Anesthesia Boards+True Learn
|EKG leads corresponding to RCA territory?|
The RCA supplies which part of the heart?
|II, III, aVF|
RA, the entire RV except for the APEX, posterior/inferior LV, posterior 1/3rd of interventricular septum, SA (50%) & AV (90%) node, posteromedial pappillary muscle
|EKG leads corresponding to LAD territory|
The LAD supplies which part of the heart?
|V1, V2, V3, V4|
LAD supplies anterior LV, anterior 2/3rds of IV septum, Bundles
|EKG leads corresponding to Circumflex territory|
The LCx supplies which part of the heart?
|I, V5, V6|
LCx provides for posterior and lateral LV wall, and anterolateral papillary muscle
|Nerve supply for Cricothyroid Muscle||External Branch of Superior Laryngeal Nerve|
|Nerve supply for everything but Cricothyroid Muscle||Recurrent Laryngeal Nerve|
|Postoperative Complications of Thyroid Surgery||1) Airway obstruction due to laryngeal edema (PACU)|
2) Airway obstruction due to hematoma (can present in PACU if arterial or within 24 hours if venous – this is the most common cause of airway obstruction)
3) Airway obstruction due to bilateral damage to RLN (results in laryngospasm immediately post extubation)
4) Hypoparathyroidism (24-96 hours later) – laryngeal stridor leading to laryngospasm
|Posterior Pituitary produces which hormones||Vasopressin and Oxytocin|
|MELD Score||INR, Bilirubin, Creatinine, Sodium; Determines who has the highest priority to receive a liver transplant. The higher the number, the more elevated the risk. “CRIB NA”|
|Child Pugh Score||INR, Bilirubin, Albumin, Ascites, Encephalopathy; Useful to determine prognosis in patients with cirrhosis. Class A (5-6 points) low risk, Class C (10-15) high risk.|
|Glascow Coma Scale||Eye response (4), Verbal (5), Motor (6); Extra value Meal costs $4.56|
|APGAR||Appearance, Pulse, Grimace, Activity, Respiration|
a wave = atrial contraction
c wave = ventricular contraction
x descent = pulmonic valve opening
v wave = venous return of flow with tricuspid closed
y descent = TV opens, atrium empties into the ventricle (diastasis)
|Innervation of Larynx (sensory)||Anterior Tongue –> Vallecula (includes soft palate and oropharynx): CN IX|
Vallecula/Hypopharynx –> Vocal cords: Internal Branch of SLN
Vocal cords –> Trachea –> RLN
|Innervation of Larynx (motor)||Cricothyroid Muscle: External Branch of SLN|
Everything else: RLN
|Regional Anesthesia for FOI (3 blocks)||1) Anterior Tonsillar Pillar – Glossopharyngeal|
2) Inferior Aspect of Greater Cornu of Hyoid – Internal Branch of SLN
3) Transtracheal – RLN
|Atracurium metabolite||Laudanosine (excreted renally). Can cause seizures and hypotension in patients with renal failure.|
Side effect of atracurium: can cause histamine release (transient flushing, hypotension, tachycardia)
Metabolism: Eliminated via Hoffman Elimination and Ester Hydrolysis
|Morphine active metabolite||Morphine-6 Glucuronide – accumulates in patients with kidney failure causing respiratory depression. THERE ARE 6 LETTERS IN THE WORD ‘ACTIVE’|
|Meperidine active metabolite||Normeperidine (excreted renally) – accumulates in patients with renal failure causing seizures|
|Hydromorphone active metabolite||Hydromorphone 3 Glucuronide (excreted renally) – accumulates in patients with renal failure causing cognitive dysfunction and myoclonus|
|Free Water Deficit equation **corrected**||(0.6 x Kg) x (Serum Na/140 – 1)|
|Diabetes Insipidus vs Cerebral Salt Wasting vs SIADH||Tx of Central DI – Desmopressin|
Tx of Nephrogenic DI – HCTZ (counterintuitive)
Tx of SIADH – fluid restriction + demeclocycline (interferes with the action of ADH)
Tx of Cerebral Salt wasting – replacing urinary loses of sodium + free water with fluids **Do not correct hypernatremia too fast (no more than 0.5mEq/L/hr)
|Plavix Mechanism of Action||Blocks ADP receptor (Activation of ADP leads to surface expression of IIb/IIIa receptor on platelets – where fibrinogen and vWF binds). It is non competitive and irreversible.|
|Warfarin Mechanism of Action||Blocks Vit K epoxide reductase. Leads to depletion of clotting factors II, VII, IX, X, protein C and protein S. Factor VII will be depleted first|
|Argatroban Mechanism of Action||Direct Thrombin Inhibitor. Hepatic clearance. t1/2: 40-50mins|
|Bivalrudin Mechanism of Action||Direct Thrombin Inhibitor. Cleared by plasma proteases – can be used in patients undergoing CPB who cannot be given heparin; it is monitored by ACT levels|
|Hirudin Mechanism of Action||Direct Thrombin Inhibitor. Renal elimination.|
|Fondaparinux Mechanism of Action||Factor Xa inhibitor. Renal elimination.|
|Dabigatran mechanism of action?||Direct thrombin inhibitor; renally cleared|
|Rivaroxiban (xarelto) mechanism of action?||Direct Xa inhibitor, use with caution in hepatic and renal insufficiency|
|DDAVP||Antagonizes V2 receptor. Regulates water reabsorption and can cause a release of vWF. Indicated in DI and vWD and mild hemophilia A.|
|TXA and Aminocaproic Acid Mechanism of Action||Binds to plasminogen and blocks the activation of plasmin (pro-thrombotic)|
|HIT Type I vs Type II||Type 1: Non immune mediated. Seen after 1st day of exposure. Transient and insignificant|
Type 2: Immune mediated. IgG binds to PF4, activates platelets and causes aggregation. Seen 5-10 days after exposure. Management: switch to direct thrombin inhibitors (bivalrudin, argatroban, fondaparinux
|vWD Type 1 vs Type 2 vs Type 3||Type 1: Quantitative decrease in vWF. AD. Tx: Desmopressin|
Type 2: Qualitative abnormality in vWF. AD
Type 3: Rare, undetectable levels of vWF. Body does not produce it.
|Lambert Eaton Syndrome sensitive/resistant to Succinylcholine/NMBDs?||Sensitive to both Succinylcholine and NMBDs.|
|Myasthenia Gravis sensitive/resistant to Succinylcholine/NMBDs?||Resistant to Succinylcholine but sensitive to NMBDs.|
|How to tell the difference between Myasthenic Crisis vs Cholinergic Crisis?||Give Edrophonium –> Increased weakness points to cholinergic crisis; Improvement or Decreased weakness points to Myasthenic crisis|
|Tx of Myasthenia Gravis||Anticholinesterase inhibitors – Pyridostigmine|
|Malignant Hyperthermia Diagnosis||Gold standard – Halothane-caffeine Test|
|Treacher Collins Syndrome||Difficult airways, autosomal dominant, genetic mutation, 1:50,000 live births|
– Mandibular/Maxillary Hypoplasia (micrognathia, absent cheekbones)
– Cleft or Arched Palate
– Fish like facies
– Choanal Atresia
– Cor Pulmonale
– Conductive hearing loss, malformed ears
|Pierre Robin Sequence||Triad (Disappears after 2 years of age):|
1) Hypoplastic Mandible
2) Glossoptosis – posterior displacement of the base of the tongue over epiglottis
3) Cleft palate
Associated with Cor pulmonale, OSA
Can be seen in Stickler syndrome, Velocardiofacial syndrome, Treacher-Collin syndrome
|1cm elevation = what change of mmHg?||0.74mmHg; Example 10cm elevation = reading will be 7.5mmHg higher than baseline|
|Types of Heat Loss? #1 cause of intraop heat loss?||Convection, Conduction, Evaporation, Radiation. Radiation is the #1 cause of heat loss intraoperatively|
|Anterior/Posterior Ischemic Optic Neuropathy Associations||Associated with:|
Cardiopulmonary Bypass cases
Increased Venous/Eyeball pressure
|Vessel Rich Organs vs Vessel Poor Organs||Rich = Brain, Kidney, Heart, Liver, Adrenals (does NOT include lungs because normally the lungs receive 100% of CO)|
Med = Muscle, Skin
Poor = Bone, Cartilage, Ligaments
|Meperidine Facts||– Meperidine is a strong anticholinergic, causes tachycardia|
– Causes Histamine Release
– Metabolite Normeperidine – accumulates in renal patients potentially causing seizures
– MAO inhibitor + Meperidine can lead to serotonin syndrome (confusion, hyperthermia, shivering, myoclonus, and hyperreflexia)
– Kappa receptor agonism to oppose shivering
– Potency 0.1 compared to Morphine
|Baclofen binds to which receptor||GABA-B. Benzodiazepines bind to GABA-A.|
|Opioid Receptors||Mu1: analgesia, skeletal muscle rigidity|
Mu2: respiratory depression
Kappa: sedation, dysphoria, miosis. Antagonizes shivering
|Venous systems that bypass the R Heart||Thesbian, bronchiolar and pleural veins|
|Full term newborn’s Total Blood Volume|
Premature neonate’s Total blood volume
|Neonatal Airway Differences|
The Larynx is positioned at ____ level.
The epiglottis is long/short?
The tongue is smaller/larger?
The narrowest part of the airway is the ____.
