Neurophysiology pharmacology Flashcards
Alpha 1 agonists may cause
bolus: may transiently change CBF & cerebral SaO2
continuous: little effect on CBF & cerebral SaO2
- maintenance of CPP with these vasopressors does not have an adverse effect on the brain
Alpha 2 agonists may cause
decreased CBF (up to 25-30%) results from reduced CMRO2 leading to reduced CBF small doses= little effect on CBF large doses+ phys stress= increased in CMRO2 & CBF up to 20%*******
Beta blockers have
little to no effect on CBF & CMRO2
Ace inhibitors & ARBs have
little to no effect on CBF & CMRO2
autoregulation is maintained
Do not give ________ prior to any intracranial procedure.
benzos
may prolong emergence… unable to do post op neuro exam
less reduction than barbiturates, propofol, or etomidate
Barbiturates are associated with
the robin hood effect (reverse steal phenomenon)**
CBF redistributed from normal to ischemic areas in the brain
Propofol leads to
dose-dependent reduction in CBF & CMR*
anticonvulsant
short elimination half-life**
Etomidate can
activate seizure foci in patients with epilepsy*****
-decreases the CMR, CBF, & ICP
has been used to treat seizures although not the first choice
Ketamine is the only intravenous anesthetic that
dilates cerebral vasculature & increases CBF****
can potentially increase ICP markedly if decreased intracranial compliance
CMR does not change
Ketamine as a sole agent can
increase ICP
when co-administered with other anesthetics, increased in CBF & ICP is blunted or eliminated
may result in stormy emergence*
NMDA antagonism in brain injury patient may be
protective against neuronal cell death**
functionally “dissociates” the thalamus from limbic cortex
Opioids have
minimal effects on CBF, CMR & ICP
morphine & meperedine is traditionally avoided
Most anesthetics have ___________
favorable effect on CNS*****
In general, anesthetic drugs ______
suppress the CMR with EXCEPTION of ketamine & nitrous oxide
_______ & ________ blunts increase CBF/ICP from ketamine & volatile agents
hyperventilation & PaCO2
Effects on CNS are complicated by
other drugs, surgical stimulation, intracranial compliance, BP & PaCO2
The delivery of energy substrates is dependent on
CBF
Modest alterations in CBF can substantially influence
neuronal outcome in the setting of ischemia
Control & manipulation of CBF are central to the management of
ICP
CBF does not parallel CBV when
there is normal BP (MAP 70-150 mmHg): autoregulation intact
cerebral ischemia: CBV increases but CBF decreases
MAP=
CBF, but cerebral vasoconstriction limits in CBV
Initial increases in CBV do not increase ICP due to
compensatory adjustment
- venous blood shift to extracerebral vessels
- CSF shift to spinal compartment
