LIVE VALLEY REVIEW DAY 1 Flashcards
The only fused vertebrae is the
Sacral
C8 nerve runs under
T1
A Caudal block is an
Epidural
When you do caudal block the ligament you cross is the
Saccrococcygeal Ligament
Adults Spinal cord ends at
L1
Pediatric spinal cord ends at
L3
SIFEDSASP
Skin Subcutaneous Supraspinous ligament Interspinous ligament ligamentum Flavum Epidural Dura Arachnoid Subarachnoid Pia
Other names spinal
SAB
Other names spinal
SAB, intrathecal
When does the infant SC ends at L1?
20-24 months
Toughest layer is the
Dura mater
Offer the most protection
Dura mater
Spinal web is the
Arachnoid mater
Spinal cord Layer that is tightly attached to the spinal cord
Pia
Delicate and highly vascular
Pia
At any time how much CSF in the body
100-150 ml
Per day how much CSF is produced
500 ml per day
Normal pressure of the CSF
10-20 cm H2O
Is the CSF high or low pressure
Low pressure (in healthy individuals)
Where is the CSF produced?
Choroid plexus third and fourth ventricle
Where is the CSF produced?
Choroid plexus third and fourth ventricles
***** Principle site of action of neuraxial blockade (SPINAL OR EPIDURAL) is the
Nerve root (Branch that sticks out of the picture)
Last ligament when you’re doing midline paramedian approach?
Ligamentum Flavum
Action of epinephrine with LA
Vasoconstriction, decreases absorption leading to a LONGER DURATION
Anatomical shape that can affect spinal/epidural?
Kyphosis or scoliosis
Angulation of needle can affect
Distribution
In a pregnancy , do you increase or decrease dose of LA
Decrease the dose
In a pregnant or morbidly obese, you decrease the dose why?
Increase abdominal mass which decreases the space.
If you don’t think the spinal is enough for a pregnant person, you think you underdose
Underdose redose can lead to TOTAL SPINAL
Do an epidural instead
To change density of the block you can change the
Change the concentration of the block
What can differentiate a Sensory vs motor block with choosing the local anesthetics?
Is the concentration .
SG of the CSF
1.004 - 1.009 (just remember 1.007)
Hyperbaric to CSF
Heavier than CSF (Sink)
Hypobaric to CSF
Lighter than CSF (Float)
To make hyperbaric mix with
Dextrose 5% to 8%
To make hypobaric mix with
STERILE water
To make isobaric mix with
CSF
Hypobaric laying down going
Cephalad
Hyperbaric laying down going
Caudal
If patient laying on affected side
use hyperbaric
Best for patient with hip fracture
HYPOBARIC
The most important factor affect SPINAL
Position
The most important fact for EPIDURAL
VOLUME
After spinal what do you get dilation vs constriction
Venous and arterial vasodilation
CV effect of sympathetic blockade
Massive vasodilation Decrease preload Decrease Venous return Decrease CO Decrease BP
CV effect of sympathetic blockade treatment necessary
BEST treatment with hypotension to spinal is PHYSIOLOGIC not pharmacological .
Maternal hypotension associated with
Late Decelerations
Late decelerations is associated with
maternal hypotension
If not normovolemic use
Fluids
If normovolemic use
EPHEDRINE
Before fluid loading, need to know
EF (heart pumping status)
If LV not functioning you will get
pulmonary edema
Cardiac changes occur to
Sick, very young, and elderly
THEY LACK RESERVE
Cardiac reserve decrease
1% every year after the age of 30.
High spinal vs Total spina
High spinal: Greater than T4
Total spinal :
High spinal vs Total spina
High spinal: Greater than T4
Total spinal : ALL THE WAY PAST T
Common reason of total spinal
Epidural dose for a spinal dose
Respiratory changes with neuraxial techniques
Severe chronic lung disease OR use of accessory muscles.
Interscalene block (ISB) for patients with respiratory issues?
No because of ISB possible adverse effects phrenic nerve palsy
High points
C3 and L3
Low points
T6 and S2
Widest level of spine
L2
Narrowest level of spine
C5
Cutting needle disadvantages
Bigger cut of dura
More at risk for PDPH
How long epidural set up
about 20 minutes
Spotte vs whitacre
Sprotte takes longer to setup
Cutting needle perpendicular to the fibers
Takes out lot of fibers.
Cutting needle bevel towards the
Flank
Aspirin and Neuraxial
NON issues
SC heparin or LMW, loo
ACT or PTT
Coumadin therapy
PT/INR
INR level for neuraxial
< 1.5 ok
>1.5 NO PROBLEM
Pulling a catheter , what to ask
Why is it in?
Anticoagulation reason
Fibrinolytics or thrombolytics therapy , about to have surgery, can they have neuraxial
NO , none for 10 days
Patient receive this should not receive neuraxial for 10 days
Fibrinolytics or thrombolytics therapy
Generic of plavix
Clopidogrel
Generic of eliquis
Apixaban
Generic of Pradaxa
Dabigatran
Aside from stopping AC , should know when to
Restart the medication
Xiphoid level
T6
L4 is the
illiac crest
Tuffiers line
intercristal lie
Absolute contraindications of neuraxialL: CHIP
CHIP Coagulation Hemodynamic instability Infection at site Patient refusal.
Assault vs battery
Verbal ASSAULT
Physical BATTERY
No absolute __________ for Neuraxial
Indications
Considerations that support using subarachnoid block- FATO
Full stomach
Anatomic distortions of the upper airway
TURP
Obstetrics.
Meningitis or increased ICP
Possible herniation , No neuraxial
Only aortic stenosis not to do neuraxial
Severe Aortic stenosis
Reason of the tight fitting styelet
27ga,
Enough body to bounce through tissue. Solid needle when stylet needle, and hollow without it
Predisposing factors to infections
3 AAAs CD Advanced age] Alcoholism AIDS Cancer Diabeters
3 main signs of Meningitis
High fever
Nuchal rigidity
Headaches
Laying down, headaches gets better with
PDPH
Definitive symptoms that differentiate PDPH from meningitis
High fever
Risk factors to know for PDPH
Perpendicular needles Large cutting needles Female > men Young > Elderly Pregnant women
Epidural anesthesia can be done at
ANY LEVELS
Epidural anesthesia at the sacral
Caudal
Safest entry point into epidural space is the
Midline lumbar region
Binds the epidural space
dural posterior
and ligamentum flavum ANTERIOR
Why is epidural needle curve and noncutting?
A potential space
Loss of resistance -> thread the catheter
Crawford needle of the Epidural is the
STRAIGHT NEEDLE
and CUTTING
Tuohy needle of the epidural is
CURVE needle
non-cutting
Increase risk of epidural puncture is the
Crawford needle
Most epidural catheter is
Multi port or orifice
Agents for epidural ONSET FAST TO SLOW (2-2-2)
Chloroprocaine Prilocaine Lidocaine Mepivacaine Bupivacaine Ropivacaine
WEISS has
WINGS
During an epidural if you get a blood return?
Remove and start it over.
Epidural air vs saline
use either .
How much catheter you want in the epidural space?
4 cm
How do you fix a one sided epidural )
Take tegaderm off
Withdraw catheter about 1 cm
inject extra medication .
Neuraxial acts on the
Nerve rootlets, nerve roots and spinal
Easiest to block : myelinated vs unmyelinated
Myelinated nerve
The order in which nerves are blocked following epidural
BC ADGBA
Sensory order: Myelinated and unmyelinated
Large myelinated
Small myelinated
Unmyelinated
Why do B fibers get blocked first.
B fibers gets blocked first because of their location
Sensitivity of LA vs order of Blockade
Page 400.
