Grab Bags!! Flashcards
What is BMI
kg divided by square of patient’s height in meters
Is it important to know what liposuction technique is planned?
Yes b/c different morbidity and mortality for different techniques
tumescent: large volumes of lidocaine and epinephrine are injected into subcut tissues. Fat removed is less than 3000 mL
semitumescent: more fat is removed and it is associated with fluid overlaod, pulmonary edema, local anesthetic toxicity and fat emboli
Treatment of nerve injuries :
Risks for nerve injury:
usually resolve within 5 days, but ALWAYS seek neurologic consultation.
Extremes in weight
DM
Pre-existing neuro dysfunction
certain positions: lithotomy-common peroneal nerve
Toxic dose of lidocaine: How much is usally given during liposuction:
How can you decrease risks of local anesthetic toxicity?
Pts at increased risk of lido tox?
While the maximum safe dose of lidocaine with epinephrine is often
reported as 7 mg/kg, Dermatology recs: mac dose of 55 mg/kg of lido alone using diluted tumescent solution, adding epinephrine, and
limiting the surgery to less than 3000 ml of fat removal. Moreover, I would ensure
the availability a lipid rescue kit and carefully monitor the patient for signs and
symptoms of local anesthetic toxicity (patients should be monitored throughout the
perioperative period and for at least 30 minutes postoperatively since signs and
symptoms of toxicity may be delayed for over 15 minutes following tumescent
procedures).
pts at increased risk:
extremes of age, cardiac disease, renal dysfxn
IV fluids during lipo:
be cautious, use foley to better balance recognizing that there may be intravascular fluid overload, pulmonary edema or CHF
Treatment of cancer pain: pt already on morphine. Having inadequate pain control, nausea, vomiting and constipation-what do you recommend?
antidepressants and anticonvulsants for neuropathic pain; corticosteroids to reduce
inflammation; bisphosphonates and calcitonin for bone pain; and octreotide to relieve
pain due to bowel obstruction. ANd celiac plexus block
How would you perform celiac plexus block?
prone position, at the level of the Ll vertebral body. Needles are placed approximately 5-7
cm lateral to the midline, and advanced under :fluoroscopic guidance to lie anterior to
the vertebral body.A test block is usually performed with local anesthetic to ensure
benefit from the procedure. If the patient achieves good pain relief from the local
anesthetic, a neurolytic block, with either alcohol or phenol, is then performed.
complications of celiac plexus block:
most serious complication is paralysis, due to spread of the neurolytic
agent into the spinal or epidural space, or secondary to damage of vital arterial supply
to the spinal cord (i.e., the artery of Adamkiewicz). Other complications include
postural hypotension (most common), accidental intravascular injection,
retroperitoneal hemorrhage, sexual dysfunction; pneumothorax, diarrhea, and damage
to the kidneys or pancreas. A celiac plexus block is contraindicated in the presence of
systemic anticoagulation, sepsis, local infection, or bowel obstruction.
Gabapentin works how?
increases GABA in brain (inhibitory neurotransmitte)
Celiac plexus nerves:
T5-T12
A 35-yr-old man has diffuse burning pain in his left arm that began 6 months ago
after suffering blunt trauma to his hand during a pick-up basketball game. His left
finger tips are cyanotic.
1) What is your differential diagnosis?
complex regional
pain syndrome type soft tissue injury, nerve injury (brachia! plexopathy),
vascular insufficiency (Raynaud disease), peripheral neuropathy, or nerve entrapment
syndrome (carpal tunnel syndrome).
Diagnostic criteria of CRPS-1
Diagnostic testing?
initiating noxious event,
followed by burning pain; allodynia or hyperalgesia disproportionate to the degree
and type of injury; cyanosis; edema; cutaneous vasomotor instability (changes in
blood flow); and sudomotor instability (sweating).
With time-smooth and glosy skin, stiff painful joings and NO OTHER CAUSE FOR PAIN OR DYSFUNCTION
Diagnostic testing that may help identify: thermography (to detect vasomotor instability),
sweat testing (to detect sudomotor instability), and radiography (to detect bone
demineralization).
