Professional Documents
Culture Documents
Sensory:
X internal laryngeal nerve ABOVE vocal cords
X recurrent laryngeal nerve below vocal cords
Sniffing position:
Pharyngeal and laryngeal axis parallel
Oral axis at 30 degree relative to these 2
IJ Vein
Lies between 2 heads of SCM (superior to clavicle, lateral to carotid
artery)
Interlaminar foramen
Lumbar level: at the level of interspace
Thoracic: 1-3 cm cephalad to the interspace
Innervation of the UE
Median nerve: C5-C7 (lateral cord) + C8-T1 (medial cord)
o Travels medial to brachial artery
o Sensation to palmar surface of thumb, index/middle fingers,
lateral of 4th finger, small distal portions of dorsal surface of
thumb/middle/index
o Motor to abductor pollicis brevis, opponens pollicis, 1-2 lumb
Local anesthetic toxicity by site:
Intercostal > caudal > epidural > brachial plexus > sciatic
M5 Cardiac Phys 4/29/2016 7:09:00 PM
Pathologic splitting:
due to increased RV volume
o R L ASD or pulm stenosis
CVP waveform
a wave:
o end diastole
o atrial contraction
c wave
o early systole
o isovolumic ventricular contraction, TV moving toward RA
x descent
o mid systole
o atrial relaxation
v wave
o late systole
o systolic filling of atrium
y descent
o early diastole
o early ventricular filling
Coronary distribution
LCX: V5-V6, aVL (perpendicular to left lateral wall)
LAD: V1-V4, V5-V6
RCA (inferior MI)
o II, III, aVF
5 ways to Increase coronary perfusion
Increase aortic diastolic pressure
o Con: afterload, LV wall tension and O2 consumption
Decrease LVEDP
HR
Decreasing contractility
Dilating coronary arteries
ANTI-ARRHYTHMICS:
Amiodarone: Class III antiarrhythmic K-blocking agent
Delay phase 3 repolarization
Also has some Class Ia, II and IV effects
AV nodal blocking agent
Large Vd (requires bolus + drip)
o 150 mg bolus (over 15 min)
o Drip: 1mg/min over 6 hours
Side Effects:
o Pulm fibrosis
Restrictive lung disease ( DLCO)
o Hypothyroidism
o Transaminitis and jaundice
o Peripheral neuropathies
CI is maximized at HR of 90
SV is greatest at HR 60
Vasovagal reflex
Stimulus from mesenteric retraction or distention leading to vagal
afferents, sending signal to brainstem and then the brainstem (nucleus
tractus solitarii) sending out vagal efferents w/ resultant bradycardia,
hypotension, apnea
Baroreceptor reflex
blood pressure will lead to firing of action potentials from
barorecptors in carotid sinus
Afferent signal carried by: Hering nerve (glossopharyngeal)
Net effect: inhibition of sympathetic activity, parasympathetic
outflow, HR, contractility, vascular tone
Alpha-mediated vasoconstriction:
Alpha-1: Gq receptor phospholipase C activated
o PLC IP3 formation. IP3 allows calcium release from SR into
cytosol
Phenylephrine alpha-1 receptor PLC IP3 Ca release from SR
contraction
Starling Equation
Q = kA * [(Pc Pi) + (i c)]
o Q = net filtration
o K = capillary coefficient of water
o = reflection coefficient (of albumin)
o Pc = capillary hydrostatic
o Pi = interstitial hydrostatic
o i = interstitial colloid osmotic pressure
o c = colloid osmotic pressure
SVR= afterload
Arterial impedence to ejection of blood
Afterload = Vaso-elastic properites of aorta + arteriolar tone +
density/viscosity of blood + returning pulse waves in blood
SVR is only the arteriolar tone
Diastolic dysfunction
Higher LVEDP
Pulm edema
a/w concentric hypertrophy (from high pressures)
E to A ratio < 0.8 (E less than A)
o Doppler pattern across mitral valve demonstrates characteristic
patterns of early diastolic flow (E) and peak atrial flow (A)
A wave larger than E wave only consistent w/
impaired relaxation
Acute MI 2/2 PDA occlusion, left-dominant coronary circ -- > Q waves in
lead III
Right ventricle is perfused in diastole/systole (b/c RV systolic pressures are
less than aortic diastolic pressure)
Endocardium is more likely to suffer ischemia
presenting w/ ST depressions
V-fib
Chest compressions
Defibrillation at 360 J monophasic or 200 biphasic
Unstable A-fib
Cardioversion with biphasic 120 J
SVT
6 mg adenosine then 12 mg (twice) then cardioversion
Mitral Regurgitation
Diagnosis via Echo:
o Regurgitant jet > 2/3 length of left atrium
o Regurgitant stroke volume > 65 cc
o Pulmonary vein flow reversal during systole
Results in eccentric hypertrophy due to volume overload
Goal of management:
o regurgitant SV, favor forward flow
o Afterload reduction!
o High HR (80-100) is goal
Low HR. diastolic timecan further distort annulus
Pressor Choice
o Neo: may worsen by SVR and HR
o Levophed: although modest in HR, primarily alpha-1
o Esmolol: HR regurtitant fraction
CARDIO-PULMONARY BYPASS
Benefits of Off-pump bypass:
Decreased pulm infections
incidence of A-fib
less inotrope use
fewer blood transfusions
Digitalis Toxicity:
PVC (bigeminy MC), Salvador Dali mustache sign on ECG
AV nodal block
Anorexia/nausea
Exacerbated by:
o Hypokalemia
o Hypomag
o Hypoxia
o Hypercalcemia
BETA-BLOCKERS
1) Beta-1 Receptor: Myocardium
STIMULATION: HR, contractility, conduction velocity & CARDIAC
OUTPUT
2) Beta-2 Receptor: Skeletal/coronary arteries, bronchioles, uterus, kidneys,
liver
STIMLATION: Vasodilation, bronchodilation, uterine relaxation, renin
secretion, glycogenolysis, gluconeogenesis
BB w/ ISA
Penbutolol
Pindolol
Acebutolol (beta-1)
WPW
Short PR int, wide QRS, delta wave
Accessory pathway (bundle of Kent)
AVNRT: most common tachydysrhythmia
o DOC: Procainamide or amio
Avoid drugs that slow conduction thorugh AV node
o CCB, BB, dig, adenosine
Antiplatelet drugs:
ASA: Cox inhibitor
Dipyridamole: adenosine reuptake inhibitor
Plavix: ADP receptor inhibitor
Ticlodipine: ADP receptor inhibitor
Abciximab: GIIb/IIIA inhibitor
HOCM goals:
Preload: Full
Afterload:
Contractility: , avoid inotropes
Rate: Normal
Rhythm: sinus, atrial pacing if required
Effects of Insulin
protein synthesis
Glut-4 transporter (translocation to cell surface
Glycogenesis
glycogen destruction
gluconeogenesis
activity of Na/K/ATPasewhich decreases serum K
Insulin Receptor:
Tyrosine kinase receptor
o Adds phosphate to tyrosine residues of proteins
Downstream signaling
o Activation of protein kinase B
o PIP 2 PIP3
(no cAMP involved directlybut cAMP does insulin secretion)
What cAMP?
