Neurointensive & Perioperative care Flashcards
- Which one of the following statements regarding cerebral blood flow is LEAST accurate?
a. Cerebral blood flow to white matter is
approximately 25 ml/100 g/min
b. Total cerebral blood flow is approximately 750 ml/min in adults
c. Regional cerebral blood flow tends to
track cerebral metabolic rate of oxygen
consumption rather than cerebral metabolic rate of glucose consumption
d. Cerebral blood flow to gray matter is
approximately 80 ml/100 g/min
e. Brain tissue accounts for 20% of basal
oxygen consumption and 25% of basal
glucose consumption
c—Regional cerebral blood flow tends to track cerebral metabolic rate of oxygen consumption rather than cerebral metabolic rate
of glucose consumption
Despite its relatively small size (about 2% of total
body mass; adult brain weighs approx 1.4 kg), the
high metabolic activity of the brain (20% of basal
oxygen consumption and 25% of basal glucose
consumption) requires reliable and responsive
cerebral blood flow (CBF). The brain receives
15% of cardiac output (750 ml/min in adults) at
rest, which equates to an average CBF of about
50 ml/100 g/min. Mean CBF values for white
and gray matter vary between 20-30 and 75-
80 ml/100 g/min, respectively. Regional CBF
therefore parallels metabolic activity and varies
between 10 and 300 ml/100 g/min. Transmission
of electrical impulses by the brain is achieved by
energy-dependent neuronal membrane ionic gradients. Increases in local neuronal activity, therefore, are accompanied by increases in the regional
cerebral metabolic rate. CBF changes parallel
these metabolic changes (i.e. flow-metabolism
coupling). However, increases in regional CBF
during functional activation tend to track the
cerebral metabolic rate of glucose utilization
but may be far in excess of that required for the
cerebral metabolic rate of oxygen consumption
(CMRO2). The regulatory changes involved in
flow-metabolism coupling have a short latency
(about 1 s) and may be mediated by regional metabolic or neurogenic pathways. In health, flow
and metabolism are closely matched, with
remarkably little variation in the oxygen extraction fraction (OEF) across the brain despite wide
regional variations in CBF and CMRO2.
- Which one of the following statements
regarding intracranial compliance is LEAST
accurate?
a. Increase in the volume of one intracranial
compartment will lead to a rise in ICP
unless it is matched by an equal reduction
in the volume of another compartment
b. Cerebral compliance is equal to intracranial volume displaced divided by the resultant change in intracranial pressure
c. CSF and CBV compartments normally
represent a volume of approximately
1400 ml
d. Additional intracranial volume is initially
accommodated with little or no change
in ICP
e. Once craniospinal buffering capacity is
exhausted further small increases in intracranial volume lead to substantial rises
in ICP
c—CSF and CBV compartments normally represent a volume of approximately 1400 ml
The volume of intracranial contents is approximately 1700 ml and can be divided into three
physiologic compartments: Brain parenchyma
1400 ml (80%, of which10% is solid material
and70% is tissue water), Cerebral blood volume
(CBV)150 ml (10%), CSF 150 ml (10%).