Occiput is larger/smaller?
|– C3-C4 in children. C5-C6 in adiults|
– Longer, floppy, omega/u shaped
– Cricoid cartilage; it is conically shaped. The narrowest part in adults is the glottis
– Larger occiput – may benefit from shoulder roll
|Neonates are more likely to drop temperature intraop due to:||Increased surface to body ratio|
|When does the Foramen Ovale close? Ductus Arteriosus? Ductus Venosus?||Functionally:|
FO: Immediately, DA: 1 day, DV: 1 week
Note: Foramen Ovale remains patent in 25% of population
|Adult SPINAL CORD ends at what level? Infant spinal cord ends at what level?||Adult spinal cord ends at L1-2|
Infant (<12 months) spinal cord ends at L3-4. After 12 months it is similar to that of an adult.
|Adult DURAL SAC ends at what level? Infant dural sac ends at what level?||Adult dural sac ends at S2|
Infant dural sac ends at S4
|Where would you place a pulse oximeter in a newborn?||The R Hand is the only preductal choice and it is recommended to place it on the R hand to monitor lung function.|
|Delay ambulatory/elective surgery in infants after what age?||Post conceptual age >50weeks. Delay surgery because of increased risk of post anesthesia apnea. Risk of apnea can be decreased with IV caffeine or aminophylline.|
|Apnea of Prematurity||– Defined as >10s of apnea or 15s of apnea with desaturations or bradycardia|
– Risk factors:
1) Prematurity (<37 week gestation) 2) HCT < 30% 3) GA 4) Preoperative apnea- Tx Caffeine 10mg/kg IV
|Omphalocele vs Gastroschesis||Omphalocele|
– Midline defect
– Covered in membranous sac
– More likely to be associated with other defects (75% of time – VSDs [most common], Trisomy 21, Beckwith Wiedmann syndrome
|Tracheoesophageal Fistula||– Most common type is Type C|
3. GI abnormalities
5. Renal/GU Abnormalities
– Intraop management
|How much ml/kg of pRBC can raise a patient’s Hgb by 1?||4mL/kg|
|Do muscle relaxants cross the placenta?||No, both succinylcholine and NMBDs do not cross the placenta because they are charged particles.|
|Anesthesia Dolorosa||Pain in an area that lacks sensation|
|A successful Stellate Ganglion Block should cause what?||– Ipsilateral Horner’s Syndrome (anhidrosis, miosis, ptosis, nasal stuffiness)|
– Increased temperature of ipsilateral arm
– Hyperemia of ipsilateral arm
|Celiac Ganglion Block at what level?||L1|
|1st Stage of Labor (Latent and Active) is covered at what dermatome?||Covered by T10-L1.|
Latent Stage = 2-3cm dilated
Active stage = 3cm-complete dilation
|2nd Stage of Labor is covered by what?||Covered by S2-S4. It is due to distention of the pelvic floor. Covered by Epidural, Spinal, Caudal and Pudendal nerve blocks|
|Why would you need avoid NSAIDS in the pregnant population?||It can cause closure of the Ductus Arteriosus in the fetus which can be fatal.|
|Acute Intermittent Porphyria can be triggered by?||Avoid barbiturates, BZDs, glucocorticoids, etomidate, toradol, alcohol, stress/dehydration. AIP can be exacerbated by inducers of the CYP450 system|
Present with confusion, anxiety, autonomic instability, abdominal pain and emesis.
Porphyria cutanea tarda is not affected by anesthetic medications.
|Fetal Heart Monitoring: Early, Variable and Late Decels?||Early could be due to head compression due to uterine contractions (reassuring)|
Variable could be due to uteroplacental cord compression (reversible)
Late due to uteroplacental insufficiency (not resassuring, needs OB evaluation). Deceleration >30secs after contraction
|Mild Preeclampsia? Severe Preeclampsia? Ecclampsia?||Mild preeclampsia: BP >140/90, proteinuria (>300mg/day), edema (Management: IF TERM, INDUCE; IF NOT, BEDREST)|
Severe preeclampsia: BP >160/110, proteinuria, edema, HA, blurry vision, RUQ pain, hyperactive reflexes, HELLP syndrome (Management: DELIVER IMMEDIATELY)
Ecclampsia: Severe preeclampsia + SIEZURES
|Magnesium Toxicity||Loss of DTRs, Resp depression, complete heart block, VASODILATION (Tx: Calcium gluconate, lasix + isotonic fluids, dsialysis).|
Additional info for reference:
**Remember that magnesium potentiates NMBDs and LA and can prolong succinylcholine.
|Define Placenta Accreta, Increta and Percreta|
What conveys the highest risk of abnormal placentation?
|Accreta — chorionic villi attach to the myometrium, rather than being restricted within the decidua basalis.|
Increta — chorionic villi invade into the myometrium.
Percreta — chorionic villi invade through the PERImetrium, sometimes invading the bladder or rectum
Risk factors include advanced maternal age, prior CS, and placenta previa. Placenta previa carries the highest risk.
|Placenta Previa||Positioning of the placenta at or near the cervical os. Causes painless bright red bleeding. If it is non-obstructing, trial of labor can be allowed|
|Abruptio Placenta||Separation of the placenta from the uterus. Causes mild to severe pain with dark red blood (venous bleeding). Risk factors: chronic HTN, cocaine, preeclampsia, multiparity, smoking, trauma.|
|Calculating depth of ETT?||3 x Diameter of ETT|
|Croup aka laryngotracheobronchitis||– MCC Parainfluenza, RSV, Influenza A/B|
– Well looking patient
– Slow onset
– Mild-moderate stridor
– Barking Cough
– Able to swallow
– Hoarse voice
– “Steeple sign” on XR
– Treatment: Racemic epinephrine, no intubation needed
|Epiglotitis||– MCC H. Influenzae, Staph, Strep|
– Toxic and unwell apperance
– Abrupt onset
– High fever
– Moderate-severe stridor
– Unable to speak
– Unable to swallow
– “Thumb print sign” on XR
– Treatment: Intubate in the OR with ENT available, no time for XR or any imaging, Give ABx. Do not give racemic epi (its contraindicated)
|Racemic Epinephrine||Helpful in Croup, Bronchiolitis or post intubation croup in the PACU|
|Flow volume Loops||EXPiratory Blunting is due to INTRAthroacic Obstruction (i.e. Mediastinal mass, lower tracheomalacia, lower tracheal mass)|
INSPiratory Blunting is due to EXTRAthoracic Obstruction (i.e. Vocal cord paralsis, thyroid mass, laryngomalacia, epiglotitis)
INSP- & EXPiratory Blunting is due to a FIXED lesion (i.e. Tracheal stenosis or choanal atresia)
Cardiac disease (TOF)
Due to Deletion of Chromosome 22
|Rigidity associated with Neuroleptic Malignant Syndrome OR Malignant Hyperthermia resolves after administration of muscle relaxant?||NMS|
|Where do you perform a needle thoracotomy?||Second intercostal space, midclavicular line (below 2nd rib)|
|True or False? Factor 7 administration can overcome a relative deficiency of factors in the intrinsic pathway?||True. Factor 7 couples with tissue factor to activate the common pathway (10–5–>2–>1—>Fibrin clot). The main job of the intrinsic pathway is to synergistically support the continued formation of thrombin once the extrinsic pathway is started.|
|Vitamin K is needed for production of which factors?||Factors 2, 7, 9, 10, protein C and protein S|
|Fat Embolism Syndrome presents how and when?||SOB, respiratory failure, RHF, mental status changes, coagulopathic changes, petchiae (pathognomic). It usually occurs 1-3 days postop. Diagnosis of exclusion but BAL can show fat droplets in macrophages.|
|Oculocardiac Reflex Pathway?||Afferent: Ciliary nerves/Trigeminal Nerve – Ophthalmic division (through ciliary ganglion and gasserian ganglion)|
Efferent: Vagus Nerve
|Following administration of Sulfur hexafluoride, what anesthetic should you avoid intraoperatively and for how many days after should this be avoided?||Nitrous oxide; Lasts 10 – 28 days! But avoid for 4-6 weeks after use (per UK anesthesia)|
|Carbon Monoxide Poisoning Affect on Pulse oximetry? Tx?||COHgb will overestimate SpO2 showing slightly low to normal oxygen levels. Diagnosis to be made with ABG co-oximetry. Treatment with 100% oxygen.|
|Methemoglobinemia affect on Pulse oximetry/ABG? Tx?||MetHgb will overestimate SpO2 showing O2 levels in the 80%s. ABG will show normal PaO2 levels but the patient will be cyanotic (highly suggestive of MetHgbemia). Definitive diagnosis is to be made with co-oximetry. Treatment with Methylene Blue.|
|Functional Residual Capacity = what?||ERV + RV|
|What factors decrease FRC?||Restrictive lung disease, obesity, pregnancy, posture (FRC greatest to least: standing > sitting > prone > supine > trendelenberg)|
Not obstructive lung disease
|Laminar flow is directly related to ____ where as turbulent flow is directly related to ____.||Viscosity; Density|
“Las Vegas is Too Dense”
|Laminar flow is seen in the ____ airways whereas turbulent flow is seen in the ____ airways.||Distal; proximal/larger|
|A high Reynolds number (>2000) is more consistent with turbulent or laminar flow?||Turbulent Flow|
R = (Velocity x Diameter x Density) / Viscosity
|Heliox will reduce work of breathing how?||Helium has decreased density compared to air so it will decrease the resistance caused by turbulent flow.|
|Ventilation and perfusion are maximal at what part of the lungs?||Both are maximal at the base of the lungs. Perfusion is higher than ventilation at the base. Ventilation is higher than perfusion at the apex.|
|What is the Alveolar gas equation?||Palv = FiO2 (Patm – Ph2o) – PaCO2/RQ. This equation can explain why elevated PaCO2 can cause hypoxemia.|
|Cushing’s Triad?||Response to elevated intracranial pressures which involves:|
1) Elevated BP
3) Irregular respirations (slow and irregular)
|What EKG changes would you see during a massive pulmonary embolism?||You would see ischemic changes in the anterior leads, esp V1 and V2 indicating R heart strain. RBBB could also be seen with V1-V2 RR’ complexes. The classic finding is S1Q3T3 (S wave in lead I, Q wave in lead III, and inverted T wave in lead III) but is rarely seen.|
|Absolute Contraindications to Extracorporeal Lithotripsy?||Absolute:|
2) Coagulation disorder/Anticoagulation
3) Distal Obstruction of Renal Calculi
|What is Autonomic Dysreflexia?||In a patient with spinal cord injury (usually T6 or above), noxious stimulus below the level of injury causing an amplified sympathetic response below the level. There will be a strong parasympathetic response to follow. The patient will be hypertensive and bradycardic. You will see flushing above the lesion and pale, white skin due to vasoconstriction below. It can be caused by surgical stimulation, bladder distension, or fecal impaction. Consider spinal anesthesia, arterial line and sodium nitroprusside available.|
|Major side effect of CYCLOSPORINE||Nephrotoxicity|
|Cryoprecipitate contains what?||Factor VIII|
FFP contains all the plasma proteins that is found in whole blood including all factors.
Cryoprecipitate is prepared by thawing FFP and allowing the larger molecules to precipitate which is the centrifuged and frozen.
|Major side effect of CISPLATIN||Nephrotoxicity|
|Major side effect of DOXORUBICIN||Cardiotoxicity|
|Major side effect of VINCRISTINE||Neurotoxcity|
|Major side effect of BLEOMYCIN||Pulmonary fibrosis|
|Type 1 Error||False Positive|
|Type 2 Error||False Negative|
|To measure ICP the correct level to place the transducer is the _____.||External auditory meatus|
|TV = ___mL/kg||7mL/kg|
|FRC = ___mL/kg||30mL/kg|
|Vital Capacity = ___mL/kg||60mL/kg|
|Total lung capacity = ___ mL/kg||90mL/kg|
|At what % of CO would you give supplemental oxygen?||>10%; 10% or less is normal for smokers|
|Which antibiotic has the potential to prolong neuromuscular blockade?||Aminoglycosides (i.e. gentamycin, amikacin, tobramycin, stretomycin, neomycin). NOT erythromycin, PCN or cephalosporins.|
|The carotid sinus|
Manipulation can cause what?