CRPS 2 vs CRPS 1:
CRPS-2 is different from CRPS-1 only in the nature of the inciting
event. Differentiating the two syndromes, therefore, requires a careful history. Some
of the events that can lead to the development of CRPS-1 include, crush injuries,
lacerations, fractures, surgery, sprains, or burns. CRPS-2, on the other hand,
develops following nerve injury, with the characteristic symptoms not necessarily
limited to the distribution of the injured nerve.
JW-what to do first:
Identify what they will accept, we will respect religious beliefs (until-in kids-it is absolutley necessary), Mention you will have to seek a court order authorizing the admin of those blood products
Pedi Pt crying and says they don’t want surgery:
talk to pt and family about why. If due to anxiety, consider removing pt from periop area, discuss giving midaz with pt and family. If it still escalates, have a discussion with surgeon about possible rescheduling
What is SLE?
SLE is an autoimmune disease resulting in systemic chronic inflammation
(i.e. vasculitis) and tissue damage. Diagnosis is often difficult and is usually made based on
the presence of 3 or more of the following criteria: (1) antinuclear antibodies; (2)
characteristic rash (i.e. malar rash and/or discoid rash); (3) nephritis; ( 4) polyarthritis
(symmetrical arthritis involving the hands, wrists, elbows, knees, and/or ankles); (5)
hematologic disorder (i.e. thrombocytopenia, hemolytic anemia, etc.); (6) serositis (i.e.
pericarditis and/or pleuritis); (7) neurologic disorder (i.e. seizures and/or psychosis); and (8)
photosensitivity.
Pt has lupus anticoagulant-you doing neuraxial?
Lupus anticoagulant is a misnomer because this immunoglobulin does not
result in clinical coagulopathy but, rather, is a prothrombotic agent that only causes a
prolonged aPTT because of a laboratory artifact.
So as long as other labs wnl, (of course consider clinical course KIM that lupus. can cause thromboyctopenia jsut like PET)
Antiphospholipid syndrome: Associated with what?
What lab would you see? Increased risk of bleeding? Seizures in these pts?
acquired autoimmune disorder characterized by venous and or arterial thrombosis. CAn happen with lupus or RA or in isolation. prolongation of PTT, but still no increased risk of bleeding. Consider this diagnosis in pts with isolated PTT
Seizures could be due to cerebral embolsim. keep this in mind with pregnat pts who have it and PET
14 yo pt preggo test comes back positive-wyd?
I would first attempt to determine whether my state law would
declare her emancipated in regards to medical decisions involving her pregnancy,
recognizing that this would confer upon her the right to complete confidentiality.
I would most likely inform only the
minor of her positive pregnancy test, encourage her to make her mother aware of the
pregnancy, and attempt to facilitate the appropriate follow up care for the patient (i.e.
obstetrician and social worker)- in order to maintain the trust in the physician-patient relationship
Concerns about anesthesia for MRI?
(1) the unintentional transfer of a
ferromagnetic object (i.e. gas cylinders, keys, scissors, etc.) into the scanner room, leading to
projectile-induced injury to the patient or hospital personnel; (2) dislodgement or
malfunction of an implantable device with exposure to the scanner’s magnetic field (i.e.
pacemaker, AICD, implanted infusion pump, spinal cord stimulator, and/or mechanical heart
valves); (3) magnet-induced equipment malfunction (i.e. monitors and infusion pumps); (4)
thermal injury, secondary to magnetic field affects on monitoring equipment like ECG pads
or the pulse oximeter (monitoring cables should be straight where in contact with the
patient. .. i.e. no coiling); (5) temporary or permanent hearing loss secondary to the loud
banging produced by the MRI scanner (ear plugs should be utilized to prevent this type of
injury); (6) patient anxiety,
Would you do an MRI in preggo? Braces in preggo?
The evidence does not currently suggest that the magnetic fields generated
during MRI are harmful to the baby in utero,
While the presence of braces is not a contraindication to MRI, they could
potentially degrade the quality of the image. Therefore, I would discuss this with the
radiologist to determine if MRI is still the optimum modality for this patient. If I had any
doubt about the safety of an object, I would use a small hand-held magnet to test whether the
object was ferromagnetic prior to entering the scanner room.
