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Notes from the 2010 FLCC Critical Care Transport Paramedic class as was recorded solely by Marcus LaBarbera- NYS
Paramedic. I do not apologize for any spelling or grammar errors, lack of completeness, or recording errors. These are
primarily personal notes but I am offering them to the community as an additional study resource. I will take no
responsibility for persons who fail any quiz or test as a result of this document. Always consult the text books
recommended specifically by UMBC for this course.
Day 2 CCEMTP
Class
TT airway in burns- now controversial from provider to provider
Cormack-Lehane scale
With King LT-D, suction well before insertion to decrease problems later
Passing bouge to transfer King to TT, may not work as well as company reports
Bougie as a stylette may facilitate faster intubation if it’s a known or potentially difficult airway
7- P’s:
Lidocaine is thought to decrease ICP but no good studies to prove either way
Peds: (up to 10yoa) dose 0.01mg/kg, if you give below 0.1mg/kg it may cause reflex
bradycardia because of enhanced vagal tone
Depolarizing gents:
Siccinocholine- beware previous history of muscular pathology (Guilian-baret, MS) malignant
Hyperthermia
30-5 min onset for paralysis
Wait for flaccidity before starting the procedure (test there jaw for relaxation)
People do better on a vent than on a manual BVM, rate is more consistent and volumes are
uniform.
Sedation:
Etomidate- singal dose for induction
Propofal- good for pt with steady or high B/P
Versed-
Fentanyl- analgesia and sedation and wares off fast
LAB VALUES
Make flash cards with lab data!
The body doesn’t do well with abrupt value changes (don’t drop a bg of 1200 to 90)
Blood samples that stay stagnant too long before analysis may self-metabolize and show high K
and low bg…
CBC
WBC- Leukocytosis:
Infection
Dehydration (hemo-concentration)
Trauma
Leukemia
Steroid
Inflammatory process
MI
Leukopenia:
Viral infections
Radiation
Immunosupression
Bonemaro depression
Eosinophils-
Lymphocytes 20-40%-
Vacutainer tubes:
Purple- EDTA
Green- Na Heparin
Blue- ??
“tiger top”- surum separator (with a “clot enhancer”)
Gray top- (ETOH test)
Yellow- cultures
Dark blue- heavy mettles
Red cell:
4.5-6.0 x10⁶
Hgb/ Hct
Anemia:
Blood loss
Liver disese
Malneutrition/ malabsorption
Menstration
Pregnancy
Hemolytic reaction
Polycythemia:
Seveer dehydration
Pulmonary disese
Altitude compensation
Renal malignancy
Platlet:
150-400 x103
\_HGB_/PLT
WBC/ HTC \
CPK- createnan phosphokynase (CKMB- for heart but also in other muscles)
Liver enzymes- TP, Alb, AST, ALT, GGTP, ALP, T –bil. D-bil
Pancreas- Amylase, Lipase (high suggests pancreatitis) ** may be on UMBC exam on what
organ system this
New tests:
BNP:CHF/ abnormal ventricular function
Glucose:
70-110
Power source, important for cellular respiration
Hyperglycemia:
DM
Pituitarry
Trauma
Hyperthyroidism
Acute stress
Brain trauma
K⁺ deficiency
Hypoglycemia:
Islet cell cancer
BUN:
8-20 mg/dl
A break down in bybroducts
Azothemia
Impaired renal function
Shock/ dehydration
GIB
Excessive protine intake/ catabolism
Creatinine:
0.5-1.2 mg/.dl
A good indicator of kidney function
(BUN/Creat, 24Hr creat. Clearance)
Electrolytes:
Must be in balance…
Sodium
135-145 mEq/L
Hyponat.
Usually results from too much water in the body
Malnutrition
Severe burns
Severe vomiting
Severe diarrhea
edema
HyperNa.
Dehydration
Diabetes insipidus (lack of ADH from the pituitary) where we can’t concentrate urine
Cussing’s disease
Treachobronchitis
Potassium:
3.5-5 mEq/L
Hypo K:
Loop diuretics
IV fluids without supliments
Malnutrition/ malabsorbtion
Hyper K:
Renal failure
Tissue damage
Chloride:
91-110 mmol/L
Hypo Chlo.
Vomit/ diarrhea
Ulcerative colitius
Burns
Acute infections
Fever
Hyper Chlo.
Na I Cl BUN/ GLU
K I CO2 I Creat\
Anion gap:
8-16 mEq
(Na +K)-(Cl+HCO3)
Inc. gap =metabolic acidosis
Urinalysis:
Spec gravity: 1.005-1.020 SG
pH 4.5-8.0
all other values should be neg. or trace
casts usually indicate some amount of kidney failure
COAG. Studies:
PT, PTT (heparin therapy)
INR
Guiac:
ABG:
pH is normal- (if you have acid/ base balance)
tells us about metabolic and respiratory status
PO₂:
80-100 mm/Hg
Measures effency of Oxygen thearpt
pCO₂:
35-45 mm/Hg
An acid, a waste product
A/A gradiant (usually the same as ETCO₂ but if there is a descrepance use ABG values)
36 ATP (Creb cycle)
Glucose+0₂=H₂O, …
HCO₃
19/25 mEq/L
pH:
7.35-7.45 (mean in 7.4
Acid Base system:
The big 3-
Buffer system: (many buffer but we wil stay on the Bicarb pair)
Respiratory: fast, works in minute
Renal: slow
--all 3 are required to maintain balance—
Metabolic acidosis:
(bicarb is less, CO₂ is normal)
Diarrhea
Renal failure
Metabolic alkalosis:
Partially compensated-
Day 3
Breathing management
C₆ H₁₂ O₆ + 6O₂ 6H₂O + 6 CO₂ + ~36ATP (Glucose met.)
Know Hilus structure- point of entry for airway, blood vessels, and lymph pathways
2 separate blood supplies to lungs, 1 for gas exchange, 1 for lung tissue perfusion
As long as there is a pressure gradient in the lungs respiration will continue to occurs- i.e.: hyper
ventilate … then stop and gas exchange will continue to occurs for a period of time.
Sputum:
Rusty- pneumococcal p.
As the blood becomes more acidic the hemoglobin has less affinity to hold Oxygen, (a shift of the curve
to the right of the scale).
ETCO2 is ~3mm less than that of a ABG sample taken at the same time
ETCO2 for a patient is a shock state may be inaccurate because of poor blood perfusion in relation to
ventilation (VQ)
Mechanical Vent
Inc in PEEP is also inc. FRC
Shouldn’t normally let the I:E get below 1:2 to 1:3 (inverse ratio therapy is sometimes used though)
(C= comlpliance)
(R= resistance)
(V*= flow)
PIP=Vt/C + (R x V*)
A TT ID reduction of 1mm = a resistance increase of 4 (i.e.: place the largest tube possible)
PIP x I/C= (compliance) (change compliance by augmenting the chest position and movement)
Plateau pressure (insp hold and read circuit pressure), this will give you the alveolar pressure*
Modes of ventilation:
4 basic modes:
CMV- (controlled mand. Vent
(Ve=Vt x RR)
SA node region I supplied usually by RCA (59%) but may be supplied by LCA or both (3%)
Different cardiac cells have a variation in Ca+ leakage into the cell which accounts for inherent rates in
different regions of the heart.
Contractile cells center around Na+ for depolarization (i.e.: sodium channel blockers)
Contraction of myocites centers around actin and myosin, Ca++ attaches to Troponin causing
contraction (i.e.: Calcium channel blockers)
Troponin I/ T-
Retevase pharmicodynamics
MCL1 question on final exam… (lead III and move (+) to V1 position)
Don’t use ventricular (or paced) rhythms for MI diagnosis
In RCA infarcts- common to see AV blocks 1°, 2°, 3° with junctional escape (less serious)
Ventricular aneurysm- diskenetic wall 2° to dead tissue and may show up on an ECG as persistent ST
elevation (usually in v1-v4)
BER- benign early repolarization, produces tall T waves and some ST elevation (seen in anterior and
lateral in males –esp black-, 20-40 years). (ST segment and J point makes a “fish hook” appearance) and
will gradually dissipate in prominence as you age
** Bifascicular block- start with RBBB (wide and upright in v1) with.. axis deviation (RAD or LAD)
This is important in if this is due to a LARGE infarct (and active MI) affecting both pathways, and may
destroy ALL ventricular pathways and lead to ventricular standstill.
