Pulm Pharmacology/Pharmacokinetics
 Anatomy  Laryngospasm
 1) Nose  Superior laryngeal afferent
 Nasal cavity  Recurrent laryngeal efferent
 Roof = cribiform plate  Laryngospasm Highest risk = ketamine
 Ethmoid Nerve = nares and septum  Larson maneuveur
 Palantine nerves = spheropalantine ganglion = turbinates  Medial and cephalad pressure
 Narrowest at Nasal vestibule @ main nasal cavity  Behind earlobe
 Just anterior to tip of inferior turbinate  Base of skill = superior
 Nasal oral/Oral cavities pharynxlarynx/esophagus  Mastoid = posterior
 Nasal Vasoconsrictor  Ramus of mandible = anterior
 Minimize mucosal bleeding  In pediatric
  Diameter of nasal passage  Succinylcholine may cause?
 Plus bradycardia and MH
 2) Pharynx: Subdivisions; Innervation
 Pharyngeal wall muscles=genioglossus & artenynoid  b) Vocal Cords, Positions with Paralysis
 Posterior Cricoarytenoids abduct vocal cords
 Upper airway patency
 Anterior Cricoarytenoids adduct vocal cords
 Middle ear Eustachian tubes Nasopharynx
 Equalize pressure with atmosphere  Su perior Laryngeal Nerve
 Velopharynx = separates oral and nasal cavities = most  Aryepiglotic folds, posterior eppiglotis, aretynoids base of
common site of obstructive collapse (tongue falling back is 2 nd most tongue
common)  Unitlateral paralysis = minimal effect
 Bilateral paralysis = hoarseness
 3) Larynx = epiglottis  cricoid (C3-C6)
 Branch of vagus
 a) Innervation; Muscles; Blood Supply; Cartilages
 B2 innervation via thoracic plexus  External Branch = cricothyroid muscle (tense/adduct cords)
 Most common injured in thyroid surgery
 Not innervated (non-sympathetic)
 Indirect Sympathomimetics have no effect  Internal Branch = sensory above cords
 Larynx = 9 cartilage  Afferent for laryngospasm
 SIME = sensory internal Motor external
 2x(artenyoid, corniculate, cuniform)
 (thyroid, cricoid, and epiiglotic)  Superlaryngeal nerve block
 sternothyroid (infrahyoid) = depressor or larynx  1) superioir cornu of hyoid (greater horn of hyoid)
 2) superior cornu of thyroid cartilage
 Epiglottitis: very high temp  3) superior notch of thyroid
 Age 3-7 y.o.  Trigeminal
 Drooling, dysphagia, Dysphonia, Dyspepsia  Nasal mucosa, anterior tongue
 Inspiratory stridor  Superior and inferior hard and soft palate
 Vagus
 Unilateral hoarsness, bilateral = aphonia
 Glossopharyngeal Nerve (IX)
 Tonsils, pharynx, anterior superior epiglottis, vallecula,
posterior tongue
 Gag reflex Afferent
 Glosspharyngeal nerve ‘block
 Base of tonsillar pillar
 Sensory = Posterior 1/3 of tongue
 Tonsils, pharynx,
 Innervates carotid sinus, carotid body,
 Parasymp to carotid gland
 Recurrent Laryngeal Nerve = branch of vagus
 Intrinsic laryngeal muscles below cords(except cricothyroid),
upper trachea
 Unilateral injury = hoarseness
 Bilateral = stridor/respiratory distress = fixed adducted
paramedian
 Left nerve under aortic arch
 Laryngospasm efferent
 Injury = hoarse voice, weak voice
 Recurrent Laryngeal Nerve Block
 Cricothyroid membrane (transtracheal)
 c) Differences between Infant and Adult
 Breath hold time >18 seconds = good
 Cannot hold breath for feeding = bad
 P50 increase till 1 y.o.
 Fetal hemoglobin insensitive to 2,3 DPG
 Lung compliance Increase till 8 y.o.