How will you give a pt anesthesia in MRI if you do NOT have an MRI compatible machine or monitors?
in the absence of an MRI-compatible anesthesia machine, I would: (1) ensure that
an Ambu bag was connected to an oxygen source in the scanner room; (2) apply the
appropriate monitors with sufficiently long cables to reach the area just outside the scanner
room; (3) administer a B2-agonist; (3) induce the patient with lidocaine, fentanyl, versed, and
propofol; (4) secure her airway with an ETT, to provide a definitive airway in this obese
asthmatic patient (an LMA may be considered to reduce the risk of bronchospasm, but would
be inferior in the management ofbronchospasm should it occur); and (5) maintain anesthesia
with either propofol or a volatile agent delivered through lengthy tubing that allows the
anesthesia machine and/or infusion pump to remain outside of the scanner room.
Pt with heart transplant has 2 p waves on EKG:
The non-conducted P-wave is unlikely to represent atrioventricular block, but
rather, is originating from residual native atrial tissue. The impulse from the native sinus
node is unable to traverse the anastomotic line and, therefore, does not result in ventricular
contraction and the generation of a QRS complex on ECG.
Monitors for pt with heart transplant:
Pretty much the same, but this is a preload dependent patient because the denervatedheart primarily
increases cardiac output by increasing stroke volume via the Frank-Starling mechanism,
rather than heart rate),
These pts at risk for coronary atherossclerosis, arrhythmias, So make sure you place an A line, and a 5 lead EKG. Consider placement of CVP, but weigh that with risk of infection in transplant patients.
Frank Starling:
increase in SV that results from more forceful cardiac contraction in response to increased cardiac filling. Helpful in transplanted heart physiology
Nasal intubation in heart transplant pts?
increased risk of infection from nasal flora-so no if possible
Induction in transplanted heart pts:
Good med for pt with transplanted heart?
Slow controlled to avoid drops in SVR-use etomidate
Good med: Isoprterenol: potent beta 1 and beta 2 adrenoreceptor agonist-excellent choice in pts with cardiac transplant
You’re going to reverse a transplanted heart pt with neostigmine: do you need to give glyco?
Yes. even though it wont’ change the HR< it can help reduce bronchospasm and increase salivation. KIM that neostigmine can cause bradycardia in transplanted hearts, so be ready
NSAID post op for transplanted heart pt:
If on nephrtoxic immunosuppressive drugs-NO. could exacerbate kidney damage, and also increase risk of gastritis (pts have gastritis with immunosuppressive drugs)
You’re called to be present for possible sick baby being delivered-what do you need to have ready?
Prior to delivery I would ensure that the appropriate support personnel
and equipment were available for neonatal resuscitation (i.e. a self-inflating bag
attached to 100% oxygen, a neonatal oxygen mask, wall suction, a radiant warmer or
other heat source, warmed linens, appropriately sized laryngoscopy blade and ETTs,
resuscitation medications, and blow by oxygen capabilities).
When are you suctioning out meconium?
(tracheal suctioning
should be performed if the baby does not demonstrate strong respiratory effort,
good muscle tone, and a heart rate > 100 beats/minute).
Neonatal resuscitation outline”
below 100, he
remained apneic, or he was gasping, I would provide positive mask ventilation with
air, or an air/oxygen mixture, and consider applying a pulse oximeter. If after 30
seconds of positive mask ventilation the HR was less than 60, then I would INTUBATE
increase the oxygen concentration to 100%, begin chest compressions (3
compressions to 1 breath for a total of 120 events/minute), and establish venous(umbilical·vein catheterization).~r intraosseous ac~~~~ (risks include tibial fracture
and osteomyelitis). If after another 30 seconds there were still no improvement, I
would administer 0. 01-0. 03 mg/kg of epinephrine via the umbilical vein or
established intraosseous access, and consider volume expansion.
Let’s say baby is not doing well due to magnesium toxicity-wyd?
what about hypoglycemia?
what about if baby has mom on opioids?
Why do you have to be careful with calcium?
If
magnesium toxicity were confirmed, I would administer calcium (100 mg/kg of
calcium gluconate or 30 mg/kg of CaCh), recognizing that calcium therapy has been
associated with cerebral calcification and decreased survival in stressed newborns
(therefore, it should only be administered to reverse the effects of magnesium
toxicity). In the case of hypoglycemia (glucose< 35 mg/dL), glucose should be
administered (8 mg/kg/minute of 10% solution). While placental transfer of
maternally administered narcotics could potentially be exacerbating this neonate’s
condition, I would not administer naloxone unless all other resuscitative efforts had
failed; as this drug is no longer recommended during the initial resuscitation in the
delivery room (can worsen the neurologic damage caused by asphyxia).