Beta agonism
Phosphodiesterase inhibitors inhibit cAMP breakdown
Insulin:
SQ:
o Onset: 15 min
o Peak: 1-2 hr
o Duration: 4-6 hrs
IV
o Onset: 1 min
o Duration: 1 hour
NPH:
o Onset: 2-4 hrs
o Peak 4-10 hrs
o Duration: 18 hr
Glargine:
o Onset: 2-4 hour
o Duration: 24 hrs
1 unit of insulin should glucose 25 points (goal glucose < 180)
Hyperthyroidism
Avoid Ketamine, ephedrine, pancuronium
Esmolol gtt often used for hemodynamics
o Also helps conversion of T4 to T3
Goiter = awake FOB
Pre-op: Tx w/ K iodide & propranolol
Hypothyroid
Heart: CO, HR, SV
Lungs: pleural effusions -- restriction
Post-op hypoparathyroidism
calcium
presents 6-12 hrs post-op
Cushing Syndrome
Due to primary tumor in adrenal gland, ACTH secretion
Pituitary = DISEASE
Tumors = ectopic ACTH syndrome
Results in:
o Insulin resistance/hyperglycemia
o Hypertension 2/2 hypervolemia
o Osteoporosis
o Hypokalemic alkalosis
o sensitivity to muscle relaxants
o difficult intubation 2/2 obesity/swelling
o
Supplemental steroids:
Normal production: 300 mg cortisol/day when max stressed out (20mg
on normal day)
Pheochromocytoma
Most are solitary tumors on 1 adrenal glad (right side)
o 5% MEN IIA (medullary carcinoma of thyroid, parathyroid
hyperplasia) or IIB (medullary carcinoma of thyroid)
alpha-blocker: 10-14 days before surgery
o phenoxybenzamine: long-acting (24-48 hrs), noncompetitive
presynaptic (alpha 2) and postsynaptic (alpha 1) blocker
o Doxazosin-selective alpha1 blocker
Drugs to avoid
o Ephedrine/ketamine
o Drugs w/ vagolytic activity
Pancuronium
o Histamine releasing drugs
Morphine, Meperidine, reglan, glucagon, naloxone
Ligation of adrenal vein hypotension as it removes the
catecholamines
Carcinoid Syndrome
Release vasoactive substances (serotonin, kallikrein, histamine) which
lead to hypotension/bronchospasm
S/Sx:
o Flushing/diarrhea
o Some have bronchospasm
o Tricuspid regurg
Chronic effects
o Fibrotic patches on right heart
o Tricuspid regurgitation/pulm stenosis
Anesthetic management
o Avoid catecholamine surges
o Avoid hypotension
o Avoid histamine releasing drugs
Morphine/meperiddine
o Octreotide gtt may release of carcinoid mediators
o
Anaphylactoid vs anaphylaxis
Both result in mast cell release of histamine, tryptase, proteoglycans
Anaphylaxis IgE mediated
Tx:
o Volume
o Epinephrine
o H1/H2 blockers
o Steroids
o Refractory to all medsadd glucagon if on beta blocker
Rheumatoid Arthritis
Atlanto-axial instability: 25%
Pericarditis, endocarditis, valvulitis and LVH w/ diastolic dysfunction
Vasculitits, MI, conduction block, stroke
O2 cylinder:
625 L
2200 psi
Critical temp: -119C
US color: White
Nitrous oxide
1590 L
745 psi
Critical temp 36 (above RTbelow this temp exists as liquid)
Safety:
Pin index safety system (PISS): E&H cylinders
Wall connections: Diameter index system (DISS)
Color coding
OXYGEN ELECTRODES
Clark Electrode: polar-graphic electrode
Amount of current correlates to concentration of O2
Consumable parts
Needs frequently calibrated (electrode gels are consumed)
Anode: silver
Cathode: platinum or gold
Paramagnetic Device
no consumable parts
faster response time
self-calibrating
more expensive
Anode: Lead
Cathode: silver or gold
Capnography:
http://www.capnography.com/new/index.php?option=com_content&vie
w=article&id=99&Itemid=61/
Electrical Safety
Line Isolation Monitors (LIMS): measures the amount of current that
could flow if a second short circuit should develop and sounds the
alarm if current exceeds 2mA or 5mA
Microshock: 10-100 microampere
Vent Check
A: Prolonged Phase II, II, increased angle, and steeper phase III suggest
bronchospasm or airway obstruction.
D, Capnogram with normal phase II but with increased slope of phase III.
This capnogram is observed in pregnant subjects under general anesthesia
(normal physiologic variant and details in reference 9).
F: Rebreathing EtCO2
G: Esophageal intubation
H: Spontaneously breathing
I: Dual capnogram after lung transplant. First peak from new lung, second
peak from native lung.
J: MH
K: Ripple effect during expiratory pause w/ cardiogenic oscillation
L: Sudden raise in baseline and ETCO2 due to contamination of sensor or
water vapor.
M: Intermittent mechanical ventiatlion w/ spontaneous breathing.
N: CPR
O: Rebreathing during inspiration. Normal in Mapleson D or Bain
(rebreathing circuits)
EEG findings:
Deep sleep: low frequency delta waves, increased amplitude
Spectra Edge = method of processing complex raw EEG data into simple
term, which is the frequency at which 95% of the power exists below.