Sensory block most sensitive to
Alcohol swab to assess loss of temperature
Epidural hematoma most important issue
PARALYSIS
Incidence of epidural hematoma
1 : 150,000 blocks
Majority of epidural hematoma occur in patients with
ABNORMAL COAGULOPATHY
ABNORMAL COAGULOPATHY patients at risk for epidural hematoma
Disease state ( Factor VIII deficiency) Pharmacological therapy
S/s of epidural hematoma
SHARP BACK and leg pain
Numbness
Motor weakness
SPHINCTER dysfunction .
Only way to diagnose EPIDURAL HEMATOMA
Imaging (CT, MRI) It ‘s an emergency you need it.
Definitive treatment is EPIDURAL HEMATOMA
Surgery
2 main complications of Epidural
Penetration of a blood vessel
Epidural hematoma
Signs and symptom of PDPH
Headches Double vision (Diplopia) because of traction on the cranial nerve.
Headache with PDPH why
When the lay down medulla and brainstem to drop into the foramen magnum, stretching the menin
Differential diagnoses for PDPH:
SAH Subdural hematoma Meningitis Anxiety Dehydration Hypoglycemia Lack of caffeine Loss of resistance with air (pneumocephalus)
Definitive treatment for PDPH
Epidural blood patch
PDPH is
Self limiting
Epidural blood patch process
10-30 cc of aseptically drawn blood
blood is injected into epidural space until the patient can feel pressure in the back
After the epidural blood patch, bed rest 1-2 hours before ambulating
Caffeine is a ______in the cerebral bed
Vasoconstrictor
First blood patch injecting resolves : (success rate)
89-95% of headaches may repeat in 24 hours.
How much blood to inject
14-18 ml OR when patient say feel pressure
What does the blood do when injected?
Compressing SAH with the injected blood.
Most common regional anesthetic in children
Caudal
Caudal can be done
Awake or sleeping
You don’t want to get
CSF
Brachial plexus blocks
Interscalene
Supraclavicular
Infraclaviular
Axillary
Supraclavicular/ infraclavicular
Pneumothorax
Interscalene block best for
Shoulder
Nerve roots of Brachial Plexus
C5-T1
Branches of Brachial Plexus
MARMU Musculocutaneous Axillary Radial Median Ulnar
Cords and divisions of brachial plexus.
3 cords
6 Divisions
Appears black of image
LIQUID (anechoic)
Appears white of image
BONE (hyperechoic)
Safer to work (in plane or out of plane)
In plane
Commit to memory pg.
409
Pain to pinky finger, what dermatome?
C8
Radial nerve stick gives you ______when stimulated everything else______
EXTENSION : FLEXION
Radial nerve stick gives you ______when stimulated everything else______
EXTENSION ; FLEXION
Cervical plexus block
Unilateral procedure of the neck
Complications of Cervical plexus block
Unilateral phrenic nerve paralysis (ONLY see with DEEP)
Horner’s syndrome
Hoarseness
Accidental subarachnoid or epidural injection .
Complication, Only seen with DEEP cervical block
Unilateral phrenic nerve paralysis
How much to inject for Cervical plexus block ?
4 ML (think C2-C4)
Interscalene is between
Between 2 scalene muscles
Level of C6
Cricoid Cartilage
Where it crosses interscalene groove
Level of C6
Best way to prevent intravascular injection
Aspirate first
Occurs in 100% patients undergoing interscalene block
Ipsilateral phrenic nerve block resulting in diaphragmatic paresis.
ISB is a ____volume block? how much ?
Large ; 40
Most inferior part of the interscalene groove
2 cm from MidPoint of clavicle on the medial side.
Landmarks to know Interscalene Groove
Anterior scalene
Middle scalene
Clavicle
1st rib
Complications of Supraclavicular
Pneumothorax. (hemothorax as well)
Horner’s syndrome
Phrenic nerve block
Supraclavicular volume
20-30 mL
Axillary bundle, nerve missing (muscle associated)
Musculocutaneous nerve (Costcobrachialis muscle)
Injection site for axillary block
Find axillary pulse as high as possible
Move to rope of muscle.
Most popular of the ISB
Axillary block
For axillary block, do this to the arm
90 deg out and 90 degrees up
Lies outside of axillary sheath
MCTN
For axillary block, what can cause incomplete spread.
Fascial septa result in INCOMPLETE SPREAD of LA
Median and radial nerve inject
3-4 cm
Radial where do you inject your LA.
Radial flexor muscle and extending to the dorsal surface of the ulna styloid
NO epi where with the elbow
Below elbow
NO epineprhine in 4 areas
Nose , toes, fingers, penis
Median and radial nerve blocks at elbows
Insert B bevel needle slighly medial to the brachial artery .
Radial nerve at elbow
Inject
Femoral nerve becomes the
Saphenous nerve
Lumbar plexus levels
L1 - L4 an some T12
Ulnar block of the elbow
Insert between the medial condyle of the humerus and the olecranon of the ulna
Ulnar block at the wrist
Insert B bevel needle slighly adjacent to the ulnar artery
Median nerve block at the wrist
Between long palmar muscle and the radial flexor muscle of the wrist.
Popliteal is a
Sciatic nerve block
Ankle block vs popliteal interchangeable
Saphenous is missing
Most difficult to block
Posterior tibialis
Superficial nerve of lumbar
All that starts with S
Radial nerve block at the wrist
Inject beginning at the radial flexor muscle and exendin to the dorsal surface of the ulnar styloid.
Webspace between 1st great toe and 2nd toe
DEEP peroneal nerve.
BLOCK REVIEW
421` 423
Retrobulbar
Up and away or down an dway s
Bier block , need to stay up for at least
20 minutes
Ilioinguinal and iliohypogastric nerve block
Inject 8-10 ccc
Most common complication
Most common complication of Ilioinguinal and iliohypogastric nerve block
Patient discomfort.
Maternal changes : lungs parameters unchanged
TLC, VC, IC unchanged
Maternal changes: decreased lung
Decreased FRC
What makes maternal desaturation fast?
Increase in Alveolar ventilation, and a decreased in FRC, desaturation quick
Makes maternal at risk for bleeding
Airway engogement
mucosal friable
Do not do this with maternal
no nasal instrumentation
Term changes of maternal : CO2 and PaO2
PaO2 increases
PaCo2 decreases
O2 consumption produces a
70% increase in alveolar ventilation at term.
Term and MAC
Decreased
Alveolar vs minute ventilation (difference between)
Dead space
Closing volume and capacity
Unchanged
Oxygen consumption at rest for maternal
20-30%
Oxygen consumption at Labor
2nd stage 100%
Uterine vasculature % of Co
10%
Blood volume and plasma volume
Dilutional anemia because plasma volume goes up greater than blood volume
Increase in Blood volume no increase in BP because
drop in SVR.
Increase in Blood volume no increase in BP because
drop in SVR and PVR
Maternal At risk for this because of an increase in blood volume
Thromboembolic events
CO =
HR x SV
Blood volume is
Up 25-40 %
Aortal caval compression aka
Maternal supine hypotensive syndrome
Best position for maternal
Left lateral tilt
Explains Aortal caval compression
Compression of IVC decrease VR and results in decrease SV and hypotension
What is the maternal response to Aortal caval compression?
TACHYCARDIA
VASOCONSTRICTION
CO increase in pregnant women is due to
Increase is SV
Stages of labor : First (four dermatomes)
Begins onset of contraction , result in complete dilation of the cervix
Stages of Labor: seconds (Sacral)
Sacral included.
Signs of fetal distress
Fetal scalp ph< 7.20
Meconium stained amniotic cluids
Oligohydramnios
Normal placental implantation
Top of the uterus
Placenta previa
Painless preterm bleeding
Plan
Pass on pushing (C-section needed)
Non-reassuring fetal heart rate pattern
Repetitive late decelerations
Late decelerations due to prolonged cord compression
Loss of beat-to beat variability associated with late or deep decelerations
Sustained fetal heart rate < 80bpm
Placenta previa ultimate goal
Keep fetus inside to as close to 37 weeks as possible
Expected management is terminated when
Active labor
documented lung maturity
Excessive bleeding
Gestational age reaches 37 weeks.