PWMI (posterior wall MI)- apply v7, v8, v9 (if you suspect reciprocal changes in v1-v4)
RVI (Right ventricular infarct)- v3, v4, v5, v6.. or v4R (always suspect a right sided MI in the presence of
an inferior wall MI).
SA node region I supplied usually by RCA (59%) but may be supplied by LCA or both (3%)
Different cardiac cells have a variation in Ca+ leakage into the cell which accounts for inherent rates in
different regions of the heart.
Contractile cells center around Na+ for depolarization (i.e.: sodium channel blockers)
Contraction of myocites centers around actin and myosin, Ca++ attaches to Troponin causing
contraction (i.e.: Calcium channel blockers)
Troponin I/ T-
Retevase pharmicodynamics
In RCA infarcts- common to see AV blocks 1°, 2°, 3° with junctional escape (less serious)
Ventricular aneurysm- diskenetic wall 2° to dead tissue and may show up on an ECG as persistent ST
elevation (usually in v1-v4)
BER- benign early repolarization, produces tall T waves and some ST elevation (seen in anterior and
lateral in males –esp black-, 20-40 years). (ST segment and J point makes a “fish hook” appearance) and
will gradually dissipate in prominence as you age
** Bifascicular block- start with RBBB (wide and upright in v1) with.. axis deviation (RAD or LAD)
This is important in if this is due to a LARGE infarct (and active MI) affecting both pathways, and may
destroy ALL ventricular pathways and lead to ventricular standstill.
PWMI (posterior wall MI)- apply v7, v8, v9 (if you suspect reciprocal changes in v1-v4)
RVI (Right ventricular infarct)- v3, v4, v5, v6.. or v4R (always suspect a right sided MI in the presence of
an inferior wall MI).
90% of all nutrients are absorbed in the small intestine, 30 cm is minimum for survival. “Short gut
syndrome” is a consequence of shortened bowel.
Liver fractures occur along the 2 ligaments that transverse the organ
The liver is the only organ that we cannot live without but it is also the only organ that has some
regenerative ability.
Morphine causes spasm of the sphincter of Odi (do not give in the presence of a gall bladder attack)
Absent BS is no BS in all 4 quadrants, 5 min in each quadrant (document as hypoactive if a full exam is
not done)
C. Diff- prominent today because of concomitant use of antibiotics and PPI for upper GI maintenance
Paracentesis isn’t done a lot, it’s better to get the fluid back where it came from.
Deep peritoneal lavage- (DPL) now replaced by “fast exam”= ultrasound exam, though it may still be
used in the presence of no ultrasound available.
Endocsopic Retrograde Cholangiopancreatography (ERCO) diagnostic x-ray with dye for gall bladder but
may also exacerbate pancreatitis.
Stress-related erosive syndrome (SRES)- neurologic/ CNS disease responsible for GI “stress” ulcer
The portal vein supplies 1,500 mL/ min, which is important when considering acute vericeal bleed.
Usually acute bleeding doesn’t change the hematocrit since Hct is a percent of the volume.
Use caution when considering placement of a NG/OG tube when veracies are present
(UMBC- Contraindication to NG/OG tube)
TPN- glucose rich nutrient (10-20%), when changing TPN the pancreas needs time to correct its self.
Switch to D10 solution for transport if TPN is DC’d
Asterexis (liver flap)- patients with liver failure, a test- bring the hand back at the wrist and when you let
the wrist go the hand “flaps” (due to high ammonia levels).
Bilirubin- conjigated (direct bilirubin)- when it’s changed by the liver to a water soluable form
NYS law- NG/OG tube may be used for tube feeding for up to 24 hours only
Nasointestinal tubes- bypass the stomach (post pyloric sphincter) for prolonged feedings
During transport slow or stop tube feed so you reduce tube feed back-up and aspiration.
Indiana pouch- Illium/ scecum are turned into a urinary bladder and a tube is placed through the ostomy
for drainage.
Renal
Kidneys receive about 25% of cardiac output (1,200 mL/min)
Nephron units almost always run hypoxic/ ischemic and aly insult will push them over the edge.
Acute Tubular Necrosis (ACN)- death of tubulals, though they usually regenerate and recovery is possible
(the most common cause of renal failure-25%)
Common infection by Group A Beta hemolytic strep, pharengitis that isn’t treated properly
BUN Creatinine ratio usually 20:1 (normal) (ratio >30:1 indicates pre renal failure)
Some glucometers will not work if patients are on a achodextran base PD solution (unusually high
readings) though patient’s are well aware of this.
Continuous veno-venous hemofiltartion (CVVHD)- very slow rate of clearance used for patients sensitive
to hemodialysis (becoming more popular inside a facility)
CFR patients tend to be anemic because of the lack of erythropoietin from the kidneys
Bicarb
Kay-exalate treatment.
Diabetes insipidus (DI)- lacking ADH, water is removed redial but all electrolytes are retained, spec. grav
is close to 1 in these patients
Treatment: DDAVP (vasopressin) self admin via nasal spray
Remember to stop the bleeding head injury, esp. in the elderly. An uncontrolled head would may need
transfusion
SCALP mnemonic
The subdural spanning vessels shear as the brain sloshes (more so in patients that have atrophied
brains .. elderly, alcohol abuse…
Brain only runs on glucose, receives 15% of blood, 20% of cardiac output
CN III (ocular mvmnt/ pupilary response) lies just below the tentorium and is pressed and results in
measurable changes.
After changes in the CN III there wil be pressure on the hypothalamus which regulates temp, vomiting
** reticular activating system KEEPS YOU CONCIOUS, maintains the sleep/ wake cycle
3 major artery sets feed the brain, a stroke to one of these will that particular area
Middle cerebral art (MCA) is the most common site of a stroke, usually “embolic” because of the path of
least resistant.
The blood brain barrier- doe not allow flow of interstitial protines
Arachnoid granulations allow CSF to exit to outside the arachnoids layer, RBC’s in the fluid can block
these and cause increased ICP, (also common in meningitis)
**CPP= MAP-ICP
The term “concussion” has fallen out of favor and now use “injury”
Indirect injury (edema, blood, pressure) are worse than the direct injury many times
Subarachnoid hemorrhage (SAH)- thunderclap “worst headache” occurring communally in circle of Willis
Diffuse brain injury- stretching forces stretch and break axons causing diffuse axional injury
(“concussion”) usually due to rapid deceleration Sx- repeated questions, a little off)
Hippocampus is most sensitive to hypoxia (the brains RAM) no short term memory
Posturing is a result of pressure pushing on the nerve tracts that exit the pons and medulla (medulla-
decorticate, Pons- decerabrate)
Keep head at 20° to 30° to keep ICP lower and still maintain perfusion
A single episode of hypoxia doubles their mortality ! (1 episode of a SPO₂ less than 90%)
D5W- hypotonic and promotes free water shifting into the tissue
topical anesthetic spray- to minimize noxious stimuli which will reduce a rise in ICP
Lidocaine controversy currently during RSI (it may blunt a rise in ICP by decreasing the cough reflex)
Propofol- be ware hypotension, may want to check for bleeding else ware before starting propofol.
(urine will change green due to dilluant if your on long term or high dose but is otherwise …)
Succx- increasing eye pressure, MS, Myatetmia gravis, any diseases that affect ACH receptors, which
shift K⁺ out and with the increasing ACH receptors causes enough K⁺ to be at a dangerous level.
