Module B-2 Flashcards
Induces the least cerebral vasodilation of inhaled anesthetics making it preferred agent for neurosurgical patients with elevated ICP
Sevoflurane
Coronary steal
Blood flow distal to a fixed, atherosclerotic lesion would decrease when the surrounding, normal vasculature dilated in response to Isoflurane, triggering ischemia
Inhalation consideration with pregnancy
Nitrous oxide is teratogenic
Volatile agents decrease smooth muscle tone-maintaining uterine tone is critical for postpartum hemostasis so volatile agents are minimized0 less than 0.5 MAC Sevoflurane and 1.0 Desflurane
Relationship between CMRO2 and CBF and impact of inhaled anesthetics
Cerebral metabolic rate of oxygen consumption and cerebral blood flow are typically coupled, as one increases the other increases.
However, IAs induced a dose dependent cerebral vasodilation (increase CBF) and a decrease in the CMRO2- we call this an uncoupling
-nitrous increases CMRO2 and CBF
Cerebral hypocapnia
Vasoconstrict
Cerebral vasculature hypercarbia
Vasodilate
Calcium and Inhaled anesthetics
Reduce intracellular free calcium in cardiac and vascular smooth muscle!!
End result is depression of contractile state of the myocardium and peripheral vasodilation
This is probably why giving calcium is cardio protective
Mechanism pg 88 Nagelhout
Explain increase in HR with inhaled anesthetics
- Trigger sympathetic response
- Baroreceptor reflex
- Antagonism of SA node automaticity
Arrhythmias and Inhaled Anesthetics
All three can lead to Bradycardia(Sevoflurane) and prolonged QTc, which can lead to torsades which is a polymorphic ventricular tachycardia
Bonus: Likely due to interruption of cardiomyocyte repolarization via inhibition of K+ through hERG channels
Cardiovascular effect of Nitrous oxide
Increase in SVR and HR but a decrease in CO
IA impact on Respiratory system
Lower tidal volumes
Higher Respiratory Rate
not enough to prevent elevations in CO2 but surgical stimulation aids with this
IA biotransformation rates:
Sevoflurane 5-8% —initially caused concern for
Everything else in trace amounts
Primarily hepatic etabolism via P450 oxidation
Problems with Nitrous
Inactivation of B12 cofactor for methionine synthase which may inhibit DNA synthesis and have teratogenic & immunosuppressive effects
Watch for cobalamin deficiency!!
DO NOT USE IN PULM HTN
Number of fluorine atoms on modern IA’s
Isoflurane- 5
Desflurane- 6
Sevoflurane- 7
Impact of Halogenation
-Flammability-reduced
-Chemical Stability-enhanced
-Arrhythmogenic potential- increased
-Potency- increased
-Biotransformation
Vapor Pressure, which has the highest?
Desflurane
The pressure were your liquid is in equilibrium with the surrounding gas in a given volume at an established pressure.
Molecules that want to evaporate with have a higher vapor pressure- due to low molecular weight/high kinetic energy/low intermolecular forces
Modern “MOA” for Inhaled Anesthetics
Multiple and diverse targets that contribute to unconsciousness, amnesia, analgesia, and immobility,
-impact brain and spinal cord in a dose dependent manner
Area of action and impact of IA’s in general
Immobility- spinal cord
Analgesia- spinothalamic tract
Unconsciousness- Cortex, thalamus, brainstem
Amnesia- Amygdala, hippocampus
Common values for MAC-Awake and MAC-BAR
0.3
1.6
What increases MAC??
High CNS Metabolic activity
Neurotransmission
Red hair lol
What decreases MAC
CNS metabolic activity and neurotransmission
Concurrent administration of other drugs
Age
Advantages/concerns of Nitrous
Rapid uptake/elimination
Odorless
Mild analgesic-NMDA
Air filled spaces
Toxic effects
PONV/environmental effects
Why is NItrous a problem in air filled spaces
More soluble than N2- both attracted to gas phase and accumulate in cavities but N2O diffuses in faster than N2can be displaced out (34xfaster)
N2O problematic air spaces:
Pneumothorax
Air emboli
Bowel
Pneumoperitoneum
Intraocular air bubbles
Equipment cuffs
Why do we avoid IA’s while monitoring evoke potentials
They decrease amplitude and increase latency
Amplitude-strength of nerve response
Latency- speed of conduction
Nitrous cardiovascular impact
Increase in SVR and HR due to SNS activation
-can be given with other agents to support MAP
Preconditioning (cardiovascular)
Mimics myocardial injury which triggers cascade of intracellular events that ends up being cardio protective for future events
Goal of HPV
Hypoxia pulmonary vasoconstriction diverts blood flow to areas of lung with greater ventilation in order to improve arterial oxygenation
-inhibited by volatile agents
What do we avoid in Pulmonary hypertension?
Nitrous Oxide- it increases pulmonary vascular resistance
Inhaled Anesthetics impact on Ventilation
Decrease Tidal Volume
Increase Respiratory rate
Impairs hypercarbia ventilatory response
Impairs hypoxic ventilatory drive
What contributes to Formation of compound A??
Low flow of Sevoflurane (less than 2L)
Older/early generation CO2 absorbents
Desiccated CO2 Absorbents
What is safe for Malignant Hyperthermia?
Nitrous Oxide and complete IV anesthetic
Minus Succ?
Neuromuscular considerations
-Additive effect with muscle relaxants
-Dosages of muscle relaxants are decreased by 25-50%
-Prolonged recovered compared to TIVA (Total IV anesthetic)
Why do we not run low flow sevo (<1-2L/min)
Compound A- nephrotoxicity