Most common cause of neonatal morbidity and mortality
Before 20 weeks
Incidence of accreta for normal
3%
Antibody serum
2- 4 hours for exact match blood
Emergency bleeding volume for labor and delivery
VOLUME, VOLUME, VOLUME
ACCESS
What to prepare for possible increase bleeding.
Large bore IV
4 PRBC
FLUID/BLOOD WARMERS (possible DIC)
Placental abruptio is the
loss of area for maternal fetal gas exchange
Known risk factors
HTN Age Parity Tobacco Trauma History of
What to order for Placenta abruptio :
RBCs
Platelets
FFPs
Cryopreciptate
Any concenrst with volume or coagulation status
No epidural
Abnormal placental implantation, worst is
percreta
Placenta Accreta
Adheres to the
Placenta Increase
INvades and is confined the myometrium
Placental Percreta
PEN”etrate the myometrium
Hemabate don’t use with
ASTHMA
Methergine don’t use with
Hypertension (High blood pressure)
If mom has had a placenta previa, previous C-section or had uterine trauma she is at risk for
developing PLACENTA ACCRETA.
The more C section the greater the incidence of
ACCRETA
Amniotic Fluid embolism
High mortality rate 50% in the first hour
Amniotic fluid embolism (A- OK)
A OK
Atropine
Ondansetron
ketorolac
MAternal heart Group I
Regional ok
Maternal heart Group II
NO regional
DIC fibrinogen
< 150
DIC platelets
Decrease
DIC times all
increase
Pre-eclampsia DEFINITIVE TREATMENT
DELIVERY of the fetus.
Maternal Heart problems Group I
MVP, AI, L to R shunts
Everything else group 2
Hemodynamically Magnesium does the
OPPOSITE OF CALCIUM
Loss of DTRs, magnesium level mg/dL
7-12
During laryngoscope , see fluid, next action
Suction
Does the risk of preeclampsia ends with delivery
NO
Normal Mag mg/dl, mEq/L
- 8-2.5
1. 5-2.1
Treat which decelerations with priority
Late
Agent with lower pka
more ionized
Nonionized form is
Lipid soluble.
3% chlorprocaine does
Not follow the rule,
VERY HIGH CONCENTRATION
The lower pKA the
the faster the onset
Speed of onset is dependent on
Degree of ionization
Lipid solubility is a measure of
potency
Duration of action is more important for
Protein binding and LIPID SOLUBILITY
But MAINLY protein binding
Oil water partition coefficient
Highest potency
The higher the Oil water partition coefficient
The higher the potency and lipid solubility
Low albumin
Increase action of highly bound drug.
What determines blood cocentration
Wheter
The only vasoconstrictor LA
Cocaine
LA goes away from site from
Absorption
What form do you need to have an effect for a conduction
BOTH (one to cross one to bind)
2 forms of esters
Procaine
Chlorprocaine
Dibucaine is an
Amide local anesthetics
80% suppression with dibucaine
Normal
Dose of Lipid
1.5 mg/kg followed 0.25 ml/kg/min
Succinylcholine to vecuronium
Make sure you check twitches before giving NDNMB
No propofol in the
Context of cardiovascular instability
ECF Liter
14 L (1/3)
ICF Liter
28 L (2/3)
Other name for ICF
Cytosol and cytoplasm
Cell membrane has a
Phospholipid bilayer
What is the role of the phospholipid bilatery
prevent things from crossing
Cell membrane
50% proteins
50% of fatty acids.
For substance to cross you need
Channel
You need Amino acids to create
proteins
Amino acids are made from
DNA
Proteins 3 main functions
- receptor
- transporter
- enzymes
Receptor with 7 seven branches in and out of the cell
GPCR
Transporter receptor is a type of
bring products in an out depending on the concentration gradient
Major ions in extracellular and concentration
Sodium (135-145}
Chloride 98-108
Calcium (8-10.2)g/dL
Bicarbonate (22-27)
Major ions in INTRACELLULAR and level
K
135-150
All Major ions in INTRACELLULAR and level
K, Mag, and phosphate and PROTEINS
Phosphate INside is
100
Proteins levels inside the cell
65
Na+ inside the cell
10-15
Any ionized gets inside cell you get
Neurotransmitter release
BICARBONATE inside the cell is
18-22
K+ outside of cells level
3.5 - 5
Phosphate and Mag outside of the cell lvels
2 and 2
Protein outside of the cell level
16
Ficks law of diffusion
Concentration gradient
Size
thickness
Surface of the molecule
NA-K pump move Na+
Against concentration gradient, so OUT , 3 NA+
NA-K pump move K+
Against concentration gradient, soIN, 2 K+
ATP broken down to ADP
Releases a phosphate
Na-K ATPase uses
ENERGY
Calcium attaches to the
RECEPTOR*(which is a protein)
When calcium or ions attach to a receptor is.
A LIGAND-GATED ION CHANNEL._
Examples of ligand
Drugs, chemical , neurotransmitter, hormones
1st messenger is the
ligand
2nd messenger is the
GPCR
Signal transduction is
RELAY of message, (tweet , retweet).
G-Protein (i)
Inhibitory
G-Protein (s)
Stimulatory
Beta adrenergic agonist would be a
Stimulatory (Gs) (stimulates production of adenylate cyclase producing cAMP)
AcH binds to
Inhibitory muscarinic , prevent production of adenylate cyclase
2nd messengers are all
TISSUE SPECIFIC
Bronchial smooth muscle : Terbutaline”:
Ligand and first messenger
Terbutaline binds to
Beta -2 receptor, activate G protein
Enzymes are generally located on the
inside
Adenylate cyclase is an
Enzyme
Substrate is
ATP
The first messenger is where?
Outside the cell
The second messenger is where
inside
Cyclic AMP
active protein kinase (all kinase add a phosphate)
Calcium and bronchial
Bronchial constriction
ATP substrate create
Cyclic AMP
Signal transduction steps 1-6
- ligand
- activates recepot
- binds to protein
- Enzyme (adenylate cyclase)
- 2nd messenger cyclic AMP
- Physiological response
Nitric oxide is not a ____why?
LIGAND; Way to small travels in the body
Nitrous oxide is not a ligand but it is
STILL a 1st messenger
Nitrous oxide is still a first messenger because
It still sends a signal from outside to the inside of the cell
Nitric oxide inside the cell
Nitric oxide synthase (NOS) , convert the substrate GTP to cyclic GMP
cGMP works on
protein kinase G and we get physiological response–> BRONCHODILATION
Cyclic GMP PDE5
Cialis , viagra
PDE 3
milrinone
Sildenafil is
viagra which is a PDE5
Phospholipase C action
Phospholipase C remove the head of the phopholipids then it becomes IP3, cut head off.
IP3 acts on ER because calcium
2nd messenger
2nd messenger with IP3
2nd , second messenger is CALCIUM
Peripheral nervous system
Efferent NS (motor)
VEM mnemonic for
Ventral
Efferent (away central to peripheral)
MOTOR
Going in or towards
Afferent
The predominant neurotransmitter in the periphery is
AcH
Cell bodies –> Axons terminal then
Dendrites, Ganglion , organ
What is a ganglion?
Peripheral collection of nerve cell bodies
Neurotransmitters list
Ach Histamine Serotonin Glutamate GABA Etc..