Calcium can cause cerebral calcification and decreased survival in stressed newborns.
Mallampati score:
Class 1: complete visualization of soft paalte
2: complete visualization of the uvula
3: Visualization of only base of uvula
4: soft palate not visible at all
Laryngoscopy grades:
1: Full view of glottis
2a: partial view of glottis
2b: only arytenoids seen
3: only epiglottis seen
4: neither glottis nor epiglottis seen
What questions do you want to ask the pt with cirrhosis?
determine the severity of his hepatic disease by
performing a thorough history and physical, focusing on the onset and etiology of his
cirrhosis, and the presence of jaundice, bleeding disorders, ascites, asterixis, and
hepatic encephalopathy. Based on my findings, I may consider additional lab work to
aid in discerning the severity of liver disease, including bilirubin, transaminases,
alkaline phosphatase, albumin, total protein, prothrombin time, INR, and hepatitis
serologies
Systemic effects of cirrhosis
Cirrhosis’ effects on the respiratory system include intrapulmonary arteriovenous
(AV) shunts, reduced PRC, restrictive lung disease, pleural effusions, and attenuation
of hypoxic pulmonary vasoconstriction. Cerebral effects include the accumulation of
ammonia and other toxins, which may lead to encephalopathy. Thrombocytopenia
and clotting factor deficiencies may result in a coagulopathy. Cardiovascular effects
include decreased peripheral vascular resistance, increased cardiac output, and
cardiomyopathy. Potential metabolic effects include dilutional hyponatremia,
hypokalemia, hypoglycemia, and hypoalbuminemia. Various additional effects of
cirrhosis include portal hypertension, esophageal varices, delayed gastric emptying,
ascites, and hepatorenal syndrome
Muscle relaxant in cirrhosis:
And what if that choice wasnt’ available?
I would prefer to use a muscle relaxant that is not dependent on
hepatic metabolism, such as Cis-Atracurium. This drug’s duration of action should
not be affected by liver failure, because it undergoes degradation in the plasma by
Hofinann elimination, and is reduced to inactive metabolites. If that choice unavailable-i would recognize potential for increased duration of action and monitor nm fxn with nerve stimulator
Signs of PDPH and what you would order before treatment?
(PDPH), I would
consider an epidural blood patch. Initially, however, I would review the patient’s
record and assess him for signs and symptoms of a PDPH, such as frontal-occipital
headache, decreased pain with recumbent positioning, nausea, vomiting, neck
stiffness, back pain, visual disturbances (photophobia, diplopia, and difficulty in
accommodation), and auditory disturbances (tinnitus, hypacusis, and hearing loss). I
would also require a coagulation profile, since he may be receiving anticoagulants
following his recent knee surgery. If a blood patch were contraindicated for any
reason, I would recommend conservative therapy, which consists of hydration,
caffeine, and pain control.
Why do pts have pain with PDPH?
The lost CSF, decreased buoyant support for the brain, and cerebral
vasodilation (increased cerebral blood flow to compensate for decreased CSF) that
accompanies significant dural puncture, can lead to the signs and symptoms of a
PDPH, which include a frontal-occipital headache, decreased pain with recumbent
positioning, nausea, vomiting, neck stiffness, back pain, photophobia, diplopia,
difficulty in accommodation, tinnitus, and hypacusis (hearing loss). Rarely, PDPH is
associated with seizures (most likely secondary to cerebral vasospasm), abdominal
pain, and diarrhea. Loss of CSF can also lead to cranial nerve stretching with
subsequent palsy.
non blood patch options for PDPH:
While less effective than blood patch, conservative treatment
consisting of hydration (no evidence of therapeutic benefit), caffeine, the placement
of an abdominal binder (increases abdominal pressure, possibly leading to an increase
in CSF pressure), and pain control provides an alternative when a blood patch is
contraindicated.