Injecting local anesthetic at the sinus can cause what?
|It is a baroreceptor that is located at the base of the internal carotid artery that functions as a baroreceptor. Manipulation of the carotid sinus can lead to profound bradycardia and hypotension that is ameliorated during a carotid artery surgery by injecting local anesthetic at the carotid bifurcation. The afferent limb of this reflex is mediated by the Glossopharyngeal nerve. Injecting local anesthetic can actually cause significant hypertension intra- and postoperatively.|
|The carotid body|
Bilateral CEA would cause what?
|Chemoreceptor cells that are located at the bifurcation of the ECA and ICA. They function mainly to respond to decreases in O2 tension <60mmHg by increasing ventilation. Afferent impulses are sent via the glossopharyngeal nerve (CN IX). It is inhibited by volatile anesthetics, BZDs or opioids. Note that a bilateral carotid endarterectomy would result in significant impairment of the hypoxic drive.|
|What would you see on an ABG in a third trimester pregnant woman?||Mild, chronically compensated respiratory alkalosis. They would have elevated ventilatory rates due to an elevation in progesterone. PaCO2 would be around 30mmHg|
|Normal ABG values?|
PaCO2: 35-45 (<35 respiratory alkalosis, >45 respiratory acidosis)
HCO3: 22-28 (<22 metabolic acidosis, >28 metabolic alkalosis)
Mechanism of action?
Major side effect?
|NMDA recepter antagonist and NE+Serotonin Reuptake inhibitor|
QTc prolongation, can lead to Torsades de point
High doses of methadone (>60mg daily) can put you at increased risk for Torsades
|Transplanted Heart Patient|
What medications act directly on a transplanted heart?
What are some examples of medications that do not?
|– Any medication that acts on B receptors directly such as Dobutamine, Isoprotenernol, Epinephrine, Norepinephrine. However, the heart rate response may be exaggerated because there is no parasympathetic innervation to counter the increased heart rate|
– Indirect drugs that affect rate will not be effective (antimuscarinics, anticholinesterases, pancuronium, digoxin). Use direct acting agents (isoproterenol, epinephrine).
– Lack of vagal tone will result in baseline rate of 90-100. About 25% of patients will develop a bradycardia that will require implantation of a permanent pacemaker.
|How does laryngoscopy affect a patient with a transplanted heart?||You will not see a vagal response to laryngoscopy. Vagal bradycardic reflexes will also be absent due to denervation of parasympathetics (laryngoscopy, hypertension, carotid sinus massage).|
What is position 1? what is position 2? What is Position 3? What is asynchronous mode?
|Position 1 = Chamber paced (A, V, Dual or O[None])|
Position 2 = Chamber sensed (A, V, Dual or O [None])
Position 3 = what the device does in response to the sensing (Inhibited, Triggered, Dual [both] or O [None])
Asynchronous mode = AOO, VOO or DOO
|Two ways of stopping the heart during EVAR?||Adenosine and rapid right ventricular pacing.|
Occurrence following amputation?
Difference between phantom pain and stump pain?
|Occurs in 90% of patients in the first 6 months following amputation surgery|
Defined as unpleasant or painful sensation in the missing body part. It is usually intermittent with intervals between 1 day – several weeks. Phantom pain that lasts > 6 months is usually refractory to treatment.
Stump pain is different from phantom pain in that stump pain is usually due to local processes such as soft tissue infection, skin lesions or provoked by traction or pressure on the remaining body part.
|Keys for treating LVAD patient?||Maintain preload, reducing afterload and preserving R heart function.|
This means: Avoid hypovolemia. Recommend MAPs between 60 and 80mmHg. Preserve R heart function by avoiding elevations in pulmonary artery pressures (avoid hypercapnia)
|Trigeminal Neuralgia (tic dolereaux)|
R or L side affected more?
Men or women more?
|R >> L side|
Women >> Men
Pain is self limited
Treatment: Anticonvulsants are first line. Baclofen and Neurontin can help as well. Surigcal treatments are available for patients who have failed medical management. Microvascular decompression (MVD), nerve lesion techniques and motor cortex stimulation are available.
Question sample: A woman presents with recurrent flashes of severe pain at the junction of her R upper lip and the nasolabial fold despite normal facial appearance and neurologic exam. Brushing her upper molars triggers these attacks. Most likely diagnosis? Classical Trigeminal Neuralgia
|What is allodynia?||It is he triggering of a pain response from stimuli which do not normally provoke pain.|
|What is the difference between CRPS Type 1 vs Type 2?||CRPS Type 1 (RSD) is a syndrome where chronic pain (normally in an extremity) appears to be associated with sympathetic nervous system dysfunction. It can be the result of a trivial injury (ie burn, ankle sprain, cut) on that extremity|
CRPS Type 2 (Causalgia) is a syndrome where chronic pain is the result of prior nerve injury.
|What are some things that cause R shift on the Oxyhemoglobin dissociation curve?||Increase in Temp, PaCO2, BPG, H ions|
Decrease in pH
|What causes a L shift on the oxyhemoglobin dissociation curve?||Decrease in Temp, PaCO2, BPG, H ions|
Increase in pH
Increase in CO
Increase in MetHgb
Increase in HbF
|Explain the sensory nerve distribution of the foot/ankle.||The POSTERIOR TIBIAL NERVE covers the heel and plantar surface of the foot.|
The medial ankle is covered by the Saphenous (femoral nerve) and the lateral surface is covered by the Sural Nerve.
The superior portion of the foot is covered by the common peroneal nerve. Only thing to note is that the webbing between the 1st and 2nd toe is covered by the deep peroneal nerve while the rest is covered by the superficial peroneal nerve.
|What metabolizes codeine, oxycodone and hydrocodone?||CYP2D6|
Codeine is active and undergoes O-demethylation by CYP2D6 to create morphine.
|Alfentanil has a higher or lower volume of distribution?||It has a lower volume of distribution which means that it has a shorter duration of action. It also has a lower pKA so it has the fastest onset and crosses the BBB quickly. It has a brief duration of action due to redistribution.|
|Onset 1-2 mins|
Dose 0.01-0.1mg/kg; 0.04mg q 3-6 mins and then infuse 4-5mcg/kg/hr
t1/2 = 30-60mins
|What is the reason for the hypercoagulable state in pregnant women?||Increased fibrinogen and factor VII levels and decreased anticlotting factors.|
|LR vs NS vs Plasmalyte|
|Non ionized = lipophilic or hydrophilic?||Lipophilic (lipid soluble).|
|pKa definition||pH at which a compound exists as 50% ionized and 50% unionized|
The lower the pKA, the more the nonionized form (the more lipid soluble and therefore the faster the onset)
|Explain ion trapping.||If there is a pH gradient, ionized substances are trapped on the side that the pH favors ionization. For weak bases, the drug will accumulate on the acidic side of the membrane.|
For example, the nonionized fraction of a local anesthetic agent (weak base) crosses the placenta, where it is changed to the ionized form in the relatively acidic fetus. The ionized form cannot leave the placenta. Further, the nonionized drug continues to enter fetal circulation.
|A patient on enoxaparin for DVT ppx, when is it appropriate to remove or place an epidural? What about in a patient receiving “treatment” dosing of lovenox?||12 hours for DVT ppx|
24 hours for “Treatment”
|A patient who is receiving subQ heparin for DVT ppx, when is it appropriate to perform neuraxial anesthesia? What about a patient receiving IV heparin?||There are no contraindications if the daily dose is <10,000units.IV heparin - delay needle/catheter placement 4 hours after last dose and document a normal aPTT. Restart after 1 hour.|
Toxic range of lidocaine?
Why is it so high compared to IV toxic range?
Peak levels of lidocaine occurs when?
|– Lidocaine 0.05%,|
– Epinephrine 1:1,000,000
– Dose range: 35- 55 mg/kg of lidocaine injected.
– The range is higher because the adipose tissue acts as a resevoir (lidocaine is highly lipophilic). Also the epinephrine vasoconstricts.
– 12-14 hours after
|Specificity = ? Sensitivity = ?||Specificity = TN / TN + FP|
Sensitivity = TP / TP + FN
|FA/FI Ratio notes||FA = Alveolar end tidal concentration|
FI = Inspired concentration
The larger blood:gas partition coefficient means a lower FA/FI ration (due to increased uptake).
The lower the FA/FI ratio the slower the onset.
|Onset of anesthesia is faster in volatile agents with lower/higher blood:gas coefficients?||Lower.|
The more soluble the gas, the higher the blood:gas coefficient, and the slower the onset
|How do the following affect FA/FI?|
Children vs Adults?
|Increased ventilation, increases FA/FI|
Decreased CO, increasees FA/FI
Children have a more rapid
|Surgical emergency: Aortic dissection type A or type B?||Type A – involves the ascending aorta and possibly the AV|
Type B – can be managed medically with combined a and B blockers. SBP goal < 110mmHg
|Why is there a resistance to NMDBs in burn patients?||It is attributed to the proliferation of extrajunctional receptors.|
|When is it unsafe to use succinylcholine in burn patients?||After 24 hours, for up to one year afterwards. It can result in fatal hyperkalemia.|
|Treatment of Transient Neurologic Symptoms?|
Increased risk of TNS with what?
How is this different from neuraxial hematoma or cauda equina syndrome?
Increased risk of TNS include:
It’s different from an epidural hematoma and CE in that the patient will not have bowel or bladder dysfunction. There will only be back pain with possible radiation to the legs.
|Myotonic Dystrophy||– Patient presents with persistent muscle contraction after voluntary contraction ie unable to let go of a handshake|
– Autosomal dominant
– Likely due to intracelluar ATP system that fails to return Ca to SR.