Intracranial pressure (ICP) is the pressure within
the intracranial space relative to atmospheric pressure. “Normal” ICP is generally less than 10-
15 mmHg and varies with age being lower in
infants and children. However, it is rarely constant
and is normally subject to substantial individual
variations and physiologic fluctuations, for example, with change in position, straining, and coughing. The generalized Monro-Kellie doctrine states
that an increase in the volume of one intracranial
compartment will lead to a rise in ICP unless it
is matched by an equal reduction in the volume
of another compartment. Because brain parenchyma is predominantly represented by incompressible fluid, the vascular and CSF
compartments play the key role in buffering additional intracranial volume by increasing venous
outflow or reducing CBF and by displacing or
reducing the amount of intracranial CSF. In
infants, an open fontanelle provides an additional
mechanism of volume compensation. Because
the size of the CBV and CSF compartments is relatively small, many pathologic processes easily lead
to increases in ICP by exceeding this compensatory capacity. The dynamic relationship between
changes in intracranial volume and pressure can
be graphically presented as a “pressure-volume”
curve. It is evident from the exponential shape of the curve that additional intracranial volume is initially accommodated with little or no change in
ICP (flat part of the curve), but when craniospinal
buffering capacity is exhausted (point of decompensation), further small increases in intracranial
volume lead to substantial rises in ICP. Intracranial
compliance can serve as measure of craniospinal
compensatory reserve (position on the pressurevolume curve) and is described by the following
equation, in which ΔV is change in volume and
ΔP is change in pressure: C¼ ΔV/ΔP. Cerebral
compliance can be measured directly with invasive
devices. A substantial increase in ICP may lead to a
reduction in cerebral blood flow (CBF), and this
finding triggered interest in estimation of cerebral
perfusion pressure (CPP¼mean arterial pressure
[MAP]ICP).
- Which one of the following statements
regarding the intracranial pressure pulse
waveform is most accurate?
a. Percussion wave, which reflects the ejection of blood from the heart transmitted
through the choroid plexus in the
ventricles
b. Third arterial wave is the percussion wave
c. First wave is the tidal wave which reflects
brain compliance
d. Second wave is the dicrotic wave that
reflects aortic valve closure
e. Intracranial hypertension increase in the
peak of the tidal and dicrotic waves
e—Intracranial hypertension increase in the peak of the tidal and dicrotic waves
Typically, the normal ICP waveform consists of
three arterial components superimposed on the
respiratory rhythm. The first arterial wave is
the percussion wave, which reflects the ejection
of blood from the heart transmitted through
the choroid plexus in the ventricles. The second
wave is the tidal wave, which reflects brain compliance; and finally, the third wave is the dicrotic
wave that reflects aortic valve closure. Under
physiologic conditions, the percussion wave is
the tallest, with the tidal and dicrotic waves having progressively smaller amplitudes. When
intracranial hypertension is present, cerebral
compliance is diminished. This is reflected by
an increase in the peak of the tidal and dicrotic
waves exceeding that of the percussion wave
- Regarding cerebral autoregulation in adults,
which one of the following statements is
LEAST accurate?
a. Increasing hypoxia results in increasing
cerebral blood flow
b. Cerebral blood flow is relatively constant
over a range of cerebral perfusion pressures from 50 to 150 mmHg
c. Cerebral blood flow is directly proportional to cerebral perfusion pressure
(CPP) when CPP is greater than
150 mmHg or less than 50 mmHg
d. A pCO2 of 4.0 kPa (30 mmHg) is associated with an average cerebral blood flow
of approximately 50 ml/100 g/min
e. Cerebral blood flow¼cerebral perfusion
pressure/cerebral vascular resistance
d—A pCO2 of 4.0 kPa (30 mmHg) is associated with an average cerebral blood flow of approximately 50 ml/100 g/min (see graph)
Cerebral blood flow (CBF) is regulated at the
level of the cerebral arteriole. It depends on the
pressure gradient across the vessel wall (which
in turn is the result of CPP) and Pa CO2 value
(which depends on ventilation). Cerebral autoregulation is dominant to ICP homeostasis and
keeps CBF constant in the face of changes in