 INC alveolar # = INC total lung volume = DEC resistance
 Resp fatigue greater in neonate = DEC type I
 Accessory muscles ineffective in neonates
 Neonate
 DEC FRC till day 4
 Nasal CPAP better at preventing broncho-pulm-dysplasia
 INC O2 consumption
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 Adult O2 consumption = 3-4 mL/kg/min
 INC tongue/mouth ratio
 DEC FRC
 More cephalad larynx
 Both bronchi bifurcate at equal angles
 Cricoid cartilage = most narrow
 Pliable rib cage (less support = Work of breathing)
 Faster induction (fraction of C.O to vessel rich areas)
 Infants = MV & C.O.  volatile uptake
 O2 consumption:FRC ratio
 R main bronchus angle becomes shallower w/ aging, l
bronchus remains at 45degrees
 Sevo>Iso = possible decreased Intelligence
 Possible apoptosis
 VS Elderly
 In healthy elderly patients, chest wall compliance is more likely
to decrease than lung compliance.
 Functional residual capacity increases with aging.
 Tracheobronchial Tree
 Tracheo esophageal fistula
 Tracheal atresia and distal fistula = most common (type C)
 Broncho-pleural fistula
 More likely after (R) pneumonectomy (single bronchial artery)
  Ipsilateral air tracheal deviation
 Contralateral = Fluid level
 Trachea fistula w/ brachiocephalic innominent artery
 Most cases within 3-4 weeks of trach
 Club cells in bronchioles
 (degrade toxins, secrete components of surfactantact as
reserve cells.
 Cartilage and goblet cells extend to end of bronchi
 Tracheomalasia = granulation tissue
  ciliary activity via ketamine, Fentanyl
 Dry Air = compliance
 ciliary motility, thicker secretions, bronchospasm
 Neck extension = align laryngo-pharnygeal axis
Pulm Pharmacology/Pharmacokinetics
 Bronchospasm
 upstroke EtCo2 during exhalation
 prevention = inhaled bronchodilator, oral steroids, topical Lido
 triggered by histamine release(morphine, aracurium)
 (sux though histamine release does NOT bronchospasm)
 NSAIDS trigger in some asthmatics
 Vagus solitary nucleaus efferent vagus M3 cGMP
 In asthma b-blockers can cause
 a) Structure and Relationships in Neck and Chest
 Carina = T4/5
 Pulm artery to bronchus at hilum Right=Anterior, Left=superior
 Carina posterior to ascending aorta, anteromedial to descend
 Common carotid biFOURcates at C4
 Trachea biFOURcates at T4 = sternal angle
 Abdominal aortia biFOURcates at L4
 5) Muscles of Respiration, Accessory Muscles
 Spontaneous = diaphragm, external intercostals, scalene
 25075% effort independent
 Accessory= Alae Nasi (nasal flaring), SCM & scalene (rib lift)  Recruit alveoli w/o over distension.
 Intercostal neurovascular bundle
 From above (vein - artery -nerve)
 Nerves -= T1-T11
 T7-T11 supply abdominal wall
 Between internal oblique and transversus abdominus
 Pulmonary Lobes,
 Left Lung is 10% smaller
 Trifurcation = RUL bronchus
 Right lung (3 upper, 2 middle, 5 lower)
 Left Lung (4-5 upper, 4-5 lower)
 Bronchial Arteries
 1 Right & 2 Left arteries
 Bronchial veinspulm veinsL AtriumO2 partial pressure  Synchronized IMV
 Elasticity of system = lung + chest wall
 Hering-Breur Reflex =  stretch  apnea
 Prevents overinflation
 Less effect in humans (neonates > adults)
 Inspiratory hold = measure plateu pressure
 Transpulmonary pressure = Palveolar – Pintrapleural
 Drives air flow
 Radiological and Ultrasound Anatomy
 Chest (Including CT and MRI)
 j. Ventilators
 1) Classifications: Flow Generation vs. Pressure Generation
 Intermittent Positive Pressure = atelectrauma
 2) Principles of Action: Assistors, Controllers,
 Assist-Control = trigger assisted breath at any time
 possible hyperventilation = hypocapnea
 Pressure-Limited, Volume-Limited;
 FiO2 Control;
 Periodic Sigh, periodic hyperinflation
 Inverse Ratio,
 Inverse Ratio Ventilation = mean airway pressure, PIP
 Risk auto-peep, breath stacking.