– Contractions are not relieved by NMBDs or deep anesthesia
– Avoid succinylchoine – can be severe enough to impair ventilation
Triggers: – Succinylcholine
|In hypothermic patients, the MAC increases/decreases?||Decreases|
|Lithotomy position is associated with which nerve injury, most commonly? How would the patient present||Common peroneal. Loss of the ability to dorsiflex (footdrop) and evert the ankle.|
|Cardiac Tamponade||Equalization of the DIASTOLIC pressure in all 4 chambers of the heart with the pressure inside the pericardium. You would see pulsus paradoxus – abnormally large decrease in SBP on inspiration. During inspiration there is increased R sided filling which causes the interventricular septum to shift to the left causing a decrease in BP. You would also see electrical alterans. Clinically you would see dyspnea, hypotension, tachycardia, distant heart sounds, orthopnea, and JVD.|
“FAST FULL AND TIGHT”
|Cerebral blood flow is influenced by what?||MAP, PaCO2, PaO2, and local brain metabolic activity.|
|HERBAL SUPPLEMENTS SIDE EFFECTS 🙁|
St. Johns Wart?
|– Ginger – inhibits thromboxane synthetase.|
– Garlic – Inhibits platelet aggregation. Discontinue for 7d prior
– Ginko – inhibits platelet aggregation. Discontinue 36h prior
– Ginseng – inhibits platelet aggregation and decreases blood sugar. Discontinue 24h prior
– Green tea – inhibits platelet aggregation. Discontinue 7d prior
– Saw Palmetto – can cause increased bleeding intraop
– Fish Oil – can cause increased bleeding intraop
– Kava – anxiolytic, causes sedation, decreases MAC, can cause HEPATOTOXICITY
– Valerian – causes sedation, decreases MAC.
– Ephedra – HTN , tachycardia, seizures
– St. Johns Wart – SNRI inhibitor; also EZYME INDUCER of cytochrome P450 systems
|Chronic opioid use can lead to increase or decrease of cortisol levels, testosterone/estrogen/LH/FSH levels?||Decrease.|
|NMDA Receptor is blocked by what 5 medications?||Ketamine, N2O, Methadone, Xenon and Magnesium|
|Fenoldopam mechanism of action?||Antihypertensive. Selective D1 agonist. Direct renal vasodilator. Causes naturesis and diuresis.|
Effective in hypertensive crisis
|Effect on MAC:|
|HypoNa – decreases MAC|
Hypercarbia – decreases MAC
Hypothermia – decreases MAC
Lithium – decreases MAC
a2 agonists – decreases MAC
Acute EtOH – decreases MAC
Chronic EtOH – increases MAC
Red hair – increases MAC
Pregnancy – decreases MAC
|Intraoperative awareness vs Dreaming vs Explicit Memory vs Implicit Memory||Intraoperative awareness – postoperative recall of events while under general anesthesia|
Dreaming – experiences that patients are able to remember postoperatively that they believe to be dreaming and that they think occurred during general anesthesia
Explicit Memory – conscious recollection of prior experiences
Implicit Memory – unconscious memory of an experience that produces a change in performance or behavior. It can usually be accessed by hints or using a word stem
|How long must you wait for elective surgery after a bare metal stent? After a drug eluding stent? After a CABG?|
Are you allowed to take care of a patient with a new stent in the surgery center?
|BMS – 4-6 weeks|
DES – 12 months
CABG – 30 days
PCI/Balloon angioplasty – 2 weeks
If out of the window, continue dual antiplatelet medications PERIoperatively unless the elective procedure is with a high risk of bleeding. Then d/c plavix 5 days prior and reload postop.
Alphabetical order: Balloon angio (2 wks) < BMS (4-6 wks) < DES (12 mo)NO; send to a facility that has cardiology service
|Dantrolene will increase or decrease MAC?||Decrease|
|Sentinel Event is defined as?||Any event that is unanticipated or with an unintended outcome that has the potential to cause patient harm. A near miss can qualify as a sentinel event. A patient complaint or an error in judgement cannot be considered a sentinel event.|
|Some indications of Hyperbaric Oxygen?|
Absolute Contraindication of HBO?
|– Carbon Monoxide Levels > 25%|
– Air or Gas embolism
– Soft tissue necrosis
– Decompression sickness
– Diabetic Wound treatment
Absolute contraindication = untreated Pneumothorax
|Dobutamine affect on PVR, SVR and MAP? What about HR and Cardiac output? Receptors?||Dobutamine decreases SVR, MAP and PVR because of its affect on B2 receptors. It increases HR and CO because of its affect on B1.|
|Milrinone affect on SVR and PVR? What about CO? Mechanism?||Milrinone causes decrease in SVR and PVR. It causes increase in CO.|
Mechanism of Action: PDE III Inhibitor (decreased cAMP breakdown –> increased Ca breakdown in myocardium)
Anesthetic plan in a patient with Aortic stenosis?
Normal valve area?
|– Maintain HR 60-90. Bradycardia can be devastating as they are HR dependent. Maintain afterload by avoiding hypotension. Treat hypotension with small doses of phenylephrine.|
– Normal valve area 2.5-3.5cm2; Symptomatic stenosis occurs at 0.8-0.9cm2 and critical AS when valve area <0.7cm2- Angina, syncope, and angina. 50% mortality at 5, 3 and 2 years respectively.
|Predisposing conditions include|
– male sex
– age greater than 60 years
– Marfan syndrome or other connective tissue disease
– congenital heart disease, including coarctation of the aorta and bicuspid aortic valve
|What is likely being compressed during a medistinoscopy and what side should you monitor SpO2 and BP?||The inominate artery. You should put the Aline and SpO2 on the R side so that you dont have undetected hypotension.|
|TEG||Thromboelastogram components shown in Figure 2 include:|
Reaction time (R) measures the time to initial clot formation. R can be prolonged when clotting factors are deficient or in the presence of heparin, low molecular weight heparin, direct thrombin inhibitors, warfarin, etc.
Kinetics (K) represents the rate at which fibrin strands form and begin to cross-link to form the fibrin meshwork.
Angle (α) represents the rate of clot formation and reflects fibrinogen activity.
Maximum amplitude (MA) represents whole clot strength and reflects many aspects of clot formation, including platelet number and function as well as the fibrin contribution to clot strength.
G is derived from the MA and is also a measure of overall clot strength. The G value is used to discuss platelet function and clot strength.
Estimated percent lysis (EPL) represents clot breakdown as seen in patients with disseminated intravascular coagulation or hyperfibrinolysis.
|Mechanism of Action: Increases cGMP|
Usually measure which nerves (which correlate to which cerebral distribution?)
What qualifies as a significant change?
False positives can be caused by what?
Do NMDBs block SSEPs?
|– Posterior tibial nerve (ACA) and Median nerve (MCA)|
– Significant changes: 50% drop in amplitude and 10% increase in latency
– False positives can be due to anesthetics, hypothermia, hypotension, and anemia
– Volatile anesthetics and N2O are most suppressive
– NMDBs do not affect SSEPs.
|What part of the spinal cord do SSEPs test and what is the spinal blood supply for these territories?||– SSEPs for the upper extremity test the dorsal column which is supplied by the Posterior Spinal Artery. For the lower extremity, it will test the dorsal lateral funiculus which is supplied by the Anterior Spinal Artery.|
|Medications that undergo ester hydrolysis?||– Succinylcholine (Plasma cholinesterase)|
– Remifentanil (non specific esterases)
– Esmolol (nonspecific esterases)
– All ester local anesthetics i.e. 2-Chloroprocaine, Procaine, Cocaine
Due to a deficiency in what neurotransmitter?
This causes excessive amounts of ____?
What medications should you avoid?
What medications are ok to use?
|– Dopamine (due to loss of substantia nigra)|
– Avoid dopamine blocking medications such as:
3) Antipsychotics (haldol, chlropromazine, etc)
– OK to use:
3) Cannabinoids (Dronabinol)
|Familial Hypokalemic Periodic Parlysis||– HypoK+ periodic paralysis is a disorder characterized by episodes of weakness when serum K drops|
– Lasts anywhere from hours to days
– Spares muscles of respirations
– Avoid glucose containing solutions, hypothermia, or any medications that cause intracellular shifts of K+ (such as B blockers)
– Remember, insulin causes K to move into the cells
– Muscle relaxants (including succinylcholine) are OK
– Low dose acetazolamide may prevent attacks
|Familial Hyperkalemic Periodic Paralysis||Management:|
– Give glucose and insulin
– Give Calcium
– Give diuretics
– Avoid succinylcholine
|Innervation of the abdominal viscera?||Distal esophagus to the Transverse colon is supplied by the CELIAC PLEXUS|
Descending colon to the rectum is supplied by the SUPERIOR HYPOGASTRIC PLEXUS (which also covers GU and perineum)
|Conditions that will increase DLCO?|
Conditions that will decrease DLCO?
|Conditions that increase DLCO:|
– L–>R shunt
Conditions that decrease DL CO will be anything that impairs gas exchange across the alveolar membrane.
|In a patient who is in her third trimester, are you expected to find an increase or decrease in the following:|
Minute ventilation (due to what hormone?)
|Minute ventilation – increased due to progesterone|
Tidal volume – increased
Respiratory rate – more or less the same
Vital Capacity – more or less the same
FEV1 – more or less the same
FRC – decreased
ERV – decreased
RV – decreased
|Cytochrome P450 inducers or inhibitors?||Carbamazepine – inducer|
St. Johns Wort – inducer
Omeprazole – inducer
Phenytoin – inducer
Phenobarbital – inducer
Nicardipine – inhibitor
|Diseases linked to MH?||Central core disease, King-Denborough syndrome, and Evans myopathy are clearly linked to MH.|
|Best preoperative tests prior to thoracotomy to assess LUNG PARENCHYMAL FUNCTION? To assess CARDIOPULMONARY RESERVE? To assess RESPIRATORY MECHANICS? (include minimum values that would result in pulmonary complications)||Lung Parenchymal Function: DLCO (ppo >40%)|
Cardiopulmonary Reserve: VO2max (>15mL/kg/min)
Respiratory Mechanics: FEV1 (ppo >40%)
|What are some examples of medications that cause uterine smooth muscle relaxation?||Terbutaline, magnesium sulfate, nitroglycerine, and inhaled inhalation anesthetics relaxes uterine smooth muscle.|
|What are some medications that cause uterine smooth muscle contraction?||Oxytocin, Carboprost (Hemabate), Methergine, Cytotec|
Oxytocin – causes hypotension
|What is Hepatopulmonary Syndrome?||Hepatopulmonary syndrome (HPS) is defined by the presence of liver dysfunction, unexplained hypoxemia, and abnormal vasodilation of intrapulmonary vessels. There is also a phenomena called orthodeoxia which is manifested by hypoxia when standing that improves when lying supine. This resolves following liver transplantation.|
|Opioid Induced Pruritis treatment?||Zofran|
|Opioids other effects?|
|Opioids suppress resistance to infection by modulation of immune cellular activity (T Cells, macrophages, NK cells)|
|Which medications do you dose using Ideal Body Weight? Total Body Weight? Lean Body Weight?||Ideal Body Weight: NMDBs|
Total Body Weight: Succinylcholine and Propofol (infusion)
Lean Body Weight: Opioids and Propofol (induction)
|E Cylinder Volume Pressure|
O2 ?? ??
