ECC Final Exam with Complete
Solutions
What is the definition of cerebral perfusion pressure and the equation? - ANS-The blood
pressure in the vessels of the cranial vault. MAP-ICP= CPP
what is the Monroe Kellie doctrine - ANS-the cranial vault contains 3 components within
a fixed space:
1. Tissue (brain, meninges)
2. Blood
3. CSF
an increase in one will require a decrease in one or both of the others or else there will
be an increase in ICP
what is the Cushing's reflex? - ANS-A response to increase CPP driven by SNS
efferents from the brainstem resulting in systemic vasoconstriction:
1. Hypertension
2. Reflex Bradycardia
What is a primary brain injury? - ANS-the insult to the brain itself (ex. gsw to head). We
cannot treat this, it already happened.
What is a secondary brain injury? - ANS-refers to the "after effects" of the primary injury;
resulting from intracranial and extra cranial events. We can potentially treat these.
What is involved in triaging a head trauma case? - ANS-same as every other patient:
ABC.
Then move to the neurological system.
Other indicators of and concurrent injuries with TBI - ANS-upper airway trauma, ocular
trauma (proptosis, scleral hemorrhage), skeletal fracture, etc
Intracranial events (3 of them). (we CANNOT do much about these) - ANS-1. increased
activity of excitatory neurotransmitters (glutamate, others)--> ATP depletion-->disrupted
ion homeostasis--> cytotoxic edema--> further depolarization.
2. pro inflammatory cytokines and leukocyte chemotaxis --> vasodilation and loss of
pressure auto-regulation
3. Generation of ROS
Extra-cranial events (we can modulate these with therapy) - ANS-1.
Hypotension/hypoperfusion (auto regulation maintains flow during MAP of 50-
, 150mmHg...regulation impaired with TBI and blood flow more depended on CPP).
AVOID HYPOTENSION!!!
2. Hypoxemia
3. Hyper/hypocarbia (hyper--> vasodilation, hypo--> constriction). Keep PvCO2 at 30-
40mmHg.
4. Hyperthermia
5. hyper/hypoglycemia (hyperglycemia is a poor Px indictor)
what do intra-and extra-cranial events lead to?? - ANS-neuronal cell damage and
death--> cerebral edema, increased ICP, and BBB distruption
Treatments to target secondary injury? (extra-cranial vs intra-cranial) - ANS-Extra-
cranial: optimize MAP (restore and maintain perfusion) and Adequate ventilation and
oxygenation. Ex: optimize cerebral perfusion/ O2 delivery, optimize PvCO2, prevent
large increase in excitatory NT, ROS scavenging, prevent hyperthermia, glycemic
control.
intra-cranial: reduce ICP (reduce cerebral edema)
how do we reduce ICP?? - ANS-Hyperosmolar agents, elevate head 15-30 degrees,
check if surgical problem
what are the two hyperosmolar agents? And how do they work? - ANS-mannitol and
hypertonic saline. They pull fluid into the vascular space from the extravascular space
causing initial volume expansion followed by diuresis
Hypertonic saline - ANS-hypertonic to plasma (>0.9% NaC; usually use b/t 3-7%)
when is hypertonic saline contraindicated? - ANS-In hypernatremia or severe
dehydration, or chronically hypoNa patients
what is the first line therapy in TBI patients with hypovolemia? - ANS-hypertonic saline
what prophylactics prevent sudden increases in ICP? - ANS-anti-emetics,
anticonvulsants (keppra)
what should the target MAP and systolic BP be in TBI cases? - ANS-between 75-
80mmHg or a systolic of 120mmHg in order to maintain cerebral blood flow.
