prolonged Q- T interval, and arrythmogenesis,
can decrease cardiac output. Chronic hypocalcemia
can cause heart failure. e heart failure, however, is
in most cases reversible and can be corrected by the
administration of calcium.
FOLLOW- UP OFCLINICAL CASE #1
(HYPOCALCEMIA)
e history of the recent total thyroidectomy raised a strong
index of suspicion for hypocalcemia. Blood samples were
immediately obtained for measurement of ionized calcium
and parathyroid hormone level. e EKG showed a long
Q- T interval and T wave inversion. e ionized calcium
was 0.5mmol/ L, and she received 30 mg/ kg of calcium gluconate via a peripheral IV. e muscle weakness improved
quickly aer the administration of calcium, and the ECG
normalized. e parathyroid hormone level was 7 pg/ mL
(normal > 13 pg/ ml). Since the initial dose of calcium will
only maintain normal calcium levels for 2 to 3 hours, a calcium gluconate infusion was initiated.
e presence of detectable parathyroid hormone is a
good indicator that parathyroid function may return in 4
to 6 weeks. She was treated with calcium and vitamin D for
6 weeks. e repeat parathyroid hormone level at 6 weeks
was 16 pg/ mL. Calcium supplementation was discontinued
at thattime.
2. What are the ECG changes associated with
hypocalcemia and hypercalcemia? e classic change in
the EKG that occurs with hypocalcemia is prolongation
of the Q- T interval. Because the heart rate aects
the duration of the Q- T interval, the corrected Q- T
interval (QTc) can be calculated with the Hodges
formula:QTc=QT + 0.00175 (ventricular rate − 60).
e upper limit of normal for QTc is 0.46 seconds. e
QTc is slightly longer for adult females, and increases
with age. Hypocalcemia also produces terminal T wave
inversion in some leads. If the calcium level continues
to decline, tachydysrhythmias develop. Hypercalcemia
shortens the QTc and produces a sharp rise in the rst
part of the T wave that may obscure the ST segment.
Severe hypercalcemia causes bradydysrhythmias.
3. Should ondansetron be administered for antiemesis
to patients with long Q- T syndrome? ere are more
than 40 case reports of perioperative torsades de
pointes most likely associated with prolongation of
the Q- T interval. Many things that may occur in the
perioperative period can prolong the Q- T interval.
FOLLOW- UP OFCLINICAL CASE #2
(HYPERCALCEMIA)
Since there was no evidence of malignancy, the presumptive diagnosis was primary hyperparathydoidism. Imaging
studies performed the day aer therapy for hypercalcemia
was begun detected a probable adenoma in the parathyroid
gland. Aer 5days of treatment, the ionized calcium level
decreased to 1.7mmol/ L and the patient was referred for
surgical removal of a parathyroid adenoma.
ere are also congenital causes of a prolonged Q- T
interval. Drugs known to prolong the Q- T interval
are droperidol, ondansetron, sevourane, antibiotics,
and antihistamines. Electrolyte disturbances such as
hypokalemia, hypomagnesemia, and hypocalcemia
can also prolong the Q- T interval. It is highly likely
that those 40 case reports are a consequence of
interactions between medications and electrolyte
changes that trigger torsade de pointes. It would be
dicult in an individual patient with a long Q- T
interval to know if ondansetron could provoke a fatal
CASE- BASED LEARNING DISCUSSION
ventricular dysrhythmia. It is also likely that most
cases of prolonged Q- T interval are not recognized
preoperatively. It would be prudent to avoid the use
1. Can hypocalcemia cause heart failure? Cardiac
contraction is highly dependent on the inux of
of drugs that can prolong the Q- T interval in patients
with a preexisting long Q- T interval. Second- generation
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279
5- HT3 receptor antagonists such as palonosetron may
not prolong the Q- T interval. is quality would be a
welcome advantage for newer antiemetics.
4. What are common causes of hypercalcemia? Ninety
percent of the cases of hypercalcemia are caused
Calcitonin lowers calcium in 4– 6 hours by 0.5mmol/L
by inhibition of bone- resorbing osteoclasts.
Bisphosphonates inhibit osteoclast activity and can be
expected to lower calcium in 2 to 4days. Hypercalcemia
secondary to malignancy has a very poor prognosis.
by primary hyperparathyroidism and malignancy.
