MH, PONV, temp control Flashcards
Postoperative Nausea and Vomiting (PONV)
Nausea, retching, or vomiting
In PACU & w/in 24H postop
Post discharge nausea and vomiting (PDNV)
Symptoms that occur after discharge for outpatient procedures
_______ is a frequent cause of “unexpected hospital admission” after ambulatory surgery
Prolonged vomiting
T/F
Patients often rate PONV as worse than postoperative pain
True
POV affects __ % of all surgical patients.
The incidence of nausea is __%.
PONV in high-risk patients can be up to __%.
30
50
80
High Risk of PONV in Adults
Female
History of PONV or motion sickness
Nonsmokers
Younger
Type of surgery
Opioid analgesia
T/F
PONV can delay PACU discharge
True
Risk Score of PONV in Adults
(Apfel Simplified Risk Score)
2+ points = high risk
Postdischarge Nausea and Vomiting (PDNV)
risk factors
Female Gender
History of PONV
Age <50
Use of opioids in PACU
Nausea in PACU
Risk Score For PDNV in Adults
PONV
Potential Consequences
Increased cost
Increased admission rates (ambulatory care)
Suture dehiscence
Aspiration
Increased ICP
Pneumothorax
Patient Dissatisfaction
Factors that increase PONV
Hypercarbia, Gastric insufflation
Sympathetic stimulation
Methohexital
neostigmine?
Etomidate
Volatile anesthetics (↑ 2-3%)
(Limited to early postoperative period (30-60 mins))
Nitrous
Opioids
HypoTN, Dehydration, Fasting
Duration of anesthesia
Anesthetic technique
Experience of the anesthetist
Placement of airways
PONV
Surgeries that can increase risk
Cholecystectomy
Gynecologic (GYN)
Laparoscopic Procedures
Eye and Ear surgery
Shoulder?
In Children:
Strabismus surgery
Adenotonsillectomy
Inguinal, scrotal or penile procedures
On Apfel scoring, what is considered high and low risk?
Pediatric APFEL Score
0= 10%
1= 10%
2= 30%
3= 50%
4= 70%
Pathophysiology of PONV includes ____ & ____ mechanisms.
Central and Peripheral mechanisms
Five principal neurotransmitter receptors
-Anticholinergic/Muscarinic M1
-Dopamine D2
-Histamine H1
-5-hydroxytryptamine (5HT-3) serotonin
-Neurokinin 1 (NK1) or Substance P
All may be targets for prevention or treatment
Chemoreceptor Zone (CTZ)
4th ventricle in the area postrema
Dopamine D2 and 5HT-3
Susceptible to drugs and toxins (Chemo), anesthetic agents, opioids
T/F
The CTZ is protected by the blood brain barrier
False
not protected
Vestibular System
Histamine H1 and Muscarinic M1
Motion and equilibrium, middle ear
Vomiting Center
in nucleus tractus solitarius in postrema and lower pons
Physiologic Areas involved
Chemoreceptor Zone (CTZ)
Vestibular System
Vomiting Center
Cerebral cortex
GI tract
GIT features involved in N/V
-Afferent vagus nerve
-Enterochromaffin cells release serotonin
Strategies to Reduce Baseline Risk
-Avoid GA & use regional instead(A1)
-Adequate hydration(A1)
-Sugammadex instead of neostigmine (A1)
-Avoid nitrous in surgeries lasting over 1h (A1)
-Use propofol for induction & maintenance(A1)
-Avoid volatiles (A2)
-Minimize intraop (A2) & postop opioids (A1)
Opioid sparing/Postop pain control (ERAS)
Celebrex and Neurontin, Tylenol (IV or PO)
NSAIDS
Ketamine
Precedex
Robaxin
T/F
Avoiding hypertension will help prevent N/V.
False
avoid hypotension
Instead of GA, use….
regional
TIVA
T/F
Supplemental O2 concentration can help prevent PONV.