Air ?? ??
N2O ?? ??
|E Cylinder Volume Pressure|
O2 625L 2000psi
Air 625L 2000psi
N2O 1590L 750psi
N20 will only start to drop in pressure at ~400L. Only way to reliably estimate the volume is to weight the cylinder
PSI / (200x flow) x 60
|Most common serious adverse event following a celiac plexus block?||Paraplegia|
|Maternal Physiologic Changes|
Factor VII and Fibrinogen?
|Blood volume? Up|
Plasma volume? Up
Factor VII and Fibrinogen? Up
|Maternal Physiologic Changes|
Serum Cr/BUN? Down
HCO3? Down to compensate for resp alk
|Maternal Physiologic Changes|
|Rate? No change|
Tidal volume? Up by 50% (due to progesterone)
ERV? Down by 25%
RV? Down by 15%
FRC? Down by 20-80%
TLC, VC, CC unchanged
|Maternal Physiologic Changes|
CO? Up (up 40% to meet metabolic demands of mom and baby)
CVP? No change
|What neuromonitoring technique is most affected by volatile anesthetics?||MEP > SSEP > VEP > BAER|
They are not altered by narcotics.
EMG and nerve stimulation are not affected by volatiles but avoid NMBDs
|Subq Fentanyl Patch|
Time to therapeutic onset?
Systemic effects after removal?
|Type to therapeutic onset? 12 hours|
Time after removal? 16 hours – 3 days
|Weight change side effects:|
|TOPAMAX = weight loss|
LYRICA, NEURONTIN = weight gain
|Bainbridge Reflex||Increase in heart rate in response to increase venous return. The reflex is mediated by stretch receptors in the walls of the atria. Stimulation of sympathetic fibers and inhibition of vagal outflow from the medulla is thought to|
be the primary efferent pathway in the Bainbridge reflex to produce an increase in heart rate.
|Reverse Bainbridge Reflex||Decrease in venous return results in bradycardia, occurs during spinal anesthesia. Otherwise known as Bezold Jarisch Refelx|
|Of the IV anesthetics, the only medications to cause BURST SUPPRESSION are what?||Etomidate, Propofol and Barbiturates.|
Inhaled anesthetics also can induce burst suppression
|Critical Illness Myopathy||Distal weakness and muscles of respiration first. Depressed DTRs and slightly elevated CKs.|
More prevalent in patients who are receiving NMBDs + steroids in the ICU
Mechanism of action with what side effects.
|TCA with anticholiergic effect.|
|Postpartum Foot drop due to||Lumbosacral Nerve Injury|
|NPO Guidelines for the following?||Clear liquid 2h|
Breast milk 4h
Non human milk 6h
Light non fatty food 6h
Fried food 8h
|Bupivicaine Toxicity in Infants||2.6|
|Urinary specific gravity for a patient who is hypovolemic/dehydrated?||>1.010 = dehydration/hypovolemia|
|Strong ion difference =||SID= [Na + K + Ca + Mg]-[Cl+Lactate]|
Disturbances that increase SID increase the blood pH causing alkalosis; also dehydration can cause increase in SID
Disturbances that lower SID cause acidosis
Normal SID = 40
|Hyperkalemia – diagnosis and treatment?||Classic EKG changes include peaked T waves, shortened QT intervals, long PR|
Severe – most rapidly treated by hemodialysis
1) insulin/glucose to facilitate intracellular transfer of potassium
2) Calcium to stabilize the cardiac membrane
3) Kayexelate and loop diuretics to eliminate potassium
4) B agonists
|Are peribulbar blocks safer than retrobulbar blocks? Why?||Peribulbar blocks are generally safer because the needle transverses a shallower path without directly advancing the needle towards the optic nerve or the central retinal artery|
|Aldosterone effects on sodium and potassium? How would a Conns syndrome patient present? What medicine would directly counter aldosterone?||Aldosterone is released following activation of renin angiotensin pathway in response to hypovolemia or renal hypoperfusion. Aldosterone works on the distal tubules and collecting ducts to upregulate Na/K pumps. It promotes the reabsorption of Na and excretion of K. Supraphysiologic aldosterone secretion leads to HTN and hypokalemia. Spirinolactone is an aldosterone receptor antagonis.|
|Sodium deficit formula? ***skip||(140 – serum sodium) x (kg x 0.6)|
Typically, 50% of the Na deficit should be corrected in the first 24hrs and the rate of hypertonic saline should never be higher than 100mL/hr.
|Magnesium toxicity levels and symptoms|
Treatment of toxicity?
|5-6: Hypotension and bradycardia|
6-12: Prolonged PR
12: DTR loss, weakness, can progress to respiratory depression
18: SA/AV node block
Tx of Toxicity with IV Calcium
|Celiac plexus block||Innervates the stomach, small bowel, proximal large bowel, spleen, gallbladder, pancreas, kidneys, and adrenal glands|
Complications include orthostatic hypotension (MOST COMMON), back pain, retroperitoneal hematoma, hiccups, diarrhea, abdominal aortic dissection, paraplegia (due to subarachnoid injection).
|In a patient receiving heparin for 5 days or more, what study should be done prior to neuraxial anesthesia?||Platelet count in case of HIT.|
|Differences between aortic and radial arterial waveforms?||A radial waveform will have:|
1) a higher systolic pressure
2) a wider pulse pressure
3) a more pronounced diastolic wave
4) a more delayed and slurred dicrotic notch
|What is meralgia paresthetica?||Entrapment of the lateral femoral cutaneous nerve.|
|VACTERL stands for?||Vertebral defects|
Typically infants undergo repair of TEF first. Then, if there are cardiac abnormalities they will be repaired next. Imporforate anus is repaired next. Prior to considering a caudal for this procedure, consider a lumbosacral MRI to evaluate for neural tube defects (the v in vacterl). These defects are contraindications for caudal anesthesia.
CHD are the most common defect associated with TEF, occurring in up to 75%
|Hyperalimentation is commonly associated with what lab abnormalities?||Hypophosphatemia|
Acute liver injury/elevated PTT – usually requiring vitamin K supplementation
|Pregnancy effects on coagulation?|
Which factors increase?
Which factors decrease?
|Factors that increase include I (fibrinogen), VII, VIII, IX, X, XII and vWF.|
Factors that decrease include XI, XIII, antithrombin III, tPA and protein S
Factors that develop resistance = Protein C
Dilutional thrombocytopenia usually results in a decrease in platelets by 10%.
|The first presenting sign of an intrathecal injection in an infant is what?||Apnea. Not hypotension because infants’ have a relatively underdeveloped sympathetic nervous system. You would not see bradycardia until late hypoxemia.|
|Confirmatory tests for brain death||Positive apnea test, EEGs (2 isoelectric tests 24 hrs apart) and determination of the absence of blood flow (via cerebral angio, MRI/MRA, transcranial Doppler). All reversible tests must be ruled out.|
Note: Brain death is a clinical diagnosis and confirmatory testing is not mandatory
|List neuromonitoring that is least to most sensitive to volatile anesthetics||Least to most sensitive to anesthesia: BAEP < SSEP < MEP < VEP (BAEP = BArely affected, SSEP = Somewhat affected, MEP = Mostly affected, VEP = VEry affected|
|Changes in physiology in response to altitude?|
|The most important immediate adaptation is increased HR and then hyperventilation and thus increase in minute ventilation due to the decrease in PaO2, this via stimulation of the peripheral chemoreceptors (central chemoreceptors are not sensitive to falls in PaO2). This results in a respiratory alkalosis. This would normally suppress ventilation but in the next 48-96 hours, the pH of the CSF compensates via bicarbonate loss and bicarbonate is further excreted by the kidneys to return blood to normal pH.|
In the first 12-24 hours also note that there is a right shift in the OH curve caused by an increase in 2-3 DPG.
Over 1-3 weeks, the body further compensates by increasing EPO secretion causing an increase in hematocrit.
The increased minute ventilation remains increased as long as the person remains at a higher altitude
|Peripheral chemoreceptors (carotid and aortic bodies) sense/respond to ____ while central chemoreceptors (medullary) sense/respond to _____.||Peripheral receptors respond to hypoxemia and hypercarbia.|
Body needs oxygen and makes co2
Central receptors respond to hypercarbia.
|What do you do for hypoxemia during OLV?||First give CPAP to the nondependent (nonventilated) lung to allow ventilation to the down lung. Second, you can give PEEP to the dependent (ventilated) lung or increasing FiO2. If still hypoxemic consider unclamping the down lung. If this is not possible at the time, clamping of the branch PA on the non-dependent side to decrease intrapulmonary shunting. If absolutely necessary, institution of CPB would be the final option.|
|ACA stroke would present how?|
MCA stroke would present how?
|MCA – upper extremity and facial weakness|
ACA – lower extremity weakness
|Conn’s syndrome/Hyperaldosteronism affect on:|
|Hyperaldosteronism causes hyernatremia, hypokalemia, metabolic alkalosis.|
Aldosterone causes sodium reabsorption in exchange for potassium and hydrogen ions. It’s net effect is an expansion in ECF volume caused by fluid retention. It is stimulated by RAS.
They should be on spirinolactone.
|What is the most common congenital heart defect?||Perimembranous VSDs – VSDs are the most common and perimembranous VSDs represent 70% of all VSDs|
|What is Ebstein’s Anomaly?||It is a rare congenital anomaly characterized by downward displacement of the tricuspid valve. It is basically atrialization of a portion of the R ventricle causing a larger RA and a hypoplastic RV. The baby would present with cyanosis.|
It is associated with Wolff-Parkinson White syndrome.
|How to differentiate between DIC and Liver disease?||Factor VIII because VIII will be normal in cirrhotics.|
|Acute Epiglottitis management?||Transport to the OR immediately and perform an inhaled induction. It is crucial to maintain spontaneous ventilation with PPV. Avoid N2O because of the potential for air trapping in the lungs via a ball-valve effect (meaning that air can go in but not out)|
|Surfactant is produced when and by what cells?||It is made primarily after 32 weeks gestation. It is produced by type II pneumocytes.|
Infants born prematurely are at risk for RDS because of surfactant deficiency. Treatment with exogenous surfactant may reduce intrapulmonary shunting in RDS and hypoxemia.
|Absolute contraindications for TEE?|
Relative contraindications for TEE?