CPP or mean arterial pressure (MAP). It does
this through alterations in cerebral vasomotor
tone (i.e. cerebrovascular resistance [CVR])
such that CBF¼CPP/CVR¼[MAPICP]/
CVR. Chronic hypertension or sympathetic activation shifts the autoregulatory curve to the
right, whereas sympathetic withdrawal shifts it
to the left. Cerebral autoregulation is normally
functional for CPP values of 50-150 mmHg
and is impaired by intracranial and extracranial
(e.g. chronic systemic hypertension) pathologic
conditions and anesthetics. Tissue perfusion will
decrease proportionally when CPP is below the
lower limit of autoregulation (e.g. <50 mmHg
if normal autoregulation is intact). Above the
upper autoregulation limit, the high CPP causes
forced dilation of cerebral arterioles with resultant increases in CBV and ICP, disruption of
the blood-brain barrier, reversal of hydrostatic
gradients, and cerebral edema or hemorrhage
(or both). CBF is proportional to arterial carbon
dioxide tension (PaCO2), subject to a lower limit,
below which vasoconstriction results in tissue
hypoxia and reflex vasodilation, and an upper
limit of maximal vasodilation. As such, target
pCO2 in head injury is 4-4.5 kPa (30-35 mmHg),
and hyperventilation is avoided as brining CO2
down further to vasoconstrict can reduce CBV
because dangerously low regional CBF and resultant cerebral ischemia can develop. CBF is
unchanged until arterial oxygen tension (PaO2)
falls below about 7 kPa (53 mmHg) but rises
sharply below that, such that raised ICP may
occur in hypoxic individuals. However, the actual
threshold may vary based on arterial oxygen content (CaO2) related primarily to hemoglobin
oxygen carriage (and thus oxygen saturation)
rather than PaO2. Because of the shape of the
hemoglobin-oxygen dissociation curve, CaO2 is
relatively constant over this range of PaO2. Below
about 7 kPa, CBF exhibits an inverse linear relationship with CaO2. Hypoxemia-induced vasodilation shows little adaptation with time but may be
substantially modulated by PaCO2 levels. Other
global factors affecting CBF include hematocrit;
sympathetic tone, with β1-adrenergic stimulation
causing vasodilation and α2-adrenergic stimulation causing vasoconstriction predominantly in
the larger cerebral vessels; and elevated central
venous pressure, which may elevate ICP and
reduce CPP. Temperature changes CBF by about
5% per 1° C and also decreases both CMRO2 and
CBF, whereas autoregulation, flow-metabolism
coupling, and carbon dioxide reactivity remain
intact. Ischemia results at levels of CBF below
20 ml/100 g/min unless CPP is restored (by
increasing MAP or decreasing ICP) or cerebral
metabolic demand is reduced (through deepened
anesthesia or hypothermia). Increased ICP resulting in reduced CPP is met by cerebral arteriolar
relaxation; in parallel, MAP is increased via the
systemic autonomic response. As a result, a vicious
cycle can be established, particularly in the presence of impaired intracranial homeostasis, as
cerebral vessel relaxation increases cerebral blood
volume (CBV), thus further raising ICP. In addition, an acute reduction in CPP or MAP tends to
acutely increase ICP (the so-called vasodilatory
cascade). Reductions in PaCO2 induce vasoconstriction, reducing CBF, CBV, and thus ICP Conversely, hypercapnia increases ICP and should be
prevented in the perioperative period. This makes
hyperventilation a useful tool for the acute control
of intracerebral hyperemia and elevated ICP
- Which one of the following statements
regarding control of cerebral vascular tone
is LEAST accurate?
a. CO2 causes vasoconstriction at low tensions in the blood, and vasodilatation at
higher tensions
b. Alpha2 and beta-1 adrenergic stimulation
cause vasodilatation
c. Prostaglandins PGE2 and PGI2 are
vasodilators
d. Increase in perivascular K+ causes
vasodilatation
e. Thromboxane A2 is a potent
vasoconstrictor
185
b—Alpha2 and beta-1 adrenergic stimulation
cause vasodilatation
Multiple factors can regulate regional cerebral
blood flow. Vasodilatation may be due to beta-1
adrenoceptor stimulation, high pCO2, nitric
oxide, prostaglandins (increase in ECF/CSF during hypotension), perivascular K + (rises due to
hypoxia and seizures), and local adenosine (hypotension and hypoxia). Vasoconstriction may be
related to alpha-2 adrenergic stimulation, free
calcium ions, thromboxane A2, and endothilin
(via action of vascular smooth muscle endothilin A receptors)
- Maintenance of which one of the following
requires the highest proportion of energy
expenditure in the brain?