Type D TEF:
esophageal pouch communicates with trachea, but is otherwise the same as c
(esophageal atresia with blind upper pouch and lower segment tracheal fistula)
Where should ETT be in TEF? How can you do this? What can surgeon help you with?
Ideally the tip of the ETT should be placed distal to the fistula and
proximal to the carina, allowing positive pressure ventilation of both lungs without
excessive airflow through the fistula
One method of properly positioning the ETT is to advance the ETT
into the right main-stem bronchus and then slowly withdraw it until breath sounds are
heard through a stethoscope placed in the left axilla.
If excessive airflow through fistula occurs surgeon can perform a gastrostomy to decompress the stomach
Epiglottitis symptoms:
If pt presents with severe respiratory distress, are you getting radiographs?
SUDDEN ONSET, fever, drooling, stridor, substernal retractions. Radiographs should only be done when child is stable and when appropriate people can accompany child. Severe should immediately be transferred to OR with Anesthesiologist and the Surgeon
Pediatric pt with epiglottitis has a family Hx of MH-wyd?
100% O2
Emergency drugs and airway stuff ready
No versed
Parents come with me
stan ASA monitors, emergency airway cart and surgeon in room-an intramuscular dose of ketamine (2-3 mg/kg) with the goals of
providing sedation and maintaining spontaneous ventilation while securing
intravenous access.
Then deepen anesthesia with IV medications, place tube 1/2 size smaller than normal. Let the surgeon do their thing and then consider switching to nasal intubation as it is typically tolerated better in children.
When would you extubate kid with epiglotkfjd?
I would only consider extubation once the child’s fever, neutrophilia,
and epiglottic swelling had resolved (these patients usually remain intubated for 24-
48 hours following the initiation of treatment). The resolution of airway edema is
suspected with the return of swallowing and when a significant leak around the
nasotracheal tube is present (10-20 cm. H20 peak inflation pressure). Prior to
extubation, I would transfer the patient to the operating room, induce general
anesthesia, and confirm the resolution of airway edema by visual inspection with a
flexible fiberoptic bronchoscope. I would then extubate the child and continue to
monitor her for post-extubation edema.
In pituitary tumors, dont’ forget to ask:
What kind is it? Cushings, acromegaly, see if there is suprasellar extension (ha, blurry vision, rhinorrhea)
During infiltration of local anesthesia, you notice multiple premature ventricular
contractions (PVCs). What would you do? (LA for tumor resection) why do you think it happened?
The PVCs are likely to be the result of the injection of epinephrine-
containing local anesthetic or the use of cocaine pledgets. With this in mind, I would
alert the surgeon to stop the infiltration, ensure adequate ventilation with 100%
oxygen, check blood pressure, and examine the EKG for signs of myocardial
ischemia. I would then be prepared to treat any hypertension and/or significant
arrhythmias that may occur.
4) What do you think was the cause?
UBP Answer: As I mentioned, the most likely cause is systemic uptake of
epinephrine contained in the local anesthetic. However, other potential causes
include, hypoxia, cardiac ischemia, air embolism, electrolyte abnormalities, or
anesthetic induced cardiac depression.
A 23-year-old pregnant patient at 33 weeks gestation, who is receiving terbutaline
for premature labor, presents with respiiratory distress. On exam, you hear crackles
bilaterally. Why do you think she is in distress?
The bilateral crackles on exam are suggestive of pulmonary edema,
which could be associated with the use of terbutaline, preeclampsia (increased vascular permeability), pulmonary
embolism, or a previously unrecognized cardiac condition. Although a rare
complication, terbutaline use has been associated with pulmonary edema.
How would you tx pulmonary edema in the preggo pt? Pt in resp distress
It would depend on identifying and treating the cause. cardiogenic in origin (i.e. myocardial ischemia,
cardiomyopathy, or a dysrhythmia), I would consider using diuretics, inotropic
agents, beta-blockers, or afterload reducing agents, as indicated.non-cardiogenic in origin, I might simply provide diuretic
therapy and fluid restriction. In either. case, I would consider providing ventilatory
support with PEEP. While intubation and mechanical ventilation may prove
necessary, I would first consider using CPAP.
How does PEEP help with pulmonary edema? KIM what with PEEP and cardiac stuff?