SSEPs:
Peripheral nerve--> dorsal column--> sensory cortex
Meds w/ little effect: Opioids, ketamine, etomidate, droperidol
Look at Miller Table 38-9
Etomidate can latency and amplitude
Sensitivity to volatiles from least to most: BAEPs > SSEPSs> MEPS >
VEPS
Neuro 4/29/2016 7:09:00 PM
Nitrous:
CMRO2
CBF
cerebral vasodilation
Halo/Iso/Sevo/Des
CMRO2
CBF if > 1 MAC
Cerebral vasodilation
PaCO2 20-80:
CBF 1-1.5cc x 100g/brain wt/min for each 1 mmHg in PaCO2D
CBV 0.05 cc x 100g/brain wt/min for each 1 mmHg in PaCO2
Spinocerebellar Tract
Cerebral blood flow & CMRO2
Inhaled anesthetics: cause uncoupling & CBF
o Halothane the most
CBF: Propofol/etomidate/thiopental
EEG
Delta rhythm (03 Hz) Deep sleep, deep anesthesia, or pathologic
states (e.g., brain tumors, hypoxia, metabolic encephalopathy)
Theta rhythm (47 Hz) Sleep and anesthesia in adults, hyperventilation
in awake children and young adults
Alpha rhythm (813 Hz) Resting, awake adult with eyes closed;
predominantly seen in occipital leads
Beta rhythm (>13 Hz) Mental activity, light anesthesia
Treating VAE:
Stop more air entrapment
o Flood field w/ fluid
o Bone wax etc
o Compress IJ vein
Aspirate
Turn off Nitrous
Cardia support
SSEP path
Dorsal column
Brain stem
Medial lemniscus
Internal capsule
Contralateral somatosensory cortex
Normal VS:
Preterm: HR 160, SBP 50, DBP 30, RR 50
Term: HR 130, SBP 60, DBP 40, RR 50
1 YR: HR 120, SBP 80, DBP 60, RR 25
Toddler: HR 90, SBP 100, DBP 60, RR 20
Blood Volumes:
Newborn: 90 cc/kg
Infant: 75 cc/kg
Toddler: 70 cc/kg
ABG:
Birth: pH 7.2, paO2 50, paCO2 50
1 wk after birth: pH 7.4, paO2 70, paCO2 35
Toddler: pH 7.4, paO2 95, paCO2 40
Fetal circulation: placenta --> vein --> heart --> arterial --> placenta
F-Hb (fetal hemoglobin) --> affinity for oxygen. Unable to bind 2,3 DPG
P50 = 19 (adult = 27)
FRC = point at which outward elastic recoil of chest matches inward recoil of
lung (at end-expiration)
Both decreased in neonates
FRC
PRIS:
Inhibits proteins that allow transfer to FA into mitochondriamito are
starved of energy
Lactic acidosis..necrosis
Retinopathy of prematurity:
Pathophysiology: retinal artery constrictionproliferation of abnormal
vesselts resulting in scar/hemorrhage and retinal detachment
Risk factors:
o O2
o Genetic: sex/Caucasian
Chemical pneumonitis
Pulm edema
Hypoxia
Pulmonary hypertension
ACLS FOR NEONATE:
Hypoxia w/o bradycardia--> supplemental O2
HR < 100 --> ppv
HR < 60--> Chest compressions at 120min but FIRSTmask ventilation
Chest compression:ventilation ratio = 90:30 (3:1)
o Adults = 3:2
Epinephrine:
o Tracheal epi: 10 x the IV dose 0.1mg/kg
o IV: 0.01-0.03 (ALWAYS USE 1:10,000 for IV)
APGAR
Appearance
Pulse
Grimace
Activity
Respiration
Tetralogy of Fallot
Most common CHD
4 features:
o VSD
o RVH
o Over-riding aorta
o Right ventricular outflow tract obstruction
ECG: RAD, RVH
CXR: pul vascular markings, rt aortic arch
Tet spell: hypercyanotic attack, peak 2-6 mo (feeing, crying,
defecating)
o SVR = hypoxemia
Tx: O2, chest-knee position, morphine
o Anesthetized pt: SVR = Lft to right shunt (Neo, BB, fluids)
Hemodynamic goals:
o preload
o Slow sinus rhythm
o contractility
o SVR
o PVR
ANESTHESIA:
o No spinal! Early epidural is goodmay PVR
Down Syndrome:
CHD
ASD
Upper Airway Obstruction/Sleep Apnea
Hypothyroidism
NPO guidelines
Clears: 2 hrs
Breast milk: 4 hours
Infant formula: 6 hours
Solids/non-human milk: 6-8 hrs
o
Platelet Function:
Adhesion:
GP 1b: vWF bound to collagen in exposed endothelium binds to GP 1b
Activation
Plt changes shape, exposing GP IIb/IIIa and degranulation of plt
Granules release thromboxane A1 and platelet activating factor which leads to
aggregation and vasoconstriction
Aggregation
GP IIb/IIIa BINDS TO FIBRINOGEN
Intrinsic Pathway (PTT/ACT): 12--> 11 --> 9 --> 8 --> 10 --> 5--> 2-->1
Haemophilia A
Factor 8 deficiency, X-linked coagulopathy
50% activity required for minor surgery
100% required for major
Factor 8 concentrate: 40 units per cc
Cryo: 5-10 units/cc (100 u per bag)
DDAVP upregulates natural production of Factor 8 and vWF
vWD
Type I: quantitative defect in vWF. Responsive to DDAVP
Type IIB: DDAVP can cause paradoxical thrombosis/platelet consumption
Type III: DDAVP is ineffective
Tx: Cryo, Humate-P (factor 8/vWF), FFP
Monitoring: bleeding time
PRODUCTS
RBC:
RBC 35-42 days at 2-6deg.
Stored blood: looses ATP, 2-3DPG, increased K
FFP:
Contains ALL plasma proteins and clotting factors
Frozen to -18 tp -30, volume 250cc, stored up to 1 year
ABO identical or compatible required
Indications:
o Rapid reversal of warfarin
o Correct factor deficiencies (if factor concentrates not available)
o Correct antithrombin III deficiency
o Microvascular bleeding (if received a lot of PRBC)
Transfuse w/in 6 hours
Platelets
Store at room temp (20-24)
ABO compatibility not necessary but compatible have longer lifespan
Indications not clear but rarely for count > 100,000
CRYO
Cold insoluble portion of plasma, remains after FFP thawed.
Contains (3): Factor VIII (100 IU), vWF, factor XIII, fibrinogen
Indications:
o Hemophilia - Used for emergency back up when factor concentrates are not
available.
o von Willebrands's disease - Not currently recommended unless last reserve.
dDAVP is first line, followed by factor concentrates.
o Hypofibrinogenemia (<100)
o Bleeding from excessive anticoagulation - FFP contains most of the
coagulation factors, and is a much better choice when anticoagulation has to
be quickly reversed.
o Massive bleed - RBCs and volume expanders are preferred therapies.
o DIC
Administered as a pool of 4-6units.