a. Transmembrane electrical and ionic
gradients
b. Membrane structure and integrity
c. Synthesis and release of neurotransmitters
d. Neurogenesis
e. Axonal transport
a—Transmembrane electrical and ionic
gradients
The human brain accounts for only approximately 2% of total body weight but receives about
15% of resting cardiac output (750 ml/min) and
consumes about 20% (150 μmol/100 g/min) of
the oxygen and 25% (30 μmol/100 g/min) of
the glucose required by the body at rest. This
high energy expenditure results mainly from
maintenance of transmembrane electrical and
ionic gradients (60%), but also from maintenance of membrane structure and integrity and
the synthesis and release of neurotransmitters
(40%). Although the energy requirements of
the brain are substantial, it has a very small
reserve of metabolic substrates. Therefore, normal functioning of the central nervous system is
highly dependent on adequate and continuous
provision of energy substrates and removal of
the waste products of metabolism. Glucose is
the brains main substrate for generating ATP,
with its oxidation into pyruvate generating
2ATP molecules, but subsequent conversion of
pyruvate into acetyl-CoA and oxidation in the
citric acid (Krebs) cycle resulting in a net yield
of approximately 30 ATP molecules (compared
to 2ATP molecules for anaerobic respiration).
The brain has a high metabolic requirement for
oxygen (40-70 ml O2/min) that must be met by
delivery within blood, which depends on the
oxygen content of the blood (typically, 20 ml
per 100 ml blood) and blood flow (typically,
50 ml per 100 g brain per minute). Therefore,
under normal circumstances, delivery (150 ml/
min) is much greater than demand (40-70 ml/
min), and around 40% of the oxygen delivered
in blood is extracted. This oxygen extraction fraction (OEF) can be increased for short periods
when either delivery is reduced or demand is
increased. In states of prolonged starvation and
in the developing brain, ketone bodies (acetoacetate and β-hydroxybutyrate) can become important metabolic substrates within the brain. In
addition, some amino and organic acids can be taken up and metabolized within the brain. Overall, these are minor energy substrates except during periods of metabolic stress, such as during
acute hypoglycemia and ischemia. The brain can consume lactate as a substrate, particularly
during periods of hypoglycemia or elevated blood lactate.
- Immediately below which one of the following regional cerebral blood flow values does
the onset of infarction occur if sustained for
more than 2-3 h?
a. Less than 50 ml/100 g/min
b. Less than 23 ml/100 g/min
c. Less than 17 ml/100 g/min
d. Less than 10 ml/100 g/min
e. Less than 5 ml/100 g/min
c—Less than 17 ml/100 g/min
Under normal circumstances, CBF is maintained at a relatively constant rate of 50 ml/
100 g/min. With a reduction in cerebral perfusion pressure, CBF declines gradually. Physiologic indices of ischemia are not apparent until
CBF is reduced to about 20-25 ml/100 g/min;
at that time, electroencephalographic (EEG)
slowing is apparent. Such slowing indicates that
the brain has a substantial blood flow reserve.
Below a CBF of 17 ml/100 g/min, the electroencephalogram is suppressed and evoked potentials
are absent. It is not until the CBF is less than 10
that ATP energy failure occurs resulting in neuronal depolarization, excitotoxicity, cytotoxic
edema and cell death. Within the ischemic territory, the region supplied by end arteries
undergoes rapid death and is referred to as the
core. Surrounding the core is a variable area of
the brain called the penumbra. The penumbra
is rendered sufficiently ischemic to be electrically
silent but has not yet undergone ischemic depolarization. The penumbra is viable for several
hours and can be salvaged by restoration of flow.
If reperfusion is not established, the penumbra is
gradually recruited into the core. Depending on
the severity of the injury, blood-brain barrier
breakdown occurs about 2-3 days after injury.