Mallory Weiss Tear
Active/Recent Variceal Bleed
Recent GI surgery
|Tourniquets – how much do you inflate them?||Upper extremity: 50mmHg above SBP|
Lower extremity: 100mmHg above SBP
|B2 agonists (ritodrine and terbutaline) affect on uterine muscle?||B2 agonists are tocolytics and relax uterine contractions and increase uterine blood flow.|
Other uterine relaxants: magnesium sulfate, nitroglycerine, and inhaled inhalation anesthetics
|Treatment for uterine atony?||(Don’t need to know doses)|
Pitocin/Oxytocin: 10-20 U infusion over 10 mins – causes hypotension
|Treatment for Cyanide toxicity?||Hydroxocobalamin (first line) & Amyl nitrate|
Elevated cyanide levels can be seen with smoke inhalation from residential or industrial fires.
Elevated cyanide and thiosulfate levels can also be seen with administration of sodium nitroprusside. Thiosulfate is seen in long term administration of SNP, especially in pts with renal insufficiency.
You would see elevated SvO2 and metabolic acidosis (cyanide will decrease utilization of O2 for ATP production and decrease VO2 thus increasing SvO2)
|ARDS Severity||P/F = PaO2/FiO2 ratio|
Mild: P/F ratio 200-300
Moderate: P/F ratio 100-200
Severe: P/F ratio <100Strategies for ARDS1) Maintain PaO2 >60mmHg with adequate Hgb
2) PEEP (up to 20mmHg)
3) Minimize FiO2 (<50%)4) Minimize tidal volumes (6mL/kg)
|Does atropine cross the placenta?||Yes. It is a tertiary amine and is used if fetal bradycardia is a concern. It is usually given with neostigmine in the pregnant population.|
|Pacemakers placement is indicated in which AV node blocks?||Second degree, Mobitz Type II & Third degree block|
First degree = prolonged PR
|Simple HR determination||300, 150, 100, 75, 60, 50 etc|
|Median Nerve||– C5-C7|
– Motor: flexors of the wrist except for flexor carpi ulnaris
– Sensory: palmar side of thumb, index, middle finger, and half of ring finger
– Rescue block at the elbow – medial to the brachial artery in the AC fossa
– It runs through the carpal tunnel and compression causes CTS
|Use of Fetal Heart Rate Monitoring is feasible at the earliest when?||The soonest you can do FHR monitoring is at 18-20 weeks gestation. Prior to this, the fetus is too small to monitor.|
|Treatment of stable SVT in patients with WPW?||Procainamide is the drug of choice for patients with AVRT. Patients with AVNRT can be treated with adenosine, verapamil, B blockers, Diltiazem|
|Alkalosis does what to potassium?|
Insulin does what to potassium?
|Alkalosis drives potassium into cells. So less hydrogen ions = less potassium ions|
Insulin drives potassium into cells.
|Neuraxial Block ASRA guidelines?|
– For the patient on ASA?
– For the patient on Plavix?
– For the patient on Heparin subQ?
– For the patient on Unfractioned Heparin IV?
– For the patient on prophylactic Lovenox?
– For the patient on therapeutic Lovenox?
– For the patient on Coumadin?
|– ASA? No contraindications|
– Plavix? Should be discontinued 7 days
– Heparin SQ? No contraindications if dose is <10,000 units - Unfractioned Heparin IV? Heparin gtt must be stopped 2-4 hours before needle placement with aPTT documented to be normal, can be restarted 1 hour after procedure - Lovenox ppx? Delay procedure for 12 hours from last prophylactic dose - Therapeutic Lovenox? Delay procedure for 24 hours, removal should be 12 hours after last dose - Coumadin? Should be discontinued for 4-5 days and check an INR
|Lidocaine with epi toxic dose?||7mg/kg of lidocaine with epi|
What do you give for the following:
|Prolonged R = FFP|
Prolonged K = Cryo
Decreased MA = platelets
Teardrop = Antifibrinolytics ie TXA, eproetin
|HOCM intraop strategy?||1) Maintain preload|
2) Optimize diastolic time by decreasing heartrate (beta blockers)
3) Maintain afterload (phenylephrine)
|Alveolar gas equation?|
Which energy substrate is most effective for a ventilator wean?
|PAO2 = FiO2 x (Patm – PH2O) – CO2/RQ|
RQ = 0.8
Lipids result in the lowest increase in CO2 production. So they would be most ideal for ventilator weaning by reducing the amount of CO2 that needs to be removed by ventilation.
|Mixed Venous Oxygen (SvO2) – what causes an increase in SvO2? What causes a decrease?||SvO2 is a measure of global oxygen delivery.|
|Causes of Metabolic Acidosis|
GAP metabolic acidosis?
NONGAP metabolic acidosis?
|Normal Anion gap = 8-12|
Methanol, Uremia, DKA, Propylene glycol, INH/Infection, Lactic acidosis, Ethanol/Ethylene glycol, Salicylates
Fistula, Uretero-enterostomy, Saline admin, Endocrine (hyperPTH), Diarrhea, Carbonic anhydrase inhibitors, Ammonium chloride, RTA, Spirinolactone
There are three major etiologies of nongap acidosis:
|Afferent vs Efferent||Afferent is the nerve arriving to the spinal cord, efferent is the nerve exiting the spinal cord. Afferent ARRIVES, Efferent EXITS.|
|In a patient with muscular dystrophy who receives succinylcholine, why would they have hyperkalemic cardiac arrest?||Not because of extrajunctional receptors but because of rhabdomyolysis.|
Patients with Duchenne or Becker would present with muscle weakness, pseudohypertrophy of calves, and elevated CK. They might also have dilated CMP. They are not more susceptible to MH.
|Tumescent Liposuction dose/kg of lidocaine?||35-55mg/kg is allowed because the majority is aspirated during the procedure, because it is not absorbed, and because it is given with Epi. Concentrations peak at 12 hours.|
0.05% Lidocaine with Epi 1:1,000,000
|ABGs are generally run at ___ degrees C. To correct for colder patients||37 degrees C|
For each degree Celcius temperature decrease, the pH of the blood increases by 0.02.
For example, a sample on a patient who was at 32 degrees came back with a pH of 7.20, what would the corrected pH be? 7.30
What is the Bezold Jarisch Reflex?
What is the Bainbridge Reflex?
What is the normal Baroreceptor Reflex?
|Bezold Jarisch – hypotension sensed in the LV leads to bradycardia and further hypotension|
Bainbridge – paridoxical tachycardia in response to fluid bolus
Baroreceptor – stretch receptors in the carotid results in decreased HR and decreased BP
|Risk factors for Post Dural Puncture Headaches (PDPH)?||Age < 40Prior PDPHBMI < 30 Hx of Air TravelMultiple AttemptsThe use of Cutting Needles (Quincke, Pitkin, Rovenstine)Puncture with a large bore needle|
|Inhaled Nitric Oxide can cause what?||Methemoglobinemia and a left shift on the oxygen disassociation curve.|
It will improve VQ mismatch by decreasing PVR, thus increased PaO2
|ECT Autonomic Effects?||Initially following seizure activity, there is an increase in parasympathetic stimulation which can manifest as increased secretions, bradicardia and sometimes transient asystole. The increased parasympathetic stimulation is quickly followed by an increase in sympathetic stimulation which will present as hypertension and tachycardia. You can sometimes see ST changes which is usually transient.|
|B2 agonism effect on:|
|B2 agonists causes HYPERglycemia and HYPOkalemia.|
It also is used off label as a tocolytic/uterine relaxation.
|Goals for Aortic and Mitral Insufficiency?||Decrease afterload|
Avoid bradycardia – any medication that would decrease heart rate is not recommended because it will allow for more time for regurgitant flow.
A mnemonic for Aortic Insufficiency and Mitral Insufficiency is “fast, full and forward” – avoid bradycardia, optimize preload, and minimizing afterload.
Can use nitroprusside to decrease afterload
|Goals for Aortic Stenosis?||Avoid hypotension|
Maintain sinus rhythm avoiding both bradycardia and tachycardia
Optimize intraventricular filling
Avoid sudden increases or decrases in SVR
|Goals for MV Stenosis?||Avoid sinus tachycardia or Afib with RVR|
Avoid marked increases in CVP
Avoid drug induced decreases in systemic vascular resistance
Avoid hypoxemia or hypoventilation which might precipitate increases to PVR and eventual right sided failure
|Goals for HOCM?||1) Ensuring adequate preload and CO,|
2) Reduce contractility – halothane used in the past but no longer because of arrhythmogenicity
3) Maintain SVR
Etomidate is a good choice for induction because of its ability to maintain SVR.
|Neonatal Fluid management – Things to Keep in Mind||1) Neonates have reduced GFR and are prone to fluid overload because their nephrons are immature and underdeveloped.|
2) Neonates are sodium wasters because they do not respond as strongly to aldosterone.
3) TBW is highest in preterms and lowest in adults.
4) A high body surface area:body weight ratio pre disposes neonates to increased evaporative losses.
5) Immature sympathetic nervous system and baroreceptors are the reason for a reduced response to low BP
6) Infants and neonates have a higher volume of distribution.
7) Infants and neonates have a LOW plasma protein content which means that they have increased plasma concentration of unbound/active molecules/hormones/medications.
8) Enzyme immaturity leads to slower metabolism but remember that they have a higher volume of distribution
|The best medicine to improve CPP?||Vasopressin is actually better at improving CPP compared to phenylephrine or NE. Not only does vasopressin increase MAPs but it also reduces ICP.|
CPP = MAP – ICP
|Coronary Perfusion pressure = ?||Coronary Perfusion Pressure = Aortic DBP – LVEDP|
|What factors increase in pregnancy?||1, 7-10, 12 and vwf|
11, 13 and at3 decrease
|Substrates that are metabolized by butrylcholinesterase||Heroin|
Other ester local anesthetics
**Remifentanil and esmolol are not metabolized by butylcholinesterase
|Caused by mutation in the ryanodine receptor (normally responsible for release of calcium into muscle cell) that causes prolonged release of calcium.|
Earliest signs are masseter muscle rigidity, tachycardia and hypercarbia. Hyperthermia and myoglobinuria is a late sign.
Triggers: Volatile anesthetics only (NOT nitrous) and succinylcholine
Clear associations with Central Core Disease, Multi-minicore myopathy and King Denborough syndrome.
