PoA1 Flashcards
Where does hypobaric solutions gravitate toward?
C3 (phrenic nerve) and L3, the high points when a patient is supine
What arteries supply the cord? Where do they originate
Anterior Spinal Artery (from vertebral artery 75%), 2 Posterior Spinal Arteries (25%), and segmental spinal arteries
Dura Mater origin and endpoint
Foramen magnum and to the end of Dural Sac S2
CSF Factors
150ml total
decreased CSF amount means increased LA spread and to use a lower amount
Common causes are low weight increased abdominal pressure
Thumb Dermatome
C6
Spinal Considerations: Lidocaine
It’s pretty short acting, used for outpatient
Which spinal is goated for duration
Bupivacaine (0.75% in 0.5% dextrose)
Morphine Neuraxial Adjunct key points
Water soluble hydrophilic and will lead to delayed respiratory depression from slow spread in CSF
Opioid Neuraxial side effect and prevention
Pruritus use <300 mcg morphine, 50-75mcg it’s absent, give 4mg zofran or Nubain prophylactically
Respiratory Depression lipophilics will occur sooner (Fent and Sufent) later with hydrophilic agents (morphine)
They DO NOT prolong block, only enhance density
And urinary retention
Alpha 2 Agonist Neuraxial Effect
Intensifies and Prolongs the block and analgesia (Dex, Clonidine)
Differential Blockade
nerve fibers withing a nerve means we see a progression of block onset
B sympathetic fibers, then C & A delta fibers (i.e. slow pain,touch and temp are blocked second),
B-Sympathetic, then C and A delta (pain, temp, touch), followed by A Gamma (Motor tone/NOT SENSORY) then A Beta (touch, pressure) then A Alpha (motor and proprioception) Recovery is inverse so B Sympathetic fibers are blocked longest
LA Drug/Controlable Factors affecting (Spinal) block height
Dose (increase dose, increase duration), baracity, site of injection, patient position
LA Patient/Non Controlable Factors affecting Spinal block height
CSF volume, age, baracity, increased intra-abdominal pressure (fluffy or pregnant)
Greater Cephalad spread with greater age(greater neural nerve sensitivity), baracity(?) and less CSF
Bezold-Jarisch Reflex
Protects LV when active, leads to bradycardia and hypotension
BJR is treated by Zofran as it’s mediated by 5HT3 receptors in vagus nerve
Respiratory Response to Neuraxial
If high thoracic (T4) block, loss of Abdominal Muscle contribution in forced expiration-limits ability for active exhalation
Thermo response to Neuraxial
shivering-Meperidine and Precedex and clonidine will treat it
LAST/Failed Block get out of jail free card
1.5ml/kg 20% intralipid bolus for LAST, followed by 0.25ml/kg/min gtt
Most probable LA anaphylaxis cause
PABA in Ester LA
Block height for C-Section
T4
Block for Knee Tourniquet
T10
Needle Insertion Layer Path
Skin, subQ fat, supraspinous, interspinous, ligamentum flavum, dura mater, subdural space, arachnoid mater, subarachnoid space
What spinal approach for metal rods or scoliosis
Paramedian-10-15 angle difference from midline
“Total or High” Spinal
Unexpected cephalic spread of LA to high cervical/cranial nerves
caused by excessive dosing (and why you should check dermatomes frequently) or Rapid LA injection
Postdural Punction Headache
Failure of dura puncture site to heal
Headache is when pt is upright
PDPH Treatment
2-3 days after Headache when upright
Supine bedrest, NSAIDs, Fent, Caffeine/Methylxanthine (vasoconstriction), blood patch ~48 hours post onset
More likely with an Epidural as the gauge required is larger
Cauda Equina Syndrome
L2-S5 coccygeal nerves are affected by LA procedure
**2/2 High dose 5% lido, Microcatheter use-causes lido to pool in cauda equina, and Small Whiticare 25/26 needle **
**IF DISC COMPRESSION, LAMINECTOMY IS NEEDED IN UNDER 6 HOURS
symptoms range from back pain, saddle anesthesia, to ED, GU/GI dysfunction
Auditory/Facial/Ocular Effects
Horner’s syndrome- ptosis, miosis, anhydrosis
Epidural Pregger Concern
Baston’s plexus is engorged in the Lateral epidural space
Dont inject into them, blood upon CSE entry means youre too lateral
**Be a Chad and inject inert fluid to open the epidural space prior to catheter insertion
Blood in the catheter is also seen with multiple attempts, stiffer catheters or trauma to the epidural vein
Why is 3% Chloroprocaine the fastest onset with a pK of 9?
High 3% concentration leads to quicker onset, whats used in surgical anesthesia
very short-duration is 45min and is an ester
What is the order of LA route onset greatest to least?