 May decrease CO 2/2 INC intrathoracic pressure
 High Frequency Ventilation
 High Frequency Ventilate= >150 breaks/min defined byFDA
 High frequency positive pressure ventilation = 60-120
 High Frequency oscillation = 400-2400
 Basal continuous flow
 leaks
 High Frequency Jet ventilation = 60-300
 INC CO2
 reduces risk of airway fire during YAG laser excision of a
laryngeal tumor
 Intermittent Mandatory Ventilation (IMV)= no trigger support
 Does not assist spontaneous breaths
 Pressure Support, Pressure control
 High initial inspiratory flow
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 Pulm Pharmacology/Pharmacokinetics
 Square waves  Methods of Measurement;  Nitrogen Washout
 Airway Pressure Release Ventilation (APRV)  Normal Values;  test for measuring anatomic dead space
 continuous positive airway pressure (Phigh)  Time Constants  reveals closing capacity
 time cycled release to lower set pressure (Plow)  time constant is volume divided by flow
 Pediatric Adaptation  volume of the circuit divided by the fresh gas flow rate  O2 Uptake,
 Non-Invasive Techniques: (BIPAP)  takes three time constants for 95% of a concentration change  Oxygen
 IPAP (imporoves ventilation) and EPAP  One = 63%, two to 86%; three to 95%  Healthy a dult consumption = 0.25L/min
 Positive pressure effects  O2 consumption from work of breathing in healthy = 2%
 blood return & preload, R. ventricular afterload = CO  b) Spirometry;
 afterload  FRC  CO2 Production
 3) Monitors;  Supine DEC FRC 1L, GA DEC FRC 0.5L  1 meq/L INC in bicarb = 0.5 INC in PaCO2
 Pressure (Plateau, Peak),  TV = 0.5L
 airway resistance = determines the peak pressure  FRC = 2.2L (1L RRV + 1.2 RV)  Exercise Testing
 plateau pressure = determined by the lung compliance  Resrictive lung disease  normal = TV (inspiratory reserve), capillary bed recruitment
 inspiratory hold  Normal FEV1/FVC  exercise = CO2, O2 consumption, MV, VQ ration from
 equal to alveolar pressure in absence of flow  Obstructive lung disease apex to base more uniform
 FEV1/FVC  Pulmonary blood flow 2/2 CO (, capillary recruitment)
 The alveolar pressure should not get above 30 cmH2O.
 Normal vital capacity = 5L for 70kg man
 Oxygen,
 FEF 25%-75%=least dependent on patient effort  2) Ventilation:
 Apnea,
 Inspiratory/Expiratory Ratio,  Respirometers = measures expiratory volume
 Static and Dynamic Volumes;  Inspiratory Force,
 normal 1:2
 Dead Space;  Spirometry,
 prolonged in asthmatiics/COPD: if too short = breath stacking   CO2 A-a gradient=dead space (PE, obesity, COPD)  Wont give residual volume or FRC
 adjust by changing flow rate  INC w/: PEEP (hyperinflated alveoli), Hypotension (pulm  Can be measured with helium dilution
perfusion), inc in circle system distal to Y-piece
 2. Respiratory System
 PaCO2 to EtCO2 gradient is result of dead space  Flow-Volume Loops
 a. Physiology: Lung Functions and Cellular Processes
 Anatomic = neck extension. Bronchodilators  Restrictive disease = shift right
 1) Lung Volumes
 Alveolar = upright position, PPV, C.O.  Obstructive disease = shift left
 FRC =residual volume + expiratory reserve
 Dead Space  Variable intrathoracic obstruction
 Volume at end of tidal volume
 Distal to Y piece  Tracheal tumor, mediastinal mass
 FRC = PANGOS = Pregnancy, Ascites, Neonate, G.A.,
 Extending inspire or expire limb does NOT  dead space  Variable Extrathoracic Airway Obstruction
Obesity, Supine
 One way valve prevents  Low inspiratory plateu
 Supine DEC FRC 1L, GA DEC FRC 0.5L
 Hyperinflation = alveolar dead space  Vocal cord paralysis
 FRC = Emphysems
 In healthy 70kg man = 150mL  Normal expiratory flow-volume
 FRC = 30mL/kg
 FEV & FEV1 normal usually
 FRC increases with height, age
 Air trapping  Limits peak inspiratory flow
 Disconnect expiratory limb, increase expire time, RR, TV  (intraluminal P > intraluminal P)
 a) Definitions;
 Fixed ExtraThoracic Airway Obstruction
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 Pulm Pharmacology/Pharmacokinetics
 Larynx carcinoma, Obstructive goiter, bronchial stenosis
 Abnormal inspiratory & expiratory flow
 Fixed large airway obstruction=foreign body, tracheal stenosis,  Release cytokines and alveolar proteases
large tumor
 2) Lung Mechanics
 DEC PVR
 EPI, N.O., Angiotensin, prostaglandins
 Pleural Pressure Gradient,
 3 mechano receptors
 1) slow adapting stretch receptors
 2) rapid adapting stretch receptors
 3) bronchopulmonary C fibers
 Hysteresis, = Δ inflation/deflation volumes at a given pressure  Resistance highest when lung volumes highest or lowest.