Dosing: 1 unit per 10kg body weight (LBW)
o 1 unit contains 250 mg fibrinogen
o Increases fibrinogen by 50-75 in 70kg adult
o 1unit cryo= 3 units FFP (900 cc)
Transfuse at Room temp, NOT through warmer w/in 4 hrs
DRUGS
Argatroban/Lepirudin = direct thrombin inhibitor
Prevent fibrinogen formation at the last step in the cascade
Transfusion Reactions:
Massive transfusion
> 10u PRBC in 24 hrs
Replacement of half a patients blood volume in 3-4 hours
> 4 units in 1 hour
Metabolic complications
o Hyperkalemia
o Citrate toxicity
Binds Ca & Mg
Hypocalcemia: Hypotension, narrow pulse pressure, prolonged QT
int, inc. intraventricular EDP
o Metabolic alkalosis: citrate in stored blood is metabolized to bicarbonate by
liver via Krebs
o Avoid LETHAL TRIAD: Hypothermia Acidosis coagulopathy
Clotting factor deficiency:
o Dilutional
o Factor V & VIII have short t1/2 in FFP & not present in PRBC or platelets
Acute
TRALI: Non-cardiogenic pulm edema, hypoxemia, hypotension, fever, cyanosis
Leading cause of blood related mortality: 13-21% (35-58% in critically ill)
2 possible mechanisms:
o Immune: Reaction b/w donor anti-HLA or antileukocyte Abs & recipient
leukocytes sequestration in microcirculation of lungs capillary endothelial
damage/leak.
o Non-immune: transfusion of non-leukocyte elements, biologically active
lipids, cause alveolar damage
Risk Factors:
o Plasma-containing products (Plat > FFP > RBC)
o transfusion from multiparous female ( HLA)
o sepsis, liver disease, EtOH abuse, mechanical vent
Diagnosis: ALI + recent transfusion
o ALI:
Timing: Acute
Hypoxemia: PaO2/FiO2 </= 300 or SpO2 < 90% on RA
CXR: Bilateral infiltrates
Edema (not hydrostatic): No evidence of elevated LAP
ABG changes
Acute diarrhea: non-anion gap metabolic acidosis with hypokalemia
RTA type IV (aldosterone deficiency): non-anion gap acidosis w/ K
Thoracic epidural (T10) has been shown to reduce ileus
strength of LES
Anti-cholinergics: Glyco/scopolamine
Opioids
Thiopental
volatiles
Reglan is the only med that has proven to reduce gastric vlumes
H2/PPI gastric pH & reduce volume
Propranolol
Nonselective, beta-1 antagonist ( HR, CO), beta-2 anagonist
(peripheral vasoconstriction, bronchoconstriction)
Portal Hypertension
Gradient between IVC and portal vein > 5
> 12mmHg = symptomatic
Child-Pugh score (score C = high perioperative mortality)
Plasma albumin
Bilirubin
PT or INR
Ascites/encephalopathy
Portopulmonary Hypertension
PAH + portal HTN
Mean PAP > 25
PAOP < 15
Refeeding syndrome:
Phos
Mg
K
Hyperglycemia
Vd = dose / concentration
Hydrophillic drug = small peripheral volume of distrubtion
Propofol is completely metabolized by the liver on a single passand
concentration post liver will be zero
G-protein mediated
Opioids
Alpha and beta agonists
Serotonin
Prostaglandins
histamines
Gprotein + PKA:
Beta receptors
Gprotein mediated decrease in cAMP
Alpha-2 and opioids
Gprotein + IP3
Myotonic Dystrophy
Autosomal dominant
Myotonia = persistent contracture after muscle contraction or electrical
stimulation, progressive weakness/wasting due to abnormal calcium
metabolism
Steinerts disease (MD1) most common, (1:8,000)
Clinical:
o Pulmonary: cranial muscle weakness, aspiration, hypoventilation
o Cardiac: conduction abnormalities (AV blocks, cardiomyopathy)
o Inc. sensitivity to opioids
o Normal response to NDNMB
o Prolonged contraction w/ Sux
o Etomidate/Prop/methohexital and neostigmine may provoke
myotonia
o Myotonia w/ hypothermia, shivering, meds, electrical/mechanical
stimuli
Tx:
o Muscle infiltration w/ local anesthetic
o Phenytoin
o Procainamide
o Quinine (300-600mg IV)
Eaton-Lambert Syndrome
Antibodies to PREsynaptic voltage-gated Calcium channels results in
Ach release
Exercise improves strength
Anticholinesterases dont help
Strong association w/ neoplasm
Sensitive to both depolarizing and ND NMB
For morbidly obese patients..use LBW for induction doses of propofol and
TBW for continuous infusion
Use LBW for infusion of remifentanil
TWB for Sux
Answer: 3 hrs
SIADH
Na < 130
Plasma osmolality < 270
Urine is hypertonic relative to plasma
UOP is low or normal
Parkland Formula:
4 cc x pt wt (kg) x % body burned
o Ant. Upper trunk/lower trunk/each leg = 9 %
o Entire arm/head = 9%
Tourniquet Use
Release can cause PCWP
Release of metabolic waste: CO2, lactic acid, K arterial pressure
minute ventilation
Long times can cause neuro injury, loss of motor function and rhabdo,
compartment syndrome
Autonomic hyper-reflexia:
Common w/ injuries above T6
Hypertension + vasoconstriction
Baroreceptor-mediated reflex bradycardia + vasodilation
Visceral & muscle spasm, sweating, piloerection, uncontrolled motor
activity
Unmodulated sympathetic NS can lead to cerebral hemorrhage, seizure
Incompetent Inspiratory valve:
CO2
linearly prolonged expiratory plateau phase (III)
Prolonged phase I and progressively EtCO2 at baseline
HR values
< 24 h: 120
1-7 days: 135
1 week-1month: 160
3-12 mo: 140
Hyperkalemia:
ECG:
o P amplitude
o Peak T waves
o Widened QRS
o Sinusoidal
Tx:
o Calcium chloride
o Insulin + dextrose
o Na HCO3
o Hypervent
o Inhaled beta 2
o Loop diuretics
o Kayexalate
o HD
Anticholinesterase Poisoning
Parasympathetic stimulation:
o Miosis
o Abodminal cramping
o Excess salivation
o Loss of bowel/bladder control
o Bradycardia
o bronchoconstriction
Benzodiazepines
Lipid solubility: Midazolam > Diazepam > Lorazepam
High protein binding
Midazolam is 2x, LORAZEPAM 5-6x more potent than diazepam
Versed:
o Metabolized in liver: oxidative hydroxylation to active 1- and 4-