This permits the entry of plasma proteins into
the brain substance, which further increases
cerebral edema significantly and is called vasogenic edema. The development of post-ischemic
edema can be significant enough to result in
substantial increases in ICP and neurological
deterioration. In the region surrounding the
infarction, autoregulation and CO2 reactivity
are re-established in most situations in about
4-6 weeks.
- Which one of the following statements regarding neuroprotection during anesthesia is LEAST accurate?
a. Burst suppression must be achieved before any neuroprotective effects are seen with barbiturates
b. Hyperglycemia exacerbates ischemic injury
c. Mild hypothermia for low-grade aneurysm clipping and for head injury may not be of benefit
d. Hyperthermia should be treated
e. Volatile anesthetics reduce the vulnerability of the brain to ischemic injury
a—Burst suppression must be achieved before any neuroprotective effects are seen
with barbiturates
An anesthetized brain is less vulnerable to ischemic injury. There do not appear to be any differences among anesthetic agents with respect to
their neuroprotective efficacy.
* Barbiturates, propofol, and ketamine have
been shown to have neuroprotective efficacy. With regard to barbiturates, doses less
than those that produce burst suppression of
the electroencephalogram achieve the same
degree of protection as higher doses do
* Volatile anesthetics reduce the vulnerability
of the brain to ischemic injury
* Maintenance of CPP within the normal
range for a patient who is at risk for cerebral
ischemic injury is essential.Modest increases
in blood pressure (5-10%) may be of benefit
to those who have suffered from an ischemic
insult. Hypotension is deleterious
* Arterial pCO2 should be maintained in the
normal range unless hyperventilation is used
for short-term brain relaxation. Prophylactic hyperventilation should be avoided
* Hyperglycemia exacerbates ischemic injury
and should be treated with insulin. A reasonable threshold for treatment is 150 mg/dl. If
insulin treatment is initiated, blood glucose
should be closely monitored and hypoglycemia prevented
* The routine induction of mild hypothermia
for low-grade aneurysm clipping and for
head injury may not be of benefit. In
high-grade SAH patients (WFNS 4-5),
the utility of mild hypothermia for purposes
of brain protection remains to be defined
* Hyperthermia should be avoided
* Seizures can worsen cerebral injury and
should be treated with anticonvulsants
- Which one of the following statements
regarding successful strategies for cerebral
protection during cerebrovascular surgery is
LEAST accurate?
a. For a given total vessel occlusion time,
brief-repetitive occlusions rather than a
longer-single occlusion where possible
should be the goal
b. Collateral blood flow can be increased by
inducing hypertension (e.g. target MAP
150 mmHg)
c. Preoperative perfusion imaging to help
identify patients who have low cerebrovascular reserve and may be at higher risk
for iatrogenic ischemia
d. Intraoperatively, vessel or graft patency
can be confirmed by
e. IHAST2 trial showed improvement in
outcome for clipped ruptured aneurysms
(WFNS1 and 2) given mild hypothermia
compared to normothermia
e—IHAST2 trial showed improvement in
outcome for clipped ruptured aneurysms
(WFNS1 and 2) given mild hypothermia
compared to normothermia
Several strategies may be used in an attempt to provide cytoprotection during cerebrovascular procedures with use of temporary arterial occlusion for
dissection of aneurysms and permanent clipping.