IV, tracheal, intercostal, caudal, paracervical, epidural, brachial, sciatic, subQ
I Told Immediately Chelsea Please Eat Big Scallop Subs
Epidural Dosing per segment
1-2mL per segment
give 5mls at a time to avoid High Spinal
Neuraxial Alkanlinization
Speeds up onset, bicarb (1mEq/10ml) decreases [H+]/Increases nonionized drug
increases diffusion of drug AND speed of block onset
Epidural Procedure Unique steps
Loss of Resistance with the air or saline
Test dose with 3mL of 1.5% Lido + (1:200,000) Epi to see if IT or IV
uses 45mg Lido and 15mcg Epi
If HR jumps 20% or patient has metalic taste in mouth O O F
If dense motor block within 5 minutes occurs-you did a spinal essentially whomp whomp
Positive Test Dose Signs
Tinnitus, circumoral numbness, metallic taste
Why are esters metabolized quickly
Plasma Cholinesterases are how they are metabolized
Patients allergic to Tetracaine, Benzocaine, and cocaine have cross reactivity to?
PABA, and other Esters
ANAA monitoring frequency standards
BP, HR, and RR are q5 min
pulse ox is continous/mandatory, most do q3 min
What is the SpO2 if PaO2 is 40mmHg
75%
at 60 mmHg it’s 90
at 27 mmHg its 50
How is SaO2 estimated in pulse oximetry
Pulsatility of Arterial Blood
Carboxyhemoglobin Pulse Ox Concern? What is the % COHb in smokers?
Falsely elevates SpO2
typically over 6%- they desat quickly and youll need to adjust accordingly
Every 1% COHb increases, SpO2 increases 1%
due to COHb absorbing light in the 660nm range as O2Hb does
Pulse Ox Artifact Causes
IV dyes (methelyne blue will cause it to drop), Venous pulsatility (clots/transpo of great vessels)
ambient light, low perfusion, nail polish, and other Hb forms will mess it up
Korotkoff Sounds
Phase I: the most turbulent/audible (SBP)
Phase II: softer and longer sounds
Phase III: crisper and louder sounds
Phase IV: softer and muffled sounds
Phase V: sounds disappear (DBP)
Artline Waveform Periphery effect
Steeper upstroke, higher systolic peak, later dicrotic notch, lower End-Diastolic Pressure
Distal pulse amplification is from impedance
Square wave test
no more than two oscililations after fast flush and should get smaller
to look for good resolution- System dynamic response
Overdampening Waveform
absent dicrotic notch, lower sBP, narrowed PP with accurate MAP
Less detail
Pressure Waveform Analysis
identifies residual preload reserve and fluid status
looks at cyclic artieral BP change from respiratory cycle with PPVenting and Lung voume change
Positive Pressure Ventilation Effects on Pressure
Early Inspiratory phase- greater intrathoracic pressure, increased total lung volume - leads to less LV afterload and increased LV preload causing SV, CO, MAP to increase
Decreased venous return, increased PVR- leads to increased RV afterload causing decreased RV SV
Stroke Volume Variation
Normal is 10-13%
Computer calculates the stroke volume variation based on patient factors
if greater than 10-13% GIVE FLUID-youll see SVV of 12%
Pulse Pressure Variation
Max and min PP over the entire respiratory cycle
Normal is LESS than 13-17%
On the exam, if a patient is 13-17% GIVE THEM FLUID, YOULL SEE 14% PPV ON EXAM, GIVE VOLUME
Side-stream Gas Mixture Analysis
Most common, Lag time causes longer rise time
affected by tube diameter, length, sampling rate-bigger diameter, faster interpretation
Gas must be brought to analyzer, most common
Infrared Analysis/Absorption
O2 doesnt absorb IR radation (no dipole)
*measures CO2, N2O, H2O, and volatiles based on the asymmetry of molecules absorbing light at different lengths
measures energy absorbed of a IR band as it passes through a gas sample
What facial Nerve reflects laryngeal muscle block?