 Greater pressure during inflation (less volume per pressure)
 Expiration = lung volume decreases due to derecruitment.
 Surfactant less effective during inflation. Need to overcome
surface tension forces in inflation
 Surfactant,
 Type II alveolar cells = surfactant
 Precursor to type I cells.and others (stem cell function)
 Proliferate during lung damage
 Surfactant
 Lipoprotein complex. Lechithins (DPPC) (L/S ratio > 2)
 Hydrophilic and hydrophobic region
 DEC surface tension
 Prevents alveolar flooding, atelectasis
 Starts at 20 weeks, mature levels at 35 weeks
 TYPE 1 alveolar cells = alveolar surfaces.
 Atelectasis =when closing capacity > FRC
 Atelectasis = DEC FRC, DEC lung compliance
 Nitrogen stents open alveoli so 100% O2 microatelectasis
 Colising capacity = voluime below which airway collapses
 Alveolar macrophages
  closing capacity
 Age, Chronic bronchitis, COPD, CHF, LV failure, Smoking,
Surgery, Obesity
 b) Resistances; Principles of Gas Flow Measurement
 FLOW
 Turbulent = proportional to P2
 Laminar = proportional to P
 More turbulent in small airways
 Most resistance in medium sized bronchi (3-5 divisions)
 Greatest Airway resistance = medium sized bronchi
 Pulmonary vasc resistance lowest at FRC
 Laminar to turbulent flow
 Gas Flow, sharp tube angles, tube diameter, gas
density, viscosity
 c) Methods of Measurement
 d) Work of Breathing
 Asthma and Bronchospasm = small airways
 Chronic obstructive disease = medium airways
 Dead space, tubular resistance, valvular resistance
 e) Regulation of Airway Caliber
 M2, M3=cGMP = Bronchoconstriction
 Parasymp = antimuscarinic=cGMP= bronchdilate
 Bonchostrict via parasymp(vagus)
 excitatory NANC neurons via substance P, neurokinin A
 3) Ventilation: Perfusion
 Lung blood volume = 900cc
 30% total pulmonary blood flow shunted
 a) Distribution of Ventilation
 b) Distribution of Perfusion,
 Zones,
 Zone 1 = PA > Pa > Pvenous = V/Q >1
 Zone 2 = Pa > Pa > Pv = V/Q ~1
 Zone3/4= Pa > Pv > PA = V/Q < 1
 Shunt in zone 3
 Inspiration  pulm blood flow ~500-1000cc
 Transpulmonary pressure = intrapleural – alverolar pressure
 V/Q mismatch
 alveolar anesthetic partial pressure
 arterial anesthetic partial pressure
 Hypoxic Pulmonary Vasoconstriction
 hypercapnea, hypoxia, acidosis
 V/q mismatch, Co2
 Hypercarbia causes pulm vasoconstrict
 Direct Inhibit = hypocarbia, vasodilating drugs, infection,
volatile > 1 MAC,
 Indirect inhib = hypovolemia, vasoconstrict drugs,
hypothermia, thromboembolism
 Inhibited by: nitroglycerin, nicardipine, nitroprusside
 Hypoxic Pulmonary Vasoconstriction (HPV) = biphasic
 Endothelial O2 sensor K+ out Ca+Vasoconstriction
 Phase 1= within seconds, max at 15 min
 Phase 2 = >30-60min, max at 2 hrs
 In hypoxic lung = acidosis, alkalosis
 PVR
 Redirects ~50% PBF from poorly ventilated
 INC efficacy with acidosis (separately pulm vasoconstrict)
 DEC w/ hypothermia, ether, halothane, N20, anesthetics > 1
MAC, iron
 INC pulm HTN & INC altitude (global HPV)
 4) Diffusion
 a) Pulmonary Diffusion Capacity
 DLCO < 40% = complications
