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116 Cards in this Set

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Pulmonary Complications Risk Factors [5]
advanced age
pre-existing pulmonary disease
reactive airway disease
morbid obesity
significant and common pulmonary complications are: [5]
pulmonary embolism
pleural effusions
Aspiration Pneumonitis
A rare event related to anesthesia
incidence: 0.3-4.7 /10,000 anesthetics
Pulmonary Aspiration mechanism:

acidotic gastric contents damage alveoli & pulmonary capillaries
aspiration of large volumes produces hypoxemia similar to near drowning

Ph less than 2.5, 25-30cc
Pulmonary Aspiration Pathophysiologic changes depend upon the composition of the aspirate
acid solutions cause atelectasis, alveolar edema and loss of surfactant
particulate aspirate will also cause small airway obstruction and alveolar necrosis
granulomas may form around food or antacid particles
Aspiration Pneumonitis Risk Factors: [8]
recent oral intake (primary)
upper GI obstruction
recent n/v
symptomatic hiatal hernia
second or third trimester pregnancy
significant ascites
morbid obesity
depressed gag reflex
Aspiration Pneumonitis Signs/Symptoms: [6]
recognized or unrecognized gastric contents in trachea
hypotension (indicates significant fluid shifts into alveoli and is associated with massive lung injury)
Pulmonary Aspiration Signs & Symptoms: [3]
ABG’s reveal respiratory acidosis, hypoxemia and hypercapnia

fluffy infiltrates on chest x-ray within 24 hrs

volume loss on chest x-ray indicating large particle aspirate obstructing a large bronchus
Aspiration Pneumonitis Treatment- Premedication
Histamine H1 blockers
Diphenhydramine (Benadryl)
Dimenhydrinate (Dramamine)
Action: Prevent the bronchoconstrictive response to histamine,anticholinergic effect, prevent motion sickness,antiemetic
limited use/ low risk patient
not a set tx
Aspiration Pneumonitis Treatment- Premedication
H2 Receptor Antagonists:
H2 Receptor Antagonists:
inhibit gastric acid secretion and H+ ion content (affect pH of only those gastric secretions given after their administration)
Cimetadine ( Tagamet, 300 mgm IV, po or IM)
Rantidine(Zantac, 150 mg po, 150 mg IV or IM)
Famotidine (Pepcid, 20 mg po or IV)
Aspiration Pneumonitis Treatment- Premedication
neutralize the acidity of gastric fluid by providing a base (usually hydroxide, carbonate, bicarbonate, citrate or trisilicate) that reacts with H+ ions to form water.
They raise the pH!
They work immediately.
They also raise gastric volume.
Aspiration of particulate antacids damages alveoli if aspirated.
Best to use non-particulate antacids e.g., sodium citrate, sodium bicarbonate
Loose their effectiveness 30 -60 minutes after ingestion, timing is crucial
Bicitra (0.3 M solution of sodium citrate)
Polycitra (15-30 ml, po, 15-30 minutes prior to induction)
Bicitra----all c-sections and full stomachs
Aspiration Pneumonitis Treatment- Premedication
By enhancing the stimulatory effects of acetylcholine on intestinal smooth muscle, it increases lower esophageal sphincter tone, speeds gastric emptying & lowers gastric volume.
Dose:10-20 mg (0.25mg) po, IM or IV
Onset of action: 3-5 mins. IV v.s. 30-60 mins. po
Aspiration Pneumonitis Treatment- Premedication
Serotonin 5 HT3 blockers:
Blocks the action of 5 HT3 receptors located peripherally (abdominal vagal afferents ) & centrally (chemoreptor trigger zone) which appear to play an important role in the initiation of the vomiting reflex
They are safe drugs with superior efficacy.
Aspiration Pneumonitis Treatment- Premedication
Odansetron (Zofran)
provides superior prophylaxis compared to Reglan or droperidol
patients at high risk of n/v due to previous history, type of surgery(timing important)
No significant drug interactions have been reported.
Dose: 4mg IV
4mg, if under 40 kg, then .1mg KG