hydroxymidazolam
o Active metabolites build up in renal failure
o Substrate of CYP450
o Versed itself is a weak inhibitor of CYP3A4
Post-op shivering:
Clonidine
Precede
Propofol
Ketanserin
Tramadol
Magnesium
Narcotics
Physostigmine
Metabolites of alfentanil, meperidine, tramadol are prolonged in LIVER
failure
Hypothyroidism:
A/w other autoimmune disease: SLE, RA, DM, hypoparathyroidism,
Addisons, amyloidosis
Cardiac changes due to diminished function of beta-adrenergic
receptors ( inotropy & chronotropy)
o Resulting imbalance favors alpha receptor activity = SVR,
diastolic pressure, pulse pressure
o afterload = o2 consumption
o prolonged QT
o associatedwith autoimmune adrenal insufficiency is termed
Schmidt's syndrome
ANGIODEMA
Causes:
o Hereditary: C1 esterase deficiency
o PCN/sulfa drugs
o ACE inhibitors
o NSAID ( prostaglandin)
Treatment:
o Airway involvement: Epi, Benadryl, steroids, intubation
o Epsilon-aminocaproic acid & danazol may prevent in hereditary
form
Doxorubicin: Cardiomyopathy
PCN allergy
Cross-reactivity w/ cephalosporin due to common beta-lactam ring
Alternative: Vanc/Clinda
VTACH in pediatric
w/ pulse = synchronized cardioversion
IV amio 5mg/kg over 20-60 min or 15mg/kg IV procainamide
Autonomic hyperreflexia
Commonly caused by bladder/GI distension
Ascending reflex via spinothalamic tract (sympathetic response)
Baroreceptors detect Hypertensive response in carotid sinus
Vasodilate ABOVE level of lesion but below is still vasoconstricted
Reflex bradycardia
Methemoglobinemia:
Produced when iron in Hgb is oxidized from ferrous to ferric
NADH reductase reduces to Hgb
DLCO
COPD
Sarcoid
Asbestosis
TB
Heart failure
Anemia
DLCO
Exercise
Asthma
Polycythemia
Left to right intracardiac shunting
Pulm. hemorrhage
PFTs w/ COPD:
FEV1, ratio FEV1/FVC, FRC, TLC
Pregnancy
FRC ~ 500 cc due to
o RV
o ERV
Cardiac: SA conduction, HR
Cutaneous: vasoconstriction, flushing
GI/GU: Constipation/urinary retention, gastric acid secretion, LES tone
CNS: agitation/confusion
Eye: OP
INDICATIONS FOR BI-PAP
Post-op thoracic/abdominal surgery
Pulm edema 2/2 decom heart failure
Acute exacerbation of COPD
Immunosuppression
CONTRAINDICATED for:
AMS
resp drive
aspiration risk
HD instability
PTX
Patient refusal/noncompliance
Anatomy
Glomerulus contains Bowmans capsule which filters blood
Quantity of filtrate is dependent on blood flow and pressure w/in
glomerulus
Afferent artiole constriction decreases pressure and decreases filtrate
o Caused by sympathetic activation, ANG II, mesangial
constriction and endothelin
o Afferent dilation: prostaglandins, NO, ANP, dopamine and
bradykinin
Efferent constriction increases pressure w/in capsule, increases
filtrate
Angiotensin II (vasoconstrictor) works on both afferent and efferent.
Efferent are more sensitive. Low levels of ATII efferent affected more
and GFR increases
Autoregulation
Occurs between arterial pressure 70-120
Maintains RBC 1.25L/min
Maintains GFR at 125cc/min
Furosemide
MOA: Inhibits Na-K-2Cl transporter in the thick ascending loop of henle
(excreted in tubular lumen)
Transporter normally allows reabsorption of Na, K and chloride ions
Decreases tonicity of medullary interstitium and Increases tonicity of
the ultrafiltrate
Decreases gradient and decreasing water reuptake in the kidney and
diluting the urine
Weakly inhibits carbonic anhydrase and weakly inhibits Na-Cl transport
system
Inhibits tubuloglomerular feedback
Causes renal vasodilation by affecting prostaglandin levels
Oral bioavailability is 50%
Can cause deficiencies in Na, K, Mg and Calcium
Metabolic alkalosis due to hypochloremia
Ototoxicity
Can cause digoxin toxicity
Aldosterone:
Mineralocorticoid, controls sodium secretion
ANG II stimulates release from adrenal cortex w/ BP, RBF,
hypovolemia, hyponatremia, hyperkalemia, ACTH , surgical stimlus
enhances Na uptake and potassium release into the urine at the
collecting duct
Tx of Hyperkalemia
Calcium: decreases resting potential of myocardial cells and raises
threshold potential
Insulin: stimulates many intermediaries including protein kinase B
o Increases number of Na/K ATPase on cell surface and increases
intracellular uptake of K
Bicarbonate: increases pH, drives H+ out of the cell and Na
inintracellular Na then stimulates Na/K ATPase
Beta-2 agonists: increases Na/K ATPase activity (K shifted inside cells)
Goal of ACE/ARB in CHF: stop the pathological increases in Na retention
caused by the heart failure
Diuretics
Proximal Tubule:
Acetazolamide
Mannitol
Thick ascending limb: NKCC2 (sodium potassium di chloride inhibitor)
inhibition
Lasix
Ethacrynic acid
DCT: Na/Cl cotransporter inhibited
HCTZ
Metolazone
Collecting duct
Amiloride (epithelial Na channel inhibition), spironolactone (aldosterone
inhibition)
Thiazide diuretics increase calcium reabsorption
Loop diuretics lead to hypocalcemia
Digoxin:
Cardiac glycoside used to control HR in Afib
Reversibly inhibits N/K/ATPase in cardiac myocyte
o Ion pump normally generates extracellular Na gradient that
drives the Na/Ca exchanger which normally removes Ca from the
cellw/o Na gradient, more Ca accumulates resulting in inc
contraction of heart muscle
o Also inhibits Na/K/ATPase in renal tubuli- reduced Na
reabsorption and increased diuresis
o Low doses: decreases renin, aldosterone and norepi levels
Toxicity
o Arrhythmias (ventricular)
o Malaise
o Vision changes
o Salvodor Dali ECG signs
o Medications that causes HYPOKALEMIA inc. risk of toxicity
CRRT vs HD
CRRT: pressure driven
o Fluid can be given back
o Less effective?