This is a relative contraindication, depending on the level of function; there is more of a problem as the
patient’s inactivity increases.
Phenytone is slowly being replaced with phos-phenytone because it uses a different dilluant and doesn’t
cause arrhythmias.
Steroids in head injuries are out of favor, though decadron is used for in the setting of brain tumors.
CN VII palsy, (facial nerve) may mimic CVA unable to wrinkle forehead=CN VII, able to winkle- central
(CVA)
Think Aortic dissection if there are unusual CVA type Sx, usually in younger patients
Blowout fractures causing trapping of the inferior rectus muscle (no upward gaze)
Transverse process spine injury can impinge corroded art. And needs to be evaluated
Spinal cord injury without radiographic abnormality (SCIWORA) usually kids <9 who have incre4ased
stretch in spinal cord so.. spinal injury .. good outcome usually
Remember older patients with osteoporosis in low speed MVC’s
Rectal nerves are centrally located and their for are usually last to loose tone
NEXUS study (NYS has taken the field clearing of C-spine from this study)
Remember to pad splints and backboards, pad in void spaces (small of back)
Dopamine in spinal cord injury for better perfusion in the spinal cord (to increase MAP)
Neuro Assessment
DTR- 0- +4 (+2 is normal) one of the first senses to be diminished in spinal cord trauma
ICP
Post traumatic hydrocephalis- arachnoid granulation is congested due to white or red blood cells,
correction by placing shunt
Codman external drainage system for measuring and maintaining CSF canula
(when moving or any time the device is not leveled close the stop cock)
Burn Management
SMH decreases rate 10% every hour they meet there fluid requirement (titration gradually)
Make sure you know who has rights to make medical decisions. Have guardianship documented in
writing if there are unusual custody situations.
Sinus arrhythmias in teens are normal (it should correlate with respirations)
Normal:
90+(2x the child’s age (in years)
Hypo
70+(2x the child’s age (in years)
*Do not draw off more than 5% of normal circulating blood volume in 24 hours
Towel support under shoulders to maintain airway position (up to 8-9 sometimes)
Infants are prone to bradying down during suctioning and airway maintenance
Remember propofol is in a soy base and may cross react with soy/ peanut
Push fentynal slowly (potential of “ridged chest” which will sustain for several minutes)
Murmur is not uncommon in peds because of a more lateral position of the heart with blood flow
towards the chest wall.
Diaper count may not be accurate with the high absorbent diapers and relatively high cost of diapers
Fencing reflex- turn the head toward one side and that side arm will extend
Hemangeoma seen in the beard section of the face you should consider additional hemangeomas in the
airway and be careful with intubation
Pain scales: Wong Baker faces, number 1-5, objective scoring.. overall it is difficult to get a good results
Obstetrical
CO increases 25-30%
HR increases 10-15% SV increases 10%
Plasma volume increases 50% (probably to prepare for the blood loss during delivery)
Art. pH increases
Pregnancy produces a hypercoagulable state
Nagel’s rule: First day of the last menses, subtract 3 months and add 7 days
20 weeks the top of the fundus should be at the umbilicus (<20 weeks the fetus is not likely to be viable)
Flight Physiology
Physiologic zone- 10,000 Ft., normally not a problem living in this zone
Dalton’s Law- all the parts equal the sum (Dalton Gang)
Henry’s Law- when you pop the top the CO2 comes out (Heiniken)
Hypoxia:
4 forms-
Hypoxic
Anemic
Stagnant
Hystotoxic
Anything that makes the cell more positive (or less neg.) stimulates a reaction
The more negative a cell is the more stimulation it takes to make the cell react
Antiarrhythmics:
Na= depolarization
K= repolarization
Na/K ATP-ase pump works to reset the cell to it’s original state
As cells are used they become more accustom to reaction (i.e.: tachycardia)
The longer the cell is at rest the more K can leak and the more stimulation is needed to cause a new
reaction
**Vaughn- Williams Classification
Ca Channel blockers- works best on pacemaker cells but also enhances conduction through the
accessory pathway responsible for WPW
Antimicrobials
PCN- bacterialcidal (punch holes in the bacterial cell wall), though now the cells start to make
penicilinase that changes the receptor sites making it less effective.
Bactariaostatic antibiotics- stop the bacteria cells from dividing to allow the patient’s own immune
system a chance to work (if the patient has one)
Macrolides (Z-pak)
Sulfa drugs- good for GI infections, poorly absorbed, stay in systems a long time, good for UTI
Has a tendency to cause Stevens Johnsons.
Quinalones/ Cipro- headache/ dizzy/ ataxia. Will stop cell division in children therefore not for use in
children.
NMB
It takes 2 acetylcholine into 2 receptors to open 1 channel
Depolarization- Succx.
Non-depolorizing- rest and stay at rest (longer to work and last longer)
** dose for Succinylcholine 1.5-2mg/kg (kids always get 2mg/kg because of faster metabolism)
Degenerative neuro diseases (due to increasing nicotinic receptors resulting in a prolonged uptake),
renal pt’s, burn patients
May cause Bradicardia/ tachycardia, always have atropine at hand pre-treat children and pt’s on Ca
Channel blockers
** vech/ Norcuron- a defasciculating (0.01mg dose) (1/10 th dose for pre treating)
Onset 3-5 min duration 15 min, doe not cause histamine release (no vasodilation)
**always give sedative first and paralytic second … except:: patients already in a rapid downward
decline give succx first and sedative right after so both onset at the same time.
Volume Expanders
Crystaloid:
NaCl/ LR
Colloids:
Protines- PPF/ Albumin
Or
Carbsp Hespan
Colloids exerts a low hydrostatic pressure (high oncottic pull) so it pulls extracellular fluid back in.
Altered permeability- colloids may leak and the other fluids go with them
Usual treatment.. start with a couple liters of crystalloid then colloid or blood
Albumin (plasma protine), ha a negative charge and redially binds with many drugs.
Considered salt-poor (vs old time “salt rich” which was used to preserve fluid in WW I)
Hetastarch:
(large glucose mol. And makes clotting increase, then after clotting factors are used up, DIC)
Increases serum amalase
Thrombolytics
ST elevation that is greater in aVR than in v1 = Left main disease
ASA acetalates the COX enzyme for the life of the thrombocite
Heparin- binds antithrombin III (AT III) and makes it 1,000x more potent and halts further thrombus
formation.
Glycoprotine IIb IIIa is the point that the glycoprotine attaches to via vonwillobrans factor
(Integrlin) … must do a creatatin clearance
Vasopressors
In shock,
treat by fix the rate
fill the bucket (look at their neck veins for distension)
Squeeze the bucket (pressors)
Fix the pump
** dose range is meaningless.. there is no max dose (of dopamine) (is it doing what it’s supposed to?).
the common side effect is tachycardia
Epi:
1mg-250/ 2mg 500
Levophed- (doesn’t have the effect on the lungs and increases SVR), good as a secondary agent in shock.
As a rule look at the first pressor the patient was on (usually dopamine) start there at cutting it back
Na Nitropruside- if given too fast it may drop the blood pressure so fast it will “suck the blood”
(coronary steel) out of the coronary art.
Metabolized to cyanide
Very UV reactive
If you do treat hypertension decrease by no more than 10%/ hr unless they have brain herniation
In treating HTN, treat pain first and see what it does to reduce the overall BP
Anyone with Cerebrial edema gets manitol (usually given with lasix)
Sedatives
Whatever they were on in the ICU is ¼ of what they will need in route
Versed if they’re on more than 24 hours the drug lasts up to a week.. unless they’re an alcoholic then no
dose is high enough
Examples:
Haloperidol
Great for hepatic encephalitis, (dopamine antagonist)
Benzos
Midazolam- longer onset, longer duration less side effects than valium
(plan to redoes q-15 min for continued sedation)
Diprivan
Versed
Fentynal
Ativan
Long acting (1-2mg)
Mixed in propylene glycol, kidneys die w glycol metabolism
Demerol lowers the seizure threshold, DO NOT USE IN CCT
Antianginals
Nitro IV:
Lo-sorb sets are not required but you will have to increase the dose and retitrate when the IV line is
changed again.