Corrugator Supercilii is goated-reflects laryngeal adductor and abdominal muscles better than the adductor pollicis
Ulnar Nerve is gold standard
Deep Non-depolarizing blockade
Absent TOF, post tetanic stim present
Reversed with 4mg/kg Sugammadex
Intense block- no response, 3-6 minutes after intubation dose of ND NMBD, reversal impossible unless 16 mg/kg sugamma
moderate- gradual return of 4 responses of TOF stimulation, neostimine reversal is good and sugammadex is 2mg/kg
Depolarizing Blockade Phase II
Presence of post-tetanic facilitation
How many channels does BIS use
4, 2 per hemisphere
What nerve picks up heat/warmth
Unmyelinated C
Hypothermia Complications
Coagulopathy-reversible platlet aggregation
Decreased O2 delivered to tissues
wound healing will take longer
Decreased Drug metabolism-NMB can be prolonged
Gotta be hot to clot
*increases transfusion need by 22%, blood loss by 16%
post thermal discomfort is a thing
What is the order of heat transfer greatest to least
Radiation (40%), Convection (30%), Evaporation (10%), Conduction (ask a magic 8 Ball)
Hypocarbia concerns
decreases CBF (cerebral vasoconstriction), blunts respiratory drive, decreases PVR, K goes extra to intracellular
ETCO2 of 28 mmHg, below is risky dingo
Bohr Equation
measures deadspace to tidal volume
Increased ETCO2 causes
is measured at the end of phase 3, largest just before inspriation
Caused by:
increased metabolism(Fever/MH/sepsis/seizures)
Bicarb
Decreased alveolar ventilation-hypoventilation/NM dz/High spinal
Equipment issue-rebreathing, CO2 absorber spent, leak in circuit, or faulty inspiratory/expiratory valve
Decreased ETCO2
Hypothermia
Cardiac Arrest
Hypotension
Hemorrhage
PE
HYPERventilation or Pain
Equipment wise- vent disconnect, goose egg intubation, complete airway obstruction(laryngospasm), poor sampling-the breathing rate cant be too fast for the line to grab a sample, ETT cuff leak-room air will dilute the expired sample
ETCO2 Phase 1
Respiratory baseline at 0, exhalation of anatomic deadspace/apparatus
1/3 of tidal volume is exhaled
No CO2 should be present unless rebreathing
ETCO2 Phase II Alpha Angle
110ish degrees- widened with expiratory airflow obstruction (COPD looks sharkfin, Bronchospasm, kinked ETT)
Causes slanted Phase 2, separates phase 2 and 3
Faulty Inspiratory Valve Effects
Widened Beta Angle, decreased slope of inspiratory downstroke (phase 0)
Can cause Rebreathing when not going back to 0 baseline
Cardiac Oscillations
More common in Peds, heart proximity to trachea causes this during inspiratory phase
rapid heartrate causes timing of various lung fields to be different
Re-breathing and Soda Lime exhaustion effect
CO2 rebreathing/Inspiration and baseline increases
phase 0 doesnt change
This and faulty valve will be on the exam
Curare Cleft
NMB is wearing off
Patient is spontaneously breathing during mechanical ventilation
reparalyze or flip off the vent if its the end of the case
Esophageal Intubation capnography
Wounded Pride Intensifies
spontaneous waveform then goes away, but if a tubes in it should be regular
if wave form has right ETCO2 peaks and regular rate then falls off, tube fell out or got kinked
What monitoring is continous in OR
BP and RR
What is my SpO2 if PaO2 is 40mmHg
75%
What causes slanted phase 2 in capnography
Faulty equipment, rebreathing
Phase 2 is the expiratory upstroke, CO2 Rich alveolar gas and is steep
What is the sensory portion of Oculocardiac Reflex?
CN V (Trigeminal Nerve)
Common cause of high spinal
Too high of a dose
rapid administration
incorrect positioning
misplaced epidural catheter
What is the mechanism of action of LAs
Na channel blockade, specifically from inside
What layer of the spinal column is responsible for the “Pop” during spinal/epidural
Penetration of the Dura Mater, entering the sub dura layer
Epidural Space Rostral, Caudal, Anterior, Posterior and Lateral borders
Rostral/Caudal: Foramen magnum to near S5/Sacrococcygeal ligament
Lateral: Vertbral Pedicles
Anterior: Posterior Longitudinal Ligament
Posterior: Ligamentum Flavum and Vertebral Lamina
Epidural Space Contents
Nerves, Fatty tissue, Lymphatics, Blood Vessels
Fatty tissue can absorb and decrease bupivcaine availabilty compared to Fent/Lido/Morphine
Plica Mediana Dorsalis
Lateral connective tissue band in the Epidural Space thought to cause epidural catheter placement issues and unilateral blocks
How many Cervical, Thoracic, Lumbar, Sacral, and Coccal nerves are there
Cervical 8
Thoracic 12
Lumbar 5
Sacral 5
Coccal 1
Where are Sensory information carried and Motor information carried?
Anterior Nerve Roots: Motor and Autonomic information from cord to body
Posterior Nerve Roots: Sensory information from the body to the cord
Umbilicus Dermatome Level
T10 Sensory Level
Are there spinal nerves innervating the face for sensory fields?