PEEP improves oxygenation and pulmonary function by redistributing
alveolar fluid to areas that are less involved in gas exchange, and by recruiting
collapsed alveoli that are contributing to pulmonary shunting. KIM that PEEP can worsen cardiac fxn secondary to decreased preload
Doesn’t PEEP just hyperinflate the already open alveoli and risk barotrauma?
While PEEP has the potential to hyperin:flate already open alveoli, the
goal is to achieve optimum PEEP where collapsed alveoli are recruited
Shortly after receiving a stellate ganglion block with bupivacaine, a 28 year old
female patient is noted to have difficulty speaking and reports dizziness, difficulty
swallowing, and shortness of breath. DDX?
Also-what is a stellate ganglion block used for? where? side effects/risks?
LAST
Total spinal (with resp sxs to follow) 1) paralysis of the recurrent laryngeal nerve, which is located near the stellate
ganglion (would result in hoarseness); 2) pneumothorax could lead to respiratory
distress and hypotension (the latter occurring with a tension pneumothorax);
Indications: CPRS. Also angina, phantom limb pain, vascular insufficiency, hyperhidrosis
Anatomy: Inferior cervical + T1 sympathetic ganglia @ C7. Lays under the SCM/carotid, above the lung
Side Effects: Horner’s (intentional), hoarseness (RLN), eleveated hemidiaphragm (phrenic)
Complications: hematoma, brachial plexus injury, pneumothorax, esophageal perforation, intrathecal/epidural/intravascular injection
If a pt had last, but was not unconscious-tell me how you would proceed? What are you avoiding? When do you make the decision to give intralipid?
(1) call for help and a lipid rescue kit; (2) ensure adequate
ventilation and oxygenation to correct and/or avoid factors that enhance the systemic
toxicity of local anesthetics, such as hypercarbia (increased cerebral blood flow, intra-
neuronal ion trapping of the drug, and decreased plasma protein binding of the drug),
acidosis (decreased plasma protein binding of the drug), and hypoxemia; (3)
administer a benzodiazepine to stop the seizure (seizure activity increases
metabolism, which may lead to hypoxemia, hypercarbia, and acidosis); ( 4) administer
succinylcholine and intubate her if ventilation were inadequate, the risk of aspiration
was significant (history of GERD or hiatal hernia), or if tonic-clonic movements
persisted despite benzodiazepine administration (succinylcholine would minimize the
metabolic acidosis associated with seizure-induced.muscle activity, it would not,
however, affect the acidosis that develops secondary to seizure-induced increases in
cerebral metabolism); (5) alert the nearest facility with cardiopulmonary bypass
capability; and ( 6) treat hypotension, bradycardia, and dysrhythmias as indicated
(avoid procainamide, lidocaine, j3-blockers, vasopressin, and calcium channel
blockers when treating bupivacaine-induced cardiac arrhythmias). Moreover, I
would (7) initiate lipid emulsion therapy if the signs and symptoms of local anesthetic
toxicity appeared to be rapidly progressing, she experienced prolonged seizure
activity, or she developed signs of cardiac toxicity (i.e. bradycardia, heart block,
hypotension, asystole, or ventricular arrhythmia). Finally, if the patient did not
respond adequately to these therapies, I would (8) consider utilizing cardiopulmonary
bypass to provide “bridging” therapy until her tissue levels of local anesthetic were
no longer toxic.
Dosing for last? Can you repeat it? What is the max dose?
Bolus 1.5 mL/kg of 20% lipid solution over 1
minute (roughly 100 mL in adults) and start a continuous infusion at 0.25
mL/kg/minute. If cardiovascular instability persists after 5 minutes, repeat the
bolus and double the infusion rate. Maintain the infusion for at least lO·minutes
after attaining circulatory stability. The recommended upper limit for initial lipid
dosing is approximately 10 mL/kg over 30 minutes.
DON’T FORGET TO CALL FOR WHAT IN EMERGENT SITUATIONS?
HELP!
LAST pt progresses to asystole-now what? What do you give less of in LAST?