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 Pulm Pharmacology/Pharmacokinetics
 DLCO INC w/ Asthma, polycythemia, INC pulm blood flow  Right shift =thyroxine(hyperthyroid), phosphate, high altitude,  70% bicarb, 23% bound to Hgb(terminal of globin), 7%
 Dec w/ anemia, PE, emphysema hypoxia, HF, liver cirrhosis, sleep apnea, propranolol in CAD, dissolved
exercise  PaCO2 by 10 =  PH 0.08 (vis-versa)
 b) Apneic Oxygenation,  O2 P50  PaCO2 by 1 = CBF 2%
 passive flow 2/2 differential between alveolar O2 absorption  PaO2 requred for 50% saturation of hemoglobin  CO2
and CO2 excretion producing a mass flow of gas from the upper  Volatiles shift Right  w/ thyrotoxicosis, IV bicarb, carbs in TPN
respiratory tract into the lung  For adult hemoglobin =25mmHg  Peripheral vasoconstriction
 Sickle cell = 31  >45 = tachypnea
 Diffusion Hypoxia  >90 = respiratory distress
 O2 and CO2 in the alveolus are diluted by this NO2  Respiratory Enzymes;  CO2
 Hemoglobin (Hb) As A Buffer  Nitrous dilutes =  resp drive
 5) Blood Gas  Buffer for H+ ions
 a) O2 Transport;  Respiratory acidosis intial buffering = plasma proteins  Drop in EtCO2
  O2 Gradient = pulmonary edema, shunts  35% buffering (bicarb is 50%)  Impaired elimination, CV collapse, Venous air embolism
(etNO2), PE (EKG S1-Q3 pattern), Kinked ETT (spO2),
 A-a gradient  Respiratory Alkalosis Esophageal intubation
 If A-A<15 interstitial space is normal  Ca+, K, Phos(glycolytic pathway)   Production: hypothermia, hypothyroid, NMB
 A-a  causes: stroke, ASA, anxiety, pain, progesterone, PE,  Endobronchial intub
 VQ mismatch pneumonia, asthma  Desat
 Pulmonary Edema = perfusion w/o ventilation
 INC PIP
 Shunt = affect A-a gradient  6) Regional Blood Flow and Its Regulation
 Reduced air entry
 R to L shunt = decreased lung time  hypoxia causes vasoconstriction
 Hyperdynamic circulation, sepsis, liver failure  SubQ emphysema
 No change in pulse ox
 Pulmonary Perfusion Pressures
 O2 Physical Solubility;  No change airway pressure
 solubility decreases w/ increasing temp  b) CO2 Transport;  Swelling or crepitus
 Blood CO2 Content;  Capnothorax
 Oxyhemoglobin (Hb-O2) Saturation,  Carbonic Anhydrase;  Desat
 Hemoglobin  CO2 Dissociation Curve;  INC PIP
 Shift Left (INC O2 carrying capacity) = alkalosis  Bohr Effect = arterial > venous O2 affinity  Recuded air entry/ hyperresonance
 hypothyroid =respiratory alkalosis  in CO2/H+, Hgb less affinity for O2  CO2 embolism
 PaO2 50mmHg = Hgb 80% saturated  Haldane Effect = o2 on makes easier for CO2 off  Desat
 Hgb 50% saturated = PaO2 27mmHg  Deoxy hemoglobin increased affinity for CO2  No change PIP
 O2 = tense to relaxed  Murmur, hypotension, EKG change
 Hb-O2 Dissociation Curve; (2,3-DPG), P50  CO2
 Left shift = stored pRBCs, CO poison, fetal hemoglobin, bicarb  CO2 + H20 >(carbonic anyhrdase)>H2CO3 > Hco3- + H+   EtCo2
 H+ buffered by histadine on Hgb  MH, hyperthermia, HYPERthroid, Sepsis, shivering

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 c) Systemic Effects of Hypercarbia and Hypocarbia
 d) Systemic Effects of Hyperoxia and Hypoxemia