Confirmation test: Muscle biopsy – caffeine-halothane contracture test (10-20% false positive rate but near 0% false negative rate – it is 100% sensitive)
|Call for help|
1) Stop triggering agent
2) 100% O2 – high flows
3) Dantrolene 2.5mg/kg – give early and ok to give rapidly
4) Change circuit tubing, soda lime
5) Get Arterial access for lab draws – ABG q5 mins, check BMP and clotting studies
6) Bicarbonate 1-2mEq/kg
7) Treat symptoms – cool if necessary, antiarrhythmics (procainamide), diuretics (furosemide 1mg/kg or mannitol 0.25mg/kg)
Dantrolene + CCBs are contraindicated because myocardial depression has been demonstrated in animal studies
|What is the earliest most sensitive sign for MH?|
What is the earliest most specific sign for MH?
|Earliest most sensitive: Hypercarbia|
Earliest most specific: Muscle rigidity
|Known Triggers for post op OSA in Pediatric Population||Severe OSA on Polysomnography|
Age < 3 years oldHx of prematurityNeuromuscular disordersURI in the past 4 weeksNasal pathologySystemic HTNObstruction during Inhaled InductionHx of Snoring, Frequent awakenings, Daytime restlessnessCor Pulmonale
|Do hyper-/hypothyroidism affect MAC?||NO|
What to expect in the PACU?
|Alpha blockade first followed by beta blockade. If you do beta blockade first, you will get unopposed alpha causing hypertension.|
Treat first with phenoxybenzamine (irreversable alpha blocker) or phentolamine or prazosin (alpha 1 blocker).
Combination of phenoxybenzamine, prazosin, beta blocker, ACEi, CCBs, and magnesium sulfate to attain HD stability.
In the PACU, they will be hypotensive, sedated, hypertensive (if part of the tumor persists), and hypoglycemic. Not hyperglycemic.
|Smoking Cessation||12-24 hours to decrease CO levels and decrease sympathetic outflow caused by nicotine (t1/2 of 1-2hrs)|
1-2 weeks to decrease sputum production, normalization of mucociliary function
3-4 weeks to decrease wound healing complications
>4 weeks to decrease respiratory complications (ie bronchospasm or pneumonia)
|Hepatic Blood Flow is derived from?||The portal vein provides about 75% of total hepatic flow and the hepatic artery only provides about 25%.|
|In obesity, what changes would you see in lung mechanics?||Decreased FRC (due to decreased ERV)|
RV and closing capacity are unchanged
FEV 1 and FVC are usually normal.
|Which lung volumes remain constant from infancy to adulthood?||FRC (30mL/kg) and Tidal volume (7mL/kg)|
|Pierre Robin vs Apert Syndrome vs Klippel-Feil syndrome vs Beckwith-Wiedeman syndrome vs Hurler syndrome||Pierre Robin: Micrognathia/mandibular hypoplasia, glossoptosis and cleft palate|
Apert: MAXillary hypoplasia and choanal stenosis = mouth breathers but not a difficult airway
Klippel-Feil: limited neck extension due to fused cervical vertibrae
Beckwith-Wiedeman: macroglossia; associated with CHD and omphalocele
Hurler: airway difficulty due to infiltration of mucopolysaccharide into pharyngeal and laryngeal soft tissue
|Tet Spell Management||Knee-chest position (increases SVR)|
Phenylephrine (increases SVR)
Fluid bolus (increases preload)
Morphine (decrease agitation and decrease RVOT obstruction)
B blocker (decreases RVOT obstruction)
|Uptake of volatile agents is faster in infants why?||Because they have a higher alveolar ventilation:FRC ratio. Infants also have a larger proportion of vessel rich tissues such as brain, liver and heart which also contributes to a more rapid uptake.|
This explains why an inhaled induction is faster in infants, compared to adults.
|Umbilical Vein Blood Gas|
Umbilical Artery Blood Gas
|7.35 / 40 / 30|
7.20-7.30 / 50-55 / 18-25
|Estimated Allowable Blood Loss equation?||EABL = EBV (Hcti-Hctf/Hcti)|
EBV = 80mL/kg infants, 70mL/kg adults
|Risk factors for developing Preeclampsia?||Advanced maternal age|
Family history of Preeclampsia
NOT CIGARETTES or TABACCO
|How does magnesium affect the NMB and the NM junction?||It inhibits the release of ACh at the NMJ|
It decreases sensitivity at the NMJ to ACh
It depresses the excitability of the muscle fiber membrane
It increases potency and duration of NMDBs
|Meds that do/do not cross the placenta||Do not: Heparin, glycopyrrolate, muscle relaxants (minimal placental transfer)|
Do: Atropine, scopalamine, thiopental (highly lipid soluble), opiates (morphine the most, fentanyl the least), volatile anesthetics, local anesthetics (depend on pKA, maternal/fetal pH, degree of protein binding) – mainly lidocaine will cross, bupi and ropi have high protein binding and chlorprocaine is metabolized quickly.
|P50 of neonates?|
P50 of 10 month old?
P50 of adult Hgb?
|neonate – 20mmHg, left shift because of decreased interaction between HbF and 2,3 DPG|
10mo – 30mmHg, the P50 decreases to adult values at about 10-12yo
adult – 27mmHg
|Beginning at what week gestation should you start to implement left uterine displacement?|
When can you start monitoring fetal heart tones?
|18-20 weeks for both|
|Up to what month can you use NSAIDs during pregnancy?||Up to the end of the 2nd trimester|
|Avoid elective surgery when during pregnancy? When is the optimal time for elective surgery?||Avoid it in the 1st trimester because of organogenesis (occurs between days 30-70). The second trimester is the optimal time to perform surgery|
|t-test vs ANOVA?||t-test is used for comparing continuous outcomes in 2 groups.|
ANOVA is used to compare more than 2 groups
|What is the leading cause of mortality in pregnant women?||Pulmonary embolism – due to an increase in factor I, 7-10, 12 and vWF and a decrease in protein S (mainly hypercoagulable state is due to increased VII and fibrinogen)|
Risk of venous thromboembolism in pregnancy increases with the following additional risk factors: obesity, smoking, multiple gestations, advanced maternal age, increased parity, cesarean section, as well as the presence of a concomitant thrombophila.
|Preservatives in LA solutions possible toxicity?|
|Sulfites – added to 2-chloroprocaine is associated with arachnoiditis or anaphylaxis. Pts who have had accidental large intrathecal volume injection can develop bilateral lower extremity paralysis|
EDTA – added as a chelating agent that can cause back pain at the injection site
Methylparaben – bacteriostatic agent that has a chemical structure similar to PABA and can cause anaphylaxis.
|Absorption of LA from greatest to least?||IV, Tracheal, Intercostal, Caudal, Epidural, Brachial plexus, Sciatic, SubQ|
“IT ICE BS”
|Lidocaine max dose?||4-5mg/kg without epi|
7mg/kg with epi
|Bupivicaine/Ropivicaine max dose?||3mg/kg|
|Cocaine mechanism of action?||1) Na channel blocker|
2) NE reuptake inhibitor
3) Stimulates presynaptic NE + dopamine release
Metabolized by butrylcholinesterase
What part of the brachial plexus?
What side effects or complications?
|Upper and middle trunks mainly, the lower trunk is often spared|
Blocks the entire brachial plexus with occasional ulnar sparing
Good for shoulder or proximal – mid humerus surgery
Phrenic nerve paresis in 100% of patients, unsuitable for COPDs or elderly who cannot tolerate 25% reduction in pulmonary function
What part of the brachial plexus?
What side effects or complications?
Blocks the Radial, ulnar, median, musculocutaneous and axillary nerves so good for surgeries of the mid humerus, elbow, forearm and hands
Risk of PTX requires caution. Phrenic nerve paresis in 30%
|Infraclavicular Block||Blocks at the level of the cords|
What part of the brachial plexus?
What side effects or complications?
|Terminal branches/peripheral nerves|
Blocks the radial, ulnar, median and musculocutaneous (unreliably blocked)
Good for operations of the forearm and hand
Supplimental intercostobrachial nerve block needed for TNQT pain
|The intercostobrachial nerve is responsible for what nerve distribution?||The medial surface of the arm in the axilla|
|What formation of Bupivicaine is the most cardiotoxic? R+, S- or Racemic?||R+ isomer is 7 times more potent than S-|
Levobupivicaine is the same as S-
|Why do you get decreased HR in a high neuraxial block?||1) you could have blockage of the cardioaccelerator fibers (T1-T4)|
2) unoposed vagal tone from high sympathectomy
3) Reverse bainbridge reflex/Bezold Jarisch reflex (decresaed HR due to decreased intracardiac stretch receptors)
|What effects on lung mechanics do you get from neuraxial anesthesia?||TV is not impaired as long as C3-C5 are not blocked|
VC is decreased due to decreased ERV from abdominal muscle weakness
Apnea during spinal is due to medullary ischemia from hypotension rather than motor block of the phrenic
|In cases of MRI equipment malfunction, the liquid helium (which is used to cool the superconducting materials) can boil off in what is known as a _____. If the helium does not escape through the safety valve, the large amount of helium can pose a risk for_____.||Quench|
Asphyxiation to personal and patients due to displacement of O2 in the room.
|WPW – what are the two types of tachyarrhythmia?|
What are the pathways of the two types?
|AVNRT is the most common tachyarrhythmia seen in pts with WPW. AVNRT is classified as either ORTHODROMIC or ANTIDROMIC.|
Orthodromic is more common and has a narrow QRS – the impulse is conducted from atrium to AV node to His to Purkinje and then return from ventricle to atria using an accessory pathway. Treatment should begin with vagal maneuver. If unsuccessful give B blockers, verapamil, adenosine or amio.
Antidromic has a wide QRS – impulse is conducted from the atrium to the ventricle through the accessory pathway and returns from the ventricles to the atria via the normal AV node. Treatment with PROCAINAMIDE. Meds that slow AV node conduction such as adenosine, CCBs, B blockers, lidocaine and digoxin can actually increase conduction through the accessory pathway and are contraindicated.
Cardiovert if unstable
|Treatment of Long QT syndrome||B-blockers, potassium supplementation, Mexilitine, ICD placement|
|Neurolysis for cancer pain: what are the two methods?||1) Alcohol – burns on injection|
2) Phenol – does not burn
|Celiac plexus block is used for what?||Cancer of organs from the distal esophagus to the transverse colon|
|Superior Hypogastric Plexus is used for what?||Bladder ca, cervical Ca, prostate Ca|
|What is the caudal block dose in infants?||0.5-1mL/kg of 0.25% bupi or ropi with or without epi|
0.5mL/kg covers sacral dermatomes
1mL/kg covers low thoracic dermatomes
1.25mL/kg covers mid thoracic dermatomes
|Signs of Uterine rupture?||Atypical abdominal pain, shoulder pain, vaginal bleeding, uterine tenderness, hypotension, tachycardia, shock.|
|What type of nerve fibers are the most susceptible to LA blockade?||Small myelinated B fibers|
|What is the anesthetic site of action for lipophilic opioid epidural infusions? Lipophilic epidural bolus?||Opiate epidural infusions site of action = systemic|
Opiate epidural bolus site of action = spinal
|Neuraxial hydrophilic opioids move cephalad or caudad?||Hydrophilic opioids (ie morphine dilaudid) meds move more cephalad compared to fentanyl|
|Lidocaine Bier Block dose?||3mg/kg of 0.5% Lidocaine will provide anesthesia for up to 90 mins|
|Most common cause of transfusion related mortality?||TRALI – caused by recipient antibodies to donor HLA causing an influx of neutrophils into the lungs with subsequent activation causing inflammatory response and increased pulmonary microvascular permeability|
|Hemophilia A is a deficiency in ___?|
Hemophilia B is a deficiency in ___?
|A = factor eight|
B = factor nine
|In regards to local anesthetics:|
Lipid solubility is the determinant of what?
pKA is a determinant of what?