Neurotransmitters list
Ach Histamine Dopamine Serotonin Glutamate GABA Epinephrine Norepinephrine Glycine
A-alpha most of the work done with what neurotransmitter
Ach
Dopamine neurons are called
Dopaminergic neurons
Autonomic divisions
Visceral : heart , gut ,stomach,
Long pre-ganglionic and short post ganglionic neurons
parasympathetics neurons
Short pre-ganglionic and Long post ganglionic neurons
Sympathetic neurons
All preganglionic neurons release
ACH
Release of NE are called
Adrenergic nerve
Preganglionic neurons act on adrenal medulla
ACH
Because NE is release into the adrenal medulla it is a
HORMONE
Muscarinic is a
GPCR
Muscarinic is a _____receptor
GPCR
All Adrenergic receptors are
GPCR
SAME for remembering afferent vs efferetn
Sensory –> Afferent
Motor- EFFERENT
To know where you are look for the
Ganglion (it is the posterior)
Where does the action potential start
Dendrites , send signal –> Dorsal root ganglion =–> goes to dorsal horn –> axon collaterals
Axon collaterals stay on the same
Side (ipsilateral pathWAYS)
90%
PSEUDOpolar
SAD to remember
SENSORY
AFFERENT
DORSAL
Dorsal horn has what ?
Bunch of layers called REXED LAMINAE
A-delta travel ? which lamina
Travel pass dorsal root ganglion, will synapse as fast as they can REXED LAMINAE I or REXED LAMINA V
How many rexed laminae
10 (I-X)
Fast and sharp pain fibers go up to the brain using
LATERAL SPINOTHALAMIC PATHWAYS
Slow and chronic pain travel using
VENTRAL spinothalamic pathways.
Lamina for slow and chronic pain
Lamina II and III
Slow and fast pain
Anterior and lateral pathway
C fibers
Slower burning throbbing pain pathway
Substantia Gelatinosa found in
Rexed lamina II and /or III
Neurotransmitter release from A delta is
GLUTAMATE which binds to AMPA and NMDA receptors on the receptors on the postsynaptic membrane
Neurotransmitter released from C fibers is
Substance P which binds to NK-1 neurokinin 1 receptors on the postsynaptic membrane.
Anterolateral system
Lateral spinothalamic tract
Ventral spinothalamic tract
Tracts looking lines are on the
DORSAL
SSEPs
Dorsalateral fasciculus
Slower pathway is the
Ventral Spinothalamic tract
Crude touch and pressure
Ventral spinothalamic (spinal to thalamic)
Where are pain impulses attenuated?
Susbstantia Gelatinosa
Pain in the body
Endorphins
Enkaphelins
Dynorphins
Opiods receptors
Mu-1
Mu-2
Kappa
Delta
**The predominant opioid receptor is
Mu-2
Mu-2 receptor action
Pain transmission/sensation is decreased
Mu-2 creates ____Analgesis
SPINAL
Supraspinal analgesia
you feel it but you dont care
Spinal analgesia
Mu-1
Spinal analgesia
Perception of pain is diminished
Opioids acts on the
Periventricular gray or Periaqueductal gray ,
Spinal analgesia results fromthe action of opioids in the
Substantia Gelatinosa or in the periventricular (after epidural or intrathecal administation) /periaqueductal gray (after IV admnistration )
Nuclei
Central bodies collection
Ganglia
Peripheral nerve bodies collection
Key term for Vd is
Theoretical volume
Elimination Half Life
TOTAL AMOUNT of the drug
Elimination half time
T 1/2 beta
Vd =
Quantity / plasma concentration (at time =0)
Large volume of distribution
Induction agent like propofol
Charged and ionized
Water soluble.
Drugs with small Vd
Muscle relaxants
MR are water soluble due to their
POLAR nature.
CHARGED NATURE>
Induction agents are
Lipid soluble because NONPOLAR and UNCHARGED NATURE
Neonates need more succinylcholine ____why?
MORE; IMMATURE NMJ
Neonates and NDNMA
Less , immature NMJ
Zero order kinetics aka
Michaelis Menses
Linear order kinetics
Linear (constant)
First order kinetics
LOG (constant FRACTION)
Most drug eliminated through
FIRST ORDER KINETICS
Distribution is
Alpha
Elimination is
B”e”ta
Contraindicated in patients receiving dandrolene therapy
CCBs
Weak acids and weak bases important concept
pKa
Weak bases LA when is pka/pH relevant
Patient is septic
If pH < Pka for WA
Nonionized
If pH > Pka for WA
Ionized
If pH < Pka for WB
Ionized
If pH > Pka for WB
Nonionized
Follow 3 steps for acids bases questions
- WA or WB
- Look at pKa
- pH of the target solution
Renal effects of nitrous oxide include:
decreased renal blood flow secondary to increased renal vascular resistance
Nitrous oxide appears to decrease renal blood flow by increasing renal vascular resistance. This results in
decreased glomerular filtration and decreased urine output.
Most drugs are
Neither weak acids or weak bases
Barbiturates are
Weak acids
Weak acids is an
molecule that give up hydrogen ions incompletely
HBarb examples of weak acids breakdown
[H+] + [Barb - ]
SA node location
Posterior Right atrium
Internodal pathway : Anterior
Bachmann RA to Left atriuj
Internodal pathway : Middle
Wenckeback tract
Internodal pathway: Posterior
Thorel tract
AV node located on
Floor of the right atrium , near tricuspid valve.
Triangle of Koch is in the
heart
AV node delay allows
Proper conduction of action potential
allow the heart to be synchronous
Right and Left bundle branches small branches called
Fascicle
Action potential sequence of propagation
SA node, AV node,s Bundle of HIs, R+L BB , purkinje fibers.
Nodal action vs ventricular myocytes action potential
No phase 1
No phase 2 in nodal
RMP for the nodal is (stable vs unstable)
Not stable
What ECG represents
Electrical activity
P wave
Atrial depolarization
QRS complex
Ventricular depolarization
U wave may represents
hypokalemia
RMP ventricular myocytes
-90 mV
RMP SA nodal cells
-70 mV
RMP is maintained by
Potassium Efflux (Leaky channels)
Depolarization is caused what ions
sodium influx
Ventricular myocytes Phase 0
Sodium influx
Ventricular myocytes Phase 1
Transient repolarization (Chloride influx) Inactivation of the fast sodium channels
Plateau phase is
Phase 2
PHase 2 of ventricular myocytes
Calcium L-types channels open , and calcium influx
Phase 3 of ventricular myocytes
Late/ delayed repolarization
Delayed rectifier potassium channels
Phase 4 of ventricular myoctyes
Back to RMP
Na-K pump only responsible for about
6 mV
Helps maintain and restore RMP
Na-K- ATPase
Ohm’s law states
Voltage = Current / Resistance
V = (voltage)
IR (current x resistance)
For nodal phase 4 , what channels are responsible to maintain
Funny sodium channels
What type of Calcium channels for nodal phase 0
T-type calcium channels (transient)
For phase 3 what is the channel working
L-type calcium channels
Delayed rectifier potassium efflux
With release of ACH, it binds to
muscarinic receptor M2
Excitatory M receptors are
M1, M3, M5
Inhibitory M receptors are
M2, M4
NE binds to
B1, GPCR
Transplanted heart: parasympathetic innervation
no parasympathetic innervation
SA node beating at
110 for transplanted heart because of a lack of parasympathetic stimulation .
Potassium leaky channel is a
2 port
Primary cause of negative charge is
Protein
Phase 2 also has a
conformational change to sodium channels, shuts the H-gates
The conformational changes that occurs to the sodium channels is responsible for the
Absolute Refractory period (plateau phase)
Repolarization phase 3 , the
Relative Refractory period (strong enough stimulus can cause an action potential).