Also anzomet 12.5mg (1/2cc)
Aspiration Pneumonitis Treatment- Premedication
Dolasetron (Anzemet)
Need to administer 2 times the recommended dose of Dolasetron to be as equally effective as 1 dose of Zofran
Costs less??
12.5 mg. IV
_________ is still the mainstay of attempts to minimize the risks of regurgitation & aspiration during general anesthesia for elective surgery.
Preoperative fasting
Aspiration Pneumonitis Treatment- [10]
Place patient immediately in a head down,lateral position
Suction pharynx & trachea
Oxygen Rx & Positive Pressure ventilation (mainstay of Rx)
PEEP or continuous positive airway pressure
Bronchodilators for bronchospasm
Bronchoscopy for removal of particles obstructing bronchi
Pulmonary Lavage
Intravascular volume replacement in the event of massive pulmonary capillary leak
Prophylactic antibiotics & steroids no longer required, antibiotics only for specific microbes
Does aspiration consistently result in aspiration pneumonia?
Not necessarily.
The seriousness of the lung damage depends on the volume and composition of the aspirate.
Patients are considered to be at risk if their gastric volume is > 25ml (0.4ml/kg.) and their gastric pH is < 2.5.
Some researchers feel acidity is more important than volume
The seriousness of the lung damage depends on the ______ and _______ of the aspirate.

Patients are considered to be at risk if their gastric volume is _______.
> 25ml (0.4ml/kg.)

_______ and their gastric pH is < 2.5.
If risk factor (full stomach) is not reversible or it’s an emergency, then consider the following:
If risk factor is not reversible or it’s an emergency, then consider the following:
Rapid sequence induction unless difficult airway (then perform awake intubation first)
Regional anesthetic
Never use an LMA
Never extubate patient until wide awake
Aspiration aka ________
mendelson’s syndrome
Pulmonary Embolus Incidence:
low or unknown
One study in Scandinavia (1992,1997) cited an annual incidence of1.6-1.8/1000 people
However, studies show that many patients have tiny pulmonary emboli that go unnoticed.
The body has a built in mechanism to dissolve these small emboli
Pulmonary Embolus Cause:
Results from the entry of blood clots, fat, tumor cells, air, amniotic fluid or foreign material into the venous

deep leg veins (90% cases)
elective hip surgery (3% cases)
elective general surgery (1% cases)system.
Clots from the lower extremities, usually above the knee, pelvic veins or right side of heart
Pulmonary Embolus Pathophysiology:
Embolic occlusions in the pulmonary circulation increase dead space. The affected area loses its surfactant within hours and may become atelectic within 24-48 hours.
Pulmonary Embolism=The cross sectional area of the pulmonary vasculature is _____, Thus causing sympathetic reflex and humoral _______.
in Pulmonary Embolism PVR is __________
Pulmonary Embolism hallmark sign
Rapid, shallow respirations ensue from a reflex response (vagal receptors in the pulmonary wall)
Pulmonary Embolism

Hypoxia develops in the ________ alveoli beyond the obstruction
Pulmonary Embolism

Hypoxia causes __________,
shunting blood away from the obstructed area
Pulmonary Embolism

If the patient survives, the embolism usually resolves within _______.
1-2 weeks
Risk Factors for Pulmonary Embolus [7]
oral contraceptive use
varicose veins
prolonged immobility
congestive heart failure
Pulmonary Embolus other pearls
type of surgical procedure
length of surgical procedure
hypercoagulability (e.g. antithrombin III deficiency)
postpartum state
fracture of lower extremities
heart failure
Pulmonary Embolism Emphasis should be on __________ not Rx
Pulmonary Embolism

66% of patients who die from the disease do so within __________ after the acute event!
30 mins.
Most cases of Pulmonary Embolism are diagnosed __________!
Pulmonary Embolus Treatment Regimen for Postoperative Prophylaxis
low-dose Heparin (5000u SQ, q 8 -12 hrs)
adjusted Dose Subcutaneous Heparin
Enoxaprin (Lovenox)
graduated compression stockings
intermittent pneumatic leg compression (* place before induction of anesthesia)
oral anticoagulants in combination therapy
Enoxaprin (Lovenox)
class: thrombolytic, unfractured porcine heparin
action: acts on factor 10 alone! enhances inhibiting effects of antithrombin III, prevents conversion of fibrinogen to fibrin & prothrombin to thrombin
use: deep vein thrombosis, pulmonary emboli in hip & knee replacement surgery
dose: 1 mg/kg. Bid , SQ, continue for 7-14 days
1/2 life 12 hours
Remember:Do not give immediately postop!
Initial dose should be given 12-24 hours postop
This predisposes the patient to an unnecessary risk of postoperative hemorrhage. Must wait until hemostasis ensues!
Not interchangeable with heparin..
Pulmonary Embolism Signs & Symptoms:
often absent, mild or nonspecific unless massive PE has occurred
Unexplained & sudden hypotension
sudden hypoxemia
sudden bronchospasm
elevated CVP (right heart failure) or PAP
sudden tachypnea
chest pain or hemoptysis (implies infarction)
Cardiac signs:
wide fixed splitting of second heart sound
acute cor pulmonale (new RAD, RBBB, talll peaked T waves)
Pulmonary Embolism Treatment:supportive
elastic hose
leg exercises
PE Treatment once diagnosed
Once diagnosis confirmed:
vena cava filters
pulmonary embolectomy
Airway Obstruction Causes:
Pharyngeal obstruction from tongue or epiglottis (most common cause) or improperly placed airway
Endotracheal tube problems-kinking, mainstem intubation
Foreign bodies