Cardio selective beta blockers aren’t cardioselective at doses normally seen in the ICU, they become
general beta blockers
Bronchodilators
Bata Agonists:
Also stimulate the heart
Theophyline:
Has a narrow therputic window, patient’s have been known to become toxic while in fever
Everything reacts to it
Mg:
Start at 2gms and titrate up
CN: X (Vagus) (a branch of the superior laryngeal) provides strong sensory innervations to the
larynx which may produce sympathetic stimulation.
The trachea is approximately 9-15 mm in diameter and approximately 12-15 cm long, not quite
cylindrical and contains 12-15 cartilaginous “C” shaped rings to maintain it’s structure
The trachea divides at the carina into the right and left mainstem bronchi and continue for 23
divisions and terminate at the alveolar ducts where gas exchange occurs.
There are 300 million alveoli that each make contact with a pulmonary capillary (the junction is
referred to as the alveolar capillary membrane (AC).
Normal pulmonary artery pressure is 25/10 (normal systemic pressure being 120/80)
VQ ratio is the ratio between blood flow and gas exchange, normal VQ ratio is 0.8 for the entire
lung. For every 4 L of gas (V), there must be 5 L of blood (Q).
Pediatric patients should have a towel placed under their shoulders to compensate for their
proportionally large Occiput. They are obligate nose breathers and their tongue is
proportionally larger.
The glottic opening is more cephalad and anterior and the epiglottis is larger and lies at a 45°
angle. Large adenoidal tissue especially in infants.
In the AC membrane
(in the capillary) the partial pressure of Oxygen (PO₂) is 40 mm/Hg and the partial pressure of
Carbon dioxide (PCO₂) is 45 mm/Hg
(in the alveolus) the (PO₂) is 100 mm/Hg and the (PCO₂) is 40 mm/Hg
Normal blood returning via the pulmonary vein contains a 100 mm/Hg of Oxygen and 40
mm/Hg of CO₂ (these are normal ABG values).
The patient can experience hypoxia even if PaO₂ and Oxygen saturations are normal.
Carbon monoxide has 240 times the affinity for hemoglobin as Oxygen does.
Resistance is the amount of force needed to move a gas or fluid through a tube
(Poiseuille’s Law: Viscosity, length of the tube, driving pressure and radius contribute to the
work required to move the fluid through the tube).
The normal drive to breath comes from the need to remove CO₂ from the blood.
CO₂ combines with water to produce carbonic acid which is then broken down to H⁺ and HCO₃.
As CO₂ increases so does H⁺ which causes the pH to fall. This change is transmitted through the
blood brain barrier and simulation of the respiratory centers occurs.
As a back-up there are chemoreceptors located in the Aortic arch and carotid arteries that
activate when they sense a PaO₂ less than 60 mm/Hg and stimulate increased breath rates.
The respiratory center is located in the brain stem which comprises the Medulla and Pons.
The diaphragm is innervated by the Phrenic nerve which exits the spinal column at the level of
C3 to C5.
Minute volume- the amount of air breathed in 1 minute (Respiratory rate x average V T)
Normal minute volume is 5-10 L/min.
Dead space (VD) is air not exchanged in the upper airway and is approximately 2mL/Kg
Shunt effect (Qt)- a condition where the airway is not able to participate in gas exchange
(i.e.: pneumonia). Normal Qt ranges are 3% to 5%, a range above 20% is critical.
Stagnant hypoxia- reduced cardiac output resulting in tissue hypoxia due to lack of circulation.
Examples: heart failure, shock, CPAP, increased G forces, PE
Hystotoxic hypoxia- when cells are unable to use Oxygen due to inactivation or destruction of
key enzymes.
Examples: Cyanide, Strychnine, and later stages of CO poisoning.
I:E ratio- normal is 1:2, 1:5 is seen in airway obstruction, 1:1 is seen in Tachypnea
LEMON pneumonic:
L- Look externally
E- Evaluate 3-3-2
3- Fingers Mouth Opening
3- Fingers Hypomental Distance between the tip of the jaw and the beginning of the neck
(under the chin)
2- Fingers between the thyroid notch and the floor of the mandible (top of the neck)
M- Mallampati classification
O- Obstruction
N- Neck mobility
Mallampati Classification:
Table of Contents
Skeletal muscle relaxants Pharmacodynamics
Spasticity Clinical Uses
Anti-spasmolytic drugs Depolarization Neuromuscular-
o Other clinical uses blockade
Drugs for acute local spasm Succinylcholine (Anectine)--
Neuromuscular-blocking agents adverse effects
Pharmacokinetics: Nondepolarizing blockers
Neuromuscular-blocking drugs Clinical Pharmacology
Introductory comments about Some neuromuscular-blocking
specific nondepolarizing agents drugs
Depolarizing neuromuscular-
blocking drugs
Spasmolytic agents
Spasticity-characteristics
o Increased in tonic stretch reflexes
o Increased flexor muscle spasm
o Muscle weakness
Clinical conditions associated with spasticity: Cerebral palsy, Multiple sclerosis,
Stroke
Clinical spasticity -- mechanisms:
o Reflex arc involvement
o Higher center involvement ("upper motor neuron disease") affects descending
pathways leading to alpha motoneurons hyperexcitability
Mechanisms of drug action {diminishing spasticity}
o Alteration in stretch reflex arc
o Attenuation of excitation-contraction coupling
Anti--Spasmolytic Drugs
botulinu
carisoprod
baclofen m toxin
ol (Soma,
(Lioresal) type A
Rela)
(Botox)
chlorzoxa
chlorphen cyclobenza
zone
esin prine
(Paraflex,
(Maolate) (Flexeril)
generic)
dantrolene
diazepam metaxalone
(Dantrium
(Valium) (Skelaxin)
)
Diazepam (Valium)
o Enhances CNS GABA inhibitory activity; active at most (all) GABAA synapses.
o Anti-spasmolytic effect in part due to action in the spinal cord {effective in
patients with cord transection}
o Tends to be sedating
Baclofen (Lioresal)
o Mechanism: GABA agonist at GABAB receptors
Receptor activation causes increased K+ conductance (hyperpolarization)
in the brain and spinal cord
Spinal cord effects probably occur following increased presynaptic
inhibition which reduces transmitter released by reducing calcium influx.
o Similar anti-spasticity compared to diazepam (Valium) but with less sedation
o Pharmacokinetics:
Orally active;well absorbed
half-life: 3-4 hours
o Adverse Effects:
drowsiness; increased seizure activity in patients with epilepsy
o Intrathecal Baclofen (Lioresal) use:
Management of severe spasticity/pain when nonresponsive to
medication by other routes of administration.
Few peripheral symptoms; higher concentrations may be used
Partial tolerance may develop
Major disadvantage: maintaining the integrity of the delivery
catheter.
Advantage: significant improvement of quality of life in some
patients
Tizanidine (Zanaflex)
o Overview
Tizanidine (Zanaflex) is related to clonidine (Catapres)
Enhances both pre-& postsynaptic inhibition in the spinal cord
o General anesthesia
o Neuromuscular blocking drugs
Clinical Presentations:
"The open and closed states of the Ca2+-release channel are shown side by side
in three different views: top, side and bottom. Important details are marked: the
clamp-shaped domain (C), the handle (H) which connects the clamp shaped
domain to the central part of the cytoplasmic side (CY) of the tetramer. The
putative transmembrane (TM) part of the assembly resembles the stem of the
mushroom-shaped protein. In the open-state reconstruction the transmembrane
region of the channel appears open towards the SR, whereas in the closed state
a central opening is not seen in this region. As is clearly visible in these images,
the clamp-shaped domains (C) are open in the open-state reconstruction
whereas the fingers of the clamps touch in the closed state
reconstruction." From Orlova, E. et al. Nature Structural Biology v3(6) 547-52.