SV will be determined
EDV- ESV
EDV is primarily determined by
Preload (volume)
Ejection fraction formula
EF = SV/ EDV x 100
EF =
EF = EDV- ESV/ EDV
Lusitropy meaning
myocardial relaxation
Preload is dependent on
Compliance
venous tone
Venous return
Blood volume
Extravascular volume determined by
Sodium
3 types of reflex
Baroreceptors
Bain bridge
Bezold -Jarisch
Angiotensinogen is made in the
LIVER
ACE is in the
lung
Precursor of angiotensin I
Angiotensinogen
Force at end diastole, right before contraction is
Preload
The more filling the more
Preload
Contractility is determined by the
CHEMICAL environment of the cardiac cell
Atrial kick
20-30%
Frank Starling mechanism
Increase preload
Decrease Venous return states all the hemodynamic changes
Decrease Preload Decrease filling Decrease EDV Decrease SV Sam
After fluids administration , what parameter is increased?
Increased preload
EDV increase
ESV unchanged.
When you give a loop diuretic, what parameter is increased?
Decreased preload
EDV increase
SV decrease
ESV unchanged.
Cardiac tamponade : filling
Decrease ability to fill the heart.
Afterload is associated with
pressure.
Can increase SVR
Alpha 1 agonist
If you increase afterload what happens to EDV, ESV, SV, BP and HR
EDV increase ESV increase SV decrease BP increase HR decrease due to reflex. (which reflex?)
What happens after you give nitroprusside?
EDV decrease ESV decrease SV increase BP decrease HR increase due to reflex. (Baroreceptor? )
After given a vasopressor, what happens to EDV, ESV, SV, BP and HR
Afterload increase
SV decreases
BP increase
Phosphodiesterase Inhibitors OR DIGITALIS administration: EDV, ESV, SV, BP and HR
Increase in contractility Decrease EDV Decrease ESV Increase SV BP increase HR decrease (BaroReflex) LV decrease
CHF what happens ?
EDV increased ESV increased SV decreased BP decrease and HR increase ( Baroreceptor reflex)
Bezold Jarisch in response to
(hypotension) Low HR
Concentric remodeling is associated with
Pressure overload. (AS)
Eccentric remodeling is associated with
Volume Overload
Wall stress / wall tension on questions think
LAPLACE’s law
Hypertrophic cardiomyopathy is associated with
LV outflow tract obstruction .
Hypertrophic cardiomyopathy is inherited in the
Autosomal dominant pattern
Most common cause CARDIAC death for young adults and peds
Hypertrophic cardiomyopathy
Hypertrophic cardiomyopathy is not a result of
HTN
CAD
Valvular disease
Pericardial disease.
Hypertrophic cardiomyopathy dysfunction
Asymmetrical septal hypertrophy (ASH)
Hypertrophic cardiomyopathy motion
Systolic anterior motion (SAM)
Dilated LA associated with
Atrial fibrillation
Hypertrophic cardiomyopathy may have atrium
LA enlargement
Management of patient with Hypertrophic cardiomyopathy: HR
Maintain HR, not slow not fast
Management of patient with Hypertrophic cardiomyopathy: RHYTHM
Keep it sinus
Regurgitant management FFF
Fast, Full, forward
Management of patient with Hypertrophic cardiomyopathy: Preload
Increase
Management of patient with Hypertrophic cardiomyopathy: Afterload
iNcrease, Pure vasoconstrictor is the 2nd line of defense for hypotension
***Management of patient with Hypertrophic cardiomyopathy: CONTRACTILITY you want
DECREASE
Blood going trough LVOT is , what effect?
Venturi effect
LVOT with Hypertrophic cardiomyopathy
Increased contract
Decrease preload
Decrease LV ventricular afterload (hypotension, vasodilation)
Do not give with Hypertrophic cardiomyopathy
Lasix, NTG, PEEP nitroprusside.
Medications to decrease contractility with Hypertrophic cardiomyopathy
Beta blockers
CCBs
OLD CATs PEE Alot
Obstruction
Contractility
Preload
After loading
Hypertrophic cardiomyopathy patient have this
AICD (if you disactivating you need the external defibrillator)
Venturi effects draws the anterior leaflet of the mitral valve out as blood rushes by whose principles is this
Bernoulli’s principle.
If the patient goes to a funny rhythm
Take the magnet off
Magnet put pacemaker mode
Asynchronous mode ;
Hypertrophic cardiomyopathy S/S (SAD)
Syncope
Angina
Dyspnea
Notched P waves
Atrial enlargment
Main.Goal intraoperative Hypertrophic cardiomyopathy
Prevent release of Catecholamines
Hypertrophic cardiomyopathy prevents
Stimulation that can cause an increase in the HR and sympathetic stimulation
No spinal or epidural with this condition
Hypertrophic cardiomyopathy
A line with Hypertrophic cardiomyopathy shows
Biferiens pulse
Vasopressor of choice for Hypertrophic cardiomyopathy
Phenylephrine
If they ask about a valvular lesion in doubt pick
Rheumatic fever
Severe Coronary artery disease
You want MORE TIME in diastole
Decrease HR
Most prominent end point of severe cardiac issue
PULMONARY EDEMA
Why fast HR with regurgitation?
Because diastole time you want lower for less regurgitation.
Can cause regurgiation
Aortic annulus dilation
Acute aortic regurgitation triad:
Severe dyspnea
Hypotension
weakness
Acute AR LV has not
Compensate
AR presents as
Sudden onset of pulmonary edema and HYPOTENSION
Aortic regurgitation minimal vs severe
When regurgitnat volume remains < 40% SV
But severe if it > 60% SV
Aortic regurgitation SPINAL and EPIDURAL
OK
Aortic regurgitation Best vasopressor
EPHEDRINE
RRRE
Regarding Regurgitation Reach Ephedrine.
PCWP estimation of LV
Indirect
Chronic MR is usually due to
Rheumatic fever
incompetent fever
Acute MR cause
Acute MI ,
Papillary muscle rupture
As much as ________% of the SV may be regurgitant with MR
50%
LV compensates in MR by
Dilating and increasing EDV
Filling to a greater volume emptying in the same
Frank Starling law
In MR End Systolic volume remains
normal but eventually increases as the disease process progresses.
In mild MR
regurgitant factors < 30 %
Valvular lesion of MR radiates to the
Axilla
In moderate MR
regurgitant factors 30-60 %
In severe MR
> 60%
Regurgitant disease is AR, and MR tolerates spinal or epidural
YES
AS ventricles gets thicker what happens
There is subendocardial ischemia.
Rhythm for AS wanted VERY IMPORTANT
NSR (b/c atrial kick)
From least to most invasive to restore
Meds
EP labs
Atrial ablation
Important to Aortic stenosis
NEED ATRIAL KICK (without it , 40% decrease in CO)
Aortic Stenosis and afterload
maintain normal
Aortic Stenosis and Contractility
Maintain
Most common valvular disease in the US
AS
Most common cause of AS
Calcification
Aortic valve is a (bi/tricuspid)
TRICUSPID VALVE
Normal size of Aortic Area
2.5 - 3.5 cm
Severe stenosis , and surface area
75 % of decrease surface area
Criticial AS
< 0.8 cm^2
Concentric hypertrophy its because trying to decrease
WALL TENSION (La place law)
La place law formula
(2 x Thickness x Tension)/Radius
Epidural vs spinal for AS
Epidural, raise level of LA
The higher the pressure gradient
The worst the patient
Mean transvalvular pressure gradient : mild to mod
Mild to moderate , < 20
Mean transvalvular pressure gradient : severe
20-50
Mean transvalvular pressure gradient critical
> 50
Peak transvalvular pressure gradient : mild to mod
< 36
Peak transvalvular pressure gradient severe
> 50
Peak transvalvular pressure gradient critical
> 80
Aortic valve area, Mild to mod
1 - 1.5
Aortic valve area, severe
0.8-1
Aortic valve area,critical
<0.8
Once angina from Aortic stenosis
Angina 5 years
Syncope 3 years
Dyspnea 2 years
RV failure
Cor pulmonale
The elimination half-time of a drug: related to clearance
is inversely proportional to the clearance
The elimination half-timeof a drug is proportional to the v
Volume of distribution
Delayed complication of rheumatic fever
mitral stenosis
Mitral normal size
4-6 cm
Most common cause of right side HR
Left side HF
ARDS
Aortic regurgitation Diastolic sternal border
MRSA
Mitral regurgitiaton systolic Apex
MSDA
Mitral stenosis Diastolic Apex
ASS ARCh
Aortic Stenosis systolic Aortic Arch
Anesthesia Risks: GREATER DETERMINANT of postop complication
co- morbidities are the best prediction
Surgical risk and outcome in patients 65 years and older primarily on 4 factors (APET)
Age
Patients status and coexisting
Emergency or elective
Type of procedure.
