Week 2 PONV (everything) Flashcards
2 intraop factors that influence PONV
type of surgery and duration of surgery
what 3 surgeries have the high incidence of PONV
cholecystectomy, gynecological and lap surgeries
how would increasing surgical time (duration) by 30 minutes effect the risk for PONV?
increasing surgical duration increases risk of PONV by 60%
what inhaled anesthetic increases the risk for PONV?
Nitrous Oxide:
avoiding NO significantly decreases vomiting in Lap procedures and PONV
Nitrous oxide’s association with PONV is suggested to be due to what 3 factors?
Simulation of sympathetic system with catecholamine release
Middle ear pressure changes stimulating the vestibular system
Increased abdominal distension. This is from the exchange of Nitrous oxide and nitrogen in gas introduced into GI tract by mask ventilation
effect of Ether and Cyclopropane on PONV
Ether and Cyclopropane cause higher PONV d/t increase in endogenous catecholamines
effect of volatile gases on PONV in the early stage (0-2hr) vs delayed stage (2-24hr) of surgery
Volatiles gases were primary cause of early PONV (0-2 hours)
Volatile gases have no impact on delayed PONV (2-24 hours)
which volatile anesthetics are asociated with a lower risk for PONV
Sevoflurane, Enflurane, Desflurane, and Halothane
all but Ether and Cyclopropane: Iso was not mentioned
effect of volatile gases on PONV depends on what?
the effect is dose dependent
Etomidates effect on PONV
Continuous infusion markedly increases post-op emesis
why does ketamine increase the risk for PONV
related to release of endogenous catecholamine release:
ketamine causes hallucinations, vivid dreams and increased risk for PONV
Of Barbiturates, Nitrous Oxide and Ketamine which has a higher risk for PONV
Ketamine
how does Propofol effect PONV
reduces the risk
Nitrous-Opioid-Relaxant technique: how does it effect PONV
increases the incident of PONV d/t directly stimulating the CTZ
MOA of opioids contribution to increased risk for PONV.
Emesis caused by stimulation of opioid receptors in the CTZ.
Using intraoperative opioids shows a weak contribution to PONV.
DOSE DEPENDENT EFFECT
Do neuromuscular reversal agents increase risk for PONV?
it is unknown/uncertain
regional vs general anesthesia: what is the risk for PONV
GA is 9x more likely to cause PONV compared to Regional
do central neuraxial blocks or peripheral blocks cause a greater risk for emesis?
central neuraxial blocks
why is Emesis with central neuraxial blocks greater than with peripheral blocks
d/t SNS block contributing to postural hypotension induced N/V
what would decrease the risk for nausea with epidurals
nausea is less with lipid soluble opioids such as fentanyl and sufentanil
why does using lipid soluble opioids in epidurals decrease the risk for nausea
d/t less rostral spread from lumbar epidural injection site to CTZ and vomiting center than the less lipid soluble such as morphine
what type of pain is more commonly related to PONV
visceral or pelvic pain
how does movement or transport effect PONV
Sudden motion, changes in position, and/or transport from PACU to patient floor can precipitate n/v after receiving opioids
during what point in the surgical process would we use Non steroidals and why do we use them
used perioperatively to reduce need for opioids
what is no longer recommended for PONV prevention
supplemental O2
Genes/receptors regarded as r/t PONV or opioid induced N/V:
8
5-HT3
D - Dopamine type 2
A - Alpha-2 adrenoceptor
M - Muscarinic type-3
C - Catechol-o-methyl transferase
A - Adenosine triphosphate (binding cassette subfamily B member)
U - Uridine 5’-diphospho-glucuronosyltransferae
C - Cytochrome P450 superfamily enzyme
*5 DAM CAUC (s)
5 Primary Afferent Pathways involved in vomiting stimulation:
- Chemoreceptor Trigger Zone (CTZ)
- Vagal mucosal pathway in the GI system
- Neuronal Pathways from the Vestibular system (Inner ear)
- Reflex afferent pathways from the cerebral cortex
- Midbrain afferents
Stimulation of the afferent pathways stimulating vomiting can be activated by four receptor types:
- Cholinergic (muscarinic)
- Dopaminergic
- Histaminergic
- serotonergic
Vomiting center is located within:
the reticular formation of the brainstem
Flood says medulla oblongata and consists of nucleus of the tractus solitaires and parts of the reticular formation
The vomiting center received afferent inputs from
the 5 afferent pathways
Efferent signals are directed to the following nerves:
Flood states V, Vii, IX, X, Xii
Glossopharyngeal Hypoglossal Trigeminal Accessory Spinal segmental
the gut, oropharynx, movement, pain, hypoxemia, and hypotension can all do what
stimulate the vomiting center
CTZ is located
Outside the BBB
What has contact with CSF and allows substances in blood and CSF to interact.
CTZ
Toxins and/or drugs in the blood can stimulate the CTZ causing ____ .
This stimulation may send :
Cause: N/V
Send: emetogenic triggers to the vomiting center activating the vomiting reflex