1996.
Drugs for Acute Local Spasm
o Sedatives acting at the brain stem or spinal cord level include:
1. Carisoprodol (Soma, Rela)
2. Chlorphenesin (Maolate)
3. Chlorzoxazone (Paraflex,generic)
4. Cyclobenzaprine (Flexeril)-- not useful for muscle spasms secondary to
spinal cord injury or cerebral palsy; strong antimuscarinic and sedative
effects
5. Metaxalone (Skelaxin)
6. Methocarbamol (Robaxin)
7. Orphenadrine (Norflex)
Katzung, B.G.., Skeletal Muscle Relaxants, in Basic and Clinical Pharmacology, (Katzung, B.
G., ed) Appleton-Lange, 1998, pp 434-449;White, P. F. "Anesthesia Drug Manual", W.B.
Saunders Company, 1996
Chemistry/Structure
o NMJ blockers: Structural similarity to acetylcholine
Succinylcholine (Anectine) {depolarizing blocker, SCh} -- two linked
acetylcholine molecules
Nondepolarizing agents also contain a "double-acetylcholine" form;
however this form is hidden by ring systems-- e.g. pancuronium
(Pavulon)
Contains 1-2 quaternary nitrogens which result in limited lipid-solubility
{limited CNS penetration}
Major classes of nondepolarizing blocking drugs:
Isoquinoline
Isoquinoline derivatives
o Tubocurarine
o Atracurium (Tracrium)
o Doxacurium (Nuromax)
o Mivacurium (Mivacron)
Steroid derivatives -- e.g.
o Pancuronium (Pavulon)
o Vecuronium (Norcuron)
o Pipecuronium (Arduan)
o Rocuronium (Zemuron)
Isoquinoline derivatives
Duration of action
Drug Elimination mechanism
(minutes)
ester hydrolysis (enzymatic
Atracurium (Tracrium) 20-35
& nonenzymatic)
spontaneous (Hoffmann
Cisatracurium (Nimbex) 25-44
elimination)
Doxacurium (Nuromax) renal > 35
Metocurine (Metubine
renal (40%) > 35
Iodide)
plasma
Mivacurium (Mivacron) 10-20
pseudocholinesterase
Tubocurarine renal (40%) > 35
Steroid Derivatives
Drug Elimination mechanism Duration of action (minutes)
Pancuronium (Pavulon) renal (80%) > 35
Pipecuronium (Arduan) renal (60%) & hepatic > 35
Rocuronium (Zemuron) hepatic (75-90%) & renal 20-35
Cecuronium (Norcuron) hepatic (75-90%) & renal 20-35
*-- adapted from Table 27-1: Miller, R.D., Skeletal Muscle Relaxants, in Basic and Clinical
Pharmacology, (Katzung, B. G., ed) Appleton-Lange, 1998, p. 438
Rocuronium (Zemuron)
o Most rapid onset among nondepolarizing blockers
o A drug of choice for rapid-sequence anesthesia induction and intubation (when
succinylcholine is contraindicated or clinical circumstances suggest that it not be
used)
Atracurium (Tracrium) (isoquinoline derivative) -- similar characteristics as
vecuronium (Norcuron)
o Hoffman elimination inactivation {spontaneous breakdown}
o Atracurium (Tracrium) breakdown product --laudanosine may accumulate due
to very slow hepatic metabolism and upon crossing into the brain may
cause seizures
Seizures occur at laudanosine concentrations above that obtained
during surgical procedures; however long-term use of atracurium
(Tracrium) within the intensive care setting may result in concentration
sufficient to induce seizures
Cisatracurium (Nimbex) {atracurium (Tracrium) stereoisomer}
o Similar to atracurium (Tracrium), but less laudanosine formed and less
histamine released
Mivacurium (Mivacron): shortest duration of action among nondepolarizing agents
o Rapid clearance of isomer mixture by plasma cholinesterase
(pseudocholinesterase, i.e. butrylcholinesterase) activity
Prolonged duration of mivacurium (Mivacron) action in patients with
renal failure {renal failure is associated with reduced plasma
cholinesterase activity}
Depolarizing Neuromuscular Blocking Agents
Pharmacodynamics
More rapid laryngeal muscle onset is probably due to a more rapid drug
plasma: drug muscle equilibration
Reduced initial intensity of effect at laryngeal muscle (fast fibers)
follows from the requirement for more complete receptor blockade for
effect then for muscles mainly composed of slow fibers, e.g. adductor
pollicis.
o Neuromuscular diaphragm blockade:
Requires 2 times the dose required for adductor pollicis muscle blockade
Adductor pollicis monitoring: poor indicator of cricothyroid muscle
(laryngeal) relaxation
Facial nerve stimulation with orbicularis oculi muscle response monitoring
is a better reflection of neuromuscular diaphragm blockade onset
Orbicularis oculi muscle monitoring is preferable to monitoring adductor
pollicis as indicator of laryngeal muscle blockade
Adductor Pollicis
Cricothyroid Muscle
Cricothyroid Muscle: Vesalius Site, used with permission
(http://www.vesalius.com/graphics/archive/archtn_lar.asp)
Clinical Uses
Miller, R.D., Skeletal Muscle Relaxants, in Basic and Clinical Pharmacology, (Katzung, B. G.,
ed) Appleton-Lange, 1998, pp 434-449. Stoelting, R.K., "Neuromuscular-Blocking Drugs", in
Pharmacology and Physiology in Anesthetic Practice, Lippincott-Raven Publishers, 1999, pp
182-219. White, P. F. "Anesthesia Drug Manual", W.B. Saunders Company, 1996.
Succinylcholine (Anectine)
Time course:
o rapid onset (30-60 seconds) -- IV
o short duration of action: 3-5 minutes
Applications
o Skeletal muscle relaxation, facilitating intubation
Mechanism of Action:
o Succinylcholine (Anectine) binds to nicotinic cholinergic receptors
Promotes post synaptic membrane depolarization causing a relatively
long-term depolarization (compared acetylcholine) due to reduced
synaptic breakdown.
Blockade occurs because depolarized membrane is unresponsive to
subsequent acetylcholine-receptor interaction
Phases -- Phase I
o Depolarization component is the phase I blockade
o Prolonged phase I blockade may be associated with potassium transport (from
inside cell out): which may increase serum potassium by 0.5 mEq/L.
o Properties of phase I blockade:
Reduced amplitude; sustained response to continuous electrical
stimulation
Reduced contractile-response to single twitch stimulus
Enhanced neuromuscular-blockade following anticholinesterase drug
administration
Train-of-four (TOF) ratio of > 0.7 (the height of the 4th twitch to that of
the 1st twitch); a measure of presynaptic membrane effects. When the
single twitch height has recovered to about 100%, the train-of-four ratio is
about 70%.
No post-tetanic facilitation
Skeletal muscle fasciculations are associated with initial (onset)
succinylcholine (Anectine) action.