head & neck trauma associated with hemorrhage & dental fractures
structural damage to trachea from trauma
vomitus or poorly chewed food, especially in patients who can’t protect their airway
loose dentures
Airway Obstruction Signs & Symptoms
partial obstruction:
audible wheezing or inspiratory stridor
appearance of panic
activation of accessory muscles
suprasternal retractions /tracheal tug
nasal flaring, especially in children
Airway Obstruction s/s Complete obstruction:
unable to cough, speak or breathe
clutches the throat (universal distress signal)
Airway Obstruction Risk Factors:
Anatomy: obesity, large tongue, short neck, no jaw
Poor muscle tone: excessive narcotics or residual muscle relaxants, neuromuscular disease
Airway swelling: anaphylaxis,surgical manipulation, edema
Airway Obstruction Treatment
head tilt and jaw thrust or chin lift
insertion of an oropharyngeal or nasopharyngeal airway in unconscious person
call for help
reintubation may be indicated
reversal of pharmacological agents, muscle relaxants, opiods, etc.
encourage patient to cough forcefully
Airway Obstruction tx If complete obstruction:
perform Heimlich maneuver immediately (subdiaphragmatic thrusts) to forcefully push air out of lungs to dislodge the foreign body and clear the airway
Laryngospasm Definition
reflex response, i.e., forceful involuntary spasm of laryngeal musculature caused by sensory stimulation of SLN
can be partial or complete spasm of laryngeal muscles blocking flow of air in and out of lungs
form of upper airway obstruction
Laryngospasm Signs & Symptoms:
decreased O2 saturation/hypoxia
if complete obstruction- absence of air movement
if partial obstruction- stridor or crowing sounds
Laryngospasm Risk Factors:
Pharyngeal secretions (blood, vomitus,)
passage of ETT through larynx during extubation
insertion of oral airway
frequent suctioning
smoking history
traumatic or difficult intubation
recent cold, coughing, URI
Asthma, COPD, irritable airway
Laryngospasm Treatment :
Order of Importance
1. Jaw thrust
2. Notify anesthesia provider, call for assistance
3. Positive pressure ventilation with 100% O2
4. Decadron or lidocaine or both to reduce airway irritation and swelling, if relieved
Laryngospasm If Persists-
1. Succinylcholine (subparalytic dose, .15-.30mg/kg, to paralyze laryngeal muscles and allow CV)
2. Reintubate -give additional succinylcholine, full intubating dose
3. Assisted ventilation
4. Sedate the patient
5. If laryngeal edema present- administer racemic epinephrine & steroids
Laryngospasm Prevention
Hemostasis during surgery
Suctioning after administration of reversal agents
Suctioning before extubation
minimize stimulation of airway during extubation (extubate deep or when pt. is fully awake)
minimize stimulation of airway after pt. extubated, e.g., oral airways, stimulating gag reflex
administer steroids &/or lidocaine beforehand (remember: inhibits protective reflexes)
Bronchospasm Definition:
form of lower airway obstruction
characterized by smooth muscle contraction and increased resistance to airflow through the bronchial tree
reflexive response
Bronchospasm Causes:
airway secretions/ aspiration
foreign body /airway manipulation/ tracheal intubation
pulmonary edema
Bronchospasm Causes:
obstructed endotracheal tube at the carina or down a mainstem bronchus
allergic or anaphylactic reaction to drugs
medications: ASA, beta blockers, muscle relaxants
light anesthesia
Bronchospasm Signs & Symptoms:
anesthetized individual-
wheezing on both inspiration & expiration
increase in peak inspiratory pressure due to decreased lung compliance
capnograph- low CO2
Bronchospasm Signs & Symptoms:
awake individual-
marked tachypnea
Severe Bronchospasm Signs & symptoms:
chest retractions
shalllow noisy respirations
air trapping
hypoxemia/ decreased SaO2
impaired venous return
decreased cardiac output
Bronchospasm Treatment:
Primary Goal: Prevention!
smooth, deep, induction of GA with minimal attempts at laryngoscopy
judicious use of rapid sequence induction
avoidance of histamine releasing drugs (Mg So4, demerol, morphine, curare, atracurium, mivacurium, barbituates, beta blockers,)
Bronchospasm Preventive Treatment:
pretreatment with lidocaine & aerosolized bronchodilators before airway manipulation
increase FIO2
if light anesthesia is suspected, deepen anesthesia (if appropriate)
Bronchospasm Treatment:
remove irritant
assess airway patency and tube position
administer drugs
Bronchospasm Drug Therapy
Intra venous/subcutaneous agents
Epinephrine 0.25-1 ug/min (low dose- beta effect)
Terbutaline 0.25mg sc(repeat in 15 mins., do not exceed 0.5mg in a 4 hr. period)
Bronchospasm Drug Therapy