True
PONV
Treatment/Pretreatment
Scopolamine patch
Reglan
Decadron
Zofran
Propofol
Vistaril (Histamine 1)/Ephedrine 25/25 mg IM
Scopolamine patch
MoA
When to apply
When to remove
(competitive inhibitor at muscarinic sites)
2 hours prior to induction of anesthesia and remove 24 hours after use
Reglan MoA
Dopamine 2 antagonist
Decadron dosing
4-8 mg on induction (steroid)
Zofran
dose
MoA
4 mg at the end of surgery
(5-HT3 receptor antagonist)
used to treat Chemo-induced N/V (CINV)
Neurokinin 1/Substance P antagonists
Aprepitant PO (half-life of 40 hours)
Fosaprepitant IV
Rolapitant PO/IV (half life of 180 hours)
Phenergan (phenothiazine)
Butyrophenones for N/V
Droperidol
Haldol
(Effects of Opioids on N/V)
Incidence of PONV is greater than __% following balanced anesthesia
50
Opioids cause PONV by their effects on
the chemoreceptor zone (CTZ) in the area of the postrema of the brainstem
(Opioids)
Moving the patient (transport to the PACU) can exacerbate N/V d/t…
increased sensitivity of the vestibular system
CTZ receptors
dopamine (D2)
serotonin (5HT3)
histamine
opioid
muscarinic acetylcholine
these structures send neural projections to the vomiting center in the medulla
CTZ, vagal nerve, and vestibular organs
CTZ & vomiting center
location
CTZ: 4th ventricle of postrema (brainstem)
vomiting center: medulla
Opioid-Free Anesthesia
components
-Exparel (liposomal bupivacaine)
-Magnesium, Lidocaine IV
-Ketamine drip
-Propofol drip
-Antiemetics
-NSAID, Tylenol, Gabapentin, Celebrex
Enhanced Recovery After Surgery (ERAS)
components
-No NG tube!
-Carbohydrate rich clear drink
-Regional Anesthesia/Transabdominal Blocks (TAP block)
-TIVA
-Ketamine, Precedex, Lidocaine, Magnesium
-Gabapentin, Celebrex, Robaxin
-IV/PO Tylenol
-NSAIDs
-Exparel (liposomal bupivacaine)
Thermoregulation
3 phase process
Afferent thermal sensing
Central regulation or control
Efferent responses
Autonomic responses to heat & what mediates it?
sweating and active cutaneous vasodilation
sweating is mediated by postganglionic cholinergic nerves
Autonomic response to cold:
-Cutaneous vasoconstriction
(alpha-1 adrenergic receptors)
-Synergistically augmented by hypothermia-induced alpha-1 and 2 receptors
4 mechanisms of Heat Loss
Radiation
Conduction
Evaporation
Convection
1 & #2 source for heat loss
1: radiation
Radiation
Dissipation of heat to cooler surroundings
greatest heat loss (between 40-60%)
Depends on cutaneous blood flow & exposed surface area
Head
Convection
Airflow over exposed surfaces
Accounts for about 15-30% of intraoperative heat loss
Evaporation
Heat loss thru conversion of water → gas (body perspires)
8-10% of heat loss during surgery
Major open wound surgery
Conduction
Heat loss through physical contact with another object (cold surface; bed, mattress)
5% heat loss
Mechanisms of heat loss
%’s of heat loss
Radiation 40-60%
Convection 15-30%
Evaporation 8-10%
Conduction 5%
Hypothermia consequences
Wound infection & delayed healing
↑ O2 consumption (shivering)
↑ risk CV incidents (3x incidence of VT & cardiac events)
↑ sickling (sickle cell pts)
↓ platelet function
impairs coagulation cascade activation
(coagulopathy is the most well-studied complication of hypothermia)
Patients at high risk for hypothermia
Elderly: less subQ fat & altered hypothalamic fxn
Neonates
Intoxication: vasodilation & depressed heat regulatory center
Female
Certain drugs that cause alterations in thermoregulation
vasodilators, NSAIDs and phenothiazines
Neonates
-immature thermoreg center
-high surface area: body mass
-absent response to shivering (nonshivering thermogenesis)
If temperature falls from 37 to 35 by how much does the risk of infection increase?
2-3 times
How does hypothermia increase infxn risk?
Vasoconstriction
↓
Decreased blood & O2 delivery to the wound
Decreased superoxide production
If intraop temp falls to ___ degrees will increase the hospital stay by 2.5 days
35
Perioperative period and Hypothermia
General anesthesia:
Peripheral vasodilation
altered thermoregulation
inability to generate heat by shivering
(Neuraxial anesthesia)
Perioperative period and Hypothermia
d/t:
sympathetic blockade
muscle relaxation
lack of afferent sensory input → central thermoregulatory centers
Perioperative period and Hypothermia
OR practices
Cold fluids and blood, prep solutions, exposure
⭐️
fall in temperature during GA
3 phases:
1) initial rapid decrease ~0.5 - 1.5°C in ~30 min
2) slow linear reduction of about 0.3°C per hour
3) plateau phase as shown
Chapter 13 in Anesthesia equipment read and understand how anesthesia affects the body
🤨😒
Redistribution
-Internal distribution of body heat after GA induction
-Hypothermia after SAB or Epidural induction = added redistribution to legs
If the temperature falls from 37 to 35.5, what is the average increase in estimated blood loss (EBL)?
~500 cc
Decreased activity of clotting factors
T/F
Coag panels will show hypothermia induced coagulopathy
False
Labs run at inconsistent temps
you wont see hypothermia-induced coagulopathy on your coag panel
TEG (tests the strength of the clot) is usually warmed, but not mandatory
Why is hypothermia BAD for the heart?
(As pt rewarms after surgery)
Shivering
Arrhythmias
Hypertension
Tachycardia
(note: hypothermia causes hypoTN and brady<3 but we’re talking about going from cold to warm in this instance)
Compared to temperature of 35 degrees, normothermia is associated with a reduction in cardiac morbidity by ___%
55
Hypothermia and the ECG
mild & moderate
Mild hypothermia: sinus brady
Moderate hypothermia: prolonged PR, widened QRS, prolonged QT
Hypothermia and the ECG
severe
(below 32 degrees)
hypothermic hump/J-wave (Osborne)
elevation at the junction of the QRS and ST segments
⭐️
MAC is decreased ___% per degree C decrease in core body temperature
5-7%
hypothermia DECREASES MAC
Hypothermia
liver and renal fx
↓ renal blood flow and clearance
↓ hepatic blood flow can decrease metabolism
Hypothermia (decreases/increases) Protein binding
increases
Hypothermia & NMBs
Prolongs muscle relaxants
These drugs can depress voluntary shivering that generates heat
Opioids and muscle relaxants
During the first hour after induction of anesthesia, core body temperature can drop by 1.5° C due to what?
redistribution of body heat from core to periphery
What is the definition of hypothermia?
core temp 36 C or less within 1H of start of case
Which of the following is not an adverse effect of intraoperative hypothermia?
Increased risk of DVT/PE
Hypertension and tachycardia
Peds
methods of heat loss %’s
Radiation 39%
Convection 34%
Evaporation 24%
Conduction 3%
(note: same order from greatest to least as adults; just diff %’s)
Room temperature should be increased to at least ___℃ before nonfebrile neonates and infants arrive
26
The 4 heat loss mechanisms
How can we prevent or decrease the drop in patient temperature from redistribution after induction?
Increasing mean body temp
via
Pre-warming
usually need 30 min to be effective
(60 mins for large spinal surgeries)
⭐️
most effective non-invasive method of warming a patient?
Forced air warming blanket
⭐️
overall most effective method for warming a patient (invasive and noninvasive)?
Cardiopulmonary bypass
Pre-warming
-prevent/decrease drop in temp from redistribution after induction
-Increases mean body temp
-30 min to be effective
(60 mins for large spinal surgeries)
Where is the most accurate place to measure body temperature (closest to what the hypothalamus sees)?
Distal esophagus
45 cm from nose
Temperature Monitoring
Sites
🏆 Pulmonary artery (PA)
Distal Esophageal
Skin
Nasopharynx
Rectal
Bladder
External auditory canal
Distal Esophageal Temp monitor
optimal position
45cm from the nose
Hyperthermia
definition
⬆️ body temp 2C/hr
-or-
Core > 38C
Hyperthermia vs Hypothermia
which is uncommon in the OR?
hyperthermia
⭐️
Hyperthermia
Usual causes
sepsis or overheating due to active warming
other causes:
Malignant Hyperthermia (MH) or other syndromes
Manifestations of Hyperthermia
Increased metabolic requirements
Increased O2 consumption
Increased minute ventilation
Sweating and vasodilation
Tachycardia
Conditions associated with Hyperthermia
MH and Neuroleptic Malignant Syndrome
Pheochromocytosis, sepsis
Transfusion reaction
Serotonin syndrome
Malignant Hyperthermia
Inherited clinical syndrome
characterized by:
elevated core temperature
tachycardia
tachypnea
hypercarbia
muscle rigidity
rhabdomyolysis
acidosis
hyperkalemia
⭐️
Malignant Hyperthermia
Underlying abnormality relates to
uncontrolled release of intracellular calcium from the sarcoplasmic reticulum
Those susceptible to MH have a mutation of the _________ that allows ________ of calcium from SR
ryanodine receptor
uncontrolled release
Malignant Hyperthermia
Leads to activation of:
muscle contractile elements
hypermetabolism
MH
Mode of Inheritance
70% + of MH cases are linked to RYR1
(on chromosome 19)
The channel is the RYR1 because it binds to plant alkaloid ryanodine
MH is an inherited in an autosomal dominant manner
Does NOT skip generations
RYR1
calcium channel in the membrane of the sarcoplasmic reticulum of skeletal muscle
MH = defective
Why is it called the RYR1 receptor?
it binds to plant alkaloid ryanodine
⭐️
T/F
MH can skip a generation
FALSE
MH
Pathophysiology
abnormal/uncontrolled elevation of intracellular calcium levels in skeletal muscle
RYR1 calcium channel locked open
↓
uncontrolled Ca release (ICF Ca high)
↓
Continuous muscle activation
↓
ATP breakdown (even more heat production)
↓
SR Ca pump unable to reuptake Ca
Family History significance in MH
Any Family history
especially first-degree relative
MH
Associated skeletal muscle diseases:
Central core disease
King-Denborough syndrome
Multiminicore disease
Centronuclear myopathy
Congenital fiber-type disproportion
Native American myopathy
MH
Specific Clinical Features
Uncontrolled, exaggerated, hypermetabolic state triggered by inhaled anesthetics and/or succinylcholine
Unexplained ↑ETCO2 during constant ventilation
Generalized & Masseter rigidity
↑ T (rarely >40 degrees C)
MH
most sensitive and specific sign
Unexplained Increase in end-tidal carbon dioxide during constant ventilation
Generalized rigidity vs Masseter muscle rigidity
which is more specific?
Generalized rigidity (HIGH specificity)
Masseter rigidity (not as specific)
MH
Non-Specific Clinical Features
Tachycardia (earliest & most consistent sign, but not specific)
Tachypnea
Arrhythmias
Skin Mottling
Profuse sweating
Altered blood pressure
Tachycardia as a sign in MH
earliest and most consistent sign, although not specific
MH
Hyperkalemic Cardiac Arrest
Sudden hyperkalemic cardiac arrest after MH triggering agents in children with undiagnosed myopathy
especially dystrophinopathies, Duchenne or Becker’s muscular dystrophy
T/F
Hyperkalemic Cardiac Arrest is a result of pathophysiologic changes typical of MH
False
not a result of this
MH
Hyperkalemic Cardiac Arrest is r/t…
muscle membrane destruction leading to hyperkalemia
MH
Hyperkalemic Cardiac Arrest
Treatment
Treatment for hyperkalemia
Lab Findings of Acute MH
MH
Preop Evaluation
Detailed medical history:
Previous surgery and issues
Family history
History of heat stroke or exaggerated reactions to heat and exercise
MH
Preparing the anesthesia machine
1) Disable/remove/cover vaporizers
2) new breathing circuit & reservoir to y-piece of circle system
3) inflate (10L/min of fresh gas for up to 60-90 min; older machines 10L/min FGF for 20 min)
4) Change the CO2 absorbent
5) Activated charcoal filters to both limbs of the anesthesia breathing circuit before and during the procedure to reduce vapor [ ] to <5 ppm (increases washout period)
MH
Med cart preparation
Cover/Tape the succinylcholine or remove it
How does Dantrolene/Ryanodex work?
Direct-acting skeletal muscle relaxant
hydantoin derivative (anticonvulsant – Dilantin derivative)
Directly interferes w/ contraction
-inhibits Ca release from SR
? binds to the RYR1r
Dantrolene/Ryanodex
temp control
Can lower temp in
-neuroleptic malignant syndrome
-thyroid storm
MH Algorithm
Most accurate diagnostic for MH
exposure of biopsied skeletal muscle to halothane, caffeine, and ryanodine
MH
skeletal biopsy testing
-Thigh biopsy
-suspended in awater bath at 37C
-exposed to halothane, caffeine, or ryanodine
diagnosis of MH is based on:
Isometric contracture measured w/ strain gauge
(threshold & height of contracture)
MH
muscle biopsy test statistics
highly sensitive and close to 100%
20% of positive results are false-positives
Neuroleptic Malignant Syndrome
Signs/Symptoms
Muscle Rigidity and rhabdomyolysis, acidosis and tachycardia
Increased temperature
Depressed consciousness
Autonomic instability
⭐️
Neuroleptic Malignant Syndrome
Underlying pathophysiology
R/t central dopaminergic blockade at hypothalamus
Neuroleptic Malignant Syndrome
Triggers:
neuroleptics (Haldol)
antidopinergics
phenothiazines
other centrally acting drugs (Compazine, Reglan, Droperidol, and Phenergan)
Neuroleptic Malignant Syndrome
Treatment
Benzodiazepines
Dopamine agonist (bromocriptine)
May respond symptomatically to dantrolene
Serotonin Syndrome/Toxicity
excess serotonin in the CNS
Serotonin Syndrome/Toxicity
S/S
Mental status changes
Autonomic hyperactivity (fever, tachy🩷, HTN, diaphoresis)
Neuromuscular abnormalities (tremor, hyperreflexia)
Serotonin Syndrome/Toxicity
r/t pts on…
SSRIs, MAOI, tricyclics, amphetamines, Demerol
methylene blue
(acts as MAOI; increases serotonin levels, can be a trigger for serotonin syndrome)
Serotonin Syndrome/Toxicity
Treatment
Active cooling
IV fluids
↑ anesthetic depth to ↓ autonomic hyperactivity
Serotonin antagonist
(Chloropromazine IV, Cyproheptadine PO)
T/F
Avoid antipyretics in Serotonin Syndrome/Toxicity
True
Antipyretics have no role in this syndrome and should be avoided
Use NMB to help reduce rising body temperature
Drugs that can Increase risk for Hyperthermia
↑ basal metab rate & heat production:
-Sympathomimetic drugs
-Monoamine oxidase inhibitors
-Cocaine
-Amphetamines
-Tricyclic antidepressants
↑ T by suppressing sweating:
-Anticholinergics
-Antihistamines
How to treat Hyperthermia
Expose skin surfaces
Cooling blankets
Ice packs
Cool fluids
Antipyretics
Treat the cause
TURN OFF THE BAIR HUGGER
Dantrium/Revonto vs Ryanodex