Nope, dat der CN5/Trigeminal nerve with the following branches:
V1-Opthalmic Nerve
V2-Maxillary Nerve
V3-Mandibular Nerve
Spinal/SAB/Intrathecal Block site of action
Subarachnoid space of the cord, specifically the myelinated preganglionic fibers of the spinal nerve roots
Also inhibits neural transmission in the superficial layers of the cord
Epidural site of action
In the epidural space outside the dura mater diffuses through the dural cuff to reach nerve roots to work
can leak thorugh the intervertebral foramen to the paravertebral space
Factors NOT affecting Spinal/SAB spread
Barbotage
Speed of injection
Bevel orientation
Vasoconstriction (e.g. Epi or Phenylephrine)addition
Gender
ALL DO NOT AFFECT SPREAD
EPIDURAL Factors affecting spread and block height
Controlable with significant effect:
LA volume
Level of injection
LA Dose
Controllable with less effect:
Local anesthetic concentration
Patient Position (has a significant effect but whatever)
Plica maybehaps
Epidural NON CONTROLABLE factors affecting spread
Greater affect: Pregnancy
Older age
Meh effect: Height(Taller may need 2 ml per segement, shorter lesser per)
Epidural factors that DO NOT affect spread
Additives (though they do intensify or prolong block)
direction of needle bevel
injection speed
Differential Blockade Zones
Sensory level is 2 levels higher than motor
Sympathetic level is 2-6 levels
So a T8 block has T10 motor blocked below and T2-T6 Sympathetic block-will need Phenylephrine/Ephedrine as HR and BP will drop
Bromage Scale
PACU Motor Blockade monitoring scale 0-3
0-gucci, born to run
1-slight block cant raise extended leg
2-moderate cant raise leg or move knee, CAN move feet
3-complete motor block cant move legs, knee, or feet
CV Systemic effects of Neuraxials
Preload is decreased from sympathetomy and venous pooling
Afterload decreased from partial arterial dilation-SVR decreases 15% in healthy people and 25% in elderly/trash EF patients
Cardiac Output is reduced from SV decreasing from the SVR/Venous Return effects
Intially CO may rise from the vessel dilation then proceeds to fall off a cliff
Reverse Bainbridge Reflex
Bradycardia triggered by reduced stretching of RA
Sudden Cardiac Arrest Cause and Incidence
Young adults with high parasympathetic unopposed from our acctions, occurs 20-60 minutes after
7:10,000 spinals
1:10,000 epidurals
Which drugs are indicated for hypotension with bradycardia secondary to SAB/Epidural? Hypotension solo?
Ephedrine dose, for bradycardia alone a dose phenylephrine/Neo
Wait for your HR to change before cycling the cuff, otherwise it’ll be another cattywampus read
Prevention of Spinal induced Hypotension
Vasopressors like Phenylephrine
5-HT3 antagonist Zofran to counter BJR
Fluids we move away from preloading and Co-load with 15mL/kg 700-1Lish. Please dont tank someone with trash EFs by fluid overload. Or kidney injury with colloids and making the blood too viscous
Positioning slight pelvic tilting/Head up to prevent Hyperbaric solutions to tank your pressures further
Atropine for bradycardia alone, however tachycardia in someone with CAD is a bad time
Pulmonary Effects of Neuraxial
Minimal Impact, even with T4, only ERV is decreased and by extension Vital Capacity
Pickwickian Syndrome
BMI 40-50 when laid flat they panic as ERV and VC are low from baseline
Reassure them and raise the HOB and get Semi Fowler Action going
putting on a nasal cannula will be a dice throw, some will be bothered more by it
Diaphragm Innervation
C3, C4, C5
GI Sympathetic innervation
T5-L2
Sympathetic afferent-sends visceral pain
Sympathetic efferent-inhibits peristalsis, gastric secretion also causes sphincter contraction, and vasoconstriction
GI Parasympathetic
Afferent-sends saitey, distention, nasuea
Efferent-tonic contraction, sphincter relaxation, peristalsis, and secretion
GI Neuraxial Effect
Increases Parasympathetic and reduces Sympathetic tone
Increases Peristalsis, 20% incidence of N/V
Reduces post op ileus in abdominal surgery
GU Neuraxial Effects
RBF is stable if MAP is maintained
If you block above T10 urinary sphincter tone is relaxed
addition of Neuraxial Opioids decreases detrusor contraction and Increases bladder Capacitance
PACU will probably need a reminder to bladder scan
Neuraxial Metabolic Effect
Surgical stimulus elevates catecholeamines, cortisol, and RAAS
can partially suppress or totally block (in lower extremity cases) neuroendocrine response if it’s placed before surgical stimulus
What determines the hydrophilicity of LA?
Tertiary Amine, it is what accepts protons
LA intermediate chain big deal
determines drug class and allergic potential cough cough Esters and PABA cough cough