Pathologic increases in parathyroid hormone secretion
can be caused by parathyroid adenomas, parathyroid
REFERENCES
hyperplasia, or parathyroid carcinoma. Malignancyinduced hypercalcemia is usually secondary to
production of parathyroid hormone related protein
by the tumor, especially squamous cell carcinoma.
Hematologic malignancies can produce hypercalcemia
by direct osteolysis, and lymphoid malignancies
produce excessive calcitriol. Drugs that can cause
hypercalcemia include lithium, thiazide diuretics,
vitamin A, and increased intake from taking calcium
supplements in too many forms, producing milk- alkali
syndrome (calcium + antacids).
5. What is the treatment for acute hypercalcemia? Severe
hypercalcemia (>3.5mmol/ L) requires rapid therapy.
Severe hypercalcemia causes renal dysfunction (direct
renal vasoconstriction), hypovolemia, and a shortened
Q- T interval and promotes bradydysrhythmias.
erapy should be initiated with volume repletion
with normal saline to promote diuresis and calcium
excretion. Volume expansion typically lowers the
blood calcium level by 0.5mmol in minutes to hours.
1. Bers DM. Cardiac excitation- contraction coupling. Nature.
2002;415:198– 205.
2. Bers DM. Cardiac sarcoplasmic reticulum calcium leak: basis
and roles in cardiac dysfunction. Annual Review of Physiology.
2014;76:107– 27.
3. Christou N, Mathonnet M. Complications aer total thyroidectomy. Journal of Visceral Surgery. 2013;150:249– 56.
4. Youngwirth L, Benavidez J, Sippel R, Chen H. Postoperative parathyroid hormone testing decreases symptomatic hypocalcemia and
associated emergency room visits aer total thyroidectomy. Surgery.
2010:148:841– 46.
5. Nijjer S, Ghosh AK, Dubrey SW:Hypocalcemia, long QT interval and atrial arrhythmias. British Medical Journal Case Reports.
2010;doi:10.1136/ bcr.08.2009.2216.
6. Singh DN, Gupta SK, Kumari N, et al. Primary hyperparathyroidism presenting as hypercalcemic crisis:twenty year experience.
Indian Journal of Endocrinology and Metabolism. 2015;19:100– 5.
7. McCurdy MT, Shanholtz CB. Oncologic emergencies. Critical
Care Medicine. 2012;40:2212– 22.
8. Aguilera IM, Vaughan RS. Calcium and the anaesthetist.
Anaesthesia. 2000;55:779– 90.
9. Carroll R, Matn G. Endocrine and metabolic emergencies.
erapeutic Advances in Endocrinology and Metabolism.
2010;1:29– 33.
10. Ahmad S, Kuraganti G, Steenkamp D. Hypercalcemia crisis:a clinical review. American Journal of Medicine. 2015;128:239– 45.
HYPOCALCEMIA/HYPERCALCEMIA 279
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40.
HYPOMAGNESEMIA/ HYPERMAGNESEMIA
AaliShah
CLINICAL CASE#1
A 72- year- old, 93- kg man was scheduled for an exploratory laparotomy for resection of an ascending colon tumor.
His medical history included long- standing hypertension
treated with losartan (100 mg daily) and chronic reux
esophagitis treated for several years with omeprazole (20
PATHOPHYSIOLOGY
Magnesium is the second most common intracellular cation
and is fundamental to more than 600 enzymatic reactions
important to energy metabolism and protein synthesis.
Magnesium is also critical to neuromuscular excitability
and regulation of parathyroid hormone secretion.
1,2
mg twice daily). Preoperative vital signs were:heart rate, 76
beats per minute; blood pressure, 136/ 78mmHg; respiratory rate, 12 breaths per minute; SpO2, 96%. e preoperative EKG was interpreted as normal.
Anesthesia was induced with propofol (2 mg/ kg), fentanyl (1 mcg/ kg ) and cis- atracurium (0.8 mg/ kg). Aer
induction, ventilation was controlled via facemask with 5%
sevourane in oxygen. Following muscle relaxation, the trachea was intubated without diculty. Five minutes aer
tracheal intubation, a wide complex, polymorphic ventricular tachycardia developed. Sevourane was discontinued,
and the patient was ventilated with 100% oxygen. Sinus
rhythm was successfully restored aer two electrical countershocks. Aretrospective review of his preoperative EKG
revealed a prolonged Q- T interval.