I would immediately: (1) start chest compressions, (2) call for a
defibrillator (in case a shockable rhythm developed during resuscitation), (3) secure
the airway with an endotracheal tube, and ( 4) provide 100% oxygen. Next, I would
(5) attempt to confirm true asystole (make sure all cables are connected properly,ensure adequate monitor gau;, check another lead, ‘check for pulse - very fine
ventricular fibrillation can look like asystole), (6) initiate lipid emulsion therapy (if
not already done), (7) administer a 1 μg/k:g intravenous bolus of epinephrine,
recognizing that higher doses of epinephrine have been associated with poorer
outcomes in the setting ofbupivacaine-induced asystole (epinephrine is highly
arrhythmogenic and may reduce the efficacy of lipid emulsion therapy), and (8)
correct any potential contributing factors, such as hypoxia, hypercarbia, and acidosis.
I would then (9) continue to monitor the patient for the development of a shockable
rhythm, (10) notify the nearest facility with cardiopulmonary bypass capabilities, and
(11) consider placing her on bypass if she remained inadequately responsive to these
interventions.
Continue CPR for at least 60 min
If Epi isn’t working in last-you giving vasopressin?
NO!!! No vasopressin in LAST
What are the most important factors affecting systemic absorption of local
anesthetic?
What determines onset of local anesthetics? How can you make this faster?
What determines amount of systemic absorption?
the amount of blood flow at the site of injection (intravenous>
tracheal > intercostal > caudal > paracervical > epidural > brachial plexus >
sciatic/femoral> subcutaneous), (2) the dose, (3) the properties of the injected local
anesthetic (the higher the lipid solubility and protein binding of a drug, the lower the
rate of systemic absorption), and ( 4) the addition of vasoconstrictors to the local
anesthetic solution (the vasoconstriction associated with the addition of epinephrine
decreases the rate of systemic absorption).
The closer to physiologic pH that the pKa is, the more anesthetic exists in the uncharged base form. With the exception of benzocaine, the pKa’s of all local anesthetics are greater than tissue pH (7.4). Lower pKa results in a more rapid onset. Onset is also reduced by increasing the solution pH.
Onset can also be shortened by increasing the concentration or dose. Chloroprocaine, despite having a pKa of 9, has a rapid onset because of its use in high (as high as 3%) concentrations.
More lipophilic and protein bound a local anesthetic is, less systemic absorption
Ways to prevent LAST?
limit the administered dose of
local anesthetic drug,Other preventative measures include the use of
ultrasound, aspiration prior to injection, the use of small incremental drug dosing, avoidance of excessive sedation during block
Heart transplant pt has 2 p waves-why? will this affect conduction?
The ECG of patients with a transplanted heart often shows two sets of
P-waves, with the origin of one P-wave being the native sinoatrial node, while the
origin of the other is the donor’s sinoatrial node. While the native sinoatrial node
may continue to be affected by autonomic influences, it does not alter cardiac
function because the generated impulse is unable to traverse the suture line between
the native heart and transplanted heart
Pregnant lady has decreased in FHR immediately after placement of spinal analgesia. Why? And what are some other causes? When is it more pronounced? Does it lead to increase rate of c section?
The onset of fetal bradycardia following the initiation of spinal
analgesia suggests that the (1) rapid onset of analgesia has resulted in an abrupt
decrease in circulating epinephrine, with subsequent uterine hypertonus .
(tachysystole) and decreased uterine perfusion (spinal anesthesia –> rapid decrease in
pain —> abrupt decrease in plasma epinephrine - decreased stimulation of beta-
adrenergic receptors in the uterus —> increased uterine tone —> reduced uterine blood
flow (most uterine blood flow occurs during uterine relaxation/diastole) —>
diminished fetal oxygen delivery —-> fetal bradycardia).
other less likely causes: maternal hypotension secondary to sympathectomy (spinal
anesthesia), aortocaval compression (inadequate left uterine displacement),
hypovolemia
The increase in uterine tone that can occur with the initiation of neuraxial
anesthesia to control labor pain is more pronounced when: (1) oxytocin is utilized,
(2) spinal anesthesia is employed rather than epidural (more rapid
sympathectomy), (3) the height of sensory blockade is relatively higher, and (4)
when there is a greater difference between pre and post-analgesia pain scores.
• The, fetal bradycardia following neuraxial anesthesia is usually transient and
readily treatable. Moreover, it does not increase the incidence of emergency
cesarean section or the overall risk for adverse outcome.