Can decrease incidence of VAP
Subglottic suctioning
Decline in organ function –>
1% decline per year in organ function after age 30 years . For example 70 year old has a 40% decline in general function
DNA/RNA changes
Change in DNA/RNA replication, decrease in function.
Elderly and thermoregulation
They shiver at 35C
Young adults and thermoregulation
They shiver at 36.1
Elderly and body fat
Increase body fat
Elderly and total body water
Decrease body fat.
Blood volume and Elderly
Decrease
Collagen and skin elasticity is
Decrease
Increase SVR in elderly cause
reduce arterial compliance
Circulation time and elderly
Reduced myocardial pump function leads to reduced CO which prolong circulation time.
Adrenergic receptors and elderly
A decrease in adrenergic receptor response.
Decrease all drugs doses EXCEPT : why?
Atropine and beta agonist (like isoproterenol) because of a decrease adrenergic response.
Increase risk of aspiration in elderly why?
Due to vocal cord stimulation being elevated.
Sensitivity of need to clear secretion in the elderly is
Decreased
FB close to carina , elderly response
Low stimulus to cough , more likely to aspirate
Work of breathing in elderly is _____why?
Because of skeletal calcification and increased airway increase the work of breathing, predisposes them to ACUTE POSTOP VENTILATORY FAILURE
What can put the elderly patient at risk for Acute postop ventilatory failure?
Increase WOB due to skeletal calcifications.
Chest wall compliance for the elderly patient?Pulmonary compliance?
Decrease: Increase
Respiratory changes in elderly mimics (obstructive/restricvie)
Restrictive
Most sensitive indicator for renal function in the elderly
CrCl
With decreased albumin
Give less
MAC decrease is reduced by
4-6% decade of age over 40 years
Summary box pg 507
507
Elderly and Decrease vascular volume anesthetic consequence
Results in high initial plasma concentration
Dose to stay the same for the elderly, 2 medications:
Neogstimine, Edrophonium
Elderly and Decrease protein binding anesthetic consequence
increase availability of free drug
Elderly and Increase body lipid storage sites
Prolonged action of lipid soluble drugs
Decrease renal and hepatic blood flow
Prolonged actions of drugs dependent on kidneys and liver for elimination
Pediatric larynx level
C2-C4
Adult larynx level
C3-C6
Narrowest function location for adult vs pediatric
Adult Vocal
Pediatric cricoid
Pediatric emergency know when it is a
Medical vs surgical emergency
V shaped epiglottis
Adult
Omega shaped epiglottis
Pediatric
ETT tube ID UNCUFFED
Age (years) / 4 + 4
ETT tube ID for CUFFED
Uncuffed minus 3.5
Defining hypotension in kids: at Term:
<60 mmHg
Defining hypotension in kids: 1- 12 months
<70 mmHg
Defining hypotension in kids:1-10 years
< 70 mmHg + (2x age in years)
Ducturs arteriorsus shunt is
RIGHT to LEFT
Syndrome think of –>
Craniofacial anomalies.
Greatest risk of apnea
<46-60 weeks
Diaphragmatic herniation highest occurrence on the
LEFT foramen of Bochdalek.
CHD you can cause a
CONTRALETERAL PNEUMOTHORAX (small underdeveloped lung)
First apgar in CHD
usually fine
Between first and 2nd apgar, what happens to the baby
transitioning from high PVR, low SVR to low pVR high SVR
CHD issues what preop information we need
ECHO, Heart disease, and conditions?
CHD abdomen
SCAPHOID ABDOMEN ,
BOWEL IN THE THORAX
CHD hallmark signs
Profound arterial hypoxia due to Right to left shunt
Barrel-shaped chest,
SEVERE RESTRATIONS
CHD treatment goal
Preductal saturation over 85% using peak inspiratory pressure below 25 cm H2O and allowing PCo2 to rise to 45-55 mmHg
CHD concern Respiratory
RIGHT SIDED PNEUMOTHORAX
Increase PVR 3 things:
Hypothermia
Hypoxia
Acidosis
Sings of TEF Feeding leads to
CCC
Choking
coughing
Cyanosis
Most common variation is the form that ends in a
BLIND
More likely for aspiration : TEF
TEF D
Less likely for aspiration TEF
TEF A
TEF is associated with what mnemonic
VACTERL Vertebral defect Anal atresia CArdiac anomalies TEF Esophageal atresia Renal dysplasia Limb anomalies
TEF anesthesia considerations: Key to successful anesthetic management
Correct positioning of the ETT
TEF and PPV
Avoid PPV which will distend the stomach, thereby increasing the risk for reflux and ventilatory compromise.
What should you avoid in a patient with TEF?
Avoid instrumentation of the esophagus.
What should you avoid in a patient with TEF?
Avoid instrumentation of the esophagus increase the risk for reflux and ventilatory compromise.
Describe the most common TEF
Noncommunicated blind pouch and a lower esophageal connection to the trachea
How do you suction a patient with pyloric stenosis
Suction supine, left decubitus, and right decubitus
CHD more at risk for pneumothorax
Lung is small can’t carry normal tidal volume.
Most common cause of acute airway obstruction in otherwise healthy kids
CROUP
With croup , what problem becomes evident and requires the patient to be intubated ?
Increase PaCO2.
Treatment croup
2.25% epi in 3 ml of NS 0.05 ml.kg up to 0.5 ml/kg repet 1-4
Edema of supraglottic structures (croup vs epiglottidis)
ACUTE EPIGLOTTIDIS
Inspiratory stridor associated with
Epiglottidis
Signs of Epiglottitis
Sitting forward and upright, , chin up, mouth open , drooling.
Epiglottitis what vaccine to prevent?
Hemophillus influenza type B
DO NOT ATTEMPT to do this with epiglottidis
Not attempt to visualize glottis
Tube size with Epiglottidis
1-3 mm smaller
Epiglottitis extubation usually
2-3 days
Epiglottidis extubation, readiness?
Do an AIR leak
Use Glidescope.
Pediatric fiberscope
Omphalocele covered?
Covered
Gastrochisisis covered?
Sausage (not covered)
Mortality Gastrochisis vs omphalocele
Mortalitiy related to cardiac and chromosomal abnormalities.
Worst combination.
Macroglossia and MICROGNATHIA
Survival omphalocele vs gastrochisis
Gastrochisis > 90 %
Omphalocele > 70-90
Pierre Robin and treacher collins syndrome Anesthesi
Intubation very difficult
use awake technique
Fully awake before extubation
Pierre Robin and treacher collins syndrome
ASD
VSD
PDA
Tetralogy of fallot.
Pierre Robin and treacher collins syndrome : glottis
ASSOCIATED WITH SUBGLOTTIC STENOSIS
Trisomy 21 most common issues.