MECHANISM
Less than 1% of the total body magnesium is found in the
extracellular space, and 70% of that is in the ionized form.
e normal total serum magnesium is 0.8 to 1.2mmol/ L
(1.5 to 2.4 mEq/ L). Magnesium is absorbed in the small
intestine by active and passive transport mechanisms.
Eighty percent of magnesium is ltered by the glomeruli,
but more than 95% is reabsorbed in the renal tubules.
e eects of magnesium are seen in many organs
including the brain, lung, pancreas, liver, bone, and
immune system. Two functions of magnesium that are of
special interest to the anesthesiologist concern neuromuscular excitability and the inuence of magnesium on cardiac rhythm.
Magnesium functions as a calcium antagonist in the
CLINICAL CASE#2
muscle. At rest, calcium- binding sites in the myoplasm
are occupied by magnesium. e stimulus for muscle con-
A 37- year- old female was admitted to the labor ward for
treatment of preeclampsia with magnesium. Aer 24 hours
of labor, the decision was made to perform a cesarean section because of labor arrest and nonreassuring fetal heart
tones. Upon arrival to the operating room, the patient complained of severe weakness and was unable to sit up for the
spinal anesthetic. At that time, it was noted that the patient
had inadvertently received a bolus of intravenous magnesium sulfate. A spinal anesthetic was quickly performed
with the patient in the le lateral decubitus position. Soon
aer insertion of the spinal anesthetic, she complained of
severe dyspnea. General anesthesia was initiated and tracheal intubation performed.
traction releases calcium from the sarcoplasmic reticulum,
which in turn displaces magnesium and starts the contraction process. Hypomagnesemia, consequently, results in
muscle hyperexcitability and hypercontractility. In contrast,
hypermagnesemia inhibits release of presynaptic acetylcholine and decreases postsynaptic sensitivity to acetylcholine.3
Magnesium aects phase 2 (plateau phase) and phase 3
(repolarization) of the cardiac action potential by inhibiting
calcium channels. is modulation of calcium entry prevents
cell toxicity. Hypomagnesemia causes cardiac hyperexcitability and dysrhythmias. Hypermagnesemia slows cardiac
conduction and causes heart block. Magnesium also promotes vasodilation of the peripheral vasculature.
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RISK OFHYPOMAGNESEMIA (CLINICAL CASE#1)
Hypomagnesemia is relatively common in critically ill
patients (>65%), but the clinical signicance is unclear.
Symptoms secondary to a low magnesium level do not
generally develop until the serum magnesium level is less
than 0.50mmol/ L. Neuromuscular manifestations include
weakness, tremor, and tetany. Drowsiness, seizures, and
coma are likely to occur when the serum magnesium levels
decreases to 0.40mmol/ L.
4
e EKG changes that occur with hypomagnesemia
include a prolonged Q- T interval, attened T waves, prominent U waves, and a widened QRS complex. Apotentially
fatal ventricular dysrhythmia (torsades de pointes) can
occur (Figure 40.1, Box 40.1). Several drugs may accentuate
the prolongation of the Q- T interval induced by hypomagnesemia (Table40.1).
RISK OFHYPERMAGNESEMIA (CLINICAL
BOX 40.1 EKG CHANGES CAUSED BYABNORMAL
MAGNESIUMLEVELS
Hypomagnesemia
Prolonged Q- T interval
Prominent Uwaves
Widened QRS complex
Polymorphic ventricular tachycardia
(Torsades de pointes)
Hypermagnesemia
Prolonged P- R interval
Prolonged QRS interval
Third- degree atrioventricularblock
CASE#2)
e most common cause of hypermagnesemia that anesthesiologists confront is inadvertent magnesium overdose in
pregnant patients being treated with magnesium. e risks
are progressive muscle weakness and cardiac dysrhythmias.
When magnesium levels reach 4– 5mmol/ L, deep tendon
reexes are lost. Respiratory insuciency develops when
magnesium levels exceed 6.5mmol/ L. Progressive eects of
hypermagnesemia on the EKG include prolongation of the
P- R and QRS intervals, T wave changes, and third- degree
atrioventricular block (Box40.1).
is required. Arterial oxygen saturation, end- tidal carbon
dioxide, heart rate, and blood pressure were all normal
until the ventricular tachycardia developed. Changes in
electrolyte levels are also common causes of cardiac dysrhythmias, but must be measured for an accurate diagnosis.
Correction of any signicant changes in serum electrolytes
can rapidly decrease the likelihood of future dysrhythmias.
Serum electrolytes obtained immediately aer resumption of sinus rhythm in this patient were:Na 135mmol/ L,
K3.5mmol/ L, ionized calcium 1.2mmol/ liter, and magnesium 0.4mmol/ liter. Intravenous magnesium 25 mg/ kg was
ASSESSMENT OFHYPOMAGNESEMIA (CLINICAL
CASE#1)
administered. e serum magnesium level 30 minutes later
was 0.8mmol/ L.
e initial manifestation of severe hypomagnesemia in this
patient was a life- threatening ventricular dysrhythmia. e
rst step is correction of the rhythm; this patient responded
promptly to cardioversion. When the etiology of a cardiac
dysrhythmia is not evident, a systematic diagnostic plan
Figure40.1 Torsades de Pointes (polymorphic ventricular tachycardia) typical
of hypomagnesemia. SOURCE:From Omar HR, Sprenker C, Karlnoski R, Mangar D,
Camporesi EM. American Journal of Emergency Medicine. 2014;32:683.e5– 683e7. With
permission.
HYPOMAGNESEMIA/HYPERMAGNESEMIA 281
ASSESSMENT OFHYPERMAGNESEMIA (CLINICAL
CASE#2)
Magnesium is recommended for the treatment of severe
preeclampsia and eclampsia. Antepartum administration
of magnesium to women in premature labor is also recommended for neuroprotection of the fetus. Magnesium
reduces blood pressure (vasodilation), decreases bloodbrain barrier permeability (limits cerebral edema) and has
anticonvulsant eects. Patients are normally loaded with 4
to 6 grams of magnesium sulfate over 30 minutes. e loading dose is followed by an infusion at 1 to 2 grams per hour.
Although plasma magnesium levels are not routinely measured during magnesium therapy for preeclampsia, the target plasma level is 2mmol/ L. Monitoring of deep tendon
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TABLE40.1 DRUGS THAT PROLONG THEQ- T INTERVAL
However, a cogent argument for routine measurement of
magnesium levels can bemade.
Proton- pump inhibitors Antiarrhythmics
Omeprazole
Esomeprazole
Pantoprazole
Droperidol Amiodarone
Ondansetron Cocaine
Antidepressants Methadone
Bupropion
Quinidine
Fecainide
Sotalol
e Q- T interval is the time from the start of the Q
wave to the end of the T wave. Heart rate aects the Q- T
interval. e Q- T interval is longer with a slower heart rate
and shorter with a fast heart rate. e corrected QT interval is designated as the QTc. Some drugs may change the QT interval by an eect on heart rate. is change may not,
however, increase the likelihood of a cardiac dysrhythmia.
4
Prolongation of the Q- T interval by magnesium can
be worsened by halogenated, inhaled anesthetics. e
eect is varied and depends on age of the patient, rapidity
of induction, and rate of change in the inhaled anesthetic
Fluoxitene
Peroxetine
concentration.5 Elderly patients are especially susceptible to
prolongation of the Q- T interval by sevourane.6 Propofol
and opioids in usual clinical doses have little eect on the
Antimicrobials
Amphotericin B
Ciprooxacin
Fluoconazole
Er ythromycin
Q- T interval. Adjuvant perioperative drugs such as droperidol, ondansetron, dolasetron, antidepressants, and protonpump inhibitors can prolong the Q- T interval. In addition
to acquired changes in the Q- T interval, there are patients
with congenital syndromes characterized by long Q- T
intervals. ese patients are at risk for ventricular dysrhythmias and sudden death.
7,8
e perioperative period may increase the likelihood of
Cyclosporine
Tacrolimus
torsade de pointes in susceptible patients because of exposure to multiple drugs with eects on the Q- T interval,
changes in autonomic balance, congenital disorders, and
coexisting electrolyte abnormalities. Increased awareness of
reexes, blood pressure, respiratory rate, heart rate, and
level of consciousness is used to gauge adequacy of treatment and potential toxicity.
When the magnesium overdose was discovered, the
the risks associated with prolongation of the Q- T interval
during the perioperative period is warranted. Amore thorough review of his preoperative EKG might have detected
the prolonged Q- T interval.
patient was very somnolent but arousable, and her blood
pressure was 90/ 60mmHg. Her blood pressure prior to the
overdose was 130/ 75mmHg. Blood levels of calcium and
potassium should also be measured, as hypocalcemia and
hyperkalemia oen occur with hypermagnesemia.
CONSIDERATIONS
FORANESTHESIA— HYPERMAGNESEMIA
As long as coagulation is normal, regional anesthesia is the
anesthetic of choice for patients with preeclampsia. Despite
CONSIDERATIONS
FORANESTHESIA— HYPOMAGNESEMIA
is case is an example of a subtle, underlying metabolic
abnormality in a patient with no preoperative clinical manifestation. Administration of anesthesia produced an eect
that magnied the coexisting hypomagnesemia and led to
a signicant intraoperative event. is type of situation is
a relatively common way that underlying electrolyte abnormalities present in the perioperative period. Although magnesium levels can be readily measured, it has not become a
standard component of perioperative laboratory evaluation.
the fear of hypotension, spinal or epidural anesthesia is associated with less hypotension in preeclamptic women and a
decreased risk of peripartum central nervous system complications.9 e severe weakness of this patient posed the threat
of respiratory failure, and tracheal intubation was indicated.
General anesthesia was induced with propofol (1.5 mg/ kg)
and rocuronium (0.5 mg/ kg). e onset of muscle relaxation
was rapid and tracheal intubation was performed without
diculty. e eect of hypermagnesemia on the neuromuscular junction is very similar to the action of nondepolarizing muscle relaxants. Even pregnant patients receiving
therapeutic doses of magnesium are exquisitely sensitive
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to nondepolarizing muscle relaxants. It should be anticipated that this patient will have a prolonged response to
rocuronium and postoperative ventilation will be required.
or ventricular pacing may be benecial.10 For this patient,
cardioversion and the administration of 25 mg/ kg of intravenous magnesium was successful. Since surgery had not
commenced, the procedure was canceled and the patient
TREATMENT FORCLINICAL CASE #1
(HYPOMAGNESEMIA)
e treatment of torsades de pointes, like the treatment of
most cardiac dysrhythmias, is inuenced by the eect of
was awakened. Amagnesium level measured 60 minutes
aer the initial dose of magnesium was 0.7mmol/ L. Acontinuous, intravenous infusion of magnesium was initiated,
and repeat magnesium levels were measured. Aer 48 hours,
the patient’s magnesium level stabilized at 1.2mmol/ L.
the dysrhythmia on cardiac output (Box 40.2). Torsades de
pointes typically occurs in self- terminating bursts, and the
administration of magnesium is eective. If cardiac output
is compromised, the treatment of choice is electrical cardioversion. Antiarrhythmics that prolong repolarization may
aggravate the situation. Increasing the heart rate shortens
repolarization. Administration of isoproterenol, atropine,
TREATMENT FORCLINICAL CASE #2
(HYPERMAGNESEMIA)
e treatment of hypermagnesemia depends on the domi-
nant clinical eects. Severe muscle weakness and impend-
ing respiratory failure mandated tracheal intubation and
ventilatory support. Adverse cardiac eects of hypermagne-
semia are best treated with calcium. e administration of
BOX 40.2 TREATMENT OFTORSADES DE POINTES
loop diuretics will increase magnesium excretion. Dialysis
is indicated for patients with renal dysfunction and signi-
If Little or No Effect ofTorsades de Pointes
onCardiacOutput
cant hypermagnesemia (Box40.3).
Magnesium sulfate 20– 30 mg/ kg intravenously
If Signicant Effect ofTdP onCardiacOutput
Electrical cardioversion
PharmacologicAgents
Isoproterenol
Atropine
Increase HeartRate
Decrease repolarizariontime
Decrease Q- T interval
PHENYTOIN
Decreases ventricular automaticity
Increases A- V conduction velocity
LIDOCAINE
Decreases ventricular automaticity
FOLLOW- UP OFCLINICAL CASE#1
Since chronic administration of proton- pump inhibitors
(omeprazole) can cause hypomagnesemia, this medication
was discontinued and therapy with ranitidine was initiated.
His magnesium level remained normal for the next 3 weeks,
and surgery was rescheduled. e patient subsequently had
an uneventful perioperative course.
Hypomagnesemia is more common than previously
thought, and magnesium levels are oen not routinely
measured. Patients receiving medications that can increase
magnesium excretion may benet from preoperative measurement of magnesium levels.
FOLLOW- UP OFCLINICAL CASE#2
At the conclusion of the cesarean section, the patient was
still very weak. Train- of- four measured with a peripheral
BOX 40.3 TREATMENT OFHYPERMAGNESEMIA
Ventilatory support for skeletal muscle weakness
CardiacPacing
Increases heartrate
Decreases repolarizationtime
HYPOMAGNESEMIA/HYPERMAGNESEMIA 283
Calcium for cardiac conductiondelay
Loop diuretics to increase magnesium excretion
Dialysis if there is signicant renal dysfunction
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nerve stimulator showed only 3 of 4 twitches. Her plasma
magnesium level was 4.2mmol/ L. She was transferred to
the obstetric intensive care unit for postoperative mechanical ventilation. Aer 10 hours of mechanical ventilation, she
regained signicant strength and met extubation criteria.
e neonate was oppy and weak aer delivery and
required tracheal intubation in the delivery suite with
subsequent transfer to the neonatal intensive care unit
(NICU). e baby was extubated 12 hours aer admission
to the NICU and was observed for 72 hours aer delivery.
torsades de pointes. Magnesium is rapid acting
and readily available in the operating room. Many
antiarrhythmics such as quinidine, ecainide, and
amiodarone prolong the Q- T interval and may make
the situation worse. Although experience in humans
is limited, lidocaine and phenytoin may be eective
for treatment of torsades. Isoproterenol increases the
heart rate, which decreases the QT interval and may be
eective treatment for drug- induced torsades. However
isoproterenol may also prolong the Q- T interval and
increase the number of EADs in patients withcLQTS.
CASE- BASED LEARNING DISCUSSION
1. What conditions other than hypomagnesemia cause a
prolongation of the Q- T interval? ere are acquired
and congenital causes of Q- T prolongation. Acquired
causes are predominantly drug induced. Drugs
that might be used in the perioperative period that
can prolong the Q- T interval include sevourane,
propofol, ondansetron, amiodarone, amitriptyline,
methadone, cocaine, and erythromycin. Congenital
forms of long QT syndrome (cLQTS) include RomanWard syndrome, Jervell- Lange- Nielsen syndrome,
and Brugada syndrome. Nearly 20 genes have been
associated with cLQTS. Despite the long list of drugs
that prolong the Q- T interval and congenital causes,
the incidence of torsades de pointes in the perioperative
period is low. It is likely that a combination of multiple
factors may need to occur in the perioperative period
in order to cause ventricular dysrhythmias. ese
factors may include hypomagnesemia, hypokalemia,
hypocalcemia, Q- T prolonging drugs, and increased
4. What are common causes of hypermagnesemia?
Hypermagnesemia is almost always secondary to
increased ingestion and/ or renal failure. ere are
numerous case reports of hypermagnesemia from
ingestion of large amounts of magnesium citrate
for a bowel prep or self- administration as a laxative.
ese cases frequently occur in elderly patients with
inammatory bowel disease and renal dysfunction.
e other cause and the one that anesthesiologists are
most likely to encounter is an overdose of intravenous
magnesium to a pregnant woman with preeclampsia.
5. Why does hypermagnesemia increase the eect of
nondepolarizing muscle relaxants? Magnesium inhibits
the action of calcium within the muscle cell, and
hypermagnesemia interferes with calcium- stimulated
muscle contraction. Magnesium decreases the onset
time of nondepolarizing neuromuscular blockers and
prolongs their eect. Administration of calcium may
block some of the eect of hypermagnesemia, but
tracheal intubation and mechanical ventilation until the
magnesium level declines is usually required.
adrenergic stimulation.
2. Why does a prolonged Q- T interval predispose
to ventricular dysrhythmias? e Q- T interval
represents the time for ventricular depolarization and
repolarization. Repolarization occurs from the J point
to the end of the T wave. Ventricular dysrhythmias
occur as a result of early aerdepolarizations (EAD)
that produce aberrant automaticity, and any drug or
condition that prolongs the QT interval increases the
likelihood of torsades de pointes. Although not rmly
established, the administration of magnesium most
likely blocks the calcium ux that triggers automaticity
fromEADs.
3. What are the therapeutic options for torsades de
pointes? Magnesium is the best initial therapy for
284 SECTION C. ELECTROLYTE DISTURBANCES
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