o 2 types: CVVH and CVVHDf
convection vs ountercurrent diffusion
HD: high volumes/flows
Decrease K:
Insulin
Raising serum pH
Hypothermia
Beta 2 sympathetic stim
Strong Ion gap (SIG) measure of all cations (Na, , Ca, Mg) - anions (Cl,
HCO3, lactate) and conj bases (A-) of strong acids
Normal: 40 mEq/L = 40 of unmeasured anions
When Cl levels inc. SIG decreases
SIG: Metabolic alkalsis
SIG: Metabolic acidosis
Bladder innervation:
General visceral afferentsderived from hypogastric plexus (which
itself receives innervation from T10)
TURP syndrome:
S/S: restless, SOB, dizzy, seizure, coma, HTN, brady
Classic Triad: SBP, DBP, HR
Common:
o Hyperammonemia (glycine solutions)
o Hypernatremia
o Hyperglycemia (sorbitol and glycine)
o Transient blindness
Distilled H20--> Hemolysis
Sorbitol--> converted to fructose--> hyperglycemia --> acidosis
Glycine (inhibitory neurotransmitter): transit blindness--> ammonia-->
encephalopathy
TURP
Regional Anesthesia:
o Sensory: T9-10
Bladder perforation:
o Bradycardia
o Hypotension
o Diaphoresis
o Nausea
o Pain suprapubic, inguinal
o Shoulder pain
o Hiccups
o dyspnea
NMB 4/29/2016 7:09:00 PM
Succinylcholine:
Only depolarizing muscle relaxant
Partial agonist at AChR, binds alpha subunit
Bind both nicotinic and muscarinic
ED95 = 0.3 0.6 mg/kg
o RSI = 2x ED95
o Intubation dose: 1-1.5 mg/kg
o Single dose = Phase 1 block
o Phase II block when doses > 3-5 mg/kg w/ volatile or >8mg/kg
w/ TIVA
Does not bind pre-synaptic receptors (unlike NDNMB)
Metabolized by plasma cholinesterase (PChE) to Suxmonochline
(active)
Adverse effects (4 large categories)
o 1) Ant-muscarinic Action
Muscarinic receptors are found in brain, heart, PNS
Can cause bradycardia, idioventricular rhythm
risk with high vagal tone (kids, manipulation of
cervix)
Atropine only prevents bradyarrhythmias, not
ventricular
o 2)Potassium release: 0.5 mmol/L
o 3) Allergic reaction: IgE mediated
o 4) Nonspecific
Fasciculations/myalgia
ocular pressure
IP
Pseudocholinesterase = Butyrlcholinesterase
Serine hydrolase, alpha-2 receptor globulin
Metabolizes Ach, Sux, mivacurium, trimethaphan, ester-local
anesthetics
Dibucaine number
Dibucaine inhibits plasma cholinesterase
Heterozygote atypical: inhibits 40-60%
Homozygote atypical: 20% --- 4-8 hr blocked
Metabolized by different esterase compared w/ esmolol
o Esmolol is metabolized by RBC esterase (t1/2 10-20 min)
Homozygous typical:
o Di #: 70-80
o Response to Sux/Miva: normal
Heterozygous, atypical
o Di#: 50-60
o Response to Sux/Miva: Lengthened by 50-100%
o Occurs in 1/480
Homozygous atypical:
o Di#: 23-30
o Effects prolonged 4-8 hrs
Myasthenia gravis
Autoimmune, auto-Ab to acetylcholine R
Decreased number of functional Ach receptors
response to depolarizing NMB
o ED50 = 2x, ED95 = 2.6 x normal
o More likely to have phase II block
o Patients take anti-cholinesterases for treatment = prolonged
activity
Sensitivity to NDNMB
Physostigmine inhibits pseudocholinesterase to a lesser extent than
neostigmine
Edrophonium does not effect pseudocholinesterase
Tensilon test: Edrophonium
o Used to differentialte myasthenia gravis and cholinergic crisis
and Eaton-Lambert syndrome
o MG: improve strength
o Cholinergic crisis will become worse
Cisatracurium
Metabolized by organ-independent Hoffman elimination in plasma
o Slowed by hypothermia
Laudanosine is a byproduct, metabolized by liver, excreted in kidney
o levels can cause seizure
not associated w/ histamine release
NM metabolized by pseudocholinestersase
Mivacurium ad sux
Extubation Criteria
Tetanus > 5 sec, sustained head lift
TV > 5 cc/kg
VC > 10 cc/kg
NIF more neg than -20
PaCO2 < 50
RR < 30
RSBI < 105 (RR/TV)
MUSCARINIC STIMULATION BY ACH
Myosis
Salivary secretion
Bradycardia
Bronchospasm
Insulin secretion
Bowel motility
Bladder sphincter relaxation
Cerebral excitation (only tertiary/pass BBB physostigmine)
MONITORING NMJ
* NMJ Transmission
voltage-gated ion channel
influx of calcium
Ach vesicles fuse w/ membrane and ach released
Bind to nicotinic receptors on motor end plate
Opens ion channels and epolarizes
Modes of stimulation:
Single twitch: supramaximal stimuli, 0.1-1Hz
TOF: 4 supramaximal stimuli at 2Hz, may be repeated at min every 10
sec
o 4th response lost = 75-80 blocked
o 3rd response lost= 85%
o 2nd lost = 90% blocked
o T4/T1 = 0.9 --- GOLD STANDARD
TETANUS
Differential blockade:
Large myelinated neurons are more resistant to LA (A-alphja, motor)
o A-delta (pain, temp)thin, myelinated
o C (pain, temp)small, unmyelinated
Plain tetracaine/bupivacaine/ropivacaine: 1.5-2hr block
Adding epi has minimal effects on ropiv/Bupiv
Epi+ tetracaine: extends 1 hour
Chloroprocaine: short acting agent (also procaine)
Lidocaine: intermediate
Lido + Epi: surgical block 90 min
ASRA guidelines and spinal/epidural
D/C Plavix 7 days prior
INR < 1.5 = ok
PTT > 40 = not ok
PPX Lovenox: 12 h after last dosethen restart low cdose 6 hours later
BID Lovenox (therapeutic)-place block 24 h after last dose, restart 24
hours later
Intrathecal morphine:
Hydrophilic
Crosses dura slowerlonger lifespan w/in CSF
Greater rostral spread
Lumbar intrathecal injection will produce analgesia into HIGH
THORACIC levels
2 peaks of respiratory depression:
o 2nd peak: 6 hrs after injection
o Peak analgesis effects are at 6-12 hours..lasts 24 hours
Meperidine
Atropine like effects
Cardiac depressant effects