Macroglossia and MICROGNATHIA
Trisomy 21 associated anomalies
CHD
SUBGLOTTIC STENOSIS
Right to left shunt you need to
NO AIR BUBBLES IN IV LINE
SHORT IV TUBING< WITH FEWEST CONNECTIONS>
Malignant Hyperthermia triggers
All VA (halogenated) and succinylcholine
Early MH signs
Masseter spasm
Tachypnea
Tachycardia
Early MH SYMPTOMS
Masseter spasm
Tachypnea
Tachycardia
Intermediate MH SYMPTOMS
CLASSIC MOTTLED CYANOSIS
EARLY SIGNS of MH
Increased ETCO2
Peaked t waves
Exhausted CO2
Not going back to baseline
CO2 increase with MH is
Abrupt and very high
Incidence of MH
1: 50,000
MH increase in temperature
Increase 1C every 5 minutes
MH is associated with increase
CO2
Leading cause of death with MH
Vib
Renal failure
DIC
Interventions:
Cooling pads
Dandrolene will cause
Diuresis because of the mannitol
Why do you need foley?
because dandrolene has mannitol
Ryanodex mixing vs Dandrolene
Dandrolene: 20 mg in 60 ml; 3000mg manniotr
Ryanodex: 250mg in 5 ml . 125 mg mannitol each vial
Testing for MH
Genetic
muscle biopsy: CAFFEINE (Caffeine Halothane contracutre test)
First step in coagulation is
Endothelial damage
Platelets: What promotes platelet adhesion
Von willebrand’s factor.
Platelet binds to von willebrands via
Glycoprotein Ib (GP Ib)
Problem with glycoprotein Ib
Platelet adhesion does not occur
Most common inherited coagulation defect.
Von willebrand’s disease
Type I von willebrand’ disease
insufficient amount of von willebrands production
Most common von willebrand’s type is
Type I
Increase in bleeding time with normal platelets and others
Von willebrand’s disease.
Standard treatment for von willebrand’s disease
DDVAP (work 80% of the cases) if doesn’t work CRYOPRECIPITATE
Platelet adhesion to VWF via GPIB now we need activation how?
Thrombin receptor –> located on the platelet, Precusor of thrombin is
Platelet adhesion to VWF via GPIB now we need activation how?
Thrombin receptor –> located on the platelet, Precusor of thrombin is prothrombin, activated by thrombin (activate self)
When platelet activated,
It changes shape, allows aggregation
Thromboxane A2 and ADP
Signaling molecules that are released by platelets.
Thromboxane A2 and ADP
Signaling molecules that are released by platelets,
Promotes Platelet aggregation
2 that promotes platelet aggregation
Thromboxane A2 and ADP
Thrombin role
thrombin activates self to promote more thrombin.
Platelet aggregation feedback loop.
Positive feedback loop
When platelet start aggregated , a platelet plug is formed, which is called
A white thrombus.
How does the platelet plug formed? what is used
Fibrinogen is used.
Prevent fibrinogen from sticking to platelets
Fibrinogen receptor GLYCOPROTEIN IIB/IIIa
Fibrinogen receptor GLYCOPROTEIN IIB/IIIa is capped to prevent fibrinogen from sticking to it, which can remove the cap
ADP and Thromboxane A2.
Most effective way to protect from coagulation
Intact endothelium
Once platelets activated,we use
Phospholipase A2
Phospholipase A2 (easy to remember)
Amputates leg (remove lipids)
Phospholipase A2 after legs removes turns into
Arachidonic Acid
The most common acquired blood clotting defect is due to
Inhibition of Cyclooxygenase production by ASA or NSAIDS.
Common antiplatelet
ASA
ASA is (reversible/irreversible)
Irrreversible for lifetime of the platelets.
NSAIDS recommendation no more than
5 days
3 antiplatelets other ASA or NSAIDS
Clopidogrel (Plavix)
Prasugrel (Effient)
Ticagrelor (Brillinta)
Dipyridamole (persantine) increase
cAMP in platelets
Dipyridamole (persantine) acts
by prevents aggregation of platelet via cyclic AMP (cAMP)
Antifibrinogen receptor drugs are
GIIb and IIIa
CAP and BLOCK fibrinogen receptor.
GIIb and IIIa drugs
Eptifibatide (intergrillin)
abciximab (Reopro)
Tirofiban (Aggrastat)
Stimulates creation of platelets
Thrombopoietin.
Tissue factor aka
Thromboplastin
Fibrin what do you use
Intrinsic
Extrinsic
Final common pathways
Fibrinogen to fibrin conversion done by
Thrombin
Fibrin stabilizing factor (Factor XIII)
Secure clots
Factor XIII bond is a
Covalent
Activates factors XIII to XIIIa
Thrombin
When in doubt think
Thombin for activation.
Thombin impacts
Itself (Factor II) Helps activate factor XIII Fibrinogen to fibrin Factor V Factor VIII Factor XI
Final common pathway factors
1, 2, 5, 10, 13.
Extrinsic pathway (extrinsic
3, 7
Intrinsic pathway
Cant buy for 12 but for 11.98
Glue
Fibrin
Activator
13
I
II
Activated C is an
anticoagulant
Activated protein S
stabilizes it.
Direct thrombin inhibitors
Dabigatran
Argatroban
Bivalirudin
Determinant of osmolality: Primarily
Sodium
Concentration is
Amount/ volume
Determinant of how much sodium we have
Aldosterone.
Hormone that deal with water
ADH (vasopressin) arginine vasopresor. (AVP
Volume determinant
ADH
Normal Osmolality
270-310
End products of metabolism is
Excreted
End products of metabolism is
Excreted by kidneys
OTher name for VITAMIN D
1,25 dihydroxycholecalciferol
Calcium is involved in homeostasis
Vitamin D3
Functional unit of nephron
nephron
Kidney location
retroperitoneal space
Nephron per kidney
about 1 Million
Lose how much of nephron
65% of nephron before needing therapy
Afferent arteriole
Toward the kidney
Efferent arteriole
away from the kidney
Efferent arteriole is associated
Peritubular capillaries
Vasa recta is responsible for the
Hyperosmotic concentration
Kidney receive CO
25%
Pressure in the kidney
HIGH PRESSURE 80 mmHg
Glomerular capillaries pressure is about
60 mmgh
High pressure in glomerular capillaries and low pressure of bowman’s capsule favor
Filtration
Fitration rate
125 ml/min then rest to efferent arteriole
Filtration amount
180 L/ day
Aldosterone acts on the
collecting duct
Aldosterone acts on the
collecting duct (think AC)
Reabsorbed most of the ions in
Proximal tubule
Proximal tubule absorption of
Mag, Chloride, water, Glucose
% of water absorbed in Proximal tubule
65%
Majority of ions absorbed where?
Proximal tubule.
Impermeable to sodium
Descending loop of Henle
Thick ascending loop of henle
Sodium , Potassium - 2Chloride pump
The juxtaglomerular apparatus
Juxtaglomerular apparatus
In tubules, structure that sense fluid, sodium concentration
Macula densa
Juxtaglomerular cells can communicate with
Macula densa
Renin leads to the production on
Aldosterone
Aldosterone role at the collecting tubule.
Sodium reabsorped
Potassium excretion
PTH deals with
Calcium, Mag and Phosphate
PTH acts on
Distal convoluted tubule.
From distal nephron
Distal nephron–>Cortical collecting ducts –>
Medullary nephron have
Aquaporin-2 channels.
Aquaporin-2 channels need this hormone to function
ADH
Aquaporin-2 helps with the
reabsorption of water
Medications for blood pressure : HCTZ works where in the nephron ?
Early part of the distal tubule
Loop diuretics work where do they work in nephron ?
Thick ASCENDING LOOP of HENLE
Potassium sparing where do they work in nephron?
LATE PART OF THE DISTAL TUBULE
Potassium sparing agents most common agent
Spironolactone
Carbonic anhydrase inhibitors work where in the nephron?
Proximal tubule
Osmotic diuretic(mannitol) work where in the nephron?