 e) Basic Interpretation of Arterial Blood Gas
 6) Control of Ventilation
 Ventilation Control
 Medulla (no afferents)
 By Dorsal Resp Group - tractus solitarius
 Effect Time and pacemaker
 Inspiration
 Ventral Reticular formation - Fourth Ventricle
 Effect contractility
 Inspiration & expiration
 Hypothalamus = modulate respiration in emotional states
 Pons
 Vent rates more susceptible to Resp acidosis (vs metabolic)
 Brain Stem = generates respiratory rhythm
 Central Resp = regulates Vt, inspiratory & expiratory time
 Carotid body = hypoxic drive via glossopharyngeal
 Glomus cells > dopamine
 Sense PaO2 < 100
 Maximally responds when PaO2 = 32
 30% of ventilator drive
 Decreased by 0.1 MAC (DEC 90%)
 Decreased by benzos opioids
 INC ALT = DEC CSF CO2 = Resp Alk
 In pregnancy Progesterone is a respiratory stimulant
 Vital capacity unchanged
 Inhaled CO2 increases miute ventilation 2-3 L/min/mm PaCO2
 a) Respiratory Center
 b) Central and Peripheral Chemoreceptors;
 Proprioceptive Receptors; Respiratory
 Muscles and Reflexes; Innervation
 c) CO2 and O2 Response Curves
 PaCO2 response curve
 Slope = carbon dixode sensitivity
 Shift left=hypoxia, acidosis, surgical stimuli,  ICP
Pulm Pharmacology/Pharmacokinetics
 Shift Right = volatiles < asleep, opioids, benzos, propofol, N20
 Slope = benzo, propofol,
 right shift = opioids
 slope + right shift = volatiles
 ketamine does not affect
 7) Non-Respiratory Functions of Lungs: Metabolic, Immune
 IgA in upper respiratory
 IgG in lower respiratory
 Lung Endothelium = Plasmin activator
 Plasminogen Plasmin = fibrin breakdown
 Thromboplastin = prothrombin  thrombin
 Metabolism
 Activated = angiotensin I, arachadonic acid
 Inactivated = bradykinin, Norepi, serotonin
 None = apinephrine, isoproterenol, dopamine, histamine
 8) Perioperative Smoking
 a) Physiologic Effects
 b) Cessation of Smoking
 1-2 days = Right shift
 short = carboxy hemoglobin.mucuous clearance
 2-3 months = sputum, ciliary function, closing capacity
 c. Pharmacology
 1) Bronchodilators
 PDE inhib = cAMP = bronchodilation
 Theophylline
 Inhibit PDE = INC cAMP =bronchodilation
 Cariotoxic, neurotoxic
 Metabolized by cyto – P450
 Blocks actions of adenosine
 Sildenafil –phosphodiasterase-5 inhibitor
 cGMPintracellular Ca+, Muscle relaxation = PVR
 Inhaled Nitric Oxide = PVR = guanylyl cyclasecGMP
Ca  vasodilation
 Vasoactive Intestinal Peptide(VIP)=bronchodilation
 Protects against histamine bronchoconstrict in athmatics
 Vasodilator
 Inhibitory nANC neurons = bronchodilation
 Bosetan=block
endothelil-1 receptor = pulm vasodiation
 Prostacyclins=cAmpPKAPDE myosin lgt chain PVR
 Inhibit PLT aggregation
 a) β-Agonists = Albuterol, , salmeterol, formotero
 B2 = adenylate cyclase = cAMP = bronchodilation’
 b) Anticholinergics
 M2, M3=cGMP = Bronchoconstriction
 Tiotropium(long-acting), Ipratroprium
 Competitively block musacinic receptors
 Preventing bronchoconstriction. Also used in COPD
 2) Anti-inflammatory medications
 a) Steroids
 Fluticason, budesonide
 Inhibit the sythesiss of cytokines.
 Inactive NF-kB (TNF-a transcription factor)
 1st line for chronic asthma
 b) Leukotriene Modifier Drugs
 Montelukast, Zafirlukast
 Block leukotriene receptors
 Good for aspiring induced and exercise induces asthma
 Zileuton
 5-lipogenase pathway inhibitor
 blocks conversion of arachdonic acid to leukotrienes
 hepatotoxic
 Inhibits cyto p450= INC warfarin, propranolol,theophylline
6

 c) Mast Cell Stabilizers
 Cromolyn = prevent mast cell degranulation
 d) Immunoglobulin E (IgE) Blockers
 Omalizumab = can cause anaphylaxis @ 24 hrs
 Blocks unbound serum IgE and blocks binding
 Anesthetics-Gases and Vapors
 1) Physical Properties
 2) Mechanism of Action
 enhance inhibitory receptors (GABAA and glycine)
 dampen excitatory pathways (nicotinic and glutamate)
 3) Effects on Central Nervous System (CNS)
 volatile uncoupling (except nitrous: CMRO2)
 CBF(via direct dilation) and CMRO2
 desflurane=  CSF production
 all volatiles INC ICP counteracted w/ hypocapnea
 Nitrous INC ICP counteract by hypocap + narcoitcs,
barbiturate
 DEC aplitude INC latency of SSEP
 Isoelectric silence at 1.5 – 2.0 mac, burst suprresion >2MAC
 4) Effects on Cardiovascular System
 HR increase with all volatile
 Sensitize myocardium to epinephrine and depress myocardial
contractility
 Avoid Sevo in history of long QT
 Isoflurane has coronary vasodilating properties
 Nitrous INC C.O.
 5) Effects on Respiration
 blunt ventilator stim caused by hypoxemia and hypercarbia
 DEC tidal volume and INC RR
 6) Effects on Neuromuscular Function
 Potentiate NMB via  post-junctional receptor sensitivity to
depolarization and skeleton muscle blood flow (drug delivery)
 NDNMB potentiation des> sevo> iso> halo> TIVA
 MAC at 1.3 eliminate motor response in 99%of people
Pulm Pharmacology/Pharmacokinetics
 Dose dependent motor/sensory evoked potentials
 7) Effects on Renal Function
 dose dependent reduction in RBF, GFR, urine output
 2/2 DEC BP and CO
 compound A (sevo + soda lime) = nephrotoxic
 8) Effects on Hepatic Function
 small chance for immune mediated liver injury=require prior
drug exposure
 9) Effects on Hematologic and Immune Systems
 SEVO
 Highest incidence of emergence delirium
 ISO
 @ 1 MAC = HR, SVR/BP, MV/TV/RR
 unique = no  in CO @ < 1 MAC
 slightly soluble in rubber and plastic
 Halothane
 SBP ( via C.O.)
 others directly decrease SBP w.o decreasing C.O.
 Metabolism SEVO > ISO > DES
 Mycoarial contractility
 hepatitis type 1 = mild direct effect
 hepatitis type 2 = immune mediate. 50% fatal. INC TFA
(trifluoroacetylchloride)
 has a preservative
 slightly souble in rubber and plastic
 Desflurane
 Afterload (arterial pressure), HR, dose dependent
myocardial depression (C.O. maintained)
 requires an external heat source 2/2 its boiling point
 rapid increase= sympathetic responses = BP HR
 Nitrous
 Alpha-adrenergic (analgesia, sympathomimetic)
 C.O. SVR
 NMDA antag (analgesia, CNS depression)
 Dopamine (analgesia, downstream opoid
 Inhibit methionine synthase = B12=agranulocytosis,
megaloblastic anemia, myelin
 CBF, CMRO2 (no decoupling), ICP
 Sulfur hexafluoride = 3 wks, preflouropropane = 8 wks
 solubility is similar in fat and the vessel rich group
 Nitric Oxide
 no effect on systemic BP because it binds to hemoglobin
 Methemeglobinemia (Fe2+ Fe3+)
 Falsely Low O2 sat, high PaO2
 Local anesthetics can cause(benzocaine, prilocaine)
 Nitrites cause
 Pulse-ox 85-88
 Chocolate colored blood
 cynosis
 TRT w/ methylene blue
 MAOI
 Hemolysis in G6PD (use Vit C in this population)
 Fe3+ INC affinity for Cyanide
 Cyanide Toxicity
 Tachycardic, Anion gap metabolic acidosis, flushing, elevated
mixed venous,
 Nitroprusside causes
 Inhibits cytochrome c oxidase(complex IV)
 Trt w/ hydroxycobalamin or sodium thiosulfate, sodium nitrite
 Impairs cellular respiration
 Weakness, headache, seizues, “cherry red” blood,
 O2 present but not utilized, elevated mixed venous
 TRT Amyl Nitrate
 Breath has bitter almond odor
 Metabolic acidosis more reliable than an elevated SvO2 value
 Thiocyanate toxicity
 Hypoxia, nausea, tinnitus, muscle spasm, psychosis/disorient
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 Pulm Pharmacology/Pharmacokinetics
 Carboxyhemoglobin
 Falsely elevates SpO2  Cough/laryngospasm block  Pregnancy changes
 Trt w/ 100% O2, hyperbaric O2  Afferent superior laryngeal  MV (TV), FRC, MAC, CO, SVR, HR
 Half life 4-6 hrs (1hr on 100%) (15-30min hyperbaric)  Efferent motor recurrent laryngeal  right shift (fetal hemoglobin shift left)
 Headache, dizziness
 Bilateral globus pallidus lesions on MRI  ARDS  K+ increases 0.6 / 0.1 decrease in PH
 Not associated with cyanosis  PaO2/FiO2 ratio <300
 Left shift  4-6 ml/kg  Extubation
 Sulfhemoglobinemia  N.O. improves V/Q mismatch  Vital capacity = 15ml/kg
 Cyanosis  Improves flow to ventilated ares  PaO2 > 60 (on FiO2 < 50%)
 Low O2 sat, high PaO2  Intrapulm shunt  PH > 7.3
 Supportive care (till RBCs destroyed)  O2 of limited value  Max inspiratory pressure at least -20
 PaCO2 < 50
 One Lung Ventilation  Insufflation
 Poor outcomes= Pre-op Normal spirometry (fev1 or FVC)  Lung compliance, PIP, V/Q mismatch(atelectasis,  Resting tone of airway smooth muscle is primarily mediated by
 Lungs less adjusted to Supine (vs. lateral) FRC), reduced diaphragmatic excursion parasympathetic neurons
 Predictive Post OP FEV1: >40% low risk, <30 high risk
 Capnography graph with double peak  Epidural Increase TV in patients with pain
 When hypoxemia occurs during thoracoscopy with one lung
 T-berg
ventilation, applying CPAP to the collapsed lung is less appropriate
 FRC, TLC, Compliance, risk main stem
as an initial intervention than applying PEEP to the ventilated lung.
 Supine
 During one lung ventilation, ACE inhibitors can attenuate
 FRC, compliance
hypoxic pulmonary vasoconstriction
 Obesity

 Expiratory reserve, lung compliance, FRC
 Ascites
 Post-thoracotomy atrial arrhythmia
 Volumes, normal FEV1/FVC,
 flow resistance between pulm vascular bedR heart
strain
 PEEP
 Sympathetic stimuli
 Intrathoracic pressure, RV afterload (CVP, PAP)
 Adenosine Antagonist
 Preload  C.O. (beneficial in CHF)
 S.E. = seizure, cardiac arrhythmia

 Potency= Halothane > Iso

 Inspiration = increased chest wall diameter= increase
resistance to electric flow = RR EKG monitoring
 Apnea hyponea index = correlate w/ periop morbidity
 Hyperventilation = Ca+ due to increase protein binding
 Progesterone = LES tone