Malnurition clinically may occur and worsen outcomes such as - ANS-increase morbidity
(infection and dehiscence), increase mortality, decrease response to treatment
(prolonged hospital care times)
patients that benefit from assisted feeding - ANS-- malnourished
- when long period of malnourishment is anticipated
Solutions
What is the definition of cerebral perfusion pressure and the equation? - ANS-The blood
pressure in the vessels of the cranial vault. MAP-ICP= CPP
what is the Monroe Kellie doctrine - ANS-the cranial vault contains 3 components within
a fixed space:
1. Tissue (brain, meninges)
2. Blood
3. CSF
an increase in one will require a decrease in one or both of the others or else there will
be an increase in ICP
what is the Cushing's reflex? - ANS-A response to increase CPP driven by SNS
efferents from the brainstem resulting in systemic vasoconstriction:
1. Hypertension
2. Reflex Bradycardia
What is a primary brain injury? - ANS-the insult to the brain itself (ex. gsw to head). We
cannot treat this, it already happened.
What is a secondary brain injury? - ANS-refers to the "after effects" of the primary injury;
resulting from intracranial and extra cranial events. We can potentially treat these.
What is involved in triaging a head trauma case? - ANS-same as every other patient:
ABC.
Then move to the neurological system.
Other indicators of and concurrent injuries with TBI - ANS-upper airway trauma, ocular
trauma (proptosis, scleral hemorrhage), skeletal fracture, etc
Intracranial events (3 of them). (we CANNOT do much about these) - ANS-1. increased
activity of excitatory neurotransmitters (glutamate, others)--> ATP depletion-->disrupted
ion homeostasis--> cytotoxic edema--> further depolarization.
2. pro inflammatory cytokines and leukocyte chemotaxis --> vasodilation and loss of
pressure auto-regulation
3. Generation of ROS
Extra-cranial events (we can modulate these with therapy) - ANS-1.
Hypotension/hypoperfusion (auto regulation maintains flow during MAP of 50-
, 150mmHg...regulation impaired with TBI and blood flow more depended on CPP).
AVOID HYPOTENSION!!!
2. Hypoxemia
3. Hyper/hypocarbia (hyper--> vasodilation, hypo--> constriction). Keep PvCO2 at 30-
40mmHg.
4. Hyperthermia
5. hyper/hypoglycemia (hyperglycemia is a poor Px indictor)
what do intra-and extra-cranial events lead to?? - ANS-neuronal cell damage and
death--> cerebral edema, increased ICP, and BBB distruption
Treatments to target secondary injury? (extra-cranial vs intra-cranial) - ANS-Extra-
cranial: optimize MAP (restore and maintain perfusion) and Adequate ventilation and
oxygenation. Ex: optimize cerebral perfusion/ O2 delivery, optimize PvCO2, prevent
large increase in excitatory NT, ROS scavenging, prevent hyperthermia, glycemic
control.
intra-cranial: reduce ICP (reduce cerebral edema)
how do we reduce ICP?? - ANS-Hyperosmolar agents, elevate head 15-30 degrees,
check if surgical problem
what are the two hyperosmolar agents? And how do they work? - ANS-mannitol and
hypertonic saline. They pull fluid into the vascular space from the extravascular space
causing initial volume expansion followed by diuresis
Hypertonic saline - ANS-hypertonic to plasma (>0.9% NaC; usually use b/t 3-7%)
when is hypertonic saline contraindicated? - ANS-In hypernatremia or severe
dehydration, or chronically hypoNa patients
what is the first line therapy in TBI patients with hypovolemia? - ANS-hypertonic saline
what prophylactics prevent sudden increases in ICP? - ANS-anti-emetics,
anticonvulsants (keppra)
what should the target MAP and systolic BP be in TBI cases? - ANS-between 75-
80mmHg or a systolic of 120mmHg in order to maintain cerebral blood flow.
Malnurition clinically may occur and worsen outcomes such as - ANS-increase morbidity
(infection and dehiscence), increase mortality, decrease response to treatment
(prolonged hospital care times)
patients that benefit from assisted feeding - ANS-- malnourished
- when long period of malnourishment is anticipated