Proximal tubule or anywhere water is involved
Ventricular Myocytes
Leaky K+ RMP
-60MV set
Ca++ outside threshold
RMP move from -90mV to -100mv cell is
HYPERPOLARIZED (further from threshold potential)
Hyperpolarized K level
HypOkalemia
When cell is hyperpolarized distance further from
RMP
Hypokalemia cell is hyperpolarized, arrhythmia why
Reduction in potassium channel conduction, delay and increase in action potential duration. PURKINJE FIBERS MORE LIKELY TO FIRE> (Torsade, vtach)
Threshold potential set by ____at __mV
Calcium ; -60 mV
RMP becomes LESS negative (hypopolarized) what happens?
Due to HYPERkalemia
Excitability with HYPERKALEMIA
VERY HIGH because RMP is close to threshold
RMP close to threshold makes cell more
EXCITABLE (more likely for VFIB, Torsades)
When the RMP is move UP past threshold ____what happens
(-40 for example) RMP move over the threshold
Cardioplegia K level
15-40 K + mEq/L
Cardioplegia puts the cardiac cells
Put in Absolute Refractory period( cannot fire)
Threshold potential increase with
HyperCALCEMIA
RMP Increase and Threshold potential increase
HyperKALEMIA and HYPERCALCEMIA (after treatment of hyperkalemia)
Cells is hyperpolarized, calcium stabilizes, LESS EXCITABLE , it raises the threshold potential level.
RMP of nerve cell
normal at -70 mV
Decrease threshold potential of nerve cell
HYPOCALCEMIA
Hypocalcemia increases
Excitability
Acute hyperkalemia treatment FIRST
Calcium chloride (works in 1-2 min)
Acute hyperkalemia BICARB (work in how long)
Reduction in plasma concentration of K+ (3-5min)
Hyperventilation and acute hyperkalemia (work in how long)
15 minutes
Each 10 mmhg decrease in PaCo2 , serum K+
decrease 0.5 mEq
Loop diuretics for hyperkalemia how does in
Work on distal nephron to increase K+ excretion
Insulin, glucose and hyperkalemia
Acts on Na-K pump and drives potassium into the cells.
Administer B2 agonist for hyperkalemia does what
Stimulates the Na-K pump
The law of place states
For cylindrical shaped structures with an infinitely thin wall
Law of Laplace formula
T= wall tension, P = pressure of liquid R= radius
As structure expands, the radius _______, the tension in the wall of the structure ____. This law applies to
Increases; Increases; blood vessels and the left ventricle which also may be considered a cylinder.
The law of Laplace has two applications to alveoli
Normal alveoli and alveoli deficient in normal surfactan.
The smaller the radius of the bubble,
The greater the pressure inside of the bubble.
No normal surfactant what happens to wall tension?
wall tension becomes constant and independent of the radius
Smaller radius ____pressure
Higher pressure.
Smaller alveoli empties into the
LARGER ALVEOLI.
What causes atelectasis with ARDS?
Smaller alveoli empties into larger alveoli causing atelectasis.
Flow 2 types
laminar / turbulent
Flow is
Concentric ring of fluid.
Flow is __________ to the fourth power of the radius
Directly proportional
What has the most dramatic effect on floww?
Changing radius
Flow is ____________to the hydrostatic pressure gradient
Directly proportional
Flow and fluid viscosity
FLow is inversely proportional to fluid viscosity
Property of a fluid that largely determines flow when flow is Laminar is
VISCOSITY .
Trippling the radius increases flow to
81 times.
What is more difficult when flow is turbulent
Ventilating patients.
Resistance is _________to fluid viscosity
Directly proportional
The greater the blood viscosity the greater the
Resistance.
O2 dissociation curve x axis is
PO2
O2 dissociation curve y axis is
Hgb Saturation.
PaO2 clinical meaning of less than 60 mmhg
Hypoxemia
CADET MS RIGHT
Increased Co2 Acidosis 2,3 DPG Exercise Increase in temperature Maternal hemoglobin Sickle cell.
BOhr effect deals with
Unloading and loading to O2 from tissues
Bohr effect shifts curve to the
Rightt
IN pulmonary capillary , BOhr effect
CO2 moves up and the dissociation curve shifts to the left and facilitates loading of O2.
Total oxygen carrying capacity of the blood
(O2 Bound to hgb) + (O2 Dissolved in blood
How to find how much Hgb bound to O2
1.34 x 15g / hg x100 ml of blood X % O2
How to find O2 content that is DISSOLVED in blood?
0.003 x 90
The solubility coefficient of O2 is
0.003
The solubility coefficient of CO2
0.67
Gas inversely related to
Temperature
More gas will be given if patient is
Hypothermic , dissolves quicker/
How much (%) of CO2 is transported in blood as HCO3- (bicarb) in WHOLE BLOOD
90% (whole blood)
How much (%) of CO2 is transported in blood as HCO3- (bicarb) in WHOLE BLOOD
90% (whole blood) general accepted
Hydrate CO2 you get
Carbonic Acid (H2CO3)
CO+ H2O to get –
Carbonic acid
Enzyme that convert the reaction of CO2 + H2O to carbonic acid
Carbonic anhydrase.
Le Chatelier principle
Law of mass action
More reactant will facilitate more reaction as per the law of
Mass action
H2CO3 will lead to
HCO3 + H+
O2 unloading is favored by an _______in Co2
Increase
Major muscle for inspiration of
Diaphrgam
Diaphragm is a
Skeletal muscle.
Internal intercostal muscles from rib 1-7 help
INSPIRATION MOve ribs up and up
Internal intercostal muscles from Ribs 8-12 they are located in a way that they help with
EXPIRATION
VRG deal both with
Inspiration and expiration
Everything originates in the
DORSAL RESP GROUP
Everything originates in the
DORSAL RESP GROUP and goes to the DRG
DRG is the
Inspiratory pacemaker.
Apneustic Center + Pontine respiratory ROLE
Fine tune rate and depth of respiration
Pneumatix center now known as the
Pontine respiratory group
Pneumataxic center now known as the
Pontine respiratory group
Hering Bruer reflex
Lung distention , stretch receptors
Hering Bruer reflex more active in
Neonates.
By when do people have adult number of alveoli
By 2 years of age.
By when do people have adult number of alveoli
By 2 years of age. (though immature)
Aortic arch we have
We have chemoreceptors
Carotid bifurcation has
Peripheral chemoreceptors.
Aortic sends message via
VAGUS NERVE
Carotid send message via
GLOSSOPHARYNGEAL Nerve.
What drives NORMAL Ventilation
CO2
STRONGEST drive for ventilation
O2
PaO2 less than 60, hypoxemia
Chemoreceptors will kick in
When asked about dependent, vs nondependent.
Upright, normal TV quiet breathing
FRC range
2-3L
V/Q infinite
Extreme dead space
Obstrcutive SLEEP APnea
KNOW EVERYTHING
Obesity hyperventilation Syndrome
Know everything
Know reversal of opioid
narcan Dose and infusion
Know reversal of bnzo
Flumazenil Dose and infusion
OHS worst than
OSA
Alveoli are windows to the
Brain
Lipid solubility is related to
Potency
Pathophysiologic changes associated with metabolic alkalosis include: (Select 2)
hypokalemia, reduced tissue oxygen availability
Metabolic alkalosis is associated with
hypokalemia, ionized hypocalcemia, secondary ventricular arrhythmias, increased digoxin toxicity, and compensatory hypoventilation (hypercarbia).
Alkalemia may reduce tissue oxygen availability by
shifting the oxyhemoglobin dissociation curve to the left and by decreasing cardiac output.
The use of long-acting beta-2 agonists without the concomitant use of ______ is associated with fatal and near fatal asthma attacks.
Inhaled Corticosteroids