Limiting the duration of ischemia is probably the
most intuitive and direct method of reducing ischemic injury. The duration of focal ischemia that can
be tolerated safely without clinically evident
sequelae varies between individuals and vascular
territories. The current consensus for temporary
vessel occlusion is brief repetitive clipping periods,
which provides increased safety and less risk for
postoperative neurological deficit than a single episode of occlusion does, but variation in other
intraoperative parameters means no single occlusion time is accepted as “safe.” Collateral blood
flow can be increased by inducing hypertension
(e.g. target MAP 150 mmHg). Preoperative measurement of flow rates through cerebral vessels
can be achieved with perfusion imaging to help
the surgeon identify patients who have low cerebrovascular reserve and may be at higher risk for
iatrogenic ischemia. Intraoperatively, vessel or
graft patency can be confirmed by a number of
modalities, including direct microvascular Doppler
or transcranial Doppler (TCD) ultrasound, ultrasonic flow probe, intraoperative angiography,
EEG, electrocorticography, multimodality evoked
potential (MEP) and somatosensory evoked potential (SEP) monitoring, brain tissue oxygenation,
and fluorescent angiography (e.g. fluorescein
sodium, indocyanine green). Decreasing the metabolic activity of tissue at risk can be achieved by
mild hypothermia (33-34.5 °C) and by the use of
certain anesthetic agents to induce EEG burst suppression (e.g. pentobarbital, propofol, etomidate).
The role of mild hypothermia in neurovascular
surgery is less clear after Intraoperative Hypothermia After Aneurysm Surgery Trial (IHAST2), an
international double-blind trial in which 1001
WFNS1-3 aneurysmal SAH patients undergoing
aneurysm clipping were subjected to mild hypothermia (33 °C at clip placement) versus normothermia (36.5 °C) with no difference in outcome.
Hypothermia with circulatory arrest is most often
used during aneurysm surgery for giant and complex posterior circulation aneurysms including:
those not amenable to endovascular treatment;
those with significant intra-aneurysmal thrombus,
broad necks, or a projection endangering dissection and preservation of perforators; those adhering to vital structures; and fusiform aneurysms
with a distal vessel not suitable for arterial bypass.
- Which one of the following statements
regarding the role of hypothermia in the
management of traumatic brain injury is
LEAST accurate?
a. Eurotherm trial showed a significant
increase in odds of unfavorable outcome
but not death at 6 months in the mild
hypothermia group
b. Two trials of hypothermia therapy in children with TBI have shown no improvement in neurologic or other outcomes
one pediatric trial showed a nonsignificant
increase in mortality
c. Eurotherm trial RCT included patients
with TBI last 10 days and hypothermia
was induced if the ICP climbed above
20 mmHg for 5 min refractory to tier 1
management
d. Statistically significant increase in the odds
of an unfavorable outcome in the group
allocated to therapeutic hypothermia
e. Statistically significant increase in the odds
of death at 6 months (HR 1.45 (1.01-2.10))
hence discontinued due to futility
a—Eurotherm trial showed a significant
increase in odds of unfavorable outcome
but not death at 6 months in the mild
hypothermia group
Induced hypothermia has been a proposed treatment for TBI based upon its potential to reduce
ICP as well as to provide neuroprotection and
prevent secondary brain injury. Induced hypothermia has been shown to be effective in
improving neurologic outcome after ventricular
fibrillation cardiac arrest. National Acute Brain
Injury Study: Hypothermia II, plus two trials
of hypothermia therapy in children with TBI
have shown no improvement in neurologic or
other outcomes; one pediatric trial showed a
nonsignificant increase in mortality. Eurotherm
RCT looked at hypothermia in patients with
TBI (last 10 days) admitted to a critical care
environment with invasive ICP monitoring
and an approach to participate was triggered if
the ICP climbed above 20 mmHg for 5 min
refractory to tier 1 management (usually
includes head elevation, encouragement of
venous drainage, intubation, sedation and ventilation to appropriate targets). Cooling protocol
was a 20-30 ml/kg bolus of cold saline followed
by maintenance of hypothermia as they saw fit
but directed to a duration of at least 48 h, with
additional time as needed to control ICP. Temperature was optional between 32 and 35 °C in
the intervention arm, titrated to ICP. All
patients were followed up for 6 months and
the Extended Glasgow outcome scale (EGOS)
was used as the primary outcome measure. From
387 patients, the data committee found a statistically significant increase in the odds of an unfavorable outcome and death at 6 months in the
group allocated to therapeutic hypothermia,
hence it was discontinued due to futility. Criticisms of this trial include very early use (i.e. tier
2) of hypothermia with high potential variability
of subsequent management, inclusion criteria
any head injury in previous 10 days, only ICP
used as a guide (not CPP).