Inhaled B-adrenergic agonists
(Proventil, Ventolin)
Metaproteronol (Alupent).
Bronchospasm Drug Therapy
Intra venous/subcutaneous agents
Aminophylline 5 mg/kg over 30 mins. (loading dose), IV drip 0.5-1.0mg/kg/hr
Pulmonary Edema Stage I.
Only interstitial pulmonary edema is present;
patients become tachypneic
pulmonary compliance begins to decrease
chest x-ray shows increased interstitial markings & peribronchial cuffing
Pulmonary Edema Stage 2.
fluid fills interstitium
fluid begins to fill alveoli
gas exchange is preserved
Pulmonary Edema Stage 3.
alveolar flooding occurs, alveoli contain no air
flooding most predominant in dependent lung areas
blood flow through capillaries of flooded alveoli, result in shunting
hypoxemia and hypocapnia ensue due to dyspnea & hyperventilation
Pulmonary Edema Stage 4.
marked alveolar flooding spills over into airways as froth
gas exchange severely compromised (shunting & airway obstruction)
severe hypoxemia and hypercapnia
Hypervolemic Pulmonary Edema Rx:
vasodilators, diuretics, inotropes
goal: - reduce preload to relieve pulmonary congestion
reduce afterload to improve cardiac output
Pulmonary Edema Usual Cause:
2. An increase in the permeability of the alveolar-capillary membrane (permeability edema) ,i.e. protective effect of plasma oncotic pressure is lost as increased amounts of albumin “leak in” the pulmonary interstitium; usually the alveolar epithelial membrane is permeable to water & gases only!
e.g. acute lung injury, ARDS, sepsis, trauma
Negative Pressure Pulmonary Edema Cause:
patient vigorously tries to breathe against a partially closed glottis or occasionally a small ETT
-A large negative intrathoracic pressure is generated by the struggling patient which produces pulmonary edema in usually healthy, young patients
Negative Pressure Pulmonary Edema Signs & Symptoms:
coarse breath sounds/ rales
production of pink frothy sputum
hypoxia & hypertension precede the telltale physical signs
Negative Pressure Pulmonary Edema Patient presentation:
young muscular individual
may occur in any pt. with some degree of laryngospasm after extubation
often reversal of opiods (with narcan) has been required for extubation
Chest x-ray shown a normal sized heart with no lung parenchymal changes
Chest x-ray may show pulmonary infiltrates
Negative Pressure Pulmonary Edema Treatment:
supportive measures:
Oxygen therapy
CPAP via mask
intubation & MV with PEEP & high FIO2
minimal diuretic Rx
Hypoventilation Risk factors:
advanced age
long operations
high dose muscle relaxant use
high dose opiod use
Hypoventilation Causes:
airway obstruction
residual effects of medications
anesthetic agents
muscle relaxants
Hypoventilation Signs & symptoms:
residual muscle relaxant-
unresponsive pt. , appears “floppy” with poorly effective & coordinated intercostal & abdominal muscles
pt. may complain breathing is restricted
pt. willing to respond to commands but can’t
unable to sustain hand grasp &/or head lift
inadequate train of four response
decreased SaO2 (most frequent event)
increased PCO2
Hypoventilation Treatment:
ventilatory assistance with nasal/oral airway, intubation may also be needed
increasing FI02, switch from cannula to mask
tactile & verbal stimulation
elevate head of bed
reversal of sedatives, narcotics, muscle relaxants
Emergence Delirium Definition:
a state of delirium in which responsiveness to commands is obtunded & primitive responses to pain, hypoxia & disorientation predominate
if lasts > few minutes, termed emergence delirium
state of agitation, disturbances in thought, attention and cognition
Emergence Delirium Who is susceptible?
children/adolescents/young adults
drug or alcohol withdrawal
pain or anxiety
visceral distension: bowel, bladder
temperature alterations
Emergence Delirium Risk Factors
hypoxemia or hypercapnia
anesthetic agents: ketamine
adverse reactions to medications
metabolic disturbances: acid-base; electrolyte disturbances
Emergence Delirium Causes:
certain drugs have been implicated
anticholinergics (e.g., atropine, glycopyrolated) crosses the BBB producing CNS stimulation
opiods may cause predominately dysphoria in susceptible individuals
Emergence Delirium Signs/Symptoms
pt.s. do not remember this phase of recovery
Emergence Delirium Treatment
protect pt. from harm
wait until a more lucid period of conscious awareness arises
administer physostigmine (.5-2 mg IV) produces dramatic improvement Always rule out hypoxemia
Pseudocholinesterase Deficiency Cause:
Succinylcholine is typically broken down by pseudocholinesterase within 3-5 mins.!
Always check the TOF after the sux before giving another paralytic…