Phases -- Phase II
o Continued succinylcholine (Anectine) administration results in a transition
from endplate depolarization to endplate repolarization.
o However, this repolarization state is not susceptible to acetylcholine
depolarization provided succinylcholine (Anectine) remains present
Blockade, even following repolarization, has led to the description of
phase II block as "a desensitization blockade".
o Transition from a phase I to a phase II blockade may be rapid (following a
succinylcholine (Anectine) dose of 2-4 mg/kg IV)
Phase II onset: initial manifestation -- tachyphylaxis with need to increase
succinylcholine (Anectine) infusion rate or to administer larger doses
Various degrees of phase I & phase II blockade may coexist
Mainly phase I: -- anticholinesterases enhance neuromuscular-
blockade
Mainly phase II: --anticholinesterases antagonize phase II blockade
Small doses of edrophonium (Tensilon) (0.1-0.2 mg/kg, IV) may
be useful in discriminating phase I vs. phase II block
Time course/Duration of Action -- Succinylcholine (Anectine)
o Duration of action determined by plasma cholinesterase-mediated
succinylcholine (Anectine) hydrolysis
Plasma cholinesterase: hepatic enzyme
Initial succinylcholine (Anectine) metabolite: succinylmonocholine (very
weak neuromuscular-blocking)
o Plasma cholinesterase activity determines the amount of succinylcholine
(Anectine) reaching the endplate {most succinylcholine (Anectine) is
hydrolyzed by plasma enzyme}
o Factors influencing plasma cholinesterase (pseudocholinesterase) activity
Reduced hepatic enzyme synthesis
The presence of atypical (genetic) plasma cholinesterase which exhibits
reduced succinylcholine (Anectine) hydrolytic capacity
Liver disease (severe)
Drug effects, e.g. neostigmine (Prostigmin) -- a carbamylating
cholinesterase inhibitor
Drugs which may prolong succinylcholine (Anectine) action due to effects on
pseudocholinesterase:
o Insecticides
o Nitrogen mustard, cyclophosphamide (Cytoxan) -- plasma cholinesterase
inhibition
o Metoclopramide (Reglan) (10 mg IV)
o High estrogen levels (parturients)
Resistance to succinylcholine (Anectine)
Miller, R.D., Skeletal Muscle Relaxants, in Basic and Clinical Pharmacology, (Katzung, B. G.,
ed) Appleton-Lange, 1998, pp 434-449. Stoelting, R.K., "Neuromuscular-Blocking Drugs", in
Pharmacology and Physiology in Anesthetic Practice, Lippincott-Raven Publishers, 1999, pp
182-219 White, P. F. "Anesthesia Drug Manual", W.B. Saunders Company, 1996.
Miller, R.D., Skeletal Muscle Relaxants, in Basic and Clinical Pharmacology, (Katzung, B. G.,
ed) Appleton-Lange, 1998, pp 434-449; .Stoelting, R.K., "Neuromuscular-Blocking Drugs", in
Pharmacology and Physiology in Anesthetic Practice, Lippincott-Raven Publishers, 1999, pp
182-219; White, P. F. "Anesthesia Drug Manual", W.B. Saunders Company, 1996.
Table of Contents
Mechanism of action Diuretics
Cardiovascular effects Magnesium
Myopathy associated with critical Phenytoin (Dilantin)
illness Lithium
Factors altering patient responses Cyclosporine (Sandimmune,
to nondepolarizing drugs Neoral)
Interaction of nondepolarizing Ganglionic blocking drugs
neuromuscular agents with Hypothermia
anesthetics Burns
Differential effects based on
duration of action
Antibiotic effect on
neuromuscular-blockade
Local anesthetics:enhancement of
block by nondepolarizing agents
Antiarrhythmic drugs:
interaction with nondepolarizing
blockers
Drugs
ganglionic blocking aminoglycoside
diuretics magnesium
agents antibiotics
antiarrhythmic
local anesthetics volatile anesthetics lithium
agents
Phenytoin (Dilantin):
o Patients chronically treated with phenytoin (Dilantin) are resistant to
neuromuscular-blockade produced by nondepolarizing agents
o Mechanism: pharmacodynamic {higher neuromuscular blocker-plasma
concentration are required to produce a given level blockade in patients treated
with phenytoin (Dilantin) than to produce same level of blockade in untreated
patients}
Lithium: (used to treat bipolar disorder) -- possible enhanced neuromuscular-blockade
by both depolarizing & nondepolarizing drugs
Cyclosporine (Sandimmune, Neoral) -- possible prolongation of neuromuscular-
blockade by nondepolarizing drugs
Ganglionic blocking drugs (e.g., mecamylamine (Inversine)) may affect duration of
neuromuscular-blockade by:
o Reduced skeletal muscle blood flow
o Plasma cholinesterase in addition
o Reduced post-junctional, nicotinic cholinergic receptor sensitivity
Hypothermia:
o Increased neuromuscular-blockade duration (pancuronium (Pavulon) &
vecuronium (Norcuron))
Mechanism: decreased hepatic inactivating enzyme activity (temperature
dependency); decreased biliary & renal drug clearance
o Increased neuromuscular junctional sensitivity to pancuronium
o Increased duration of atracurium (Tracrium) action {also reduces infusion rate
necessary to maintain stable neuromuscular-blockade}
Atracurium (Tracrium) effect: probably caused by decreased rate of
Hoffmann elimination & reduced ester hydrolysis
Burns:
o Prolonged resistance to nondepolarizing neuromuscular blockers
Starts about 10 days following injury
Peaks about 40 days later
Declines after about two months {may last considerably longer > one-
year}
o Mechanism: -- probably pharmacodynamic {higher plasma drug
concentration required to cause a given extent of twitch suppression
compared to similar extent in non--burn patients}
Clinical Pharmacology
Role of neuromuscular blockade in anesthesia.
o Dose guidelines:
Facilitation of tracheal intubation -- 2 x ED95 dose of nondepolarizing
muscle relaxant
Laryngospasm: effectively treated with succinylcholine (Anectine)
Optimal intraoperative conditions -- 95% single twitch response
suppression
o Neuromuscular-blocking drugs: -- no CNS depression; no analgesia therefore they
do not substitute for anesthetic agents
o Other clinical uses:
in managing patients requiring mechanical ventilation (intensive care
environment)
Adult respiratory distress syndrome
Tetanus
Suppression of spontaneous respiration
Doxacurium (Nuromax)
o Overview: Doxacurium (Nuromax)
Nondepolarizing agents; ED95 -- 30 ug/kg
Time to onset: 4-6 minutes
Duration of action: about 60-90 minutes
Renal clearance (similar to pancuronium (Pavulon))
Extended duration in elderly patients
No histamine release; no cardiovascular effects
o Drug interactions:
Volatile anesthetics
Reduce doxacurium (Nuromax) dose requirements by 20%-40%
compared to blocking doses for nitrous oxide-fentanyl (Sublimaze)
anesthesia
Pancuronium (Pavulon)
o Overview: pancuronium (Pavulon)
Commonly used long-acting nondepolarizing agent
Low-cost advantage
Cardiovascular side effects {doxacurium (Nuromax) & pipecuronium
(Arduan) -- similar to pancuronium (Pavulon) but without cardiovascular
side effects}
Pancuronium (Pavulon) and related agents have replaced older, long-
acting nondepolarizing drugs such as:
tubocurarine
metocurine (Metubine Iodide)
gallamine (Flaxedil)
No enhancement of histamine release
No autonomic ganglia blockade
o General properties: pancuronium (Pavulon)
nondepolarizing agent: ED95 = 70 ug/kg
onset: 3-5 minutes
duration: 60-90 minutes
Pancuronium (Pavulon) block enhanced by respiratory acidosis which
opposes neostigmine (Prostigmin) antagonism
o Pharmacokinetics: pancuronium (Pavulon)
Renal excretion: 80% of dose excreted unchanged
Renal dysfunction: pancuronium (Pavulon) clearance may decrease by
33%-50%
Hepatic metabolism (10%-40%)-with at least one potent metabolite
Pancuronium (Pavulon) elimination halftime: affected by hepatic
cirrhosis/total biliary obstruction
Aging: decreased pancuronium (Pavulon) plasma clearance
Mechanism: -- probably reduced renal function
o Cardiovascular Effects: pancuronium (Pavulon)