- A patient in the emergency department has
been intubated and ventilated. CT head has
shown a rightEDHwith significantmass effect.
His right pupil is larger than the left and the
anesthetist is concerned about hemodynamic
instability. What ASA grade is this patient?
a. 1
b. 2
c. 3
d. 4
e. 5
f. 6
e—ASA 5
American Society of Anesthesiologists Physical
Status classification is as follows: 1—a normal
healthy patient (non-smoker, minimal/no alcohol);
2—a patient with mild systemic disease (smoker,
pregnancy, obesity); 3—a patient with severe
systemic disease (e.g. uncontrolled diabetes/
hypertension, alcoholism, dialysis, >3 months
since MI/TIA/CVA); 4—a patient with severe
systemic disease which is a threat to life (e.g.
<3 months since MI/TIA/CVA, ongoing cardiac
ischemia, sepsis); 5—moribund patient not
expected to survive without the operation (e.g. ruptured AAA, massive trauma, intracranial bleed
with mass effect, bowel ischemia with organ failure); 6—declared brain dead patient undergoing
organ harvesting.
- A 27-year-old man undergoes general anesthesia for a hernia repair. As the anesthesia
begins, his jaw muscles tense and he becomes
generally rigid. He becomes febrile, tachycardic, and tachypneic. Which one of the following treatments is most appropriate?
a. Atropine
b. Procyclidine
c. Succinylcholine
d. Dantrolene
e. Thiopental
d—Dantrolene
Malignant hyperthermia is characterized by acute
severe fever, tachypnea, tachycardia, and rigidity,
and high mortality rate if left untreated. It is typically precipitated by volatile anesthetics, especially halothane, or muscle relaxants such as
succinylcholine. Patients may become severely
acidotic and develop rhabdomyolysis. Pathology
shows diffuse segmental muscle necrosis. It
appears to be a metabolic myopathy in which
there is abnormal release of calcium from the sarcoplasmic reticulum and ineffectual uptake afterward. Genetic defects in the ryanodine receptor,
involved in calcium flux in the sarcoplasmic reticulum, are responsible for about 10% of cases,
although as yet unidentified abnormalities of this
or related proteins probably play a role in most
cases. It is inherited in an autosomal dominant
fashion. Certain other myopathies, including
Duchenne muscular dystrophy and central core
myopathy, are associated with this condition as
well. Treatment consists of discontinuation of
anesthesia, administration of dantrolene, which
prevents release of calcium from the sarcoplasmic
reticulum, and supportive measures.
- Which one of the following is LEAST likely to
be associated with massive blood transfusion?
a. Iron overload
b. Hyperkalemia
c. Hypocalcemia
d. Hypothermia
e. Coagulopathy
a—Iron overload
A massive transfusion is defined as a transfusion
equaling the patients’ blood volume within 12-
24 h. The specific additional problems related
to this scenario include:
* Volume overload resulting in noncardiogenic pulmonary edema
* Thrombocytopenia: following storage
there is a reduction of functioning platelets,
so that there is a dilutional thrombocytopenia following a large transfusion
* Coagulation factor deficiency (relative)—
leading to a coagulopathy if concomitant
cryoprecipitate/FFP not also transfused.