May also effect esmolol and mivacurium…………


Atypical Psudocholinesterase is unable to break down succinylcholine!!!!
Psudocholinesterase or plasma cholinesterase: (PChE)
1. Responsible for metabolism of succinylcholine (Sch), ester anesthetics , mivacurium and trimethaphan (an anti-hypertensive)
2. Produced by the liver
Succinylcholine Important Difference!
ScH is normally hydrolyzed by plasma cholinesterase (pseudocholinesterase)

ScH is not hydrolyzed by acetylcholinesterase (non depolarizers)
Duration of Action of ScH is prolonged by:
high doses / prolonged exposure (7-10mg/kg)
abnormal metabolism (e.g., low enzyme levels of pseudocholinesterase, doubles or triples duration of blockade)
genetically aberrant enzyme
Dibucaine Variant
Most commonly recognized abnormal genetic variant.
Dibucaine: a local anesthetic
Dibucaine # is a qualitative measurement

This is how it is tested.

The dibucaine level is to test for pseudocholinesterse difficiency
Causes of Low Levels of Pseudocholinesterase
certain drug Rx
*beta blockers
*local anesthetics
cytotoxic drugs
*collagen vascular diseases
*renal failure
*liver failure
*severe anemia
Pseudocholinesterase Deficiency Treatment:
Keep patient intubated & ventilated until efficient respirations obtained
administer sedative
Educate pt. and family of need to avoid ScH in the future
Obtain lab studies to determine Db #
Hypotension Interventions
Rx the cause (replace fluids, administer inotropes or chronotropes, repair bleeders)
place in Trendelenberg or shock position
Place pregnant patients in left lateral tilt to relieve vena cava pressure
Hypertension Patients at Risk
Patients with increased C.O. caused by:
Volume overload
Patients with increased vascular resistance caused by:
Full bladder
Chronic hypertension
Signs and Symptoms
Signs and Symptoms
blood pressure deviates from patient’s normal reading by 20% S
Intervention usually not required unless blood pressure is 180/100 or higher
Rx the cause (rewarming, diuretics, analgesics, antihypertensives, oxygen, inserting a urinary catheter, ventilating)
PONV Incidence:
The overall incidence for all surgeries is 25-30%
Pediatric population incidence is 40% in children> 3 yrs. Of age
In high risk patients the incidence is 60 to 70%
0.2% patients may experience intractable PONV leading to delay in PACU discharge and admission
One of the most unpleasant experiences after surgery and one of the most common reason for poor patient satisfaction
________ is also associated with wound dehiscence, pulmonary aspiration, hematoma formation beneath skin flaps, dehydration, electrolyte disturbances, Mallory-Weiss tear and esophageal rupture
Risk Factors for PONV
Nitrous may or may not cause N/V
Anesthetic Factors:
Volatile agents
Nitrous oxide
High doses of neostigmine
Patient Factors:
Female gender
h/o PONV or motion sickness
High levels of anxiety
Surgical Factors:
Long surgical procedures (ea. 30mins increases risk by 60%)
Certain types of surgeries: intrabdominal (70%), major gynecologic (58%), laparoscopic (40-77%), breast (50%), ENT (71%), strabismus(85%), tonsillectomies and middle ear
Physiologic Basis of Antiemetics:
Vomiting center located in lateral reticular formation of medulla
It receives input from chemoreceptor trigger zone (CTZ), vestibular apparatus, cerebellum, solitary tract nucleus and the higher cortical centers
Currently available antiemetics act by blocking one or more of the four major receptor systems:
1. Dopaminergic (D2)
2. Cholinergic (muscarinic)
3. Histaminergic (H1)
4. Seratoninergic (5-HT3)
PONV Anticholinergics – [2]
(blocks muscarinic cholinergic receptors)