Slight increase (10%-15%):
Heart rate
Mean arterial pressure
Cardiac output
Mechanism:
Atropine-like effect on cardiac, muscarinic cholinergic receptors
Sympathetic, autonomic nervous system activation
Adverse Effects:
Increased incidence of cardiac arrhythmias following pancuronium
(Pavulon) (but not succinylcholine (Anectine)) in patients treated
chronically with digitalis glycosides
Increased cardiac arrhythmias may occur due to enhanced
sympathetic nervous system activity
Pipecuronium (Arduan)
o Overview: pipecuronium (Arduan)
nondepolarizing neuromuscular for; ED95 -- 50-60 ug/kg
time to onset: 3-5 minutes
duration of action: 60-90 minutes
Enhanced potency increased/duration of action shortened in infants
{relative to adults or children}
No histamine release; no cardiovascular changes associate with
pipecuronium (Arduan) administration
o Pharmacokinetics:
similar to pancuronium (Pavulon) in terms of renal clearance
Hepatic cirrhosis -- no effect on pipecuronium (Arduan)
pharmacodynamics/ pharmacokinetics
Atricurium (Tracrium)
o Overview:atracurium (Tracrium)
Nondepolarizing, neuromuscular blocker (multiple isomers)
ED95: 0.2 mg/kg
Time to onset: 3-5 minutes
Duration of action: about 20-35 minutes
Site of action:
Presynaptic & postsynaptic membrane nicotinic receptors
Degradation: spontaneous, in vivo (Hofmann elimination)
More stable in acid pH (storage --pH 3.25-3.65)
Should not mix atracurium (Tracrium) with alkaline drugs
(e.g. barbiturates) or expose to solutions of more alkaline
pH
alkaline pH: accelerated breakdown
o Clearance-- two mechanisms
Hofmann elimination -- nonenzymatic; accounts for one-third of the
degradation
Hydrolysis catalyzed by plasma esterases (nonspecific, i.e. not plasma
cholinesterase); accounts for about two-thirds of degraded atracurium
(Tracrium)
Clearance not dependent on hepatic or renal function
Clearance not affected in patients with atypical cholinesterase
o Laudanosine -- major metabolite of both catabolic atracurium (Tracrium)
pathways
CNS stimulant --even with long, continues atracurium (Tracrium)
infusions in the surgical setting--laudanosine concentrations remain below
those apparently required for cardiovascular/CNS action; in the ICU
setting with longer durations seizure potential becomes much more likely
o Cumulative effects
No significant cumulative effect due to rapid clearance from plasma
(hydrolysis + Hofmann elimination)
o Cardiovascular Effects:
With these background anesthetics: nitrous oxide, fentanyl (Sublimaze),
halothane (Fluothane), isoflurane (Forane)
no BP/heart rate change associated with rapid IV atracurium
(Tracrium) up to (2 X ED95)
With nitrous oxide-fentanyl (Sublimaze) anesthesia, IV atracurium
(Tracrium) (3 X ED95): slight increase in heart rate (8%); decreased in
mean arterial pressure (20%)
Cardiovascular effects: transitory (< 5 minutes)
Facial/truncal flushing may be due to histamine release (no
circulatory effects if patients are pretreated with H1/H2 receptor
blockers)
H1/H2 receptors may be activated by prostacyclin (not histamine)
o Special Patient Populations
Pediatric patients
Similar atracurium (Tracrium) doses in adults and children (2-16
years old) when doses are calculated using mg/m2 rather than on a
mg/kg basis.
Infants -- 1-6 months: require about 50% of the atracurium
(Tracrium) dose given to older children
continuous infusion rate (to maintain steady-state
blockade): 25% less during the first month of life
Elderly patients
Increasing age: no effect on atracurium (Tracrium) continuous
infusion rate required for constant degree of neuromuscular-
blockade
Mechanism -- age independence of Hofmann elimination &
plasma ester hydrolysis inactivation processes
{renal/hepatic state independent}
Cisatracurium (Nimbex)
o Overview: cisatracurium (Nimbex)
nondepolarizing neuromuscular blocker
ED95: 50 ug/kg
Time to onset: 3-5 minutes
Duration of action: 25-30 minutes
Similar pharmacological profile to atracurium (Tracrium) compared
atracurium (Tracrium)
Cisatracurium (Nimbex)(Tracrium) onset slightly slower
Cisatracurium (Nimbex) much less likely to cause histamine
release, compared atracurium (Tracrium)
Spontaneous neuromuscular blockade recovery not affected by
prolonged infusion (80 hr) to patients requiring ventilation in the
intensive care environment-- by contrast to vecuronium (Norcuron)
Recovery: accelerated by the use of anticholinesterase agents
o Clearance: cisatracurium (Nimbex)
Hofmann elimination (77% cisatracurium (Nimbex) clearance)
16%: renal
Neuromuscular-blockade characteristics not affected by hepatic or renal
dysfunction
Cisatracurium (Nimbex) pharmacokinetics: not appreciably affected by
advanced age (slight delay in time to onset)
o Cardiovascular Effects: cisatracurium (Nimbex)
No histamine-releasing effects (by contrast yo atracurium (Tracrium))
Large doses (8 X ED95, IV) do not typically induce cardiovascular changes
Less change in cerebral hemodynamics compared to equal potent
atracurium (Tracrium) dosage
Vecuronium (Norcuron)
o Overview: vecuronium (Norcuron)
Nondepolarizing neuromuscular blocker
ED95: 50 ug/kg
Time to onset: 3-5 minutes
Duration of action: 20-35 minutes
Structurally resembles pancuronium (Pavulon) -- vecuronium (Norcuron)
reduced anti-vagal properties compared to pancuronium (Pavulon)
Unstable in solution; supplied as lyophilized powder
o Clearance
Overview
hepatic metabolism & renal excretion
metabolites generally much less active than vecuronium
(Norcuron)
More lipid-soluble compared pancuronium (Pavulon) -- promotes
biliary excretion & significant hepatic uptake
Rapid hepatic uptake may be responsible for short duration of
action
Reduced renal function
Vecuronium (Norcuron) action prolonged in patients with renal
failure -- increased concentration of metabolites also contribute to
prolonged skeletal muscle paralysis following long-term
vecuronium (Norcuron) infusion
Reduced liver function
When used in patients with hepatic cirrhosis, vecuronium
(Norcuron) at 0.2 mg/kg IV, longer duration of action (longer
elimination halftime); not observed that the 0.1 mg/kg IV dose
level
In patients with cholestasis, undergoing biliary surgical
procedures: vecuronium (Norcuron) duration of action is increased
(at the 0.2 mg/kg IV dosage)
o Cardiovascular Effects
Minimal even at 3 X ED95, with rapid IV administration
No vagolytic action
apparently no/minimal histamine release
possible vagotonic vecuronium (Norcuron) effect if administered nearly
concurrently with potent opioids (e.g. sufentanil (Sufenta))
vagotonic action may be serious -- promoting sinus nodal exit
block & cardiac arrest
o Use in pediatric patients
Vecuronium (Norcuron) potency {during nitrous oxide-halothane
(Fluothane) anesthesia}: similar in --
infants (7-45 weeks)
children (1-8 years)
adults (18-38 years)
Onset of action: more rapid in infants compared to adults; (infants have
high cardiac output -- promoting rapid onset)
Duration of action: longest in infants; shortest in children-- (infants have
less/immature enzyme systems -- increased volume of distribution)
o Use in Elderly patients
With increased age: decreased continuous infusion rate required to
maintain a given level of block
Mechanism:
Age-related hepatic blood flow decrease;
Age-related decreased renal blood flow;
Age-related reduced hepatic microsomal enzyme system
activity (possibly)
With increased age: prolonged recovery time if vecuronium (Norcuron)
was administered by continuous infusion (recovery from individual IV
doses of vecuronium (Norcuron): not age sensitive)
o Use in Obstetric patients
Clinically significant fetal effects not observed with nondepolarizing
neuromuscular-blocking drugs.