* Ineffective tissue oxygenation due to
reduced volume of 2,3 bisphosphoglycerate,
which does not store well
* Hypothermia unless blood adequatelywarmed
* Hypocalcemia: Due to chelation by the citrate in the additive solution and may worsen
coagulopathy
* Hyperkalemia: Due to progressive potassium leakage from the stored red cells
- Which one of the following statements
regarding intraoperative blood loss management techniques applied in patients refusing
blood product transfusion is LEAST
accurate?
a. Meticulous attention to hemostasis and
technical blood losses during surgery are
not usually important
b. Phlebotomy should be rationalized
c. Jehovah’s witnesses generally accept prothrombin complex concentrate
d. Intraoperative cell saver use should be
considered if appropriate
e. DDAVP (vasopressin) can be used as a
procoagulant
c—Jehovah’s witnesses generally accept prothrombin complex concentrate
In general, while a hemoglobin (Hgb) between 7
and 8 g/dl appears to have no immediate adverse
effect on mortality, there is a clear risk of death in
the 30-day postoperative period when hemoglobin fell much below 7 g/dl. Where transfusion
is not an option (e.g. Jehovah’s witnesses, multiple alloantibodies) the key emphasis is on optimizing hematopoiesis, minimizing bleeding and
blood loss (blood conservation), and harnessing
and optimizing physiological tolerance of anemia
(through application of all available therapeutic
resources). Meticulous attention to hemostasis
and technical blood losses during surgery (e.g.
use of hemostatic surgical devices, fibrin glue
and tissue adhesives; controlled hypotension; elevating the surgical field above the rest of the
body), minimizing phlebotomy are important.
In addition, clarity must be sought (and documented) from the individual about each available
blood product and extracorporeal procedure that
is acceptable to them in the following groups:
* Allogenic human blood and blood products.
Whole blood, RBC, plasma, platelets, white
blood cells, blood from specific donors
* Human blood fractions and medications
that contain human blood fractions: cryoprecipitate, cryosupernatant, albumin, plasma protein fraction, human immunoglobulin (e.g. Rh immune globulin, IVIG),
plasma derived clotting factor concentrates
(e.g. fibrinogen, VIII, IX), tissue adhesive/
fibrin glue
* IV fluids and medications not derived from
human blood: hydroxyethyl starch (hetastarch, pentastarch), balanced salt solutions,
recombinant clotting factor concentrates
(rVIII, rIX, recombinant VIIa), recombinant erythropoietin, antifibrinolytic chemicals (e.g. tranexamic acid, aminocaproic
acid), procoagulant chemicals (e.g.
DDAVP, vitamin K)
* Extracorporeal techniques for blood conservation or treatment: intraoperative
hemodilution, intraoperative blood salvage
(cell saver), autologous banked blood (selfdonation), cardiopulmonary bypass, chest
drainage autotransfusion, plasmapheresis,
hemodialysis
- Which one of the following statements
regarding the oxygen-dissociation curve is
LEAST accurate?
a. It is sigmoidal due to cooperative binding
of oxygen to hemoglobin
b. The Bohr effect is a shift of the dissociation curve to the left
c. Reducing pH shifts the oxygendissociation curve to the left
d. The fetal oxygen-dissociation curve is
shifted to the left reflecting the increased
oxygen affinity of fetal hemoglobin caused
by the presence of the gamma subunit of
hemoglobin
e. Increased temperature shifts the oxygendissociation curve to the left
b—The Bohr effect is a shift of the dissociation curve to the lef
The sigmoidal shape of the oxygen dissociation
curve reflects the progressive nature with which
each oxygen molecule binds to hemoglobin such
that the binding of one oxygen molecule facilitates the binding of the next. The Bohr effect is
a shift of the dissociation curve to the right, signifying a reduction of the oxygen affinity of the
hemoglobin molecule and thus a greater tendency to off-load oxygen into the tissues (i.e. in
acute or chronically underperfused tissue). This
change is caused by increased body temperature,
acidosis, chronic hypoxia (increased 2,3-BPG)
and hypercapnia. The fetal oxygen-dissociation
curve is shifted to the left, reflecting the increased
oxygen affinity of fetal hemoglobin compared to
maternal hemoglobin molecule and allowing oxygen transfer (gamma subunit instead of the alpha
that cannot form covalent bonds with 2,3-BPG).