Euphoria
Local anesthetic properties
Post-op shivering
Sacral Sparing: patchy epidural or less dense in L5-S2 due to large size of
nerve roots
Remedy: bolus in reverse trendelenburg
KNOW THESE:
Abciximab: 2 days
Argatroban/Bivaliriudin/Lepirudin: PTT < 40
Alteplase: 10 days
Plavix: 7 days
Dabigatran: 3 days
Dalteparin (ppx)/full dose: 12/24 hrs
Fondaparinux (PPX/full): 48/72 hrs
Ticlopidine: 14 days
Tirofiban/Eptifibatide: 8 hrs
Interscalene block
Primary use: shoulder surgery (ALSO arm/elbow)
Target: nerves of upper brachial plexus: C4-C7
o Distal roots or proximal trunks
o Blocks suprascapular nerve (C4)top of shoulder
LANDMARKS: Anterior/ middle scalene muscles, Subclavian artery
o Pleura lies anteromedial to inferior trunk
o Posterior border of clavicular head of SCM
o Thyroid cartilage
o EJ (anterior)
Ulnar nerve sparing (C8, T1) (4th/5th fingers)
Side Effects:
o Phrenic nerve paralysis (100%)
o Horners syndrome (stellage ganglion)
Myosis, ptosis, anhydrosis, nasal stuffiness
o Recurrent laryngeal nerve block: hoarse voice
o Vertebral artery injection: too deep/directed more caudad
o Carotid artery injection: too anterior
o Epidural/subdural/intrathecal injection: too caudad
o Pneumothorax
o Bezold-Jarisch reflex: hypotension, bradycardia, coronary
vasodilation
Supraclavicular:
Purpose: Elbow, wrist, hand surgery
Target: Distal trunks/divisions
Side effects:
o Phrenic nerve paralysis (but as often as interscalne)
o PTX
Landmarks:
o bundle of grapes, lateral & superficial to Subclavian artery
o posterior/lateral to Subclavian artery
Infraclavicular:
Purpose: same as supraclavicular block (wrist/hand)
o Spares C5-C6
Performed at level of CORDS: medial/lat/post
o Nerves located around axillary artery
o Lateral cord: SUPERIOR
o Posterior cord: POSTERIOR
o Medial cord: POSTERIOR/MEDIAL
Complications comparable to axillary
Contraindicated w/ coagulopathy
Advantages:
o Pt does not have to abduct arm
o Bilateral blocks can be done--> phrenic nerve not involved
o Continuous catheter can be placed
o Musculocutaneous does not have to be supplemented
Axillary Block:
Nerves: Median, ulnar, radial (misses musculocutaneous &
coracobrachialis)
Target: 3 terminal branches
Must supplement musculocutaneous
Clockwise around axillary artery under ultrasound: MUR
o Median (supero-LATERAL, crosses at elbow then medial)
o Ulnar: Superior-Medial
o Radial: posterior
Problems: Neuropathy
Uses: Hand/wrist surgery
NERVE INJURY
Radial nerve
Axilla injury: unable to extend forearm (triceps)
Spiral groove: wrist drop
Prominent Landmarks:
Prominent cervical thoracic process: C7
Inferior tip of scapula: T7
Superior iliac: L4
Posterior superior iliac spine: S2
In supine position: hyperbaric local anesthetic will not move above T5-T7
Surface Anatomy
C2 1st palpable spinous process
C7 most prominent
T7 inferior tip of scapula
L4 or L4/L5 interspace: superior point of iliac crests
S2: posterior-superior iliac spine
Dermatomes
C8 - 4th/5th digits of hand
T4- Nipple
o Required for upper abdominal surgery
o T6 is required for lower intestinal, uro/gyn
T7-xiphoid
T10-umbilicus
o Required for labor/vaginal delivery/hip surgery
S2-S5 saddle block for anl surgeries
Caudal space
Continuous w/ lumbar epidural space
Located on sacrum
5 fused spinal processesbut the 5th one is only fused
anteriorly..leaving the SACRAL hiatus posteriorly
Sacral hiatus is covered by the sacrococcygeal ligamentextension of
ligamentum flavum
How to locate:
o Find coccyx and travel superiorlyabove gluteal cleft, until
palpate 2 sacral cornua
o
5 nerves of ankle to block
Posterior tibial (heel, plantar foot, toes)
o Motor: Flexors of foot, Sensory: Sole of foot
o Located posterior to medial malleolus
Sural lateral foot (S1-S2)
o Motor: none; Sensory: lateral foot
o Located posterior to lateral malleolus
o Sensory to posterolateral leg, lateral foot, 5th toe
Superficial peroneal: L4-S1
o Motor: extensors, sensory: dorsum of foot (except webspace of
big toe)
Deep peroneal: L4-L5 (web space of big toe)
o Motor: extensors of foot; Sensory: 1st web space
o Located lateral to dorsalis pedis artery & extensor hallicus
longusinnervates flexors to toes, sensation between great and
2nd toe
Saphenous (L3-L4): only nerve from femoral
o Motor: none; Sensory: medial leg & foot
o Located anterior to medial malleolus
o Sensoty to anteromedial leg/medial foot
Pneumatic tourniquet:
Must be inflated to excess 100mmHg
Pain: due to unmyelinated, slow-conducito C fibersresistant to local
anesthetic
Can cause DVT
Cuff deflation: CVP, MAP , PaCO2, ETCO2 ,Lactate and K
TENs Unit
Produces tingling or vibratory sensation
MOA: produces analgesia by releasing endogenous endorphinsthese
activate inhibitor neurons
Increasing dose of LA will hasten onset and duration of epidural
Bupivacaine Toxicity:
Mechanism
o -Dose-dependent blockade of sodium channels. Of note,
o 1) bupivacaine binds more strongly to resting/inactivated Na
channels as compared to lidocaine, and
o 2) bupivacaine dissociates from Na channels during diastole
more slowly than lidocaine.
Diagnosis of LA Systemic Toxicity
o -CNS signs: Circumoral numbness, Slurred speech, Muscle
twitching, restlessness, agitation drowsiness seizures
o -Cardiovascular signs: Bradycardia, dysrhythmias, Hypotension,
Heart block arrest
Treatment
o Supportive
o -Seizures: treat with GABA agonists.