Vecuronium (Norcuron) clearance: increased during late pregnancy;
possibly due to enhance microsomal enzyme activity {by progesterone}
Vecuronium (Norcuron)-induced neuromuscular blockade: prolonged
immediately postpartum
o Obesity:
Vecuronium (Norcuron) duration of action (but not atracurium
(Tracrium)) prolonged in obese (> 130% of ideal body weight) compared
with nonobese adults
o Malignant Hyperthermia
Not associated with vecuronium (Norcuron) or atracurium (Tracrium)
administration in animal models
In a patient susceptible to malignant hyperthermia and therefore
pretreated with dantrolene (Dantrium): duration of vecuronium
(Norcuron) action prolonged
Mechanism: Dantrolene (Dantrium) may prolonged action of
neuromuscular-blocking agents secondary to dantrolene
(Dantrium)-mediated impairment of presynaptic calcium release
Rocuronium (Zemuron)
o Overview: rocuronium (Zemuron)
Nondepolarizing agent; ED95 -- 0.3 mg/kg
Time to onset: 1-2 minutes
Duration of action: 20-35 minutes
reduced potency (relative to vecuronium (Norcuron)) probably responsible
for relatively rapid onset [lower potency requires higher dose {more
molecules administered} -- more molecules increased the likelihood of
initial blockade]
o Time to onset: Clinical implications --
Time to onset of maximal single twitch depression (following 3-4 X
ED95): similar to time to onset for succinylcholine (Anectine) (when
mg/kg, IV)
Rocuronium (Zemuron): only nondepolarizing agent which may
substitute for succinylcholine (Anectine) when:
Succinylcholine (Anectine) is contradicted
Rapid onset is required to promote tracheal intubation
Differences between rocuronium (Zemuron) & succinylcholine
(Anectine)
Laryngeal muscles more resistant to rocuronium
(Zemuron) than adductor pollicis: large dose rocuronium
(Zemuron) effects resemble succinylcholine (Anectine) at
adductor pollicis but will be delayed relative to
succinylcholine (Anectine) effects at laryngeal adductors.
o Duration of action:
Similar to other intermediate-acting agents-- at normal doses
With large dose rocuronium (Zemuron) --3-4 X ED95-- to achieve onset
rates similar to succinylcholine (Anectine)-- duration is prolonged (more
similar to long-acting nondepolarizing drugs, e.g. pancuronium (Pavulon))
Large IM doses (rocuronium (Zemuron)) -- 1-8 mg/kg given to
infants/children to support rapid tracheal intubation results in relatively
long durations (sixty minutes) -- This long duration may limit clinical
utility.
o Effects on muscle groups
Laryngeal adductor muscles and diaphragm: more resistant to rocuronium
(Zemuron) than adductor pollicis muscles
Therefore, complete single twitch response suppression of adductor
pollicis is not sufficient to ensure paralysis of laryngeal muscles and
diaphragm.
Maximal paralysis of laryngeal muscles may not be recognized if
suppression of adductor pollicis single twitch response is being
monitored as the clinical sign for optimal conditions supporting
intubation.
Direct laryngoscopy for intubation performed at peak laryngeal
muscle paralysis may result in abdominal muscle/diaphragmatic
motion when the tracheal tube is positioned -- because the
diaphragm and abdominal muscles are not yet fully paralyzed:
This condition is undesirable especially in those cases
when pulmonary aspiration gastric contents is considered a
risk.
o Pharmacokinetics -- Clearance:
Rocuronium (Zemuron)
-- up to 50% excreted in the bile {animal studies}
-- > 30% renal excretion (in 24 hours)
Liver disease: possible increased drug effect duration due to increased
volume of distribution
Elderly patients:
similar time to onset (compared to young adults)
prolonged duration (compared to young adults)
o Cardiovascular Effects --
No histamine released (as with other non-polarizing agents)
Small anti-vagal effect -- may be useful in certain surgical procedures
which cause vagal stimulation (e.g. opthalmological, laproscopic
procedures)
Bradycardia (reflex) may occur with atracurium (Tracrium) or
vecuronium (Norcuron) in patients undergoing these procedures
Review Class
[ - will be on the test]
Propofol will be on test
Inflate at the dicrotic notch and deflate just prior to the next systole (the end of the R wave)
Not Bad: Late inflation and early deflation (may be used safely if you have an eratic
rhythm)
normal CO = 4-6
Invasive lines:
Components: transducer, flush system (300mmHg), stop cock, central line
PACING:
V-O-O (pacing without sensing or inhibiting)
V-V-I (vent. Paced, vent sensed, a spike inhibits the next pace)
IABP:
Rupture
Platelet damage
Misplacement (high=CVA Sx – occludes Left breachial cephalic, Left..)
(Low, decreased renal output, decreased GI motility, abdominal pain)
Remember to keep the arterial lines safe and patent, don’t forget patient safety
When pregnant females get dehydrated they release ADH (but it pitosin is also released along with it out
of default)
20mg/kg is a pediatric fluid bolus (trauma, vomiting, etc.) kids can usually handle excess fluids well
Magnesium given IV causes decreased DTR (Mg toxicity may hinder diaphragm movement)
CVP= Preload
Treatment of hyper K:
Pretreat with calcium (to stabilize cardiac membraine)
Bicarb
Insulin R/ Glucose
Albuterol
Dialysis
Kay-exelate (potassium binder that acts in the gut)= GI will become mobile!
ABG values:
CBC
Na, K, Cl, Creat.
ABG
Shock:
Distributive (septic, anaphylactic, Neurogenic)
Obstructive
Cardiogenic
Neurogenic shock- lack of sympathetic tone, fix with a pressor (epi, neo, dopamine, levophed)
Colloids- large particles, used to draw fluid into vascular space (albumin, blood) (is manitol???)
Breathing management:
High PEEP may decrease preload via compressing the venicava, correct this by increasing fluid if you cant
lower PEEP
Chest tubes:
Water seal unit: 3 sections, collection, water seal, suction (water column/ 20 mm, H₂O) (add water to
increase suction... in older units)
If chest tube is pulled out, seal the site, monitor for Pneumothorax
If water seal is broken during transport, place the tube in a bottle of saline
Suctioning:
Is a sterile technique
RSI:
Prepare- (meds drawn up, 2 ETT, back-up tube, 10cc syringe on the tube), make sure the suction works
Airway assessment
Preoxygenate- NRB 1-2 min, BVM with Oxygen (cautiously)
Premedicate- atropine, lidocaine, sedative (ketamine, atomadate, propofol, fentynal)
Paralytic- succinicoline 1-2mg/kg, (2mg in kids) (the only depolorizing paralytic, onset 30 sec,
duration 5 min). (increases free Potassium, patient with neuromuscular diseases may have a
lower uptake in the neurons, may have paralysis up to days), contraindication burns and crush
injuries, malignant hyperthermia (Dantraline is a treatment for..), increased interoccular
pressure
Pass the tube and confirm
Post intubation care- analgesia and sedation
study the big medications, study the classes (classs I Na Channel blockers, II Beta, III Potassiun, IV Ca, V
nucleoside- Adenocard) (the periodic table- Na, Boron, K, Ca, …)
Trebutuline, Ketamine (ketamine is only listed in the pediatric section)
ICP monitoring:
0-15 is normal range
MAP-ICP=CPP (CPP should be >70)
Monro-Kellei doctrine- if the patient has a inter-ventricular catheter you can decrease the 10% of fluid,
but there is a high risk of infection
Axis to level the cranial catheter is the tragus of the ear
ICP Waves: (remember this is seen in trending over time, hours)
A waves- high with a plateu, sustaining with >60 mm/Hg, seen in brain herniation
B waves- sharp pulsations,up to 50mm/Hg high pressure increases, poor compensation
B waves need to be treated before this point optimally.
C waves- rhythmic, small amplitude, 4-8/min, clinically insignificant
Neuro assessment- the key is to continuously recheck, DTR (graded 0-4, 2 is normal)
Pupilary assessment-
Vital signs-
Inline position of the neck may decrease drainage and flow of CSF (C-Collar)
To manage ICP:
Oxygen
Sedation (will lower ICP)
Manitol (crystallizes very easy, use filtered needle)
levophed for sepsis, dopamine is never the first answer for CC transports
TEST: