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A 76-year-old man is scheduled for a hemicolectomy. His past medical history is
significant for third degree heart block treated with a permanent pacemaker.
Problems with electrocautery use in this patient can be minimized by:
• placing the grounding pad near the pacemaker
• using infrequent bursts of longer duration
• the use of a bipolar cautery
• reducing the surface area of the return electrode
the use of a bipolar cautery.
Electrical interference from the electrocautery can be interpreted by the pacemaker
as myocardial activity and suppress pacemaker activity. These problems can be
minimized by limiting use to short bursts, placing the grounding pad as far from
the pacemaker as possible and using a bipolar cautery.
Effects of lidocaine include:
a. increased intracranial pressure
b. increased refractory period of cardiac muscle
c. decreased fibrinolysis
d. myonecrosis
d. myonecrosis
Intravenous lidocaine decreases cerebral blood flow unless seizure activity
develops. Lidocaine decreases the refractory period of cardiac muscle and
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decreases platelet aggregation while enhancing fibrinolysis. Local anesthetics have
been shown to cause lytic degeneration and necrosis of muscle fibers when directly
injected into the muscle (trigger point injections).
During fetal monitoring, Type III decelerations are thought to be related to:
• head compression
• umbilical cord compression
• uteroplacental insufficiency
• placental abruption
umbilical cord compression
Type III, or variable, decelerations are the most common type of decelerations.
They are thought to be related to umbilical cord compression and intermittent
decreases in umbilical blood flow.
The arteria radicularis magna, or artery of Adamkiewicz, most commonly arises
from:
• T4 - T8
• T8 - L2
• L2 - L4
• L4 - S1
T8 - L2.
A major complication of thoracic aortic surgery is paraplegia, occurring in up to
20% of elective cases, and is secondary to spinal cord ischemia. The arteria
radicularis magna supplies blood to the anterior spinal artery. The arteria
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radicularis magna has a variable origin from aorta, arising between T5 - T8 in
15%, between T9 - T12 in 60% and between L1 - L2 in 25% of individuals.
A 55-year-old woman with a history of congenital long QT syndrome is
undergoing a hysteroscopy for abnormal uterine bleeding. She had uneventful
induction of general anesthesia but after paracervical block with lidocaine develops
ventricular tachycardia with morphological appearance of torsades de pointe.
Which of the following medications should be AVOIDED in the treatment of her
arrhythmia?
• Amiodarone
• Calcium chloride
• Esmolol
• Magnesium sulfate
Amiodarone.
Congenital long QT syndrome may occur in conjunction with other hereditary
syndromes, such as Jervell, Lange-Nielsen or Romano-Ward syndrome, or
acquired as a result of pharmacologic or metabolic etiologies. It is an issue of
cellular repolarization which precipitates tachyarrhythmias, most commonly
polymorphic ventricular tachycardia or torsades de pointe. There are multiple
subtypes that affect both potassium and/or sodium channels. The arrhythmias may
be precipitated by sympathetic activation, auditory stimuli or at rest. Family history
may be positive for sudden cardiac death and the ECG significant for prolonged
corrected QT interval > 430ms or bizarre odd-appearing T waves. Treatment
includes magnesium for arrhythmias, possible permanent pacemaker, or beta
blockers for subtypes 1 and 2, but amiodarone is considered contraindicated as it
prolongs the QT interval.
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A 35-year-old woman who underwent orthotopic heart transplantation 2 years ago
for nonischemic cardiomyopathy presents after a motor vehicle accident for
exploratory laparotomy under general anesthesia. Intraoperatively, her blood
pressure is 75/35 mmHg and heart rate is 90 bpm. After the administration of
phenylephrine, which of the following hemodynamic responses do you MOST
expect?
• HR decreased, BP increased
• HR decreased, BP no change
• HR no change, BP increased
• HR no change, BP no change
HR no change, BP increased.
After heart transplantation, the heart is completely denervated. The normal resting
heart rate is relatively tachycardic at 90-100 bpm due to lack of vagal tone. Vagal
bradycardic responses (to laryngoscopy, hypertension, carotid sinus massage) will
also be absent. Over time, however, many patients require permanent pacemaker
placement for treatment of significant bradycardia. After heart transplant, patients
are not able to respond to demands for increased cardiac output with increased
heart rate. Thus in this situation of a trauma with potentially significant blood loss,
a normal patient would have tachycardia but a heart transplant patient has no
change in heart rate, only hypotension. Instead for heart transplant patients, cardiac
output is augmented by increased stroke volume. For this reason it is important to
maintain adequate intravascular volume. The transplanted heart is not able to
respond to medications that block the parasympathetic system. Bradycardia and
hypotension have to be treated with medications that have a direct effect such as
epinephrine and isoproterenol. Phenylephrine will result in increased blood
pressure, but no change in heart rate. Indirect and mixed indirect/direct-acting
drugs have minimal effect or have the effect of their direct components.
The postretrobulbar block apnea syndrome:
• is likely secondary to intravascular injection