o -Convulsions: treat with paralytics and airway management
o -Hypotension: vasopressors may be indicated, although at
decreased doses
o -CV collapse: CPR + 20% Intralipid [1.5- 4mL/kg, then 0.25-0.5
mL/kg/min infusion for 10-60 min]
Topical anesthesia
Lidocaine
Tetracaine
Cocaine
Dibucaine
Benzocaine
Lido + Prilo = EMLA cream
IV regional/Bier Blocks
Esters are NOT used
Bupivacaine can cause cardiac problems
Use Lidocaine or Prilocaine
Intermediate:
Lidocaine
Mepivacaine
Prilocaine
Long Duration:
Bupivacaine
Tetracaine
Ropivacaine
A-alpha:
efferent to skeletal muscle
A-beta:
Afferent from skin/joints
Touch, proprioception
A-gamma: Efferent to muscle spindles for tone
3-6 um, CV 15-35 m/sec
A-delta: Afferent
Myelinated
Sharp/localized pain/temp/touch
1-4um, CV 5-25
B fibers
Myelinated, preganglionic sympathetic
<3um, medium CV 3-15
autonomic nervous system control
C fibers:
Unmyelinated, post-ganglionic sympathetic, free nerve endings
Slow CV, 0.1-2 m/sec
Diameter = 1-4 nm
Afferent sensory
Nonlocalized pain, temp, touch
Spinal anesthetic in kids: requires larger volume and does not last as long
S1-2: ankle
L3-4: knee
C5-6: biceps, supinator
C7-8: triceps
Infraorbital Block:
Used for analgesia after cleft lip repair
Terminal branch of maxillary division of trigeminal V1
o A = fascia lata
o B= fascia iliaca
3 structures that are essential to visualize:
o Femoral artery
o Fascia lata
o Fascia iliaca
Axillary Block: The axillary block is frequently performed for surgeries distal
to the elbow.
Brachial plexus, superior to clavicle, coursing next to subclavian artery
Side effects:
o Phrenic nerve blockade
o Horner syndrome
o PTX
BRACHIAL PLEXUS:
The brachial plexus is composed of the 5 nerve roots (C5-T1) that combine
to form the superior, middle, and inferior trunks. These trunks further divide
to form the lateral, medial, and posterior cords, which then branch off into
the peripheral nerves of the upper extremity (Table 1).
Appendectomy T6-8
Inguinal Herniorhaphy
Pelvic procedures
All nerves of the foot (except saphenous) are derived from sciatic nerve
Normal VS:
Preterm: HR 160, SBP 50, DBP 30, RR 50
Term: HR 130, SBP 60, DBP 40, RR 50
1 YR: HR 120, SBP 80, DBP 60, RR 25
Toddler: HR 90, SBP 100, DBP 60, RR 20
Blood Volumes:
Newborn: 90 cc/kg
Infant: 75 cc/kg
Toddler: 70 cc/kg
ABG:
Birth: pH 7.2, paO2 50, paCO2 50
1 wk after birth: pH 7.4, paO2 70, paCO2 35
Toddler: pH 7.4, paO2 95, paCO2 40
Fetal circulation: placenta --> vein --> heart --> arterial --> placenta
F-Hb (fetal hemoglobin) --> affinity for oxygen. Unable to bind 2,3 DPG
P50 = 19 (adult = 27)
FRC = point at which outward elastic recoil of chest matches inward recoil of
lung (at end-expiration)
Both decreased in neonates
FRC
PRIS:
Inhibits proteins that allow transfer fo FA into mitochondriamito are
starved of energy
Lactic acidosis..necrosis
Retinopathy of prematurity:
Pathophysiology: retinal artery constrictionproliferation of abnormal
vesselts resulting in scar/hemorrhage and retinal detachment
Risk factors:
o O2
o Genetic: sex/Caucasian
Chemical pneumonitis
Pulm edema
Hypoxia
Pulmonary hypertension
Acls FOR NEONATE:
Hypoxia w/o bradycardia--> supplemental O2
HR < 100 --> ppv
HR < 60--> Chest compressions at 120min but FIRSTmask ventilation
Chest compression:ventilation ratio = 90:30 (3:1)
o Adults = 3:2
Epinephrine:
o Tracheal epi: 10 x the IV dose 0.1mg/kg
o IV: 0.01-0.03 (ALWAYS USE 1:10,000 for IV)
APGAR
Appearance
Pulse
Grimace
Activity
Respiration
Tetrology of Fallot
Most common CHD
RIGHT LEFT shunt, pulm blood flow, hypoxemia
o SVR or spasm of unfundibular cardiac muscle causes pulm
blood flow & r to left shunt
4 features:
o VSD
o RVH
o Over-riding aorta
o Right ventricular outflow tract obstruction
ECG: RAD, RVH
CXR: pul vascular markings, rt aortic arch
Tet spell: hypercyanotic attack, peak 2-6 mo (feeing, crying,
defecating)
o SVR = hypoxemia
Tx: O2, chest-knee position, morphine
o Anesthetized pt: SVR = Lft to right shunt (Neo, BB, fluids)
Hemodynamic goals:
o preload (squatting, Neo, fluid bolus)
o Slow sinus rhythm (beta blockers)
o contractility (volatile?)
o SVR (Neo)
o PVR (Hi FiO2, hyperventilate)
ANESTHESIA:
o No spinal! Early epidural is goodmay PVR
o AVOID: Atropine, nitrous, iso ( HR), Epi, dop
Down Syndrome:
CHD
ASD
Upper Airway Obstruction/Sleep Apnea
Hypothyroidism
NPO guidelines
Clears: 2 hrs
Breast milk: 4 hours
Infant formula: 6 hours
Solids/non-human milk: 6-8 hrs
Induction : FA/FI
Solubility: less soluble = faster induction
Cardiac output: decreased = faster induction
o CO ----FA lags behind FI
o Increasing ventilation
FA increases and FI does not change
Ratio increases
Shunt (right to left)
o Blood bypasses lungs, dilutes mixed venous blood returning from
pulm circulation causing increased gradient between alveoli and
arterial blood slows induction
Concentration effect = at igh concentrations, speed of induction
increases as FA approximates FI
Right mainstem intubation:
Shunt increases
Dec. concentration of gas in mixed venous blood
Greater concentration difference from alveoli to venous blood
More anesthetic will be pulled from alveoli into blood BUT less blood is
being exposed to lungs
Altogether, FA continues to approximate FI yet the arterial partial
pressure of volatile is decreased
Soluble agents are less affected
Nitrous
Preserved minute ventilation, no rise in apneic threshold
at 50-70%, stimulate sympathetic nervous system
small increase or no change in HR, MAP, CO
Mild myocardial depressing effects, outweighed by sympathetic
stimulation
PVR increases.can exacerbate pulm HTN
Preserved minute ventilation, no rise in apneic threshold
Inhibits enzymes
o Methionine synthetase myelin formation
o Thymidylate synthetase DNA synthesis
Peripheral neuropathies, pernicious anemia, megaloblastic anemia,
depressed bone marrow
35x MORE SOLULB THAN NITROGEN IN BLOOD
Metabolism of Volatiles
Sevoflurane ismetabolized the most @ 5%
Iso: 0.2%
Nitrous <0.2%
Halothane: 20%
CO has more effect on the rate of change of FA/Fi for POORLY SOLUBLE
AGENTS (ISOFLURANE)(
Iso: 1.46
SEvo: 0.65
Des: 0.42
Nitrous
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