Protein binding is a determinant of what?
|Lipid solubility is the primary determinant of intrinsic local anesthetic potency (increased lipid solubility indicates increased potency)|
Speed of onset is related to the pKa (lower pKA indicates shorter onset of action)
Protein binding is implicated in the duration of action (high protein binding indicates longer duration of action)
Normal regional cerebral blood flow?
Ischemia seen with what cerebral blood flow?
EEG changes seen with what cerebral blood flow?
Cerebral tissue death is seen with what CBF?
EEG changes 15-20mL/min/100g
Cell death 10mL/min/100g
16 lead EEG is the gold standard
|Paired t-test: compare study subjects means at 2 different times|
Unpaired t-test: compares means of two different subjects
Fisher test: compares 2 proportions
Chi-square: compares >2 proportions
|SVR formula? PVR formula?||SVR = 80 * (MAP-CVP) / CO|
PVR = 80 * (mPAP – PCWP) / CO
|Abdominal compartment syndrome:|
When do you see it?
What bladder pressures would you see?
|– Can be the result of major abdominal surgery or following massive fluid resuscitation for massive trauma or burns. This is because of massive intra-abdominal edema secondary to shock induced inflammatory mediators or surgical manipulation|
|Alpha stat vs pH stat||During pH stat the patient’s pH is maintained my managing the pH at the current temperature.|
***pH stat infuses extra CO2 into the blood causing improved CBF***
During alpha stat the patient’s pH management is not temperature corrected. Just remember that in a cold patient, the patient’s PaCO2 will be LOWER than what is seen on the alpha stat.
|In the prone head/neck case, patient wakes up with unilateral blindness, proptosis and retinal exam shows a cherry red spot, what is the diagnosis?||Central retinal artery occlusion|
“Prone case with pressure on the eyeball”
This is different from Posterior/Anterior IOP in that the optic disc is normal.
|Extracorporeal Membrane Oxygenation|
|VA ECMO = can provide near full support of heart and lungs|
VV ECMO = gas exchange of 80% of cardiac output, does not provide any cardiovascular support
AV ECMO = gas exchange is driven by arterial flow through extracorporeal membrane
|Vaporizer output at alitutde||Modern conventional vaporizers are temperature compensated variable bypass vaporizers. This means that these vaporizers divert a certain amount of FGF through the liquid volatile anesthetic. Therefore the amount of volatile exiting the vaporizer is subject to change based on the atmospheric pressure. They automatically compensate for changes in altitude.|
However, the desflurane vaporizer is different in that it is heated to 39 degrees C. No FGF flows through a desflurane sump, rather a certain volume of desflurane is released into the circuit based on the percentage set on the control dial. Therefore, the output of desflurane from the anesthesia circuit will be the SAME weather at sea or at altitude.
An example of a question: If a machine is set at 6% in two operating rooms. One machine is set at sea level (Patm 760mmHg) and the other is set at 8000ft above sea level (Patm 570mmHg), what would be the expected anesthetic depth of the patient at 8000 feet?
Answer: Relatively lighter because the partial pressure of desflurane in the sea level pt would be 760 x 0.06 = 45.6mmHg and the partial pressure of the desflurane in the 8000ft pt would be 570 x 0.06 = 34.2mmHg. So the 8000ft pt would be getting less desflurane.
|For a sciatic nerve block, what three anatomical landmarks are required?||1) Greater trochanter of the femur|
3) Sacral Hiatus
|What is the most common congenital cardiac anomaly?||Bicuspid aortic valve|
|Cirrhosis: increased or decreased?|
Total body water?
|Intravascular volume decreased|
Total body water increased
Intracellular volume unchanged
CO increased – cirrhosis causes a hyperdynamic state
|Amniotic Fluid Embolism risk factors?||Multiparity|
|GI changes in 3rd trimester: increased or decreased?|
– Gastric pH?
– Gastric emptying?
– Gastric volume?
– LES tone
|Gastric pH down due to increased gastrin|
Gastric emptying decreases in active labor
Gastric volume up due to increased gastrin
LES tone decreases due to progestin & upward displacement of the stomach
|Neonatal resuscitation||Not breathing or crying? Dry, warm, stimulate, clear airway secretions|
HR <100, gasping or apneic? PPVHR < 60 after 30 seconds of PPV? Continue PPV - intubate, start chest compressionsHR still < 60 after 60 secs? GIVE EPI 10-30mcg/kg IV, IT, or via umbilical arteryFor meconium: If adequate RR, HR and activity, do NOT intubate, just suctionIf not adequate HR, irregular RR, poor tone - intubate and suction
|Conditions associated with Meconium||Postmaturity (>42 weeks)|
Maternal conditions (ie HTN, Placenta previa, PHTN, Abruptio placenta)
|Arrhythmia associated with SAH?|
Also, in the setting of SAH an echo might show what?
Global LV hypokinesis
|What period of the cardiac cycle is most shortened in sinus tachycadia?|
When does most of the LV filling occur?
|Diastasis (slow filling prior to atrial contraction, the y descent)|
Early diastole upon opening of the mitral valve. Atrial systole is responsible for 15% of LV filling
|How does hetastarch affect anticoagulation?||It binds to Factor VIII and vWF.|
|First you will get direct stimulation of respiratory centers leading to respiratory alkalosis due to hyperventilation|
Metabolic acidosis to follow with an increased anion gap acidosis due to accumulation of lactate and excretion of bicarb (the kidneys have been wasting bicarb to compensate for resp alkalosis)
Clinically, TINNITIS, tachypnea, hyperthermia, nausea/vomiting, seizures, CV collapse
Tx: Activated charcoal within 1-2 hours, gastric lavage, bowel irrigation; sodium bicarb, HD, IV fluids
|Congenital Long QT syndrome|
Medications to avoid?
Acute management of torsades?
Chronic management of LQTS?
|Avoid quinidines, procainamide, amio, macrolides, TCAs, SSRIs, ondansetron, methadone, volatile anesthetics|
Acute management: Magnesium, correct electrolytes
Chronic management: B blocker and possibly a pacemaker
|Separation anxiety does not begin until what age?||6 months|
|What ETTs are the most flammable?||PVC > silicone > red rubber|
|If a patient presents with MI and is found to have severe mitral regurg, what happened?||There was likely posteromedial papillary muscle rupture due to RCA infarction.|
|Renal failure electrolytes?||Elevated Electrolytes: potassium, phosphate, and magnesium|
Decreased Electrolytes: sodium, calcium
Other Increases: urea, creatinine, uric acid, sulfate, phosphorus, lipids, cholesterol
Other Decreases: albumin
Acid/Base: anion gap metabolic acidosis
|IE prophylaxis||Previous IE|
Heart transplant pts with valve issues
|Most likely cause of intraop anaphylaxis?||NMBDs|
|Elderly PFTs/Age related changes|
Chest wall rigidity
Response to hypercapnia/hypoxia
Volume of distribution
Recovery from anesthesia
Levels of catecholamines
Sensitivity to B receptor
|Closing pressure increased|
Residual volume increased
Gas exchange decreased due to collapse of smaller airways and decreased alveolar surface area
Dead space increased
Chest wall rigidity increased
Response to hypercapnia/hypoxia blunted
Volume of distribution increased
Hepatic function decreased
Recovery from anesthesia due to increased Vd and decreased hepatic function
There is increased levels of catecholamines but decreased sensitivity to B receptor
Affect on SVR?
Affect on HR?
|Decreases SVR and HR.|
|Tetanus toxin mechanism?||Tetanus – travels retrograde up the motor neuron to the spinal cord where it enters the inhibitory interneurons and blocks the release of glycine.|
|Botulism toxin mechanism?||Botulism inhibits the release of ACh at the NMJ by cleaving SNARE proteins – this stops the fusion of vesicular ACh.|
|FENa values||<1% = prerenal>1% = intrinsic (ATN or AIN)|
>4% = post renal
|Acetazolamide||Wastes sodium and HCO3|
Clinical use: Acute mountain sickness (to compensate for resp alkalosis), glaucoma, urinary alkalinization
Can in hyperchloremic metabolic acidosis
|Etomidate/Ketamine affect on evoked potentials?||Increased amplitude|
|Cyanide toxicity||Hydroxocobalamin: combines with cyanide, forming cyanocobalamin (vitamin B12), which is renally excreted; few side effects, well-tolerated by critically ill|
Amyl nitrite: inhaled formulation, rapidly enters circulation generating methemoglobin which has higher affinity for CN than cytochrome oxidase
Sodium Nitrite: slower onset, longer lasting nitrite, as above frees up cytochrome oxidase to resume aerobic metabolism
Sodium Thiosulfate: regenerates sulfur-dependant rhodanese activity; this enzyme converts CN to thiocyanate, which is renally excreted; recommended co-administration with hydroxocobalamin or nitrites, especially in prolonged exposures
|1) WPI score >7 OR SS scale score of >5 OR WPI 3-6 + SS scale of >9|
2) Symptoms >3 months
3) No other explanation of pain
Treatment CBT, sleep hygeine, strength training, meds – fda approved meds = Cymbalta, Lyrica or Savella
|Each facet joint is innervated by the MEDIAL BRANCH of the posterior rami of the spinal nerves above and below|
Pain may be near midline and can radiate to gluteal region, thigh and knee.
Worse with hyperextension and lateral rotation of spine
Diagnostic medial branch block
Tx Medial branch rhizotomy
Worse with? Better with?
|90% of the time it is L4-L5 or L5-S1.|
Occurs from flexion injuries or heavy lifting
Aggravated by bending, lifting, sitting.
Relieved by lying down
+/- numbness or weakness or DTRs
L4-L5 = weakness in dorsiflexion
L5-S1 = weakness in plantar flexion
Acute back pain tx: NSAIDs and APAP
|Spinal stenosis||Progressive narrowing of neural foramina and spinal canal.|
It is improved with flexion of the spine (squatting) and worsened with extension of the spine (walking up a hill)
|Sciatic nerve is derived from what?||L4-S3|
|Obesity||Decrease in TLC|
Decrease in FRC (due to loss of ERV)
Retardation of growth or development