atropine, scopolomine
PONV Antihistamines-
(blocks acetylcholine receptors and H1 receptors) ethanolamines (dimenhydinate, diphenhydramine) and piperazines (clyclizine, hyroxyzine, meclizine)
PONV Phenothiazines
(blocks D2 receptors in CTZ) alphatic group: promethazine, chlopromazine have less antiemetic and more sedative effects v.s. heterocyclic group: perphenazine, prochlorperazine
PONV Butyrophenones-
(D2 receptor antagonists act on CTZ & area postrema) droperidol, haloperidol Note: Nov. 2001 FDA issued “black box” warning on droperidol, most serious warning of FDA, its use was associated with QT segment prolongation &/or torsades de pointes and in some cases resulted in fatal cardiac arrhythmias, after its administration EKG should be monitored for 2-3 hrs.
PONV Benzamides-
Metaproclamide (most common) prokinetic agent that blocks D2 receptors in the GI tract and centrally in CTZ and area postrema, increases LEST and enhances gasric motility, has short duration of action 1-2 hrs. Recent study 2002 showed most efficacious dose was 20mg and not 10mg
PONV 5 Ht3 Receptor Antagonists-
-highly specific and selective for n/v
-bind to 5-HT3 receptor in the CTZ & at vagal afferents in GI tract
-effective for both prevention and treatment
-often used as a rescue drug
PONV Dolasetron
– chemically related to tropisetron (5mg) & granisetron (3mg)
- 12.5 mg IV (30 mins. Before end surgery)
-po dose 100 mg.
-efficacy compared to odansetron ongoing debate
-studies show no difference in discharge time from PACU between the two drugs
PONV Odansetron-
- chemically related to metoclopramide
-optimal effective dose: 4mg
- po dose 8 mg. 1-2 hrs. before surgery
- antivomiting efficacy better v.s. antinausea efficacy
- side effects: headaches, diziness, flushing, elevated liver enzymes & constipation
PONV Unconventional Antiemetics
1. steroids
2. propofol
3. benzodiazapines
4. ephedrine
5. supplemental oxygen
6. hydration
7. NK-1 recptor angagonists
PONV Nonpharmacologic Techniques
1. sea bands-acupressure/acupoint stimulation
2. acupuncture (1996 – change from Class III (experimental) to Class II medical device)
3. hypnosis
4. electroacupuncture
5. laser stimulation of P6 point
(ginger root has not been found to work)
PONV Acupuncture
-3000 years in China
1999 Lee & Done meta analysis
Findings: significant reduction in PONV v.s placebo in early prevention
Acupuncture techniques results ~ antiemetics in preventing late or early PONV
In children, no benefit was found
PONV Multimoddal Approach
Attack several receptor sites at once to get best results!
Concept introduced in 1988 for chemotherapy pts.
Most frequently studied combination therapy: 5HT3-receptor antagonist with droperidol or dexamethasone
PONV Patient risk Factors:
h/o PONV or motion sickness
Use of opiods
PONV/Risk Factors Surgical Factors:
Surgical Factors:
Gynecologic surgery
Breast surgery
According to a 2001 FDA black box warning droperidol has been associated with:
Q-Tc segment prolongation &/or torsades de pointes